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Pharmacology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Risk factors for Primary Hypertension aka Essential

A 
Obesity
Stress
Smoking
Age
Diet
Race
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2
Q

Define Secondary Hypertension

A

Has definitive cause like stenosis or renal artery, or pheochromocytoma

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3
Q

Complications of HTN

A 
CAD
Cardiac/Renal Failure
Stroke
TIA's
MI
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4
Q

Centrally acting hypertensives action

A

Decrease sympathetic outflow to HRT which decrease HR which decreases myocardial contractility which decreases CO which decreases BP

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5
Q

Centrally acting hypertensives work on which receptor?

A

A2 receptors in the CNS

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6
Q

Alpha-adrenergic blockers action

A

Block A1 receptors which cause vasodilation which decreases peripheral resistance which decreases BP

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7
Q

Name an Alpha-adrenergic blocker

A

Prazosin (Minipress)

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8
Q

Beta-adrenergic Action

A

Blocks B1 receptors which decreases HR and myocardial contractility with decreases CO which decreases BP

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9
Q

Name Beta adrenergic drugs

A 
Propranolol - B1 &B2 blocker
Metoprolol - cardio selective B1
Atenolol - Cardio selective
Labetolol - also blocks A receptors
Cavedilol - also blocks A receptors
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10
Q

Ganglionic Blocker action

A

At high doses it blocks ganglia which block the sympathetic outflow to BV’s which decreases BP

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11
Q

Name a Ganglionic Blocker drug

A

Mecamylamine

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12
Q

Name Postganglionic adrenergic neuronal blockers

A

Reserpine

Guanethidine

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13
Q

Reserpine Action

A

Blocks the uptake of dopamine in the synaptic vesicles blocking the formation of norepinephrine (doesn’t work on adrenergic receptors)

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14
Q

Guanethidine Action

A

Inhibits release of NE

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15
Q

Types of Diuretics?

A

Thiazide Diuretics
Loop Diuretics
Potassium Sparing Diuretics

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16
Q

Example of Thiazide diuretics?

A

Hydrochlorothiazide

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17
Q

Example of Loop diuretic?

A

Furosemide

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18
Q

Example of Potassium Sparing diuretic?

A

Spironolactone

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19
Q

Structural unit of the kidney?

A

Nephron

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20
Q

Why are diuretics used?

A

Decrease blood volume which decreases BP

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21
Q

What’s the action of diuretics?

A

Blocks reabsorption of NA

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22
Q

Where on the nephron is 65% of Na reabsorbed?

A

Proximal Convulated Tubule (PCT)

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23
Q

Where on the nephron is 20% of Na reabsorbed?

A

Loop of Henle

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24
Q

Where on the nephron is 10% of Na reabsorbed?

A

DCT

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25
Q

Where on the nephron is 1-5% of Na reabsorbed?

A

Collecting Duct (Spironolactone)

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26
Q

Where on the nephron do Thiazide diuretics work?

A

DCT = Weak diuretic

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27
Q

Where on the nephron do Loop Diuretics work?

A

LOH (20%) greater diuresis

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28
Q

Indications of Thiazide Diuretics?

A

Mild to moderate HTN

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29
Q

MOA of Thiazide diuretics?

A

Block reabsorption of NA, Cl in the early segment of DCT which blocks reabsorption of H2O (where sodium goes water follow). Will only work with decent renal function

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30
Q

Adverse Effects of Thiazide Diuretics?

A
  • HYPONATREMIA
  • HYPOCHLOREMIA
  • HYPOKALEMIA (^NA reabsorption at CD, aldosterone secreted, some NA reabsorbed in exchange for K secreted)
  • HYPERGLYCEMIA ( inhibition of insulin releases, promotion of glycogenolysis, inhibition of glycogen genesis)
  • HYPERURICEMIA (^ urine acid in the blood)
  • ALTERATION OF LIPID PROFILE (LDL ^ - high cholesterol, HDL decreases)
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31
Q

Indications of Loop Diuretics?

A

Pulmonary edema

Edema associated with cardiac, renal or hepatic origin

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32
Q

Adverse effects of Loop Diuretics?

A
  • HYPONATREMIA
  • HYPOCHLOREMIA
  • HYPOKALEMIA (^NA reabsorption at CD, aldosterone secreted, some NA reabsorbed in exchange for K secreted)
  • HYPERGLYCEMIA ( inhibition of insulin releases, promotion of glycogenolysis, inhibition of glycogen genesis)
  • HYPERURICEMIA (^ urine acid in the blood)
  • ALTERATION OF LIPID PROFILE (LDL ^ - high cholesterol, HDL decreases)
  • OTOTOXICITY (damage to ear)
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33
Q

Loop diuretics and other drug interactions?

A

Patients taking amino glycoside antibiotics (Gentamicin) cause ototoxicity

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34
Q

Potassium sparing diuretics indication?

A

To avoid side effects, use K sparing diuretics - acts at the level of the Collecting Ducts

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35
Q

Someone on Digoxin what should you give to maintain K levels elevated?

A

Spironolactone

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36
Q

Action of Spironolactone?

A

Blocks aldosterone (NA not reabsorbed, is eliminated with H2O, K is retained - K levels should be 3.5-5.5 meq/L)

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37
Q

Name Vasodilators used for HTN?

A
  • Hydralazine
  • Minoxidil
  • Sodium Nitroprusside
  • Calcium Channel Blockers
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38
Q

Hydralazine, Minoxidil MOA?

A

Hyperpolarize vascular smooth muscle by opening up K channels > away form threshold > no contraction of smooth muscle in the blood > vessels dilate (affects mainly the arteries)

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39
Q

Adverse effects of Hydralazine and Minoxidil?

A

[] Hydralazine - Lupus like reactions (butterfly rash)

[] Minoxidil - Pericardial effusion (fluid in the pericardium) leading to cardiac tamponade (pressure on the heart)

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40
Q

Indications for Sodium Nitroprusside?

A

Drug of choice for emergency HTN

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41
Q

Sodium Nitroprusside MOA?

A
  • Increases levels of cGMP > dilates BV’s (both arteries and veins)
  • When metabolized cyanide is released > can lead to cyanide poisoning (rhodanese reduces level of toxicity for cyanide poisoning > cyanide detoxification)
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42
Q

Name Calcium Channel Blockers Drugs used to treat HTN?

A

Verapamil (Calan)
Amlodipine (norvasc)
Nifedipine (Aldolat, Procardia)

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43
Q

Action of Verapamil?

A
  • Dilates peripheral arteries to ↓ BP
  • Dilates arteries going to myocardium (coronary vessels)
  • Has a cardio suppressant effect → ↓HR, ↓AV nodal conductions, myocardial contraction (but body’s baroreceptors ↑ actions on the heart canceling the effects on the heart)
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44
Q

Adverse effects of Verapamil?

A
  • Constipation

- Edema of ankles and feet

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45
Q

Indications for Verapamil?

A
  • Used for angina pectoris, HTN, cardiac dysrhythmias
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46
Q

Nifedipine action?

A
  • Acts like Verapamil, but it doesn’t suppress the heart

- If we get a baroreceptor reflex → reflex tachycardia (give ß blocker to prevent tachycardia)

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47
Q

Name ACE Inhibitors to treat HTN?

A
  • Captopril (Capoten)

- Enalapril (Vasotec)

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48
Q

Antiotensin → Angiotensin II Mechanism?

A

Angiotensin converting enzyme (ACE) makes Angiotensin II from Angiotensin I

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49
Q

Systemic Vasoconstrictor that increases BP?

A

Angiotensin II

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50
Q

Stimulates aldosterone secretion and NA retention by kidneys. ( ↑ H2O reabsorption → ↑blood volume → ↑BP)

A

Angiotensin II

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51
Q

Stimulates ADH. (↑ H2O reabsorption → ↑blood volume → ↑BP)

A

Angiotensin II

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52
Q

When you give ACE inhibitors BP decreases because?

A

Angiotensin II is no longer produced?

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53
Q

What else does ACE work on?

A

Bradykinin

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54
Q

What’s Bradykinin?

A

A vessel dilator, won’t be broken down when given ACEi it decreases BP

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55
Q

What is ACE called when working on Bradykinin?

A

Kinase II

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56
Q

What adverse effects can Bradykinin have when accumulated?

A
  • Cough > take patient OFF ACEi, put patient on Angiotensin II receptor blocker - losartan
57
Q

Adverse effects of ACEi?

A
  • Possible angioedema (swelling of tongue, glottis, pharynx) can be fatal
  • Hyperkalemia (normally Angiotensin II stimulates aldosterone secretion, K excreted)
58
Q

Name an Angiotensin II receptor antagonist?

A

Losartan

59
Q

Types of drugs used to treat CHF?

A
  1. Cardiac Glycosides
  2. Bipyridine Derivatives
  3. Beta-adrenergic Agonists
  4. Vasodilators
  5. Diuretics
  6. ACE inhibitors
  7. Angiotensin II Receptor Agonists
  8. Beta-Adrenergic Blockers
60
Q

Name a Cardiac Glycoside drug

A

Digoxin

61
Q

Name Bipyridine Derivative drugs

A

Inamrinone

Milrinone

62
Q

Name Beta-adrenergic agonists

A

Dobutamine

Dopamine

63
Q

Name Vasodilator Drugs

A

Nitroglycerin
Sodium Nitroprusside
Hydralazine

64
Q

Name Diuretic Drugs

A

Thiazide Diuretics
Loop Diuretics
K Sparing diuretics

65
Q

Name ACE inhibitor drugs

A

Captopril

Enalapril

66
Q

Name Angiotensin II Receptor Antagonist drugs

A

Losartan

67
Q

Name Beta-Adrenergic Blocker drugs

A

Metropolol

Carvedilol

68
Q

What is CHF?

A

When CO is inadequate to meet the metabolic demand of the body

69
Q

Causes of CHF?

A
  • CAD
  • MI
  • Chronic HTN
70
Q

Signs of CHF?

A
  • If left sided HF, fluid may build up in lungs causing pulmonary edema which results in SOB
  • If right sided HF, fluid may build back up into your abdomen, legs and feet, causing swelling.
71
Q

How does the body try to compensate for back flow?

A
  1. ↑sympathetic outflow to the heart, to arteries, and veins. ↑ venous return.
  2. ↑H2O retention which ↑ blood volume
72
Q

Treatments for CHF?

A
  1. ↑ Myocardial contractility
  2. Decrease preload (venous return to the heart)
  3. Decrease afterfload (dilate arteries)
73
Q

Digoxin Indications?

A
  • CHF
  • Atrial fibrillation
  • Atrial Flutter
74
Q

Digoxin MOA?

A
  • Inhibits Na-K pump leading to ↑ Na & decreased K
  • Reverses Na/Ca exchanger
  • ↑ in Ca = ↑ myocardial contraction
75
Q

Digoxin Contraindications?

A

Bradycardia

Ventricular Fibrillation

76
Q

Digoxin Adverse Effects?

A
  • Digoxin toxicity due to decreased K - hypokalemia (K and Digoxin compete for Na-K pump)
77
Q

Early signs of Digoxin toxicity?

A
  • Blurred vision
  • yellow tinged to the vision
  • halos around dark objects
78
Q

What do you give to keep K levels therapeutic?

A

K sparing diuretics

79
Q

Digoxin drug-drug interactions?

A
  • Diuretics
  • ACE inhibitors (hyperkalemia)
  • Angiotensin II antagonist (hyperkalemia)
80
Q

Bipyridine derivatives MOA?

A
  • inhibit phosphodiesterase (enzyme that breaks cAMP), increases levels of cAMP which ↑ intracellular Ca which ↑ contractility of the heart
  • Vasodilate - unclear MOA
81
Q

Dopamine binds to adrenergic receptors and stimulates B1 receptors increasing what?

A

↑ myocardial contractility which ↑CO

82
Q

At high doses what does Dopamine do?

A
  • could stimulate A1 receptors (negative effect because that would cause vasoconstriction which would increase after load on the heart making it difficult for the heart to pump blog out)
83
Q

Dopamine also works of Dopaminergic Receptors by doing what?

A
  • Dilating renal blood vessels with ↑ renal blood flow which ↑ urinary output which decreases preload (less work for heart)
84
Q

Dopamine is used to treat?

A

Acute CHF

85
Q

Dobutamine MOA?

A

More selective for B1

86
Q

Dobutamine treats?

A

Acute CHF

87
Q

Define Angina Pectoris?

A

Sudden intense substernal pain cause by reduced coronary artery flow to the myocardium (imbalance between myocardium needs and what coronary arteries can supply)

88
Q

Action of Vasodilator Drugs?

A

Dilate veins - ↓ preload

Dilate arteries - ↓ afterload

89
Q

Action of Metropolol & Carvedilol?

A

↓ HR & Myocardial activity which ↓CO which ↓BP

90
Q

Types of Angina Pectoris?

A
  1. Stable Angina: 90% patients, sudden pain brought on by physical exertion, pain stops when patient rests
  2. Unstable angina: 10% patients
  3. Ptinzmetal’s angina: spasm of coronary arteries
91
Q

Treatments strategies for Angina pectoris?

A
  • ↑ O2 delivery to myocardium

- ↓ demand for O2 by myocardium

92
Q

Antianginal Drug types?

A
  • Nitrates: Nitroglycerin
  • Calcium channel blockers: Procarda, Verapamil, Cardizem
  • Beta Blockers: Atenolol, Timolol, Metoprolol
93
Q

Action of Nitrates?

A
  • when metabolized its converted to nitric oxide (NO)

- Nitric Oxide (NO) activates guanylate cyclase system which ↑ cGMP > dilating vessels

94
Q

Nitrates at Hight doses?

A

Dilates the arteries ↓ after load

95
Q

Nitrates at Low doses?

A

Dilates veins > ↓ preload > ↓ myocardial demands for O2

96
Q

Indications for Nitrates?

A
  • Acute Attack, give sublingual

- To prevent attack, give orally or transdermal

97
Q

Adverse effect of Nitrates?

A
  • Orthostatic Hypotension
  • Reflex tachycardia
  • tolerance common, give drug holiday
98
Q

Contraindications for giving Nitrates?

A

Viagra - also dilates vessels, can significantly ↓ BP

99
Q

Action of Calcium Channel Blockers?

A
  1. Inihbits influx of Ca into myocardial cells, ↓ myocardial contractility
  2. Inhibits influx of Ca into BV’s causing dilation
100
Q

Action of Beta Blockers?

A
  1. Reduce mortality in patients with MI

2. Blocks reflex tachycardia

101
Q

Antiplatelet Drug types?

A
  1. Aspirin
  2. ADP Receptor Antagonists: Ticlopidine (Ticlid), Clopidrogel (Plavix)
  3. Glycoprotein IIB/IIIa Receptor Antagonists: Abciximab (Reopro)
  4. Dipyridamole (Persantine)
102
Q

Define Arterial thrombus

A
  • platelet rich clot
  • tend to form in medium sized arteries
  • Fatty plaques (atheromas)
103
Q

Define Venous Thrombus

A
  • Fibrin rich
  • Forms as a result in bed rest patients
  • Can lead to pulmonary embolism
104
Q

Thrombus formation steps (7)

A
  1. Damage to endothelial cells → chemical mediators releases (Von Williebrand factors)
  2. V factor renders vessel wall which becomes sticky
  3. Platelets adhere “platelet adhesion”
  4. The exposed collagen fibers of the connective tissue bind to platelet membrane receptors → triggers production of TXA2
  5. TXA2 leads to platelet degranulation → ADP, serotonin and platelet derived growth factors are released
  6. ADP (adenosine dipophate) binds to other platelet receptors (aggregin) causing platelet activation of Glycoprotein IIb/IIIa
  7. Glycoprotein IIb/IIIa change shape. Fibrinogen can now bind to receptors and bridge platelets together (platelet aggregation)
105
Q

Aspirin action

A
  • irreversibly inhibits COX → blocks production of TXA2 (no degranulation of the platelets)
  • Lasts 7-10 days (lifespan of platelets), must stop aspiring before surgery
106
Q

Aspirin Indications

A

[] Longterm myocardial prophylaxis (81-162mg/day)
[] Stroke prophylaxis (50-325mg/day)
[] Acute MI (162-325mg/day)

107
Q

Adverse effects of Aspirin?

A

GI Bleeding

108
Q

Aspirin drug interactions

A

[] Don’t use enteric coated. Ask patient to chew it
[] Other NSAIDS have anti platelet properties too
[] Don’t take while taking Ibuprofen

109
Q

Indication for Ticlopidine?

A

Prevent stroke

110
Q

Adverse effects Ticlopidine?

A

Agranulocytosis

TTP (Thrombotic Thrombocytopenic Purpura)

111
Q

What is TTP?

A

Blood disorder that causes blood clots to form in small blood vessels around the body, and leads to low platelet count

112
Q

TTP characterized by?

A 
Fever
Anemia
Renal dysfunction
Thrombocytopenia
Neurobiological disturbances
113
Q

Indications for ADP receptor Antagonists?

A

Prevent thrombolytic events following a recent MI, stroke, or unstable angina

114
Q

Action of Plavix?

A
  1. Blocks ADP receptor → no platelet activation → no aggregation
  2. Blocks glycoprotein IIb/IIIa
115
Q

ABCiximab MOA?

A

Inhibit binding of fibrinogen to the Glycoprotein IIb/IIIa receptor

116
Q

Indication for Glycoprotein IIb/IIIa receptor antagonist?

A

Prevent thrombolytic events following a recent MI, stroke, or unstable angina

117
Q

Dipyridamole MOA?

A

[] Inhibits Phosphodiesterase → ↑ cAMP → prevents platelet degranulation

[] mimics actions of prostaglandin known as PGI2 (prostacyclin) which prevents platelet degranulation

118
Q

Thrombin inhibitor types?

A

Parenteral: Heparin, Lovenox
Oral: Warfarin

119
Q

Heparin action?

A
  1. Binds to antithrombin III (AT), inhibits active factors 2 & 10
  2. Activated AT then inactivates thrombin
120
Q

Heparin Indication

A

↬ Pulmonary Embolism
↬ evolving stroke
↬ DVT
↬ DIC
↬ Prevent post op venous thrombus
↬ Adjunct to thrombolytic therapy of acute IM
↬ in dialysis machines to prevent thrombus
↬ Anti-coagulant of choose for pregnant women (doesn’t cross placenta)

121
Q

Heparin Limitations?

A

↬ given IV, subQ
↬ prevents thrombus BUT doesn’t break down preexistent ones
↬ Monitor lab tests closely. aPTT

122
Q

Heparin contraindications?

A

↬ Thrombocytopenia
↬ Bleeding
↬ During surgery and after surgery of eye, brain, spinal cord

123
Q

For Heparin OD give?

A

Protamine Sulfate (antidote)

124
Q

LOVENOX differs from Heparin how?

A

⇥ binds to Antithrombin III to inactivate factor 10 only
⇥ dosage is fixed, as opposed to based aPTT with Heparin
⇥ administered Orally, no constant monitoring needed
⇥ greater bioavailability, longer 1/2life than heparin
⇥ less likely to cause thrombocytopenia

125
Q

Liver needs vitamin K to produce what?

A

Clotting factors 2,7,9,10

126
Q

Warfarin Action?

A

Interferes with actions of VIT. K → liver doesn’t produce clotting factors

127
Q

Warfarin indications?

A

Longterm anticoagulant therapy

128
Q

Drugs that ↑ effects of warfarin?

A

➻ anti-seizure drugs
➻ oral contraceptives
➻ Vitamin K (also used for Warfarin OD)
➻ Lipid/cholesterol lowering drugs

129
Q

Contraindications of warfarin?

A

same as Heparin

130
Q

Differences between Warfarin & Heparin?

A 
➻ W is a small lipid soluble molecule (crosses placenta - Teratogenic)
➻ H is a large lipid insoluble molecule
➻ W delayed onset of action (HRS)
➻ H rapid onset of actin
➻ W orally
➻ H subQ or IV
➻ W monitor prothrombin time (PT)
➻ H monitor aPTT
131
Q

Action of Fibronolytic type drugs?

A

Breaks down actual clot, administered IV

132
Q

Types of Fibrinolytic drugs?

A
  1. Streptokinase (streptase)
  2. Tissue Plasminogen Activator (Alteplase)
  3. Tenectaplase (TNKase)
133
Q

Define Plasmin

A

Enzyme in blood that degrades fibrin clots (Plasminogen is a pre-cursor to plasmin)

134
Q

Streptokinase MOA?

A

⇝ Binds plasminogen - leads to rapid conversion to Plasmin

⇝ Degrades fibrinogen in systemic bleeding

135
Q

Tissue Plasminogen Activator action?

A

Endothelial cells put out TPA

136
Q

Indications for Fibrinolytic drugs?

A

⇝ Acute MI
⇝ DVT
⇝ Pulmonary embolism

137
Q

Fibrinolytics contraindications?

A

⇝ Intracranial hemorrhage
⇝ Recent surgery
⇝ GI bleeding
⇝ aneurysm (weakening of BV walls)

138
Q

Tx of Fibrinolytic OD?

A

Aminocaproic Acid (prevents Plasmin from binding to the fibrin mesh - clot)

139
Q

Where does Streptokinase come from?

A

Bacteria

Pharmacology (8 decks)

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