Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Year 1: Patho/Pharm > CAD and ACS Patho > Flashcards

CAD and ACS Patho Flashcards

1
Q

Arterioscelerosis
Definition

A

Disease of arteries where injury/inflammation results in :
1. thickening/narrowing
2. loss of elasticity

Occurs in
1. intima layer (endothelial)
2. medial layer (muscular)

Example:
Atheroscelerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Atheroscelerosis
Definition

A

A type of arterioscelerosis
1. narrowing/thickening
2. loss of elasticity

Results from injury, inflammation, and deposition of cholesterol/lipids in the endothelial/intimal layer of the artery

Arteries involved:
Aorta
Coronary arteries
Carotid arteries
iliac
mesenteric
femoral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Coronary Arteries
Physiology

A

Coronary ostia
- site where coronary arteries originate
- off of the aorta
- 2 branches

  1. LCA
    - left coronary artery (Left atrium, ventricle)
    - Left anterior descending coronary artery (anterior, septum, apical)
    - Left circumflex artery (lateral, posterior)
  2. RCA
    - right coronary artery (right atrium, ventricle, SA, AV node)
    - right posterior descending artery (back of right side of heart)
    - right marginal artery (lateral side of heart)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Physiological Function of the Endothelium

A

Endothelium
- intima
- inner lining of the blood vessels

Functions (homeostasis: vascular tone, coagulation, immune response)

  • Anti-platelet (prostaglandins inhibit platelet activation)
  • Vasodilation (production NO)
  • Anti-coagulation(activate protein C anti-coagulation, produce heparin)
  • inflammation (P-Selectin, attachment for platelets and WBC diapedesis)
  • angiogenesis (new blood vessels)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pathophysiology CAD
Step 1

A
  1. Endothelial injury and dysfunction

Injury
- virus, toxins, smoking
- inflammatory cytokines
- hypertension
- hyperglycemia, dyslipidemia, hyperuricemia

Endothelial dysfunction

  1. Narrowing
    - cannot produce NO
  2. Clotting
    - cannot produce anti-platelet (heparin, C protein)
    - cannot produce anti-coagulation (PGE)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pathophysiology CAD
Step 2

A
  1. Formation Fatty Streak (earliest lesion)
  • endothelial cell injury
  • inflammatory response
  • expression P selectins
  • recruitment of WBC (neutrophils, macrophages)
  • deposition LDL (lipids deposit)
  • Neutrophils release ROS which oxidize lipids
  • oxidized lipids increase endothelial expression of adhesion molecules (diapedesis WBC)
  • macrophages phagocytose the oxidized LDL
  • Foam cell = macrophage + oxidized LDL
  • signal cytokines to recruit T cells
  • cytokines TNF alpha, IFN gamma, IL1 stimualte expression adhesion molecules and procoagulation activity
  • formation fatty streak = T cells (WBC) + foam cells (Macropahges + oxidized lipids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pathophysiology CAD
Step 3

A
  1. Formation fibrous plaque
  • Pro-inflammatory cytokines recruit vascular smooth muscle cells and fibroblasts
  • proliferation, hypertrophy, increase deposition ECM
    1. thickening of the intima layer / narrowing
    1. loss of elasticity
  • (aterioscelerosis)
  • Formation of the thin fibrous plaque over the foam cell core (proinflammatory)

Unstable plaque
- thin fibrous cap
- large foam cell core (proinflammatory)
- NEW
- Prone to rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathophysiology CAD
Step 4

A
  1. Complicated lesion = ruptured fibrous cap = hemorrhage + thrombi + emboli
  • Thin fibrous cap ruptures
  • hemorrhage (bleed)
  • exposure of ECM results in platelet activation (collagen activates platelet IIb/IIIa receptors)
  • thrombus formation
    1. narrow lumen (thrombi)
    1. Ischemia at site
    1. Formation emboli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diseases that lead to endothelial injury and dysfunction

A
  • hypertension
  • diabetes
  • chronic kidney disease
  • gout
  • dyslipidemia
  • hyperglycemia/hypoglycemia
  • viruses
  • inflammatory cytokines
  • toxins
  • obesity
  1. injury
  2. inflammation
  3. oxidization lipids, fatty streaks
  4. fibrous cap/scelerosis/thikening/narrowing VSM
  5. unstable lesion/complicated lesion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acute Coronary Syndrome

A
  1. Unstable Angina
  2. NSTEMI
  3. STEMI

*medical emergency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Stable Angina
Definition

A

Pain < 5 minutes
reversible with rest, medication
Trigger (vasoconstriction): emotions, exercise

Pathphysiology
- atheroscelerosis of the coronary arteries
- Thickening/narrowing intima
- Decreased elasticity
- unable to vasodilate under stress
- ishemia (demand for oxygen > supply)

Laboratory findings
- normal troponin
- normal ECG (unless stress ECG / exercise ECG)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Unstable Angina
Definition

A

Pain > 5 minutes and < 20 minutes
reversible if < 20 minutes
Occurs at rest (no trigger)

Pathophysiology
- Unstable, complicated plaque
- rupture, thrombus formation
- blocks blood flow at rest
- ischemia at rest
*high risk of MI

Laboratory findings
- Normal or slightly elevated troponin
- normal or ST depression, T wave inversion ECG (when in pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

NSTEMI
Definition

A

Non ST elevated MI
> 20 minutes cardiac ischemia -> Necrosis
Troponin elevated
ECG changes (ST depression, T wave inversion)
*endocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

STEMI
Definition

A

ST elevated MI
> 20 minutes cardiac ischemia -> necrosis
troponin elevated
ECG changes (ST elevation)
*transmural necrosis (more serious than NSTEMI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Interventions ACS

A
  1. Reperfusion of cardiac muscle (time is muscle)

MONA
- morphine
- oxygen
- nitroglycerin
- anti-platelet therapy (ASA)

PCI
- percutaneous coronary intervention

Anti-fibrinolytic therapy
- TNK or Tissue plasminogen activator
- dissolve the clot if PCI is not available

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Unstable Angina
Clinical Signs and Symptoms

A
  • crushing substernal chest pain
  • increase frequency and severity of the angina pain
  • lasts > 5 minutes
  • unprovoked (occuring at rest when calm)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

STEMI/NSTEMI
Typical Clinical Signs and Symptoms

A

Ischemia:
Crushing substernal chest pain
pain in back
referred pain back, shoulder, arm, neck, jaw
nausea, vomiting
arrhythmias

SNS activation:
pale
diaphoresis
tremor
anxiety
tachycardia

Decreased CO:
fatigue
confusion
hypotension
syncope
pulmonary edema (SOB), dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Atypical
STEMI and NSTEMI

A

Older > 85 years
DM
female
*neuropathy results in no SNS signals

Decrease CO:
Hypotension
fatigue
weakness
confusion
shortness of breath

Referred pain:
abdominal indegestion like pain
neck, back

*Higher mortality as it is missed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pathophysiology
Acute Coronary Syndromes

A

CAD leads to decrease blood flow (ischemia)

  1. Stable angina
    - trigger: vasoconstriction
    - < 5 minutes pain
    - reversible
  2. Unstable angina
    - No trigger: at rest
    - ruptured plaque: complicated lesion, thrombosis ischemia
    - < 20 minutes
    - reversible
    - no death of cardiomyocytes
  3. MI
    - ischemia > 20 mintues, infarct
    - Change in 1. function 2. structure of the heart
    - cardiomyocyte stunning (loss of contraction due to anaerobic metabolism, low pH, electrolyte imbalance, activation SNS, change in contractility/HR/conduction)
    - cardiomyocyte hibernation (change in metabolism to survive, occurs if frequent ischemia, adaptive)
    - cardiomyocyte remodelling (inflammation, myofibroblasts/VSM proliferation/hypertrophy/ECM; SNS, RAAS, cytokines)
  4. Change conduction pathways
    - dysrhythmias
  5. change in size, shape, function
    - hypertrophy
    - heart failure
    - dissections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

CVD
Modifiable risk factors

A

CVD = injury/inflammation (endothelial dysfunction)

  • virus
  • toxins (smoking, alcohol)
  • obesity (pro-inflammatory)
  • diabetes (hyperglycemia)
  • dyslipidemia
  • hyperuricemia (gout)
  • HTN
  • stress/depression (pro-inflammatory)
  • diet
  • exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

CVD
Non-modifiable risk factors

A
  1. Age
    - older
    - women > 65 years
    - men > 55 years
    - before this is premature CVD
  2. gender
    - males > females (early in life)
  3. family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Social Determinants of Health
CVD

A
  • housing
  • food
  • stress
  • employment
  • racisim/sexism/discrimination
  • environment pollution

Influences endothelial injury, dysfunction, CVD development and disease progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Indigenous Peoples
CVD

A
  • Higher HTN
  • Higher DM
  • Higher CVD

*discrimination, racism, SDOH -> CVD

  • poor access to care, cost of care
  • bias in assessment, not screened
  • emergency PCI vs. planned
  • higher morbidity and mortality post operatively
24
Q

PQRSTUAAA
Chest Pain

A

Provokes: at rest? trigger?

Quality: crushing? heavy?

Radiation: jaw, neck, back, shoulder, arm

Region: substernal

Severity: Severe

Timing: with exercise? in morning? with stress? all the time? with movement? without movement? > 5 mintues?

Understanding:
Associated S&S: SNS (diaphoresis, tremors, anxiety, pale, tachycardia), CO (fatigue, confusion, dizziness, syncope, hypotension, bradycardia)

Alleviation: rest?

Aggrevation: exercise?

25
Typical Angina Classification
3/3 Typical symptoms 1. substernal chest pain - crushing - < 5 minutes 2. provoked by - stress - exercise 3. relieved by - rest - nitroglycerin medicaiton
26
Atypical Angina Classification
2/3 classical signs and symptoms SILENT - women, > 85 years, DM can present with atypical angina - fatigue, confusion, N/V, abdominal discomfort 1. provoked 2. relieved with rest Meet 2/3
27
Non-cardiac classification
1/3 classical signs and symptoms investigate other cause - heart - lungs - MSK - mind
28
Canadian Cardiovascular Society (1976) Angina Classification I-IV
Class I-III - stable angina - Class I: strenuous exercise - Class II: exercise - Class III: normal activities Class IV - unstable angina - provoked at rest
29
Diagnostic and Laboratory Tests CAD
CBC Lytes (Na, K, Mg, Ca, Phosphate) Lipid pannel (TC, TG, LDL, HDL) A1C and FPG Creatinine INR and PTT (preparation for PCI) ECG (12 lead) Troponin I and T Hs-cTN
30
Troponin I vs. T vs. hs-cTN
Troponin - Actin (thin filament) = actin, tropomyosin (covers myosin binding site), troponin (I, T, C) - indicators of MI (or muscle breakdown) cTnI - Cardiac troponin I - one isoform, only expressed in cardiomyocytes - most specific marker for MI - rises 2-4 hours post MI - can take up to 12 hours to appear - remains elevate for 10-14 days TnT - not specific to cardiac muscle damage - however can be used to indicate MI hs-cTn - high sensitivity cardiac troponin - can be elevated in unstable angina
31
Disorders with elevated troponin
- MI - Unstable angina - atrial fibrillation - myocarditis - heart failure - structural heart disease (cardiomyopathy) - depression - rhabdomyolysis - sepsis - renal failure *inflammation and muscle damage leads to the release of troponin from the muscle cell
32
Information obtained from ECG
1. rate 2. rhythm 3. conduction (Bundle branch block = MI) 4. ischemia / infarct (ST elevation, depression, T wave inversion) 5. necrosis (Q waves) ST: time from ventricular contraction (depolarization) to ventricular relaxation (repolarization) - isoelectric to PR - not isoelectric = ischemia NSTEMI: ST depression, T wave inversion STEMI: ST elevation
33
Alterations ECG with ACS
1. unstable angina - ischemia present then ECG changes present - ST depresison, T wave inversion 2. NSTEMI - ST depression - T wave inversion - * No Q wave - *clot dissolves, only subendothelial 3. STEMI - ST elevation - Q wave (ncrosis) *Transmural infarct
34
Diagnostic work up pathways Angina 1. typical 2. atypical 3. non-cardiac
STABLE chest pain syndrome - typical 3/3 - atypical 2/3 - non-cardiac 1/3 1. substernal chest pain< 5 mintutes 2. provoked by stress/activity 3. relieved by rest Not emergency, perform labs: - CBC, lytes, lipid pannel, A1C, FPG, Cr - ECG 1. Typical (3/3) or atypical (2/3) - non invasive testing - choice of test dependent on ECG 2. non-cardiac 1/3 - males > 40 years, females > 60 years, CVRF present: non-invasive testing - males < 40 years, females < 60 years, no CVRF present: watch and wait
35
Non invasive CAD testing
Questions: Is your ECG normal? Can you exercise? (no HTN > 200mmHg SBP; MI; HF; electrolyte imbalances; PE; arrhythmias) 1. Exercise stress test - ECG while exercising (vasoconstriction induced) 2. Exercise echocardiography (ECG abnormal, can excercise) - echocardiography: wall motion, LV ejection fraction, and ECG 3. Exercise perfusion imaging (ECG abnormal, can exercise) 3. Vasodilator echocardiography (cannot exercise) - pharmacological induced ischemia 4. Vasodilator perfusion imaging (branch blocks, ventricular paced rhythm) - pharmacological induced ischemia 5. cardiac computed tomography (branch blocks, ventricular paced rhythm)
36
Information obtained from cardiac CT
- extent and area of the block
37
Gold standard diagnosis CAD
Coronary angiography - contrast dye SE: - 1/1000 MI, CVA, death
38
Physiological Function Cholesterol
1. Cell/organelle membranes (fluidity, rigidity) 2. Bile salts (absorption/digestion fat, GI, Liver) 3. prevent water loss skin 5. Steroid hormones (estrogen, progesterone, testosterone) *LDL delivers cholesterol to non-hepatic cells
39
Cholesterol Endogenous vs. Exogenous
Majority of cholesterol is ENDOGENOUS - made by liver - HMG CoA reductase (3 hydroxy 3 methyl glutaryl co enzyme A) - rate limiting step Minority cholesterol is DIET - dietary intake - liver stops synthesis
40
What type of fat intake increases endogenous cholesterol synthesis?
Saturated fats Reduce intake = reduce cholesterol synthesis by 15-25%
41
Lipoproteins Components, Function
Lipoproteins 1. phospholipid 2. Triglyceride and cholesterol core 3. Apolipoprotein - circular structure - soluble transport of lipids in the blood Apolipoprotein function - structure - receptor attachment site (uptake) - activate enzyme for metabolism Types of lipoproteins - VLDL - LDL - HDL
42
Structure and Function VLDL, LDL, HDL
VLDL - TG core - *predictive pancreatitis LDL - Cholesterol core - transport cholesterol to non-hepatic tissues - tissues increase LDL receptors when they need cholesterol -*predictive CAD and ASCVD - 1% reduction = 1% reduction HDL - Cholesterol core - Transport cholesterol back to liver - good cholesterol - Protective
43
Role of LDL oxidation in Atheroscelerosis (ASCVD)
LDL deposits in intima (below endothelial cells) Oxidation LDL - cytotoxic = inflammation - signals monocytes - engulphed by macrophages - causes vacuolation of macrophages = foam cells - prevents their mobility - macrophages signal for WBC - accumulation = atheroma - lumpy = turbulent blood flow = pro-coagulation
44
What is more likely to rupture Mature or immature plaque?
Immature plaque Thin fibrous cap unstable and more likely to rupture
45
What causes a plaque to rupture?
Accumulation inflammatory cells Turbulent blood flow shearing forces high blood pressure
46
ASCVD Risk Factors
- age - black - hypertension (BP > 130) - smoking - HDL, Total cholesterol, LDL DM is EQUIVALENT to having ASCVD
47
3 principle presentations of unstable angina
1. rest angina > 5 minutes 2. new onset class III (regular activities) 3. more frequent, more severe, longer duration, lower threshold trigger
48
Management unstable angina hospital
1. hospital 2. MONA - morphine, oxygen, nitrates, anti-coagulation therapy 3. PCI (reperfusion) or anti-thrombotic therapy or both 4. beta blocker + ACEi + statin + hyperglycemic control
49
Functional impairment Post MI and complications
- contractility & conduction - end diastolic pressure - ejection fraction - dysrhythmias - 6 weeks for scar tissue to heal
50
Complications of MI
dysrhythmias; 90% post MI LV HF pericarditis rupture heart wall, vessels thromboembolism sudden death (> 65 years, HTN, shock, DM, dysrhythmia, prior MI)
51
Peripheral Artery DIsease (PAD) Pathophysiology
Atheroscelerosis of the arteries of the lower extremities - iliac - femoral 1. acute or 2. gradual ONSET Clinical S&S - intermittent claudication
52
Lipids that predict CVE
Lipoprotein B (structural protein on LDL, allows for deposition into tissue) non HDL C (atherogenic lipids) LDL low HDL Lipoprotein A (genetically pre-determined at birth) - predictive for women
53
Non pharmacological ways to raise HDL
fish oil exercise weight loss moderate alcohol intake
54
Diagnostic labs for ACS
ECG Labs: CBC and WBC diff ESR, CRP high sensitivity troponin other: lipid pannel A1C, RPG Chest x ray
55
Treatment STEMI and NSTEMI
MONA morphine oxygen nitroglycerine ASA
56
ICU orders for MI
Continuous monitoring ECG, oxygen Blood work trends: CBC, WBC, high sensitivity troponin, CRP every 24 hours Bed rest for 14 days Continuous medicaitons ACEi/ARB + Beta blocker Statin Anti-coagulant (heparin/LMWH, DOAC) Treatment glucose stool softeners
57
ECG indications
Q wave - necrosis ST elevation - Injury myocardium T wave inversion - ischemia

Year 1: Patho/Pharm (45 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions