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Blood Vessels > Pharmacology > Flashcards

Pharmacology Flashcards

0
Q

Mechanism of statins? Major side effects of statins?

A

inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
huge drop in LDL levels, some drop in TGs, some increase in HDL

Side effects:
hepatotoxicity (increased LFTs) and myopathy/rhabdomyolysis

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1
Q

Pt with history of acute MI 6 months ago appears with fatigue, muscle pain, and increased creatine kinase activity – what drug effect?

A

Statins
lower cholesterol and stabilize plaques to decrease 2nd MI incidence and mortality; commonly prescribed for MI pts

Side effects: MYOPATHY and hepatotoxicity
risk of myopathy increased with concomitant use of fibrates and/or niacin!!

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2
Q

Why might you want to decrease fatty acid oxidation in treatment of stable angina?

A

fatty acid oxidation results in greater ATP production, but REQUIRES MORE OXYGEN USE vs. glycolysis

  • shifting energy production from fatty acid oxidation to glucose oxidation may be more oxygen efficient (and thus beneficial in treating angina)
  • also decreases potentially toxic fatty acid metabolite production
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3
Q

Best agent for pt with diabetes, HTN, microalbuminuria?

A

ACE inhibitors and angiotensin receptor blockers (ARBs)
slow the progression of diabetic nephropathy in Type I and Type II diabetics

useful both prior to onset of proteinuria as well as after proteinuria documentation

antihypertensive effect is also useful because normal BP limits are lower in diabetics

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4
Q

Flushing in niacin mediated by what molecules? How can it be prevented?

A

mediated by prostaglandins

can be prevented with aspirin pre-treatment
also slow-release, with meals, and with long-term use

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5
Q

What is Substance P? What is the function of capsaicin?

A

Substance P is a pain neurotransmitter in the PNS and CNS

Capsaicin reduces pain by decreasing levels of Substance P in the PNS

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6
Q

What enzyme is responsible for the inactivation of bradykinin? What drugs interfere with this process and what side effects result?

A

ACE
angiotensin converting enzyme

ACE inhibitors prevent inactivation of bradykinin (potent vasodilator), leading to side effects like cough and angioedema due to increased bradykinin levels.
These side effects can be avoided by use of an ARB, which preserves ACE function and thus does not increase bradykinin levels.

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7
Q

What receptor is blocked by ARBs? What are the effects? Bradykinin levels?

A

block angiotensin-1 (AT-1) receptors to block the effects of AT II
competitive inhibition

results in arterial vasodilation and decreased aldosterone secretion
bradykinin degradation and levels stay normal

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8
Q

How does fenoldopam act in hypertensive emergencies? What pts is it particularly effective in?

A

dopamine D1 receptor agonist (no effect on alpha or beta receptors)

activates AC and increases cAMP levels to vasodilate most arterial beds (especially coronary, renal, splanchnic):

  • decreases systemic vascular resistance to decrease BP
  • increases renal perfusion and promotes natriuresis

Exceptionally beneficial in HTN pts with concomitant renal insufficiency!!

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9
Q

Use and mechanism of action for nitroprusside? Side effects?

A

quick-onset, short-acting agent
most effective agent for most cases of HTN emergency

NO release to cause increased cGMP and vasodilation

Side effects:

  • cyanide toxicity (greatest limiting factor)
  • slight reflex sympathetic activation
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10
Q

What is the first-line treatment for hypertriglyceridemia? Mechanism? Second-line and mechanism?

A

Fibrates are 1st-line

  • upregulate lipoprotein lipase (LPL) to increase TG clearance
  • activate peroxisome proliferator-activated receptor alpha (PPAR-alpha) to induce HDL synthesis

Niacin is 2nd line

  • inhibits lipolysis in adipose tissue
  • decreases synthesis of hepatic triglycerides and VLDL
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11
Q

How do bile acid resins work? Ezetimibe? Use?

A

Bile acid resins bind bile acids in GI tract (forces liver to use cholesterol to replace)

Ezetimibe selectively inhibits intestinal absorption of cholesterol at brush border (used with statins)

Both used for hypercholesterolemia.

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12
Q

First-line drugs for isolated systolic hypertension?

A

Thiazide diuretics and DHP calcium channel blockers (amlodipine)

For pts with ISH and diabetes, ACE inhibitors or ARBs used first-line.

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13
Q

What are the side effects of calcium channel blockers like amlodipine? Which are used for vascular smooth muscle? For heart?

A

cardiac depression, AV block (relaxes heart muscle)
Heart/non-DHP: diltiazem and verapamil

peripheral edema, flushing (relaxes vascular smooth muscle)
Vascular/DHP: amlodipine, nefedipine, nimodipine

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14
Q

What is cilostazol? Mechanism and uses? Other agents in its class?

A

phosphodiesterase III inhibitor
increases cAMP levels

1) inhibits platelet aggregation
2) direct arterial vasodilator

Uses: intermittent claudication, vasodilation
prevention of stroke or TIAs, angina prophylaxis

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15
Q

How are statin drugs metabolized? Consequences?

A

Statins (except pravastatin) are metabolized by liver CYP-450

inhibitors of CYP-450 system will increase toxicity (e.g., risk for rhabdomyolysis and myopathy)

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16
Q

Name inducers of CYP450. Inhibitors?

A 
Inducers:
Carbamazepine
Phenobarbital
Phenytoin
Rifampin
Griseofulvin
Inhibitors:
Cimetidine
Ciprofloxacin
Erthyromycin (macrolides)
Azole antifungals
Grapefruit juice
Isoniazid
Ritonavir (protease inhibitors)
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17
Q

Vd of a drug is 4.5L – what are likely properties of this drug?

A

features that tend to trap drug in plasma compartment:

  • high MW
  • high plasma protein-binding
  • high charge
  • hydrophilicity
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18
Q

What is the Vd for a drug that has a small MW and is hydrophilic?
What is the Vd for a drug that has a small MW and is hydrophobic?

A

small MW and hydrophilic – can distribute into the interstitial fluid compartment outside of the blood vessels in addition to plasma
- ECF volume is about 15 liters (1/3 of total body water)

small MW and hydrophobic/lipophilic – can cross cell membranes and reach intracellular compartments to reach entirety of total body water
- total body water is 41 liters

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19
Q

What lipid lowering agents can have an effect of increasing triglycerides?

A

bile acid resins

cholestyramine, cholestipol, colesevelam

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20
Q

What do statins do to hepatic cholesterol synthesis? Bile acid resins?

A

statins – lowers

bile acid resins – increase

21
Q

What lipid lowering agents are associated with an increased risk of gallstones?

A

fibrates (gemfibrozil, etc.) and bile acid-binding agents (cholestyramine, etc.)

22
Q

What conversion does ACE catalyze?

A

Angiotensin I to Angiotensin II

also inactivates bradykinin

23
Q

Pt taking ceftriaxone for pneumonia develops difficulty breathing, hypotension, rash? Treatment?

A

Anaphylactic shock

Epinephrine is the drug of choice for treatment of anaphylactic shock!!
(stimulates beta2 receptors/bronchodilation, which NE does not – NE cannot be used as a substitute!)

24
Q

Pt treated with hypertension having spells of lightheadedness, frequent falls? Reason?

A

Orthostatic hypotension
due to blockade of alpha1 receptors (normally mediate vasoconstriction)

all alpha1-blockers cause orthostatic hypotension!

25
Q

Which lipid-lowering agents are most likely to precipitate gallstone formation? What is the rate-limiting enzyme that converts cholesterol to bile acids?

A

fibrates and cholestyramine (bile acid resins)
both increase cholesterol excretion by the liver – increased risk of cholesterol stones

7alpha hydroxylase

26
Q

Cholesterol lowering med that causing flushing and pruritis? Mediator? Drug mechanism of action? Major use? Other notable side effects?

A

Niacin (caused by prostaglandins)

Niacin:

  • decreases synthesis of hepatic VLDL
  • inhibits lipolysis in adipose tissue

Major use is to increase HDL levels!!

27
Q

Pt on a cholesterol-lowering agent develops coagulation problems?

A

bile acid resins cause malabsorption (decreased uptake of fat-soluble vitamins like vitamin K)

vitamin K deficiency – coagulopathy

28
Q

Pt put on ramipril sees a rise in serum creatinine levels – why?

A

ACE inhibitors inhibit conversion of AngI to AngII

AngII is a potent vasoconstrictor of the efferent arteriole
Normally, kidney maintains GFR by dilating afferent arteriole and constricting the efferent arteriole

29
Q

What is the affect of beta-blockers on the renin-angiotensin-aldosterone system?

A

beta-1 receptor pathway normally increases renin secretion

BLOCKADE of beta-1 receptors leads to decreased renin, and thus decreased RAAS activation.

30
Q

What are the three major pathways that regulate the renin-angiotensin-aldosterone system?

A

1) macula densa
2) intrarenal baroreceptors
3) beta-adrenergic receptors (sympathetic stimulation of beta-1 receptors on juxtaglomerular cells leads to renin release)

31
Q

What is vitamin B3? What is it used for as a lipid-lowering agent?

A

Niacin = vitamin B3

increases HDL choelsterol levels

32
Q

What agents are used for hypertriglyceridemia? What is the mechanism? What are the side effects?

A

fibrates (gemfibrozil, fenofibrate)

  • increases PPARalpha expression
  • increases lipoprotein lipase activity (lipolysis/clearance of lipoprotein TGs)

Side effects:

  • myositis (increased risk with statins)
  • hepatotoxicity
  • cholesterol gallstones (increased risk with bile-acid resins)
33
Q

Pt with HTN and elevated CK – what drug combination responsible?

A

statins and fibrates

34
Q

IV drip of NE found to blanch vein with surrounding tissue cold, hard, pale? Treatment?

A

NE extravasation – causes intense alpha1 vasconstriction that can leads to local tissue necrosis

Treat with alpha receptor blocker (like phentolamine)

35
Q

What causes angioedema associated with ACE inhibitors? Presentation?

A

increased bradykinin
(potent vasodilator that increases vascular permeability to cause angioedema)

Most commonly involves swelling of tongue, lips, or eyelids and laryngeal edema and difficulty breathing (but can affect any tissue).

36
Q

What is the effect of a competitive inhibitor on a drug receptor binding curve? Noncompetitive antagonist?

A

Competitive:

  • shifts curve to the right, but not change in size or shape
  • decreases POTENCY but no change in efficacy of drug

Noncompetitive:

  • shifts curve down – maximum reduced
  • decrease in efficacy
37
Q

Efficacy vs. potency? How is potency measured?
Which applies to drugs that bind their receptors with a higher affinity?
Which applies to drugs that are better able to gain access to their target tissues?

A

Efficacy - maximum pharacodynamic effect achievable by drug
Potency - amount of drug needed to produce given effect (lower ED50 = more potent)

Drugs that
- bind receptors with higher affinity
- better access target tissues
have greater POTENCY

38
Q

What are the side effects of niacin? What adjustments to anti-HTN drugs may have to be made?

A
  • redness, flushing
  • hyperglycemia/insulin resistance
  • hyperuricemia

Vasodilation caused by niacin can potentiate some anti-HTN drugs so may have to reduce doses.

39
Q

What is nitroprusside used for and what is its mechanism? Toxicity and treatment?

A

most effective agent for most cases of hypertensive emergency (quick-onset and short action)

releases NO to increase cGMP levels and vasodilate

Causes cyanide toxicity (metabolized to NO and CN), which can be treated with nitrites and thiosulfate:

  • nitrites convert Hb to methemeglobin which binds CN better than cytochromes in mitochondria do
  • thiosulfate transfers a sulfur to cyanate for form thiocyanate (less toxic form that can be excreted in urine)
40
Q

Pt with hyperlipidemia with gout – what precipitated?

A

niacin (hyperuricemia)

other drugs that can cause hyperuricemia:

  • hydrochlorothiazide
  • cyclosporine
  • pyrazinamide
41
Q

Drug for pt with BPH and HTN?

A

alpha1-selective antagonist (-zosin)

doxazosin, prazosin, terazosin

42
Q

What is streptokinase and what is it used for medically? Side effect? Antidote?

A

thrombolytic agent (like t-PA)
protein synthesized by beta-hemolytic streptococci
- forms a complex with plasminogen that cleaves it to form plasmin
- plasmin cleaves fibrin to dissolve thrombi

Most common side effect = hemorrhage
Antidote = aminocaproic acid (Lys analogue that inhibits plasmin)

43
Q

What is amiloride? Amlodipine? Amiodarone?

A

Amiloride = K+sparing diuretic

Amlodipine = Ca2+ channel blocker (DHT/vascular smooth muscle)

Amiodarone = K+ channel blocker (Class III antiarrhythmic)

44
Q

What are the effects of dopamine at low, moderate, and high doses?

A

Dopamine: D1 = D2 > beta > alpha

Low doses:

  • D1 stimulation in renal vasculature and tubules
  • increased GFR, renal blood flow, sodium excretion

Higher doses:
- beta-1 stimulation increases cardiac contractility, PP, systolic BP

Even higher doses:

  • alpha1 stimulation causes systemic vasoconstriction
  • leads to decreased cardiac output (due to increased afterload)
45
Q

What are D1 agonists used for? Name a D1 agonist.

A

used for shock – at high doses acts on beta2 and alpha1 in addition to D1 receptors (alpha1 effects predominate at high doses)

Fenoldopam is a D1 agonist

46
Q

What are the effects of epinephrine? What predominates at low doses vs. high doses?

A
  1. increases systolic blood pressure (alpha1 and beta1)
  2. increases heart rate (beta1)
  3. EITHER increases or decreases diastolic blood pressure
    - at low doses, the beta2 effect predominates = vasodilation and decreased diastolic BP
    - at high doses, the alpha1 effect predominates = vasoconstriction and increased diastolic BP

Diastolic BP determined by the amount of total peripheral resistance and afterload (increased TPR = increased afterload = increased diastolic BP)

47
Q

What side effect of ACE inhibitors are you worried about upon first dose? What predisoposes to risk?

A

first-dose hypotension

Predisposing risk factors:

  • hypovolemia secondary to diuretics
  • low baseline BP
  • hyponatremia
  • high renin/aldosterone levels
  • renal impairment
  • heart failure
48
Q

What is the mechanism of statins reducing LDL levels?

A
  • statins reduce cholesterol synthesis
  • cholesterol-starved hepatocytes upregulate LDL receptors
  • increased LDL uptake by hepatocytes is used for cholesterol
49
Q

How can ACE inhibitors precipitate acute renal failure in at-risk pts?

A

pts with renal artery stenosis are dependent on efferent arteriole constriction to maintain renal perfusion

  • ACE inhibitors block AngII production, leading to dilation of the efferent arteriole
  • reduction in renal filtration fraction can precipitate acute renal failure

CONTRAINDICATED in pts with renal artery stenosis (especially bilateral)

Blood Vessels (3 decks)

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