Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm Exam 7 > Drug Info > Flashcards

Drug Info Flashcards

1
Q

only insulin suitable for IV use - human sequence

A

Regular insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

B28 proline replaced by aspartic acid

A

Insulin Aspart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Duration of action/Time course of Insulin Aspart/Glulisine/Lispro

A

Onset .25h, Peak 1h, Duration 4-5h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

B3 asparagine replaced by lysine and B29 lysine replaced by glutamic acid

A

Insulin Glulisine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

B28 and B29, proline-lysine residues are reversed

A

Insulin Lispro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Side Effects of Insulin

A

Hypoglycemia, weight gain, allergic reaction, insulin resistance (neutralizing Ab’s), hypertrophy of subQ fatty tissue (repeated injections at 1 site), increased cancer risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Treatment for hypoglycemia

A

sugary snack, IV glucose or IM glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

NPH Insulin

A

Human sequence insulin + aggregates of protamine and zinc (cloudy solution). Aggregate breakdown takes time causing delay, longer time course and variable rate of absorption. Onset 2-5h, Peak 4-9h, Duration 10-16h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which Insulin related drugs mimic postprandial states

A

Normal Insulin, Insulin Aspart/Glulisine/Lispro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which Insulin related drugs basal insulin secretion

A

NPH, Insulin Glargine/Detemir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Insulin Glargine

A

Aspargine at A21 replaced by glycine and 2 argininesare added to the C-terminus of the B chain. Soluble at pH 4, poorly soluble at pH 7, and forms fine precipitant in the interstitial fluids when injetced subQ. Onset 1-4h, Duration 24-36h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Insulin Detemir

A

Threonine at B30 is omitted, C14-fatty acid chain is attached to B29. Self-association at subQ site and binding to albumin in the blood. Onset 1-2h, Duration 20-24h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Prevents hyperglycemia, but does not induce hypoglycemia (euglycemic agent)

A

Metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Metformin mechanism

A

reduction in hepatic gluconeogenesis through activation of the AMP-activated protein kinase (AMPK) in hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Metformin SE

A 
anorexia, n/v, abdominal discomfort, diarrhea
Lactic acidosis (prevented by avoiding contraindications: alcoholism, renal insufficiency, hepatic disease, hypoxic pulmonary disease)

Does not cause hypoglycemia or weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Contraindications for Metformin

A

alcoholism, renal insufficiency, hepatic disease, hypoxic pulmonary disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

First-line Tx for Type II Diabetes

Reduced circulating LDL and VLDL and decreases the risk of macrovascular and microvascular disease, may also decrease risk of certain cancers

A

Metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Glyburide Mechanism

A

requires functioning pancreatic beta cells: increase insulin release by binding to the K-atp channel on beta cell membranes and inhibit their activity, leading to depolarization, influx of Ca2+, and insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Metformin metabolism

A

excreted unchanged in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Repaglinide mechanism

A

requires functioning pancreatic beta cells: increase insulin release by binding to the K-atp channel on beta cell membranes and inhibit their activity, leading to depolarization, influx of Ca2+, and insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Glyburide SE

A

Hypoglycemia, weight gain (increased appetite), sulfur allergy

Long-term use associated w/ increased CV mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Glyburide Contraindications

A

Hepatic impairment, renal insufficiency, pregnant & breastfeeding women, elderly or acute CV disease patients (susceptible to hypoglycemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Repaglinide SE

A

Hypoglycemia (esp if subsequent meal is skipped/delayed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Repaglinide Contraindications

A

Renal insufficiency, Hepatic impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which drugs are best for early stage Type II Diabetes to prevent progression

A

Glyburide & Repaglinide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Pioglitazone Mechanism

A

increasing insulin sensitivity in target tissues; Mechanism: acting as PPAR-gamma agonist, to modulate expression of lipid and glucose metabolism genes, primarily in the adipose tissues. Effect: differentiation of adipocytes, resulting in increased sensitivity to insulin-stimulated uptake of glucose and fatty acids and altered adipokine production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Rosiglitazone Mechanism

A

increasing insulin sensitivity in target tissues; Mechanism: acting as PPAR-gamma agonist, to modulate expression of lipid and glucose metabolism genes, primarily in the adipose tissues. Effect: differentiation of adipocytes, resulting in increased sensitivity to insulin-stimulated uptake of glucose and fatty acids and altered adipokine production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Long-term use of Rosiglitazone & Pioglitazone

A

decreased TG, slightly elevated LDL and HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Rosiglitazone & Pioglitazone SE

A

Weight gain, edema, osteoporosis and bone Fx in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Rosiglitazone & Pioglitazone Contraindications

A

Pregnancy, hepatic impairment, Heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Pioglitazone SE

A

risk of bladder cancer w/ high dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Rosiglitazone special warning

A

black box warning removed (increased risk of CV events -MI/stroke)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Type II Diabetes (effect takes 1-3 months to be seen - altered gene expression)

A

Rosiglitazone & Pioglitazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Acarbose Mechanism

A

Competitive inhibition of enteric alpha-glucosidase, enzyme that breaks down complex carbohydrates and oligosaccharides, delays postprandial absorption of glucose since only monosaccharides can be absorbed; insulin-sparing agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Pramlitidine Mechanism

A

Amylin is a peptide released concurrently w/ insulin form the pancreatice beta cells, and acts on the hindbrain to promote satiety, delay gastric emptying, and suppress glucagon release; Amylin analogs act as an insulin-sparing agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Acarbose SE

A

Gastrointestinal disturbances: flatulence, diarrhea, abdominal pain (due to bacterial metabolism of undigested carbohydrates, diminish w/ usage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Acarbose Contraindications

A

Inflammatory bowel disease, Renal impairment, Gastrointestinal conditions worsened by distention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Pramlitidine SE

A

Hypoglycemia, gastrointestinal disturbances (nausea), weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Which drug is used an as adjunct for Type I and II diabetes Tx

A

Pramlitidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Sulfur allergy

A

Glyburide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Exenatide Mechanism

A

Glucagon-like polypeptide-1 (GLP-1) is an incretin; Exenatide activates GLP-1, which results in increased insulin synthesis and secretion in a glucose-dependent manner, delays gastric emptying and decreased appetite due to GLP-1 activation in the periphery, CNS and GIT; also suppresses glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Exenatide SE

A

nausea, weight loss, hypoglycemia (esp w/ sulfonylurea), pancreatitis, altered pharmacokinetics of drugs (due to delayed gastric emptying)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Exenatide Contraindications

A

pancreatitis

44
Q

Sitagliptin Mechanism

A

Dipeptidyl peptidase (DPP-4) is an enzyme that degrades incretin hormones, DPP-4 inhibitors increase the circulating level of both GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) resulting in increased postprandial insulin secretion and a decrease in glucagon levels

45
Q

Sitagliptin SE

A

Increased rate of infection (DPP-4 is expressed in lymphocytes), HA, Hypoglycemia (esp w/ sulfonylurea), hypersensitivity rxn, pancreatitis

46
Q

Canagliflozin Mechanism

A

Sodium-glucose cotransporter 2 (SGLT2) transports filtered glucose from the proximal renal tubule into the tubular epithelial cells, inhibition of SGLTs reduced glucose reabsorption; SGLT2 inhibition in the kidney results in decreased glucose reabsorption, increased urinary glucose excretion, and lowering of blood glucose levels

47
Q

Canagliflozin SE

A

Genital mycotic infectionss, urinayr tract infections, diuretic effects; increases serum concentration of digoxin

48
Q

Canagliflozin Contraindications

A

renal impairment

49
Q

Emergency treatment of severe hypoglycemia; Overdose of b-adrenoreceptor blocker

A

Glucagon

50
Q

Glucagon Mechanism

A

pancreatic alpha cells; Glucagon binds to a G-protein coupled receptor -> A.C. -> cAMP -> glycogen phosphorylase activity and a decrease in glycogen synthase activity; Glucagon raises blood glucose levels by stimulating the breakdown of hepatic glycogen stores, stimulates gluconeogenesis and ketogenesis in the liver; glucagon has no effect on glycogen stores in skeletal mm.

51
Q

Glucagon SE

A

Transient n/v, tansient tachycardia and HTN (inotropic and chronotropic effects similar to b-adrenergic agonists)

52
Q

Digoxin Mechanism

A

direct inhibition of cell membrane bound Na/K-ATPase, reducing the transport of Na out of the cell -> increased intracellular [Na+] -> reduced action of Na/Ca exchanger -> increase in [Ca2+]i -> moreCa2+ available for contraction -> increased contractility (positive inotropic action)

53
Q

Digoxin SE

A

GI: anorexia, n/v, diarrhea (vagal slowing)
Cardiac: arrhythmias (bradycardia, paroxysmal atrial tachycardia, ventricular tachycardia and fibrillation)
CNS: HA, fatigue, drowsiness, mental disorientation, confusion, delirium, convulsion
Vision: blurred vision, white borders or halos on dark objects

54
Q

Digoxin Drug Interactions

A

Phenylbutazone- displaces Digoxins
Phenobarbital and Phenytoin- decrease plasma levels of Digoxin and increase its metabolism by inducing hepatic microsomal enzymes
Quinidine and Verapamil: increase plasma levels of Digoxin by displacing it from skeletal mm binding sites and inhibiting its renal clearance
Antacid gels, Sulfasalaine, and bile acid being resins reduce the bioavailability of Digoxin

55
Q

What electrolyte imbalances can increase Digoxin toxicity

A

Increased Ca and Decreased K and Mg

56
Q

Digoxin OD Tx

A

Gigoxin Immune Fab or KCl

57
Q

Digoxin Immune Fab Mechanism

A

Antigen binding fragments that bind to the molecules of Digoxin and the resulting Fab-Fragment-Digitalis complex is excreted in the urine

58
Q

Severe, refractory CHF (ICU pts only via IV)

A

Dobutamine, Dopamine, Inamrinone, Milrinone

59
Q

Dobutamine Mechanism

A

Synthetic catecholamine-like cardioselective beta-1-adrenergic agonist given IV; Increases CO by increased ventricular beta-1-receptor action

60
Q

Dopamine Mechanism

A

Endogenous catecholamine given IV; Direct activation of beta-1-adrenergic receptors; Increases HR and Cardiac O2 demand more than Dobutamine

61
Q

Inamrinone & Milrinone Mechanism

A

inhibition of phosphodiesterase resulting in cAMP inactivation inhibition -> increased ventricular cell cAMP and increased free Ca availability, relaxation is improved by stimulating more SR Ca2+ uptake during diastole

62
Q

What drugs are used once a tolerance has been built to Dobutamine and Dopamine

A

Inamrinone & Milrinone (independent of b-receptor #s)

63
Q

Inamrinone SE

A

Thrombocytopenia, Increased myocardial O2 demand (fatal w/ ischemic heart disease)

64
Q

Milrinone SE

A

Increased myocardial O2 demand (fatal w/ ischemic heart disease)

65
Q

Captopril SE

A

Sulfydryl group - rash, loss of taste, proteinuria, renal abnormalities

66
Q

If GFR drops below 30 in CHF then

A

switch from thiazide to Loop diuretic

67
Q

ACE-II not only decreases preload and after load but also prevents

A

cardiac remodeling (aldo - fibrosis, A-II - hypertrophy)

68
Q

Which dry can increase ovulation in insulin resistant women

A

Metformin

69
Q

Inhibits liver output of glucose

A

Metformin

70
Q

ACE-I SE

A

Non-productive cough

71
Q

Which ACE-I is a prodrug and requires functioning liver for activation?

A

Enalapril

72
Q

Losartan, Valsartan, Candesartan mechanism

A

ARBs - preventing A-II mediated vasoconstriction, and decreased TPR/preload; Decreases A-II synthesis of Aldosterone -> decreased Na/H2O retention/afterload; Greater ability to inhibit A-II cardiac remodeling (hypertrophy )bc it prevents ACE-independent pathways as well as ACE-dependent

73
Q

Which is better at preventing cardiac remodeling ARB or ACE-I

A

ARB

74
Q

Hydralazine Mechanism

A

arterial vasodilator - afterload reduction

75
Q

Nitroprusside Mechanism

A

Preload AND Afterload Reduction; IV administration - only for ICU use

76
Q

Nitroglycerin Mechanism

A

Venodilation -> Preload Reduction; Tolerance may develop

77
Q

Isosorbide Dinitrate Mechanism

A

Venodilation -> Preload Reduction; Tolerance may develop

78
Q

Nesiritide Mechanism

A

Vasodilator + Diuretic - decreases both arterial and venous SM tone by increasing intracellular cGMP; Diuretic action due to its natural natriuretic capability as a natriuretic peptide; IV administration - only for ICU use

79
Q

Which drugs are useful in pts w/ less severe CHF, but contraindicated in severe CHF

A

B-Blockers (Bisoprolol, Carvedilol, Metoprolol)

80
Q

Antioxidant; alpha- and beta-blocker

A

Carvedilol

81
Q

Metoprolol Mechanism

A

Lower arterial BP mainly by reducing CO (decreasing contractility and HR), decreased HR and contractility results in lowered O2 demand; Inhibit renin release from JG cells; Specific beta-1 antagonist

82
Q

Hospitalized pts w/ CHF hyponatremia Tx

A

Conivaptan and Tolvaptan

83
Q

CHF pts w/ severe condition refractory to other therapies

Pts right after a MI, who have pre-existing chronic CHF Tx

A

Hydralazine, Nitroprusside, Nitro, Dinitrate, Nesiritide

84
Q

Decreases rise in phase 0 Na channels to slow conduction velocity, but doe snot effect ERP duration

A

Flecainide

85
Q

Inhibits Cardiac K channels to prolong AP duration, cell-cell coupling to decrease conduction velocity, Tx all types of arrhythmias

A

Amiodarone

86
Q

Interstitial pulmonary fibrosis SE of

A

Amiodarone

87
Q

Na channel inhibitor for Tx of ventricular arrhythmias

A

Lidocaine

88
Q

Lupus Syndrone SE

A

Procainamide

89
Q

May cause TdP arrhythmias due to prolonging of ventricular AP duration (AT prolongation);
N/V, diarrhea, cinchonism;
Decrease BP and increase regular sinus rhythm

A

Quinidine

90
Q

________ increases serum levels of Digoxin by displacing it from plasma proteins

A

Quinidine

91
Q

Na inhibitor; Shortens phase 3 repolarization, decreasing AP duration and ERP, w/o much decrease in conduction veolocty/phase 0 slope

A

Lidocaine

92
Q

Emergency treatment of ventricular arrhythmias arising acutely during a MI;
Suppresses ventricular arrhythmias caused by abnormal automaticity;
Stops TdP precisely by decreasing AP duration

A

Lidocaine

93
Q

Decreasing the slop of phase 4 =

A

decreased automaticity

94
Q

Decrease phase 4 Ca2+ and decrease automaticty

A

Class 2 - Propanolol, acetbutol, esmolol

95
Q

Phase 0 decrease =

A

slowed conduction

96
Q

Severe arrhythmias resistant to other drugs

A

Flecainide

97
Q

Acute arrhythmias during surgery or emergency situations Tx

A

Esmolol

98
Q

Which class inhibits K channels to increase AP duration and ERP

A

Class 3 - Amiodarone, Dofetilide

99
Q

Niacin lowers lipids but

A

aggravates hyperglycemia

100
Q

Inhibits only K+ channels, similar to NAPA, to prolong ADP and ERP

A

Dofetilide

101
Q

Ventricular TdP as a SE

A

Dofetilide and Quinidine

102
Q

Block voltage-sensitive L-type Ca2+ channels to decrease inward current carried by Ca2+; Phase 0 and 4 suppression thus slowing conduction and suppressing automaticity, primarily in tissues highly dependent on Ca currents (AV node); Increase APD and ERP in phase 3 of the AV node

A

Verapamil & Diltiazem

103
Q

Apprehension, fear of impending doom, flushing, SOB, chest pain (bronchospasm)
SE

A

Adenosine

104
Q

Tx for PSVT

A

Adenosine

105
Q

Adenosine Mechanism

A

Decreased conduction velocity and decreased abnormal impulse formation in the AV node partly by inhibiting Ca2+ influx and by activating ACh-sensitive phase 4 K+ current

106
Q

Which may worsen arrhythmias of WPW + Afib

A

Class 4

Pharm Exam 7 (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions