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OPT 541 > Final Material > Flashcards

Final Material Flashcards

1
Q

Why does the heart need its own blood supply?

A

The cardiac muscle is too thick for blood in atria and ventricles to perfuse through to supply the heart.

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2
Q

Types of Angina

A
  1. Classical or typical angina
  2. Unstable angina
  3. Prinzmetal, variant, angina
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3
Q

Classic or typical angina

A

This is occurs due to plaque building up over time. Will not have enough oxygen supply during exercise. Goes away with rest

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4
Q

Unstable Angina

A

A type of acute coronary syndrome. A different type of angina where the plaque begins to flap off and can sometimes partially occlude the vessel. Very unpredictable and doesn’t only occur during exercise.

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5
Q

Prinzmetal/variant angina

A

Due to vasospasm. Occurs at night or rest. Not related to exercise, HR, or BP.

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6
Q

Acute Coronary Syndrome

A

Occurs when atherosclerotic plaque ruptures and resulting thrombus partially/completly occludes coronary arteries. Include 1. STEM 2. NSTEM 3. Unstable angina

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7
Q

How long does it take for heart muscle to die without oxygen

A

greater then 20 minutes

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8
Q

Causes of heart attack

A
  1. Clot completely blocks vessel

2. Embolize block off downstream vessel

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9
Q

What is the medical treatment for a heart attack?

A

Morphin, Oxygen, Nitrates, Asprin. EGG monitor to diagnoise.

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10
Q

What are the classes of drugs for treatment of angina

A

Nitrates, beta-blockers, CCB, Na channel blockers.

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11
Q

Drugs to give post MI

A

Betablockers, Nitrates, anticoagulant, acei, Statin.

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12
Q

What do Organic nitrates do?

A

Dilate veins, coronary vasculature, decrease MI oxygen consumption.

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13
Q

Mechanism of organic nitrates.

A

On a cellular level nitrates->nitrites->nitric oxide->increse CGMP->increased cGMP causes increased dephospho rylation of myosin light chain. This causes vascular smooth muscle relaxation.

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14
Q

Adverse effects of Organic nitrates?

A

HA, postural hypertenion, tachycardia, flushing, Contraindicted with PED51. Tolerance develops radily.

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15
Q

How do Beta blockers treat Angina?

A

Decrease the oxygen demand for myocardium. Drug of choice for effort induced angina. Gradually taper over 2-3 weeks.

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16
Q

Propranolol

A

Beta blocker used to treat Angina.

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17
Q

Calcium Channel Blockers

A

Relieves angina by reduction of free Ca which decreases heart rate (decreases rate of depolarization at SA nodes) and thus decreasing oxygen demand by the heart

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18
Q

SE of CCB

A

Constipation

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19
Q

Calcium Channel Blockers

A

Relieves angina by reduction of free Ca which decreases heart rate (decreases rate of depolarization at SA nodes) and thus decreasing oxygen demand by the heart Used with exercise induced angina.

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20
Q

What drugs should be used with concomitant angina and HTN?

A

BB and CCB

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21
Q

Arrhythmias

A

Dysfunction cause abnormalities in impulse formation and condition in the myocardium.

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22
Q

Nodal AP

A

Ca channels open and cause a fast depolarization. Slow to depolarize due to long standing open in calcium channels.

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23
Q

Cause of arrhythmias

A

Arise either from aberrations in impulse generation or from a defect in impulse conduction.

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24
Q

Re-entry

A

Most common cause of arrhythmia. Occurs when impulse travels in retrograde direction and reenters the conduction pathway.

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25
Q

Bradycardia

A

Slow heart beat. SA node is slow or doesn’t generate AP since it gets parasympathetic stimulation or not enough sympathetic stimulation

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26
Q

Tachycardia

A

A very high heart beat. Can occur by increase pacemaker activity in the SA node due to too much stimulation or not enough parasympathetic stimulation. Can also be due to SA node dysfunction.

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27
Q

How to remember the classes of the drugs?

A

South Beach Pol-Ka

Sodium channel blocker, BB, Potasioum, CCB

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28
Q

How to remember the classes of anti arrhythmic drugs?

A

South Beach Pol-Ka

Sodium channel blocker, BB, Potasioum, CCB

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29
Q

Class I anti-arrhythmic drugs

A

Block sodium channels so it takes longer for depolarization to occur. It makes the refractory period longer which increases HR.

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30
Q

Lidocaine

A

A class I anti-arrhythmic drug. The sodium channel blocker.

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31
Q

Class II anti-arrhythmic drugs

A

Beta blockers. Drugs like propanolol

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32
Q

Class III anti-arrhythmic drugs

A

Inhibits K channels widens the action potential and leading to increased refractory period to slow heart beat. Leads to increased risks of ventricular tachyarrhythmias.

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33
Q

Class IV anti-arrhythmic drugs

A

Used for CCB.

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34
Q

Verpamil

A

Class IV anti-arrhythmic drugs. Shows greater action on the heart.

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35
Q

Nifedipine

A

Class IV anti-arrhythmic drug. Exerts a stronger effect on the vascular smooth muscle.

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36
Q

Verpamil

A

Class IV anti-arrhythmic drugs. Shows greater action on the heart. Treats supra ventricular tachycardia.

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37
Q

HF

A

Decreased ability of the heart to fill with or eject blood

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38
Q

Congestive Heart Failure

A

HF with signs of symptoms of HF (feel congestion in the lungs and has problem breathing)

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39
Q

LHF

A

Dyspnea (shortness of breath upon exertion), cough, orthopnea (shortness of breath upon rest), paroxysmal nocturnal dyspnea (shortness of breath at night)

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40
Q

RHF

A

Problem getting enough back to the RA. peripheral edema (swollen legs and ankles), ↑ liver size, ascites (fluid in abdominal cavity)

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41
Q

LHF

A

Dyspnea (shortness of breath upon exertion), cough, orthopnea (shortness of breath upon rest), paroxysmal nocturnal dyspnea (shortness of breath at night). Past the lung and left side of heart cannot pump out efficiently. Will get back up in the lungs.

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42
Q

RHF

A

Problem getting enough back to the RA. peripheral edema (swollen legs and ankles), ↑ liver size, ascites (fluid in abdominal cavity).

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43
Q

What regulates Cardiac Output?

A

HR and Stroke volume.

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44
Q

What regulates Stroke Volume

A

Afterload, contractility, preload

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45
Q

What decreases stroke volume?

A

Chronic hypertension (increases after load) Coronary artery disease (increases contraction) Constrictive pericarditis (decreases preload)

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46
Q

NYHA HF classification

A
  1. no limit on exercise, no symptoms
  2. decreased exercise ability with symptoms during normal exercise
  3. further decreased ability to exercise and symptoms with less than normal exercise
  4. symptoms at rest
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47
Q

AHA/ACC HF Classification

A

A. person at risk, no structural disease and no symptoms
B. structural disease and no symptoms
C. structural disease with symptoms
D. structural disease with symptoms and medically refractory

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48
Q

Corellation of NYHA and AHA/ACC HF Classification

A

I:B
II: C
III: C
IV: D

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49
Q

What is involved with remodeling of cardiac tissue?

A

Chronic activation of the sympathetic nervous system and the renin-angiotensin-aldosteron axis. Associated with remodeling of cardiac tissue characterized by loss of monocyte, hypertrophy, and fibrosis. The heart become less elliptical and more spherical.

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50
Q

What classes of drugs are used to treat HF

A

BADRID

  1. Beta-adrenoreceptor blocker
  2. Aldosteron antagonist
  3. Diuretics
  4. Reinin-angiotensin inhibitor
  5. Ionotropic agents
  6. Direct vasodilators
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51
Q

Compensatory physiological responses in HF

A
  1. increases sympathetic activity-an increased HF and cardiac preload
  2. Activation of the renin system-retention of sodium and water
  3. Myocardial hypertrophy-chambers dilate
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52
Q

Therapeutic strategies in HF

A

Reduction in physical activity, low sodium. Avoid NSAIDS, alcohol, CCBs.

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53
Q

Angiotensin-converting enzyme inhibitors

A

Drugs of choice for HF. Reduce angiotensin II and secretion of aldosterone. Decreases morbidity and mortality. Initiate ASAP after MI.

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54
Q

Ramipril

A

ACEi. Prodrug. Use for Heart failure

55
Q

ACEI SE

A

Persistant dry cough, angioedema, teratogenicity

56
Q

ARB

A

Use for those resistant to ACEi.

57
Q

Losartan

A

ARB. The prototype drug.

58
Q

Carvedilol

A

Beta blockers. Used in HF.

59
Q

Most commonly used diuretics in HF

A

Loop diuretics

60
Q

Nitrates

A

Direct vasodilators. Reduces preload.

61
Q

Ionotropic Drugs

A

Increase contraction of the heart. Mess with the ions in the heart.

62
Q

Digoxin

A

Inotropic drugs. Has a low therapeutic index. Inhibits the NA K exchange by Na/K ATPase

63
Q

Digoxin

A

Inotropic drugs. Has a low therapeutic index. Inhibits the NA K exchange by Na/K ATPase. Decreased K increases the potential for cardiotoxicty. SE: arrhythmia, blurred vision, alteration of color preception

64
Q

What drugs to use during stage A?

65
Q

What drugs to use during stage B?

A

ACEi + beta blocker and digoxin

66
Q

What drugs to use during stage C

A

ACEi, beta blocker, diuretics (loop and aldosteron antagonist)

67
Q

What drugs to use during stage D?

A

Hospice care or heart transplant

68
Q

Primary HTN

A

Cause is indirect like smoking, obesity, hyperlipidemia, Diabeties

69
Q

Secondary HTN

A

Caused by a direct disease like kidney disease or aortic concretion

70
Q

HTN Symptoms

A

Patients won’t have symptoms of HTN for a long time

71
Q

Malignant HTN

A

Anything above 240/120. Will take time for damage as well.

72
Q

Hypertension effects on blood vessels

A

Stretch and tears vessels which turn to scar tissue. Damage the endothelial cells of vessels.

73
Q

Baroreceptors

A

In carotid sinus and sensor in aortic arch. If bp is too high the sinus baroreceptors will stretch and send signal to midbrain to cause heart to slow. Release more parasymp. If bp is low barorecptor will not fire as much and this will decrease parasympathetic innervation to raise BP.

74
Q

Lifestyle modification in HTN

A

Eating less salt, exercising more, lowering primary risk factors.

75
Q

Drugs to use in HTN

A

ABCD: ACEi/ARB, Betablockers, CCB, diuretics

76
Q

First line therapy with HTN

A

Diuretics! Commonly use hydrochlorathalidone

77
Q

GO TO QUIZ DECK TO GET OTHER HTN AND DYSLIPIDEMIA INFO!

A

NOOOOOOOWWW!

78
Q

Thrombus

A

A clot that adheres to a vessel wall

79
Q

Embolus

A

An intravascular clot that floats in the blood

80
Q

Response to vascular injury

A

Vasospasm of the damaged blood vessels and formation of a platelet-fibrin clot

81
Q

Prostacyclin

A

Act as inhibitors of platelet aggregation. Elevate levels of intracellular cAMP when inactive. Decrease in intracellular calcium

82
Q

Nitric Oxide

A

Act as inhibitors of platelet aggregation. Elevate levels of intracellular cAMP when inactive. Decrease in intracellular calcium

83
Q

Thromboxanes

A

An agent that will lead to platelet aggregation. Collagen is covered in sub endothelial layers and will send message when it is exposed from damage.

84
Q

Thrombin (factor IIA)

A

Acts to To convert fibrinogen into fibrin (the coagulation cascade) to form a clot

85
Q

What do activated platelets release?

A

ADP, 5HT2 (serotonin), thromboxane A2, Platelet-activation factor, thrombin, also increase calcium levels.

86
Q

How are platelets actives?

A

By collagen binding.

87
Q

Glycoprotein IIB/IIIA

A

Cross-linking and platelet aggregation. Fibrinogen binds to GP receptors on two separate platelets (this causes the cross linking)

88
Q

How is arachnoid acid made?

A

It is a normal part of phospholipid membrane but it can be cleaved from the membrane by phospholipase A2.

89
Q

Asprin

A

Irreversibly inactivates cyclooxygenase preventing platelete aggregation.

90
Q

ADP receptor inhibitor

A

Irreversibly inhibit the binding of ADP to its receptor. This stops platelet aggregation

91
Q

Ticlopidine

A

ADP receptor inhibitor. SE: neutropenia, TTP(low level platelet) and aplastic anemia.

92
Q

Clopidogrel

A

ADP receptor inhibitor. A prodrug! If you have CY-450 or 2C19 may need to adjust dose

93
Q

Dipyridamole

A

Inhibits cyclic nucleotide phosphodiesterase (decrease amt. of cAMP so there will be more AMP). Decrease thromboxane A2 synthesis. Is used prophylactically to treat angina. In combination with aspirin or warfarin.

94
Q

Extrinsic clotting system

A

Occurs with trauma. Acts more to start intrinsic pathway. Factors involved are VII and X.

95
Q

Plasmin

A

Acts to break down clots

96
Q

Intrinsic clotting system factors involved

A

XII, XI, IX, X.

97
Q

How is extrinsic system of blood coagulation initiated?

A

Clotting factor VII

98
Q

How is intrinsic system of blood coagulation initiated?

A

Clotting factor XII

99
Q

Heparin

A

Activates antithrombin III. Interferes with thrombin factor II to inhibit formation of fibrin. Injectable and rapidly acting. Prevent venous thrombosis, treat pulmonary embolism and acute myocardial infarction.

100
Q

Enoxaparin.

A

LMWH. Longer half life, more predictable, more bioavaailability, less frequent bleeding, and hospital and outpatient.

101
Q

Heparin SE

A

Bleeding, hypersensitivity, thrombocytopenia

102
Q

Warfarin

A

Vitamin K antagonist. Factors II, VII, IX, and X require vitamin K for their synthesis. Delayed onset 8-10 hours. A narrow TI. Old anticoagulant.

103
Q

Coumarin

A

Vitamin K antagnoist. Factors II, VII, IX, and X require vitamin K for their synthesis.

104
Q

Thrombolytic drugs

A

Get rid of the clot. Activate conversion of plasminogen to plasmin (help to digest fibrin). Dissolution is more successful with new clots.

105
Q

Alteplase

A

Thrombolytic drug. Tissue plasminogen activator. Activates plasminogen that is bound to fibrin. Treatment of MI, massive pulmonary embolism, and acute ischemic stroke.

106
Q

Different forms of hemophilia

A 
Type A (Def. in factor VIII)
Type B (def. in factor IX)
Type C (def. in factor XI)
107
Q

Aminocaproic acid

A

Treats bleeding. Inhibits plasminogen activation.

108
Q

Protamine Sulfate

A

Treats bleeding. High in arginine, positively charged. Antidote to heparin.

109
Q

Vitamin K

A

Antidote for warfarin

110
Q

Anemia

A

A below normal plasma hemoglobin concentration. Can be due to deficiency in iron, folic acid, or vitamin B12.

111
Q

Iron Deficiency

A

Microcytic anemia

112
Q

Folic and B12 deficiency

A

macroblastic anemia

113
Q

Erythropoietin

A

Glycoprotein. Regulates RBC production. Used to treat anemia SE: HTN, Arthralgia

114
Q

Folic Acid

A

Used to treat anemia.

115
Q

Hydroxyurea

A

Drugs used to treat sickle cell disease. Increases fetal hemoglobin levels

116
Q

Pentoxifylline

A

Drugs used to treat sickle cell disease. Increases the deformability of RBC (make them more flexible)

117
Q

Toxicology

A

The study of adverse effects of chemicals on living organisms.

118
Q

Actions of chemicals

A
  1. Selective-warfarin-attacks one system
  2. nonselective-will active whatever is exposed. Acid
  3. immediate action-alkaline.
  4. Delayed-obestos-causes lung cancers over time.
119
Q

Halogenated hydrocarbon effects

A

Irritation of the eyes, irritation of respiratory system, nausea, dizziness, HA, death.

120
Q

Aromatic hydrocarbons

A

volatile, inhalation and ingestion, CNS depression, cardiac arrhythmias, tobacco smoke, toluene

121
Q

Methanol

A

Can have intermediate formaldehyde and then formic acid and can lead to permanent

122
Q

Ethylene glycol

A

Anti-freeze. Toxic to liver

123
Q

Pesticides

A

Organophosphates.

  1. Carbamates-inhibition of acetylcholinesterase. Indirect inhibitor.
  2. Rotenone-inhibits oxidation of reduced NAD+. Affects the ETC
124
Q

Heavy Metals

A

Lead, Mercury, cadmium. Functional groups: hydroxyl, carboxylic acid, sylfhydryl, and amino. Chronic exposures to low levels.

125
Q

SE of Lead

A

GI disturbance, Insomnia, HA, fatigue

126
Q

Mercury

A

DDX: parkinson dz or alzheimer dz.

127
Q

CO

A

Colorless, odorless, and tasteless. Cyanide binds to many metalloenzymes and interfere with ETC.

128
Q

Silica

A

Progressive lung dz.

129
Q

Atropine

A

Antidote for organophosphates, nerve gases, carbamates.

130
Q

Fomepizole

A

Antidote for methanol or ethylene glycol.

131
Q

Flumazenil

A

Antidote for benzodiazepine

132
Q

N-acetylcysteine

A

Antidote for acetaminophen

133
Q

Sodium Nitrate

A

Antidote for cyanide

134
Q

Succimer

A

Antidote for lead poisoning.

OPT 541 (3 decks)

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