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hi guys...my score arrived today and i got 221/90.
it feels great to touch 90 Smile)
now about my preparation hoping it would help a few of you.
i studied for about 2 1/2 months.
one reading of FA. i am bad at pharma and anat but goljan 100 pages was more than enough for me.
goljan 100 pages twice...once halfway during preparation
and once the night before the exam.
i also read goljan 35 pages.
heard the goljan audio during the initial days of preparation.
did almost all the 3000 odd questions from BRS.
did about 1000 and more q's from kaplan q bank downloaded in the site.
did q's from NMS and every source i could lay my hands on.
(did not do any usmle world q's)
did not subscribe for nbme but did all the 4 forms downloaded from the site.
some did not have answers for which i searched googleSmile
for histo and neuro anat i searched google for relavant websites and looked at very few pics.

initially i thought my prep was inadequate but the score shows otherwiseSmile)
i took the exam on 25th sept in india.
the day before the exam i had good sleep and was pretty happy that i was going to
finish off with it. i had tea in the morning.
my exam started at around 9 and i did 2 blocks at a stretch. i took a 10 min break for breakfast.
got back to the exam and did 2 more blocks.
then a 5 min break for some sweetsSmile
then the last 3 blocks. my mind was sooo numb by the time i did the 5th block that i wanted
to be out of there as soon as possible. so i did not break for the next 2 blocks.
i left the hall with more than half an hour break timeSmile

the questions were more like those in nbme forms. some q's repeated from them too.
do know them well. there were a few q's to which i had no clue about what they were asking...
make a guess and move on. i had about 8 min left on average in each block...i marked more than
half the q's thinking i would ponder over them in the remaining time but i stuck to the first answer mainly.
to q's i had no clue at all...i would not even mark them...i would make a choice and never return back to those questions...
if we keep going back to past q's in a block..we could end up wasting a lot of time.
at home i normally would take about 30-35 min to finish of a block but on the exam i took about 50 min.
so while practicing do keep an eye on the clock and try to do q's as fast as possible.
even on the exam we don't have to be 100 % sure of an answer...if you feel it looks right..it most probably isSmile

for the first block take a deep breath and start off right away...because we don't yet have a feel of the exam.
adjust yourself to the chair( which isn't very comfy) and put on the earplugs even if u don't need them...for me...the hall was filled
with students writing other exams and they were hitting the key board with a vengance...so its always better to have the earplugsSmile


also doing a whole lot of q's from any good source helps a lot. the main exam would feel like
another of the practice exams we take at home then.
be very confident....i came out of the hall ok but after about 15 days, i would get flashes of a few q's which i
thought were wrong .its ok...none of us can do all 350 q's right...right?!
i checked oasis on deewali. it said score reported and the oasis trick worked.

for a summary i would say...do FA and goljan...notes, pics ,audio and comprehensive test.loads and loads of q's.make good use of the break time on the exam and be confident...
i don't know about 99 but these materials will definitely help you guys with a score better than mine.

wishing all of you a very very good luck.
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wish u 99
can someone add more to these path derm notes
#329967
fawn - 08/20/08 22:25

scarlet fever = strawberry tongue,blanching sandpaper rash sparing palms & soles,circumoral pallor
honey coloured crusts on childs face = Impetigo
staph = abcess,hydradenitis suppurativa & surgical wound inf
TSS = Shock in tampoon users,SSS = sunburn rash includes palms & soles
HSV “ type 1 at mouth, type ll in genitalia. Dx Tzank
HPV = warts(1 & 4),condylomata accuminata anogenital (6 & 11)
pox virus = molluscum contagiosum,keratin filled umbilicated lesion,eosinophilic molluscum bodies
Rubeola = C's conjunctivitis,cough,coryza.rash follows kopliks spot.SSPE.WF multinucleated giant cell Pn
Rubella = 3 day measles,painful post auricular LN,blueberry muffin baby.1st TM to prevent triad: visual (cataracts), hearing loss, heart (PDA) defects.

Varicella=all stages lesion in crops Tzanck a/w reye synd. In 1st TM, causes microcephaly, chorioretinitis, IUGR and cataracts. Treat neonates with VZIG if mom contracted varicella within 5 days of delivery.

painful vesicles & blisters sensory dermtome,reactivated at dorsal nerve root = zoster

parvovirus B19 = slapped cheeks & lacy body rash.Aplastic crisis,Pure red cell Aplasia,Abortion
HH6 = roseola infantum,
tuberculoid Lep=granuloma,no bac,+ve Lepromin test,ulnar n enlarged
lepromatous Lep=no granuloma,lots of bac,-ve Lepromin test,leonine facies,nasal septum,eyebrows
Sporotrichosis=rose gardening,chain of S/C nodules
Seb.dermatitis = M.furfur greasy scales on scalp,eyebrow,ears,nasal cleft
M.furfur = pityriasis versicolor on KOH shows spagetti & meatballs
C.albicans = diaper rash & inframammary KOH shows yeasts & pseudohyphae
black dot bald scalp spot = fungal inf
Trichophyton tonsurans = inside hair shaft,-ve Woods.Microsporum Canis = outside Hair shaft,+ve Woods
T.rubrum=barbae,ubguinum,cruris,corporis,pedis

Acne Vulgaris=propionibac acnes.androgen related
Acne roscea=red pustules on cheeks + Rhinophyoma (Seb hyperplasia)

Pityriasis-herald patch later christmas tree prupitic trunk rash,spont remits

Psoriasis=candle wax scales,Auspitz sign +ve,Keobners
nail pepper pot pitting,grease spots,discolourations & Onycholysis
Epidermal hyperplasia,hyperkeratosis,Parakeratosis,elongated broadened Rete ridges,Munros microabcess(N)

Solar or Actinic keratosis=whitish grey pearly recurring lesion on sun exposed dorsal wrist.risks SCC
LichenPlanus= pruritic,violaceous,plaque,oral Wickhams stria,Koebners,Alopecia
dermo epidermal junction obscured with saw tooth rete

Eczema=flexures.Acute=red,itchy,weepy Chronic=thick,pigmented,hyperkeratotic,lichenified,scratch marks
Atopic=typel HSR=IgE(asthma)Contact=typelV HSR(poison ivy)

polymorphous light eruption-native americans photodermatitis

Urticaria=type I HSR,dermatographism
Porphyria Cutanea Tarda=Uroporphyrinogen decarboxylase defn,wine colour urine,lanugo,fragile hyperpigmented skin,photosensitive bullae,a/w HCV, Rx 1st stop EtOH then phlebotomy


Acanthosis nigricans=Axilla,Velvety pigmented.Adenocar,Obesity,Insulin resistance

Pemphigus Vulgaris=suprabasal,desmosomes,Acantholytic keratinocytes in vesicular fluid,Nickolsky's -ve
Bullous Pemphigoid=subepidermal,basement memb,no Acantholysis,Nickolsky's +ve

Dermatitis Herpetiformis=blisters,asso with coeliac dis,IgA-antibody complex Rx gluten-free diet and dapsone (r/o G6PD first)
Factitial Dermatitis “ no rash in nonreachable areas (midback, butterfly sign)

Erythema nodosum=panniculitis;red,raised,painful on shins
TB,Lep,Histoplasmosis,Coccidodomycosis,Sarcoidosis

Erythema Multiforme=targetoid multiple lesions
Drugs (Penicillin,Sulphonamides,Barbiturates,Phenytoin)Infections(mycoplasma,HSV)

Granuloma annulare=Idiopathic.Disseminated in Diabetics
Erythema chronicum migrans=lyme dis
Erythema marginatum=ARF

Xerosis=less skin lipid,itchy dry in elderly
Ichthycosis=AD increased thickness stratum corneum,no stratum granulosum

Seb Keratosis=Stuck on appearance,lesion has keratin filled ostiae.horn cysts Rx excision and curettage, cryotherapy
Lesar Trelat pathognomonic of gastric Adenocar
Keratocanthoma=mimics SCC,crateriform with central keratin plug,spontaneous regress with scarring
Nevus=nevocellular=benign; junctional,compound,epidermal types

SCC=radiation,burn,arsenic,Xeroderma Pigmentosa,actinic keratosis,chronic sinus,UV exposure.lower lip;nodular/ulcerated
atypical Keratinocytes,keratin pearls,intercellular bridges
Rx surgery or radiation

BCC=sunlight
upper lip,inner eye corner; rodent ulcer,pearly papule,talengiectasia.invasive rarely metastasize
basaloid cells nest,palisading growth pattern
Rx surgery or radiation

Mal Melanoma=whites,F/H,sun exposure,dyplastic nevus syndrome(>100)
ABCD (asymmetry, borders irregular, color variation, diameter >6mm
Superficial speading MC,Acral=confuse with subungual hematoma,Lentigo=on face,Nodular= invades
loves to metastasize
Atypical melanocytes,Rx excision

Albinism=oculo cut depigmentation,tyrosinase enz def
Vitiligo=patches of depigmentation,autoimmune melanocyte destruction
chloasma= cheeks of pregnant women,OCP users
lentigo=inc number of melanocytes,freckles=inc melanosomes





Got this from step 2 site....

PATH_NEOPLASIA


Q: Approximately what percentage of brain tumors arise from metastasis?
A: 0.5

Q: Are basal cell carcinomas invasive?
A: Locally invasive but rarely metastasize

Q: Are Ewing's sarcomas likely to metastasize?
A: Yes. They are extremely aggressive with early metastasis. However, they are responsive to chemotherapy.

Q: Are meningiomas resectable?
A: Yes

Q: Are squamous cell carcinomas of the skin invasive?
A: Locally invasive but rarely metastasize

Q: Are the majority of adult tumors supratentorial or infratentorial?
A: Supratentorial

Q: Are the majority of childhood tumors supratentorial or infratentorial?
A: Infratentorial

Q: Common histopathology often seen in squamous cell carcinomas of the skin?
A: Keratin pearls

Q: Define anaplasia
A: Abnormal cells lacking differentiation; like primitive cells of the same tissue. Often equated with undifferentiated malignant neoplasms. Tumor giant cells may be formed.

Q: Define dysplasia
A: Abnormal growth with loss of cellular orientation, shape, and size in comparison to normal tissue maturation. It is reversible but is often a preneoplastic sign.

Q: Define hyperplasia
A: Increase in the number of cells (reversible)

Q: Define metaplasia
A: One adult cell type is replaced by another (reversible). It is often secondary to irritation and/or environmental exposure (e.g. squamous metaplasia in the trachea and bronchi of smokers)

Q: Define neoplasia
A: Clonal proliferation of cells that is uncontrolled and excessive

Q: Do oncogenes cause a gain or loss of function?
A: Gain of function

Q: Do tumor suppressor genes cause a gain or loss of function?
A: Loss of function. Both alleles must be lost for expression of disease

Q: Does a melanoma have a significant risk of metastasis?
A: Very significant risk! The depth of the tumor often correlates with the risk of metastasis.

Q: From what cells do meningiomas most commonly arise?
A: Arachnoid cells external to the brain

Q: Give 2 examples of a benign tumor of epithelial origin.
A: 1. Adenoma 2. Papilloma

Q: Give 2 examples of a malignant tumor of epithelial origin.
A: 1. Adenocarcinoma 2. Papillary carcinoma

Q: Give 2 examples of malignant tumors of blood cell (mesenchymal) origin.
A: 1. Leukemia 2. Lymphoma

Q: Give an example of a benign tumor of blood vessel (mesenchymal) origin.
A: Hemangioma

Q: Give an example of a benign tumor of bone (mesenchymal) origin.
A: Osteoma

Q: Give an example of a benign tumor of more than one cell type.
A: Mature teratoma

Q: Give an example of a benign tumor of skeletal muscle (mesenchymal) origin.
A: Rhabdomyoma

Q: Give an example of a benign tumor of smooth muscle (mesenchymal) origin.
A: Leiomyoma

Q: Give an example of a malignant tumor of blood vessel (mesenchymal) origin.
A: Angiosarcoma

Q: Give an example of a malignant tumor of bone (mesenchymal) origin.
A: Osteosarcoma

Q: Give an example of a malignant tumor of more than one cell type.
A: Immature teratoma

Q: Give an example of a malignant tumor of skeletal muscle (mesenchymal) origin.
A: Rhabdomysarcoma

Q: Give an example of a malignant tumor of smooth muscle (mesenchymal) origin.
A: Leiomyosarcoma

Q: Give an example of a neoplasm associated with Down's Syndrome.
A: Acute Lymphoblastic Leukemia (ALL)

Q: How are tumor markers used?
A: Tumor markers are used to confirm diagnosis, to monitor for tumor recurrence, and to monitor the response to therapy. They should not be used as a primary tool for diagnosis.

Q: How is prostatic adenocarcinoma most commonly diagnosed?
A: Digital rectal exam (detect hard nodule) or by prostate biopsy

Q: How often do primary brain tumors undergo metastasis?
A: Very rarely

Q: In what population is osteochondroma most often found?
A: Usually men under the age of 25

Q: In which age group is prostatic adenocarcinoma most common?
A: Men over the age of 50

Q: Is malignant transformation in osteochondroma common?
A: Malignant transformation to chondrosarcoma is rare

Q: Name 1 common tumor staging system.
A: TNM system T= size of tumor, N=node involvement, and M=metastases

Q: Name 3 herniation syndromes that can cause either coma or death when the herniations compress the brainstem
A: 1. Downward transtentorial (central) herniation 2. Uncal herniation 3. Cerebellar tonsillar herniation into the foramen magnum

Q: Name 4 factors that predispose a person to osteosarcoma.
A: 1. Paget's disease of bone 2. Bone infarcts 3. Radiation 4. Familial retinoblastoma

Q: Name 4 possible routes of herniation in the brain
A: 1. Cingulate herniation under the falx cerebri 2. Downward transtentorial (central) herniation 3. Uncal herniation 4. Cerebellar tonsillar herniation into the foramen magnum

Q: Name 5 primary brain tumors with peak incidence in adulthood.
A: 1. Meningioma 2. Glioblastoma multiforme 3. Oligodendroglioma 4. Schwannoma 5. Pituitary adenoma

Q: Name 5 primary brain tumors with peak incidence in childhood.
A: 1. Medulloblastoma 2. Hemangioblastoma 3. Ependymomas 4. Low-grade astrocytoma 5. Craniopharyngioma

Q: Name 5 sites from which tumor cells metastasize to the brain.
A: 1. Lung 2. Breast 3. Skin (melanoma) 4. Kidney (renal cell carcinoma) 5. GI

Q: Name a common histopathological sign of basal cell carcinoma nuclei
A: The nuclei of basal cell tumors have 'palisading' nuclei

Q: Name a population at a greater risk for melanoma.
A: Fair-skinned people (blue eyes and red hair have also been considered as factors)

Q: Name the 5 primary tumors that metastasize to the liver
A: 1. Colon 2. Stomach 3. Pancreas 4. Breast 5. Lung

Q: Name two of the most common sites of metastasis after the regional lymph nodes
A: The liver and the lung

Q: Name two presenting sequelae of a pituitary adenoma.
A: 1. Bitemporal hemianopsia (due to pressure on the optic chiasm) 2. Hypopituitarism

Q: On which chromosome is the p53 gene located?
A: 17p

Q: On which chromosome is the Rb gene located?
A: 13q

Q: On which chromosomes are the BRCA genes located?
A: BRCA 1 is on 17q and BRCA 2 is on 13q

Q: Out of the 6 primary tumors that metastasize to bone, which two are the most common?
A: Metastasis from the breast and prostate are the most common

Q: What 2 cancers are associated with EBV?
A: 1. Burkitt's lymphoma 2. Nasopharyngeal carcinoma

Q: What 2 neoplasms are associated with AIDS?
A: 1. Aggressive malignant lymphomas (non-Hodgkins) 2. Kaposi's sarcoma

Q: What 2 neoplasms are associated with Autoimmune disease (e.g. Hashimoto's thyroiditis, myasthenia gravis, etc.)?
A: Benign and malignant thymomas

Q: What 2 neoplasms are associated with Paget's disease of bone?
A: 1. Secondary osteosarcoma 2. Fibrosarcoma

Q: What 2 neoplasms are associated with Tuberous sclerosis (facial angiofibroma, seizures, and mental retardation)?
A: 1. Astrocytoma 2. Cardiac rhabdomyoma

Q: What are 2 characteristic findings in carcinoma in situ?
A: 1. Neoplastic cells have not invaded the basement membrane 2. High nuclear:cytoplasmic ratio and clumped chromatin

Q: What are 2 characteristic findings of an invasive carcinoma?
A: 1. Cells have invaded the basement membrane using collagenases and hydrolases 2. Able to metastasize if they reach blood or lymphatic vessels.

Q: What are 2 neoplasms associated with Xeroderma pigmentosum?
A: 1. Squamous cell carcinoma of the skin 2. Basal cell carcinoma of the skin

Q: What are 3 disease findings associated with Alkaline Phosphatase?
A: 1. Metastases to bone 2. Obstructive biliary disease 3. Paget's disease of bone

Q: What are 6 primary tumors that metastasize to bone?
A: 1. Kidney 2. Thyroid 3. Testes 4. Lung 5. Prostate 6. Breast

Q: What are a common histopathological finding of meningiomas?
A: Psammoma bodies. These are spindle cells concentrically arranged in a whorled pattern.

Q: What are ependymomas?
A: Ependymal cell tumors most commonly found in the 4th ventricle. May cause hydrocephalus

Q: What are the steps in the progression of neoplasia?
A: 1. Normal 2. Hyperplasia 3. Carcinoma In Situ/Preinvasive 4. Invasion

Q: What are two signs of bone metastases in prostatic adenocarcinoma?
A: An increase in serum alkaline phosphatase and PSA (prostate-specific antigen)

Q: What are two useful tumor markers in prostatic adenocarcinoma?
A: Prostatic acid phosphatase and prostate-specific antigen (PSA)

Q: What can be associated with the risk of melanoma?
A: Sun exposure

Q: What cancer is associated with HBV and HCV (Hep B and C viruses)?
A: Hepatocellular carcinoma

Q: What cancer is associated with HHV-8 (Kaposi's sarcoma-associated herpes virus)?
A: Kaposi's carcinoma

Q: What cancer is associated with the HTLV-1 virus?
A: Adult T-cell leukemia

Q: What cancers are commonly associated with HPV (human papilloma virus)?
A: Cervical carcinoma, penile, and anal carcinoma

Q: What causes the local effect of a mass?
A: Tissue lump or tumor

Q: What causes the local effect of a nonhealing ulcer?
A: Destruction of epithelial surfaces (e.g. stomach, colon, mouth, bronchus)

Q: What causes the local effect of a space-occupying lesion?
A: Raised intracranial pressure in brain neoplasms. Also seen with anemia due to bone marrow replacement.

Q: What causes the local effect of bone destruction?
A: Pathologic fracture or collapse of bone

Q: What causes the local effect of edema?
A: Venous or lymphatic obstruction

Q: What causes the local effect of hemorrhage?
A: Caused by ulcerated area or eroded vessel

Q: What causes the local effect of inflammation of a serosal surface?
A: Pleural effusion, pericardial effusion, or ascites

Q: What causes the local effect of obstruction in the biliary tree?
A: Jaundice

Q: What causes the local effect of obstruction in the bronchus?
A: Pneumonia

Q: What causes the local effect of obstruction in the left colon?
A: Constipation

Q: What causes the local effect of pain?
A: Any site with sensory nerve endings. Remember that tumors in the brain are usually painless.

Q: What causes the local effect of perforation of an ulcer in the viscera?
A: Peritonitis or free air

Q: What causes the local effect of seizures?
A: Tumor mass in the brain.

Q: What causes the localized loss of sensory or motor function?
A: Compression or destruction of nerve (e.g. recurrent laryngeal nerve by lung or thyroid cancer causes hoarseness)

Q: What causes the paraneoplastic effect gout?
A: Hyperuricemia due excess nucleic acid turnover (secondary to cytotoxic therapy of various neoplasms)

Q: What causes the paraneoplastic effect of Cushing's disease?
A: ACTH or ACTH-like peptide (secondary to small cell lung carcinoma)

Q: What causes the paraneoplastic effect of hypercalcemia?
A: PTH-related peptide, TGF-a, TNF-a, IL-2 (secondary to squamous cell lung carcinoma, renal cell carcinoma, breast carcinoma, multiple myeloma, and bone metastasis)

Q: What causes the paraneoplastic effect of Lambert-Eaton syndrome?
A: Antibodies against presynaptic Ca2+ channels at NMJ (Thymoma, bronchogenic carcinoma)

Q: What causes the paraneoplastic effect of Polycythemia?
A: Erythropoietin (secondary to renal cell carcinoma)

Q: What causes the paraneoplastic effect of SIADH?
A: ADH or ANP (secondary to small cell lung carcinoma and intracranial neoplasms)

Q: What chemical carcinogen is commonly associated with the centrilobar necrosis and fatty acid change?
A: CCL4

Q: What chemical carcinogen is commonly associated with the esophagus and stomach?
A: Nitrosamines

Q: What chemical carcinogen is commonly associated with the lungs?
A: Asbestos (Causes mesothelioma and bronchogenic carcinoma)

Q: What chemical carcinogen is commonly associated with the skin (squamous cell)?
A: Arsenic

Q: What chemical carcinogen(s) are commonly associated with the liver?
A: Aflatoxins and vinyl chloride

Q: What is a chondrosarcoma?
A: Malignant cartilaginous tumor.

Q: What is a common genetic finding in Ewing's sarcoma?
A: 11;22 translocation

Q: What is a common gross pathological sign seen in Ewing's sarcoma?
A: Characteristic 'onion-skin' appearance of bone

Q: What is a common origin of a chondrosarcoma?
A: May be of primary origin or from osteochondroma

Q: What is a common sign found on the x-ray of a person with osteosarcoma?
A: Codman's triangle (from elevation of periosteum)

Q: What is a craniopharyngioma?
A: Benign childhood tumor. Often confused with pituitary adenoma because both can cause bitemporal hemianopsia. Calcification of the tumor is common.

Q: What is a Ewing's sarcoma?
A: Anaplastic small cell malignant tumor.

Q: What is a giant cell tumor?
A: Locally aggressive benign tumor around the distal femur, proximal tibial region.

Q: What is a gross pathological sign of basal cell carcinoma?
A: Pearly papules

Q: What is a helpful mnemonic to remember the neoplasm associated with Down's Syndrome?
A: We ALL go DOWN together.

Q: What is a helpful mnemonic to remember the site of metastasis to the brain?
A: Lots of Bad Stuff Kills Glia

Q: What is a helpful mnemonic to remember the types of cancer that metastasize to the liver?
A: Cancer Sometimes Penetrates Benign Liver

Q: What is a helpful mnemonic to remember what tumors metastasize to bone?
A: BLT with a Kosher Pickle

Q: What is a Hemangioblastoma?
A: Most often a cerebellar tumor. Associated with von Hippel Lindau syndrome when found with retinoblastoma.

Q: What is a low-grade astrocytoma?
A: Diffusely infiltrating glioma. In children, it is most commonly found in the posterior fossa.

Q: What is a medulloblastoma?
A: Highly malignant cerebellar tumor. A form of primitive neuroectodermal tumor (PNET). Can compress 4th ventricle causing hydrocephalus

Q: What is a neoplasm associated with actinic keratosis?
A: Squamous cell carcinoma of the skin

Q: What is a neoplasm associated with Barrett's esophagus (chronic GI reflux)?
A: Esophageal adenocarcinoma

Q: What is a neoplasm commonly associated with chronic atrophic gastritis, pernicious anemia, and postsurgical gastric remnants?
A: Gastric adenocarcinoma

Q: What is an oligodendroglioma?
A: A relatively rare, slow growing, benign tumor.

Q: What is CEA (carcinoembryonic antigen)?
A: Very nonspecific antigen produced by 70% of colorectal and pancreatic cancers and by gastric and breast carcinoma

Q: What is considered a precursor to squamous cell carcinoma?
A: Actinic keratosis

Q: What is considered to be a precursor to malignant melanoma?
A: Dysplastic nevus

Q: What is meant by the term tumor grade?
A: Histologic appearance of the tumor. Usually graded I-IV based on degree of differentiation and number of mitoses per high-power field.

Q: What is meant by the term tumor stage?
A: Based on site an size of primary lesion, spread to regional lymph nodes, and presence of metastases.

Q: What is the characteristic appearance of a giant cell tumor on an x-ray?
A: Characteristic 'double bubble' or 'soap bubble' appearance

Q: What is the common histopathology associated with Ependymomas?
A: Characteristic perivascular rosettes. Rod-shaped blepharoblasts (basal ciliary bodies) found near the nucleus.

Q: What is the common histopathology associated with Hemangioblastoma?
A: Foamy cells and high vascularity are characteristic. Can produce EPO and lead to polycythemia.

Q: What is the common histopathology associated with medulloblastomas?
A: Rosettes or perivascular pseudorosette pattern of cells

Q: What is the common histopathology associated with oligodendrogliomas?
A: Fried egg' appearance of cells in tumor. Often calcified.

Q: What is the common histopathology associated with schwannoma?
A: Antoni A=compact palisading nuclei; Antoni B=loose pattern

Q: What is the common histopathology found in Glioblastoma multiforme?
A: Pseudopalisading' tumor cells border central areas of necrosis and hemorrhage

Q: What is the differentiation pattern of normal cells?
A: Basal to apical differentiation

Q: What is the histopathology commonly associate with giant cell tumors?
A: Spindle-shaped cells with multi-nucleated giant cells.

Q: What is the most common benign bone tumor?
A: Osteochondroma

Q: What is the most common location of basal cell carcinoma of the skin?
A: Usually found in sun-exposed areas of the body.

Q: What is the most common location of osteosarcoma?
A: Commonly found in the metaphysis of long bones

Q: What is the most common organ to 'send' metastases?
A: The lung is the most common origin of metastases. The breast and stomach are also big sources.

Q: What is the most common organ to receive metastases?
A: Adrenal glands. This is due to their rich blood supply. The medulla usually receives metastases first and then the rest of the gland.

Q: What is the most common population to have chondrosarcoma?
A: Men age 30-60 years old

Q: What is the most common primary brain tumor?
A: Glioblastoma multiforme (grade IV astrocytoma)

Q: What is the most common primary malignant tumor of bone?
A: Osteosarcoma

Q: What is the most common type of pituitary adenoma?
A: Prolactin secreting

Q: What is the most likely population to have Ewing's sarcoma?
A: Boys under 15 years old.

Q: What is the origin of a craniopharyngioma?
A: Derived from the remnants of Rathke's pouch

Q: What is the origin of a Pituitary adenoma?
A: Rathke's pouch

Q: What is the origin of the Schwannoma?
A: Schwann cell origin. Often localized to the 8th cranial nerve (acoustic schwannoma). Bilateral schwannoma found in NF2.

Q: What is the peak incidence of giant cell tumor?
A: 20-40 years old

Q: What is the peak incidence of osteosarcoma?
A: Men 10-20 years old

Q: What is the prognosis for Glioblastoma multiforme?
A: Prognosis is grave. Usually only have a year life expectancy.

Q: What is the second most common primary brain tumor?
A: Meningioma

Q: What is the third most common primary brain tumor?
A: Schwannomas

Q: What neoplasias are associated with a-fetoprotein?
A: Hepatocellular carcinoma and nonseminomatous germ cell tumors of the testis.

Q: What neoplasias are associated with B-hCG?
A: Hydatidiform moles, Choriocarcinomas, and Gestational trophoblastic tumors.

Q: What neoplasias are associated with CA-125?
A: Ovarian and malignant epithelial tumors

Q: What neoplasias are associated with S-100?
A: Melanoma, neural tumors, and astrocytomas

Q: What neoplasm is associated with Cirrhosis (due to alcoholism, Hep B, or Hep C)
A: Hepatocellular carcinoma

Q: What neoplasm is associated with Dysplastic nevi?
A: Malignant melanoma

Q: What neoplasm is associated with Immunodeficiency states?
A: Malignant lymphomas

Q: What neoplasm is associated with Plummer-Vinson syndrome (atrophic glossitis, esophageal webs, and anemia; all due to iron deficiency)
A: Squamous cell carcinoma of the esophagus

Q: What neoplasm is associated with ulcerative colitis?
A: Colonic adenocarcinoma

Q: What oncogene is associated with breast, ovarian, and gastric carcinomas?
A: erb-B2

Q: What oncogene is associated with Burkitt's lymphoma?
A: c-myc

Q: What oncogene is associated with colon carcinoma?
A: ras

Q: What oncogene is associated with Follicular and undifferentiated lymphomas (inhibits apoptosis)?
A: bcl-2

Q: What tumor marker is associated with Prostatic carcinoma?
A: PSA (Prostatic acid phosphatase)

Q: What tumor suppressor gene is associated with Retinoblastoma and osteosarcoma?
A: Rb gene

Q: What type of metastases are common in the late stages of prostatic adenocarcinoma?
A: Osteoblastic metastases in bone

Q: What type of neoplasm is associated with Acanthosis nigricans (hyperpigmentation and epidermal thickening)
A: Visceral malignancies (stomach, lung, breast, and uterus)

Q: What type of skin cancer is associated with excessive exposure to sunlight or arsenic exposure?
A: Squamous cell carcinoma

Q: Where are chondrosarcomas usually located?
A: Pelvis, spine, scapula, humerus, tibia, or femur.

Q: Where are Ewing's sarcomas most commonly found?
A: Diaphysis of long bones, pelvis, scapula, and ribs

Q: Where are Glioblastoma multiformes found?
A: Cerebral hemispheres

Q: Where do giant cell tumors most commonly occur?
A: At epiphyseal end of long bones

Q: Where do meningiomas most commonly occur?
A: Convexities of hemispheres and parasagital region

Q: Where do oligodendrogliomas most often occur?
A: Most often found in the frontal lobes

Q: Where do osteochondromas commonly originate?
A: Long metaphysis

Q: Where do squamous cell carcinomas most commonly occur?
A: Hands and face

Q: Where does prostatic adenocarcinoma most commonly arise?
A: From the posterior lobe (peripheral zone) of the prostate gland

Q: Which has more prognostic value: tumor stage or grade?
A: Stage

Q: Which is more common: metastasis to bone or primary tumors of bone?
A: Metastatic bone tumors are far more common than primary tumors

Q: Which is more common: metastasis to the liver or primary tumors of the liver?
A: Metastasis to the liver is more common

Q: Which tumor suppressor gene is associated with most human cancers and the Li-Fraumeni syndrome?
A: p53

Q: Which tumor suppressor genes are associated with breast and ovarian cancer?
A: BRCA 1 and 2
PATH_CNS
Q: Define epilepsy.
A: Epilepsy is a disorder of recurrent seizures.

Q: Define syrinx.
A: Tube, as in syringe

Q: Describe a myoclonic seizure.
A: Quick,repetitive jerks

Q: Describe a tonic-clonic seizure.
A: Alternating stiffening and movement (grand mal)

Q: Describe a tonic seizure.
A: Stiffening

Q: Describe an absence seizure.
A: A blank stare (petit mal- it's in 1st aid this way!!)

Q: Describe an atonic seizure.
A: drop' seizures

Q: Describe Broca's aphasia.
A: Broca's is nonfluent aphasia with intact comprehension.
A: BROca's is BROken speech.

Q: Describe Horner's syndrome.
A: Sympathectomy of face (lesion above T1). Interruption of the 3-neuron oculosympathetic pathway.

Q: Describe Wernicke's aphasia.
A: Wernicke's is fluent aphasia with impaired comprehension.
A: Wernicke's is Wordy but makes no sense.

Q: How do patients present with a subarachnoid hemorrhage?
A: Worst headache of my life'

Q: How do pts present with MS?
A: -Optic neuritis (sudden loss of vision)
A: - MLF syndrome (internuclear ophthalmoplegia)
A: -Hemiparesis
A: -Hemisensory symptoms
A: -Bladder/bowel incontinence

Q: How does it spread?
A: Through the bloodstream to the CNS

Q: How does Werdnig-Hoffman disease present?
A: At birth as a 'floppy baby'

Q: How is Huntington's disease inherited?
A: Autosomal dominant

Q: How is the polio virus transmitted?
A: Fecal-oral route

Q: How is the prevalence of MS geographically distributed?
A: Higher prevalence with greater distance from the Equator

Q: In what persons is subdural hemorrhage often seen?
A: Elderly individuals, alcoholics, and blunt trauma

Q: T/F. Partial seizures can not generalize.
A: False- Partial seizures can generalize.

Q: What are 2 common organisms that target the brain in AIDS pts?
A: 1. Toxo!Toxo!Toxo!
A: 2. Cryptococcus

Q: What are 2 degenerative diseases of the cerebral cortex?
A: 1. Alzheimer's
A: 2. Pick's disease

Q: What are 2 degenerative diseases that affect the basal ganglia and brain stem?
A: 1. Huntington's disease
A: 2. Parkinson's disease

Q: What are 3 degenerative disorders of the motor neuron?
A: 1. Amyotrophic lateral sclerosis (ALS)
A: 2. Werdnig-Hoffman disease
A: 3. Polio

Q: What are associated with Guillain-Barre?
A: 1. Infections (herpesvirus or C. jejuni)
A: 2. Inoculations
A: 3. Stress

Q: What are neurofibrillary tangles?
A: Abnormally phosphorylated tau protein

Q: What are some demyelinating and dysmyelinating diseases?
A: 1. Multiple sclerosis (MS)
A: 2. Progressive multifocal leukoencephalopathy (PML)
A: 3. Postinfectious encephalomyelitis
A: 4. Metachromatic Leukodystrophy
A: 5. Guillain-Barre syndrome

Q: What are the 4 types of intracranial hemorrhages?
A: 1. Epidural hematoma
A: 2. Subdural Hematoma
A: 3. Subarachnoid hemorrhage
A: 4. Parenchymal hematoma

Q: What are the 5 types of generalized seizures?
A: 1. Absence
A: 2. Myoclonic
A: 3. Tonic-clonic
A: 4. Tonic
A: 5. Atonic

Q: What are the clinical symptoms of Huntington's disease?
A: Dementia, chorea

Q: What are the clinical symptoms of Parkinson's disease?
A: TRAP= Tremor (at rest)
A: cogwheel Rigidity
A: Akinesia
A: Postural instability
A: (you are TRAPped in your body)

Q: What are the clinical symptoms of Tabes dorsalis?
A: -Charcot joints
A: -Shooting pain
A: -Argyll-Robertson Pupils
A: -Absence of deep tendon reflexes

Q: What are the common causes of seizures in adults?
A: -Tumors
A: -Trauma
A: -Stroke
A: -Infection

Q: What are the common causes of seizures in children?
A: -Genetic
A: -Infection
A: -Trauma
A: -Congenital
A: -Metabolic

Q: What are the common causes of seizures in the elderly?
A: -Stroke
A: -Tumor
A: -Trauma
A: -Metabolic
A: -Infection

Q: What are the lab findings in Guillain-Barre syndrome?
A: Elevated CSF protein with normal cell count ('albumino-cytologic dissociation')

Q: What are the lab findings in poliomyelitis?
A: -CSF with lymphocytic pleocytosis with slight elevation of protein
A: -Virus recovered from stool or throat

Q: What are the pathological signs of glioblastoma multiforme (GBM)?
A: -Necrosis
A: -Hemorrhage
A: -Pseudo-palisading

Q: What are the signs of LMN lesions seen in poliomyelitis?
A: -Muscle weakness and atrophy
A: -Fasciculations
A: -Fibrillation
A: -Hyporeflexia

Q: What are the symptoms of Horner's?
A: 1. Ptosis
A: 2. Miosis
A: 3. Anhidrosis and flushing of affected side of face

Q: What are the symptoms of poliomyelitis?
A: -Malaise
A: -Headache
A: -Fever
A: -Nausea
A: -Abdominal pain
A: -sore throat

Q: What area of the brain is affected by generalized seizures?
A: Diffuse area

Q: What artery is compromised in an epidural hematoma?
A: Middle meningeal artery

Q: What blood vessels are affected in subdural hemorrhages?
A: Rupture of bridging veins

Q: What causes a parenchymal hematoma?
A: -HTN
A: -Amyloid angiopathy
A: -Diabetes Mellitus
A: -Tumor

Q: What causes poliomyelitis?
A: Poliovirus

Q: What chemical can Parkinson's disease be linked to?
A: MPTP, a contaminant in illicit street drugs

Q: What clinical symptoms are present with syringomyelia?
A: Bilateral pain and temperature loss in the upper extremities with preservation of touch sensation

Q: What clinical symptoms are present?
A: -Symmetric ascending muscle weakness beginning in the distal lower extremities
A: -Facial diplegia in 50% of cases
A: -Autonomic fx may be severely affected

Q: What congenital malformation is often associated with syringomyelia?
A: Arnold Chiari Malformation

Q: What damage does cryptococcus cause in the brain?
A: Periventricular calcifications

Q: What damage does toxoplasma cause in the brain?
A: Diffuse (intracerebral) calcifications

Q: What diseases are berry aneurysms associated with?
A: -Adult polycystic kidney disease
A: -Ehlers-Danlos syndrome
A: -Marfan's syndrome

Q: What do partial seizures affect?
A: One area of the brain

Q: What does rupture of a berry aneurysm lead to?
A: Stroke

Q: What does the spinal tap show in a subarachnoid hemorrhage?
A: Bloody or xanthochromic

Q: What event is the rupture of the middle meningeal artery secondary to?
A: Temporal bone fracture

Q: What genes is the familial form of Alzheimer's associated with?
A: Genes are chromosomes 1, 14, 19 and 21

Q: What is a complex partial seizure?
A: Impaired awareness

Q: What is a degenerative disorder of the Spinocerebellar tract?
A: Friedrich's ataxia (olivopontocerebellar atrophy)

Q: What is anhidrosis?
A: Absence of sweating

Q: What is another name for Guillain-Barre syndrome?
A: Acute idiopathic polyneuritis

Q: What is another symptom of Werdnig-Hoffman disease?
A: Tongue fasciculations

Q: What is another term for Broca's aphasia?
A: Expressive aphasia

Q: What is another term for Wernicke's aphasia?
A: Receptive aphasia

Q: What is miosis?
A: Pupil constriction

Q: What is PML associated with?
A: JC virus

Q: What is ptosis?
A: Slight drooping of the eyelids

Q: What is the classic triad of MS?
A: SIN
A: 1. Scanning speech
A: 2. Intention Tremor
A: 3. Nystagmus

Q: What is the common name for ALS?
A: Lou Gehrig's disease

Q: What is the course of a subdural hemorrhage?
A: Venous bleeding (less pressure) with delayed onset of symptoms

Q: What is the course of MS?
A: In most pts, the course is remitting and relapsing

Q: What is the incidence of brain tumors in adults?
A: Metastases> Astrocytoma (including glioblastoma)> Meningioma

Q: What is the incidence of brain tumors in children?
A: Astrocytoma> Medulloblastoma> Ependymoma

Q: What is the most common cause of dementia in the elderly?
A: Alzheimer's disease

Q: What is the most common complication of a berry aneurysm?
A: Rupture of the aneurysm

Q: What is the most common site for a berry aneurysm?
A: The bifurcation of the anterior communicating artery

Q: What is the pathogenesis of Guillain-Barre syndrome?
A: Inflammation and demyelination of peripheral nerves and motor fibers of ventral roots (sensory effect less severe than motor)

Q: What is the pathogenesis of Tabes dorsalis?
A: Degeneration of the dorsal columns and dorsal roots due to tertiary syphilis.

Q: What is the pathology of Alzheimer's?
A: Associated with senile plaques (beta-amyloid core) and neurofibrillary tangles

Q: What is the pathology of Huntington's disease?
A: Atrophy of the caudate nucleus

Q: What is the pathology of MS?
A: -Periventricular plaques
A: -Preservation of axons
A: -Loss of oligodendrocytes
A: -Reactive astrocytic gliosis
A: -Increased protein (IgA) in CSF

Q: What is the pathology of Parkinson's disease?
A: Associated with Lewy bodies and depigmentation of the substantia nigra

Q: What is the pathology of Pick's disease?
A: Associated with Pick bodies, intracytoplasmic inclusion bodies

Q: What is the pathology of poliomyelitis?
A: Destruction of anterior horn cells, leading to LMN destruction

Q: What is the pathology of syringomyelia?
A: Softening and cavitation around the central canal of the spinal cord.

Q: What is the prognosis for a pts diagnosed with a GBM?
A: Very poor

Q: What is the second most common cause of dementia in the elderly?
A: Multi-infarct dementia

Q: What is the shape of GBMs?
A: Butterfly' glioma

Q: What is the usual cause of a subarachnoid hemorrhage?

Q: What neural deficits are present in Tabes dorsalis?
A: Impaired proprioception and locomotor ataxia

Q: What neural tracts are damaged?
A: Crossing fibers of the spinothalamic tract

Q: What neurons are affected in ALS?
A: Both the upper and lower motor neurons

Q: What neurons are affected in Polio?
A: Lower motor neurons only

Q: What seizures are categorized as simple partial?
A: Awareness intact
A: -Motor
A: -Sensory
A: -Autonomic
A: -Psychic

Q: What tumor is Horner's syndrome associated with?
A: Pancoast's tumor

Q: Where are most brain tumors located in adults?
A: 70% are supratentorial (cerebral hemispheres)

Q: Where are most childhood brain tumors located?
A: 70% below tentorium (cerebellum)

Q: Where do berry aneurysms occur?
A: At the bifurcations in the Circle of Willis

Q: Where does it initially replicate?
A: The oropharynx and small intestine

Q: Where does the 3 neuron oculosympathetic pathway project from?
A: The hypothalamus

Q: Where does the 3 neuron oculosympathetic pathway project to?
A: 1. Interomediolateral column of the spinal cord
A: 2. Superior cervical (sympathetic) ganglion
A: 3. To the pupil, smooth muscles of the eyelids and the sweat glands

Q: Where is Broca's area located?
A: Inferior frontal gyrus

Q: Where is Pick's disease specific for?
A: The frontal and temporal lobes

Q: Where is the aopE-4 allele located?
A: Chromosome 19

Q: Where is the most common site of syringomyelia?
A: C8-T1

Q: Where is the p-App gene located?
A: 21

Q: Where is Wernicke's area located?
A: Superior Temporal Gyrus

Q: Which demyelinating disease is seen in 2-4% of AIDS patients?
A: PML
PATH_KIDNEY
Q: Define renal failure.
A: Failure to make urine and excrete nitrogenous wastes

Q: How do you calculate anion gap?
A: Na-(Cl + HCO3) = 8-12 mEq/L

Q: How do you treat minimal change disease?
A: Responds well to steroids

Q: How does acute poststreptococcal glomerulonephritis resolve?
A: Spontaneously

Q: How does renal cell carcinoma spread metastically?
A: Invades the IVC and spreads hematogenously

Q: How does transitional cell carcinoma present?
A: Hematuria

Q: How does Wilms' tumor present?
A: Huge, palpable flank mass

Q: In what epidemiological group is renal cell carcinoma most common?
A: Men ages 50-70

Q: T/F: Ammonium magnesium phosphate kidney stones are radiopaque
A: TRUE

Q: T/F: Calcium kidney stones are radiopaque.
A: TRUE

Q: T/F: Calcium kidney stones do not recur.
A: FALSE

Q: T/F: Cystine kidney stones are radiopaque.
A: FALSE, cystine stones are radiolucent

Q: T/F: Transitional cell carcinoma is cured by surgical removal.
A: False, transitional cell carcinoma often recurs after removal

Q: T/F: Uric acid kidney stones are radiopaque
A: FALSE, uric acid stones are radiolucent

Q: What additional sx are seen in a pt with acute streptococcal glomerulonephritis?
A: Peripheral and periorbital edema

Q: What age group is poststreptococcal glomerulonephritis most common?
A: Children

Q: What are 4 causes of hypoventilation?
A: 1. Acute lung disease
A: 2. Chronic lung disease
A: 3. Opioids, narcotics, sedatives
A: 4. Weakening of respiratory muscles

Q: What are the 2 forms of renal failure?
A: Acute and chronic

Q: What are the 2 main symptoms present in Goodpasture's syndrome?
A: Hemoptysis, hematuria

Q: What are the 4 major types of kidney stones?
A: 1. Calcium
A: 2. Ammonium magnesium phosphate
A: 3. Uric acid
A: 4. Cystine

Q: What are the 5 nephritic syndromes?
A: Acute poststreptococcal glomerulonephritis
A: Rapidly progressive (crescentic) glomerulonephritis
A: Goodpasture's syndrome
A: Membranoproliferative glomerulonephritis
A: Berger's disease

Q: What are the 5 nephrotic syndromes?
A: 1. Membranous glomerulonephritis
A: 2. Minimal change disease (lipoid nephrosis)
A: 3. Focal segmental glomerular sclerosis
A: 4. Diabetic nephropathy
A: 5. SLE

Q: What are the causes and signs of calcium ion deficiency?
A: -Kids- rickets
A: -Adults- osteomalacia
A: -Contributes to osteoporosis
A: -Tetany

Q: What are the causes and signs of phosphate toxicity?
A: -Low serum calcium ion
A: -can cause bone loss
A: -renal stones

Q: What are the causes of chloride ion deficiency?
A: Secondary to emesis, diuretics, renal disease

Q: What are the causes of metabolic acidosis?
A: -Diabetic ketoacidosis
A: -Diarrhea
A: -Lactic Acidosis
A: -Salicylate OD
A: -Acetazolamide OD

Q: What are the causes of respiratory acidosis?
A: -COPD
A: -Airway obstruction

Q: What are the causes of respiratory alkalosis?
A: -High altitude
A: -Hyperventilation

Q: What are the characteristics of acute poststreptococcal glomerulonephritis seen with immunofluorescence?
A: Granular pattern

Q: What are the characteristics of acute poststreptococcal glomerulonephritis seen with the electron microscope?
A: Subepithelial humps

Q: What are the characteristics of acute poststreptococcal glomerulonephritis seen with the light microscope?
A: Glomeruli enlarged and hypercellular
A: neutrophils
A: 'lumpy-bumpy'

Q: What are the characteristics of rapidly progressive (crescentic) glomerulonephritis seen on LM and IF?
A: Crescent-moon shape

Q: What are the clinical features of renal cell carcinoma?
A: -Hematuria
A: -Palpable mass
A: -Secondary polycythemia
A: -Flank pain
A: -Fever

Q: What are the clinical symptoms of a nephritic syndrome?
A: I' = inflammation; hematuria, hypertension, oligouria, azotemia

Q: What are the clinical symptoms of nephrotic syndromes?
A: O = proteinuria
A: Hypoalbuminuria
A: Generalized edema
A: Hyperlipidemia

Q: What are the consequences of renal failure?
A: 1. Anemia
A: 2. Renal osteodystrophy
A: 3. Hyperkalemia
A: 4. Metabolic acidosis
A: 5. Uremia
A: 6. Sodium and water excess
A: 7. Chronic pyelonephritis
A: 8. HTN

Q: What are the factors associated metabolic alkalosis?
A: -Increased pH
A: -Increased PCO2
A: -Increased HCO3-

Q: What are the factors associated with metabolic acidosis?
A: -Decreased pH
A: -Decreased PCO2
A: -Decreased HCO3-

Q: What are the factors associated with respiratory acidosis?
A: -Decreased pH
A: -Increased PCO2
A: -Increased HCO3-

Q: What are the factors associated with respiratory alkalosis?
A: -Increased pH
A: -Decreased PCO2
A: -Decreased HCO3-

Q: What are the functions of calcium ion?
A: -Muscle contraction
A: -Neurotransmitter release
A: -Bones, teeth

Q: What are the functions of sodium ion?
A: -Extracellular fluid
A: -Maintains plasma volume
A: -Nerve/muscle function

Q: What are the functions of the chloride ion?
A: -Fluid/electrolyte balance
A: -Gastric acid
A: -HCO3/Cl shift in RBC

Q: What are the functions of the magnesium ion?
A: -Bones, teeth
A: -Enzyme cofactor

Q: What are the functions of the phosphate ion?
A: -ATP
A: -nucleic acids
A: -Phosphorylation
A: -Bones, teeth

Q: What are the functions of the potassium ion?
A: -Intracellular fluid
A: -Nerve/muscle function

Q: What are the signs of magnesium ion deficiency?
A: -Diarrhea
A: -Alcoholism

Q: What are the signs of magnesium ion toxicity?
A: -Decreased reflexes
A: -Decreased respirations

Q: What are the signs of phosphate deficiency?
A: -Kids- rickets
A: -Adults- osteomalacia

Q: What are the signs of potassium ion toxicity?
A: -EKG changes
A: -Arrhythmia

Q: What bugs cause ammonium magnesium phosphate kidney stones?
A: Urease-positive bugs such as Proteus vulgaris or Staphylococcus

Q: What calcium molecules form calcium kidney stones?
A: Calcium oxalate or calcium phosphate or both

Q: What can excess Na and water cause?
A: CHF and pulmonary edema

Q: What can the hyperkalemia associated with renal failure lead to?
A: Cardiac arrhythmias

Q: What causes metabolic alkalosis?
A: 1. Vomiting
A: 2. Diuretic use
A: 3. Antacid use
A: 4. Hyperaldosteronism

Q: What causes renal osteodystrophy?
A: Failure of active vitamin D production

Q: What characteristics of Berger's disease are seen with IF and EM?
A: Mesangial deposits of IgA

Q: What characteristics of focal segmental glomerular sclerosis are seen with the LM?
A: Segmental sclerosis and hyalinosis

Q: What characteristics of Goodpasture's syndrome are seen with IF?
A: Linear pattern
A: Anti-glomerular basement membrane antibodies

Q: What characteristics of Membranoproliferative glomerulonephritis are seen with the EM?
A: subendothelial humps
A: 'tram track'

Q: What characteristics of membranous glomerulonephritis are seen with IF?
A: Granular pattern

Q: What characteristics of membranous glomerulonephritis are seen with the EM?
A: Spike and Dome'

Q: What characteristics of membranous glomerulonephritis are seen with the LM?
A: Diffuse capillary and basement membrane thickening

Q: What characteristics of minimal change disease are seen with the EM?
A: Foot process effacement

Q: What characteristics of minimal change disease are seen with the LM?
A: Normal glomeruli

Q: What characteristics of SLE are seen with the LM?
A: Wire-loop appearance with extensive granular subendothelial basement-membrane deposits in membranous glomerulonephritis pattern

Q: What defines metabolic acidosis?
A: -pH less than 7.4
A: -PCO2 less than 40 mm Hg

Q: What defines metabolic alkalosis with compensation?
A: -pH greater than 7.4
A: -PCO2 greater than 40 mm Hg

Q: What defines respiratory acidosis?
A: -pH less than 7.4
A: -PCO2 greater than 40mm Hg

Q: What defines respiratory alkalosis?
A: -pH greater than 7.4
A: -PCO2 less than 40 mm Hg

Q: What diseases often cause uric acid kidney stones?
A: Diseases with increased cell proliferation and turnover, such as leukemia and myeloproliferative disorders

Q: What disorders can lead to hypercalcemia and thus kidney stones?
A: 1. Cancer
A: 2. Increased PTH
A: 3. Increased vitamin D
A: 4. Milk-alkali syndrome

Q: What disorders cause an increased anion gap?
A: 1. Renal failure
A: 2. Lactic acidosis
A: 3. Ketoacidosis (DM)
A: 4. Aspirin ingestion

Q: What disorders cause metabolic acidosis and normal anion gap?
A: 1. Diarrhea
A: 2. Glue sniffing
A: 3. Renal tubular acidosis
A: 4. Hyperchloremia

Q: What disorders make up the WAGR complex?
A: Wilms' tumor
A: Aniridia
A: Genitourinary malformation
A: mental-motor Retardation

Q: What does potassium deficiency cause?
A: -Weakness
A: -Paralysis
A: -Confusion

Q: What factors are associated with transitional cell carcinoma?
A: Exposure to cyclophosphamide, smoking, phenacetin, and aniline dyes

Q: What genetic disorder and mutation are associated with renal cell carcinoma?
A: Renal cell carcinoma is associated with von Hippel-Lindau and gene deletion in chromosome 3

Q: What genetic disorder is associated with Wilms' tumor?
A: Deletion of tumor suppression gene WT-1 on chromosome 11

Q: What is a common cause of adult nephrotic syndrome?
A: Membranous glomerulonephritis

Q: What is acute renal failure often due to?
A: Hypoxia

Q: What is Berger's disease?
A: IgA nephropathy
A: -Mild disease
A: -Often postinfectious

Q: What is chronic failure due to?
A: HTN and diabetes

Q: What is the 2nd most common type of kidney stone?
A: Ammonium magnesium phosphate

Q: What is the cause of magnesium ion deficiency?
A: Secondary to malabsorption

Q: What is the cause of metabolic alkalosis?
A: Vomiting

Q: What is the cause of potassium ion deficiency?
A: Secondary to injury, illness or diuretics

Q: What is the cause of sodium deficiency?
A: Secondary to injury or illness

Q: What is the compensatory mechanism of metabolic alkalosis?
A: Hypoventilation

Q: What is the compensatory mechanism of respiratory alkalosis?
A: Renal HCO3- secretion

Q: What is the compensatory response to metabolic acidosis?
A: Hyperventilation

Q: What is the compensatory response to respiratory acidosis?
A: Renal HCO3- reabsorption

Q: What is the course of membranoproliferative glomerulonephritis?
A: Slowly progresses to renal failure

Q: What is the course of rapidly progressive (crescentic) glomerulonephritis?
A: Rapid course to renal failure from one of many causes

Q: What is the Henderson-Hasselbalch equation?
A: pH = pKa + log [(HCO3-)/(0.03*PCO2)]

Q: What is the most common cause of childhood nephrotic syndrome?
A: Minimal change disease (lipoid nephrosis)

Q: What is the most common renal malignancy of early childhood (ages 2-4)?
A: Wilms' tumor

Q: What is the most common renal malignancy?
A: Renal cell carcinoma

Q: What is the most common tumor of the urinary tract system?
A: Transitional cell carcinoma

Q: What is the primary disturbance in respiratory acidosis?
A: Increased PCO2

Q: What is the primary disturbance of metabolic acidosis?
A: HCO3- decrease

Q: What is the primary disturbance of metabolic alkalosis?
A: Increased HCO3-

Q: What is the primary disturbance of respiratory alkalosis?
A: Decreased PCO2

Q: What is the sign of calcium ion toxicity?
A: Delirium

Q: What is the sign of sodium ion toxicity?
A: Delirium

Q: What lesions are seen on the LM in diabetic nephropathy?
A: Kimmelstiel-Wilson lesions

Q: What might an elevated anion gap indicate?
A: MUD PILES
A: 1. Methanol
A: 2. Uremia (chronic renal failure)
A: 3. Diabetic ketoacidosis
A: 4. Paraldehyde or Phenformin
A: 5. Iron tablets or INH
A: 6. Lactic acidosis (CN-, CO, shock)
A: 7. Ethanol or Ethylene glycol
A: 8. Salicylates

Q: What paraneoplastic syndromes are associated with renal cell carcinoma?
A: Ectopic EPO, ACTH, PTHrP, and prolactin

Q: What severe complications may kidney stones lead to?
A: Hydronephrosis
A: Pyelonephritis

Q: What social factor increases the incidence of renal cell carcinoma?
A: Smoking

Q: What type of hypersensitivity contributes to the pathogenesis of Goodpasture's syndrome?
A: Type II hypersensitivity

Q: Where can transitional cell carcinoma occur?
A: -Renal calyces
A: -Renal pelvis
A: -Ureters
A: -Bladder

Q: Where does renal cell carcinoma originate?
A: Renal tubule cells, polygonal clear cells

Q: Which kidney stone is often secondary to cystinuria?
A: Cystine

Q: Which kidney stone is strongly associated with gout?
A: Uric acid kidney stones

Q: Which of the nephrotic syndromes are worse in HIV pts?
A: Focal segmental glomerular sclerosis

Q: Which type of kidney stones constitute the majority of kidney stones (80-85%)?
A: Calcium

Q: Why are ammonium magnesium phosphate kidney stones often associated with UTIs?
A: Ammonium magnesium phosphate stones can form large struvite calculi that can be a nidus for UTIs

Q: Why does renal failure cause anemia?
A: Failure of EPO production

Q: Why does renal failure cause metabolic acidosis?
A: Due to decreased acid secretion and decreased generation of HCO3-
PATH_LUNGS
Q: An FEV1/FVC ratio greater than 80% indicates what form of pulmonary disease?
A: Restrictive lung disease

Q: Are bronchogenic carcinoma metastases common?
A: Yes, very common

Q: Decreased FEV1/FVC ratio are the hallmark of what kind of pulmonary disease?
A: COPD

Q: How does interstitial fibrosis create a restrictive lung disease?
A: It causes increased recoil (decreased compliance), thereby limiting alveolar expansion.

Q: How does lung cancer commonly present? (5)
A: - Cough
A: - Hemoptysis
A: - Bronchial obstruction
A: - Wheezing
A: - Pneumonic 'coin' lesion on x-ray

Q: How does surfactant deficiency cause NRDS?
A: It leads to an increase in surface tension, resulting in alveolar collapse

Q: How to you treat NRDS?
A: - Maternal steroids before birth
A: - Artificial surfactant for infant

Q: Identify: ivory-white pleural plaques in the lung.
A: Ferruginous bodies

Q: In COPD, are lung volumes increased, decreased, or normal?
A: Increased (increasedTLC, increased FRC, increased RV)

Q: In restrictive lung disease, are lung volumes increased, decreased, or normal?
A: Decreased

Q: In what occupations is asbestosis most commonly seen? (2)
A: Shipbuilders and plumbers

Q: Name three 'triggers' of asthma.
A: - Viral URIs
A: - Allergens
A: - Stress

Q: Name three characteristics of Horner's syndrome?
A: - Ptosis
A: - Miosis
A: - Anhidrosis

Q: Name two extrapulmonary (poor breathing mechanics) causes of restrictive lung disease.
A: - Poor muscular effort: polio, myasthenia gravis
A: - Poor apparatus: scoliosis

Q: Name two pulmonary (poor lung expansion) causes of restrictive lung disease.
A: - Defective alveolar filling: pneumonia, ARDS, pulmonary edema
A: - Interstitial fibrosis

Q: Patients with asbestosis are at increased risk for what? (2)
A: Pleural mesothelioma and bronchogenic carcinoma

Q: T/F Bronchiectasis is associated with bronchial obstruction, cystic fibrosis, and poor ciliary motility.
A: True

Q: T/F In obstructive (not restrictive) lung disease, FEV1 and FVC are reduced.
A: False, FEV1 and FVC are reduced in both

Q: T/F Restricted lung expansion causes decreased total lung capacity and increased vital capacity.
A: False, decreased VC and TLC

Q: T/F Smokers with asbestosis have a decreased risk of developing cancer.
A: False, it increases synergistically

Q: What are asbestos fibers coated with hemosiderin in the lung?
A: Ferruginous bodies

Q: What are the characteristics of lobar pneumonia?
A: Intra-alveolar exudate -> consolidation; may involve entire lung

Q: What are the clinical findings of chronic bronchitis? (3)
A: - Wheezing
A: - Crackles
A: - Cyanosis

Q: What are the clinical findings of emphysema? (4)
A: - Dyspnea
A: - Decreased breath sounds
A: - Tachycardia
A: - Decreased I/E ratio

Q: What are the symptoms and complications of interstitial lung fibrosis?
A: - Symptoms: gradual progressive dyspnea and cough
A: - Complications include cor pulmonale (can be seen in diffuse interstitial pulmonary fibrosis and bleomycin toxicity)

Q: What bronchogenic carcinoma is associated with ectopic hormone production (ADH, ACTH) and may lead to Lambert-Eaton syndrome?
A: Small cell carcinoma

Q: What bronchogenic carcinoma is associated with ectopic PTH-related peptide production?
A: Squamous cell carcinoma

Q: What bronchogenic carcinoma is most common?
A: Adenocarcinoma

Q: What bronchogenic carcinoma is thought not to be related to smoking?
A: Bronchioalveolar carcinoma

Q: What bronchogenic carcinomas are clearly linked to SSmoking?
A: SSquamous cell carcinoma and SSmall cell carcinoma

Q: What bronchogenic carcinomas usually express tumors that arise centrally? (2)
A: - Squamous cell carcinoma
A: - Small cell carcinoma

Q: What bronchogenic carcinomas usually express tumors that arise peripherally? (3)
A: - Adenocarcinoma
A: - Bronchioalveolar carcinoma
A: - Large cell carcinoma--undifferentiated

Q: What carcinoma occurs in the apex of the lung and may affect the cervical sympathetic, causing Horner's syndrome?
A: Pancoast's tumor

Q: What causes bronchiectasis?
A: Chronic necrotizing infection of bronchi

Q: What causes neonatal respiratory distress syndrome (NRDS)?
A: Surfactant deficiency

Q: What cells make surfactant and when is it made most abundantly in fetuses?
A: Type II pneumocytes most abundantly after 35th week of gestation

Q: What COPD has a productive cough for greater than three months in two years and hypertrophy of mucus-secreting glands in the bronchioles (Reid index greater than 50%)?
A: Chronic bronchitis

Q: What COPD is characterized by dilated airways, purulent sputum, recurrent infections, and hemoptysis?
A: Bronchiectasis

Q: What COPD is due to an enlargement of air spaces and decreased recoil resulting from destruction of alveolar walls?
A: Emphysema

Q: What COPD is due to bronchial hyperresponsiveness which causes reversible bronchoconstriction?
A: Asthma

Q: What does inhaled asbestos do to the lungs?
A: It causes diffuse pulmonary interstitial fibrosis

Q: What is the composition of surfactant:
A: Dipalmitoyl phosphatidylcholine

Q: What is the difference in FEV1/FVC ratios between obstructive and restrictive lungs diseases?
A: FEV1 and FVC are reduced in both, but in obstructive the FEV1 is more dramatically reduced, resulting in a decreased FEV1/FVC ratio

Q: What is the leading cause of cancer death?
A: Lung cancer

Q: What is the SPHERE (acronym) of complications associated with lung cancer?
A: Superior vena caval syndrome
A: Pancoast's tumor
A: Horner's syndrome
A: Endocrine (paraneoplastic)
A: Recurrent laryngeal symptoms (hoarseness)
A: Effusions (pleural or pericardial)

Q: What kind of pulmonary diseases are caused by a inhibition of air flow resulting in air trapping in the lungs?
A: Obstructive lung diseases (COPD)

Q: What organisms are is the most frequent cause of lobar pnuemonia?
A: Pneumococcus

Q: What organisms are the most frequent cause of bronchopnuemonia? (4)
A: - S. aureus
A: - H. flu
A: - Klebsiella
A: - S. pyogenes

Q: What organisms are the most frequent cause of interstitial (atypical) pnuemonia? (3)
A: - Viruses (RSV, adenoviruses)
A: - Mycoplasma
A: - Legionella

Q: What specific type of emphysema is caused by alpha-1-antitrypsin deficiency?
A: Panacinar emphysema (and liver cirrhosis)

Q: What specific type of emphysema is caused by smoking?
A: Centriacinar emphysema

Q: What test is used to measure in utero lung maturity?
A: The lecithin-to-sphingomyelin ratio in the amniotic fluid, usually less than 1.5 in neonatal respiratory distress syndrome

Q: What type of lung cancer can cause carcinoid syndrome?
A: Carcinoid tumor

Q: What type of pneumonia is characterized by acute inflammatory infiltrates from bronchioles into adjacent alveoli with a patchy distribution affecting more than one lobe?
A: Bronchopneumonia

Q: What type of pneumonia is characterized by diffuse patchy inflammation localized to interstial areas at alveolar walls and involves more than one lobe?
A: Interstitial (atypical) pneumonia

Q: Where does bronchogenic carcinoma commonly metastasize and how does it present? (3)
A: - Brain (epilepsy)
A: - Bone (pathologic fracture)
A: - Liver (jaundice, hepatomegaly)

Q: Why does alpha-1-antitrypsin deficiency cause emphysema?
A: Increased elastase activity
PATH_RHEUMATIC DISEASEA
Q: Define Ankylosing spondylitis?
A: Chronic inflammatory disease of spine & large joints, sacroilitis, uveitis, & aortic regurgitation

Q: Define Ankylosing spondylitis?
A: Chronic inflammatory disease of spine & large joints, sacroilitis, uveitis, & aortic regurgitation

Q: Define Celiac sprue
A: Autoimmune-mediated intolerance of gliadin (wheat) leading to steatorrhea.

Q: Define Celiac sprue
A: Autoimmune-mediated intolerance of gliadin (wheat) leading to steatorrhea.

Q: Define Gout.
A: Precipitation of monosodium urate crystals into joints due to hyperuricemia.

Q: Define Gout.
A: Precipitation of monosodium urate crystals into joints due to hyperuricemia.

Q: Define Scleroderma
A: Excessive fibrosis & collagen deposition throughout the body; commonly sclerosis of the skin, but also of CV & GI systems & kidney

Q: Define Scleroderma
A: Excessive fibrosis & collagen deposition throughout the body; commonly sclerosis of the skin, but also of CV & GI systems & kidney

Q: Define Sicca syndrome.
A: dry eyes, dry mouth, nasal & vaginal dryness, chronic bronchitis, reflux esophagitis

Q: Define Sicca syndrome.
A: dry eyes, dry mouth, nasal & vaginal dryness, chronic bronchitis, reflux esophagitis

Q: In what population is ankylosing sponsylitis more commonly found?
A: males (10-30 year old)

Q: In what population is ankylosing sponsylitis more commonly found?
A: males (10-30 year old)

Q: In what population is Celiac sprue more commonly found?
A: Assoc. w/ people of northern European descent

Q: In what population is Celiac sprue more commonly found?
A: Assoc. w/ people of northern European descent

Q: In what population is Goodpasture's syndrome more commonly found?
A: Men 20-40 y/o

Q: In what population is Goodpasture's syndrome more commonly found?
A: Men 20-40 y/o

Q: In what population is gout more commonly found?
A: Men

Q: In what population is gout more commonly found?
A: Men

Q: In what population is Osteoarthritis more commonly found?
A: Common in older patients

Q: In what population is Osteoarthritis more commonly found?
A: Common in older patients

Q: In what population is pseudogout more commonly found?
A: > 50 y/o, both sexes equally

Q: In what population is pseudogout more commonly found?
A: > 50 y/o, both sexes equally

Q: In what population is Reiter's syndrome more commonly found?
A: Strong predilection for males

Q: In what population is Reiter's syndrome more commonly found?
A: Strong predilection for males

Q: In what population is Rheumatoid arthritis more commonly found & what the common autoimmune factor present?
A: - Common in females
A: - 80% of RA pt's have positive rheumatoid factor (anti-IgG Ab)

Q: In what population is Rheumatoid arthritis more commonly found & what the common autoimmune factor present?
A: - Common in females
A: - 80% of RA pt's have positive rheumatoid factor (anti-IgG Ab)

Q: In what population is sarcoidosis more commonly found?
A: black females

Q: In what population is sarcoidosis more commonly found?
A: black females

Q: In what population is scleroderma more commonly found?
A: 75% female

Q: In what population is scleroderma more commonly found?
A: 75% female

Q: In what population is Sjogren's syndrome more commonly found?
A: females between the ages of 40 & 60

Q: In what population is Sjogren's syndrome more commonly found?
A: females between the ages of 40 & 60

Q: In what population is SLE more commonly found?
A: 90% are female & between ages 14 & 45. More common & severe in black females

Q: In what population is SLE more commonly found?
A: 90% are female & between ages 14 & 45. More common & severe in black females

Q: What are the 2 major categories of scleroderma & what findings are they assoc w/?
A: Diffuse scleroderma: widespread skin involvement, rapid progression, early visceral involvement. Assoc. w/ anti-Scl-70 Ab

Q: CREST syndrome:
A: Calcinosis, Raynaud's phenomenon, Esophageal dysmotility, Sclerodactyly & Telangiectasia; limited skin involvement, often confined to fingers & face. More benign clinical course - assoc w/ anticentromere Ab

Q: What are the 2 major categories of scleroderma & what findings are they assoc w/?
A: Diffuse scleroderma: widespread skin involvement, rapid progression, early visceral involvement. Assoc. w/ anti-Scl-70 Ab

Q: CREST syndrome:
A: Calcinosis, Raynaud's phenomenon, Esophageal dysmotility, Sclerodactyly & Telangiectasia; limited skin involvement, often confined to fingers & face. More benign clinical course - assoc w/ anticentromere Ab

Q: What are the associated sx's & risks for Sjogren's syndrome?
A: - Parotid enlargement
A: - incr risk of B-cell lymphoma
A: - Assoc. w/ RA

Q: What are the associated sx's & risks for Sjogren's syndrome?
A: - Parotid enlargement
A: - incr risk of B-cell lymphoma
A: - Assoc. w/ RA

Q: What are the characteristic findings in Celiac sprue?
A: Blunting of villi, lymphocytes in the lamina propria, & abnormal D-xylose test

Q: What are the characteristic findings in Celiac sprue?
A: Blunting of villi, lymphocytes in the lamina propria, & abnormal D-xylose test

Q: What are the common characteristics of Sarcoidosis?
A: immune-mediated, widespread noncaseating granulomas & elevated serum ACE levels

Q: What are the common characteristics of Sarcoidosis?
A: immune-mediated, widespread noncaseating granulomas & elevated serum ACE levels

Q: What are the common gross findings in Goodpasture's syndrome?
A: pulmonary hemorrhages, renal lesions, hemoptysis, hematuria, crescentic glomerulonephritis

Q: What are the common gross findings in Goodpasture's syndrome?
A: pulmonary hemorrhages, renal lesions, hemoptysis, hematuria, crescentic glomerulonephritis

Q: What can cause gout?
A: Lesch-Nyan disease, PRPP excess, decreased excretion of uric acid, or G6PD deficiency. Also assoc. w/ the use of thiazide diuretics which competitively ingibit the secretion of uric ac

kaplan q bank HY



Anatomy “
 Drainage of ovaries/testes : left gonadal  left renal vein  IVC ¢ right gonadal vein  IVC ¢ same situation occurs for left & right adrenal veins
 Cervix drainage : cervical vein  uterine vein  internal iliac
 Uterine tubes drainage : pampiniform plexus  ovarian vein  IVC
 Radial nerve injury : inability to extend the wrist ¢ digits (= wrist drop) ¢ weakness of grip ¢ anesthesia of dorsal surface of the arm, forearm and hand
 Axillary nerve injury : fracture at the surgical neck of humerus ¢ supplies teres minor , deltoid and skin of shoulder
 Musculocutaneous nerve injury : innervates the flexors of the arm ¢ weakness of arm flexion at the shoulder (biceps, brachialis, coracobrachialis )¢ anesthesia of lateral forearm skin
 CNS locations : pyriform cortex :primary olfactory cortex ¢ postcentral gyrus : primary sensory cortex ¢precentral gyrus : primary motor cortex ¢ insula :primary gustatory cortex
 Friedreich™s ataxia : ataxia,tremor, kyphoscoliosis,foot deformities ¢ death by 40 yrs old ¢ AR ¢ atrophy of spinal cord “ spinocereblellar tracts, corticospinal tracts and posterior columns
Behavioral “
 Cooperative play : after 4 yrs ¢
 Regression :automatic retreat to a less mature level of behavior in times of stress
 Sublimation : turning socially unacceptable impulses into acceptable or more benign forms to allow their expression
 Minor with STD  no need to inform the parents ¢ go ahead and treat !
 Alprazolam is intermediate acting BSD ¢ primarily used for panic attacks
 Diazepam & lorazepam : status epilepticus
 Toilet training : not possible befor the age of 18 months
Biostatistics “

Biochemistry “
 PDH deficiency : pyruvate will be used in other pathways ¢ alanine & lactate will be elevated ¢ alanine aminotransferase converts pyruvate to alanine ¢ LDH converts pyruvate to lactate
 Leigh™s disease Sadsubacute necrotizing encephalomyopathy) : defective form of cytochrome C oxidase ¢ symmetric necrosis that affects central arease of the nervous sytem from the thalamus to the spinal cord ¢
 Glucagon inhibits fatty acid synthesis by a cAMP-dependent phosphorylation of acetyl-CoA carboxylase
 High carbohydrate & low fat diet would stimulate fatty acid synthesis
 cDNA library is synthesized from the mRNA of a cell using the enzyme reverse transcriptase ¢ it is used to study the DNA and the RNA message from which proteins are transcribed
 Fluorescence activated cell sorting (FACS) uses antibodies coupled to fluorescent markers to determine cell surface molecules of whole cells
 Genomic library is the chromosomal sequence of a gene including coding and non-coding regions ¢ it is synthesized directly from the DNA of a cell and it is used to study both the coding regions & the areas such as promoters, enhancers, and introns of a gene
 Deletions are detected by two methods : 1) Southern Blot 2) PCR ( 3. restriction enzymes)
 Glutamate carboxylase : catalyzes the carboxylation of glutamic acid side chains in several clotting factors ( II, VII, IX, X, protein C, S) ¢ vitamin K acts as co-enzyme
 Hemolytic anemia in newborn : as a result of vitamin E “tocopherol- deficiency
 Vitamin B12 is required for two reactions in human body : methylation of homocysteine to methionine ¢ conversion of methylmalonyl CoA  succinyl CoA (methylomalonyl CoA mutase)
 Vitamin C excess can lead to : decreased absorption of B12 ¢ increased estrogen levels in women on estrogen replacement therapy ¢ kidney stones ¢
 Vitamin A : necessary for retinal pigments  nyctalopia
 Glucose transporters are integral membrane proteins with 12 spanning domains
 Beta-adrenergic receptors for Epinephrine have 7 transmembrane segments
 Hexosaminidase A hydrolyzes a bond between N-acetylglucosamine and galactose in the polar head of ganglioside GM2
 Propionic aciduria : deficiency in biotin ¢ propionyl CoA carboxylase
 Galactosemia : the only clinical significant complication is cataract
 Fabry™s :a-galactosidase def ¢ renal failure ¢ telangiectasias ¢ skin rash ¢ ceramide trihexoside accumulation
 Farber disease : ceramidase def ¢ hoarseness, dermatitis, skeletal deformations, mental retardation, hepatomegaly
 Niemann-Pick : def of sphingomyelinase ¢ mental retardation, hepatosplenomegaly, foam cells in bone marrow, cherry red spots in macula (40%) ¢ death by 3 yrs of age
 Von Gierke™s disease : glucose 6-phosphatase def ¢ glucose 6P trapped in the liver cell is degraded to lactate & pyruvate  released into serum ¢ high serum lactate + high serum pyruvate
 Ketone bodies : acetone, acetoacetate , b-hydroxybutyrate ¢ produced by the liver by beta oxidation of free fatty acids ¢ occurs as follows :insulin deficiency  activated lipolysis  increased plasma free fatty acids  increased hepatic fatty acids  accelerated ketogenesis
 Malate shuttle : used to transport cytoplasmic NADH into mitochondria
 Southwestern blotting :involves DNA-protein interactions. ¢ a protein sample is subjected to electrophoresis, transferred to a filter, and exposed to labeled DNA
 UDP glucose phosphorylase :important in glycogen synthesis ¢ glycogen synthase is the rate limiting step in glycogen synthesis
 Alkaptonuria :def of homogentisic acid oxidase (degradation of tyrosine) dark urine ¢ dark connective tissue  ear cartilage may appear bluish
 Northern Blot : best test to determine whether a gene is expressed in a particular cell type
 DNA sequencing & Southern Blot examine the DNA of the cell
 Biochemical testing is usually used to detect a defective enzyme or a reduced amount of normal enzyme ¢ used in the detection of carriers of AR diseases such as Tay Sachs, sickle cell, thalassemias
 Vitamin C def : perifollicular hemorrhages, ecchymoses , splinter hemorrhages, hemorrhages into muscle
 Von Gierkes™s lab : increased lactate , cholesterol, TG, and uric acid
 Wernicke™s : ataxia (= difficulty walking), dementia, paralysis of lateral gaze (= opthalmoplegia) ¢ thiamine deficiency
 Transaminases require pyridoxal phosphate (vitamin B6)
 Thiolase converts acetoacetyl-CoA into acetyl CoA
 Abetalipoproteinemia : absence of apo-proteins ¢ leads to fat malabsorption ¢ complete absence of chylomicrons ¢ patient™s RBC™s are deformed (acanthocytosis)
 Glycine is not hydroxylated ¢ abundant in fibroblasts ¢ constitutes every third aminoacid in collagen structure
 Proline is hydroxylated  hydroxyproline ¢
 Serine, threonine, tyrosine can be phosphorylated post-translationally
 Cystathionine synthetase :catalyzes the conversion of homocysteine  cystathionine  cystein ¢ if enzyme is deficient  homocysteine accumulates, is methylated  methionine ¢ patients with homocystinuria are vulnerable to thrombotic episodes


Genetics “
 Fragile X : enlarged testes + mental retardation ¢ expansion of CGG trinucleotide repeat located on X chromosome
 Edwards syndrome : trisomy 18 ¢ rocker bottom feet, micrognathia, mental retardation, 2nd and 5th finger over 3rd and 4th , congenital heart disease, death within a month
 Patau syndrome : trisomy 13 ¢ mental retardation, cleftlip/palate, polydactyly, rocker bottom feet
 Smith Lemli Opitz syndrome :ambiguous genitalia ¢ failure to metabolize 7 dehydrocholesterol to cholesterol ¢ pyloric stenosis ¢ syndactyly
 Mosaic in trisomy 21 : 1% of children ¢ some of their cells are normal ¢ these individuals show only a mild expression of the trisomy 21 phenotype
 Locus heterogeneity : refers to the situation in which the same phenotype is caused by defects in different genes ¢ commonly seen in syndromes resulting from failures in a complex pathway, such as hearing ¢ - deaf parents produce nomrla hearing children,suggesting that the parents have defects in different genes. The children are heterozygous at both loci and so have normal hearing
 Pleiotropy : is observed in retinoblastoma ¢ carriers may develop other cancers such as osteosarcoma ¢ inactivation of Rb suppressor gene in chromosome 13
 SXD disorder with 60% penetrance ¢ daughters have 60% chance to be affected

Histology / Cellular Biology “
 Major basic protein : found in eosinophils ¢crystalline core of granules in eosinophils ¢destruction of parasites ¢ eosinophils contain also : histaminase, arylsulfatase
 Histamine is produced by basophils & mast cells ¢ eosinophil secretes histaminase
 Circulating RBC™s : 60 days life span
 Peroxisomes : single membrane bound organelles ¢ important in alcohol detoxification & long chain fatty acid metabolism ¢ Degradation of ethanol to acetaldehyde occurs in humans in both peroxisomes & smooth endoplasmic reticulum (P450) ¢ aldehyde dehydrogenase “blocked by disulfiram- occurs in mitochondria
 Sialic acid : is a terminal glycosylation product added to proteins (usually those destined for secretion) in the Golgi apparatus
 P450 :located in SER ¢in chronic alcoholism  growth
 Spleen : white pulp  contains collections of lymphocytes arranged around a central artery in a configuration called the periarterial lymphatic sheath (PALS).germinal centers may occur within the sheath in reaction to antigen exposure ¢ red pulp  consists of splenic cords and splenic sinuses, filters the blood
 Ito cells: found in the perisinusoidal space (space of Disse) Ito cells are hepatic adipose cells and provide primary storage site for vitamin A
 Kupfeer cells :are found in liver sinusoids and belong to the mononuclear phagocytic system ¢greatly increased function after splenectomy ¢ final breakdown of senili RBC™s
 Hemosiderin, a denatured form of ferritin, appears microscopically as yellow brown granules in cytoplasm ¢
 Masson™s trichrome is a connective tissue stain ¢ blue :nuclei ¢ green : connective tissue ¢ red :blood
 Karyorrhexis : pattern of nuclear degradation ¢ pyknotic nucleus undergoes degradation followed by complete lysis ¢ this pattern is common in neutrophils present in acute inflammation
 Liquefactive necrosis :abcess ¢ CNS infarct


Microbiology / Immunology “
 Neonate with widespread granulomas = Listeria monocytogenes (granulomatis infantiseptica)
 Neisseria gonorrhea transmitted via birth canal ¢ opthalmia neonatorum
 Chediak “Higashi : small doses of vitamin C may effectively treat this disorder
 Sporothrix schenkii : hyphae with rosettes of conidia : transmission form ¢ unequal budding yeast found in clinical speciment from a patient with sporotrichosis ¢ Rx : KI or itraconazole
 Tinea pedis /athlete™s foot :colorless, branching hyphae with cross walls and arthroconidia ¢ rx : topical azole
 Malassezia furfur : pityriasis versicolor ¢ short curved hyphae, and round yeasts = œ spapghetti and meatball œ ¢
 Common variable immunodeficiency : decreased number of plasma cells ¢ NORMAL number of B-cells ¢ low levels of all antibody classes ¢ lymph node architecture is unaltered in common variable immunodeficiency
 Giardia lamblia : infects the small intestine ¢ if biopsy : crescent shaped protozoa ¢ if smear : flagellated organism with face like appearance ¢ prolonged diarrhea ¢ may have low serum IgA ¢ river streams in mountains  giardia
 Entamoeaba histolytica : affects the large intestine ¢ may liver abcess
 Scalded skin syndrome : Staphylococcus aureus ¢ exfoliative toxin ¢ splitting of the epidermis at the level of the stratum granulosum, causing global denudation of the skin
 Impetigo & post-streptococcal glomerulonephritis : group A b hemolytic streptococci ¢eroded pustules covered by honey colored crusts
 IgA deficiency Confusedome patients with IgG2 deficiency also have IgA deficiency and may develop anaphylaxis if given IgA-containing blood products
 C4 deficiency : SLE like syndrome
 DiGeorge : tetany (facial muscles first sign  Chvostek™s sign) ¢absent thymus ¢low set ears recurrent candidal infections
 Hyper IgM syndrome : high IgM, low all other classes ¢ helper T cells defect in surface protein CD40L that interacts with CD40 on B-cell surface ¢often form antibodies to neutrophils,platelets, and tissue antigens
 Ataxia telangiectasia :prominent telangiectasias around the eyes ¢ AR ¢ chromosomal breakage syndrome ¢ increased number of translocations ¢ chromosome 11 related
 Molluscum contagiosum :cytoplasmic inclusions in the epidermal cells are pathognomonic ¢ babies & AIDS ¢ poxvirus
 Mycobacterium & Treponema cause chronic meningitis ¢ lymphocytic infiltrate
 Enterococcus faecalis : cause UTI™s “often nosocomial & classically in ICU- ¢ do NOT produce nitrites from nitrates ¢
 Nitrites + :usually a gram negative organism (enterobacteria) such as Klebsiella, pseudomonas, E.Coli, Enterobacter sp. ¢
 Omcogenesis in HPV : cervical intraepithelial neoplasia is associated with HP infection (types 16,18) ¢ produce E6 & E7 proteins inhibiting p53
 Progressive multifocal leukoencephalopathy : JC virus (papova virus) ¢ infects oligondendroglial cells in the brain ¢ eosinophilic inclusions ¢ AIDS-defining ¢ only white matter affected
 Subacute sclerosing panencephalitis ¢ may follow previous measles infection ¢ gray matter & white are affected ¢ occurs usually before the age of 18
 Yersinia pestis & plague : any previously healthy person in the Southwestern US who develops septic shcok or sever pulmonary disease shold be evaluated for plague
 Aspergilloma may be formed by tuberculosis, tumor, bronchiectasis ¢ surgically resection ¢antibiotics are ineffective
 Syngeneic graft : transfer of tissue between genetically identical individuals (identical twins)
 Allograft /homograft : graft between genetically different members of the same species
 Xenograft : e.g pig heart valve
 C5a & IL 8 most powerful chemotactic factors for neutrophils ¢ LTB4 also
 IgG subclass 2 is directed against polysaccharide antigens and is involved in the host defense against encapsulated bacteria
 C 3 nephritic factor = IgG autoantibody that binds to C 3 convertase making it resistant to inactivation ¢ persistently low serum complement levels ¢ Type II MPGN
 Scalded skin syndrome (Staphylococcus aureus phage II group ) : involves the very superficial squamus cells just beneath the granular layer
 Type II hypersensitivity : are mediated by IgG or IgM antibodies to fixed cell bound antigens ¢ this response may lead to cell destruction or cell dysfunction ¢ important in the pathogenesis of transfusion reactions, graft rejection, Graves disease, myasthenia gravis
 Type III hypersensitivity :formation of circulating immune complexes ¢ may precipitate in small blood vessels  fix complement and incite an inflammatory reaction ¢ glomerulonephritis, vasculitides, collagen vascular diseases
 Type IV hypersensitivity Confusedensitized T lymphocytes ¢ either CD4+ (helper) T lympocytes or CD8+ (cytotoxic) T lymphocytes take part in this response ¢ granulomas
 IFNγ produced by T1 helper cells instructs macrophages to become epithelioid cells
 Aspirin-induced asthma : inhibition of cyclooxygenase/ but not lipooxygenase  decreased ratio between PG™s (bronchodilators) and leukotrienes (bronchoconstrictors)
 Germ tube test :diagnostic test for candida albicans
 Cervical exudates  gram negative diplococci within neutrophils = Neisseria gonorrhea 1000%
 Cervical exudates  gram negative cocci : 1) neisseria gonorrhea 2) acinetobacter (normal flora) ¢ use DNA probe to distinquish
 Leptospirosis : abrupt onset of headache (98%) , fever, chills, conjunctivitis, muscle aches, GI symptoms, rash, hypotension ¢ this phase lasts 3-7 days ¢ asymptomatic period  recurrence of fever & generalized symptoms
 Neisseria gonorrhea arthritis : patients are continuously susceptible to reinfection b/c of antigenic variation of the pili

Molecular biology “

Pathology “
 Subcortical leukoencephalopathy (Binswanger™s disease) : diffuse loss of deep hemispheric white matter ¢ associated with hypertension ¢ widespread gliosis
 Yolk sac tumor a.k.a = infantile embryonal carcinoma/= endodermal sinus tumor : b/c of presence of endodermal sinuses that resemble primitive glomeruli ¢ cytoplasmic granules that contain alpha fetoprotein. ¢ can be used as a serum marker for recurrent disease
 Still™s disease : a.ka juvenile rheumatoid arthritis ¢ affects children younger than 16 yrs old , 1-3 yrs of age ¢ female predominance ¢fever, splenomegaly, general lymphadenopathy, leukocytosis ¢ rheumatoid factor is usually negative ¢ if +  poorer prognosis
 Henoch Schonlein purpura : preceded by an URI ¢ vasculitis, arthritis, purpura, GI pain & blood in stool , kidney  nephritic syndrome
 Kawasaki™s disease : fever, conjunctivitis, erosion of oral mucosa, lymphadenopathy, rash , coronary & aortic vasculitis  death
 Fibrinous pericarditis : post MI ¢ loud pericardial friction rub, chest pain,fever, symptoms of CHF
 Caseous pericardtitis TB
 Conn™s syndrome : hyperplasia of zona glomerulosa ¢ hypertension secondary to sodium retention ¢ hypokalemia ¢decreased serum rennin (negative feedback of increased blood pressure on rennin secretion)
 Secondary aldosteronism :increased levels of rennin ¢ due to renal ischemia
 Dermatitis herpetiformis : associated with celiac sprue ¢ type III hypersensitivity reaction ¢ immunocomplexes igA + complement
 Discoid lupus erythematosous : localized cutaneous form of SLE ¢ type III hypersensitivity reaction
 Urticaria : IgE mediated ¢ type I hypersensitivity
 ASD :prominent right ventricular cardiac impulse ¢ systolic ejection murmur heard in the pulmonic area & along the left sternal border ¢ fixed splitting of the 2nd heart sound
 Melasma :irregular patches of hyperpigmentation on the face ¢occurs in pregnancy ¢ may not regress
 Primary sclerosing cholangitis : beaded appearance on ERCP of biliary tree ¢
 Osteosarcoma : XRay : bone destruction /soft tissue with œsunburst appearance œ / Codman™s triangle (=periostal elevation) ¢ Histo : anaplastic cells with osteoid
 Exostoses (=osteochondromas), debaceous cysts, dermoid tumor™s, colonic polyps = Gardner™s
 Lymph node structure & disease :
a. Viral infection “ expansion of germinal centers without loss of normal architecture
b. AIDS “ progressive transformation of germinal centers ¢ not paracortical hyperplasia
c. Lymphomas “ destroy the architecture of the lymph node
 Complete hydatiform mole : elevated b-hCG ¢grape like cystic structures filling the uterus ¢ no embryo ¢ the genotype of a complete hydatiform mole is purely paternal (XY), caused by fertilization of an egg that has lost its chromosomes ¢ danger : choriocarcinoma
 Partial moles : triploidy / tetraploidy ¢ fertilization of an egg with two different sperm ¢ one with X & one with Y
 AFP : hepatocellular carcinoma ¢ yolk sac tumors ¢ embryonal tumors in men
 Irritable bowel syndrome : alternating constipation / diarrhea ¢ more common in young females ¢ no organic changes are evident
 Hypoaldosteronism :decrease in serum sodium increase in serum K+ ¢ retain of H+ ions  metabolic acidosis with low serum bicarbonate
 Bernard Soulier disease : prolonged BT ¢ normal PLT ¢ dysfunction in glycoprotein Ib-IX complex ¢ only treatment in acute emergency : transfusion of PLT™s
 Henoch-Schonlein : URI + purpura + abdominal pain + hematuria + child
 Cryoprecipitate would help in a case of vWF disease
 Hyaline droplets (dark staining droplets ) are found in the epithelium of PCT in cases of proteinuria
 Spongiosis : intercellular edema of the epidermis ¢ fluid accumulates between the cells, pulling the apart
 Adult form of aortic coarctation Confusedtenosis distal to the left subclavian artery ¢ collateral circulation by intercostal & internal mammary artery ¢notching of inferior margins of ribs ¢
 Infantile form of aortic coarctation is associated with patent ductus arteriosus
 Aortic stenosis : systolic hypotension throughout the body ¢ recurrent syncope ¢ hypertrophe / dilatation of LV
 Takayasu arteritis : a.k.a pulseless disease ¢ vasculitis of the aortic arch and its branches  stenosis of these arteries ¢ signs & symptoms of ischemia to the upper part of the body ¢ radial pulses are weak/ absent = pulseless disease
 Vascular proliferating skin lesions :hemangiomas ¢ Kaposi ¢ bacillary angiomatosis
 Malignant mixed mullerian tumor : tumor with 2 components : stromal & epithelial (endometrial glands) ¢ both are malignant but only the epithelial metastizes ¢ stromal component may contain metaplastic components such as cartilage & bone
 Endometrial carcinoma is derived form epithelial glandular component of endometrium ¢ abnormal bleeding is the usual presentation ¢
 Small parietal lobe abcesses : septic emboli from infective endocarditis
 Albinism & associated skin cancer : squamus cell carcinoma (multiple)
 Rheumatoid nodules are composed histologically of areas of fibrinoid necrosis surrounded by palisading epithelioid cells
 Thalassemia & sickle cell anemia do not usually present until about the 6 months of age ,when fetal hemoglobin production ceases
 Celiac disease : limited to proximal small bowel ¢ anti-gliadin antibodies ¢ granular deposits of IgA and C3 in dermal papillary tips ¢ gluten free diet as Rx ¢ tropical sprue affects the entire small bowel ( ETEC infection) ¢
 Basal cell carcinoma : œpearly papules on sun exposed skin ¢ almoste never metastize ¢ palisading of the cell nuclei ¢
 Resistance to thyroid hormone (Refetoff™s syndrome ): mutation in thyroid hormone receptor gene ¢ affects also the cells in pituitary  œno negative feedback  increased plasma TSH  increase in serum T4
 Low T3 syndrome (euthyroid sick syndrome) occurs with certain systemic illnesses such pneumonia or septicemia,afterm major surgery and with malnutrition or starvation ¢ decrease of 5™ monodeiodinase activity ¢ decreased levels of T3
 Addison™s disease : decreased secretion of cortisol, aldosterone and adrenal androgens ¢ hypotension may be present b/c arterioles are less responsive to the constrictor effects of catecholamines in the absence of cortisol ¢ hyperkalemia & hyponatremia due to lak of cortisol
 Nelson™s syndrome : usually post-adrenalectomy for Cushing ¢ extreme hyperpigmentation due to hypersecretion of ACTH from pituitary adenoma that is no longer being restrained by the supressibve effect of cortisol
 Head & neck (particularly nose,nasopharynx and orbit is the most frequent site for embryonal rhabdomyosarcoma ¢ other sites are the genitourinary tract
 Hereditary factor XIII deficiency :presentation at birth when the umbilical stump bleeds excessively ¢ factor XIII is necessary to stabilize clot formation ; in its absence clots will rapidly lyse ¢ spontaneous abortion in women is common
 Complications of MVP :atrial thrombosis, caclcification, infective endocarditis, emboli to the brain, rupture of chordae, mitral regurgitation,,arrythmias, and premature ventricular contractions
 Conn™s syndrome : hypertension, hypernatremia, hypokalemia, low rennin levels, metabolic alkalosis
 Vitamin K dependent factors : II (prothrombin), VII, IX, X, C, S ¢ deficiency in protein C would cause thrombosis NOT bleeding ¢ check hemorrhagic skin necrosis by warfarin
 Prostatic hyperplasia : periurethral zone
 Reye™s syndrome : fatty liver with encephalopathy ¢ Hx : viral illness, severe vomiting, irritability, hepatomegaly, elevation of serum ammonia ¢ aquired mitochondrial abnormality ¢may occur also without exposure to salicylates ¢ esp after influenza and cickenpox ¢ mortality rate 50%

Pharmacology “
 DMARDS for RA : MTX ¢ azathiprine ¢ penicillamine ¢hydroxycholroquine ¢ chloroquine ¢ organic gold compounds ¢ sulfasalazine
 Glucocorticoids SE : hypocalcemia, fluid retention, hypokalemia, hyperglycemia, hypernatremia , adrenal suppression, muscle weakness & atrophy, gastrtits, Cushingoid state, immunosuppression, hypertension, psychosis , osteoporosis, glaucoma, cataract
 N acetylcyteine : mucolytic used in CF to thin mucous ¢splits disulfide linkages between these mucoproteins  ↓ mucous viscosity
 Dextromethorphan is a cough depressant
 Pentamidine : used in HIV patients with PCP
 Metoclopramide Confusedtimulates motility of intestinal tract ¢ contraindicated in patients with bowel obstruction  danger for perforation
 Anticholinergic drugs : may precipitate attacks of narrow angle glaucoma b/c muscarinic receptors on the papillary constrictor muscle of the iris are blocked ¢ TCA™s “ imipramine, amitryptiline, nortriptyline, desipramine, clomipramine,doxepine- can do that !
 Decrease of blood levels of a drug : 1 half life  50 % ¢ 2 half lifes  25 % left in blood ¢ 3 half lifes  12,5 % left ¢ 4 half lifes  6,25% left in blood ¢ levels decrease by half every half life
 Retarded ejaculation : can be improved by admin a SSRI ¢ fluexitine, sertraline,citalopram, paroxetine.
 β-blockers are used in treatment of hypertrophic cardiomyopathy ¢ β1-blockers : atenolol, betaxolol, esmolol, acebutolol, metoprolol
 Bretylium : class III anti-arrythmic ¢ indicated for treatment of ventricular fibrillation and ventricular tachycardia
 Digoxin :used in atrial fibrillation ¢ atrial flutter ¢ CHF
 Lidocaine : class Ib antiarrythmic ¢ used in Rx of ventricular tachycardia
 Ventricular tachycardia : amiodarone ¢ bretylium ¢ lidocaine
 Succinylcholine : depolarizing skeletal muscle relaxant ¢ can cause hyperkalemia ¢ PR prolongation , widening of QRS , peaked T waves
 Acute interstitial nephritis : caused by ibuprofen, indomethacin, methicillin, cephalothin, sulfonamides,thiazides, furosemide, cimeridine,methyldopa ¢Clinical : ARF ( ↑ BUN, creatinine 0,6-1,2 ) fever, maculopapular rash, EOSINOPHILIA !, periorbital edema, wheezing
 Acarbose : delays glucose absoption from GI
 Metformin : causes lactic acidosis ¢ increases the binding of insulin to its receptor
 Oxybutynin : inhibits muscarinic action on smooth muscle (antimuscarinic action) ¢ Rx for bladder instability “ incontinence, persistent urinary urgency-
 Betanechol : used in urinary retention to contraction of detrusor muscle ¢
 Gabapentin : used to treat neuropathic pain in diabetic patients ¢ antiepileptic
 Primidone : anticonvulsant ¢ has two active metabolites 1) ohenobarbital 2) phenethylmalonamide ¢ associated with cross- hypersensitivity to Phenobarbital
 T3 therapy : increases serum T3 levels ¢ but NOT serum T4 b/c T3 is not converted peripherally to T4 ¢ TSH will be low due to feedback inhibition by T3 ¢ decrease of TSH causes also decrease in T4
 Salicylate intoxication : dizziness, tinnitus, hearing impairment , nausea, vomiting, hyperventilation , flushing, sweating, metabolic acidosis ¢ agents that acidify urine , such as NH4Cl are known dramatically decrease salicylate excretion and subsequently increase salicylic acid blood levels ¢ Rx : sodium bicarbonate, sodium lactate
 Jimson weed contains anti-muscarinic agents ¢ in overdose : agitation,mydriasis, hot dry skin, tachycardia , decreased bowel sounds
 Stimulants : best way to differentiate stimulatnt overdose from anticholinergic overdose is the skin ¢ sweaty  stimulants ¢ dry  anticholinergics
 Opioid intoxication : sleepiness, lethargy, miosis, cool skin , hypoventilation, hypotension, bradycardia, decreased bowel sounds ¢
 Cefoperazone : 3rd generation cephalosporin ¢can cause vitamin K deficiency ¢ disulfiram like reaction with alcohol ¢ DOC in people with impaired renal function b/c 60% is eliminated by the biliary route
 Ticarcillin : β”lactamase sensitive ¢ causes a large salt load  salt retention and hypokalemia
 Carbidopa blocks a pyridoxal dependent decarboxylase located in the mucosa of the GI tract and in systemic circulation
 Heparin is the most common cause of drug induced thrombocytopenia ¢risk for development thrombocytopenia increases as the duration of therapy increases (more than 10days e.g) ¢ no skin necrosis
 Warfarin & hemorrhagic skin necrosis : associated protein C deficiency in the patient ¢ presents on 3rd- 10th day of therapy ¢ may lead to necrosis of skin (typically on breast, thighs, and buttocks) ¢ heterozygote carriers for protein C become homozygote when given warfarin in 6~8 hrs when the half life of previously γ-carboxylated protein C disappears.Now the patient is hypercoagulable ¢ warfarin is used for prophylaxis and treatment of thromboembolic complications associated with cardiac valve replacement and atrial fibrillation, as well as the prophylaxis and treatment of venous thrombosis and pulmonary embolism ¢
 Aminoglycosides & nonoliguric RF : some patients develop a non-oliguric form of renal failure when treated with aminoglycosides such as gentamycin ¢ elevation of creatinine ¢
 Cephalothin/Methicillin interstitial nephritis : fever + rash + acute renal failure + eosinophilia
 Central pontine myelinolysis : demyelination affecting the central region of basis pontis ¢ in severe malnourished & dehydrated alcoholics ¢ from rapid correction of hyponatermia
 Hydrocarbon exposure  scrotal carcinoma
 Zolpidem : non-benzodiazepine ¢ hypnotic agent
 Buspirone : non-benzodiazepine ¢anxiolytic ¢ devoid of sedative ,hypnotic,anticonvulsant and muscle relaxant properties
 Obsessive compulsive disorder : clomipramine (TCA) or SSRI (e.g fluexitine)
 Nortriptyline  hyperplrolactinemia (methyl dopa, phenothiazines also)
 Diabetic with sulfa allergy : contraindicated sulfonylureas (chlorpropamide, tolbutamide,glyburide,glipizide)
 Methamphetamine : indirect- acting agonist ¢ acts inducing dopamine, NE, and 5HT release ¢ dopamine is believed to play an important role in the reward system of the brain and is thought to be a significant factor in the reinforcing effects of stimulants ( area involved in reward system : ventral tegmental area of midbrain to the nucleus accumbens of the forebrain)
 Hydrocortisone suppositories : indicated for treatment of distal ulcerative colitis ¢ sulfasalazine is also used in treatment of UC
 Metronidazole gold standard for pseudomembranous colitis ¢ vancomycin is another option
 Hyoscyamine : anticholinergic ¢ Rx : irritable bowel syndrome ¢ administered before the meal
 Prednisone for treatment of acute flare ups of Crohn™s
 Megestrol acetate & leuprolide : for prostate cancer ¢ GnRH analogs
 Cyclobenzaprine : centrally acting skeletal muscle relaxant ¢ structurally related to tricyclic antidepressants ¢ is has anticholinergic side effects ( blurred vision, urinary retention, constipation,tachycardia etc)
 Baclofen :centrally acting skeletal muscle relaxant ¢ inhibition of both monosynaptic and polysynaptic reflexes ¢ indicated for treatment of spasticity resulting from multiple sclerosis or secondary to spinal cord injuries ¢ also Rx for trigeminal neuralgia ¢ fatigue & hypotension
 Traveler;s diarrhea Rx : most cases of traveler™s diarrhea are caused by ETEC, Shigella species and Campylobacter jejuni ¢ treat with fluoroquinolones ( ciprofloxacin,ofloxacin, norfloxacin) ¢ TMP/SFX is used for children !
 Mebendazole : used for elminths such as Enterobius, Trichuris trichiura, Ascaris lumbricoides
 Diabetic with hypertension : ACE inhibitors ¢ ca2+ blockers
 Cefazolin & Cefadroxil : 1st generation cephalosporins ¢ used surgical prophylaxis
 SIADH & drugs : carbamazapine ¢ vincristine,vinblastine ¢ cyclophosphamide ¢ chlorpropamide ¢ TCA




Physiology “
 Glycoprotein hormones : EPO, LH, FSH, hCG, TSH ¢ bind at cell surface receptors ↑ cAMP levels
 Catecholamine hormones : epinephrine, norepinephrine, dopamine
 Oligopeptide hormones : endorphins, ADH, oxytocin, TRH, GnRH, SS, CCK, secretin, VIP, GIP
 Polypeptide hormones : PTH, calcitonin, insulin, glucagons, pancreatic polypeptide, gastrin, ACTH, IGF™s, EGF, FGF, NGF
 Baroreceptor reflex (patient stands up from supine condition) :patient stands up  less blood to brain  less firing to baroreceptors  sympathetic stimulation  increase in HR, conduction velocity and myocardial contractility  constriction of all arterioles  ↑ TPR  sympathetic stimulation of renal vasculature  decrease in renal blood flow  constriction of large veins  increases venus return to the heart  ↑ preload
 Transcutaneous electrical nerve stimulation is a method used to lessen severe,chronic pain by overly stimulating the involved neurons ¢ gate theory of pain

GL

Anatomy “
 Drainage of ovaries/testes : left gonadal  left renal vein  IVC ¢ right gonadal vein  IVC ¢ same situation occurs for left & right adrenal veins
 Cervix drainage : cervical vein  uterine vein  internal iliac
 Uterine tubes drainage : pampiniform plexus  ovarian vein  IVC
 Radial nerve injury : inability to extend the wrist ¢ digits (= wrist drop) ¢ weakness of grip ¢ anesthesia of dorsal surface of the arm, forearm and hand
 Axillary nerve injury : fracture at the surgical neck of humerus ¢ supplies teres minor , deltoid and skin of shoulder
 Musculocutaneous nerve injury : innervates the flexors of the arm ¢ weakness of arm flexion at the shoulder (biceps, brachialis, coracobrachialis )¢ anesthesia of lateral forearm skin
 CNS locations : pyriform cortex :primary olfactory cortex ¢ postcentral gyrus : primary sensory cortex ¢precentral gyrus : primary motor cortex ¢ insula :primary gustatory cortex
 Friedreich™s ataxia : ataxia,tremor, kyphoscoliosis,foot deformities ¢ death by 40 yrs old ¢ AR ¢ atrophy of spinal cord “ spinocereblellar tracts, corticospinal tracts and posterior columns
Behavioral “
 Cooperative play : after 4 yrs ¢
 Regression :automatic retreat to a less mature level of behavior in times of stress
 Sublimation : turning socially unacceptable impulses into acceptable or more benign forms to allow their expression
 Minor with STD  no need to inform the parents ¢ go ahead and treat !
 Alprazolam is intermediate acting BSD ¢ primarily used for panic attacks
 Diazepam & lorazepam : status epilepticus
 Toilet training : not possible befor the age of 18 months
Biostatistics “

Biochemistry “
 PDH deficiency : pyruvate will be used in other pathways ¢ alanine & lactate will be elevated ¢ alanine aminotransferase converts pyruvate to alanine ¢ LDH converts pyruvate to lactate
 Leigh™s disease Sadsubacute necrotizing encephalomyopathy) : defective form of cytochrome C oxidase ¢ symmetric necrosis that affects central arease of the nervous sytem from the thalamus to the spinal cord ¢
 Glucagon inhibits fatty acid synthesis by a cAMP-dependent phosphorylation of acetyl-CoA carboxylase
 High carbohydrate & low fat diet would stimulate fatty acid synthesis
 cDNA library is synthesized from the mRNA of a cell using the enzyme reverse transcriptase ¢ it is used to study the DNA and the RNA message from which proteins are transcribed
 Fluorescence activated cell sorting (FACS) uses antibodies coupled to fluorescent markers to determine cell surface molecules of whole cells
 Genomic library is the chromosomal sequence of a gene including coding and non-coding regions ¢ it is synthesized directly from the DNA of a cell and it is used to study both the coding regions & the areas such as promoters, enhancers, and introns of a gene
 Deletions are detected by two methods : 1) Southern Blot 2) PCR ( 3. restriction enzymes)
 Glutamate carboxylase : catalyzes the carboxylation of glutamic acid side chains in several clotting factors ( II, VII, IX, X, protein C, S) ¢ vitamin K acts as co-enzyme
 Hemolytic anemia in newborn : as a result of vitamin E “tocopherol- deficiency
 Vitamin B12 is required for two reactions in human body : methylation of homocysteine to methionine ¢ conversion of methylmalonyl CoA  succinyl CoA (methylomalonyl CoA mutase)
 Vitamin C excess can lead to : decreased absorption of B12 ¢ increased estrogen levels in women on estrogen replacement therapy ¢ kidney stones ¢
 Vitamin A : necessary for retinal pigments  nyctalopia
 Glucose transporters are integral membrane proteins with 12 spanning domains
 Beta-adrenergic receptors for Epinephrine have 7 transmembrane segments
 Hexosaminidase A hydrolyzes a bond between N-acetylglucosamine and galactose in the polar head of ganglioside GM2
 Propionic aciduria : deficiency in biotin ¢ propionyl CoA carboxylase
 Galactosemia : the only clinical significant complication is cataract
 Fabry™s :a-galactosidase def ¢ renal failure ¢ telangiectasias ¢ skin rash ¢ ceramide trihexoside accumulation
 Farber disease : ceramidase def ¢ hoarseness, dermatitis, skeletal deformations, mental retardation, hepatomegaly
 Niemann-Pick : def of sphingomyelinase ¢ mental retardation, hepatosplenomegaly, foam cells in bone marrow, cherry red spots in macula (40%) ¢ death by 3 yrs of age
 Von Gierke™s disease : glucose 6-phosphatase def ¢ glucose 6P trapped in the liver cell is degraded to lactate & pyruvate  released into serum ¢ high serum lactate + high serum pyruvate
 Ketone bodies : acetone, acetoacetate , b-hydroxybutyrate ¢ produced by the liver by beta oxidation of free fatty acids ¢ occurs as follows :insulin deficiency  activated lipolysis  increased plasma free fatty acids  increased hepatic fatty acids  accelerated ketogenesis
 Malate shuttle : used to transport cytoplasmic NADH into mitochondria
 Southwestern blotting :involves DNA-protein interactions. ¢ a protein sample is subjected to electrophoresis, transferred to a filter, and exposed to labeled DNA
 UDP glucose phosphorylase :important in glycogen synthesis ¢ glycogen synthase is the rate limiting step in glycogen synthesis
 Alkaptonuria :def of homogentisic acid oxidase (degradation of tyrosine) dark urine ¢ dark connective tissue  ear cartilage may appear bluish
 Northern Blot : best test to determine whether a gene is expressed in a particular cell type
 DNA sequencing & Southern Blot examine the DNA of the cell
 Biochemical testing is usually used to detect a defective enzyme or a reduced amount of normal enzyme ¢ used in the detection of carriers of AR diseases such as Tay Sachs, sickle cell, thalassemias
 Vitamin C def : perifollicular hemorrhages, ecchymoses , splinter hemorrhages, hemorrhages into muscle
 Von Gierkes™s lab : increased lactate , cholesterol, TG, and uric acid
 Wernicke™s : ataxia (= difficulty walking), dementia, paralysis of lateral gaze (= opthalmoplegia) ¢ thiamine deficiency
 Transaminases require pyridoxal phosphate (vitamin B6)
 Thiolase converts acetoacetyl-CoA into acetyl CoA
 Abetalipoproteinemia : absence of apo-proteins ¢ leads to fat malabsorption ¢ complete absence of chylomicrons ¢ patient™s RBC™s are deformed (acanthocytosis)
 Glycine is not hydroxylated ¢ abundant in fibroblasts ¢ constitutes every third aminoacid in collagen structure
 Proline is hydroxylated  hydroxyproline ¢
 Serine, threonine, tyrosine can be phosphorylated post-translationally
 Cystathionine synthetase :catalyzes the conversion of homocysteine  cystathionine  cystein ¢ if enzyme is deficient  homocysteine accumulates, is methylated  methionine ¢ patients with homocystinuria are vulnerable to thrombotic episodes


Genetics “
 Fragile X : enlarged testes + mental retardation ¢ expansion of CGG trinucleotide repeat located on X chromosome
 Edwards syndrome : trisomy 18 ¢ rocker bottom feet, micrognathia, mental retardation, 2nd and 5th finger over 3rd and 4th , congenital heart disease, death within a month
 Patau syndrome : trisomy 13 ¢ mental retardation, cleftlip/palate, polydactyly, rocker bottom feet
 Smith Lemli Opitz syndrome :ambiguous genitalia ¢ failure to metabolize 7 dehydrocholesterol to cholesterol ¢ pyloric stenosis ¢ syndactyly
 Mosaic in trisomy 21 : 1% of children ¢ some of their cells are normal ¢ these individuals show only a mild expression of the trisomy 21 phenotype
 Locus heterogeneity : refers to the situation in which the same phenotype is caused by defects in different genes ¢ commonly seen in syndromes resulting from failures in a complex pathway, such as hearing ¢ - deaf parents produce nomrla hearing children,suggesting that the parents have defects in different genes. The children are heterozygous at both loci and so have normal hearing
 Pleiotropy : is observed in retinoblastoma ¢ carriers may develop other cancers such as osteosarcoma ¢ inactivation of Rb suppressor gene in chromosome 13
 SXD disorder with 60% penetrance ¢ daughters have 60% chance to be affected

Histology / Cellular Biology “
 Major basic protein : found in eosinophils ¢crystalline core of granules in eosinophils ¢destruction of parasites ¢ eosinophils contain also : histaminase, arylsulfatase
 Histamine is produced by basophils & mast cells ¢ eosinophil secretes histaminase
 Circulating RBC™s : 60 days life span
 Peroxisomes : single membrane bound organelles ¢ important in alcohol detoxification & long chain fatty acid metabolism ¢ Degradation of ethanol to acetaldehyde occurs in humans in both peroxisomes & smooth endoplasmic reticulum (P450) ¢ aldehyde dehydrogenase “blocked by disulfiram- occurs in mitochondria
 Sialic acid : is a terminal glycosylation product added to proteins (usually those destined for secretion) in the Golgi apparatus
 P450 :located in SER ¢in chronic alcoholism  growth
 Spleen : white pulp  contains collections of lymphocytes arranged around a central artery in a configuration called the periarterial lymphatic sheath (PALS).germinal centers may occur within the sheath in reaction to antigen exposure ¢ red pulp  consists of splenic cords and splenic sinuses, filters the blood
 Ito cells: found in the perisinusoidal space (space of Disse) Ito cells are hepatic adipose cells and provide primary storage site for vitamin A
 Kupfeer cells :are found in liver sinusoids and belong to the mononuclear phagocytic system ¢greatly increased function after splenectomy ¢ final breakdown of senili RBC™s
 Hemosiderin, a denatured form of ferritin, appears microscopically as yellow brown granules in cytoplasm ¢
 Masson™s trichrome is a connective tissue stain ¢ blue :nuclei ¢ green : connective tissue ¢ red :blood
 Karyorrhexis : pattern of nuclear degradation ¢ pyknotic nucleus undergoes degradation followed by complete lysis ¢ this pattern is common in neutrophils present in acute inflammation
 Liquefactive necrosis :abcess ¢ CNS infarct


Microbiology / Immunology “
 Neonate with widespread granulomas = Listeria monocytogenes (granulomatis infantiseptica)
 Neisseria gonorrhea transmitted via birth canal ¢ opthalmia neonatorum
 Chediak “Higashi : small doses of vitamin C may effectively treat this disorder
 Sporothrix schenkii : hyphae with rosettes of conidia : transmission form ¢ unequal budding yeast found in clinical speciment from a patient with sporotrichosis ¢ Rx : KI or itraconazole
 Tinea pedis /athlete™s foot :colorless, branching hyphae with cross walls and arthroconidia ¢ rx : topical azole
 Malassezia furfur : pityriasis versicolor ¢ short curved hyphae, and round yeasts = œ spapghetti and meatball œ ¢
 Common variable immunodeficiency : decreased number of plasma cells ¢ NORMAL number of B-cells ¢ low levels of all antibody classes ¢ lymph node architecture is unaltered in common variable immunodeficiency
 Giardia lamblia : infects the small intestine ¢ if biopsy : crescent shaped protozoa ¢ if smear : flagellated organism with face like appearance ¢ prolonged diarrhea ¢ may have low serum IgA ¢ river streams in mountains  giardia
 Entamoeaba histolytica : affects the large intestine ¢ may liver abcess
 Scalded skin syndrome : Staphylococcus aureus ¢ exfoliative toxin ¢ splitting of the epidermis at the level of the stratum granulosum, causing global denudation of the skin
 Impetigo & post-streptococcal glomerulonephritis : group A b hemolytic streptococci ¢eroded pustules covered by honey colored crusts
 IgA deficiency Confusedome patients with IgG2 deficiency also have IgA deficiency and may develop anaphylaxis if given IgA-containing blood products
 C4 deficiency : SLE like syndrome
 DiGeorge : tetany (facial muscles first sign  Chvostek™s sign) ¢absent thymus ¢low set ears recurrent candidal infections
 Hyper IgM syndrome : high IgM, low all other classes ¢ helper T cells defect in surface protein CD40L that interacts with CD40 on B-cell surface ¢often form antibodies to neutrophils,platelets, and tissue antigens
 Ataxia telangiectasia :prominent telangiectasias around the eyes ¢ AR ¢ chromosomal breakage syndrome ¢ increased number of translocations ¢ chromosome 11 related
 Molluscum contagiosum :cytoplasmic inclusions in the epidermal cells are pathognomonic ¢ babies & AIDS ¢ poxvirus
 Mycobacterium & Treponema cause chronic meningitis ¢ lymphocytic infiltrate
 Enterococcus faecalis : cause UTI™s “often nosocomial & classically in ICU- ¢ do NOT produce nitrites from nitrates ¢
 Nitrites + :usually a gram negative organism (enterobacteria) such as Klebsiella, pseudomonas, E.Coli, Enterobacter sp. ¢
 Omcogenesis in HPV : cervical intraepithelial neoplasia is associated with HP infection (types 16,18) ¢ produce E6 & E7 proteins inhibiting p53
 Progressive multifocal leukoencephalopathy : JC virus (papova virus) ¢ infects oligondendroglial cells in the brain ¢ eosinophilic inclusions ¢ AIDS-defining ¢ only white matter affected
 Subacute sclerosing panencephalitis ¢ may follow previous measles infection ¢ gray matter & white are affected ¢ occurs usually before the age of 18
 Yersinia pestis & plague : any previously healthy person in the Southwestern US who develops septic shcok or sever pulmonary disease shold be evaluated for plague
 Aspergilloma may be formed by tuberculosis, tumor, bronchiectasis ¢ surgically resection ¢antibiotics are ineffective
 Syngeneic graft : transfer of tissue between genetically identical individuals (identical twins)
 Allograft /homograft : graft between genetically different members of the same species
 Xenograft : e.g pig heart valve
 C5a & IL 8 most powerful chemotactic factors for neutrophils ¢ LTB4 also
 IgG subclass 2 is directed against polysaccharide antigens and is involved in the host defense against encapsulated bacteria
 C 3 nephritic factor = IgG autoantibody that binds to C 3 convertase making it resistant to inactivation ¢ persistently low serum complement levels ¢ Type II MPGN
 Scalded skin syndrome (Staphylococcus aureus phage II group ) : involves the very superficial squamus cells just beneath the granular layer
 Type II hypersensitivity : are mediated by IgG or IgM antibodies to fixed cell bound antigens ¢ this response may lead to cell destruction or cell dysfunction ¢ important in the pathogenesis of transfusion reactions, graft rejection, Graves disease, myasthenia gravis
 Type III hypersensitivity :formation of circulating immune complexes ¢ may precipitate in small blood vessels  fix complement and incite an inflammatory reaction ¢ glomerulonephritis, vasculitides, collagen vascular diseases
 Type IV hypersensitivity Confusedensitized T lymphocytes ¢ either CD4+ (helper) T lympocytes or CD8+ (cytotoxic) T lymphocytes take part in this response ¢ granulomas
 IFNγ produced by T1 helper cells instructs macrophages to become epithelioid cells
 Aspirin-induced asthma : inhibition of cyclooxygenase/ but not lipooxygenase  decreased ratio between PG™s (bronchodilators) and leukotrienes (bronchoconstrictors)
 Germ tube test :diagnostic test for candida albicans
 Cervical exudates  gram negative diplococci within neutrophils = Neisseria gonorrhea 1000%
 Cervical exudates  gram negative cocci : 1) neisseria gonorrhea 2) acinetobacter (normal flora) ¢ use DNA probe to distinquish
 Leptospirosis : abrupt onset of headache (98%) , fever, chills, conjunctivitis, muscle aches, GI symptoms, rash, hypotension ¢ this phase lasts 3-7 days ¢ asymptomatic period  recurrence of fever & generalized symptoms
 Neisseria gonorrhea arthritis : patients are continuously susceptible to reinfection b/c of antigenic variation of the pili

Molecular biology “

Pathology “
 Subcortical leukoencephalopathy (Binswanger™s disease) : diffuse loss of deep hemispheric white matter ¢ associated with hypertension ¢ widespread gliosis
 Yolk sac tumor a.k.a = infantile embryonal carcinoma/= endodermal sinus tumor : b/c of presence of endodermal sinuses that resemble primitive glomeruli ¢ cytoplasmic granules that contain alpha fetoprotein. ¢ can be used as a serum marker for recurrent disease
 Still™s disease : a.ka juvenile rheumatoid arthritis ¢ affects children younger than 16 yrs old , 1-3 yrs of age ¢ female predominance ¢fever, splenomegaly, general lymphadenopathy, leukocytosis ¢ rheumatoid factor is usually negative ¢ if +  poorer prognosis
 Henoch Schonlein purpura : preceded by an URI ¢ vasculitis, arthritis, purpura, GI pain & blood in stool , kidney  nephritic syndrome
 Kawasaki™s disease : fever, conjunctivitis, erosion of oral mucosa, lymphadenopathy, rash , coronary & aortic vasculitis  death
 Fibrinous pericarditis : post MI ¢ loud pericardial friction rub, chest pain,fever, symptoms of CHF
 Caseous pericardtitis TB
 Conn™s syndrome : hyperplasia of zona glomerulosa ¢ hypertension secondary to sodium retention ¢ hypokalemia ¢decreased serum rennin (negative feedback of increased blood pressure on rennin secretion)
 Secondary aldosteronism :increased levels of rennin ¢ due to renal ischemia
 Dermatitis herpetiformis : associated with celiac sprue ¢ type III hypersensitivity reaction ¢ immunocomplexes igA + complement
 Discoid lupus erythematosous : localized cutaneous form of SLE ¢ type III hypersensitivity reaction
 Urticaria : IgE mediated ¢ type I hypersensitivity
 ASD :prominent right ventricular cardiac impulse ¢ systolic ejection murmur heard in the pulmonic area & along the left sternal border ¢ fixed splitting of the 2nd heart sound
 Melasma :irregular patches of hyperpigmentation on the face ¢occurs in pregnancy ¢ may not regress
 Primary sclerosing cholangitis : beaded appearance on ERCP of biliary tree ¢
 Osteosarcoma : XRay : bone destruction /soft tissue with œsunburst appearance œ / Codman™s triangle (=periostal elevation) ¢ Histo : anaplastic cells with osteoid
 Exostoses (=osteochondromas), debaceous cysts, dermoid tumor™s, colonic polyps = Gardner™s
 Lymph node structure & disease :
a. Viral infection “ expansion of germinal centers without loss of normal architecture
b. AIDS “ progressive transformation of germinal centers ¢ not paracortical hyperplasia
c. Lymphomas “ destroy the architecture of the lymph node
 Complete hydatiform mole : elevated b-hCG ¢grape like cystic structures filling the uterus ¢ no embryo ¢ the genotype of a complete hydatiform mole is purely paternal (XY), caused by fertilization of an egg that has lost its chromosomes ¢ danger : choriocarcinoma
 Partial moles : triploidy / tetraploidy ¢ fertilization of an egg with two different sperm ¢ one with X & one with Y
 AFP : hepatocellular carcinoma ¢ yolk sac tumors ¢ embryonal tumors in men
 Irritable bowel syndrome : alternating constipation / diarrhea ¢ more common in young females ¢ no organic changes are evident
 Hypoaldosteronism :decrease in serum sodium increase in serum K+ ¢ retain of H+ ions  metabolic acidosis with low serum bicarbonate
 Bernard Soulier disease : prolonged BT ¢ normal PLT ¢ dysfunction in glycoprotein Ib-IX complex ¢ only treatment in acute emergency : transfusion of PLT™s
 Henoch-Schonlein : URI + purpura + abdominal pain + hematuria + child
 Cryoprecipitate would help in a case of vWF disease
 Hyaline droplets (dark staining droplets ) are found in the epithelium of PCT in cases of proteinuria
 Spongiosis : intercellular edema of the epidermis ¢ fluid accumulates between the cells, pulling the apart
 Adult form of aortic coarctation Confusedtenosis distal to the left subclavian artery ¢ collateral circulation by intercostal & internal mammary artery ¢notching of inferior margins of ribs ¢
 Infantile form of aortic coarctation is associated with patent ductus arteriosus
 Aortic stenosis : systolic hypotension throughout the body ¢ recurrent syncope ¢ hypertrophe / dilatation of LV
 Takayasu arteritis : a.k.a pulseless disease ¢ vasculitis of the aortic arch and its branches  stenosis of these arteries ¢ signs & symptoms of ischemia to the upper part of the body ¢ radial pulses are weak/ absent = pulseless disease
 Vascular proliferating skin lesions :hemangiomas ¢ Kaposi ¢ bacillary angiomatosis
 Malignant mixed mullerian tumor : tumor with 2 components : stromal & epithelial (endometrial glands) ¢ both are malignant but only the epithelial metastizes ¢ stromal component may contain metaplastic components such as cartilage & bone
 Endometrial carcinoma is derived form epithelial glandular component of endometrium ¢ abnormal bleeding is the usual presentation ¢
 Small parietal lobe abcesses : septic emboli from infective endocarditis
 Albinism & associated skin cancer : squamus cell carcinoma (multiple)
 Rheumatoid nodules are composed histologically of areas of fibrinoid necrosis surrounded by palisading epithelioid cells
 Thalassemia & sickle cell anemia do not usually present until about the 6 months of age ,when fetal hemoglobin production ceases
 Celiac disease : limited to proximal small bowel ¢ anti-gliadin antibodies ¢ granular deposits of IgA and C3 in dermal papillary tips ¢ gluten free diet as Rx ¢ tropical sprue affects the entire small bowel ( ETEC infection) ¢
 Basal cell carcinoma : œpearly papules on sun exposed skin ¢ almoste never metastize ¢ palisading of the cell nuclei ¢
 Resistance to thyroid hormone (Refetoff™s syndrome ): mutation in thyroid hormone receptor gene ¢ affects also the cells in pituitary  œno negative feedback  increased plasma TSH  increase in serum T4
 Low T3 syndrome (euthyroid sick syndrome) occurs with certain systemic illnesses such pneumonia or septicemia,afterm major surgery and with malnutrition or starvation ¢ decrease of 5™ monodeiodinase activity ¢ decreased levels of T3
 Addison™s disease : decreased secretion of cortisol, aldosterone and adrenal androgens ¢ hypotension may be present b/c arterioles are less responsive to the constrictor effects of catecholamines in the absence of cortisol ¢ hyperkalemia & hyponatremia due to lak of cortisol
 Nelson™s syndrome : usually post-adrenalectomy for Cushing ¢ extreme hyperpigmentation due to hypersecretion of ACTH from pituitary adenoma that is no longer being restrained by the supressibve effect of cortisol
 Head & neck (particularly nose,nasopharynx and orbit is the most frequent site for embryonal rhabdomyosarcoma ¢ other sites are the genitourinary tract
 Hereditary factor XIII deficiency :presentation at birth when the umbilical stump bleeds excessively ¢ factor XIII is necessary to stabilize clot formation ; in its absence clots will rapidly lyse ¢ spontaneous abortion in women is common
 Complications of MVP :atrial thrombosis, caclcification, infective endocarditis, emboli to the brain, rupture of chordae, mitral regurgitation,,arrythmias, and premature ventricular contractions
 Conn™s syndrome : hypertension, hypernatremia, hypokalemia, low rennin levels, metabolic alkalosis
 Vitamin K dependent factors : II (prothrombin), VII, IX, X, C, S ¢ deficiency in protein C would cause thrombosis NOT bleeding ¢ check hemorrhagic skin necrosis by warfarin
 Prostatic hyperplasia : periurethral zone
 Reye™s syndrome : fatty liver with encephalopathy ¢ Hx : viral illness, severe vomiting, irritability, hepatomegaly, elevation of serum ammonia ¢ aquired mitochondrial abnormality ¢may occur also without exposure to salicylates ¢ esp after influenza and cickenpox ¢ mortality rate 50%

Pharmacology “
 DMARDS for RA : MTX ¢ azathiprine ¢ penicillamine ¢hydroxycholroquine ¢ chloroquine ¢ organic gold compounds ¢ sulfasalazine
 Glucocorticoids SE : hypocalcemia, fluid retention, hypokalemia, hyperglycemia, hypernatremia , adrenal suppression, muscle weakness & atrophy, gastrtits, Cushingoid state, immunosuppression, hypertension, psychosis , osteoporosis, glaucoma, cataract
 N acetylcyteine : mucolytic used in CF to thin mucous ¢splits disulfide linkages between these mucoproteins  ↓ mucous viscosity
 Dextromethorphan is a cough depressant
 Pentamidine : used in HIV patients with PCP
 Metoclopramide Confusedtimulates motility of intestinal tract ¢ contraindicated in patients with bowel obstruction  danger for perforation
 Anticholinergic drugs : may precipitate attacks of narrow angle glaucoma b/c muscarinic receptors on the papillary constrictor muscle of the iris are blocked ¢ TCA™s “ imipramine, amitryptiline, nortriptyline, desipramine, clomipramine,doxepine- can do that !
 Decrease of blood levels of a drug : 1 half life  50 % ¢ 2 half lifes  25 % left in blood ¢ 3 half lifes  12,5 % left ¢ 4 half lifes  6,25% left in blood ¢ levels decrease by half every half life
 Retarded ejaculation : can be improved by admin a SSRI ¢ fluexitine, sertraline,citalopram, paroxetine.
 β-blockers are used in treatment of hypertrophic cardiomyopathy ¢ β1-blockers : atenolol, betaxolol, esmolol, acebutolol, metoprolol
 Bretylium : class III anti-arrythmic ¢ indicated for treatment of ventricular fibrillation and ventricular tachycardia
 Digoxin :used in atrial fibrillation ¢ atrial flutter ¢ CHF
 Lidocaine : class Ib antiarrythmic ¢ used in Rx of ventricular tachycardia
 Ventricular tachycardia : amiodarone ¢ bretylium ¢ lidocaine
 Succinylcholine : depolarizing skeletal muscle relaxant ¢ can cause hyperkalemia ¢ PR prolongation , widening of QRS , peaked T waves
 Acute interstitial nephritis : caused by ibuprofen, indomethacin, methicillin, cephalothin, sulfonamides,thiazides, furosemide, cimeridine,methyldopa ¢Clinical : ARF ( ↑ BUN, creatinine 0,6-1,2 ) fever, maculopapular rash, EOSINOPHILIA !, periorbital edema, wheezing
 Acarbose : delays glucose absoption from GI
 Metformin : causes lactic acidosis ¢ increases the binding of insulin to its receptor
 Oxybutynin : inhibits muscarinic action on smooth muscle (antimuscarinic action) ¢ Rx for bladder instability “ incontinence, persistent urinary urgency-
 Betanechol : used in urinary retention to contraction of detrusor muscle ¢
 Gabapentin : used to treat neuropathic pain in diabetic patients ¢ antiepileptic
 Primidone : anticonvulsant ¢ has two active metabolites 1) ohenobarbital 2) phenethylmalonamide ¢ associated with cross- hypersensitivity to Phenobarbital
 T3 therapy : increases serum T3 levels ¢ but NOT serum T4 b/c T3 is not converted peripherally to T4 ¢ TSH will be low due to feedback inhibition by T3 ¢ decrease of TSH causes also decrease in T4
 Salicylate intoxication : dizziness, tinnitus, hearing impairment , nausea, vomiting, hyperventilation , flushing, sweating, metabolic acidosis ¢ agents that acidify urine , such as NH4Cl are known dramatically decrease salicylate excretion and subsequently increase salicylic acid blood levels ¢ Rx : sodium bicarbonate, sodium lactate
 Jimson weed contains anti-muscarinic agents ¢ in overdose : agitation,mydriasis, hot dry skin, tachycardia , decreased bowel sounds
 Stimulants : best way to differentiate stimulatnt overdose from anticholinergic overdose is the skin ¢ sweaty  stimulants ¢ dry  anticholinergics
 Opioid intoxication : sleepiness, lethargy, miosis, cool skin , hypoventilation, hypotension, bradycardia, decreased bowel sounds ¢
 Cefoperazone : 3rd generation cephalosporin ¢can cause vitamin K deficiency ¢ disulfiram like reaction with alcohol ¢ DOC in people with impaired renal function b/c 60% is eliminated by the biliary route
 Ticarcillin : β”lactamase sensitive ¢ causes a large salt load  salt retention and hypokalemia
 Carbidopa blocks a pyridoxal dependent decarboxylase located in the mucosa of the GI tract and in systemic circulation
 Heparin is the most common cause of drug induced thrombocytopenia ¢risk for development thrombocytopenia increases as the duration of therapy increases (more than 10days e.g) ¢ no skin necrosis
 Warfarin & hemorrhagic skin necrosis : associated protein C deficiency in the patient ¢ presents on 3rd- 10th day of therapy ¢ may lead to necrosis of skin (typically on breast, thighs, and buttocks) ¢ heterozygote carriers for protein C become homozygote when given warfarin in 6~8 hrs when the half life of previously γ-carboxylated protein C disappears.Now the patient is hypercoagulable ¢ warfarin is used for prophylaxis and treatment of thromboembolic complications associated with cardiac valve replacement and atrial fibrillation, as well as the prophylaxis and treatment of venous thrombosis and pulmonary embolism ¢
 Aminoglycosides & nonoliguric RF : some patients develop a non-oliguric form of renal failure when treated with aminoglycosides such as gentamycin ¢ elevation of creatinine ¢
 Cephalothin/Methicillin interstitial nephritis : fever + rash + acute renal failure + eosinophilia
 Central pontine myelinolysis : demyelination affecting the central region of basis pontis ¢ in severe malnourished & dehydrated alcoholics ¢ from rapid correction of hyponatermia
 Hydrocarbon exposure  scrotal carcinoma
 Zolpidem : non-benzodiazepine ¢ hypnotic agent
 Buspirone : non-benzodiazepine ¢anxiolytic ¢ devoid of sedative ,hypnotic,anticonvulsant and muscle relaxant properties
 Obsessive compulsive disorder : clomipramine (TCA) or SSRI (e.g fluexitine)
 Nortriptyline  hyperplrolactinemia (methyl dopa, phenothiazines also)
 Diabetic with sulfa allergy : contraindicated sulfonylureas (chlorpropamide, tolbutamide,glyburide,glipizide)
 Methamphetamine : indirect- acting agonist ¢ acts inducing dopamine, NE, and 5HT release ¢ dopamine is believed to play an important role in the reward system of the brain and is thought to be a significant factor in the reinforcing effects of stimulants ( area involved in reward system : ventral tegmental area of midbrain to the nucleus accumbens of the forebrain)
 Hydrocortisone suppositories : indicated for treatment of distal ulcerative colitis ¢ sulfasalazine is also used in treatment of UC
 Metronidazole gold standard for pseudomembranous colitis ¢ vancomycin is another option
 Hyoscyamine : anticholinergic ¢ Rx : irritable bowel syndrome ¢ administered before the meal
 Prednisone for treatment of acute flare ups of Crohn™s
 Megestrol acetate & leuprolide : for prostate cancer ¢ GnRH analogs
 Cyclobenzaprine : centrally acting skeletal muscle relaxant ¢ structurally related to tricyclic antidepressants ¢ is has anticholinergic side effects ( blurred vision, urinary retention, constipation,tachycardia etc)
 Baclofen :centrally acting skeletal muscle relaxant ¢ inhibition of both monosynaptic and polysynaptic reflexes ¢ indicated for treatment of spasticity resulting from multiple sclerosis or secondary to spinal cord injuries ¢ also Rx for trigeminal neuralgia ¢ fatigue & hypotension
 Traveler;s diarrhea Rx : most cases of traveler™s diarrhea are caused by ETEC, Shigella species and Campylobacter jejuni ¢ treat with fluoroquinolones ( ciprofloxacin,ofloxacin, norfloxacin) ¢ TMP/SFX is used for children !
 Mebendazole : used for elminths such as Enterobius, Trichuris trichiura, Ascaris lumbricoides
 Diabetic with hypertension : ACE inhibitors ¢ ca2+ blockers
 Cefazolin & Cefadroxil : 1st generation cephalosporins ¢ used surgical prophylaxis
 SIADH & drugs : carbamazapine ¢ vincristine,vinblastine ¢ cyclophosphamide ¢ chlorpropamide ¢ TCA




Physiology “
 Glycoprotein hormones : EPO, LH, FSH, hCG, TSH ¢ bind at cell surface receptors ↑ cAMP levels
 Catecholamine hormones : epinephrine, norepinephrine, dopamine
 Oligopeptide hormones : endorphins, ADH, oxytocin, TRH, GnRH, SS, CCK, secretin, VIP, GIP
 Polypeptide hormones : PTH, calcitonin, insulin, glucagons, pancreatic polypeptide, gastrin, ACTH, IGF™s, EGF, FGF, NGF
 Baroreceptor reflex (patient stands up from supine condition) :patient stands up  less blood to brain  less firing to baroreceptors  sympathetic stimulation  increase in HR, conduction velocity and myocardial contractility  constriction of all arterioles  ↑ TPR  sympathetic stimulation of renal vasculature  decrease in renal blood flow  constriction of large veins  increases venus return to the heart  ↑ preload
 Transcutaneous electrical nerve stimulation is a method used to lessen severe,chronic pain by overly stimulating the involved neurons ¢ gate theory of pain

GL
* My experience its long
#340067
drkyhasan - 09/19/08 08:19

Hi guys I am back with my experience albeit after quite a whileSmile sorry for that.
Anyway I started studying in February for the step 1. Gave 8-12 hours to the study material every day. My resources:

Kaplan lecture notes
Goljan for pathology

Regarding Kaplan DVDs I did biochem, anatomy, physiology, BS, pharma and immunology. I think doing them did help me a lot esp the biochem BS and anatomy. I did Goljan audio once but never completed them. I used a lot of other stuff but I guess these helped me the most. I had done both BRS and KAplan patho before i started on goljan and i think that was the best thing i did. Regarding MCQs I did all i got my hand on
Kaplan Qbank 85% subject wise
UWORLD 68% timed mixed
NBME 1 offline 154
NBME 2 offline 171
NBME 3 offline 168
NBME 4 offline 170

I gave about 3-4 reads to all subjects. I did not do First Aid I believe it is a waste of time and has too many mistakes in it totaling upto 8 pages!!!!!!!!!!!! I did Qbook about 65% and scored between 75-90% questions correctly on each block. I also did Robbins review of pathology MCQ book which is awesome. It is the best really
Week before exam i crammed up everything i got my hands on did not do any structured reading but did study goljan again. I revised some questions from uworld and kaplan qbank. Day before exam I studied till 10 pm. Took a light meal took lexotanil and still managed to sleep at 2amSmile but it was enuf. on my way to prometric center as my brother was driving I revised CTs and MRIs from WebPath, yes i did webpath too. and also goljan images. I got to the center half an hour early. started myfirst block which was horrible i think. this was nothing like i had imagined. Had a lot of blocking too. had 1 Audio visual question at the end which i missed. took a 5 min break. went to the toilet took a bite of sandwich i had taken took a gulp of redbull and started the 2nd block. It went well. from then on took 5 min breaks after every block and managed to finish all blocks before time. took a longer break after block 5 and prayed Zuhr namaz. block 7 was really tough. gave the survey and went out of the exam hall. Had no idea how the exam went. the next 3 weeks i tried to study step 2 CK Internal medicine and did Kaplan Qbank for CK but without any concentration.
Got my result on the 17th and it was beautiful. 243/99


Factors that determine ur success in this exam:
1) Pray to GOD as much as u can
2) Take ur parents blessings and make sure they are happy with u
3) Find a suitable life partner, getting married before starting the prep was the best thing i did
4) Study and study well.

Material u need:
1) Goljan audio and Goljan Rapid review is a must
2) Kaplan lecture notes are enuf for everything else
3) DO as many MCQs as u can uworld, kaplan qbank, qbook, robbins review mcqs of pathology etc etc. it really helps this forum really helped a lot man the questions were awesome.

Lastly help others and stay happy

well, thanx for every one there, specailly those sent me those supportive regards,,,,,,,,,,,,
just to make the long stroy short: honestly and honestly and honestly the exam was easier than i was expect, you are expect to be asked in everything.
now my advice, yes i didn't have enough time to study every thing bce i had only 4 mons,......
focus on usmle world and study their explanation well, believe me exam more easier than usmle world and i mean what iam saying.
practice on the increase - decrease arrows ( like in aldosteron-renin , TSH-t4-t3, BP , estrogen -progesteron, etc).
CT scans of head (know all of them).
now big topics i had: molecular biology, genetics AND oncology.
pharmacology: non even unfamiliar question, all striaght forwards.
micrology:was few, mostly slides (i had 2 one coccidio and blasto typical), others were to treat and how transmitted.
immunology:was big topic know everything.
physiology: focus on respiratory(obst and rest) and cardiac(electrolytes trasports via mb).
behavioral:most qs were ethic, some about personality dis, anorexia, child development.
pathology: big topics were hema,resp,musclo and ONCOLOGY.(each block you have at least 20 qs pathology).
anat, hist and cyto: which i didn't study they were very easy i swear, but i really missed them, most qs were about fracture and nerve injuired, blood supply, for me those qs were hard.
(but infact they are easy).
well, that all for the moment, soon i will post some of the qs i had, wish you all the best.
GLLLLLLLLLLLLLLLLLLLLLLLLLLLLLLLLLLL

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nuroanatomy HY


1. A spinal cord disorder should be considered in any patient with bilateral motor and sensory dysfunction in the extremities in the absence of signs or symptoms of brain or brainstem dysfunction.
2. Spinal cord compression due to epidural metastasis is a neurologic emergency for which urgent MRI of the entire spine is appropriate.
3. Vertebral artery dissection typically presents with neck or head pain, Horner's syndrome, dysarthria, dysphagia, decreased pain and temperature sensation, dysmetria, ataxia, and vertigo.
4. Magnetic resonance angiography is a sensitive diagnostic test for vertebral artery dissection as a cause of stroke.
5. Juvenile myoclonic epilepsy is a primary, genetic, generalized epilepsy that typically manifests with myoclonic jerks followed by a generalized tonic“clonic seizure
6. Guillain“Barré syndrome is characterized by proximal and distal weakness, autonomic symptoms, cranial nerve involvement, and respiratory failure.
7. Treatment of Guillain“Barré syndrome with either intravenous immunoglobulin or plasmapheresis is indicated in patients who cannot walk independently or who have impaired respiratory function or rapidly progressive weakness.
8. Small, stable, asymptomatic meningiomas can be followed with serial neuroimaging.
9. In large, symptomatic, or progressive meningiomas, surgical resection offers an 80% chance of cure.
10. Personality change, lost initiative, and slowing of thought, with relative preservation of recent memory, suggest frontotemporal dementia.
11. Frontotemporal dementia is usually associated with disproportionate atrophy of the anterior frontal and temporal lobes, a finding that is usually clearly demonstrated on MRI.
12. Elevation of the cerebrospinal fluid 14-3-3 protein in a patient with rapidly progressive dementia and normal structural imaging suggests Creutzfeldt“Jakob disease.
13. Treatment with interferon-beta decreases the incidence of additional attacks in patients with monosymptomatic demyelination, including optic neuritis and myelopathy.
14. Propranolol and primidone are first-line drugs in the treatment of essential tremor (postural and action tremor).
15. The diagnosis of Parkinson's disease requires the presence of at least two of the following: tremor at rest, bradykinesia, rigidity, and postural reflex abnormality.
16. The characteristics of migraine headache without aura include worsening of the headache with movement, limitation of activities, and photo- and phonophobia
17. Transverse myelitis is an acute or subacute demyelinative or inflammatory disorder of the spinal cord that causes motor, sensory, and autonomic dysfunction below a spinal cord level.
18. High-dose intravenous corticosteroids are indicated for initial treatment of acute transverse myelitis.
19. Secondary prevention of cardioembolic stroke consists of warfarin with a target INR of 2.0 to 3.0.
20. Heparin has no established role in the acute treatment of stroke.
21. The manifestations of partial seizures depend on their neuroanatomic location.
22. Frontal seizures are brief and are usually not associated with aura or postictal confusion.
23. Hereditary sensorimotor neuropathy is an autosomal dominant disorder that usually presents with clumsiness or difficulty running in the first decade of life.
24. Hereditary sensorimotor neuropathy is characterized by distal muscle atrophy, weakness, and sensory loss associated with high arches (pes cavus) and hammertoes
25. Cell type and tumor grade are the most important determinants of survival in glioma.
26. Higher-grade gliomas are more aggressive than lower grade.
27. Alzheimer's disease is characterized by primary dementia with prominent amnesia.
28. Dementia with Lewy bodies, characterized by fluctuating cognition, parkinsonism, and/or visual hallucinations, often coexists with Alzheimer's disease.
29. All patients with relapsing multiple sclerosis should be considered for immunomodulatory therapy with either a form of interferon-beta or glatiramer acetate.
30. Adult-onset idiopathic dystonia is usually focal or segmental and does not generalize to other parts of the body.
31. Botulinum toxin injections can correct the abnormal posture and alleviate the pain associated with cervical dystonia.
32. Approximately 20% of patients with migraine have headache with aura, that is, neurologic problems such as visual hallucinations or numbness or tingling before or during headache.
33. Lhermitte's sign, an œelectric shock“like sensation down the neck, back, or extremities occurring with neck flexion, is a helpful historical clue to a cervical spinal cord disorder.
34. Cervical spondylosis is a chronic disorder of degenerative and hypertrophic changes of the vertebrae, ligaments, and disks that may narrow the spinal canal and cause cervical spinal cord compression.
35. In patients with stroke not eligible for thrombolytic therapy, aspirin modestly reduces both the short-term risk of recurrent stroke and the long-term risk of stroke-related death and disability.
36. In patients with acute stroke, thrombolytic therapy must be started within 3 hours of the onset of symptoms or of the time the patient was last known to be well.
37. Elderly patients may be particularly sensitive to the cognitive, motor, and coordination side effects of phenytoin, even if the serum phenytoin level is in the therapeutic range.
38. Gabapentin, lamotrigine, and carbamazepine are equally effective at controlling partial onset seizures in the elderly, but gabapentin and lamotrigine are better tolerated.
39. Peripheral nervous system vasculitis usually presents with asymmetric weakness and sensory loss in specific nerve distributions.
40. In an elderly patient with recurrent glioblastoma and poor performance status, referral for hospice care is preferable to additional antitumor treatment.
41. The three specific criteria for dementia with Lewy bodies are fluctuating encephalopathy, parkinsonism, and visual hallucinations.
42. A centrally acting anticholinesterase agent may alleviate the inattention, hallucinations, and fluctuating encephalopathy of dementia with Lewy bodies.
43. Women taking immunomodulatory treatment for multiple sclerosis should use effective contraception, or if they want to become pregnant, stop therapy several months before attempting to conceive.
44. Involuntary brief, irregular, unpredictable movements fleeting from one body part to another are hallmarks of chorea.
45. Chorea can occur as a hereditary and degenerative disease or secondary to drugs, metabolic disorders, infections, immune-mediated diseases, and vascular lesions.
46. Tension-type headache is distinguished from migraine by the fact that patients with tension headache are not disabled and can carry out activities of daily living in a normal, expedient manner.
47. Vitamin B12 deficiency can cause dysfunction of the posterior columns and corticospinal tracts of the spinal cord, causing paresthesias, loss of vibration and position sense, sensory ataxia, weakness, and upper motor neuron signs.
48. Neurologic signs of vitamin B12 deficiency may manifest in the absence of hematologic signs of vitamin B12 deficiency.
49. In a patient with a transient ischemic attack, carotid artery ultrasonography showing a >50% stenosis of the internal carotid artery may be an indication for carotid endarterectomy.
50. A single antiepileptic drug should be used in pregnant women with epilepsy; multiple drug therapy increases the risk for birth defects.
51. Chronic inflammatory demyelinating polyneuropathy, the chronic form of Guillain“Barré syndrome, is characterized by proximal and distal weakness, areflexia, and distal sensory loss.
52. Chronic inflammatory demyelinating polyneuropathy progresses in a stepwise or relapsing course for at least 8 weeks and can occur early in the course of HIV infection.
53. In a young patient with totally resected low-grade glioma, postsurgical management consists of observation with serial neuroimaging.
54. Vascular dementia is suggested by a history of vascular risk factors, abrupt onset with subsequent improvement, periventricular white matter ischemia on imaging, and focal neurologic findings.
55. Intravenous methylprednisolone therapy followed by an oral prednisone taper speeds recovery of visual acuity in optic neuritis
56. The restless legs syndrome consists of abnormal sensations in the legs and restlessness relieved by movement.
57. Patients are at risk for developing analgesic overuse headache if they use prescription or over-the-counter medication for headache more than 2 days a week.
58. Pseudotumor cerebri is characterized by papilledema, postural change with headache, visual changes, recent report of rapid weight gain, or introduction of oral contraceptives or tetracycline.
59. Infarction of the spinal cord typically presents as sudden spinal cord dysfunction.
60. Spinal cord infarction usually affects the territory of the anterior spinal artery, causing weakness and pinprick loss of sensation with sparing of vibration and position sense.
61. CT scan may miss subarachnoid hemorrhage, especially when there is a delay in presentation after the initial hemorrhage.
62. Focal neurologic symptoms 3 to 7 days after a subarachnoid hemorrhage may be due to vasospasm with cerebral ischemia.
63. Patients with epilepsy who are most likely to remain seizure free after medication withdrawal are those with no structural brain lesion, no epileptiform or focal abnormalities on electroencephalogram, a sustained seizure-free period, and no abnormalities on neurologic examination.
64. Patients with epilepsy who discontinue antiepileptic medication should stop driving for at least 3 months and preferably 6 months from the start of the taper.
65. Critical illness polyneuropathy is a common cause of failure to wean from a ventilator in a patient with associated multiorgan failure and sepsis.
66. Critical illness polyneuropathy is characterized by generalized or distal flaccid paralysis, depressed or absent reflexes, and distal sensory loss with sparing of cranial nerve function.
67. Patients with primary central nervous system lymphoma should be evaluated for vitreal or uveal involvement before therapy is begun.
68. Aggressive resection is not recommended in primary central nervous system lymphoma; methotrexate chemotherapy is primary therapy.
69. Donepezil, an acetylcholinesterase inhibitor, may cause mild peripheral cholinergic side effects, including increased vagal tone, with bradycardia, and occasionally atrioventricular block.
70. In at least 50% of patients with relapsing“remitting multiple sclerosis, disease will evolve to a secondary progressive course.
71. In at least 50% of patients with relapsing“remitting multiple sclerosis, disease will evolve to a secondary progressive course.
72. Metoclopramide, which blocks dopamine receptors both in the periphery and inside the central nervous system, can induce parkinsonism.
73. Prednisone is the most appropriate treatment for episodic cluster headache.
74. Acute cervical spinal cord compression due to hyperextension injury is common in elderly patients.
75. Emergent MRI of the cervical spinal cord is indicated in any patient with quadriparesis after a fall.
76. The classic symptoms of cerebellar stroke are headache, vertigo, and ataxia.
77. Patients with epilepsy who fail to respond to three trials of antiepileptic drugs are unlikely to ever become seizure free with drug therapy.
78. Treatment-resistant patients with epilepsy should be evaluated for a surgically remediable epilepsy syndrome.
79. Myasthenia gravis is an autoimmune disease caused by antibodies against the acetylcholine receptor, which results in impaired neuromuscular transmission.
80. Myasthenia gravis is characterized by fatigable weakness with a predilection for ocular, bulbar, proximal-extremity, neck, and respiratory muscles.
81. Leptomeningeal spread of systemic carcinoma manifests as a cranial neuropathy or spinal polyradiculopathy, or as encephalopathy, diffuse brain infiltration, or communicating hydrocephalus.
82. Creutzfeldt“Jakob disease is suggested by subacute progression of dementia with myoclonus and other motor signs and a normal brain MRI.
83. In the setting of subacutely progressive dementia, the presence of 14-3-3 protein in cerebrospinal fluid, or electroencephalography showing periodic sharp waves, can be diagnostic of Creutzfeldt“Jakob disease.
84. Mitoxantrone therapy is of modest benefit in slowing progression of secondary progressive or severe relapsing“remitting multiple sclerosis.
85. The primary concern about mitoxantrone therapy is the risk for cardiotoxicity.
86. Progressive supranuclear palsy is characterized by parkinsonism with early gait and balance involvement, vertical gaze palsy, severe dysarthria, and dysphagia.
87. Normal pressure hydrocephalus is characterized by the classic triad of gait impairment, cognitive decline, and urinary incontinence.
88. Patients with idiopathic intracranial hypertension present with signs and symptoms of increased intracranial pressure without a mass lesion on brain imaging.
89. In patients with possible idiopathic intracranial hypertension, a diagnostic and potentially therapeutic lumbar puncture is indicated after brain imaging excludes a mass lesion.
90. Severe cerebral anoxia from cardiac arrest can cause severe diffuse cerebral hemispheric cortical injury with relative preservation of brainstem function, leading to the development of a vegetative state.
91. A vegetative state is a condition of complete unawareness of self or the environment, accompanied by sleep“wake cycles and preservation of brainstem and hypothalamic functions.
92. Intracerebral hemorrhage with extensive subarachnoid hemorrhage is the hallmark of a ruptured arteriovenous malformation.
93. Conventional angiography is the definitive diagnostic procedure for detecting arteriovenous malformations and berry aneurysms.
94. In a patient with status epilepticus, after the airway is stabilized and plasma glucose determined to be normal, parenteral antiepileptic medications should be started.
95. Lorazepam is the preferred benzodiazepine for initial therapy for a patient in status epilepticus.
96. Myasthenia gravis crisis is characterized by dysphagia requiring nasogastric feeding and/or severe respiratory muscle weakness necessitating ventilation.
97. Myasthenia gravis crisis is treated with either plasmapheresis or intravenous immunoglobulin.
98. Radiation-induced leukoencephalopathy is a subcortical process affecting white matter and characterized by the triad of gait apraxia, dementia, and urinary incontinence.
99. Radiation-induced leukoencephalopathy may occur months to years after radiation and is more common after whole-brain compared with focal brain irradiation.
100. Mild cognitive impairment consists of isolated mild amnesia with no impairment of interpersonal, occupational, or daily living activities.
101. The conversion rate from mild cognitive impairment to mild dementia is 10% to 15% per year.
102. Amantadine is the first-line pharmacologic agent for treatment of multiple sclerosis-related fatigue.
103. Multiple system atrophy is characterized by orthostatic hypotension, neurogenic bladder, constipation, and impotence, with gait-predominant parkinsonism and corticospinal tract signs.
104. Carbamazepine is the appropriate treatment for trigeminal neuralgia.
105. Patients with the locked-in syndrome are quadriplegic, have paralysis of horizontal eye movements and bulbar muscles, and can communicate only by moving their eyes vertically or blinking.
106. The locked-in state is due to a lesion of the base of the pons, usually from pontine infarction due to basilar artery occlusion.
107. Antiplatelet therapy, statins, and ACE inhibitors each reduce the risk of recurrent stroke even in the absence of chronic hypertension or a lipid disorder.
108. Headache may be a limiting factor in the use of the combination of aspirin and extended-release dipyridamole for secondary stroke prevention.
109. Nonepileptic seizures of psychogenic origin can be differentiated from epilepsy by their longer duration, normal electroencephalogram findings, and maintenance of consciousness.
110. Nonepileptic psychogenic seizures are often associated with moaning, crying, and arrhythmic shaking of the body.
111. Absence seizures are characterized by a brief loss of awareness with no movement or very subtle movements of the lips and fingers.
112. Juvenile myoclonic epilepsy is characterized by myoclonic seizures and often accompanied by absence and generalized tonic“clonic seizures.
113. Amyotrophic lateral sclerosis is characterized by pathologic hyperreflexia, spasticity, extensor plantar responses, along with atrophy, fasciculations, and weakness.
114. Muscle weakness in amyotrophic lateral sclerosis usually begins distally and asymmetrically in the upper or lower extremities or may be limited initially to the bulbar muscles, resulting in dysarthria and dysphagia.
115. Surgical resection is indicated for an accessible solitary brain metastasis in patients with limited or no systemic tumor.
116. Cholinesterase inhibitors have modest efficacy on cognitive and global function in mild to moderate Alzheimer's disease.
117. Vitamin E and selegiline may delay the progression of Alzheimer's disease, but do not alleviate cognitive or psychiatric symptoms.
118. In patients with possible multiple sclerosis, new MRI white-matter lesions or new gadolinium-enhancing lesions on serial brain or spinal cord MRI at least 3 months after an initial scan, indicate dissemination of demyelination, even without a new clinically evident attack.
119. Carbidopa-levodopa is the first-line treatment for patients older than 70 years with new-onset Parkinson's disease.
120. Complications associated with the use of dopamine agonists, such as somnolence, drug-induced psychosis, and dizziness, are more common in patients older than 70 years.
121. The risk of rupture of a small intracranial aneurysm is less than the risk of complications with clipping or endovascular coiling of the aneurysm.
122. Incidentally discovered small aneurysms should be re-evaluated periodically for enlargement.
123. Oxcarbazepine is effective monotherapy for partial onset seizures.
124. Risk factors for recurrent seizures include multiple previous seizures, a history of significant head trauma, focal electroencephalogram abnormalities, and structural abnormality on MRI.
125. Amyotrophic lateral sclerosis causes progressive respiratory muscle weakness that may present with supine dyspnea, frequent arousals, daytime fatigue, or morning headache.
126. Noninvasive positive-pressure ventilation should be started in patients with amyotrophic lateral sclerosis whose forced vital capacity is
Concepts everyone should know.
#324940
suportboy - 08/02/08 23:56

-Recognize Wolf-Parkinson-White on EKG i.e recognize "delta" wave. WPW is due to an accessory conduction pathway which bypasses the AV node.
-Know that the "J" wave is secondary to hypothermia. Patient will have a temperature usually below 95 degrees.
-Recognize ST elevation MI on an EKG and know the various treatments i.e Tissue Plasminogen Activator, PCA etc.
-Recognize pulsus/electrical alternans on EKG and know the pathophysiology.
-Recognize AV blocks on EKG; all of them.
-Recognize atrial fibrillation on EKG. In a hemodynamically stable patient the treatment of choice is rate control. Anti-coagulation is either with Aspirin or Warfarin depending on the patient's age and the following comorbidities: CHF, HTN, DM, and stroke.
* took exam today
#317639
ultradocmansu - 07/10/08 11:40

hi guys.. i took the exam today..
its not that hard an exam.. jus stay calm and go take it.. but it needs alot of basic knowledge and thats what they really test. so donot leave basic chapters of any subject..
for my exam

-- anatomy and histo was tested, embryo was not

-- reproductive system was heavily tested

-- questions were long , typically concentrated in one or 2 blocks often 6-7 liners , so that they can screw us on time in those blocks
-- autonomic pharmacology , and overall pharmacology was considerably tested

--goljan is high yield

-- respiratory system pahophysio was heavily tested , with all graphs , acid base stuff

-- ethics and behavioral were heavily tested. ethics , as usual clueless, and remaining disorders were high yield
-- biostats was toughly constructed.. some questions were intermingled with genetics , probabilities and stuff

--genetics itself was tough , but doable..

-- receptors and stuff..
-- immunology was considerably around too.. with brain teasers here and there

----expected but not tested topics

-- much of patho was not tested
-- metabolisms , hardly 4-5 qs

suggestions - improve ur stamina , many questions r thoughtfully constructed , while our mind simply stops thinkin after first 3-4 blocks..
improve reading habit , fast reading is required without getting tired..
concepts r required to be dugged in our mind.. they should always be present , even if we have gone 5 hrs tired of 250 questions , we should still be able to interpret graphs and feedbacks , as they coin all this stuff from top of their heads.. u require alot of thinking.. so, improve stamina of solving questions..
try to be calm thru out exam.. many questions u r not expected to know.. and its useless to think that we can ever know them..
nbme concepts r high yield
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