My some review points and images before exam. - medicalspirit

[ArchivalUser]

Disseminated Intravascular Coagulopathy in Acute Promyelocytic Leukemia:

http://www.medscape.com/viewarticle/583101

* DIC results from the activation of the virtually unregulated coagulation cascade, characterized by the generation of thrombin with fibrin deposition within the micro- and macrovascular systems (i.e., multiple thrombi), combined with a hemorrhagic diathesis. The counteraction by the fibrinolytic cascade is variable and is characterized by the conversion of plasminogen to plasmin, the latter functioning as a potent proteolytic enzyme, capable of degrading fibrinogen, fibrin, and several clotting factors. The kinin and complement cascades also partake in the promotion of DIC. In addition, antithrombin (AT), proteins C and S, antiplasmin, and plasminogen activator inhibitor 1, play a functional role in curtailing the activation of the coagulation and fibrinolytic mechanisms, but they too may be affected by the DIC process, particularly because a marked decrease in AT takes place in severe cases.

* lab findings of DIC include elevation of D-dimer (a product of lysed fibrin), fibrinogen degradation products (FDP), as well as prolongation of prothrombin time (PT), partial thromboplastin time (PTT), and thrombin time, accompanied by thrombocytopenia and hypofibrinogenemia (noted mostly in obstetrical cases). Because some of these assays are not specific for the diagnosis of DIC, we propose the use of a new, simple, and cost effective panel: D-dimer, FDP, and AT. Elevations in FDP and D-dimer are sensitive for the diagnosis of DIC and a marked drop in AT establishes a poor prognosis.

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http://medsci.indiana.edu/c602web/602/c6...ide135.htm

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Angiotensin Converting Enzyme (ACE) Inhibitors: PRIL's

* 1. Cause (dry) cough by inhibiting the degradation of bradykinin:
ACE breaks down bradykinin ( vasodilator substance). Therefore, ACE inhibitors like captoPRIL, by blocking the breakdown of bradykinin, increase bradykinin levels, which can contribute to vasodilator action of ACE inhibitors. Increase in bradykinin = cough
(also remember: angioedema point UW image)

*2. ACE Inhibitors ecrease the RISE in Aldosterone due to lowering of Angiotensin 2 .. As a result Sodium resorption with small rise in Serum potasium.

*3. ACE Inhibitors: Prevent EFFerent arteriolar constriction which is done by Angiotensin 2 (more than afferent) therefore decrease GFR; discontinue ACE Inhibitors if renal function worsens.

http://www.cvpharmacology.com/vasodilator/ACE.htm
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* Angiotensin 2 constricts EFFerent arterioles ; ACEI DILATE EFFerent arterioles and can cause Acute renal failure.

* PG's DILATE Afferent arterioles ; NSIAD's constrict afferent arterioles and can cause ARF.

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*2. ACE Inhibitors ecrease the RISE in Aldosterone due to lowering of Angiotensin 2 .. As a result
DECREASE in Sodium resorption with small rise in Serum potasium.

[ArchivalUser]

*Sinus bradycardia and ECG signs of hypokalemia : (U waves in leads II, V-2, V-3, and V-4, progressive flattening of T waves and depression of ST segment) may appear when the serum potassium falls below normal. Prolongation of the PR and QT intervals and T-wave flattening are associated with prominent U-waves.


http://i.quizlet.com/i/z-hOUHlYNWtJNSM7AERtQQ_m.jpg

* Thiazide diuretic develop hypokalemia bc. they induce volume depletion ; Stimulate formation of Angiotensin 2 = leading to increase in plasma aldosterone, which stimulates potassium excretion...

[ArchivalUser]

Acetazolamide carbonic anhydrase (CA) inhibitor, is commonly used for the amelioration of acute mountain sickness (AMS). acetazolamide's efficacy has been attributed to inhibition of CA in the kidneys, resulting in bicarbonaturia and metabolic acidosis. The result is offsetting hyperventilation-induced respiratory alkalosis and allowance of chemoreceptors to respond more fully to hypoxic stimuli at altitude.

*Acetazolamide significantly increase minute ventilation is due predominantly to an increase in tidal volume and not due to an increase in respiratory frequency

*It improves arterial PO2 (PaO2) and oxyhemoglobin saturation

http://jap.physiology.org/content/102/4/1313.full

http://en.wikipedia.org/wiki/Acetazolamide

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carbonic anhydrase inhibitor: Acetazolamide= in treatment for Acute angle closure glaucoma- decreases HCO3 availability and leads to Decrease aqueous humor production; it can lead to Metabolic ACIDosis = decrease HCO3 with low pH.

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http://library.med.utah.edu/WebPath/CVHTML/CV041.html

http://library.med.utah.edu/WebPath/CVHTML/CV042.html

splinter hemorrhages in a patient with infective endocarditis:

http://library.med.utah.edu/WebPath/CVHTML/CV105.html

http://library.med.utah.edu/WebPath/CVHTML/CV106.html

Osler's Nodes: Painful, erythematous nodules associated with bacterial endocarditis:
http://meded.ucsd.edu/clinicalimg/skin_oslers_nodes.htm

Janeway lesions

In contrast to Osler nodes, Janeway lesions are non-tender, often haemorrhagic (bleeding into the skin), and occur mostly on the palms and soles including the thenar and hypothenar eminences (at the base of the thumb and little finger respectively). They tend to last days to weeks before healing totally. They are more commonly seen in acute endocarditis, when bacteria such as Staphylococcus aureus may be cultured from them. The histology is usually consistent with septic micro-embolism (i.e. bacteria may be found within the blood vessels).

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http://www.cmaj.ca/content/182/10/1075.full

http://www.childrenshospital.org/cfapps/...IA_ID=1887

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Rheumatic Fever and Rheumatic Heart Disease
Jone’s Criteria:
* Major: “SPACE”

Subcutaneous nodules
Pancraditis
Migratory polyArthritis
Sydenham Chorea
Erythema Marginatum of Skin

*Minor: LEAF
Fever
Arthralgia
Leukocytosis and Raised ESR (Erythrocyte Sedimentation Rate)

http://peir.path.uab.edu/iplab/messages/598/518.html

http://images.rheumatology.org/viewphoto...umId=75683

http://medchrome.com/wp-content/uploads/...f-body.jpg

http://medchrome.com/basic-science/patho...t-disease/