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Pathophys > CAD > Flashcards

CAD Flashcards

1
Q

Left anterior descending artery

A

supplies anterior wall of both ventricles and ant 2/3 septum & ant papillary muscle

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2
Q

diagonal branches

A

supply ant surface LV

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3
Q

left circumflex artery

A

supplies left atrium, posterior and lateral lv ventricle

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4
Q

RCA

A

supplies right atrium and right ventricle , SA and AV nodes and posterior interventricular septum

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5
Q

right marginal artery

A

supplies RV

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6
Q

posterior descending artery

A

supplies inferior and post walls of ventricle and post 1/3 septum including posterior papillary muscle

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7
Q

dysfunctional endothelium

A

decrease in NO and prostacyclin ( relaxation doesnt occur) and contraction occurs via 5-HT and TXA2 and less inhibition of the coagulation bc of decrease in NO and prostacyclin

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8
Q

metabolic syndrome

A 
any of the 3: 
abdominal obesity ( men >40 in / women >35in) 
TG > 150 mg/dl
BP >= 130/85
fasting glucose >110 mg/dl 
HDL cholesterol : men < 50 mg/dl
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9
Q

biomarkers of increased risk of CAD

A

elevated lipoprotein (a)
elevated homocysteine levels
elevated high sensitivity C -reactive protein

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10
Q

ischemia VS angina

A

I->inadequate supply of blood and oxygen to myocardium

A-> clinical presentation of what is happening at the myocardial level - chest pain from ischemia

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11
Q

critical narrowing

A

70% you have symptoms with exercise or emotional distress

90% symptoms at rest

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12
Q

Stable angina

A

chronic pattern of transient angina precipitated by physical activity or emotional upset and relieved by rest within a few mins. no permanent myocardial damage

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13
Q

silent ischemia

A

asymptomatic myocaradial ischemia ; detected by EKG or lab tests

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14
Q

variant angina

A

typical anginal pain by occurs at rest due to coronary artery spasm- not do to plaques

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15
Q

unstable angina

A

increasing frequency or duration of anginal episodes with less exertion or at rest

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16
Q

MI

A

myocardial necrosis from prolonged blood loss - permanent

17
Q

EKG

A

look for signs of previous MI - Q waves

  • ST- segment depression during angina
  • inverted T waves during angina
  • absence of EKG changes during pain suggests non-ischemia etiology
18
Q

NonTransmural (subendocardial) ischemia -ekg

A

ST segments are transiently depressed and may show T wave inversion

19
Q

transmural ischemia -ekg

A

st segments are transiently elevated ( early acute mi)

- after transmural MI -> q waves are present and permanent

20
Q

what to look for changes in - RCA, LAD, Circumflex

A

RCA-> II, III and aVF - ST depression
LAD -> V1-V4
circumflex -> V5, V6 I and aVL

21
Q

acute coronary syndromes

A

unstable angina
non- st- segment elevation ( NSTEMI) - subendocardial
St-segment elevation ( STEMI)- transmural

22
Q

stable angina

A
  • > = 70% luminal narrowing of one or more coronary arteries
  • EKG : baseline often normal ; ST segment depression or T wave inversion with angina
  • exercise stress test
  • modify risk factors, drugs - decrease MVO2
  • nitrates - decrease preload , beta blockers - decrease MVO2 by decreasing contractility - calcium channel blockers - vasodilation
23
Q

prinzmetal’s or variant angina

A

pattern: angina at rest
abnormality: coronary artery spasm
EKG: transient ST -segment elevation with pain, may have AV block or vent arrhy
diagnosis: cardiac cath -> acetylcholine-> provoke acetylcholine
treatment; calcium channel blockers/ nitrates

24
Q

partially occluded thrombus

A

unstable angina or NSTEMI

25
Q

completely obstructing thrombus

A

stemi

26
Q

Unstable angina

A
  • occurs at rest >10 minutes
    -severe of new onset ( 4-6 weeks)
    -crescendo pattern
    -unpredictable
    abnormality: plaque rupture with thrombus causing worsening coronary blockage
    EKG: same as stable
  • may go onto NSTEMI or STEMI unless treated
27
Q

unstable angina - diagnosis

A

crescendo
ST depression and/or T wave inversion on EKG
no serum biomarkers

28
Q

NSTEMI - daignosis

A

prolonged chest pain

  • ST depression and/or T wave inversion on EKG
  • positive serum markers
29
Q

STEMI- diagnosis

A

prolonged chest pain

  • ST elevation ( with Q waves later)
  • positive serum biomarkers
30
Q

cardiac biomarkers

A 
cardiac specific troponins 
- reg proteins involved in actin and myosin - TnC, TnI , TNT 
- cardiac forms of troponin I and T 
-3-4 hrs after MI 
-peak 18-36 hours 
declines after 10-14 days

creatine kinase

  • myocardial specific isoenzyme
  • 3-8 hours after onset
  • peak 24 hrs
  • returns to normal by 48 hrs
  • not as sens or spec as cardiac troponins
  • used to detect early reinfarction
31
Q

Treatment

A

Same for all 3 : 1. rapid response time critical to limit damage. 2. correct intracoronary thrombus 3. restore balance of myocardial oxygen supply with demand

different: STEMI pt need immediate reperfusion therapies die to complete occlusion of vessel - NSTEMI and UA dont

anti-ischaemic, control pain ( morphine), O2, antithrombotic , adjunctive treatment ( statins, ace inhibitors)

32
Q

anti-ischemic therapy

A

b blockers, nitrates, calcium channel blockers

33
Q

antithrombotic therapy

A

antiplatelet: aspirin, clopidogrel , glycoprotein IIb. IIA inhibitors
anticoagulants : low molecular weight heparin, unfractionated IV heparin, other

34
Q

STEMI ONLY TREATMENT

A

within 90 mins -> percutaneous coronary intervention

after 90 mins 0> fibrinolytic therapy ( tPA)

35
Q

STEMI and UA treatment only

A 
risk assessment thrombolysis in MI score ( TIMI) 
-7 variables to predict risk) 
if low - conservative approach
-if high -> invasive approach 
NO FIBRINOLYTICS
36
Q

complications of MI

A 
LV dysfunction - 25% loss -> CHF 
40% cardiogenic shock 
- recurrent ischemia - 20-30% 
-arrhythmias 
-mechanical problems: pump failure, pap muscle rupture( posterior is more vulnerable)  , ventricular free wall rupture , vent septal rupture, vent aneurysm
37
Q

dressler syndrome

A

uncommon form of pericarditis that occurs weeks after MI

  • due to immune process directed at damaged myocardial tissue
  • fever malaise, sharp pleuritic chest pain
  • pericardial effusion seen
  • treat with aspirin or NSAIDS

Pathophys (1 decks)

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