Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

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
Q

Typical Angina
Classification

A

3/3 Typical symptoms

  1. substernal chest pain
    - crushing
    - < 5 minutes
  2. provoked by
    - stress
    - exercise
  3. relieved by
    - rest
    - nitroglycerin medicaiton
26
Q

Atypical Angina
Classification

A

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
Q

Non-cardiac
classification

A

1/3 classical signs and symptoms
investigate other cause

  • heart
  • lungs
  • MSK
  • mind
28
Q

Canadian Cardiovascular Society (1976)
Angina Classification
I-IV

A

Class I-III
- stable angina
- Class I: strenuous exercise
- Class II: exercise
- Class III: normal activities

Class IV
- unstable angina
- provoked at rest

29
Q

Diagnostic and Laboratory Tests
CAD

A

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
Q

Troponin I vs. T vs. hs-cTN

A

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
Q

Disorders with elevated troponin

A
  • 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
Q

Information obtained from ECG

A
  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
Q

Alterations ECG with ACS

A
  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
Q

Diagnostic work up pathways
Angina
1. typical 2. atypical 3. non-cardiac

A

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
Q

Non invasive CAD testing

A

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)
  4. Vasodilator echocardiography (cannot exercise)
    - pharmacological induced ischemia
  5. Vasodilator perfusion imaging (branch blocks, ventricular paced rhythm)
    - pharmacological induced ischemia
  6. cardiac computed tomography (branch blocks, ventricular paced rhythm)
36
Q

Information obtained from cardiac CT

A
  • extent and area of the block
37
Q

Gold standard diagnosis CAD

A

Coronary angiography
- contrast dye

SE:
- 1/1000 MI, CVA, death

38
Q

Physiological Function
Cholesterol

A
  1. Cell/organelle membranes (fluidity, rigidity)
  2. Bile salts (absorption/digestion fat, GI, Liver)
  3. prevent water loss skin
  4. Steroid hormones (estrogen, progesterone, testosterone)

*LDL delivers cholesterol to non-hepatic cells

39
Q

Cholesterol
Endogenous vs. Exogenous

A

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
Q

What type of fat intake increases endogenous cholesterol synthesis?

A

Saturated fats

Reduce intake = reduce cholesterol synthesis by 15-25%

41
Q

Lipoproteins
Components, Function

A

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
Q

Structure and Function
VLDL, LDL, HDL

A

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
Q

Role of LDL oxidation in Atheroscelerosis (ASCVD)

A

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
Q

What is more likely to rupture
Mature or immature plaque?

A

Immature plaque
Thin fibrous cap
unstable and more likely to rupture

45
Q

What causes a plaque to rupture?

A

Accumulation inflammatory cells

Turbulent blood flow

shearing forces

high blood pressure

46
Q

ASCVD Risk Factors

A
  • age
  • black
  • hypertension (BP > 130)
  • smoking
  • HDL, Total cholesterol, LDL

DM is EQUIVALENT to having ASCVD

47
Q

3 principle presentations of unstable angina

A
  1. rest angina > 5 minutes
  2. new onset class III (regular activities)
  3. more frequent, more severe, longer duration, lower threshold trigger
48
Q

Management unstable angina hospital

A
  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
Q

Functional impairment Post MI and complications

A
  • contractility & conduction
  • end diastolic pressure
  • ejection fraction
  • dysrhythmias
  • 6 weeks for scar tissue to heal
50
Q

Complications of MI

A

dysrhythmias; 90% post MI
LV HF
pericarditis
rupture heart wall, vessels
thromboembolism
sudden death (> 65 years, HTN, shock, DM, dysrhythmia, prior MI)

51
Q

Peripheral Artery DIsease (PAD)
Pathophysiology

A

Atheroscelerosis of the arteries of the lower extremities
- iliac
- femoral

  1. acute or 2. gradual ONSET

Clinical S&S
- intermittent claudication

52
Q

Lipids that predict CVE

A

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
Q

Non pharmacological ways to raise HDL

A

fish oil
exercise
weight loss
moderate alcohol intake

Year 1: Patho/Pharm (39 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions