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Drug Info Flashcards

1
Q

only insulin suitable for IV use - human sequence

A

Regular insulin

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2
Q

B28 proline replaced by aspartic acid

A

Insulin Aspart

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3
Q

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

A

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

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4
Q

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

A

Insulin Glulisine

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5
Q

B28 and B29, proline-lysine residues are reversed

A

Insulin Lispro

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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

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7
Q

Treatment for hypoglycemia

A

sugary snack, IV glucose or IM glucagon

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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

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9
Q

Which Insulin related drugs mimic postprandial states

A

Normal Insulin, Insulin Aspart/Glulisine/Lispro

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10
Q

Which Insulin related drugs basal insulin secretion

A

NPH, Insulin Glargine/Detemir

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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

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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

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13
Q

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

A

Metformin

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14
Q

Metformin mechanism

A

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

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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

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16
Q

Contraindications for Metformin

A

alcoholism, renal insufficiency, hepatic disease, hypoxic pulmonary disease

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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

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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

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19
Q

Metformin metabolism

A

excreted unchanged in urine

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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

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21
Q

Glyburide SE

A

Hypoglycemia, weight gain (increased appetite), sulfur allergy

Long-term use associated w/ increased CV mortality

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22
Q

Glyburide Contraindications

A

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

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23
Q

Repaglinide SE

A

Hypoglycemia (esp if subsequent meal is skipped/delayed)

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24
Q

Repaglinide Contraindications

A

Renal insufficiency, Hepatic impairment

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25
Which drugs are best for early stage Type II Diabetes to prevent progression
Glyburide & Repaglinide
26
Pioglitazone Mechanism
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.
27
Rosiglitazone Mechanism
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.
28
Long-term use of Rosiglitazone & Pioglitazone
decreased TG, slightly elevated LDL and HDL
29
Rosiglitazone & Pioglitazone SE
Weight gain, edema, osteoporosis and bone Fx in women
30
Rosiglitazone & Pioglitazone Contraindications
Pregnancy, hepatic impairment, Heart failure
31
Pioglitazone SE
risk of bladder cancer w/ high dose
32
Rosiglitazone special warning
black box warning removed (increased risk of CV events -MI/stroke)
33
Type II Diabetes (effect takes 1-3 months to be seen - altered gene expression)
Rosiglitazone & Pioglitazone
34
Acarbose Mechanism
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
35
Pramlitidine Mechanism
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
36
Acarbose SE
Gastrointestinal disturbances: flatulence, diarrhea, abdominal pain (due to bacterial metabolism of undigested carbohydrates, diminish w/ usage)
37
Acarbose Contraindications
Inflammatory bowel disease, Renal impairment, Gastrointestinal conditions worsened by distention
38
Pramlitidine SE
Hypoglycemia, gastrointestinal disturbances (nausea), weight loss
39
Which drug is used an as adjunct for Type I and II diabetes Tx
Pramlitidine
40
Sulfur allergy
Glyburide
41
Exenatide Mechanism
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
42
Exenatide SE
nausea, weight loss, hypoglycemia (esp w/ sulfonylurea), pancreatitis, altered pharmacokinetics of drugs (due to delayed gastric emptying)
43
Exenatide Contraindications
pancreatitis
44
Sitagliptin Mechanism
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
Sitagliptin SE
Increased rate of infection (DPP-4 is expressed in lymphocytes), HA, Hypoglycemia (esp w/ sulfonylurea), hypersensitivity rxn, pancreatitis
46
Canagliflozin Mechanism
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
Canagliflozin SE
Genital mycotic infectionss, urinayr tract infections, diuretic effects; increases serum concentration of digoxin
48
Canagliflozin Contraindications
renal impairment
49
Emergency treatment of severe hypoglycemia; Overdose of b-adrenoreceptor blocker
Glucagon
50
Glucagon Mechanism
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
Glucagon SE
Transient n/v, tansient tachycardia and HTN (inotropic and chronotropic effects similar to b-adrenergic agonists)
52
Digoxin Mechanism
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
Digoxin SE
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
Digoxin Drug Interactions
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
What electrolyte imbalances can increase Digoxin toxicity
Increased Ca and Decreased K and Mg
56
Digoxin OD Tx
Gigoxin Immune Fab or KCl
57
Digoxin Immune Fab Mechanism
Antigen binding fragments that bind to the molecules of Digoxin and the resulting Fab-Fragment-Digitalis complex is excreted in the urine
58
Severe, refractory CHF (ICU pts only via IV)
Dobutamine, Dopamine, Inamrinone, Milrinone
59
Dobutamine Mechanism
Synthetic catecholamine-like cardioselective beta-1-adrenergic agonist given IV; Increases CO by increased ventricular beta-1-receptor action
60
Dopamine Mechanism
Endogenous catecholamine given IV; Direct activation of beta-1-adrenergic receptors; Increases HR and Cardiac O2 demand more than Dobutamine
61
Inamrinone & Milrinone Mechanism
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
What drugs are used once a tolerance has been built to Dobutamine and Dopamine
Inamrinone & Milrinone (independent of b-receptor #s)
63
Inamrinone SE
Thrombocytopenia, Increased myocardial O2 demand (fatal w/ ischemic heart disease)
64
Milrinone SE
Increased myocardial O2 demand (fatal w/ ischemic heart disease)
65
Captopril SE
Sulfydryl group - rash, loss of taste, proteinuria, renal abnormalities
66
If GFR drops below 30 in CHF then
switch from thiazide to Loop diuretic
67
ACE-II not only decreases preload and after load but also prevents
cardiac remodeling (aldo - fibrosis, A-II - hypertrophy)
68
Which dry can increase ovulation in insulin resistant women
Metformin
69
Inhibits liver output of glucose
Metformin
70
ACE-I SE
Non-productive cough
71
Which ACE-I is a prodrug and requires functioning liver for activation?
Enalapril
72
Losartan, Valsartan, Candesartan mechanism
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
Which is better at preventing cardiac remodeling ARB or ACE-I
ARB
74
Hydralazine Mechanism
arterial vasodilator - afterload reduction
75
Nitroprusside Mechanism
Preload AND Afterload Reduction; IV administration - only for ICU use
76
Nitroglycerin Mechanism
Venodilation -> Preload Reduction; Tolerance may develop
77
Isosorbide Dinitrate Mechanism
Venodilation -> Preload Reduction; Tolerance may develop
78
Nesiritide Mechanism
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
Which drugs are useful in pts w/ less severe CHF, but contraindicated in severe CHF
B-Blockers (Bisoprolol, Carvedilol, Metoprolol)
80
Antioxidant; alpha- and beta-blocker
Carvedilol
81
Metoprolol Mechanism
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
Hospitalized pts w/ CHF hyponatremia Tx
Conivaptan and Tolvaptan
83
CHF pts w/ severe condition refractory to other therapies | Pts right after a MI, who have pre-existing chronic CHF Tx
Hydralazine, Nitroprusside, Nitro, Dinitrate, Nesiritide
84
Decreases rise in phase 0 Na channels to slow conduction velocity, but doe snot effect ERP duration
Flecainide
85
Inhibits Cardiac K channels to prolong AP duration, cell-cell coupling to decrease conduction velocity, Tx all types of arrhythmias
Amiodarone
86
Interstitial pulmonary fibrosis SE of
Amiodarone
87
Na channel inhibitor for Tx of ventricular arrhythmias
Lidocaine
88
Lupus Syndrone SE
Procainamide
89
May cause TdP arrhythmias due to prolonging of ventricular AP duration (AT prolongation); N/V, diarrhea, cinchonism; Decrease BP and increase regular sinus rhythm
Quinidine
90
________ increases serum levels of Digoxin by displacing it from plasma proteins
Quinidine
91
Na inhibitor; Shortens phase 3 repolarization, decreasing AP duration and ERP, w/o much decrease in conduction veolocty/phase 0 slope
Lidocaine
92
Emergency treatment of ventricular arrhythmias arising acutely during a MI; Suppresses ventricular arrhythmias caused by abnormal automaticity; Stops TdP precisely by decreasing AP duration
Lidocaine
93
Decreasing the slop of phase 4 =
decreased automaticity
94
Decrease phase 4 Ca2+ and decrease automaticty
Class 2 - Propanolol, acetbutol, esmolol
95
Phase 0 decrease =
slowed conduction
96
Severe arrhythmias resistant to other drugs
Flecainide
97
Acute arrhythmias during surgery or emergency situations Tx
Esmolol
98
Which class inhibits K channels to increase AP duration and ERP
Class 3 - Amiodarone, Dofetilide
99
Niacin lowers lipids but
aggravates hyperglycemia
100
Inhibits only K+ channels, similar to NAPA, to prolong ADP and ERP
Dofetilide
101
Ventricular TdP as a SE
Dofetilide and Quinidine
102
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
Verapamil & Diltiazem
103
Apprehension, fear of impending doom, flushing, SOB, chest pain (bronchospasm) SE
Adenosine
104
Tx for PSVT
Adenosine
105
Adenosine Mechanism
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
Which may worsen arrhythmias of WPW + Afib
Class 4

Pharm Exam 7 (2 decks)

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