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STEP1 > Blood and Inflammation Drugs > Flashcards

Blood and Inflammation Drugs Flashcards

1
Q

What is are the major side effects of heparin?

A

hypoaldosteronism, osteoporosis, bleeding, and HIT

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2
Q

What is fondaparinux?

A

a form of LMWH

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3
Q

What is argatroban?

A

a direct thrombin inhibitor

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4
Q

What is dabigatran?

A

a direct thrombin inhibitor

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5
Q

What relationship is there between warfarin and the microsomal enzyme system?

A

warfarin is primarily cleared via microsomal enzymes, thus other drugs often alter it’s metabolism

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6
Q

Describe the mechanism of action through which aspirin has an anti-thrombotic effect.

A

it acetylates and irreversibly inhibits COX-1 and COX-2, preventing the production of thromboxane A2, which promotes platelet activation and aggregation, from arachidonic acid

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7
Q

What is the mechanism of action of the “grel” drugs?

A

they are non-competitive, irreversible P2Y12 receptor inhibitors, which impair platelet aggregation by inhibiting the binding of ADP to the platelet receptor

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8
Q

What is a suitable replacement for aspirin in those who suffer a pseudo allergic reaction?

A

P2Y12 antagonists (“-grel”), which inhibit ADP binding to platelets

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9
Q

What is the aspirin “pseudoallergy” and how should it be managed?

A
  • it is reaction to aspirin characterized by urticaria and respiratory symptoms
  • it is said to be a “pseudo” allergy because it is mediated by an excess of leukotrienes rather than IgE
  • patients who suffer this reaction should be prescribed a P2Y12 antagonist (“grel”) instead
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10
Q

List four indications for anti platelet therapy with either aspirin or P2Y12 inhibitors. For which is dual therapy indicated?

A
  • reduce risk of cardiovascular events in patients with peripheral artery disease and coronary artery disease
  • reduces mortality in those suffering an acute MI or other acute coronary syndrome
  • dual therapy is used to prevent ischemic stroke in those with atherosclerosis and known cerebrovascular disease
  • dual therapy is used to prevent coronary stent thrombosis
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11
Q

What kind of aspirin should be given to those suffering an acute MI?

A

chewable aspirin

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12
Q

What is ticlopidine and what is the major adverse effect?

A

a P2Y12 platelet inhibitor that carries a significant risk for granulocytopenia and requires frequent CBCs for monitoring

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13
Q

Platelet Inhibitors

A
  • aspirin acetylates and irreversibly inhibits COX-1 and COX-2, preventing production of the thromboxane A2
  • clopidogrel and ticlopidine irreversibly bind and inhibit the P2Y12 ADP receptor on platelets
  • either can be used to prevent cardiovascular events in those with peripheral artery disease or coronary artery disease and to reduce mortality in the setting of acute MI or other acute coronary syndrome
  • dual therapy is indicated to prevent coronary stent thrombosis and ischemic stroke in those with atherosclerosis and known cerebrovascular disease
  • aspirin may induce a “pseudo” allergy due to the accumulation of leukotrienes, which presents as urticaria and symptoms of asthma
  • ticlopidine commonly causes a granulocytopenia and frequent CBCs are needed to monitor WBC counts
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14
Q

What is abciximab?

A

a monoclonal antibody against GP IIb-IIIa, which inhibits platelet aggregation

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15
Q

What is eptifibatide?

A

a GP IIb-IIIa antagonist that inhibits platelet aggregation

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16
Q

What is tirofiban?

A

a GP IIb-IIIa antagonist that inhibits platelet aggregation

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17
Q

GP IIb-IIIa antagonists share what naming convention?

A

tirofiban and eptifibatide both contain “fib” because they inhibit fibrinogen binding

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18
Q

Abciximab, eptifibatide, and tirofiban all share what major side effect?

A

they may induce thrombocytopenia and thus require frequent CBC monitoring

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19
Q

What is dipyridamole?

A

an anti platelet phosphodiesterase inhibitor

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20
Q

What is cilostazol?

A
  • an antiplatelet phosphodiesterase inhibitor which raises cAMP levels; in platelets this impairs aggregation and in arteries it causes vasodilation
  • can be used to prevent strokes or treat claudication because of it’s dual action
  • however, it may cause coronary steal
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21
Q

What is coronary steal?

A
  • the idea that in someone with coronary artery disease, the arteries distal to a narrowed lumen are already maximally dilated
  • when you give a coronary vasodilator, this dilates the other arteries and actually directs blood away from the arteries that need it
22
Q

Drugs ending “-teplase” have what mechanism of action?

A

they are fibrinolytics that activate plasmin from plasminogen

23
Q

What is streptokinase?

A
  • a virulence factor produced by streptococcal species, which can be used clinically as a fibrinolytic because it activates plasmin from plasminogen
  • it is, however, immunogenic and poses some risk for allergic reaction and/or anaphylaxis
24
Q

Name four circumstances under which fibrinolytic therapy is contraindicated.

A
  • evidence of a bleed
  • recent surgery
  • recent head injury
  • severe hypertension
25
Q

What are four ways to reverse fibrinolytic therapy?

A
  • amniocaproic acid
  • tranexamic acid
  • fresh frozen plasma
  • cryoprecipitate
26
Q

What is amniocaproic and?

A

a drug that can be administered to reverse fibrinolytic therapy because it competitively inhibits plasmin activation

27
Q

What is tranexamic acid?

A

a drug that can be administered to reverse fibrinolytic therapy because it competitively inhibits plasmin activation

28
Q

What are the time limits on percutaneous coronary intervention and fibrinolytic therapy?

A
  • PCI must occur in the first two hours

- fibrinolytic therapy must occur in 3-4.5 hours

29
Q

What lipoproteins contain apoB and apoE?

A
  • apoE is found on chylomicrons traveling from enterocytes to the periphery and liver
  • apoB is found on VLDL and LDL departing the liver for the periphery
30
Q

What is the role of chylomicrons? VLDL? LDL? HDL?

A
  • chylomicrons are formed by enterocytes and moved into lacteals in the lamina propia, which delivers them to the systemic blood supply; LPLs in peripheral capillaries then hydrolyzes and remove fatty acids, producing LDLs which are taken up by the liver
  • VLDLs are leased from the liver and deliver triglycerides/fatty acids to peripheral tissues; as it is depleted by peripheral LPLs, it becomes more dense and forms an IDL and then LDL
  • LDL from depleted chylomicrons and VLDL is cholesterol dense and delivers cholesterol to peripheral tissues before being deposited in vasculature or returning to the liver and being taken up by LDL receptors
  • HDL scavenges cholesterol from the periphery, esterifies it using LCAT, and then returns it to the liver directly via scavenger 1 receptors or transfers it to LDL and VLDL for transport back to the liver
31
Q

What are triglycerides?

A

the transport form of free fatty acids, which are composed of three fatty acids bound to a glyceride molecule

32
Q

What happens to cholesterol before it is packaged and transported by lipoproteins?

A

it is esterified

33
Q

Statins

A
  • hepatocytes produce cholesterol by converting HMG-CoA to mevalonate, but statins inhibit this conversion
  • in doing so, they lower cholesterol synthesis in the liver, causing the liver to up regulate it’s LDL receptors, removing more LDL and cholesterol from circulation
  • thus, it is the most effective drug for lowering LDL and only moderately effective at lowering HDL and triglycerides
  • it is the only lipid-lowering agent with any proven ability to reduce cardiovascular risk regardless of which lipid measure is abnormal
  • it lowers risk in diabetics, those with peripheral artery disease, and those with previous MI, stroke, or TIA
  • side effects include the fact it is a teratogen; causes myopathy with weakness, soreness, and elevated CK; and may cause liver damage, increasing LFTs
  • it is metabolized by microsomal enzymes, thus CYP inhibitors may increase serum levels and induce myopathy
34
Q

Bile Acid Resins

A
  • cholestyramine, colesevelam, and colestipol
  • all are cations that bind and prevent the reabsorption of bile acids from the terminal ileum
  • in doing so, they cause the liver to upregulate de novo bile synthesis from cholesterol, which requires up regulation of HMG-CoA reductase and hepatic LDL receptors, thus clearing more LDL from circulation
  • effective only at lowering LDL with no proven risk reduction for cardiovascular events, thus rarely used as mono therapy
  • adverse effects include increased serum triglycerides, cholesterol gall stones, constipation and bloating, poor fat and fat-soluble vitamin absorption, and inhibited absorption of statins
  • because of it’s interaction with statins, if they are used with statins, they must be taken 4 hours apart
35
Q

Ezetimibe

A
  • inhibits absorption of cholesterol from the GI tract, which forces the liver to upregulate expression of hepatic LDL receptors, clearing more cholesterol from circulation
  • effective only at lowering LDL with no proven risk reduction for cardiovascular events, thus rarely used as mono-therapy
  • adverse effects include diarrhea, steatorrhea, and elevated LFTs
36
Q

Evolocamab

A

a PCSK9 inhibitor, which blocks degradation of hepatic LDL receptors, leaving them expressed at the surface to increase clearance of LDL from circulation

37
Q

Fibrates

A
  • function by activating PPARa, which inhibits release of VLDL from hepatocytes and upregulates LPL (lipoprotein lipase) in the periphery
  • the net effect is lower levels of VLDL and chylomicrons in circulation
  • fibrates, then, are the best agent for lowering triglycerides but have little effect on LDL and HDL
  • side effects include increased risk for cholesterol gall stones and myopathy, especially when combined with statins
38
Q

Niacin

A
  • also known as B3, it’s mechanism for altering lipid metabolism isn’t entirely clear
  • it is the most effective drug for raising HDL but has little effect on LDL and triglycerides
  • may cause prostaglandin-mediated cutaneous flushing and warmth, which can be avoided by pre-medicating with NSAIDs
  • may also cause hepatotoxicity, hyperglycemia, or hyperuricemia
39
Q

What effect do omega-3 fatty acids have on lipid metabolism?

A

they’re effective at lowering triglycerides by inhibiting VLDL release and production of apoB, which is necessary for production of LDL and VLDL

40
Q

Describe the roles of COX-1 and COX-2.

A
  • COX-1 is constitutively expressed and produces thromboxane A2 as well as prostaglandins, which protect the gastric mucosa, from arachadonic acid
  • COX-2 is expressed by vascular endothelium and smooth muscle cells where it produces prostacyclin (PGI2), which promotes vasodilation and inhibits platelet aggregation, and prostaglandins, which mediate vascular permeability, pain sensitization, and fever
  • both are found in the glomerulus where they produce prostaglandins important for afferent arteriole vasodilation and maintenance of perfusion
41
Q

List the important non-selective COX inhibitors.

A
  • ibuprofen
  • diclofenac and ketorolac
  • indomethacin
  • meloxicam and piroxicam
  • naproxen
42
Q

What are the side effects of non-selective COX inhibitors?

A
  • hypertension
  • erosions or ulcers of the GI mucosa
  • GI bleeding
  • acute interstitial nephritis
  • papillary necrosis
  • lithium toxicity (limits renal elimination)
  • aplastic anemia (particularly indomethacin)
  • hypoaldosteronism and hyperkalemia
43
Q

Aspirin

A
  • acetylates and irreversibly inactivates COX-1 and COX-2
  • at low dose, it primarily inactivates COX-1 and has an antithrombotic effect but at higher doses it can be used in the treatment of Kawasaki disease
  • should be avoided in children with a viral illness for fear of Reye’s syndrome of hepatic dysfunction and encephalopathy
  • toxicity may cause an early respiratory alkalosis and then an anion gap metabolic acidosis as well as tinnitus
  • toxicity should be treated with activated charcoal and alkalization of the serum and urine with sodium bicarb
44
Q

Celoxicib

A
  • a selective COX-2 inhibitor
  • has fewer GI side effects
  • but is a sulfa drug and because it inhibits prostacyclin formation and not thromboxane A2, there is also a risk for thrombotic events
45
Q

Acetaminophen

A
  • a selective COX-2 inhibitor
  • has only antipyretic and analgesic effects without anti-inflammatory
  • so it’s use is primarily for non-inflammatory pain as in osteoarthritis (rather than RA for instance)
  • metabolized to a toxic metabolite known as NAPQI
  • toxicity should be treated with activated charcoal and N-acetylcysteine to increase glutathione levels
46
Q

In which two populations should NSAIDs be avoided?

A

those with poor renal function and those who are pregnant in the third trimester (due to possibility of closing the ductus arteriosus prematurely)

47
Q

Cholchicine

A
  • binds intracellular tubules and prevents microtubule polymerization, thus inhibiting neutrophil migration
  • serves to reduce the inflammation and symptoms of acute gout
  • effects on microtubules also affect GI system, however, causing diarrhea and other GI disturbance
48
Q

Allopurinol

A
  • a xanthine oxidase inhibitor, which limits production of uric acid
  • used as gout prophylaxis, treatment for Lesch-Nyhan hyperuricemia, and tumor lysis syndrome
  • may cause Steven-Johnson syndrome, induce DRESS syndrome, or reduce metabolism and increase the toxicity associated with purine analog antimetabolite drugs
49
Q

Febuxostat

A

a xanthine oxidase inhibitor which limits production of uric acid for the management of gout, Lesch-Nyhan syndrome, and tumor lysis syndrome

50
Q

Probenecid

A
  • a second line agent for treating hyperuricemia in those with poor elimination rather than excess production
  • probenecid inhibits reabsorption of uric acid from the proximal tubule, increasing elimination
  • adverse effects include increasing the concentration and potential toxicity of many antibiotics
  • and it is a sulfa drug which may cause allergies
51
Q

What effect does aspirin have on gout?

A
  • aspirin at low dose will increase reabsorption of uric acid from the proximal tubule, but at high dose it will reduce reabsorption
  • that said, it isn’t used at that high of dose and isn’t really used in the treatment of gout
52
Q

Pegloticase

A
  • recombinant uricase, which converts uric acid to the more soluble allantoin, promoting elimination
  • used as a second line agent for hyperuricemia in those who have impaired elimination rather than excess production
  • may induce hemolysis and bite cell formation in those with a G6PDH deficiency
  • must be administered IV in an in-patient setting because of it’s high risk for anaphylaxis

STEP1 (24 decks)

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