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

Final Exam - Section III and IV Flashcards

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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?

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

What CCB effects on the heart?

Study These Flashcards
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?

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

How are beta blockers useful for angina?

Study These Flashcards
A

decrease oxygen demand:
↓ HR
↓ BP
↓ Contractility

25
What are the 4 antihypertensive control sites? How do drugs work that act here?
* Diuretics: deplete sodium * Sympathoplegics: decrease PVR, reduce CO * Direct Vasodilators: relax vascular smooth muscle * Anti-angiotensins: block activity or production
26
What is the hydraulic equation?
BP=COxPVR
27
What are the 2 centrally acting sympathoplegics and their MOA?
* Clonidine and Methyldopa * Primary antihypertensive activity due to α agonist activity in brainstem, decreasing sympathetic stimulation. Bind more tightly to α2 than α1
28
What is the MOA of α1 blockers used for HTN? Drugs?
* 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
What is the MOA of minoxidil and hydralazine?
Minoxidil: Opens K+ channels in smooth muscles, stabilizes potential, less likely to contract. Dilates arteries, arterioles Hydralazine: Dilates arterioles (NO production)
30
What is the MOA and uses of sodium nitroprusside?
* 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
What is the MOA and uses of sodium fenoldopam?
* Agonist of D1 receptors, causing diuresis * Peripheral arteriolar dilator * HTN emergencies, post-op HTN
32
Describe the RAAS pathway and drugs that work here.
33
Describe the normal intracellular cardiac contractility cycle?
* “Trigger” calcium enters cell * Binds to channel in SR, release stored calcium * Frees actin to interact with myosin
34
Describe the differences between systolic and diastolic heart failure?
**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
What is MOA and effects of digoxin?
* Inhibits Na+/K+ ATPase * Slows down removal of calcium by NCX * Maintains normal resting potential * Positive inotrope
36
What are the EC50 and TC50 of digoxin?
EC50 – 1 ng/mL TC50 – 2 ng/mL
37
What drug is a bypyridine?
Milrinone
38
How do PDE inhibitors increase inotropy?
* Inhibt enzymes that inactivate cAMP and cGMP * Positive inotropic effects * Main action from vasodilation
39
Explain the phases of cardiac action potentials and the ion channels participating?
40
What are the 4 classes of antiarrythmics and their MOA?
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
What class are quinidine, lidocaine, and flecaninde in? Effects on cardiac cycle? Dissociation?
Class I - Na+ channel blockers
42
What is the MOA of amiodarone? Uses?
DOC for VT
43
Explain the MOA of carbonic anhydrase inhibitors? Where do they work?
Proximal convuluted tubule
44
Loop diuretics MOA? Examples?
* Inhibit NKCC2 in thick ascending loop of henle * Furosemide (sulfa) * Ethacrynic acid (non-sulfa)
45
What electrolytes are reabsorbed via the paracellular route in the ascending loop of henle? How?
Ca++ and Mg++ The secretion of K+ creates a positve lumen potential and drives Ca and Mg through paracellular route
46
Thiazaides MOA? Example?
* Inhibit NaCl transport in DCT (NCC) * Some inhibition of CA activity * Hydrochlorothiazide
47
Describe upstream diuretic effects on the collecting tubule?
* 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
How do aldosterone and spirinolactone affect the collecting tubule?
Aldosterone: * Increase Na+ and water reuptake (ENaC) * Increases blood volume Spironolactone * Block aldosterone receptors * Potassium sparing
49
What are ADH affects at the collecting tubule? Its antagonist?
* Increases water reabsorption * Adds preformed AQP2 to apical membrane * Increases blood volume * Makes more concentrated urine * Antagonist: Conivaptan
50
What are the uses and toxicities of mannitol?
* Used mainly to reduce intracranial pressure * Promote removal of renal toxins Toxicity * Extracellular volume expansion * Rapidly distributed to extracellular compartments * Dehydration

Z-Advanced Pharmacology (17 decks)

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