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68 Cards in this Set

  • Front
  • Back
What is hemostasis?
The spontaneous arrest of bleeding from a damaged blood vessel.
What is ADP?
A powerful inducer of platelet aggregation.
What is synthesized within platelets and induces thrombogenesis and vasoconstriction?
Thromboxane A2
What is Prostacyclin?
It is synthesized within vessel walls and inhibits thrombogenesis.
Released from platelets, stimulating further aggregation and vasoconstriction.
Endogenous anticoagulants, diminish amplification in the blood clotting cascade by proteolysis of factors Va and VIIIa.
Proteins C & S
Remodels the thrombus and limits the extension of thrombis by proteolytic digestion of fibrin.
What are some substances that activate the fibrinolytic system?
Tissue plasminogen activator, urokinase, and streptokinase.
What are the indirect thrombin inhibitors?
1. Unfactionated heparin
2. Low MW Heparin
3. Synthetic fondaparinux
Inhibits clotting factor protease, especially thrombin, IXa and Xa by forming equimolar stable complexes with them.
True or False?
Once the antithrombin-protease complex is formed, that heparin is no longer active.
What is the difference in affinities between HMW and LMW Heparins?
HMW fractions of heparin markedly inhibit all three factors especially thrombin and factor Xa.
LMW fractions inhibit factor Xa but have lower affinity for thrombin.
What are some LMW heparins?
Enoxaparin, dalteparin, and tinzaparin
What drug is given to reverse heparin action?
Protamine sulfate
What is the specific irreversible thrombin inhibitor from the leech that is now available in recombinant form as lepirudin?
What is the MOA of coumadin anticoagulants?
The block the gamma carboxylation of several glutamate residues in the prothrombin and factors VII, IX, and X as well as the endogenous anticoagulants Proteins C and S
How do fibrinolytic drugs work?
They rapidly lyse thrombin by catalyzing the formation of the serine protease plasmin from its precursor zymogen, plasminogen.
What are some fibrinolytic drugs?
Streptokinase, altephase, antistreplase, tissue plasminogen activator, reteplase, tenecteplase, urokinase.
What are the toxicities of heparin?
Bleeding, Thrombocytopenia,
Thrombosis (Heparin-induced antibody complex bind to Fc receptors on adjacent platelets)
Heparin does not cross the placenta
What is the difference between Hirudin and Bivalirudin?
Hirudin binds irreversibly to both sides of thrombin.
Bivalirudin binds reversibly at one active site.
Why can direct thrombin inhibitors inactivate bound and circulating fibrin where heparin can only inactivate circulating fibrin?
Heparin has too much steric hinderance to overcome.
Small DTIs have low MW.
What are some toxicities of warfarin?
Bleeding, skin necrosis (purple toe syndrome, a deficiency of protein C and S)
Birth defects -
1st tri. nasal hypoplasia
2nd tri. CNS abnormalities (bleeding in brain)
What is the INR?
International Normalized Ratio used to compare patient PT to control PT.
The usual goal is 2-3 times normal.
How do osmotic diuretics work?
They sit in the solution and extract water adn electrolytes from intracellular fluid to increase ECF. It also increases renal blood flow in the medulla.
Where does mannitol work?
The proximal tubule and descending limb.
When would you use osmotic diuretics?
To increase urine volume with a crush damage.
To decrease intracranial and intraocular pressure
Dialysis equilibrium
What are some carbonic anhydrase inhibitors?
Sulfonamide derivatives, acetazolamide, dichlorphenamide, and methazolamide.
Where do carbonic andydrase inhibitors work?
Proximal tubules
What are the 4 categories of regulating BP?
1. Diuretics
2. Sympathoplegic agents
3. Direct vasodilators
4. ACE inhibitors
What are the 4 compensating actions the body can take against blood pressure?
1. baroreflexes
2. shut down renin
3. vasopressin control
4. renal function - Increase secretion of Na
What drugs are the first choice for incomplicasted HTN?
Reduce BP 10-15 mmHg
What pressure is considered HTN?
What are the 3 pathways that control renin release?
Macula densa pathway
Intrarenal baroreceptor pathway
B1 adrenergic receptor pathway
What are the effects of AII on altered peripheral resistence?
1. Direct vaso-constriction, enhancement of noradrenergic neurotransmission (increase NE), and increase sympathetic discharge
What are the effects of AII on altered renal function?
Direct effect to increase Na reabsorption in proximal tubule, release of aldosterone from adrenal cortex, altered renal hemodynamics
What are the rapid pressor responses of AII?
increase total peripheral resistance
Increase cardiac contractility
increase Heart rate
What are the slow pressor responses of AII?
Decrease in renal excretory function, endothelin-1, aldosterone
How does AII affect cardiovascular structure?
Increase expression of proto-oncogenese, Increase growth factors, Increase collagen, chronic HTN damage (Increased afterload, increase wall tension)
What suffix refers to converting enzyme inhibitors?
~pril (~prilat for prodrug)
What suffix refers to AII receptor antagonists?
What diuretic does not work from the luminal side?
What role does Ca++ play in the kidneys?
It is a NKCC cotransporter in the thick ascending limb. When the lumen-positive electric potential is inhibited, Ca++ secretion increases.
What transporters are in the distal tubule?
Na/Cl- cotransporter
Apical Ca++ channel
Basolateral Na+/Ca++ exchanger
What is the mechanism of action of osmotic diuretics?
Increase in osmotic pressure in tubular fluid. Increase in renal blood flow (renin turned off)
What are the pharmacodynamics of osmotic diuretics?
Water excretion is greater than Na+ excretion.
ECF expansion
Decrease in blood viscosity
Suppress renin release to decrease constriction
What are the adverse effects of osmotic diuretics?
Acute ECF expansion (congestive HF and pulmonary edema)
What are the pharmacodynamics of carbonic anhydrase inhibitors?
Increase in bicarb excretion, increase in NaCl reabsorption, increase in K+ secretion, decrease in RBF and GFR because the macula densa sees more fluid and constricts AA.
What are the adverse effects of CA inhibitors?
Hyperchloremia, metabolic acidosis, renal stones, hypokalemia, allergic reactions
What are the clinical indications for CA inhibitors?
Glaucoma, urinary alkaliniation, metabolic alkalosis, acute mountain sickness, epilepsy
Where is the site of action for loop diuretics?
The thick ascending limb of the loop of henle.
What is the mechanism of action of loop diuretics?
1. Inhibit NKCC symport
-stop (+) potential and Ca++ and Mg++ reabsorption decreases
-increase GFR and increase renin release
What are some drug interactions with loop diuretics?
NSAIDS and probenacid
What are the pharmacodynamics of loop diuretics?
Decrease NaCl reabsorption
decrease ECF volume
Decrease Ca+, Mg+ reabsorption ---> hypomagnesia
stimulate renal prostaglandin synthesis
increase K+ and H+ secretion
What are adverse effects of loop diuretics?
Hypokalemia, hyperuricemia, hyperchloremia, ototoxicity
What are the indications for loop diuretics?
Chronic CHF, acute renal failure, pulmonary edema, anion overdose
What is the prototype thiazide?
Where is the site of action for thiazide diuretics?
Early distal tubule, past the macula densa
What is the mechanism of action of thiazide diuretics?
Inhibition of Na+-Cl cotransport.
Theory: If Na+ reabsorption is inhibited, Na+/Ca+ is upregulated and Ca+ is increased to regulate ICF levels
What are the pharmacodynamics of HCTZ?
Weak carbonic anhydrase inhibition.
Increase Ca+ reabsorption, decrease Mg+ reabsorption
Increase K+ and H+ secretion, renal prostaglandin synthesis
True or False?
Thiazides cause Ca+ precipitation in urine?
Thiazides cause a decrease in Ca+ secretion and decrease pH so Ca+ is poorly soluble
What are some adverse effects of thiazides?
Hypokalemia, hypochloremia, metabolic alkalosis, hypomagnesemia, hyperuricemia, carbohydrate intolerance. Increase serum lipid and lipoprotein conc.
What are the clinical indications of thiazides?
HTN, edema, nephrolithiasis, osteoporosis, nephrogenic diabetes insipidus.
What are the potassium sparing diuretics?
Organic bases - amiloride, triamterene
Mineralocorticoids - Spironolactone
Where is the site of action for potassium sparing diuretics?
Late distal tubule
What is the mechanism of action for potassium sparing diuretics?
Inhibition of Na+ channels in luminal membrane (amiloride)
Competitive antagonist at mineralocorticoid receptor (prevents aldosterone from creating proteins necessary for Na+ reabsorption)
What are the dynamics of K+ sparing diuretics?
Decrease Na+ reabsorption
Decrease K+ secretion - hyperkalemis
Decrease H+secretion - metabolic acidosis
What are some adverse effects of spirolactone and amiloride?
Hyperkalemia, hyperchloremic metabolic acidosis
Spironolactone - gynecomastia and hirusitism
Triamterene - weak folate antagonist (megaloblastic anemia and folate deficiency)
What are the clinical indications for K+ sparing diuretics?
Primary hyperaldosteronism - (Conn's syndrome, ectopic ACTH)
Secondary hyperaldosteronism - (heart failure, hepatic cirrohsis, nephrotic syndrome)