Heart Pathology Flashcards

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1
Q

What is an acute myocardial infarction?

A

usually caused by sudden thrombotic occulusion of a coronary artery at the site of an atherosclerotic plaque that has become unstable due to a combination of ulceration, fissuring and rupture.

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2
Q

25% of acute MI’s are what?

A

CHF

Left ventricle infarcted

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3
Q

What is right ventricular ischemia or infarction?

A

occurs in up 1/2 of inferior wall of infarctions

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4
Q

thrombosis

A

blocks vessels due to aggregate of plaques

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5
Q

STEMI

A

ST-segment elevation MI

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6
Q

WHAT IS A STEMI?

A

complete occlusion of blood/oxyegn to large portion of mycardium, so no O2 getting to heart

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7
Q

Stemi is based upon

A

reperfusion capacity of myocardium, and is a more rapid ST segment resolution with treatment resulted in better prognosis/ survival rate

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8
Q

absence of st

A

indicates failed reperfusion treatment

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9
Q

Where do thrombus formation occur?

A

most often at the site of atheroscelerotic lesion, thus obstructing blood flow to myocardial tissues

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10
Q

Plaque rupture

A

thrombus formed on site and occlude blood, thus causing MI

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11
Q

Zone of Infarction

A

can’t reverse or save area

ischemia and reperfusion injury is accompanied by inflamatory response

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12
Q

Zone of hypoxic injury

A

reversible

immediately surrounding the zone of infarction is region

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13
Q

Zone of ischemia

A

reversible

if blood repercussion reestablished

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14
Q

6 Factors that impact size of infarction

A
extent
severity
duration of ischemic episode
size of vessel
amt of collateral circulation
status of intrinsic fibrinolytic sys
vascular tone
metabolic demand of myocardium at the time of event
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15
Q

MI most damage is where

A

left ventricle leading to alteration in ventricular function, but can occur in right or both at same time

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16
Q

Where are MI located in left ventricle?

A
Anterior 
septal 
lateral
posterior
inferior walls of left ventrical
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17
Q

Transmural infarction

A

used to imply an infarction process that has resulted in necrosis of the tissue in al the layer of the myocardium

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18
Q

why transmural infarct?

A

Heart functions as squeezing pump, sys and diastolic efforts can be significantly changed when segment of heart muscle is necrotic and nonfunctional

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19
Q

What happens if transmural infarct is small, the necrotic wall may be . . . ?

A

dyskinetic- difficulty moving due to scar tissue

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20
Q

What happens if transmural infarct is more extensive?

A

The myocardial muscle may become akinetic meaning without motion

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21
Q

Saving hear after MI occurs ?

A

a substantial amt of myocardial tissue can be saved of flow is restored within 6 hrs after onset of coronary occlusion

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22
Q

cellular changes associated with MI include what 3 things?

A
  1. the development of infarct extension (new myocardial necrosis),
  2. infarct expansion (a disproportionate thinning and dilation of the infarct zone), or
  3. Ventricular remodeling (a disproportionate thinning and dilation of the ventricle).
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23
Q

reperfusion injury

A

supplemental oxygen support in individuals with STEMI

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24
Q

Ischemia Reperfusion injury is when?

A

cardiac myocyes more glycolytic resulting in pH shift (decreased pH/ increased acidity)

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25
Q

Ions associated with ischemia ?

A

Increase in Na+ inactivation of Na/K pump based upon pH, the Na/K pump allows rest, and this stops working and is not getting rid of sodium anymore

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26
Q

What does increased Na+ cause?

A

depolarized state with Ca2+, which is repelled everywhere and results hypercontracture of ischemic zone resulting in altered environment in cell. The cell/zone = dead can’t save

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27
Q

hypercontracture defin

A

constant depolarized state of myocyte

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28
Q

Upon reperfusion injury what happens

A

ionic injury dissipates through gap junctions (cardiac cells autorhymatcity/ juxtacrine). pH shift results in lysosomal damage and an increase in free radicals

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29
Q

change pH upon reperfusion results in

A

autolysis cell die

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30
Q

Major cardiac arrhythmias

A

referfusion injury

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31
Q

Clincial manifesstions of MI (male)

A

Sudden sensation of pressure (crushing chest pain)
Radiation to: Arm, Throat, Jaw, Neck, and mid thoracic back pain.
Constant pain lasting 30 minutes to an hour
SOB
Pallor
Profuse perspiration

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32
Q

Female clinical manifestitations of MI

A

Major symptoms: SOB (middle of night), and chronic unexplained fatigue

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33
Q

Atypical presentation of female MI

A
Continuous pain in @ mid thoracic spine
continous pain at the tight inter-scapular space
Neck/shoulder pain
stomach or abdominal pain
nausea
unexplained anxiety
heartburn not changed by antacids
34
Q

Post-infarct complications

A

Arrhthmias
CHF
Cardiogenic shock
Pericarditis

35
Q

How is post-infarct diagnosed?

A

History
ECG
serum levels of cardiac enzymes

36
Q

cardiac enzymes diagnose ones

A

CK

troponin C

37
Q

MI treatment

A
Reestablish blood flow
pain relief (drugs)
Limit infarct size
reduce vasoconstriction
prevent thrombus formation
angioplasty
stenting
stem cell implantation
cardiac rehab
38
Q

How should MI patients exercise?

A

gentle movements
Breathing exs/coughing
survivors who exercise require less meds (high self efficacy)
Reduces cardiac risk factors
require fewer invasive procedures
cool-down is required to prevent blood pooling

39
Q

What are 2 vascular complications with MI?

A

recurrent ischemia

recurrent infarction

40
Q

What are the 3 mechanical complications with MI?

A

Left ventricular free wall rupture (death)
Ventricular septal rupture
Papillary muscle rupture with acute mitral regurgitation

41
Q

7 myocardial complications with MI?

A
Diastolic dysfunction
systolic dysfunction
CHF
hypotension/ cardiogenic shock
right ventricular infarction
ventricular cavity dilation
aneurysm formation (true or false)
42
Q

pericardial comps with MI

A

Pericarditis
Dressler’s syndrome
Pericardial effusion

43
Q

Thromboembolic complications w/ MI

A

mural thrombosis
systemic thromboembolism
deep venous thrombosis (DVT)
pulmonary embolism

44
Q

Electrical comps with MI

A
Ventricular tachycardia
ventricular fib
supraventricular tachydysrhythmias
bradydysrhythmias
atrioventricular block (conduction system, so nodes)
45
Q

systemic thromboembolism

A

emboli in the (arteries) systemic circuit, can result in TIA (stroke) so it is when you have mild stroke due to emboli, but has no long lasting effects

46
Q

TIA (transient ischemic attaack)

A

precursor to bigger event

47
Q

DVT

A

huge thrombi, but usually in lower extremities such as gatrocenmius, could embolize right after surgery.

48
Q

three locations emboli can go

A

Coronary arteries
lungs
brain

49
Q

fibrolysin

A

dissolves clots

50
Q

angiotensin II

A

most potent vasoconstictor

51
Q

ANP

A

most potent vasodilator

52
Q

diuretics do what

A

increase the formation and excretion of urine

53
Q

What is the first line pharmaocological approach to HTN?

A

diuretic

54
Q

diuretics used for what?

A

mild-moderate HTN and with combo of other drugs

55
Q

Thiazide diuretics

A

inhibit sodium reabsorption and is very strong

56
Q

Loop Diuretics

A

act on loop of Henle and prevent sodium and chloride reabsorption into the systemic circulation

57
Q

K+-sparing diuretics

A

prevent the secretion of potassium into the distal tubule, used to treat very mild case. they are not as effective due to smaller osmotic pull. Prevent hypokalemia!

58
Q

Adverse Effects of diuretics

A
FD
EI
HNA+
HK+
BA
GID
F
OH
C
MDELTA
59
Q

What are sympatholytic drugs?

A

drugs that interfere with sympathetic discharge/ shut off SNS

60
Q

Sympatholytic drugs include what?

A
beta blockers
alpha blockers
Pre-synaptic adrenergic neurotransmitter depletors
centrally acting drugs
ganglionic blockers
BB, AB, PSAND, CNSAD, GB
61
Q

Beta-adrenergic blockers MOA (mech of action)

A

block b-1 recepotrs located on heart from adrengeric stimulation, decrease cardiac contracilty and rate of contraction (HR). Decrease total cardiac workload, which will normalize heart rate and decrease general sympathetic tone. limit extent of cardiac damage following MI. Decrease chance of death.

62
Q

b-1 selective

A

predominately affect B-1 receptors (cardio selective)

63
Q

beta-nonselective

A

equal affinity for B-1,2, and 3

64
Q

adverse effects of beta blockers

A
B
EDHR
EDMC
OH
D
F
GID
ARXN
65
Q

drugs ending in -olol are what kinds of drugs

A

beta blockers

66
Q

block the a-1 adrenergic receptor on vascular smooth muscle 5 things:

A

reduction in intracellular Ca2+
vaso-smooth muscle relaxtion
decrease peripheral vascular resistance
used in autonomic crisis (sympathetic shock)
promote vasodilation in condition of vascular insufficiency

67
Q

a-1 can decrease 2 blankload

A

preload and afterload

68
Q

Adverse effects of alpha blockers

A

RT
OH
CD/CHF
VASODILATION = INCREASE BV

69
Q

Presynaptic Adrenergic Inhbitors are what?

A

drugs that inhibit release of Norepinephrine from presynaptic termincal (nerve) of peipheral adrengeric neurons, thus, inhibiting catecholamine release at presynaptic junction, thus, catecholamine release inhibited at axon terminal

70
Q

Adverse effects of Presyn adr inh

A

OH

GID (nausea, vomiting, nd the best diarrhea)

71
Q

Centrally Acting Agents inhbt

A

sympathetic discharge from brainstem

72
Q

adv effects of centrally acting agents

A

dry mouth, dizziness, and sedation

73
Q

Gangllionic blockers

A

drugs that block synapse transmission at autonomic ganglions so catecholamines not synthesized

74
Q

ganglionic blockers inhbit

A

ACh nevr a discharge across nerve

75
Q

Vasodilators

A

produce their effect by directly inhibiting vaso-smooth muscle cells from contracting
a-1 dont do

76
Q

Vasodilators increase

A

the intracellular production of cGMP

77
Q

cGMP

A

inhibitss second messenger

78
Q

vasodilators inhibit

A

intracellular Ca++, thus there is no crossbridging so no muscle contraction

79
Q

adverse effects vasodilators

A
RT
PH
D
F
N
80
Q

ACE (Angiotensin converting enzyme) Inhibitors

A

inhibit the enzyme that converts angiotensin I to angiotensin II, thus, Angiotensin I never becomes angiotensin II

81
Q

Angiotensin II Receptor Blockers

A

Block angiotensin receptors on various tissues, blocking the vaso-constricting effect