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Unit 4 JG > Pharm > Flashcards

Pharm Flashcards

1
Q

heart: (inward/outward) current: the potassium current, I-K1

A

outward (contributes most to repolarization of cardiac myocyte after an AP, phase 4)

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2
Q

heart: (inward/outward) current: the fast sodium current, I-Na

A

inward (phase 0 of AP)

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3
Q

heart: (inward/outward) current: the L-type calcium current, I-Ca-L

A

inward, during plateau phase of AP, phase 2

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4
Q

heart: (inward/outward) current: the pacemaker current, I-f

A

inward (funny current–activates with hyperpolarization)

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5
Q

heart: necessary to initiate electrical activation (functioning pacemaker/autonomic innervation/electrical coupling of myocytes/electromechanical coupling)

A

functioning pacemaker

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6
Q

heart: necessary to ensure propagation of electrical activation (functioning pacemaker/autonomic innervation/electrical coupling of myocytes/electromechanical coupling)

A

excitable myocytes and electrical coupling of myocytes

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7
Q

heart: necessary to translate electrical activation into mechanical contraction (functioning pacemaker/autonomic innervation/electrical coupling of myocytes/electromechanical coupling)

A

electromechanical coupling

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8
Q

heart: (duration of P wave/PR interval/shape of QRS complex/duration of QT interval/degree of QT elevation) reflects rate of atrial activation

A

duration of P wave

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9
Q

heart: (duration of P wave/PR interval/shape of QRS complex/duration of QT interval/degree of QT elevation) reflects conduction time from atria to the ventricles

A

PR interval

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10
Q

heart: (duration of P wave/PR interval/shape of QRS complex/duration of QT interval/degree of QT elevation) reflects adaptation of myocardial cells to changing HR

A

duration of QT interval

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11
Q

heart: (duration of P wave/PR interval/shape of QRS complex/duration of QT interval/degree of QT elevation) reflects sequence and rate of activation of the ventricles

A

shape of QRS

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12
Q

heart: (duration of P wave/PR interval/shape of QRS complex/duration of QT interval/degree of QT elevation) indicative of ischemia

A

degree of QT elevation

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13
Q

heart: (Na/Ca/K current Kr/transient outward K current/K current Ks) reduces propagation velocity in ventricular myocardium when blocked

A

Na current

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14
Q

heart: (Na/Ca/K current Kr/transient outward K current/K current Ks) block of these two currents can shorten the AP without affecting propagation velocity in the ventricular myocardium

A

calcium and Ks

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15
Q

heart: (Na/Ca/K current Kr/transient outward K current/K current Ks) these two currents are activated during Phase 1 and 2 and do not affect propagation

A

transient outward K current I-to and I-Kr

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16
Q

heart: phase (0/1/2/3/4) due to activation of fast voltage gated Na channels

A

0

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17
Q

heart: phase (0/1/2/3/4) due to inactivation of fast sodium channel current and activation of transient outward K current I-to

A

1

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18
Q

heart: phase (0/1/2/3/4) due to inward calcium channels and outward K channels

A

2 (plateau)

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19
Q

heart: phase (0/1/2/3/4) due to outward K channels

A

3 (final phase of repolarization)

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20
Q

heart: phase (0/1/2/3/4) due to inward rectifier K current

A

4 (resting)

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21
Q

heart: conduction of cardiac impulse is (fastest/slowest) in nodal tissues

A

slowest (SA and AV nodes)

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22
Q

heart: conduction of cardiac impulse is (fastest/slowest) in His-Purkinje fibers

A

fastest

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23
Q

heart: conduction of cardiac impulse in which cells is intermediate velocity

A

atrial and ventricular cells

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24
Q

heart: (increases/decreases) HR: parasympathomimetic agent

A

decreases (hyperpolarize membrane potential)

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25
Q

heart: (increases/decreases) HR: less negative threshold potential

A

decreases (will take longer time to reach threshold)

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26
Q

heart: (increases/decreases) HR: vagal stimulation

A

decreases (release of ACh, hyperpolarizes membrane potential)

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27
Q

heart: (increases/decreases) HR: increased slope of diastolic depolarization

A

increases (shorter time to threshold)

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28
Q

heart: (increases/decreases) HR: ACh-esterase inhibitors

A

decreases (prolong affect of ACh, hyperpolarizes membrane potential)

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29
Q

heart: (desmosomes/intercalated disks/T tubules/Gap junctions/Bundles of Kent) are low resistance pathways that allow the propagation of the impulse

A

Gap junctions

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30
Q

heart: (desmosomes/intercalated disks/T tubules/Gap junctions/Bundles of Kent) mechanical coupling between cells

A

desmosomes

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31
Q

heart: (desmosomes/intercalated disks/T tubules/Gap junctions/Bundles of Kent) a membrane specialization between cardiac cells

A

intercalated disk (comprised of desmosomes and gap junctions)

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32
Q

heart: (desmosomes/intercalated disks/T tubules/Gap junctions/Bundles of Kent) invaginations of the sarcolemmal membrane into the cell interior

A

T tubules

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33
Q

kidney: (acetazolamide/mannitol/cholothiazide/
tramterene/spironolactone) is a carbonic anhydrase inhibitor which decreases bicarbonate reabsorption in the proximal tubule

A

acetazolamide

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34
Q

kidney: (HCTZ/amiloride/furosemide/isosorbide/indapamide) would benefit a pt taking Lithium having trouble maintaining fluid balance

A

amiloride (blocks channel mediated lithium uptake by cells in late distal tubule and collecting duct)

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35
Q

kidney: (thiazide/amiloride/furosemide/isosorbide/indapamide) may be prescribed to mitigate the effect of lithium induced diuresis, but requires an assessment of blood lithium levels

A

thiazide–due to the increase in proximal tubule lithium reabsorption when prescribing thiazides in patients taking lithium

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36
Q

kidney: (thiazide/amiloride) puts patient at risk for hypokalemia

A

thiazide

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37
Q

kidney: which nephron segment reabsorbs most of the glomerular filtrate

A

proximal tubule

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38
Q

kidney: the increase in urine volume caused by osmotic diuretics is attributed to its effect in the ______ (nephron segment)

A

proximal tubule

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39
Q

kidney: (amiloride/HCTZ/furosemide/acetazolamide/aminophylline): limits ability of kidney to conserve fluid volume and make a hyperosmotic urine

A

furosemide

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40
Q

kidney: (amiloride/HCTZ/furosemide/acetazolamide/aminophylline) decreases solute reabsorption in the medullary thick ascending limb of the LoH, which decreases the counter-current multiplication of solute concentrations

A

furosemide

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41
Q

kidney: what is the free water clearance when the ECF is neither contracted nor expanded, and the edema has been corrected?

A

0

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42
Q

kidney: (toresemide/metolazone/methazolamide/spironolactone/amiloride/isosorbide) inhibits carbonic anhydrase in the proximal tubule

A

methazolamide

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43
Q

kidney: (toresemide/metolazone/methazolamide/spironolactone/amiloride/isosorbide) inhibits Na, K, Cl Cotransport in the thick ascending limb of the loop of Henle.

A

torsemide

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44
Q

kidney: (toresemide/metolazone/methazolamide/spironolactone/amiloride/isosorbide) thiazide like diuretic which inhibits Na, Cl cotransport in the early distal tubule

A

metolazone

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45
Q

kidney: (toresemide/metolazone/methazolamide/spironolactone/amiloride/isosorbide) inhibits Na channels in the late distal tubule and collecting duct

A

amiloride

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46
Q

kidney: (hypoventilation/bicarbonate infusion/ketoacidosis/increasing titratable acid excretion/increasing ECF pCO2) promotes increased renal clearance of salicylate

A

bicarbonate infusion, raises pH of tubular fluid

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47
Q

kidney: intravascular volume = _% of body weight

A

7%

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48
Q

kidney: The Na, Cl cotransporter in the luminal membrane of the early distal tubule is the target of what type of diuretics

A

thiazide

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49
Q

kidney: Thiazide and thiazide-like diuretics block sodium reabsorption at which nephron segment

A

early distal tubule

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50
Q

kidney: what type of diuretic is chlorthalidone

A

thiazide like

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51
Q

kidney: The countercurrent multiplication of the cortical to medullary ion concentration gradient arises from active solute transport in the (thin/thick) ascending limb of the loop of Henle.

A

thick

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52
Q

kidney: renal wasting of K in the urine induced by diuretics results from an increase in (Na secretion/K secretion/Na reabsorption/K reabsorption) in the late distal tubule

A

Na reabsorption

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53
Q

kidney: (lumenal membrane Na/basolateral Na-K-Cl cotransport/basolateral K/basolateral Na-K-ATPase/lumenal membrane K) channels couple increased sodium reabsorption to increased K secretion in the cortical collecting duct

A

basolateral Na-K-ATPase

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54
Q

kidney: thiazide diuretics decrease free water clearance by (a decrease/an increase) in urine osmolarity

A

an increase

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55
Q

kidney: (mannitol/HCTZ/furosemide/spironolactone/bumetanide) corrects hypercalciuria

A

HCTZ. thiazides induce an increase in Ca reabsorption from the tubular fluid

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56
Q

kidney: Most of the sulfonamide diuretics present in the tubular fluid arise from secretion in which part of the nephron

A

proximal tubule

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57
Q

kidney: (amiloride/torsemide/methazolamide/indapamide/dichlorphenamide) most rapidly contracts ECF volume

A

torsemide (high ceiling loop diuretic which induces the greatest incrase in urine flow rate)

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58
Q

kidney: percentage of renal plasma flow normally filtered in the glomerulus is __%

A

20%

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59
Q

kidney: (amiloride/torsemide/methazolamide/indapamide/dichlorphenamide) prevents hypokalemia, is a K sparing diuretic

A

amiloride

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60
Q

kidney: The (ion-ion) cotransporter in the lumenal membrane of the early distal tubule is the target of thiazide diuretics

A

Na-Cl

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61
Q

kidney: (amiloride/torsemide/methazolamide/indapamide/dichlorphenamide) is a high ceiling/loop diuretic

A

torsemide (inhibits Na, K, 2Cl cotransport in thick ascending limb of LoH)

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62
Q

kidney: Amiloride and HCTZ both (decrease/increase) calcium reabsorption in the early and late distal tubule and lower calcium concentration in the urine.

A

increase (corrects hypercalciuria)

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63
Q

kidney: (bumetanide/indapamide/chlorothiazide/triamterene/torsemide) can cause hyperkalemia because it is a K sparing diuretic

A

triamterene by decreasing K secretion in the late distal tubule

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64
Q

kidney: lithium may induce nephrogenic diabetes insipidus by an effect on which segment of the nephron

A

collecting duct (interferes with ADH to increase water permeability)

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65
Q

kidney: (positive/negative) free water clearance is a response to dehydration

A

negative

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66
Q

kidney: acetazolamide increases the concentration of which anion in the tubular fluid

A

HCO3-

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67
Q

kidney: patient with renal dz and decreased GFR has a failure to respond to high ceiling diuretics because of (a decrease/an increase) in plasma organic anions, which prevents tubular secretion of diuretic

A

an increase

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68
Q

kidney: Aldosterone-dependent regulation of Na+ reabsorption occurs in which nephron segment

A

late distal tubule

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69
Q

kidney: (amiloride/torsemide/methazolamide/indapamide/dichlorphenamide) used to prevent stone formation in the kidney

A

indapamide (thiazide like diuretic)

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70
Q

kidney: Diuresis is a symptom of uncontrolled diabetes mellitus. This diuresis results primarily from a
decrease in fluid and solute reabsorption in which segment of the nephron?

A

proximal tubule (due to high glucose levels, the filtered load of glucose exceeds the resorptive capacity of the prox tubule)

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71
Q

kidney: High ceiling or loop diurectics induce the largest diuresis by inhibition of solute transport in which nephron segment

A

the thick ascending loop of Henle

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72
Q

kidney: (amiloride/furosemide/indapamide/chlorothiazide/acetazolamide) induces the largest diuresis in the shortest time, reversing a crisis episode of pulmonary edema

A

furosemide (high ceiling loop diuretic)

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73
Q

kidney: the urine osmolarity of someone with nephrogenic diabetes insipidus is (very high/very low)

A

very low (100mOsm/kg H2O) because the collecting ducts are unresponsive to ADH and therefore impermeable to water)

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74
Q

kidney: The kidney functions to maintain ECF osmolality constant while responding to a negative
Na+ balance by isosmotically (increasing/decreasing) the ECF volume proportionate to the negative Na+ balance while increasing Na+ reabsorption.

A

decreasing

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75
Q

kidney: Which nephron segment is constitutively “leaky” and unable to maintain an osmotic gradient?

A

proximal tubule

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76
Q

kidney: (chlorothiazide/furosemide/spironolactone/triamterene) compromises the kidney’s ability to compensate for dehydration

A

furosemide–inhibits medullary solute reabsorption in the thick ascending LoH. Over time, this decreases the cortico-medullary solute conc gradient and the magnitude of negative free water clearance.

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77
Q

kidney: (mannitol/furosemide/bumetanide/triamterene/HCTZ) compensates for diuretic induced hypokalemia

A

triamterene, a K sparing diuretic which decreases fractional excretion of K

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78
Q

kidney: (amiloride/mannitol/bumetanide/torsemide/chlorothiazide) increases negative free water clearance in patients taking lithium

A

amiloride (blocks apical membrane channel in late distal tubule and collecting duct which permits access of lithium intracellularly)

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79
Q

kidney: thiazide diuretics control polyuria from nephrogenic diabetes insipidus by an indirect effect on (corticomedullary solute gradient/LoH solute transport/glomerular filtration/collecting duct solute transport)

A

glomerular filtration. thiazide decreases ECF volume which induces a decrease in GFR (decrease GFR leads to decreased urine excretion)

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80
Q

kidney: (amiloride/spironolactone/chlorothiazide/acetazolamide/aminophylline) slows the time-dependent renal compensation to ECF volume expansion

A

chlorothiazide–inhibits solute reabsorption in the diluting segment of the nephron which raises the osmolarity of the tubular fluid and urine, decreasing the positive free water clearance in response to ECF expansion

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81
Q

kidney: (amiloride/spironolactone/HCTZ/mannitol/aminophylline) causes hyponatremia in response to excess fluid consumption

A

HCTZ–inhibits solute reabsorption in the diluting segment of the nephron, raises the osmolarity of tubular fluid and urine, decreases the positive free water clearance in response to ECF volume expansion –> risk for hyponatremia

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82
Q 
kidney: A localized increase in intravascular hydrostatic pressure will drive an ECF fluid shift
from the (interstitial/intravascular) to the (interstitial/intravascular) space.
A

from the intravascular to the interstitial

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83
Q

kidney: at normal hydrostatic pressure, ECF distribution is __% interstitial and __%intravascular

A

75% interstitial, 25% intravascular

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84
Q

kidney: Which segment of the nephron causes a reduced fractional excretion of Na+ in response to
aldosterone?

A

late distal tubule and collecting duct

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85
Q

kidney: an elevated level of ADH would result in a (higher/lower) urine osmolarity

A

higher urine osmolarity (increases reabsorption of water, negative free water clearance)

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86
Q

kidney: (furosemide/chlorothiazide/triamterene/spironolactone/amiloride) is a competitive antagonist of the cytoplasmic aldosterone receptor in the late distal tubule and collecting duct

A

spironolactone (does not interact with a membrane transport protein)

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87
Q

kidney: (amiloride/spironolactone/chlorothiazide/acetazolamide/aminophylline) prevents mountain sickness, controls intraocular fluid pressure, may cause metabolic acidosis

A

acetazolamide (carbonic anhydrase inhibitor which blocks bicarb transport in proximal tubule)

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88
Q

diuretics: (increase/decrease) excretion of sodium

A

increase, by defn (water follows solute) EXCEPT mannitol

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89
Q

diuretics: (carbonic anhydrase inhibitor/loop/thiazide/K sparring) cause acidosis, increased urinary excretion of HCO3-

A

carbonic anhydrase inhibitor (acetazolamide)

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90
Q

diuretics: (carbonic anhydrase inhibitor/loop/thiazide/K sparring) cause increased calcium excretion, alkalosis

A

loop (ethacrynic acid, furosemide, torsemide)

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91
Q

diuretics: (carbonic anhydrase inhibitor/loop/thiazide/K sparring) cause decreased Ca excretion, alkalosis

A

thiazide (HCTZ, indapamide, metolazone)

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92
Q

diuretics: (carbonic anhydrase inhibitor/loop/thiazide/K sparring) cause acidosis with decreased K excretion

A

K sparring (amiloride, triamterene, spironolactone, eplerenone)

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93
Q

diuretics: (carbonic anhydrase inhibitor/loop/thiazide/K sparring): acetazolamide

A

CA inhib

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94
Q

diuretics: (carbonic anhydrase inhibitor/loop/thiazide/K sparring) ethacrynic acid

A

loop

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95
Q

diuretics: (carbonic anhydrase inhibitor/loop/thiazide/K sparring) amiloride, triamterene

A

K sparring

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96
Q

diuretics: (carbonic anhydrase inhibitor/loop/thiazide/K sparring) spironolactone, eplerenone

A

K sparring

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97
Q

diuretics: (carbonic anhydrase inhibitor/loop/thiazide/K sparring) indapamide, metolazone

A

thiazide

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98
Q

antiHTN: if a pt is taking HCTZ already and still has HTN, why is it bad to add furosemide?

A

best to combine tx from different classes. two diuretics will magnify the side effects of diuretic therapy

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99
Q

antiHTN: (beta blockers/loop diuretics/alpha 1 antagonists/thiazide diuretics) have a neutral or beneficial effect on serum lipids

A

alpha 1 antagonists (the others may raise serum lipids)

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100
Q

antiHTN: a cardioselective beta blocker has greater affinity for beta (1/2), and this selectivity is (enhanced/lost) at high concentrations

A

greater affinity for 1 (1 heart, 2 lungs) but selectivity is lost at high concentrations

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101
Q

antiHTN: cardioselective beta blocker WITHOUT intrinsic sympathomimetic activity (metoprolol/acebutolol)

A

metoprolol. (acebutolol) has intrinsic sympathomimetic activity)

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102
Q

antiHTN: pheochromocytoma, oral contraceptives, renal parenchymal dz and renal vascular stenosis can lead to (primary/secondary) HTN

A

secondary (primary=essential=cause unknown)

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103
Q

antiHTN: pts with essential HTN may benefit from (hormone replacement tx/decreased sodium intake)

A

decreased sodium intake and other lifestyle changes (decrease alcohol, stop using OCPs)

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104
Q

antiHTN: ______ is a Zn containing metalloproteinase with two active sites that can break down bradykinin, is found in heart and brain

A

ACE. most abundant in lung, converts angiotensin I to II

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105
Q

antiHTN: recommended to tx HTN in pregnancy (enalapril/losartan/a-methyldopa/captopril/valsartan)

A

a-methyldopa

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106
Q

antiHTN: cardioselective beta blockers decrease (resorption of sodium in nephron/peripheral resistance/cardiac output)

A

cardiac output

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107
Q

antiHTN: (beta 1/beta 2/alpha 1/alpha 2) blocker will reduce vascular resistance by blocking receptors on vascular smooth muscle cells

A

alpha 1 blocker

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108
Q

antiHTN: _____ decreases blood pressure by interfering with the uptake and storage of biogenic amines resulting in depletion or norepinephrine, dopamine, and serotonin in central and peripheral neurons.

A

Resperpine

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109
Q

antiHTN: antihypertensive that may aggravate gout (enalapril/nifedipine/carvedilol/HCTZ/doxasosin)

A

HCTZ (side effect is increased serum uric acid levels)

110
Q

antiHTN: what does it mean for a beta blocker to have intrinsic sympathomimetic activity (ISA)?

A

they interact with the beta receptor in a manner
that interferes with the actions of endogenous NE but results in stimulation of the adrenergic pathway
to varying degrees. Such agents act as competitive inhibitors when endogenous sympathetic activity is high, but act as partial agonist when endogenous
sympathetic activity is low.

111
Q

antiHTN: angiotensin receptor blocker (lisinopril/a-methyldopa/losartan/doxasosin)

A

losartan

112
Q

antiHTN: ACE inhibitor (lisinopril/a-methyldopa/losartan/doxasosin)

A

lisinopril

113
Q

antiHTN: which TWO drugs are beneficial to pts with diabetes and chronic kidney disease (lisinopril/furosemide/a-methyldopa/losartan/doxasosin)

A

lisinopril and losartan

114
Q

antiHTN: which drug is associated with cough (lisinopril/a-methyldopa/losartan/doxasosin)

A

lisinopril ACEi

115
Q

antiHTN: what two classes of drugs should you use when someone with HTN also has diabetes and chronic kidney dz?

A

ACEi and angiotensin receptor blocker

116
Q

antiHTN: example of an ACEi (propranolol/HCTZ/a-methyldopa/enalapril)

A

enalapril PRIL (lisinopril)=ACEi

117
Q

antiHTN: what two types of drugs for HTN can cause harm to a developing fetus

A

ACEi and angiotensin receptor blockers

118
Q

antiHTN: what type of antiHTN is contraindicated in a pt with asthma

A

beta blocker (beta agonists are used to treat asthma)

119
Q

antiHTN: In patients with bilateral renal artery stenosis, glomerular perfusion pressure is maintained by ____ mediated vasoconstriction of the efferent arterioles.

A

angiotensin II (therefore, do not give a pt with renal artery stenosis an angiotensin receptor blocker, it could lead to decreased GFR and kidney failure)

120
Q

antiHTN: in a pt at risk of developing osteoporosis, which drug can increase serum Ca levels (enalapril/nifedipine/HCTZ/carvedilol/doxasosin)

A

HCTZ

121
Q 
antiHTN:  Hydralazine and 
amlodipine can (decrease/increase) proteinuria in chronic kidney dz
A

increase (bad)

122
Q

antiHTN: beta blockers can (improve/worsen) glycemic control in diabetes mellitus

A

worsen

123
Q

antiHTN: which antiHTN used in pregnancy can present with a lupus-like syndrome with joint pain and photosensitivity and anemia (amlodipine/losartan/lisinopril/HCTZ/methyldopa)

A

methyldopa

124
Q

antiHTN: which drug can cause dose-related peripheral edema and reflex tachycardia (amlodipine/losartan/lisinopril/HCTZ/methyldopa)

A

amlodipine

125
Q

antiHTN: (ACEi’s/Ca channel blockers/diuretics/direct vasodilators) have a renoprotective effect due to dilation of the efferent arteriole, thus reducing glomerular hyperfiltration

A

ACE inhibitors act at the efferent arteriole to decrease vascular resistance (dilate)
and therefore, prevent an increase in GFR and hyperfiltration.

126
Q

asthma: (theophylline/cromolyn/betamethasone/prednisone/ipratropium) reverses bronchoconstriction by blocking vagal stimulation

A

ipratroipium (anticholinergic)

127
Q

asthma: (theophylline/cromolyn/betamethasone/prednisone/ipratropium) anticholinergic

A

iprotropium

128
Q

asthma: (theophylline/cromolyn/betamethasone/terbutaline/ipratropium) given orally or by IV injection or by suppositories

A

theophylline (mild to moderate bronchodilator)

129
Q

asthma: (theophylline/cromolyn/salmeterol/albuterol/ipratropium) prevents asthma attacks but does not reverse asthmatic bronchospasm

A

cromolyn

130
Q

asthma: (theophylline/cromolyn/albuterol/prednisone/zileuton) used to reverse acute onset of asthmatic bronchospasm

A

albuterol (beta 2 agonist)

131
Q

asthma: albuterol is a beta 2 (antagonist/agonist)

A

agonist

132
Q

asthma: (theophylline/cromolyn/albuterol/prednisone/ipratropium) decreases reflex bronchoconstriction caused by inhaled irritants

A

ipratropium (blocks vagal pathway, mediating reflex bronchoconstriction)

133
Q

asthma: oral (beta 2 agonist/corticosteroid) has greatest side effects

A

oral corticosteroid

134
Q

asthma: (oral/inhaled) corticosteroid has greatest side effects

A

oral

135
Q

asthma: albuterol decreases bronchoconstriction by acting on (mast cells/basophils.smooth muscle/microvascular endothelium)

A

smooth muscle

136
Q 
angina: \_\_\_\_ (drug class) increase myocardial 
O2 consumption (reflex increased in heart rate and contractility), while others tend to decrease myocardial oxygen consumption (decreased preload with consequent decrease in end
-diastolic pressure, decreased systolic blood pressure and decreased ventricular volume).
A

nitrates

137
Q

cardiac: (digoxin/dobutamine/inamrione/dopamine/isoproterenol) inhibits troponin I

A

digoxin

138
Q

cardiac: (digoxin/dobutamine/inamrione/dopamine/isoproterenol) blocks alpha 2 receptors

A

isoproterenol

139
Q

cardiac: (digoxin/dobutamine/inamrione/dopamine/isoproterenol) inhibits Na-K ATPase

A

inamrione

140
Q

cardiac: (digoxin/dobutamine/inamrione/dopamine/isoproterenol) beta 1 receptor agonist, positive inotrope and chronotrope

A

dobutamine

141
Q

cardiac: (enalapril/propranolol/isosorbide dinitrate/NE/digoxin) for CHF, reduces dyspnea, pulm edema, and systolic dysfunction by decreasing left ventricular afterload

A

enalapril (ACEi that selective vasodilates arteries)

142
Q

cardiac: (enalapril/propranolol/isosorbide dinitrate/NE/digoxin) reduces cardiac output, do not use for CHF

A

propranolol

143
Q

cardiac: (enalapril/propranolol/isosorbide dinitrate/NE/digoxin) selective venodilator

A

isosorbide dinitrate

144
Q

cardiac: treat diastolic heart failure with (dobutamine/verapamil/digoxin/hydralazine/isosorbide dinitrate)

A

isosorbide dinitrate–reduces filling pressure without reducing cardiac output

145
Q

cardiac: (diastolic/systolic) heart failure: dyspnea, near normal ejection fraction

A

diastolic

146
Q

cardiac: (diastolic/systolic) heart failure: decreased ejection fraction

A

systolic

147
Q

cardiac: (dobutamine/verapamil/digoxin/hydralazine/isosorbide dinitrate) is a calcium channel blocker

A

verapamil

148
Q

cardiac: agents with positive inotropic actions (are/are not) indicated if systolic function is normal

A

are not

149
Q

cardiac: (dobutamine/verapamil/digoxin/hydralazine/isosorbide dinitrate) is a vasodilator whose major effects occur in the arterial circulation

A

hydralazine

150
Q

cardiac: (propranolol/dobutamine/carvedilol/bucindolol/inamrione) (2) third-generation beta blockers

A

carvedilol and bucindolol

151
Q

cardiac: (propranolol/dobutamine/carvedilol/aspirin/inamrione) reduces afterload to counteract the negative inotropic properties of adrenergic withdrawal, may even increase cardiac output

A

carvedilol (third gen beta blocker)

152
Q

cardiac: (propranolol/dobutamine/carvedilol/aspirin/inamrione) contraindicated in heart failure

A

propranolol

153
Q

cardiac: (propranolol/dobutamine/carvedilol/aspirin/inamrione) (2) can only be used for in-hospital treatment of heart failure that is refractory to conventional medication

A

dobutamine and inamrione

154
Q

cardiac: ST elevation in normal complexes suggest what?

A

myocardial ischemia

155
Q

cardiac: ____ rhythm: a P wave precedes each normal beat

A

sinus

156
Q

angina: nitroglycerin action (coronary vasodilation/reduced preload/reduced afterload/coronary vasoconstriction/increased ejection time)

A

reduced preload (relaxation of smooth muscle, especially in venous circulation)

157
Q

cardiac: (phenylephrine/clopidogrel/nitroglycerin/metaraminol/isoproteronol) side effect: orthostatic hypotension

A

nitroglycerin (weakness, syncope, dizziness)

158
Q

why would you see rapid HR after administration of nitroglycerin?

A

reflex sympathetic discharge due to a fall in systemic blood pressure

159
Q

atrial flutter: use digitalis to (slow rate of firing at SA node/slow conduction through AV node/decrease refractory period through AV node/decrease rate of conduction through atrial muscle)

A

slow conduction through AV node by enhancing its vagal tone and diminishing sympathetic activity, direct inhibitory effect on AV propagation

160
Q

nitrates in angina pectoris: (increase preload/decrease systolic BP)

A

decrease systolic BP. may cause reflex increase in HR, ventricular size decrease, peripheral venous pooling

161
Q

(decreased peripheral resistance/metabolic vasodilation/alpha adrenergic stimulation/release of ACh) causes increase in coronary blood flow during exercise

A

metab vasodilation

162
Q

nitroglycerin reduces myocardial oxygen needs by reducing (CO/HR/coronary flow/intramyocardial tension)

A

intramyocardial tension

163
Q

three major determinants of myocardial oxygen consumption: systolic wall tension, contractility, and ___

A

HR

164
Q

what causes lethargy and weakness in a patient taking furosemide for CHF?

A

hypokalemia

165
Q

a patient with CHF being treated with furosemide who has developed hypokalemia should receive which type of diuretic in addition?

A

K sparring, like triamterene

166
Q

when digitalis therapy is initiated, serious cardiac arrhythmias may be caused by what element deficiency? (Na/K/Cl/Ca/Zn)

A

potassium (take care when using diuretics in conjunction with digitalis)

167
Q

initial treatment of mild CHF (diuretic/Ca channel blocker/phosphodiesterase inhibitor/first gen beta blocker/catecholamine)

A

diuretic

168
Q

whenever there is an increase in oxygen demand, the coronary vascular resistance (increases/decreases)

A

decreases, with a consequent increase in coronary blood flow

169
Q

angina pectoris: immediate relief (esmolol/nifedipine/propranolol/nitroglycerin/isosorbide dinitrate)

A

sublingual nitroglycerin

170
Q

prevents tachycardia induced by a bolus IV injection of nitroglycerin: (propranolol/isoproterenol/phenoxybenzamine/phentolamine/dobutamine)

A

propranolol–blocks beta receptors in the heart

171
Q

lipids: what type of drug is colestipol

A

bile acid sequestrant

172
Q

lipids: what type of drug is prescribed for children

A

bile acid sequestrant (safe)

173
Q

lipids: what type of drug lowers serum cholesterol by inhibiting a sterol transporter in the endothelial cells of the small intestine (PSCSK9 inhib/ezetimibe/HMG CoA Reductase Inhib-statins/bile acid sequestrant/fibrates/niacin)

A

ezetimibe

174
Q

lipids: what type of drug is colesevelam (PSCSK9 inhib/ezetimibe/HMG CoA Reductase Inhib-statins/bile acid sequestrant/fibrates/niacin)

A

bile acid sequestrant

175
Q

lipids: what type of drug binds to cholesterol and causes its fecal excretion (PSCSK9 inhib/ezetimibe/HMG CoA Reductase Inhib-statins/bile acid sequestrant/fibrates/niacin)

A

bile acid sequestrant

176
Q

lipids: what type of drug is bezafibrate

A

fibrate

177
Q

lipids: what type of drug stimulates fatty acid oxidation and LPL synthesis

A

fibrate

178
Q

lipids: statins (PSCSK9 inhib/ezetimibe/HMG CoA Reductase Inhib/bile acid sequestrant/fibrates/niacin)

A

HMG CoA Reductase Inhibitor

179
Q

lipids: ___ inhibits LDL oxidation in arteries, absorbs cholesterol from cell membrane turnover, delivers cholesterol from peripheral tissues to liver

A

HDL–increased levels decrease risk of CAD

180
Q

lipids: cholesterol (increases/decreases) activity of HMG CoA reductase

A

decreases

181
Q

lipids: cholesterol (inactivates/activates) ACAT - acetyl coA: cholesterol acetyltransferase

A

activates

182
Q

lipids: cholesterol (increases/decreases) txn of the LDL receptor gene

A

decreases

183
Q

lipids: what type of drug produces its effect by binding to and activating the peroxisome proliferator-activated receptor α (PPARα)? (niacin/fibrate/bile acid sequestrant/statin/ezetimibe)

A

fibrate (ex. fenofibrate)

184
Q

lipids: _____ is a nuclear receptor expressed in skeletal muscle, cardiac muscle, hepatocytes, and macrophages, and fibrates work on this receptor

A

PPAR alpha

185
Q

lipids: resins have (many/few) side effects and are (rarely/safely) prescribed in combo with statins or ezetimibe

A

few side effects, safely combined

186
Q

lipids: a combination of fibrate with a ___ (drug type) is inadvisable due to increased risk of myositis

A

statin

187
Q

lipids: 2 resins (nicotinic acid/bezafibrate/cholestyramine/ezetimibe/colesevelam)

A

cholestyramine and colesevelam

188
Q

lipids: (nicotinic acid/bezafibrate/cholestyramine/ezetimibe/colesevelam) best agent for increasing HDL-C, lowers triglycerides, and lowers LDL-C by 25%

A

nicotinic acid

189
Q

lipids: (nicotinic acid/fibrates/ezetimibe/resins) have no effect on HDL-C levels and can actually increase serum TG’s (triglycerides)

A

resins

190
Q

lipids: (nicotinic acid/fibrates/ezetimibe/resins) insignificant effects on TGs and HDL-C levels

A

ezetimibe

191
Q

lipids: (nicotinic acid/fibrates/ezetimibe/resins) variable effects on LDL-C and modest increases in HDL-C

A

fibrates

192
Q

lipids: combination tablet of ezetimibe and ____ is marked because of their complementary mechanistic effects on lowering LDL-C levels

A

simvastatin (Vytorin)

193
Q

lipids: first statin studied in humans, but not marketed as a drug (mevastatin/simvastatin)

A

mevatatin

194
Q

lipids: how do statins work to lower serum cholesterol levels

A

increased LDL-receptor gene txn

195
Q

lipids: statins: (increased/decreased) intracellular cholesterol activates an hepatic protease, which activates a sterol regulatory element binding protein (SREBP), which increases transcription of the LDL-R gene.
Increased expression of LDL-R increases hepatocyte absorption of LDL-C, thus producing a fall in
serum cholesterol levels.

A

decreased

196
Q

antiarrhythmics: cardiac glycoside toxicity induced v tach is likely caused by (increased pacemaker activity/AV node reentry/early after depolarizations/delayed after depolarizations/atrial ectopic focus)

A

DADs

197
Q

antiarrhythmics: Increases in diastolic [__ (ion)]i activate a transient inward cation current the
produces DADs.

A

Ca2+

198
Q

antiarrhythmics: cardiac glycosides (do not affect/affect) normal automatic mechanisms

A

do not affect, and therefore will not increase pacemaker automaticity or an atrial ectopic focus

199
Q

antiarrhythmics: early after depolarizations are enhanced by (increased/decreased) QT interval duration

A

increased

200
Q

antiarrhythmics: Increasing ___ (ion) currents will suppress EAD formation.

A

K+

201
Q

antiarrhythmics: ______ are the primary mechanism for prolonged QT interval arrhythmias and are
enhanced by increases in INa or ICa,L and slow heart rates.

A

early after depolarizations

202
Q

antiarrhythmics: Mobitz Type (1/2) 2nd degree AV block, or Wenckebach phenomenon, is characterized by a gradually increasing PR interval until a ventricular beat is dropped.

A

type 1

203
Q

antiarrhythmics: Which type of cardiac arrhythmia is least likely to require an artificial pacemaker? (sick sinus syndrome/mobitz type II 2nd degree AV block/trifascicular block/3rd degree AV block/Mobitz type I 2nd degree AV block)

A

mobitz type 1

204
Q

antiarrhythmics: Mobitz Type I 2nd degree AV block is typically caused by excessive vagal tone and usually responds to _____ (M2 receptor blockade).

A

atropine

205
Q

antiarrhythmics: Wolff Parkinson White syndrome (will/will not) be terminated by vagal stimulation

A

will not–may become worse

206
Q

antiarrhythmics: v tach (will/will not) be terminated by vagal stimulation

A

will not

207
Q

antiarrhythmics: Automatic AV junctional tachycardia may be slowed, but not terminated, by vagal stimulation or ______.

A

adenosine

208
Q

antiarrhythmics: which tachycardia is most likely to be terminated by vagal stimulation? (paroxysmal SVT/atrial tach/automatic AV junctional tach/v tach/WPW syndrome tach)

A

paroxysmal SVT

209
Q

antiarrhythmics: Atrial tachycardia is usually caused by an

automatic ____ activity and will not be terminated by increased vagal tone.

A

ectopic

210
Q

antiarrhythmics: drug of choice for Mobitz type I 2nd degree AV block (quinidine/procainamide/propranolol/verapamil/atropine)

A

atropine–because Mobitz Type I is caused by excessive vagal tone, so it can be reversed by atropine

211
Q

antiarrhythmics: 2 drugs that may worsen heart block (quinidine/procainamide/propranolol/verapamil/atropine)

A

quinidine and procainamide

212
Q

antiarrhythmics: 2 drugs that further slows AVN conduction in AVN heart block (quinidine/procainamide/propranolol/verapamil/atropine)

A

propranolol and verapamil

213
Q

antiarrhythmics: Class (Ia/Ib/Ic/II/III/IV) Na channel blockers

A

Class I

214
Q

antiarrhythmics: Class (Ia/Ib/Ic/II/III/IV) quinidine, procainamide, disopyramide

A

Ia

215
Q

antiarrhythmics: Class (Ia/Ib/Ic/II/III/IV) lidocaine, mexiletine (oral)

A

Ib

216
Q

antiarrhythmics: Class (Ia/Ib/Ic/II/III/IV) flecainide, propafenone, moricizine

A

Ic

217
Q

antiarrhythmics: Class (Ia/Ib/Ic/II/III/IV) beta blockers

A

II

218
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) propranolol, carvedilol

A

non selective II

219
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) metoprolol, acebutolol

A

II beta i selective

220
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) esmolol

A

fast acting

221
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) prolong phase 3

A

III

222
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) K channel blockers, sotalol

A

III

223
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) ibutilide, dofetilide

A

III

224
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) amiodarone, dronedarone

A

III mixed

225
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) Ca channel blockers

A

IV

226
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) phenylalkamines

A

IV

227
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) verapamil

A

IV example of phenylalkamine

228
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) benzothiazepines

A

IV

229
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) diltiazam

A

IV example of benzothiazepines

230
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) dihydropyridines

A

IV

231
Q

antiarrhythmics: Class (Ia/Ib/Ic/II non selective/II beta i selective/II fast acting/III/IV) nifeidipine, amlodipine, felodipine, isradipine

A

IV example of dihydropyridines

232
Q

carhart: contraindicated in seasonal wheezing (atorvastatin/clopidogrel/enalapril/propranolol/valsartan)

A

propranolol beta blocker contraindicated in asthma

233
Q

carhart: most important ion in determining the electrophysio changes of myocardial ischmia

A

extracellular K: greatest impact on the AP

234
Q

carhart: dipyridamole increases intracellular cAMP and inhibits the uptake/degradation of (NE/renin/AT I/5-HT/adenosine)

A

adenosine

235
Q

carhart: dipyridamole inhibits the breakdown of adenosine, which leads to (vasodilation/anti-platelet action)

A

vasodilation

236
Q

carhart: dipyridamole increases cAMP, which leads to (vasodilation/anti-platelet action)

A

anti platelet

237
Q

carhart: (oxygen therapy/beta blocker) have a positive impact on mortality in acute ST elevation MI

A

beta blocker. Oxygen has not demonstrated mortality benefits.

238
Q

carhart: thrombolytic therapy in acute MI with ST elevation (reduces mortality/has no impact on mortality)

A

reduces mortality. as does aspirin

239
Q

carhart: BNP levels are measured to assess _____ status

A

volume

240
Q

carhart: lactate levels rise with poor _____

A

perfusion

241
Q

carhart: __ (ion) levels increase with the use of spironolactone and need to be monitored frequently

A

K+

242
Q

carhart: what is the effect of spironolactone used in heart failure on Na and creatinine levels?

A

the dose used in heart failure therapy does not cause significant diuresis

243
Q

carhart: (adenosine/endothelin) causes coronary artery dilation

A

adenosine

244
Q

carhart: (beta 2 agonists/endothelin) causes smooth muscle contraction and vasoconstriction of coronary arteries

A

endothelin

245
Q

carhart: peripheral edema side effect (amlodipine/furosemide/isosorbide mononitrate/metolazone/metoprolol)

A

amolodipine (15% incidence of this effect)

246
Q

carhart: dihydropyridine Ca channel blocker (amlodipine/furosemide/isosorbide mononitrate/metolazone/metoprolol)

A

amlodipine

247
Q

carhart: (dipyridamole/heparin/clopidogrel/nitroglycerin) has clear anti platelet effects

A

clopidogrel–thienopyridine derivative

248
Q

carhart: (dipyridamole/heparin/clopidogrel/nitroglycerin) anticoagulant, works on thrombin (not platelets)

A

heparin

249
Q

carhart: (dipyridamole/heparin/clopidogrel/nitroglycerin) secondary anti platelet effects, but is not considered an aspirin alternative

A

nitroglycerin

250
Q

carhart: (dipyridamole/heparin/clopidogrel/nitroglycerin) may worsen ischemia

A

dipyridamole

251
Q

carhart: four drug classes that have a mortality benefit in pt with stable angina

A

beta blockers, aspirin, ACEi’s, statins

252
Q

carhart: (sildenafil/quinidine) quality of life drug in pt with stable angina

A

sildenafil (viagra)

253
Q

carhart: (sildenafil/quinidine) anti arrhythmic which actually increases risk of death in pt with stable angina

A

quinidine

254
Q

carhart: nitrates, Ca channel blockers, ticlopidine improve symptoms in pt with stable angina. what is their effect on mortality?

A

do not demonstrate a survival benefit

255
Q

carhart: ACEi’s (increase glomerular filtration pressure/block the release of vasopressin)

A

block the release of vasopressin. (GFR decreases)

256
Q 
carhart: thrombolytic contraindications (4) 
A. Adenocarcinoma of the colon
B. Aortic dissection
C. Intracranial hemorrhage
D. Pregnancy
E. Recent facial trauma
A

B. Aortic dissection
C. Intracranial hemorrhage
D. Pregnancy
E. Recent facial trauma

257
Q 
carhart: absolute contraindications of thrombolytics (3)
B. Aortic dissection
C. Intracranial hemorrhage
D. Pregnancy
E. Recent facial trauma
A

B. Aortic dissection
C. Intracranial hemorrhage
E. Recent facial trauma

258
Q 
carhart: relative contraindication of thrombolytics (1)
B. Aortic dissection
C. Intracranial hemorrhage
D. Pregnancy
E. Recent facial trauma
A

pregnancy

259
Q

carhart: reduced in the setting of heart failure (aldosterone/melatonin/endothelin)

A

melatonin

260
Q

carhart: elevated in the setting of heart failure (tumor necrosis factor/melatonin)

A

TNF

261
Q

carhart: what should you give instead if captopril is giving a dry cough

A

ARB (sartan)

262
Q

carhart: what do statins increase that cause dry cough

A

bradykinin

263
Q

carhart: treats CAD by relaxing vascular smooth muscle by increasing intracellular cGMP (isosorbide dinitrate/bisoprolol/enalapril)

A

isosorbide dinitrate

264
Q

carhart: isosorbide dinitrate increases intracellular (cAMP/cGMP)

A

cGMP

265
Q

carhart: treats CAD by acting on the myocardium (isosorbide dinitrate/bisoprolol/enalapril)

A

bisoprolol (beta 1 selective)

266
Q

carhart: verapamil and diltiazem are in what drug class

A

non dihydropyridine Ca channel blockers

267
Q

carhart: nondihydropyridine Ca channel blocker (enalapril/bisoprolol/verapamil)

A

verapamil

268
Q

carhart: nondihydropyridine Ca channel blocker (isosorbide dinitrate/diltiazem)

A

diltiazem

269
Q

carhart: used to treat fluid retention in chronic heart failure (diltiazem/aldactone/nifedipine/furosemide)

A

furosemide

270
Q

carhart: 2 vasodilator drugs (diltiazem/aldactone/nifedipine/furosemide)

A

diltiazem and nifedipine

Unit 4 JG (5 decks)

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