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Medical Perspectives 411 > Heart Pathology > Flashcards

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
Ions associated with ischemia ?
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
26
What does increased Na+ cause?
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
27
hypercontracture defin
constant depolarized state of myocyte
28
Upon reperfusion injury what happens
ionic injury dissipates through gap junctions (cardiac cells autorhymatcity/ juxtacrine). pH shift results in lysosomal damage and an increase in free radicals
29
change pH upon reperfusion results in
autolysis cell die
30
Major cardiac arrhythmias
referfusion injury
31
Clincial manifesstions of MI (male)
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
32
Female clinical manifestitations of MI
Major symptoms: SOB (middle of night), and chronic unexplained fatigue
33
Atypical presentation of female MI
``` 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
Post-infarct complications
Arrhthmias CHF Cardiogenic shock Pericarditis
35
How is post-infarct diagnosed?
History ECG serum levels of cardiac enzymes
36
cardiac enzymes diagnose ones
CK | troponin C
37
MI treatment
``` Reestablish blood flow pain relief (drugs) Limit infarct size reduce vasoconstriction prevent thrombus formation angioplasty stenting stem cell implantation cardiac rehab ```
38
How should MI patients exercise?
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
What are 2 vascular complications with MI?
recurrent ischemia | recurrent infarction
40
What are the 3 mechanical complications with MI?
Left ventricular free wall rupture (death) Ventricular septal rupture Papillary muscle rupture with acute mitral regurgitation
41
7 myocardial complications with MI?
``` Diastolic dysfunction systolic dysfunction CHF hypotension/ cardiogenic shock right ventricular infarction ventricular cavity dilation aneurysm formation (true or false) ```
42
pericardial comps with MI
Pericarditis Dressler's syndrome Pericardial effusion
43
Thromboembolic complications w/ MI
mural thrombosis systemic thromboembolism deep venous thrombosis (DVT) pulmonary embolism
44
Electrical comps with MI
``` Ventricular tachycardia ventricular fib supraventricular tachydysrhythmias bradydysrhythmias atrioventricular block (conduction system, so nodes) ```
45
systemic thromboembolism
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
TIA (transient ischemic attaack)
precursor to bigger event
47
DVT
huge thrombi, but usually in lower extremities such as gatrocenmius, could embolize right after surgery.
48
three locations emboli can go
Coronary arteries lungs brain
49
fibrolysin
dissolves clots
50
angiotensin II
most potent vasoconstictor
51
ANP
most potent vasodilator
52
diuretics do what
increase the formation and excretion of urine
53
What is the first line pharmaocological approach to HTN?
diuretic
54
diuretics used for what?
mild-moderate HTN and with combo of other drugs
55
Thiazide diuretics
inhibit sodium reabsorption and is very strong
56
Loop Diuretics
act on loop of Henle and prevent sodium and chloride reabsorption into the systemic circulation
57
K+-sparing diuretics
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
Adverse Effects of diuretics
``` FD EI HNA+ HK+ BA GID F OH C MDELTA ```
59
What are sympatholytic drugs?
drugs that interfere with sympathetic discharge/ shut off SNS
60
Sympatholytic drugs include what?
``` beta blockers alpha blockers Pre-synaptic adrenergic neurotransmitter depletors centrally acting drugs ganglionic blockers BB, AB, PSAND, CNSAD, GB ```
61
Beta-adrenergic blockers MOA (mech of action)
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
b-1 selective
predominately affect B-1 receptors (cardio selective)
63
beta-nonselective
equal affinity for B-1,2, and 3
64
adverse effects of beta blockers
``` B EDHR EDMC OH D F GID ARXN ```
65
drugs ending in -olol are what kinds of drugs
beta blockers
66
block the a-1 adrenergic receptor on vascular smooth muscle 5 things:
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
a-1 can decrease 2 blankload
preload and afterload
68
Adverse effects of alpha blockers
RT OH CD/CHF VASODILATION = INCREASE BV
69
Presynaptic Adrenergic Inhbitors are what?
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
Adverse effects of Presyn adr inh
OH | GID (nausea, vomiting, nd the best diarrhea)
71
Centrally Acting Agents inhbt
sympathetic discharge from brainstem
72
adv effects of centrally acting agents
dry mouth, dizziness, and sedation
73
Gangllionic blockers
drugs that block synapse transmission at autonomic ganglions so catecholamines not synthesized
74
ganglionic blockers inhbit
ACh nevr a discharge across nerve
75
Vasodilators
produce their effect by directly inhibiting vaso-smooth muscle cells from contracting a-1 dont do
76
Vasodilators increase
the intracellular production of cGMP
77
cGMP
inhibitss second messenger
78
vasodilators inhibit
intracellular Ca++, thus there is no crossbridging so no muscle contraction
79
adverse effects vasodilators
``` RT PH D F N ```
80
ACE (Angiotensin converting enzyme) Inhibitors
inhibit the enzyme that converts angiotensin I to angiotensin II, thus, Angiotensin I never becomes angiotensin II
81
Angiotensin II Receptor Blockers
Block angiotensin receptors on various tissues, blocking the vaso-constricting effect

Medical Perspectives 411 (9 decks)

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