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STEP1 - TLe > firstaid - pharm(2) > Flashcards

firstaid - pharm(2) Flashcards

1
Q

Cyclosporine

A

Inhibits calcineurin –> blocks differentiation/activation of T cells –> NO IL-2 (or its receptor) is made

for organ transplant patients

adv rxn: 
nephrotoxicity
gingival hyperplasia
HYPERlipidemia/HYPERglycemia
hirsutism
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2
Q

Tacrolimus

A

Similar to cyclosporine
Inhibits calcineurin –> no IL-2 secretion

Immunosuppresive in organ transplant pts.

adv rxn: everything similar to cyclosporine EXCEPT NO gingival hyperplasia & hirsutism

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3
Q

Sirolimus (Rapamycin)

A

Inhibits mTOR
Inhibits T cell proliferation in response to IL-2

Kidney transplant pts. – use in combo w/ cyclosporine & corticosteroids

adv. rxns:
Hyperlipidemia
Thrombocytopenia
Leukopenia

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4
Q

Azathioprine

A

antimetabolite precursor of 6-mercaptopurine

interferes w/ metabolism/synthesis of nucleic acids; toxic to lymphocytes

Kidney transplants
Autoimmune disorders (glomerulonephritis & hemolytic anemia)

Bone marrow suppression; toxic effects may be increased w/ allupurinol (since mercaptopurine is metabolized by xanthine oxidase)

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5
Q

Muromonab-CD3 (OKT3)

A

Binds CD3 (epsilon chain) on T cells – blocks CD3 interaction w/ T-cell signal transduction

Prevent acute rejection after KIDNEY transplant

adv rxns: cytokine release, hypersensitivity reaction

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6
Q

Aldesleukin (IL-2)

A

Renal cell carcinoma

Metastatic melanoma

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7
Q

Epoetin alfa

A

Anemias (esp in renal failure)

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8
Q

Filgrastim

A

GCSF –> recovery of bone marrow

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9
Q

Sargramostim

A

GMCSF –> recovery of bone marrow

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10
Q

a-interferon

A

Hep B&C
Kaposi’s sarcoma
Leukemia
Malignant melanoma

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11
Q

b-interferon

A

Multiple sclerosis

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12
Q

y-interferon

A

Chronic granulomatous disease

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13
Q

Oprelvekin (IL-11)

A

Thrombocytopenia

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14
Q

Thrombopoietin

A

Thrombocytopenia

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15
Q

Digoxin Immune Fab

A

target = digoxin

andtidote for digoxin toxicity

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16
Q

Infliximab

A

target = TNF-a

Crohn’s, RA, psoriatic arthritis, anklyosing spondylitis

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17
Q

Adalimumab

A

target = TNF-a

Crohn’s, RA, psoriatic arthritis

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18
Q

Abciximab

A

target = glycoprotein IIb/IIIa

prevent cardiac ischemia in unstable angina & pts. treated w/ percutaneous coronary intervention

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19
Q

Trastuzumab

A

Herceptin
target = HER2

HER2-overexpressing breast cancer

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20
Q

Rituximab

A

target = CD20

B-cell non-Hodgkin’s lymphoma

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21
Q

Omalizumab

A

target = IgE

severe asthma

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22
Q

When must B-blockers be used w/ caution in treating HTN?

A

Pts. w/ decompensated CHF (contraindicated in cardiogenic shock - LOW cardiac output)

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23
Q

ACE inhibitor relationship w/ diabetes mellitus

A

Protective against diabetic nephropathy

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24
Q

Antihypertensives for pts. w/ deiabetes mellitus

A

ACE inhibitors/ARBs
Ca2+ channel blockers
a-blockers
b-blockers

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25
Q

DHP Ca2+ channel blockers

A

Nifedipine
Amlodipine

works on SMOOTH MUSCLE –> decrease BP (vessels relax)

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26
Q

non-DHP Ca2+ channel blockers

A

Verapamil
Diltiazem

HEART specific –> decrease contractility

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27
Q

Ad. Side effect of verapamil

A

AV block

slows down AV node
decrease contractility (due to decrease Ca2+) --> weaken heart (BAD for CHF pts.)
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28
Q

Ca2+ channel indications

A 
HTN
Angina
Arrhythmias (not nifedipine*)
Prinzmetal's angina
Raynaud's
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29
Q

Ca2+ channel adv. rxns

A 
Cardiac depression
AV block (Verapamil)
Edema
Flushing
Dizziness (low CO)
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30
Q

Hydralazine

A

Increase cGMP –> smooth muscle relaxation

VASODILATE arterioles» veins

AFTERLOAD reduced

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31
Q

Hydralazine: indications

A

Severe HTN
CHF (problem w/ afterload)

FIRST LINE therapy for HTN in pregnancy (with methyldopa)

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32
Q

What is hydralazine normally co-administered w/ to prevent one of its side effects? What additional side effects are present?

A

B-blocker co-administration w/ hydralazine to PREVENT reflex tachycardia

Compensatory reflex tachycardia makes drug CONTRAindicated in angina/CAD

Lupus-like syndrome

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33
Q

Rx for malignant HTN

A 
Nitroprusside
Labetalol
Fenoldopam
Nicardipine
Clevidipine
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34
Q

Nitroprusside

A

Increase cGMP via release of NO

Cause CN toxicity (releases CN)

Short acting

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35
Q

Fenoldopam

A

Dopamine D1 receptor agonist

Vasodilation of:
Coronary
Peripheral
Renal
Splanchnic

Decrease BP and increase natriuresis

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36
Q

Nitroglycerin

A

Vasodilate by releasing NO in smooth muscle

Increase cGMP

Dilates VEINS»arteries
(contrast w/ hydralazine)

Decrease PRELOAD
(less blood volume returning to heart from systemic system)
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37
Q

Isosorbide dinitrate

A

Same fxn. as nitroglycerin

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38
Q

Anti-anginal therapy (goal is to decrease myocardial O2 consumption - MVO2)

A
  1. Nitrates (preload)
    Dilates veins:
    –decrease EDV (amount of venous return to heart)
    –decrease BP
    –decrease ejection time
    –decrease MVO2
    – increase contractility&HR (reflex response)
  2. B-blockers (afterload)
    - -Increase EDV
    - -increase ejection time
    - - decrease contractility&HR (antiarrhythmic to counter nitrates effects)
  3. Nitrates + b-blockers
    - -decrease BP
    - -decrease HR
    - -GREAT decrease in MVO2
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39
Q

Examples of anti-anginal drugs

A

Ca2+ channel blockers:
Nifedipine ~ Nitrates
Verapamil ~ B-blockers

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40
Q

What b-blockers should NEVER be used in treatment of angina?

A

Pindolol
Acebutolol

Partial B-agonists – CONTRAINDICATED in angina

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41
Q

HMG-CoA reductase inhibitors: examples

A

“-statin”

Lovastatin
Pravastatin
Simvastatin
Atorvastatin
Rosuvastatin
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42
Q

Mechanism of HMG-CoA reductase inhibitors

A

Lowers LDL

Inhibit HMG-CoA –> mevalonate conversion

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43
Q

Toxicities of HMG-CoA reductase inhibitors

A 
Hepatotoxic
Rhabdomyolysis (breakdown of muscle fibers)
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44
Q

Niacin effect on lipids

A

Decrease LDL

Increase HDL

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45
Q

Niacin (vitamin B3): MOA

A

inhibits lipolysis in adipose

reduces hepatic VLDL secretion into circulation

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46
Q

Niacin toxicities

A

Red, flushed face (give ASA to decrease symptom)

Hyperglycemia (acanthosis nigricans)

Hyperuricemia (MAKES GOUT WORSE)

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47
Q

What lipid lowering drug should be avoided in treating gout patients?

A

Niacin –> causes hyperuricemia –> exacerbates gout

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48
Q

Bile acid resins: examples

A

Cholestyramine
Colestipol
Colesevelam

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49
Q

Bile acid resins: MOA

A

Prevent intestinal reabsorption of bile acids –> liver uses cholesterol in body to make more bile acids

DECREASES LDL

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50
Q

Side effects of bile acid resins

A

Bad taste
GI discomfort
Decrease absorption of fat-soluble vitamins
Cholesterol GALLSTONES

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51
Q

Cholesterol absorption blockers: example

A

Ezetimibe

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52
Q

Cholesterol absorption blockers: MOA

A

Decrease LDL

Prevent cholesterol reabsorption at small intestine brush border

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53
Q

Side effect of Ezetimibe

A

Diarrhea

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54
Q

Fibrates: examples

A

Gemfibrozil
Clofibrate
Bezafibrate
Fenofibrate

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55
Q

Fibrates: MOA

A

Upregulate lipoprotein lipase (LPL) –> increase TG clearance

Decrease TGs!

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56
Q

Toxicities of Fibrates

A

Myositis
Hepatotoxic
Cholesterol GALLSTONES

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57
Q

Concommitent use of fibrates + statins leads to what toxicity?

A

Rhabdomyolysis

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58
Q

Cardiac glycoside: example

A

Digoxin

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59
Q

Digoxin: MOA

A

Inhibits Na+/K+ ATPase –> inhibit Na+/Ca2+ antiport –> INCREASE intracellular Ca2+ –> positive inotropy

Increase contractility

Stimulates vagus nerve –> DECREASE HR

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60
Q

Digoxin: indications

A

CHF (increase contractility)

a. fib (decrease conduction at AV node & depression of SA node)

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61
Q

Digoxin toxicities

A

Blurry yellow vision

T wave inversion, AV block
Increase PR, decrease QT

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62
Q

Poor prognostic indicator while on digoxin treatment

A

Hyperkalemia

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63
Q

Factors predisposing pt. to digoxin toxicity

A

Renal failure
Hypokalemia
Quinidine (decrease digoxin clearance)

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64
Q

Antidote for digoxin toxicity (4)

A

Normalize K+ (slowly!)
Lidocaine
Anti-digoxin Fab fragments
Mg2+

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65
Q 
Antiarrhythmics:
Na+ channel blockers (class IA)
A

Quinidine
Procainamide
Disopyramide

Increase AP duration
Increase effective refractory period (ERP)*
Increase QT interval

For use in ventricular tachycardia, reentrant & ectopic supraventricular tachycardia

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66
Q

What phase of the ventricular action potential curve is affected by Class I antiarrythmics?

A

Phase 0

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67
Q

Toxicities: Quinidine

A

Cinchonism - headache, tinnitus

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68
Q

Toxicities: Procainamide

A

Reversible SLE-like syndrome

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69
Q

Toxicities: Disopyramide

A

Heart failure

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70
Q

Toxicities for all class IA antiarrhythmics

A

Thrombocytopenia

Torsades de pointes (due to increase QT interval)

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71
Q 
Antiarrythmics:
Na+ channel blockers (class IB)
A

Lidocaine
Mexiletine
Tocainide

Decrease AP duration

Acute ventricular arrhythmias – preferred for post-MI patients*

Digitalis-induced arhythmias*

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72
Q

What class of antiarrhythmics does phenytoin fall into?

A

Class IB

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73
Q 
Antiarrhythmics:
Na+ channel blockers (class IC)
A

Flecainide
Propafenone

Use for V. tach that progress to V. fib or intractable SVT

LAST RESORT - for pts. with no structural abnormalities

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74
Q

When is use of class IC antiarrhythmics contraindicated?

A

Post-MI patients
Pts. with no structural abnormalities

Significantly prolong refractory period in AV node

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75
Q 
Antiarrhythmics:
B-blockers (class II)
A

Metoprolol
Propanolol
Esmolol
Timolol

Decrease SA and AV node activity via decrease cAMP and decrease Ca2+ currents

AV node most sensitive*
Increase PR interval

Use for V. tach, SVT
Slows ventricular rate during a. fib & a. flutter*

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76
Q

What phase of the ventricular action potential curve is affected by Class II antiarrhythmics?

A

Phase 4

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77
Q

Toxicities of class II antiarrhythmics

A

Impotence
Asthma exacerbation
CNS sedation
cardiovascular (bradycardia, AV block, CHF)

MASK signs of HYPOGLYCEMIA
Treat toxicity w/ glucagon

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78
Q

Toxicity specific to metoprolol

A

Dyslipidemia

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79
Q

Toxicity specific to propranolol

A

Exacerbate vasospasm in Prinzmetal’s angina

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80
Q 
Antiarrhythmics:
K+ channel blockers (class III)
A 
"AIDS":
Amiodarone
Ibutilide
Dofetilide
Sotalol

Used when other antiarrythmics fail

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81
Q

Why are class III antiarrhythmics only used after other Rx have failed?

A

Prolonged QT interval –> could lead to torsades de pointes

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82
Q

Toxicity: Sotalol

A

Torsades de pointes

Excessive B block

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83
Q

Toxicity: Ibutilide

A

Torsades de pointes

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84
Q

Amiodarone toxicity

A 
Pulmonary fibrosis
Hepatotoxicity
Hypothyroidism/hyperthyroidism (due to drug composition containing 40% Iodine)
Corneal deposits
Skin deposits (blue/gray)
Photodermatitis
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85
Q

Tests to monitor what systems while patient is on Amiodarone?

A

Lungs
Liver
Thyroid

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86
Q

Why is Amiodarone a special antiarrhythmic?

A

Has class I, II, III, IV effects bc it alters lipid membrane

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87
Q

Arrhythmics: Ca2+ channel blockers (class IV)

A

Verapamil
Diltiazem

Decrease conduction velocity
Increase ERP
Increase PR interval

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88
Q

Class IV antiarrhythmics used to prevent?

A

nodal arrhythmias (SVT)

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89
Q

Adenosine indication

A

Increase K+ out of cells –> HYPERPOLARIZE cell and DECREASE influx of Ca into cell

Use to diagnose/abolish SVT

SHORT acting (~15 secs)

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90
Q

What can block effects of adenosine on cardiac conduction?

A

Theophylline

Caffeine

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91
Q

Mg2+ indication (what type of cardiac conditions?)

A

Torsades de pointes

Digoxin toxicity

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92
Q

Management of Type 1 diabetes

A

low sugar diet

insulin replacement

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93
Q

Management of Type 2 diabetes

A

dietary modification & exercise –> weight loss

oral hypoglycemics

insulin replacement (due to eventual loss of Islet cells producing adequate amount of insulin & increased insulin resistance as disease progresses)

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94
Q

Rapid-acting insulin

A

Lispro
Aspart
Glulisine

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95
Q

Short-acting insulin

A

Regular insulin

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96
Q

Intermediate acting insulin

A

NPH

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97
Q

Long-acting insulin

A

Glargine

Detemir

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98
Q

Insulin: MOA

liver, muscle, fat

A

Bind insulin receptor (tyrosine kinase activity)

Liver: increase glucose storage as glycogen

Muscle: increase glycogen & protein synthesis, K+ uptake

Fat: helps TG storage

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99
Q

Insulin indications

A

Type 1 & 2 DM, gestational diabetes

Life-threatening hyperkalemia*

Stress-induced hyperglycemia

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100
Q

Insulin toxicity

A

Hypoglycemia

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101
Q

Metformin: MOA

A

Decrease gluconeogenesis

Increase glycolysis (breaks down glucose –> makes ATP)

Increase peripheral glucose uptake (INCREASE insulin sensitivity)

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102
Q

Metformin: indications

A

1st line for Type 2 DIABETES

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103
Q

Metformin: toxicity

A

Lactic acidosis

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104
Q

When is metformin use contraindicated?

A

Pts. with RENAL FAILURE (due to lactic acidosis side effect)

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105
Q

Sulfonylurea: 1st gen (2)

A

Tolbutamide

Chlorpropamide

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106
Q

Sulfonylurea: 2nd gen (3)

A

Glyburide
Glimepiride
Glipizide

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107
Q

Sulfonylurea: MOA

A

Close K+ channel in B-cell membrane –> cell depolarize –> Ca2+ influx –> insulin release

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108
Q

Sulfonylurea: indications

A

Stimulate release of ENDOGENOUS INSULIN in Type 2 diabetes

Requires islet function (NOT effective in type 1 diabetes!)

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109
Q

Sulfonylurea: toxicity (1st gen vs. 2nd gen)

A

1st gen: disulfiram-like effects (Disulfiram is Antabuse – used for long term treatment of alcoholics)

2nd gen: hypoglycemia

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110
Q

Glitazones/thiazolidinediones

A

Pioglitazone

Rosiglitazone

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111
Q

Pioglitazone & Rosiglitazon: MOA

A

Increase insulin sensitivity

Binds PPAR-y nuclear transcription regulator

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112
Q

PPAR-y nuclear transcription regulator

A

Transcription regulator responsible for increasing insulin sensitivity & increase levels of adiponectin–fatty acid storage

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113
Q

Pioglitazone & Rosiglitazon: indications

A

Type 2 diabetes

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114
Q

Pioglitazone & Rosiglitazon: toxicity

A

Weight gain
Edema
Hepatotoxicity
Heart failure (CHF exacerbation, MI)

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115
Q

a-glucosidase inhibitors (2)

A

Acarbose

Miglitol

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116
Q

a-glucosidase inhibitors: MOA

A

Inhibit intestinal brush border a-glucosidases

DELAYS sugar hydrolysis & glucose absorption –> DECREASES availability of sugars –> DECREASE postprandial hyperglycemia

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117
Q

a-glucosidase inhibitors: indications

A

Type 2 diabetes

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118
Q

a-glucosidase inhibitors: toxicity

A

Gi disturbances (b/c they act at intestinal brush border)

don’t use these drugs much anymore

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119
Q

Amylin analogs (1)

A

Pramlintide

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120
Q

Pramlintide: MOA, indications, toxicity

A

MOA: decrease glucagon (decrease sugars)

Indication: type 1&2 diabetes

Toxicity: Hypogylcemia

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121
Q

GLP-1 analogs (2)

A

Glucagon-like peptide (opposite of normal glucagon which is anti-insulin; GLP is pro-insulin!)

Exenatide
Liraglutide

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122
Q

GLP-1 analogs: MOA

A

Increase insulin

Decrease glucagon release

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123
Q

GLP-1 analogs: indications

A

Type 2 diabetes

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124
Q

GLP-1 analogs: toxicity

A

Pancreatitis

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125
Q

DPP-4 inhibitors (3)

A

Linagliptin
Saxagliptin
Sitagliptin

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126
Q

Relationship btwn DPP-4 and GLP-1

A

DPP-4 metabolizes GLP-1

Inhibit DPP-4 to keep GLP-1 in circulation

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127
Q

DPP-4 inhibitors: MOA, indications, toxicity

A

MOA & indications (same as GLP-1):
Increase insulin
Decrease glucagon
Type 2 diabetes

Toxicity: mild urinary/respiratory tract infections

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128
Q

Propylthiouracil
Methimazole
(MOA); what extra function does propylthiouracil have?

A

Blocks peroxidase –> inhibit organification of iodide –> inhibit coupling of thyroid hormone synthesis (can’t make T3 or T4)

Propylthiouracil also blocks 5’-deiodinase (decrease peripheral converion of T4 to T3); Active form T3 isn’t made

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129
Q

Propylthiouracil
Methimazole
(Indications)

A

Hyperthyroidism

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130
Q

Propylthiouracil
Methimazole
(Toxicity)

A

Skin rash
Aplastic anemia*
Agranulocytosis (rare)

Hepatotoxicity (Propylthiouracil)
Teratogen (Methimazole)

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131
Q

Levothyroxine
Triiodothyronine
(MOA)

A

Thyroxine replacement

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132
Q

Levothyroxine
Triiodothyronine
(Indications)

A

Hypothyroidism

Myxedema

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133
Q

Levothyroxine
Triiodothyronine
(Toxicity)

A

Tachycardia
Heat intolerance
Tremors
Arrhythmias

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134
Q

Hypothalamic/pituitary drugs (4)

A

1) GH
2) Somatostatin (Octreotide)
3) Oxytocin
4) ADH (Desmopressin)

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135
Q

1) GH
2) Somatostatin (Octreotide)
3) Oxytocin
4) ADH (Desmopressin)

Indications for drugs?

A

GH: GH deficiency, Turner syndrome

Octreotide/Somatostatin: Acromegaly, Carcinoid, Gastrinoma, Glucagonoma, Esophageal varices

Oxytocin: Stimulates labor, uterine contractions, MILK LET-DOWN, controls uterine hemorrhage (contraction of uterus to stop bleeding)

ADH (desmopressin): Pituitary Diabetes Insipidus

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136
Q

Demeclocycline: MOA

A

ADH antagonist (member of tetracyclin family)

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137
Q

Demeclocycline: Indications

A

SIADH

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138
Q

Demeclocycline: Toxicity

A

Nephrogenic Diabetes Insipidus
Photosensitivity

Abnormalities in bone & teeth (b/c Demeclocycline is a tetracycline)

139
Q

Glucocorticoids (5)

A 
Hydrocortisone
Prednisone
Triamcinolone
Dexamethasone
Beclomethasone
140
Q

Glucocorticoids: MOA

A

Decrease production of leukotrienes & prostaglandins via:

1) inhibition of phopholipase A2
2) inhibition of COX-2 expression

141
Q

Glucocorticoids: Indications

A

Addison’s diesease (primary adrenal insufficiency – CAN’T make any cortisol)

Inflammation
Immune suppression
Asthma

142
Q

Glucocorticoids: Toxicity

A

Iatrogenic Cushing’s syndrome: buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruising, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic)

Adrenal insufficiency (when drug stopped abruptly) – adrenal atrophy after prolonged glucocorticoid use (due to negative feedback)

143
Q

H2 blockers (4)

A

Cimetidine
Ranitidine
Famotidine
Nizatidine

144
Q

H2 blockers: MOA

A

Blocks histamine H2-receptors (reversible) –> DECREASE H+ secreteion from parietal cells

145
Q

H2 blockers: Indications

A

Peptic ulcer, gastritis, mild esophageal reflux

146
Q

H2 blockers: toxicity

A

Cimetidine:

a) Cytochrome P450 inhibitor
b) Antiandrogenic effects* – prolactin release, gynecomastia, impotence, decrease libido
c) can cross blood-brain barrier (confusion, dizziness); cross placenta

Cimetidine + Ranitidine:
DECREASE renal excretion of creatinine

147
Q

Proton pump inhibitors (5)

A 
Omeprazole
Lansoprazole
Esomeprazole
Pantoprazole
Dexlansoprazole
148
Q

Proton pump inhibitors: MOA

A

Inhibit H+/K+ ATPase in stomach parietal cells (irreversible)

149
Q

Proton pump inhibitors: Indications

A

Peptic ulcer, gastritis, esophageal reflux

Zollinger-Ellison syndrome*

150
Q

Proton pump inhibitors: toxicity*

A

C. difficile infection
Pneumonia
Hip fractures
Decrease serum Mg2+ after chronic use

151
Q

Bismuth
Sucralfate
(MOA)

A

Binds to ulcer base - physical protection while HCO3- secretion reestablishes pH graident in mucous layer

152
Q

Bismuth
Sucralfate
(Indications)

A

Increase ulcer healing

Traveler’s diarrhea

153
Q

Misoprostol: MOA

A

PGE1 analog

Increase production and secretion of gatric mucous barrier

Decrease acid production

154
Q

Misoprostol: Indications

A

Prevent NSAID-induced peptic ulcers

Maintenance of patent ductus arteriosus

Induce labor (ripens cervix)

155
Q

Maintenance of patnet ductus arteriosus

Induce labor

Prevent NSAID-induced peptic ulcers

A

Misoprostol

156
Q

Misoprostol: Toxicity & contraindication

A

Diarrhea

Contraindicated in women with childbearing potential (abortifacient)

157
Q

Octreotide: MOA

A

Long-acting somatostatin analog

158
Q

Octreotide: Indications

A

Acute variceal bleeds, acromegaly, carcinoid syndrome

VIPOMA: produce vasoactive intestinal peptide – secretes a lot of H2O and electrolytes –> diarrhea, hypokalemia, achlorhydria, dehydration

159
Q

Octreotide: Toxicity

A

Steatorrhea

Nausea, cramps

160
Q

Antacids (3)

A

Aluminum hydroxide
Magnesium hydroxide
Calcium carbonate

161
Q

Antacid use: common side effect

A

Hypokalemia

162
Q

Aluminum hydroxide: side effects

A 
Constipation
Hypophosphatemia
Proximal muscle weakness
Osteodystrophy
Seizures
163
Q

Magnesium hydroxide: side effects

A

Diarrhea
Hyporeflexia
Hypotension
Cardiac arrest

(Mg2+ relaxes smooth muscles – hence side effects of Mg(OH)2

164
Q

Calcium carbonate: side effects; specifically – what drug interactions occur?

A

Hypercalcemia

Rebound INCREASE in acid (due to excess Ca2+ which causes increase gastrin production –> increase stomach acid)

Can chelate and decrease effectiveness of other drugs (tetracycline)

165
Q

Osmotic laxative (4)

A

Magnesium hydroxide
Magnesium citrate
Polyethylene glycol
Lactulose

166
Q

Osmotic laxative: MOA

A

Provide osmotic load –> draws water out

167
Q

Lactulose: special MOA other than just providing osmotic load (for treatment of constipation)

A

Treats hepatic encephalopathy (gut flora degrade toxic substances normally removed by liver into metabolites = lactic acid & acetic acid) –> promote nitrogen excretion as NH4+

Hepatic encephalopathy = confusion, altered level of consciousness, coma due to accumulation of toxic substances normally removed by the liver

168
Q

Osmotic laxative: Indications

A

Constipation

169
Q

Osmotic laxative: Toxicity

A

Diarrhea
Dehydration
(Abused by bulimics)

170
Q

Infliximab: MOA

A

Monoclonal antibody to TNF-alpha

171
Q

Infliximab: Indications

A

Crohn’s disease
UC
Rheumatoid arthritis

172
Q

Infliximab: Toxicity

A

Infection (reactivation of latent TB)
Fever
Hypotension

173
Q

Sulfasalazine: MOA

A

Combination of:
sulfapyridine (antibacterial)
&
5-aminosalicyclic acid (anti-inflammatory)

Has to be activated by colonic bacteria

174
Q

Sulfasalazine: Indications

A

UC

Crohn’s disease

175
Q

Sulfasalazine: Toxicity

A

Sulfonamide toxicity

Oligospermia

176
Q

Ondansetron: MOA

A

5-HT3 antagonist

Central-acting antiemetic

177
Q

Ondansetron: Indications

A

Controls vomiting postoperatively

Vomiting in pts. undergoing chemotherapy

178
Q

Ondansetron: Toxicity

A

Constipation

contrast this w/ carcinoid syndrome when an excess of serotonin –> diarrhea

179
Q

Metoclopramide: MOA

A

D2 receptor antagonist

Increase resting tone, contractility, LES tone, motility

180
Q

Metoclopramide: Indications

A

Diabetic & post-surgery gastroparesis

Anti-emetic

181
Q

Metoclopramide: Toxicity

A

Increase Parkinsonian effects (tremor, rigidity, slowness of movement)

Contraindicated in pts. w/ small bowel obstruction or Parkinson’s disease

182
Q

What drug interactions occur w/ Metoclopramide?

A

Interacts w/ digoxin & diabetic agents

183
Q

Pro-kinetic Rx to get things moving in gut:

A

Increase Ach
Increase serotonin
Decrease dopamine

184
Q

Mannitol: MOA

A

Osmotic diuretic

Increase tubular fluid osmolarity –> increase urine flow (more H2O in urine)

Decrease intracranial/intraocular pressure

185
Q

Mannitol: Indications

A

Drug overdose

Elevated intracranial/intraocular pressure (neuro procedures)

186
Q

Mannitol: Toxicity & contraindications

A

Pulmonary edema

Contraindicated in anuria (absolutely no urine production), CHF

187
Q

Acetazoladmide: MOA

A

Carbonic anhydrase inhibitor

Osmotic diuretic

NaHCO3 diuresis (since NaHCO3 can’t be broken down to CO2 + H2O to be reabsorbed from tubule lumen) –> reduction in HCO3- stores

188
Q

Acetazoladmide: Indications

A

a) Glacucoma (need to decrease pressure)
b) Urinary alkalinization (need to prevent kidney stone formation)
c) Metabolic alkalosis
d) Altitude sickness (respiratory alkalosis, appropriate metabolic acidosis compensation)

189
Q

Acetazoladmide: Toxicity

A

Hyperchloremic metabolic acidosis
(Excess H+ and Cl-)

Paresthesias

NH3 toxicity

Sulfa allergy

190
Q

Furosemide: MOA

A

Loop diuretic

Inhibits cotransport of Na+ K+ and 2Cl-

Renal medulla loses hypertonicity; urine is no longer concentrated

191
Q

Relationship of furosemide to PGE release

A

Increase PGE release –> vasodilation of afferent arteriole

can be inhibited by ASA

192
Q

Relationship of furosemide to Ca2+

A

Increase Ca2+ excretion

193
Q

Furosemide: Indications

A 
a) Edematous states:
CHF
cirrhosis
nephrotic syndrome
pulmonary edema

b) Hypertension
c) Hypercalemia (b/c furosemide Loop diuretic Loses Ca2+)

194
Q

Furosemide: Toxicity

A 
Ototoxicity
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout

“OH DANG”

195
Q

Ethacrynic acid: MOA

A

Phenoxyacetic acid

Loop diuretic that is NOT a sulfonamide (for pts. w/ sulfa allergy)

Inhibits cotransport of Na+ K+ and 2Cl- (same as furosemide)

196
Q

Ethacynic acid: Indications

A

Diuresis in pts. w/ sulfa allergy

197
Q

Ethacrynic acid: toxicity

A

Hyperuricemia

All others similar to furosemide: "OH DaNG"
Ototoxicity
Hypokalemia
Dehydration
no sulfa Allergy!*
Nephritis (interstitial)
Gout
198
Q

When is ethacrynic acid absolutely contraindicated?

A

Pts. w/ GOUT

199
Q

Hydrochlorothiazide (HCTZ): MOA

A

Inhibits NaCl reabsorption in PCT - reduce diluting capacity of nephron

Acts on DCT

200
Q

HCTZ relationship to Ca2+

A

Decrease Ca2+ excretion (keeps Ca2+)

201
Q

HCTZ: indications

A

HTN, CHF

Idiopathic hypercalciuria

Nephrogenic diabetes insipidus* (doesn’t respond to ADH)

202
Q

HCTZ: toxicity

A

Hypokalemic metabolic alkalosis
Hyponatremia

Hyper"GLUC":
HyperGlycemia
HyperLipidemia
HyperUricemia
HyperCalcemia

Sulfa allergy

203
Q

Loop diuretic to give patient w/ sulfa allergy

A

Ethacrynic acid

204
Q

Renal Rx to avoid in patients w/ gout

A

Loop diuretic

205
Q

K+ sparing diuretics (4)

A

Spironolactone, Eplerenone

Triamterene, Amiloride

206
Q

K+ sparing diuretics: MOA

A

Spironolactone & Eplerenone:
competitive aldosterone receptor antagonist

Triamterene & Amiloride:
blocks Na+ channels (same channels aldosterone acts on)

207
Q

K+ sparing diuretics: indications

A

Hyperaldosteronism
K+ depletion
CHF

208
Q

K+ sparing diuretics: toxicity

A

Hyperkalemia –> arrhythmias

Spironolactone –> gyncomastia, antiandrogen effects

209
Q

Diuretics: changes in urine NaCl

A

all diuretics INCREASE urine NaCl

210
Q

Diuretics: changes in urine K+

A

All increase K+ excretion in urine –> toxicity potential: hypokalemia (except for K+ sparing diuretics)

211
Q

Diuretics: changes in blood pH (ACIDEMIA)

A

Carbonic anhydrase inhibitors (decrease HCO3- reabsorption)

K+ sparing (aldosterone prevents K+ and H+ secretion into urine); also hyperkalemia –> K+ enters cells, H+ exits cells into blood –> acidemia

212
Q

Diuretics: changes in blood pH (ALKALEMIA)

A

Loop diuretics
Thiazides

Volume contraction –> increase ATII –> increase Na+/H+ exchange –> increase HCO3- reabsorption (contraction alkalosis)

Low K+ states… H+ is exchanged for Na+ in cortical collecting tubule –> alkalosis & “paradoxical aciduria”

213
Q

Diuretics: changes in urine Ca2+

A

Lose Ca2+ w/ loop diuretics

Keep Ca2+ w/ thiazides (HCTZ)

214
Q

ACE inhibitors (3)

A

Captopril
Enalapril
Lisinopril

215
Q

ACE inhibitors: MOA

A

Decrease ATII

Prevent constriction of EFFERENT arterioles –> DECREASE GFR

Increase bradykinin (vasodilator)

216
Q

ACE inhibitors: Indications

A

HTN, CHF
(prevent unfavorable heart remodeling due to HTN)

Proteinuria (decrease GFR)
Diabetic renal disease

217
Q

ACE inhibitors: Toxicity

A

Increase bradykinin –> increase cough (kallekrein)
Angioedema
Teratogen* (fetal renal malformation)
Creatinine (increase due to decrease GFR)
Hyperkalemia (due to less GFR)
Hypotension

218
Q

Advantage of using ATII receptor blockers (-sartans) over ACE inhibitors

A

ARBs similar actions as ACE inhibitors but: ARBs have REDUCED angioedema & cough

219
Q

When is use of ACE inhibitors contraindicated?

A

Pts. with bilateral renal artery stenosis (since ACE inhibitors further DECREASE GFR –> renal failure)

220
Q

Leuprolide: MOA

A

GnRH analog

agonist: pulsatile use
antagonist: continuous use

221
Q

Leuprolide: indications

A

Pulsatile:
Infertility

Continuous:
Prostate cancer
Uterine fibrinoids
Precocious puberty

222
Q

Leuprolide: toxicity

A

Antiandrogen

223
Q

What other drug is used w/ leuprolide to treat prostate cancer?

A

Flutamide

224
Q

Testosterone, methyltestosterone: MOA

A

agonist at androgen receptors

225
Q

Testosterone, methyltestosterone: Indications

A

Hypogonadism –> develops secondary sex characteristics

Stimulates anabolism –> recovery after burn/injury

226
Q

Testosterone, methyltestosterone: Toxicity

A

Masculinization in females

Reduce intratesticular testosterone in males (inhibits release of LH via negative feedback) –> testicular atrophy

227
Q

Testosterone, methyltestosterone: association w/ lipoproteins

A 
Increase LDL (bad!!)
Decrease HDL (also bad!!)
228
Q

Testosterone, methyltestosterone: association w/ growth in children

A

Premature closure of epiphyseal plate (pediatrics have early growth spurt but end up being shorter than their potential height bc of premature closure of growth plates)

229
Q

Antiandrogens (4)

A

Finasteride
Flutamide
Ketoconazole
Spironolactone

230
Q

Finasteride: MOA

A

Inhibits 5a-reductase

Testosterone CANNOT be converted to DHT

231
Q

Finasteride: Indication

A

Benign prostatic hypertrophy

232
Q

Alternative use for Finasteride

A

Male pattern baldness –> generates new hair growth

233
Q

Flutamide: MOA

A

Competitive inhibitor of androgens at TESTOSTERONE RECEPTOR

234
Q

Ketoconazole: MOA

A

Inhibits steroid synthesis (inhibits 17,20-Desmolase)

235
Q

Spironolactone: MOA

A

Inhibits steroid BINDING

236
Q

Rx for polycystic ovarian syndrome to prevent hirsutism

A

Ketoconazole & Spironolactone

237
Q

Side effects of Ketoconazole & Spironolactone

A

Gynecomastia

Amenorrhea

238
Q

Estrogens (3)

A

Ethinyl estradiol
DES
Mestranol

239
Q

When is ethinyl estradiol, DES, mestranol absolutely contraindicated?

A

ER positive breast cancer

History of DVTs (due to increased risk of thrombi)

240
Q

Ethinyl estradiol
DES
Mestranol
(MOA)

A

Bind estrogen receptors

241
Q

Ethinyl estradiol
DES
Mestranol
(Indications)

A

Hypogonadism
Ovarian failure
Menstrual abnormalities

Hormone replacement therapy (HRT) in postmenopausal

Men: androgen dependent prostate cancer

242
Q

Ethinyl estradiol
DES
Mestranol
(Toxicity)

A

Increase risk of endometrial cancer

Bleeding (post menopausal women)

Clear cell adenocarcinoma of vagina (females exposed to DES in utero)*

Increase thrombi risk

243
Q

Selective estrogen receptor modulators -SERMs (3)

A

Clomiphene
Tamoxifen
Raloxifene

244
Q

Clomiphene: MOA

A

Partial agonist at ER in hypothalamus

Prevents negative feedback –> increase release of LH and FSH –> ovulation

245
Q

Clomiphene: Indications

A

Infertility

Polycystic ovarian syndrome

246
Q

Clomiphene: toxicity

A

Hot flashes
Ovarian enlargement
Multiple, simultaneous pregnancies
Visual disturbances

247
Q

Tamoxifen

A

Antagonist at breast tissue

Treat/prevent ER positive breast cancer

248
Q

Raloxifene

A

Agonist on bone - reduces resorption of bone

Treats osteoporosis

249
Q

Hormone replacement therapy (for postmenopausal)

A

Relief/prevention of menopausal symptoms (hot flashes, vaginal atrophy)

Osteoporosis (increase estrogen, decrease osteoclast activity)

250
Q

Complications of HRT

A

unopposed estrogen replacement increase ENDOMETRIAL cancer –> need to add progesterone

possible increase in CV risk

251
Q

Anastrozole

Exemestane: MOA

A

Aromatase inhibitors

Inhibits conversion of testosterone to estradiol

252
Q

Anastrozole

Exemestane: Indications

A

Use in postmenopausal women w/ breast cancer

253
Q

Progestins: MOA

A

Bind progesterone receptors

Reduce growth & vascularization of endometrium

254
Q

Progestins: Indications

A

Oral contraceptives

Endometrial cancer 
(from unopposed estrogen)

Abnormal uterine bleeding

255
Q

Mifepristone (RU-486): MOA

A

Competitive inhibitor of progestins at progesterone receptors

256
Q

Mifepristone (RU-486): Indications

A

Termination of pregnancy

No more progesterone –> endometrium sheds (similar to end of menses cycle)

257
Q

What other Rx is usually administered w/ Mifepristone? What does this Rx do?

A

Misoprostol (PGE1)

Uterine contractions (labor induction)

258
Q

Mifepristone (RU-486): Toxicity

A

Heavy bleeding

259
Q

Oral contraception (synthetic progestins, estrogen): MOA on hypothalamus

A

Inhibit LH/FSH –> no estrogen surge –> no LH surge –> no ovulation

260
Q

Oral contraception: progestin specific effects

A

Progestins –> thickening of cervical mucus –> limit access of sperm to uterus

Inhibit endometrial proliferation –> endometrium less suitable for implantation of embryo

261
Q

When is oral contraception contraindicated?

A

Smokers > 35yrs of age (increase risk of cardiovascular events)

Pts. w/ history of:

a) thromboembolism & stroke
b) estrogen-dependent tumor

262
Q

Terbutaline

A

b2 agonist - relax uterus

causes PREMATURE uterine contractions

263
Q

Tamsulosin

A

a1 antagonist - inhibit smooth muscle contraction

treats BPH:
selective for a1A,D receptors (found on prostate); does NOT affect vascular a1B receptors

264
Q

Sildenafil
Vardenafil
(MOA)

A

Inhibit phosphodiesterase –> increase cGMP

Smooth muscle relaxes –> increase blood flow –> penile erection

265
Q

Sildenafil
Vardenafil
(toxicity)

A

Blue-green color vision

Hypotension (life threatening) if pt. is also on Nitrates

Headache
Dyspepsia

266
Q

Danazol: MOA

A

Partial agonist at androgen receptors

267
Q

Danazol: Indications

A

Endometriosis

Hereditary angioedema

268
Q

Danazol: toxicity

A

Masculinization (acne, hirsutism)

Decrease HDL levels
Hepatotoxic
Edema
Weight gain

269
Q

H1 blockers: MOA

A

Reversible inhibitors of H1 histamine receptors

270
Q

H1 blockers - 1st gen (3)

A

Diphenhydramine
Dimenhydrinate
Chlorpheniramine

271
Q

H1 blockers - 1st gen (Indications)

A

Motion sickness*
Sleep aid*
Allergy

272
Q

H1 blockers - 1st gen (Toxicity)

A

Sedation
Antimuscarinic

Anti-a-adrenergic (hypotension, dizziness)

273
Q

H1 blockers - 2nd gen (3)

A

Loratidine
Fexofenadine
Desloratadine

274
Q

H1 blockers - 2nd gen (Indication)

A

Allergy

275
Q

H1 blockers - 2nd gen (Toxicity)

A

DECREASED entry into CNS (far less sedating)

preferred antihistamine due to less drowsiness

276
Q

Asthma drug targets (2 processes that mediate bronchoconstriction)

A

1) inflammation

2) parasympathetic tone

277
Q

Short acting b2 agonist (acute exacerbation)

A

Albuterol - relaxes smooth muscle

278
Q

Long acting b2 agonist (prophylaxis of asthma)

A

Salmeterol

Formoterol

279
Q

Side effects of Salmeterol & Formoterol

A

Tremor

Arrhythmia

280
Q

Theophylline

Methylxanthines

A

Inhibit phosphodiesterase –> decrease cAMP hydrolysis –> increase overall cAMP concentration –> bronchodilation

281
Q

Toxicities of Theophylline

A

Narrow TI (cardiotoxic, neurotoxic)

Metabolized by P450

282
Q

Relationship of theophylline & adenosine

A

Theophylline blocks action of adenosine

283
Q

Asthma drug (muscarinic antagonist)

A

Ipratropium

Blocks muscarinic receptor –> prevent bronchoconstriction

284
Q

Muscarinic antagonist: indications

A

Tiotropium: COPD – long acting anti-muscarinic

Ipratropium: asthma (blocks bronchoconstriction)

285
Q

Increase Ach
Increase Adenosine;
relationship to asthma?

A

Both increase in Ach and increase in adenosine –> bronchoconstriction

muscarinic antagonists & theophylline used to inhibit Ach and adenosine, respectively

286
Q

Corticosteroids (2)

A

Beclomethasone

Fluticasone

287
Q

1st line therapy for chronic asthma

A

Corticosteroids

288
Q

Corticosteroids: MOA

A

Inhibit cytokine synthesis by inhibiting NF-kB

No NF-kB –> no TNF-a

289
Q

Antileukotrienes (3)

A

Montelukast
Zafirlukast

Zileuton

290
Q

Montelukast, Zafirlukast: MOA

A

Block leukotriene receptors

Esp. good for ASA-induced asthma

291
Q

Zileuton: MOA

A

Inhibit 5-lipoxygenase pathway

Blocks conversion of arachidonic acid to leukotrienes

292
Q

Omalizumab

A

anti-IgE antibody

used in allergic asthma (that is resistant to inhaled steroids and long acting b2 agonists)

293
Q

Guaifenesin

A

thins respiratory secretions; does NOT suppress cough reflex

294
Q

N-acetylcysteine

A

mucolytic - loosen mucus plugs in CF patients

also antidote for acetaminophen toxicity

295
Q

Bosentan

A

antagonizes endothelin-1 receptors (decrease pulmonary vascular resistance)

Rx for pulmonary HTN

296
Q

Dextromethorphan; MOA, indications; what is it an analog of?

A

Antitussive

Antagonize NMDA glutamate receptors

297
Q

What is dextromethorphan an analog of?

A

Analog of codeine; mild opioid effect in excess

Give NALOXONE for overdose

mild abuse potential

298
Q

Pseudoephedrine
Phenylephrine
(MOA)

A

Sympathomimetic a-agonistic nasal decongestant

299
Q

Pseudoephedrine
Phenylephrine
(Indications)

A

Reduce hyperemia, edema, nasal congestion

Open obstructed Eustachian tubes

Pseudoephedrine also used as stimulant

300
Q

Pseudoephedrine
Phenylephrine
(Toxicity)

A

HTN (a-agoonist activity)

CNS stimulation & anxiety (pseudoephedrine)

301
Q

Methacholine

A

muscarinic receptor agonist

used in asthma challenge testing

302
Q

LTB4

A

Neutrophil chemotactic

303
Q

LTC4
LTD4
LTE4

A

Bronchoconstriction
Vasoconstriction
Contraction of smooth muscle
Increase vascular permeability

304
Q

PGE2

A

increase uterine tone

decrease vascular tone, bronchial tone

305
Q

TXA2

A

increase platelet aggregation
increase vascular tone
increase bronchial tone

306
Q

PGI2

A

PGI2 = Prostacyclin

inhibits platelet aggregation
promotes vasodilation

307
Q

Aspirin (ASA): MOA

A

Irreversibly inhibit COX-1 and COX-2 via acetylation

Decrease TXA2 and prostaglandins

Increase bleeding time, no effect on PT or PTT

308
Q

ASA: Indication

A

Low dose:
decrease platelet aggregation

Intermediate:
Antipyretic/analgesic

High dose:
Anti-inflammatory

309
Q

ASA: Toxicity

A

Gastric ulceration
Tinnitus (CNVIII)

Chronic use:
Renal failure, interstitial nephritis
Upper GI bleeding

310
Q

ASA relationship w/ respiratory system

A

ASA stimulates respiratory centers –> hyperventilation –> respiratory alkalosis

311
Q

ASA: use in children

A

Reye’s syndrome in children given ASA for viral infection

Exception: can give children ASA for Kawasaki’s disease

312
Q

NSAIDs (5)

A 
Ibuprofen
Naproxen
Indomethacin
Ketorolac
Diclofenac
313
Q

NSAIDs: MOA

A

Reversible inhibition of COX

Blocks prostaglandin synthesis –> vasoconstriction occurs

314
Q

NSAIDs: Indications

A

Antipyretic
Analgesic
Anti-inflammatory

Indomethacin: closes PDA

315
Q

NSAIDs: Toxicity

A

Interstitial nephritis

Gastric ulcer: prostaglandins protect gastric mucosa

Renal ischemia: prostaglandins vasodilate afferent arteriole

316
Q

COX-2 inhibitor (1)

A

Celecoxib

317
Q

Celecoxib: MOA

A

Reversible inhibition of COX-2 –> decrease inflammation & pain

318
Q

Why is COX-2 inhibitor preferred over non-selective NSAIDs?

A

Spares TXA2 production –> platelet function remains

Spares gastric mucosa –> no gastric bleeding

319
Q

Celecoxib: Indications

A

Rheumatoid arthritis
Osteoarthritis
Pts. w/ gastritis or uclers

320
Q

Celecoxib: Toxicity

A

Increase thrombosis

Sulfa allergy

321
Q

Acetaminophen: MOA

A

Inhibits COX in CNS

322
Q

Acetaminophen: Indications

A

Antipyretic
Analgesic

Give to children w/ upper respiratory illness

323
Q

Acetaminophen: Toxicity

A

Hepatic necrosis

324
Q

Acetaminophen metabolites: how does it cause liver toxicity?

A

Metabolites deplete glutathione –> toxic tissue adducts in liver

N-acetylcysteine –> regenerates glutathione

325
Q

Bisphosphonates

A

Alendronate

and other “-dronates”

326
Q

Alendronate: MOA

A

Pyrophosphate analog

Binds hydroxyapatite in bone

Inhibit osteoclast activity

327
Q

Alendronate: Indications

A

Osteoporosis
Hypercalcemia
Paget’s disease of the bone

Pts. on corticosteroids: need prophylactic bisphosphonates

328
Q

Alendronate: Toxicity

A

Corrosive esophagitis (pt. needs to remain upright for 30mins after taking medication)

Osteonecrosis of the jaw

329
Q

Gout: chronic (4)

A

Allopurinol
Febuxostat
Probenecid
Colchicine

330
Q

Allopurinol

A

Inhibits xanthine oxidase (no conversion of hypoxanthine –> xanthine; xanthine –> uric acid)
DECREASED uric acid production

331
Q

Allopurinol: Indication

A

Chronic gout

Lymphoma & Leukemia:
prevent tumor lysis-associated urate nephropathy

Increase concentrations of azathioprine (drug given for prevention of organ rejection in pts. w/ kidney transplant) & 6-MP

332
Q

Febuxostat

A

Inhibit xanthine oxidase

333
Q

Probenecid

A

Inhibit reabsorption of uric acid in PCT

334
Q

Relationship of Probenecid & Penicillin

A

Probenecid inhibits secretion of penicillin

335
Q

Colchicine

A

Binds/stabilizes tubulin –> inhibit polymerizations –> inhibit leukocyte chemotaxis and degranulation

336
Q

Gout: acute (2)

A

NSAIDs

Glucocorticoids

337
Q

ASA administration to pts. w/ gout

A

DO NOT give salicylates –> decrease uric acid clearance in urine –> increased likelihood of gout!

338
Q

TNF-alpha inhibitors (2)

A

Etanercept

Infliximab, Adalimumab

339
Q

Use of TNF-alpha inhibitors predispose to what condition?

A

Reactivation of latent TB

TNF blockage –> no activation of macrophages –> no destruction of phagocytosed microbes

340
Q

Etanercept: MOA

A

Fusion protein serves as receptor for TNF-a + IgG Fc

Produced by recombinant DNA

Etanercept is TNF decoy receptor (binds up all TNF-a in body)

341
Q

Etanercept: Indications

A

Rheumatoid arthritis
Psoriasis
Ankylosing spondylitis

342
Q

Infliximab
Adalimumab
(MOA)

A

Anti-TNF-a monoclonal antibody

343
Q

Infliximab
Adalimumab
(Indications)

A

Crohn’s disease
Rheumatoid arthritis
Ankylosing spondylitis
Psoriasis

STEP1 - TLe (8 decks)

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