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Pharm II Unit II > REVIEW RAMBLINGS > Flashcards

REVIEW RAMBLINGS Flashcards

1
Q

What is the predominant tone of the eyes?

A

Iris radial muscle = sympathetic (a1)

Iris circular muscle = parasympathetic (m3)

Ciliary muscle = parasympathetic (m3)
(But ß also relaxes it)

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2
Q

What is the predominant tone of the heart?

A

Main tone comes from SA node = parasympathetic (m2) slows it down
(But ß1/ß2 accelerate it)

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3
Q

Predominant tone of the blood vessels

A

Predominant are the skin, splanchnic vessels = sympathetic (alpha contracts them)

Skeletal muscle vessels relax by ß2

Endothelium by NO release

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4
Q

Predominant tone of the bronchiolar smooth muscle

A

Parasympathetic (m3) —> contracts

Also relaxes by ß2 but no innervation

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5
Q

What is the predominant tone of the GI tract?

A

Parasympathetic (M3)

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6
Q

What is the predominant tone of the GU smooth muscle?

A

Parasympathetic (M3)

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7
Q

What is the predominant tone of the skin?

A

Sympathetic

Pilomotor smooth muscles and apocrine sweat glands are alpha, but eccrine is M (even though its sympathetic)

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8
Q

Describe presynaptic receptor regulation

A

IT’S A BIG KRIS-KROSS (see pic on slide 9)

Sympathetic fibers release NE, which can bind to its own a2 receptor and inhibit further release of NE

Parasympathetic fibers can also act upon sympathetic fibers by releasing ACh on M2 receptors —> inhibit NE release

Parasympathetic fibers release ACh which can act upon its own M2 receptors to inhibit further release of ACh

Sympathetic fibers can also act upon parasympathetic fibers by releasing NE on a2 receptors —> inhibit ACh release

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9
Q

How is postsynaptic regulation achieved?

A

Up-regulation of receptors (or denervation)

Down-regulation or desensitization of receptors (from excessive stimulation)

Other modulators regulating membrane potentials such as IPSP M2 or EPSP peptides

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10
Q

What are the steps of the baroreflex?

A
  1. Baroreceptor in carotid sinus senses arterial BP
  2. Signal to inhibitory interneurons in nucleus of the tractus solitarius
  3. Inhibitory interneuron signals vasomotor center
  4. Signal goes to autonomic ganglion —> motor fibers to sympathetic nerve ending —> a or ß receptor

See the animation on slide 13

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11
Q

General rules rules regarding drug effects

A

Any decrease in BP —> reflex tachycardia (immediate)

Any decrease in BP —> increased renin release —> increased Na+ and H2O retention (long term effect)

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12
Q

Name all the Carbonic Anhydrase Inhibitors

A

ACETAZOLAMIDE (Diamox)

Dorzolamide (Trusopt)

Brinzolamide (Azopt)

The last two are eye drops

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13
Q

What is the MOA for CA Inhibitors?

A

Inhibits CA enzyme —> blocks H2CO3 production —> Reduces H+ for exchange with Na+, resulting in INCREASED SODIUM (and H2O) LOSS

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14
Q

DOC for acute mountain sickness

A

Acetazolamide (Diamox)

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15
Q

How long does Acetazolamide last?

A

Diuretic effectiveness decreases in several days (why it’s not used as a regular diuretic)

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16
Q

What’s the main adverse effect of CA inhibitors?

A

HYPERCHLOREMIC metabolic acidosis

Develops b/c the Na+ loss is in the form of NaHCO3 and not NaCl

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17
Q

What is the prototype Loop Diuretic

A

Furosemide (Lasix)

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18
Q

MOA for Loop diuretic

A

Blocks the 1 Na+ 1 K+ 2 Cl- cotransporter

—> increased Na+ in the lumen —> diuresis

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19
Q

Most important indication for Furosemide

A

PULMONARY EDEMA - relieves pulmonary congestion by increasing systemic venous capacitance

HF - moves large volumes of water

Hypercalcemia - loops reduce reabsorption of Mg2+ and Ca2+ by reducing the K+ gradient

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20
Q

Most important adverse effect of Loops

A

HYPOKALEMIC METABOLIC ALKALOSIS - induces K+ and H+ loss at the DCT

Others:
Hypocalcemia
Hypomagnesemia
Hyperuricemia
Irreversible ototoxicity
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21
Q

Why makes Ethacrynic Acid a special Loop?

A

It’s not a sulfonamide derivative

It has the highest risk of ototoxicity

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22
Q

MOA for Thiazide Diuretics

A

Inhibition of sodium resorption at the early distal tubule by INHIBITION of the Na+ Cl- co-transporter

Dependent on PG synthesis

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23
Q

Major beneficial effect of thiazides

A

Relaxation of smooth muscle cells —> VASODILATION

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24
Q

Major adverse effects of thiazides

A

Reduced insulin secretion—> HYPERGLYCEMIA***

HYPOKALEMIC metabolic alkalosis***

Hyperuricemia

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25
Q

Contraindications for Thiazide use

A

SULFONAMIDE hypersensitivity

Hypokalemia —> digitalis toxicity and hepatic coma in CIRRHOTIC patients

DIABETICS (reduced insulin secretion —> HYPERGLYCEMIA

People with gout (hyperuricemia)

Those on LITHIUM (clearance reduced —> toxicity

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26
Q

What makes Metolazone a special thiazide?

A

Able to produce diuresis in patients with a reduced GFR (loops can work at low GFRs but most thiazides can’t except this one)

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27
Q

What makes Indapamide a special thiazide?

A

Pronounced vasodilation

Does not increase plasma lipids

Is metabolized by the liver and kidney 50/50

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28
Q

What are the two classes of potassium sparing diuretics?

A

Aldosterone antagonists

Direct inhibitors of Na+ flux

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29
Q

What are the side effects of Spironolactone?

A

Edema

HYPERaldosteronism

HIRSUTISM in women***

GYNECOMASTIA in men***

Occasional HYPERKALEMIA (usually only in combo with other K+ sparing drugs)

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30
Q

What is the only serious toxicity of potassium sparing diuretics?

A

Hyperkalemia

Duh

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31
Q

How are Osmotic Diuretics administered?

A

IV only

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32
Q

What is the MOA for Osmotic Diuretics?

A

Keeps water in the tubules —> produces water diuresis

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33
Q

Adverse effects of osmotic diuretics

A

Diarrhea and other GI effects (dehydration symptoms)

Excessive administration —> extracellular volume expansion —> PULMONARY EDEMA IN HF (CONTRAINDICATED)

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34
Q

Which receptors are targeted by Desmopressin

A

Activates V2&raquo_space; V1 ADH receptors

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35
Q

What is Desmopressin used to treat?

A

Central Diabetes Insipidus

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36
Q

What is the main side effect of the -vaptans (ADH antagonists)

A

Hypokalemia

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37
Q

What did Demeclocycline used to treat?

A

SIADH (used before vaptans were developed)

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38
Q

Most HF is due to __________ dysfunction

A

Left Ventricular

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39
Q

What happens to preload in HF patients?

A

Increased sympathetic and RAAS activity —> Increased venous return —> Increased blood volume and venous tone

THAT’S WHY YOU NEED VENODILATORS

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40
Q

What happens to Afterload in HF patients

A

Increased sympathetic and RAAS activity —> increased peripheral resistance via arterial constriction

THAT’S WHY YOU NEED ARTERIODILATOR DRUGS

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41
Q

What happens to myocardial contractility in HF patients?

A

Decreased contractility as the myocardial muscle fibers are stretched too far as ventricles become dilated

Beta-blockers can REDUCE contractility

Inotropic drugs can INCREASE contractility

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42
Q

MOA for Digoxin

A

Inhibition of membrane sodium pump (Na/K ATPase) leading to cardiac effects:

  • Increased intracellular Na+
  • Increased intracellular Ca2+ leads to increased SR Ca2+ stores
  • Increased actin-myosin interaction by intracellular Ca2+
  • Increased CONTRACTILITY (Positive Inotropy)
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43
Q

Earliest signs of digoxin toxicity?

A

GI effects - even at low doses

Disappear after discontinuation

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44
Q

Most common and dangerous side effect of Digoxin?

A

Arrhythmias: sinus bradycardia, ectopic ventricular beats, AV block, and BIGEMINY

Must stop and give K+ if bigeminy occurs

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45
Q

What else do you need to know about Digoxin

A

ALL OF IT. KNOW ALL OF IT.

GO BACK RIGHT NOW AND READ THOSE SLIDES AGAIN.

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46
Q

When do you use Milrinone?

A

IV only for acute HF or severe exacerbation

Basically PALLIATIVE ONLY

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47
Q

Dobutamine and Dopamine should not be given with…

A

Beta blockers

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48
Q

Which diuretics are most effective at reducing mortality in HF patients?

A

Spironolactone and eplerenone

Additional benefits over other diuretics by inhibiting aldosterone receptors

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49
Q

Main side effect that occurs with ACE inhibitors but not ARBs?

A

Dry cough

Seriously, if you don’t know this by now, we aren’t really friends

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50
Q

What is the most important role of the neprilysin inhibitor in the Sacubitril/Valsartan combo?

A

Reduced sodium retention

Also helps reduce vasoconstriction and cardiac remodeling but for some reason I circled sodium retention

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51
Q

Main side effects of Sacubitril/Valsartan?

A

Hypotension

Hyperkalemia (from the ARB)

COUGH and ANGIOEDEMA)

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52
Q

What is the main contraindication for Sacubitril/Valsartan?

A

Preggos

53
Q

When do we use beta blockers in HF patients

A

Effective only in early stages of HF - dangerous in severe, end-stage HF b/c of the NEGATIVE INOTROPIC effect

54
Q

Drug that reduces mortality if used in early HF

A

Carvedilol - b/c it’s a negative inotropic beta blocker

Just don’t give it in severe/end-stage HF

55
Q

How do the three different vasodilators differ?

A

Sodium nitroprusside - mostly effects the VEINS

Isosorbide dinitrate - precursor of nitric acid (not sure what this means but I wrote it down 🤷‍♀️)

Hydralazine - increases NO

56
Q

Which drug blocks the funny current in the heart?

A

Ivabradine (Corlanor)

It decreases HR when beta blockers can’t/won’t

57
Q

Why do we treat HTN?

A

B/c it leads to an increased incidence of renal failure, CAD, HF, and stroke

Not sure why I highlighted this but I did

58
Q

Only ______% of HTN is due to a specific cause

A

10-15%

Examples:
Renal artery constriction
Coarctation of the aorta
Pheochromocytoma 
Cushing’s disease
Primary aldosteronism (Conn)
59
Q

What do we mean by “essential” HTN?

A

Cause is not known - multifactorial

60
Q

What is the main difference between Stage 1 and Stage 2 hypertension in terms of management?

A

Stage 1 (SBP 130-139 or DBP 80-89) only needs one drug

Stage 2 (SBP ≥140 or DBP ≥ 90) needs two drugs

61
Q

What is the most common cause of HTN treatment failure?

A

Non-compliance

People don’t want to take their damn drugs

62
Q

What’s the biggest benefit of Central Acting Sympatholytics (Clonidine, Methyldopa) in treatment of HTN?

A

No reflex tachycardia

They stimulate medullary a2 adrenergic receptors —> reduced peripheral sympathetic nerve activity

63
Q

When is Methyldopa recommended?

A

In pregnancy

64
Q

Main adverse effects of central acting sympatholytics (clonidine and Methyldopa)

A

Sedation and other CNS effects

Xerostomia

ED

Methyldopa: hemolytic anemia with a (+) Coombs test

65
Q

HTN med beneficial in BPH

A

Prazosin and other a1 adrenergic antagonists

They also do not adversely effect plasma lipids. Didn’t feel like make that a separate card…

66
Q

Major adverse effects of a1 adrenergic antagonists

A

“First dose phenomenon” - postural hypotension may be pronounced with the first dose

Reflex tachycardia

67
Q

Which is the only ß-blocker that IS a vasodilator?

A

Nebivolol - b/c it also includes NO release

68
Q

Which are the non-selective beta blockers

A

Propranolol

Nadolol

Timolol

69
Q

Which are the selective ß1 blockers?

A

Metoprolol

Atenolol

Nebivolol

Acebutolol

70
Q

What are the HIP drugs?

A

Hydralazine
Isoniazid
Procainamide

All are capable of inducing SLE in slow acetylators

71
Q

When is Fenoldopam used?

A

For emergency hypertensive situations

IV only with short half-life

72
Q

Major cardiac effects of CCBs

A

Decreased contractility —> NEGATIVE INOTROPIC

Decreased impulse generation in the SA node —> NEGATIVE CHRONOTROPIC

Decreased AV node conduction —> NEGATIVE DROMOTROPIC

73
Q

Which CCB is most likely to produce reflex tachycardia

A

Nifedipine (highest vasodilation —> marked hypotension —> reflex tachycardia)

74
Q

Myocardial ischemia results from an imbalance between…

A

O2 supply vs O2 demand

Any increase in HR or contractility will increase the need for O2

75
Q

Coronary flow may be decreased by…

A

Shortening diastole when HR increases

Increased ventricular end-diastolic pressure

Reduced diastolic arterial pressure

76
Q

How do Nitrates and Nitrites work for angina?

A

Vasodilation via NO —> cGMP

UNEVEN VASODILATION - large veins are markedly dilated —> increased venous capacitance and decreased afterload

DOC for any acute angina attack - by reducing myocardial O2 requirement

77
Q

Why is nitro given sublingually?

A

To avoid hepatic destruction due to high first pass metabolism

Rapid absorption

Immediate angina release - onset in 1-3 min and duration 10-30 min

78
Q

What is “Monday Disease”?

A

Explosive manufacturers chronically exposed to nitrate would get headache and dizziness on Monday but it would go away by Friday b/c they became tolerant to exposure.

79
Q

Why are CCBs good for chronic angina treatment but not for immediate relief?

A

B/c you need VENOdilation for acute relief

80
Q

What’s one big contraindication for Sildenafil (Viagra)?

A

Administration to patients who are concurrently using organic nitrates or nitrites in any form, b/c vasodilation effects can lead to unconsciousness

81
Q

MOA for HMG-CoA Reductase Inhibitors

A

Active forms are structural analogs of HMG-CoA reductase intermediate in mevalonate synthesis

Reduce plasma LDL by inhibiting the reductase to increase high-affinity LDL receptors

MOST EFFECTIVE DRUG at lowering LDL

82
Q

Hallmark side effects of Statins

A

Increased serum aminotransferase (liver toxicity)

Myopathy and/or muscle pain (w/ increased serum creatine kinase)

Rarely - rhabdomyolysis/myoglobinuria —> renal shutdown

83
Q

Contraindications for statins

A

Preggos

Hepatic disease

84
Q

What will increase the plasma concentration of statins?

A

P450 inhibitors

GRAPEFRUIT JUICE, macrolide (esp erythromycin), cyclosporine, ketoconazole, verapamil, ritonovir

85
Q

What will decrease the plasma concentration of statins?

A

P450 activators

Phenytoin, griseofulvin, barbiturates, rifampin

Gemfibrozil will inhibit their metabolism

86
Q

MOA for bile acid binding resins (Cholestyramine, Colestipol, Colesevelam)

A

Binding to bile acids and preventing their intestinal reabsorption

Too bad they taste like shit

87
Q

In whom do bile acid binding resins have no effect?

A

Homozygous familial hypercholesterolemia (b/c no functional LDL receptors)

88
Q

Who SHOULD bile acid binding resins be used for?

A

Preggos

89
Q

Main side effect of bile acid binding resins

A

Floaty poops

90
Q

Niacin is best for …

A

Increasing HDL

Watch out for that flush tho, and hyperglycemia

91
Q

Fibrates are good for …

A

Reducing triglycerides

Too bad they give you gallstones and inhibit statins

92
Q

How does Zetia work?

A

Blocks intestinal absorption (zebra with diarrhea lol)

No decrease in CV endpoints (mortality)

Only used in combo

93
Q

Why don’t more people use PCSK9 inhibitors?

A

They’re expensive, monthly SC injections

Ain’t nobody got time for that

94
Q

MOA Class IA antiarrhythmics

A

Preferentially block open or activated Na+ channels —> lengthen the duration of action potential

Quinidine, Procainamide

95
Q

MOA Class IB antiarrhythmics

A

Block INACTIVATED sodium channels —> shorten the duration of action potentials

Lidocaine

96
Q

MOA Class IA antiarrhythmics

A

Bind to ALL sodium channels —> no effect on the duration of action potentials

Flecainide

97
Q

MOA Class II antiarrhythmics

A

Reduce adrenergic activity on the heart

BETA BLOCKERS, duh

98
Q

MOA Class III antiarrhythmics

A

K+ channel inhibitors

Amiodarone, Sotalol

99
Q

MOA Class IV antiarrhythmics

A

Calcium channel blockers —> decrease HR, contractility

Verapamil, Diltiazem

100
Q

What are the “Miscellaneous” antiarrhythmics

A

Adenosine, digoxin, Mg, K

101
Q

What is the Secondary action of the Class IA antiarrhythmics?

A

Blocking K+ channels —> prolongs the action potential duration and the effective refractory period

102
Q

DOC for Torsade de pointes

A

Magnesium

103
Q

Adverse effects of Quinidine (Class IA)

A

Low therapeutic index

Cardiac toxicity

Blocks alpha receptors

Paradoxical tachycardia

***TORSADE DE POINTES (aka “Quinidine syncope” - transient and rare to catch on ECG)

104
Q

What is the gene that leads to slow acetylation?

A

NAT2 gene

Watch out for the HIP drugs:
Hydralazine
Isoniazid
Procainamide

105
Q

DOC for acute ventricular arrhythmias

A

Lidocaine (Class IB)

But watch out for CONVULSIONS (one of it’s bad side effects)

106
Q

What is the main side effect to worry about with Flecainide (Class IC)?

A

Strong pro-arrhythmic effect

107
Q

MOA for Amiodarone (Class III)

A

Main MOA: Blocks K+ channels

Other MOAs: 
Blocks Na+ channels
Beta-blocker (like Class II)
Some Ca2+ channel blocking effect
Alpha blocker
108
Q

When DO we use Amiodarone?

A

Effective against both supraventricular and ventricular arrhythmias

DOC for ventricular arrhythmias —> used in ACLS

109
Q

Adverse effects of Amiodarone

A

Slows sinus rate, conduction and prolongs QT —> no Torsade de pointes

Bradycardia, heart block, HF

PULMONARY FIBROSIS***

Yellowish-brown cornea and grayish-blue skin***

Thyroid dysfunction***

110
Q

Non-selective beta blocker that is also a class III antiarrhythmic

A

Sotalol (Betapace)

Used in ventricular and supraventricular arrhythmias

111
Q

Main adverse effect of Sotalol

A

Torsade de pointes

112
Q

As CCBs, Verapamil and Diltiazem are only effective in…

A

The atria

Used for Reentrant supraventricular tachycardia and PSVT, a fib/flutter, and has marked effect on the SA/AV nodes

113
Q

What’s the order of treatment options for PSVT?

A

Acute:
Adenosine, then Esmolol, then CCBs (Class IV)

Chronic:
Beta blockers, then CCBs

114
Q

Where do the intrinsic and extrinsic pathways meet in the coagulation cascade?

A

Factor Xa

115
Q

How is unfractionated heparin administered?

A

Exclusively IV

IM —> hematoma

Onset of action is immediate

116
Q

What’s the benefit of LMWH over UFH?

A

Can be injected subcutaneously

Can be used in pregnancy

Lower incidence of HIT

117
Q

What’s the downside of LMWH?

A

Protamine sulfate does not completely reverse the LMW heparins

118
Q

Which anticoagulant comes from leeches?

A

Bivalirudin

119
Q

Do you have to monitor anticoagulation with Dabigatran (Pradaxa)?

A

No - predictable anticoagulant effects, not monitored by PTT (true of all new anticoagulants)

120
Q

What is the antidote to Direct Inhibitors of Factor Xa (the XaBan’s)

A

Rivaroxaban, Apixaban, Edoxaban, Betrixaban

Antidote is Factor Xa decoy (Andexxa)

121
Q

MOA of Warfarin

A

Inhibits reduction of vitamin K —> interferes with synthesis of II, VII, IX, and X, Protein C and S

Takes time to take effect but lasts 4-5 days after d/c
—> start in combo with heparin for first 5 days

122
Q

Adverse effects of Warfarin

A

Reversal of action (w/ vitamin K) takes time - can use fresh frozen plasma for immediate effects

Quickly reduces levels of Protein C —> cutaneous necrosis/infarction (warfarin-induced thrombosis)

123
Q

Contraindications for Warfarin

A

PREGGOS

LOTS of drug interactions:
Vitamin K - abx
Clotting factors - estrogen/oral bc
Platelet aggregation/function - aspirin
Displace from binding sites on plasma albumin
Inhibit/induce liver microsomes enzymes
124
Q

MOA for Fibrinolytic Agents

A

Convert plasminogen to plasminogen —> lyses thrombus from within

125
Q

How are thrombolytics different from fibrinolytic agents?

A

(Alteplase [tPA] and Tenecteplase)

Higher activity for fibrin-bound plasminogen vs plasma plasminogen —> “clot-selective”

Tenecteplase is more fibrin specific and resistant to PAI-1 than standard tPA)

126
Q

MOA for Aspirin as an anticoagulant

A

Irreversible inhibition of the COX enzyme —> reduced production of TXA2

No prostaglandin synthesis —> decreased platelet aggregation

Lasts the life of the platelet (7-10 days)

127
Q

When is aspirin useful?

A

Secondary prevention of CV events in most patients with established CVD

128
Q

MOA for Clopidigrel, Ticlopidine, and Prasugrel

A

Irreversibly blocks the ADP receptor on platelets —> decreased platelet aggregation

Used in patients who are allergic to aspirin and DOC to prevent thrombosis in patients undergoing placement of coronary stents

129
Q

What are the inhibitors of the GPIIb/IIIa receptor and what do they do?

A

Abciximab, Eptifibatide, Tirofiban

Decrease platelet aggregation by inhibiting GP IIb/IIIa receptors from binding fibrinogen

Used in angioplasty, atherectomy, and stent placement

BUT given IV (not oral like clopidigrel)

Pharm II Unit II (8 decks)

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