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Cardiology > Pharmacology quiz 3 > Flashcards

Pharmacology quiz 3 Flashcards

1
Q

Describe the dose dependent effect of DA

Indications?

A

Low - D1 receptors -> dilation of renal + splanchnic vessels

Mid - beta-1 adrenergic receptors -> tachy + inc contractility

High - alpha-1 adrenergic -> increase peripheral vascular resistance

Used for hypotensive shock and acute HF

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2
Q

Alpha-2 vs beta1,2 receptors on the presynapse in CNS

A

Alpha-2 -> inhibit NE release

Beta -> stimulate more NE release

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3
Q

Clonidine

  • MoA
  • indications
  • major adverse effects
  • compare to alpha-methyldopa
A

presynaptic alpha-2 adrenergic agonist -> reduces SANS outflow in CNS

  • also reduces renin release
  • lowers heart rate and CO (better than methyldopa)

Indications
-HTN

Adverse effects

  • rebound HTN on abrupt w/drawal due to:
    1) downregulation of central presynaptic alpha-2 receptors
    2) upregulation of peripheral post synpatic alpha-1 receptors on vascular smooth muscle

Alpha-methyldopa

  • same MoA
  • different presynaptic alpha-2 receptor (not as good)
  • used in pregnancy HTN
  • contraindicated in liver disease
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4
Q

Phentolamine vs prazosin

A

Both are alpha-adrenergic receptor ANTAGONISTS

PHENTOLAMINE -> non-selective

  • reflex tachy observed
  • given w/ beta-blocker and diuretic (retention of salt/water can occur without it)

Indications/Uses

  • pheochromocytoma
  • prevention of dermal necrosis after IV NE or DA

Contraindications
-CAD (hypoTN can evoke angina and AMI) -> make ischemic insult worse

Adverse rxn

  • HypoTN -> b-2 activation/high NE levels
  • Tachy + arrhythmia -? high NE at beta-receptors

PRAZOSIN -> alpha-1 selective

  • no reflex tachy -> alpha-2 not blocked
  • used w/ other HTN agents

Indications

  • 2nd line HTN
  • BPH

Adverse rxns

  • 1st dose hypoTN, dizziness and syncope
  • nasal congestion -> unopposed beta-receptor action of NE
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5
Q

Compare the beta-adrenergic receptor antagonist

A

First generation beta blockers - propranolol
-nonselective

Second-generation agents: metoprolol
-selective for cardiac beta-1 receptors when given in low doses

Third-generation compounds: Carvedilol and labetalol
-Block beta and alpha receptors

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6
Q

Which beta blockers reduce mortality after an MI?

A

Propanolol metoprolol timolol

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7
Q

Which beta blockers reduce mortality in patients with heart failure?

A

Carvedilol (non-selective) and metoprolol (beta-1 selective)

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8
Q

List three side effects of beta blockers

A
  1. Smooth muscle spasm
  2. exaggeration of cardiac actions including bradycardia, heart block and negative inotropic effect
  3. CNS effects including insomnia and depression
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9
Q

Which beta blocker has a high risk of sexual dysfunction

A

Metoprolol

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10
Q

Why do beta blockers decrease renin release

A

Presence of beta-1 receptors on the kidneys

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11
Q

List the vascular relaxation mechanisms and associated drug classes

A
  1. cGMP (nitrates/nitrites)
    - inc cGMP -> dephosphorylation of myosin light chain -> prevents myosin-actin ix
  2. intracellular Ca++ (calcium channel antagonists, Na channel blockers)
    - reduction intracellular Ca++ -> reduced MLC kinase efficacy -> reduces myosin-actin ix
  3. cell membrane potential (direct vasodilators)
    - inc K+ permeability -> hyperpolarization
  4. cAMP (b-2 adrenergic agonists)
    - inc cAMP -> inc rate of MLC kinase inactivation -> reduce myosin-actin ix
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12
Q

List 3 Ca++ channel blockers
-which one has the greatest suppression of contractility and conduction?
least?

A
  1. Verapamil - greatest
  2. Diltiazem
  3. Nifedipine - least
    - dihydropyridine -> vascular selectivity
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13
Q

What can dec metab of Ca++ channel blockers?

A

inhibitors of P450

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14
Q

Verapamil inc plasma levels of?

A

digoxin

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15
Q

Which Ca++ blocker can cause peripheral dependent edema?

Myocardial depression?

constipation?

reflex tachy?

Which one should NOT be given w/ beta-blocker

A

Nifedipine

verapamil and diltiazem

verapamil

nifedipine

Verapamil (diltiazem ok)

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16
Q

Hydralazine

  • administration?
  • dilates which vessels?
  • combined with what to tx HF (in which population?)
  • side effects and CIs?
A
  • orally
  • dilates arterioles
  • combined w/ isosorbide dinitrate to tx HF in AA

Side effects

  • lupus-like syndrome
  • reflex tachy
  • CI in CAD and rheumatic valve disease
17
Q

Name 2 activators of vascular ATP-sensitive K+ channels

  • dilate which vessels?
  • IV or oral?
  • tx use?
A
  • Minoxidil and Diazoxide
  • arterioles
  • diazoxide = IV and minoxidil = oral
18
Q

Minoxidil, diazoxide or both?

  1. Hypertrichosis
  2. Reflex tachy
  3. Salt+water retn
  4. hyperglycemia
  5. subendocardial necrosis (reflex catecholamine)
  6. LVH and pericardial effusion
  7. gynecomastia
A
  1. Hypertrichosis - M
  2. Reflex tachy - B
  3. Salt+water retn - B
  4. hyperglycemia - D
  5. subendocardial necrosis(reflex catecholamine)-D
  6. LVH and pericardial effusion - M
  7. gynecomastia - M
19
Q

Ranolazine

  • MoA
  • tx use
  • side effects and CI
A

Moa - blocks VG Na channel -> minimizes Na+ coming in to the cell

Tx use -> chronic angina

Side effects
-QTc prolongation

CI
-hepatic impairment

Drug-Drug ix

  • drugs that inhibit P450
  • Verapamil
  • Digoxin
20
Q

Name 2 nitrovasodilators

  • mech
  • artery vs vein selectivity?
  • indications
  • side effects/toxicities
  • tolerance?
A

NITROGLYCERIN

  • mech -> stimulates intracellular cGMP production
  • dilates veins (low conc.) and arteries (higher conc)
  • dec preload and afterload

Use

  • acute angina pectoris
  • angina prophylaxis
  • IV for CV surgery to lower BP
Adverse effects (unique to NG)
-headache 
NITROPRUSSIDE
-non-selective vasodilator 
-use -> HTN crisis (not angina!!!)
-toxicity -> cyanide with prolonged use 
NO TOLERANCE -> doesn't affect thiol stores

BOTH can cause methemoglobinemia

21
Q

How can we decrease the reflex increase in heart rate associated with nitrates?

contractility?

A

Add beta blocker or Ca++ channel blocker

22
Q

In patients with CAD which drug should never be combined with nitrovasodilators? Why?

A
  • Nitroglycerine and Sildenafil (Viagra) drug rxn
    • cGMP increase the phosphatase leading to vasodilation
    • Sildenafil blocks breakdown of cGMP
    • Double whammy combination leading to massive VSM relaxation
    • Potent lowering of BP leading to heart attack
      • Exacerbation of ischemia
23
Q

Dobutamine

  • class
  • MoA
  • side effects
A

class -> Beta1 adrenergic agonist

MoA

  • inc rate and force of contraction (Ca++ induced Ca++ release)
  • inc rate of relaxation (phospholamban-P reuptake of Ca++)

Side effects

  • arrhythmias-> can result in sudden cardiac death
  • worsen ischemic injury
  • tolerance due to beta receptor down regulation
24
Q

List the beneficial actions of beta blockers in HF (6)

A
  • Bradycardia by inhibiting conduction
  • Too much catecholamine can hurt myocytes - beta blockers reduce this
  • Blocking beta receptor leads to up regulation leading to preservation of beta signaling
  • Renin release blocks which prevents AGII from forming
    • AGII is a potent vasoconstrictor
  • Slow down the remodeling process which is bad in the long run
  • Decreasing sympathetic tone also beneficial
25
Q

List the the drug ix of metoprolol

A

1) Cimetidine (Histamine H2 antagonist): Increase the bioavailability of metoprolol by affecting hepatic blood flow
2) Hydralazine (vasodilator): Increase the bioavailability of metoprolol by affecting hepatic blood flow
3) Calcium channel blocking agents: Increase risk of conduction disturbances
4) Rifampin (antibiotic): Decrease plasma levels of metoprolol
5) Phenytoin (anticonvulsant) or Phenobarbital (anticonvulsant):
Decrease plasma levels of metoprolol
6) Cholestyramine (bile acid sequestrant): decrease absorption of metoprolol

26
Q

Carvedilol drug ix

A

1) Antidiabetic agents: The beta-blocking effect may increase the hypoglycemic effects
2) Calcium channel blocking agents: Increase risk of conduction disturbances
3) Clonidine: Potentiation of BP and heart rate lowering effects
4) Cyclosporine: Increase cyclosporine blood levels due to decrease liver breakdown
5) Digoxin: Increase digoxin levels
6) Rifampin: Decrease plasma levels of carvedilol

27
Q

Digoxin

  • indication
  • MoA
  • excretion
  • unique aspect
  • toxicities
A

Indication

  • chronic CHF + chronic afib
  • sx control in HF and systolic dysfx
  • control ventricular rate in afib

Excretion -> kidneys

MoA

  • Na/K ATPase inhibitor -> inc intracellular [Ca++] -> inc F of contraction
  • Ach release at AV node -> enhance parasympathetic tone of heart -> relaxation
  • activation of Ach-mediated K+ current -> convert atrial flutter to afib

Unique -> only oral positive inotropic drug for CHF

Toxicities
Cardiac -> arrhythmias
Extracardiac
-GI -> N/V, diarrhea, anorexia
-Neuro -> depression, disorientation paresthesias 
-Visual
-Hyperestrogenism -> gynecomastia
28
Q

List 4 hemodynamic effects of digoxin in CHF

A
  1. Positive inotropy
  2. reduction in HR
  3. Vasodilation
  4. Diuresis
29
Q

How to tx digitalis toxicity

A
  • KCl

- Digoxin-specific Abs

30
Q

Digitalis drug ix

A

1) Diuretics (thiazides and loop diuretics)
2) Sympathomimetics and catecholamines
3) Spironolactone (aldosterone receptor blocker) 4) Verapamil (Ca2+ channel blocker)
5) Insulin

31
Q

Milrinone

  • MoA
  • use
  • 3 tx actions
  • Side effects
A

MoA -> intracellular PDE-III inhibitor

indication -> IV tx for short-term management of acute HF

  1. Pos inotropy
  2. Pos lusitropy
  3. vasodilation -> inc cGMP in vascular smooth muscle

Side effects
1) Exacerbate ischemic event (increase in
myocardial O2 consumption)
2) Arrhythmogenesis (due to elevated Ca2+) 3) Thrombocytopenia
4) Hypotension
5) Headache

32
Q

Levosimendan

-MoA

A

-MoA -> sensitize contractile apparatus to prevailing level of Ca++

• At higher doses, appear to inhibit PDE-III
• Opens ATP-sensitive potassium channels on blood vessels and myocytes
o Reduces preload and afterload o Cardiomyocyte survival

33
Q

Aliskiren

  • MoA
  • CI and adverse effects
A

MoA - inhibits renin

Adverse effects
-angioedema and GI disturbances

CI

  • pregnancy
  • diabetes -> hyperkalemia when combined with ACE inhibitor
  • caution -> impaired renal fx
34
Q 
Lisinopril
MoA
clinical outcomes 
adverse effect
CI
A

ACE inhibitor

  • Decreased mortality after myocardial infarction
  • Increased cardiac performance in heart failure
  • Kidney protected from deteriorating damage associated with sustained hypertension

angioedema
cough - noncompliance
CI -> pregnancy (2nd + 3rd TM)
chronic renal failure ONLY volume depleted (temporarily stop)

35
Q

Losartan

A
  • ARB - block T1 AGII receptors

- metabolized in liver - metabolites have HIGHER potency

36
Q

Endothelin receptor antagonists

  • use
  • list 2 and compare
  • side effects
  • drug ix
  • biological actions
A

-use -> pulmonary arterial HTN

  1. Bosentan -> non-selective antagonist
  2. Ambrisentan -> selective for ETA

Adverse effects - liver injury

CI

  • pregnancy
  • metab by CYP2C9 and 3A4

Drug ix

1) Cyclosporine A (immunosuppressant): affects the activity of bosentan
2) Glyburide (anti-diabetic agent): affects the activity of bosentan
3) “Statins” (lipid-lowering agents): bosentan may decrease the effects of statins
4) Oral contraceptives: bosentan may prevent contraceptives from working properly and may result in an unplanned pregnancy

Biological actions

  • vasodilation
  • dec cardiac contractility and remodeling
  • inhibition of aldosterone and dec in blood volume
37
Q

BNP dxic of?

A

Heart failure

38
Q

physiological actions of ANP/BNP

A
  • vasodilation
  • natriuresis/diuresis
  • inhibition of the renin-angiotensin- aldosterone (RAA)
  • inhibition of the sympathetic nervous system
39
Q

Nesiritide

  • clinical effects
  • side effect
A

Clinical effect
• Dilates veins & arteries
• Reduces pulmonary
capillary wedge pressure
• Reduces systemic BP
• Increases cardiac output & stroke volume, without increasing heart rate
• Has natriuretic actions and promotes diuresis

Side effect
-hypotension (worse w/ ACEI)

Cardiology (6 decks)

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