Some imp topic review.. - medicalspirit

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http://www.pharmacology2000.com/Cardio/C...atomy6.htm

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Charcot-Bouchard pseudoaneurysms (CBA) are tiny expansions of arterioles in the small arteries of the brain that perfuse the basal ganglia or internal capsule. It is normally due to hypertension as increased blood pressure induces hyaline atherosclerosis of tiny arterioles most commonly in the basal ganglia. The vascular walls of the small arteries become weakened and prone to dilatation which expand to form (CBA). The aneurysms often at times may rupture causing small amounts of bleeding or production of a hematoma.

It must be differentiated from another kind of brain aneurysm known as Berry (Saccular) aneurysm. (BA)

CBA: assiciated with hypeterntion, located in small arteries supplying basal ganglia and internal capsule,less than 1mm in size, rupture results in intracerebral hemorrhage in the areas if basal glanglia, internal capsule, thalamus and pons. Symptoms include sudden onset of focal deficites which usually helps differenctiates it from saccular aneurysm which has neurologic symptoms that only appear later not sudden.

BA: associated with ADPKD, marfan and ehlers danlos. Located in the circle of Willis esp around anterior and posterior communicating arteries. Size varies btw 2-25mm, rupture produces sub arachnoid hemorrhage which affects the bridging veins. Symptoms include sudden onset headache and altered level of consciousness with prominent neurological deficits occurring later.

Note: you can read more from 2009 FA pg 383 or 2010 FA pg 401

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http://tube.medchrome.com/2011/05/draw-t...eliac.html

http://www.scioly.org/phpBB3/viewtopic.p...&start=240

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http://www.learningradiology.com/archive...orrect.htm

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Clinical Considerations of Upper Limb
http://home.comcast.net/~wnor/clinicalco...ations.htm


Clinical Considerations of lower limbs:
http://www.docstoc.com/docs/72628427/Cli...ower-limbs

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Deep Tendon Reflexes

Reflex Main Spinal Nerve Roots Involved
Biceps C5, C6
Brachioradialis C6
Triceps C7
Patellar L4
Achilles Tendon S1


Deep Tendon Reflexes Root Supply (nursery rhyme)
One, two-- buckle my shoe.
Three, four-- kick the door.
Five, six-- pick up sticks. S
Seven, eight-- shut the gate.

S1,2 = ankle jerk
L3,4 = knee jerk
C5,6 = biceps and brachioradialis
C7,8 = triceps

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Muscles Inserting into Humerus
"A lady between two majors"
Pectoralis major attaches to lateral lip of bicipital groove, the teres major attaches to medial lip of bicipital groove, and the latissimus dorsi attaches to the floor of bicipital groove. The "ladt" is between two "majors"


Radial Nerve Innervations
"BEST": Brachioradialis, Extensors, Supinator, Triceps.


Median Nerve Innervations
"2LOAF": Lateral 2 Lumbricals, Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis.



Hip Lateral Rotators (Femur Greater Trochanter Attachments)
“P-GO-GO-Q”: Piriformis Gemellus superior Obturator internus Gemellus inferior
Obturator externus Quadratus femoris



Vagal Nerve Path Into Thorax
“Not Left Behind”: Left is anterior (not behind), Right is posterior
Lung Vessels
“RALS”: Right lung artery is Anterior to broncus, Left lung artery is Superior to broncus

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*Serratus anterior: innervation and action "C5-6-7 raise your arms up to heaven":
Long thoracic nerve roots (567) innervate Serratus anterior.
· Test C567 roots clinically by ability to raise arm past 90 degrees.


* Ureter to ovarian/testicular artery relation "Water under the bridge":
The ureters (which carry water), are posterior to the ovarian/testicular artery.
· Clinically important, since a common surgical error is to cut ureter instead of ovarian artery when removing uterus.

* Carpal tunnel syndrome causesMEDIAN TRAP: Myxoedema Edema premenstrually Diabetes Idiopathic Agromegaly Neoplasm Trauma Rheumatoid arthritis Amyloidosis Pregnancy ·

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http://highered.mcgraw-hill.com/sites/00...ction.html


2010Fa 373

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Is OA simply a process of aging of cartilage?
A critical question is whether OA is truly a disease or a natural consequence of aging. Several differences between aging cartilage and OA cartilage have been described, suggesting the former. For example, although denatured type II collagen is found in both normal aging and OA cartilage, it is more predominant in OA. In addition, OA and normal aging cartilage differ in the amount of water content and the in ratio of chondroitin-sulfate to keratin sulfate constituents. The expression of a chondroitin-sulfate epitope (epitope 846) in OA cartilage, that is otherwise only present in fetal and neonatal cartilage, provides further evidence that OA is a distinct pathologic process. A final but important distinction is that degradative enzyme activity is increased in OA, but not in normal aging cartilage.
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What molecules are responsible for degrading cartilage matrix?
The primary enzymes responsible for the degradation of cartilage are the matrix metalloproteinases (MMPs) (slide). These enzymes are secreted by both synovial cells and chondrocytes and are categorized into three general categories: a) collagenases; b) stromelysins; and, c) gelatinases. Under normal conditions, MMP synthesis and activation are tightly regulated at several levels. They are secreted as inactive proenzymes that require enzymatic cleavage in order to become activated. Once activated, MMPs become susceptible to the plasma-derived MMP inhibitor, alpha-2-macroglobulin, and to tissue inhibitors of MMPs (TIMPs) that are also secreted by synovial cells and chondrocytes. In OA, synthesis of MMPs is greatly enhanced and the available inhibitors are overwhelmed, resulting in net degradation. Interestingly, stromelysin can serve as an activator for its own proenzyme, as well as for procollagenase and prostromelysin, thus creating a positive feedback loop of proMMP activation in cartilage.
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What factor(s) is responsible for inducing metalloprotease synthesis?
One candidate is interleukin-1 (IL-1). IL-1 is a potent pro-inflammatory cytokine that, in vitro, is capable of inducing chondrocytes and synovial cells to synthesize MMPs (slide). Furthermore, IL-1 suppresses the synthesis of type II collagen and proteoglycans, and inhibits transforming growth factor-ß stimulated chondrocyte proliferation. The presence of IL-1 RNA and protein have been confirmed in OA joints. Thus, IL-1 may not only actively promote cartilage degradation, but may also suppress attempts at repair, in OA. In addition to these effects, IL-1 induces nitric oxide production, chondrocyte apoptosis, and prostaglandin synthesis, which further contribute to cartilage deterioration. Under normal conditions, an endogenous IL-1 receptor antagonist regulates IL-1 activity. A relative excess of IL-1 and/or deficiency of the IL-1 receptor antagonist could conceivably result in the cartilage destruction that is characteristic of OA. It is likely that other cytokines or particulate material from damaged cartilage may also contribute to this inflammatory, degradative process.


http://www.ihaveosteoarthritis.com/resou...2819426312


http://www.hopkins-arthritis.org/arthrit...ology.html