Final Material Flashcards
(134 cards)
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.
2
Q
Types of Angina
A
- Classical or typical angina
- Unstable angina
- Prinzmetal, variant, angina
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
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.
5
Q
Prinzmetal/variant angina
A
Due to vasospasm. Occurs at night or rest. Not related to exercise, HR, or BP.
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
7
Q
How long does it take for heart muscle to die without oxygen
A
greater then 20 minutes
8
Q
Causes of heart attack
A
- Clot completely blocks vessel
2. Embolize block off downstream vessel
9
Q
What is the medical treatment for a heart attack?
A
Morphin, Oxygen, Nitrates, Asprin. EGG monitor to diagnoise.
10
Q
What are the classes of drugs for treatment of angina
A
Nitrates, beta-blockers, CCB, Na channel blockers.
11
Q
Drugs to give post MI
A
Betablockers, Nitrates, anticoagulant, acei, Statin.
12
Q
What do Organic nitrates do?
A
Dilate veins, coronary vasculature, decrease MI oxygen consumption.
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.
14
Q
Adverse effects of Organic nitrates?
A
HA, postural hypertenion, tachycardia, flushing, Contraindicted with PED51. Tolerance develops radily.
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.
16
Q
Propranolol
A
Beta blocker used to treat Angina.
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
18
Q
SE of CCB
A
Constipation
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.
20
Q
What drugs should be used with concomitant angina and HTN?
A
BB and CCB
21
Q
Arrhythmias
A
Dysfunction cause abnormalities in impulse formation and condition in the myocardium.
22
Q
Nodal AP
A
Ca channels open and cause a fast depolarization. Slow to depolarize due to long standing open in calcium channels.
23
Q
Cause of arrhythmias
A
Arise either from aberrations in impulse generation or from a defect in impulse conduction.
24
Q
Re-entry
A
Most common cause of arrhythmia. Occurs when impulse travels in retrograde direction and reenters the conduction pathway.
25
Bradycardia
Slow heart beat. SA node is slow or doesn't generate AP since it gets parasympathetic stimulation or not enough sympathetic stimulation
26
Tachycardia
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.
27
How to remember the classes of the drugs?
South Beach Pol-Ka
| Sodium channel blocker, BB, Potasioum, CCB
28
How to remember the classes of anti arrhythmic drugs?
South Beach Pol-Ka
| Sodium channel blocker, BB, Potasioum, CCB
29
Class I anti-arrhythmic drugs
Block sodium channels so it takes longer for depolarization to occur. It makes the refractory period longer which increases HR.
30
Lidocaine
A class I anti-arrhythmic drug. The sodium channel blocker.
31
Class II anti-arrhythmic drugs
Beta blockers. Drugs like propanolol
32
Class III anti-arrhythmic drugs
Inhibits K channels widens the action potential and leading to increased refractory period to slow heart beat. Leads to increased risks of ventricular tachyarrhythmias.
33
Class IV anti-arrhythmic drugs
Used for CCB.
34
Verpamil
Class IV anti-arrhythmic drugs. Shows greater action on the heart.
35
Nifedipine
Class IV anti-arrhythmic drug. Exerts a stronger effect on the vascular smooth muscle.
36
Verpamil
Class IV anti-arrhythmic drugs. Shows greater action on the heart. Treats supra ventricular tachycardia.
37
HF
Decreased ability of the heart to fill with or eject blood
38
Congestive Heart Failure
HF with signs of symptoms of HF (feel congestion in the lungs and has problem breathing)
39
LHF
Dyspnea (shortness of breath upon exertion), cough, orthopnea (shortness of breath upon rest), paroxysmal nocturnal dyspnea (shortness of breath at night)
40
RHF
Problem getting enough back to the RA. peripheral edema (swollen legs and ankles), ↑ liver size, ascites (fluid in abdominal cavity)
41
LHF
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.
42
RHF
Problem getting enough back to the RA. peripheral edema (swollen legs and ankles), ↑ liver size, ascites (fluid in abdominal cavity).
43
What regulates Cardiac Output?
HR and Stroke volume.
44
What regulates Stroke Volume
Afterload, contractility, preload
45
What decreases stroke volume?
Chronic hypertension (increases after load) Coronary artery disease (increases contraction) Constrictive pericarditis (decreases preload)
46
NYHA HF classification
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
47
AHA/ACC HF Classification
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
48
Corellation of NYHA and AHA/ACC HF Classification
I:B
II: C
III: C
IV: D
49
What is involved with remodeling of cardiac tissue?
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.
50
What classes of drugs are used to treat HF
BADRID
1. Beta-adrenoreceptor blocker
2. Aldosteron antagonist
3. Diuretics
4. Reinin-angiotensin inhibitor
5. Ionotropic agents
6. Direct vasodilators
51
Compensatory physiological responses in HF
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
52
Therapeutic strategies in HF
Reduction in physical activity, low sodium. Avoid NSAIDS, alcohol, CCBs.
53
Angiotensin-converting enzyme inhibitors
Drugs of choice for HF. Reduce angiotensin II and secretion of aldosterone. Decreases morbidity and mortality. Initiate ASAP after MI.
54
Ramipril
ACEi. Prodrug. Use for Heart failure
55
ACEI SE
Persistant dry cough, angioedema, teratogenicity
56
ARB
Use for those resistant to ACEi.
57
Losartan
ARB. The prototype drug.
58
Carvedilol
Beta blockers. Used in HF.
59
Most commonly used diuretics in HF
Loop diuretics
60
Nitrates
Direct vasodilators. Reduces preload.
61
Ionotropic Drugs
Increase contraction of the heart. Mess with the ions in the heart.
62
Digoxin
Inotropic drugs. Has a low therapeutic index. Inhibits the NA K exchange by Na/K ATPase
63
Digoxin
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
What drugs to use during stage A?
ACEi
65
What drugs to use during stage B?
ACEi + beta blocker and digoxin
66
What drugs to use during stage C
ACEi, beta blocker, diuretics (loop and aldosteron antagonist)
67
What drugs to use during stage D?
Hospice care or heart transplant
68
Primary HTN
Cause is indirect like smoking, obesity, hyperlipidemia, Diabeties
69
Secondary HTN
Caused by a direct disease like kidney disease or aortic concretion
70
HTN Symptoms
Patients won't have symptoms of HTN for a long time
71
Malignant HTN
Anything above 240/120. Will take time for damage as well.
72
Hypertension effects on blood vessels
Stretch and tears vessels which turn to scar tissue. Damage the endothelial cells of vessels.
73
Baroreceptors
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
Lifestyle modification in HTN
Eating less salt, exercising more, lowering primary risk factors.
75
Drugs to use in HTN
ABCD: ACEi/ARB, Betablockers, CCB, diuretics
76
First line therapy with HTN
Diuretics! Commonly use hydrochlorathalidone
77
GO TO QUIZ DECK TO GET OTHER HTN AND DYSLIPIDEMIA INFO!
NOOOOOOOWWW!
78
Thrombus
A clot that adheres to a vessel wall
79
Embolus
An intravascular clot that floats in the blood
80
Response to vascular injury
Vasospasm of the damaged blood vessels and formation of a platelet-fibrin clot
81
Prostacyclin
Act as inhibitors of platelet aggregation. Elevate levels of intracellular cAMP when inactive. Decrease in intracellular calcium
82
Nitric Oxide
Act as inhibitors of platelet aggregation. Elevate levels of intracellular cAMP when inactive. Decrease in intracellular calcium
83
Thromboxanes
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
Thrombin (factor IIA)
Acts to To convert fibrinogen into fibrin (the coagulation cascade) to form a clot
85
What do activated platelets release?
ADP, 5HT2 (serotonin), thromboxane A2, Platelet-activation factor, thrombin, also increase calcium levels.
86
How are platelets actives?
By collagen binding.
87
Glycoprotein IIB/IIIA
Cross-linking and platelet aggregation. Fibrinogen binds to GP receptors on two separate platelets (this causes the cross linking)
88
How is arachnoid acid made?
It is a normal part of phospholipid membrane but it can be cleaved from the membrane by phospholipase A2.
89
Asprin
Irreversibly inactivates cyclooxygenase preventing platelete aggregation.
90
ADP receptor inhibitor
Irreversibly inhibit the binding of ADP to its receptor. This stops platelet aggregation
91
Ticlopidine
ADP receptor inhibitor. SE: neutropenia, TTP(low level platelet) and aplastic anemia.
92
Clopidogrel
ADP receptor inhibitor. A prodrug! If you have CY-450 or 2C19 may need to adjust dose
93
Dipyridamole
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
Extrinsic clotting system
Occurs with trauma. Acts more to start intrinsic pathway. Factors involved are VII and X.
95
Plasmin
Acts to break down clots
96
Intrinsic clotting system factors involved
XII, XI, IX, X.
97
How is extrinsic system of blood coagulation initiated?
Clotting factor VII
98
How is intrinsic system of blood coagulation initiated?
Clotting factor XII
99
Heparin
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
Enoxaparin.
LMWH. Longer half life, more predictable, more bioavaailability, less frequent bleeding, and hospital and outpatient.
101
Heparin SE
Bleeding, hypersensitivity, thrombocytopenia
102
Warfarin
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
Coumarin
Vitamin K antagnoist. Factors II, VII, IX, and X require vitamin K for their synthesis.
104
Thrombolytic drugs
Get rid of the clot. Activate conversion of plasminogen to plasmin (help to digest fibrin). Dissolution is more successful with new clots.
105
Alteplase
Thrombolytic drug. Tissue plasminogen activator. Activates plasminogen that is bound to fibrin. Treatment of MI, massive pulmonary embolism, and acute ischemic stroke.
106
Different forms of hemophilia
```
Type A (Def. in factor VIII)
Type B (def. in factor IX)
Type C (def. in factor XI)
```
107
Aminocaproic acid
Treats bleeding. Inhibits plasminogen activation.
108
Protamine Sulfate
Treats bleeding. High in arginine, positively charged. Antidote to heparin.
109
Vitamin K
Antidote for warfarin
110
Anemia
A below normal plasma hemoglobin concentration. Can be due to deficiency in iron, folic acid, or vitamin B12.
111
Iron Deficiency
Microcytic anemia
112
Folic and B12 deficiency
macroblastic anemia
113
Erythropoietin
Glycoprotein. Regulates RBC production. Used to treat anemia SE: HTN, Arthralgia
114
Folic Acid
Used to treat anemia.
115
Hydroxyurea
Drugs used to treat sickle cell disease. Increases fetal hemoglobin levels
116
Pentoxifylline
Drugs used to treat sickle cell disease. Increases the deformability of RBC (make them more flexible)
117
Toxicology
The study of adverse effects of chemicals on living organisms.
118
Actions of chemicals
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
Halogenated hydrocarbon effects
Irritation of the eyes, irritation of respiratory system, nausea, dizziness, HA, death.
120
Aromatic hydrocarbons
volatile, inhalation and ingestion, CNS depression, cardiac arrhythmias, tobacco smoke, toluene
121
Methanol
Can have intermediate formaldehyde and then formic acid and can lead to permanent
122
Ethylene glycol
Anti-freeze. Toxic to liver
123
Pesticides
Organophosphates.
1. Carbamates-inhibition of acetylcholinesterase. Indirect inhibitor.
2. Rotenone-inhibits oxidation of reduced NAD+. Affects the ETC
124
Heavy Metals
Lead, Mercury, cadmium. Functional groups: hydroxyl, carboxylic acid, sylfhydryl, and amino. Chronic exposures to low levels.
125
SE of Lead
GI disturbance, Insomnia, HA, fatigue
126
Mercury
DDX: parkinson dz or alzheimer dz.
127
CO
Colorless, odorless, and tasteless. Cyanide binds to many metalloenzymes and interfere with ETC.
128
Silica
Progressive lung dz.
129
Atropine
Antidote for organophosphates, nerve gases, carbamates.
130
Fomepizole
Antidote for methanol or ethylene glycol.
131
Flumazenil
Antidote for benzodiazepine
132
N-acetylcysteine
Antidote for acetaminophen
133
Sodium Nitrate
Antidote for cyanide
134
Succimer
Antidote for lead poisoning.
