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Advanced Pharmacology > Final Exam - Section III and IV > Flashcards

Final Exam - Section III and IV Flashcards

1
Q

What are the catecholamines?
What receptors do they effect?

A
  • Epinephrine – α1, α2, β1, β2
  • Norepinephrine - α1, α2, β1
  • Isoproterenol - β1, β2
  • Dopamine – D1-5, Higher doses: α1, β1
  • Dobutamine - β1
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2
Q

What alpha antagonist is irreversibly bound?

A
  • Phenoxybenzamine
    -recovery requires new receptors due to covalent bonding
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3
Q

What is the clinical use for phenoxybenzamine? What is important to know about this drug?

A
  • Hypertension associated with pheochromocytoma (tumors producing NE)
  • It is covalently bound and irreversible
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4
Q

What are the reversible alpha antagonists?

A
  • Phentolamine
  • Prazosin
  • Tolazoline
  • Labetalol
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5
Q

Beta antagonist effect on the heart?
Blood vessels?

A

Heart:
* Negative inotropic
* Negative chronotropic
Blood vessels:
* Opposes B2 vasodilation
* Acute: increases peripheral resistance
* Chronic: decreases peripheral resistance

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6
Q

Describe MOA of propanolol, metoprolol, atenolol, and esmolol

A
  • Propanolol-Works on β1 and β2 receptors
  • Metoprolol- Mainly β1 selectivity; safer in COPD, diabetics
  • Esmolol – Beta-1 selective, ultra short acting
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7
Q

What are the direct acting cholinomimetics and their MOA?

A
  • Esters of choline
  • Alkaloids
  • Bind and activate muscarinic or nicotinic receptors
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8
Q

What are the indirect acting cholinomimetics MOA?

A
  • Inhibit action of acetylcholinesterase
  • Prolongs effects of ACh released at junction
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9
Q

What are the effects of cholinomimetics on the eye?

A
  • Muscarininc agonist cause miosis
  • Increases intraocular drainage
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10
Q

What are the cholinomimetic effects on the CV system?

A
  • Reduction in peripheral vascular resistance
  • Vasodilation – reduction in BP – reflexive increase in HR
  • Large doses - bradycardia
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11
Q

What are the classes of indirect cholinomimetics and examples?

A
  • Simple alcohols - Edrophonium
  • Carbamic acid esters of alcohols - Carbamates and Neostigmine
  • Organophosphates
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12
Q

What are the major uses for cholinomimetics?

A
  • Disease of the eye
  • GI and urinary tracts
  • Neuromuscular junction – Myasthenia gravis (autoimmune against ACh receptor)
  • Atropine overdose
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13
Q

What are the symptoms of cholinomimetic overdose?
Causes?
Treatments?

A
  • SLUDGE-M
  • Organophosphate exposure - TX: atropine, pralidoxime
  • Poisonous mushrooms (muscarinic excess) - TX: atropine
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14
Q

What can cause atropine OD?
Symptoms?
TX?

A
  • Belladona
  • Sx: BRAND (Blind, Red, Absent bowel sounds, Nuts, Dry)
  • Tx: Physostigmine
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15
Q

Describe the 3 differenent angina classifications?

A
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16
Q

What is the MOA of nitrates?

A

Activate GC, increase cGMP - Relaxation

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17
Q

WHat is the MOA of beta-2 agonists o smooth muscle?

A

GPCR – cAMP – Relaxation (mainly respiratory)

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18
Q

Describe the MOA of CCB on smooth muscle?

A

Less total calcium - Relaxation

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19
Q

Describe the MOA of sildenafil?

A

Blocks PDE5, increase cGMP - Relaxation

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20
Q

What is the good and bad of nitrates/nitrites?

A

The Good:
↑ venous capacitance, ↓ ventricular preload
↓ heart size, ↓ CO
The Bad:
Orthostatic hypotension, syncope, HA
Reflex tachycardia

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21
Q

What are the 4 mechanisms for drugs to relax vascular tone?

A
  • Block Ca influx
  • Increase cAMP
  • Increase cGMP
  • Prevent depolarization by potassium efflux
22
Q

What CCB effects on the heart?

A

↓ contractility
↓ SA node pacemaker rate
↓ AV node conduction velocity
Reduce blood pressure

23
Q

What are the 2 main classes of CCB and where they work?

A
  • Dihydropyridines: more peripheral vasculature
  • Verapamil and Diltiazem: more cardiac
24
Q

How are beta blockers useful for angina?

A

decrease oxygen demand:
↓ HR
↓ BP
↓ Contractility

25
Q

What are the 4 antihypertensive control sites?
How do drugs work that act here?

A
  • Diuretics: deplete sodium
  • Sympathoplegics: decrease PVR, reduce CO
  • Direct Vasodilators: relax vascular smooth muscle
  • Anti-angiotensins: block activity or production
26
Q

What is the hydraulic equation?

A

BP=COxPVR

27
Q

What are the 2 centrally acting sympathoplegics and their MOA?

A
  • Clonidine and Methyldopa
  • Primary antihypertensive activity due to α agonist activity in brainstem, decreasing sympathetic stimulation. Bind more tightly to α2 than α1
28
Q

What is the MOA of α1 blockers used for HTN?
Drugs?

A
  • Prazosin, Terazosin, Doxazosin, phenolamine, labetalol, phenoxybenzamine
  • Block α1 receptors in arterioles and venules
  • Dilates both resistance and capacitance vessels
  • BP is reduced more in upright position
29
Q

What is the MOA of minoxidil and hydralazine?

A

Minoxidil: Opens K+ channels in smooth muscles, stabilizes potential, less likely to contract.
Dilates arteries, arterioles
Hydralazine: Dilates arterioles (NO production)

30
Q

What is the MOA and uses of sodium nitroprusside?

A
  • HT emergencies, Cardiac failure
  • Dilates arterial and venous vessels
  • Relaxes vascular smooth muscle
  • Breaks down in blood to release NO
  • Increases intracellular cGMP

Can cause CN toxicity

31
Q

What is the MOA and uses of sodium fenoldopam?

A
  • Agonist of D1 receptors, causing diuresis
  • Peripheral arteriolar dilator
  • HTN emergencies, post-op HTN
32
Q

Describe the RAAS pathway and drugs that work here.

A
33
Q

Describe the normal intracellular cardiac contractility cycle?

A
  • “Trigger” calcium enters cell
  • Binds to channel in SR, release stored calcium
  • Frees actin to interact with myosin
34
Q

Describe the differences between systolic and diastolic heart failure?

A

Systolic: typical of acute failure, MI (Ex: thin, dilated left ventricle)
↓ CO, ↓ Ejection fraction
Diastolic (Ex: hypertrophy of myocardium)
↓ CO, Normal Ejection fraction
Does not respond well to positive inotropic drugs

35
Q

What is MOA and effects of digoxin?

A
  • Inhibits Na+/K+ ATPase
  • Slows down removal of calcium by NCX
  • Maintains normal resting potential
  • Positive inotrope
36
Q

What are the EC50 and TC50 of digoxin?

A

EC50 – 1 ng/mL
TC50 – 2 ng/mL

37
Q

What drug is a bypyridine?

A

Milrinone

38
Q

How do PDE inhibitors increase inotropy?

A
  • Inhibt enzymes that inactivate cAMP and cGMP
  • Positive inotropic effects
  • Main action from vasodilation
39
Q

Explain the phases of cardiac action potentials and the ion channels participating?

A
40
Q

What are the 4 classes of antiarrythmics and their MOA?

A

Class I – sodium channel blockade
Class II – sympatholytic
Class III – prolong action potential duration (other mechanisms besides sodium channels – K+)
Class IV – block cardiac calcium channel currents

41
Q

What class are quinidine, lidocaine, and flecaninde in?
Effects on cardiac cycle?

A

Class I - Na+ channel blockers

42
Q

What is the MOA of amiodarone?
Uses?

A

DOC for VT

43
Q

Explain the MOA of carbonic anhydrase inhibitors?
Where do they work?

A

Proximal convuluted tubule

44
Q

Loop diuretics MOA?
Examples?

A
  • Inhibit NKCC2 in thick ascending loop of henle
  • Furosemide (sulfa)
  • Ethacrynic acid (non-sulfa)
45
Q

What electrolytes are reabsorbed via the paracellular route in the ascending loop of henle?
How?

A

Ca++ and Mg++
The secretion of K+ creates a positve lumen potential and drives Ca and Mg through paracellular route

46
Q

Thiazaides MOA?
Example?

A
  • Inhibit NaCl transport in DCT (NCC)
  • Some inhibition of CA activity
  • Hydrochlorothiazide
47
Q

Describe upstream diuretic effects on the collecting tubule?

A
  • Diuretics upstream result in excess Na+ in CT
  • Some block NaCl
    Cl- leaves via paracellular route
  • Some block NaHCO3
  • HCO3 can’t exit via paracellular route - Drives K+ depletion
48
Q

How do aldosterone and spirinolactone affect the collecting tubule?

A

Aldosterone:
* Increase Na+ and water reuptake (ENaC)
* Increases blood volume
Spironolactone
* Block aldosterone receptors
* Potassium sparing

49
Q

What are ADH affects at the collecting tubule?
Its antagonist?

A
  • Increases water reabsorption
  • Adds preformed AQP2 to apical membrane
  • Increases blood volume
  • Makes more concentrated urine
  • Antagonist: Conivaptan
50
Q

What are the uses and toxicities of mannitol?

A
  • Used mainly to reduce intracranial pressure
  • Promote removal of renal toxins
    Toxicity
  • Extracellular volume expansion
  • Rapidly distributed to extracellular compartments
  • Dehydration

Advanced Pharmacology (17 decks)

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