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First Aid > Cardiovascular - Pathology (1) > Flashcards

Cardiovascular - Pathology (1) Flashcards

1
Q

Congenital heart diseases:
Right-to-left shunts

  • Characteristic findings
  • Diseases
A
  • Characteristic findings
    • Early cyanosis
    • “Blue babies.”
    • Often diagnosed prenatally or become evident immediately after birth.
    • Usually require urgent surgical correction and/or maintenance of a PDA.
  • Diseases (The 5 Ts)
    1. Truncus arteriosus (1 vessel)
    2. Transposition (2 switched vessels)
    3. Tricuspid atresia (3 = Tri)
    4. Tetralogy of Fallot (4 = Tetra)
    5. TAPVR (5 letters in the name)
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2
Q

Persistent truncus arteriosus

  • Type of disease
  • Characteristics
A
  • Type of disease
    • Right-to-left shunt congenital heart disease
  • Characteristics
    • Failure of truncus arteriosus to divide into pulmonary trunk and aorta
    • Most patients have accompanying VSD.
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3
Q

D-transposition of great vessels

  • Type of disease
  • Characteristics
A
  • Type of disease
    • Right-to-left shunt congenital heart disease
  • Characteristics
    • Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior) –>Ž separation of systemic and pulmonary circulations.
    • Not compatible with life unless a shunt is present to allow mixing of blood (e.g., VSD, PDA, or patent foramen ovale).
    • Due to failure of the aorticopulmonary septum to spiral.
    • Without surgical intervention, most infants die within the first few months of life.
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4
Q

Tricuspid atresia

  • Type of disease
  • Characteristics
A
  • Type of disease
    • Right-to-left shunt congenital heart disease
  • Characteristics
    • Absence of tricuspid valve and hypoplastic RV
    • Requires both ASD and VSD for viability.
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5
Q

Tetralogy of Fallot

  • Type of disease
  • Characteristics
A
  • Type of disease
    • Right-to-left shunt congenital heart disease
  • Characteristics
    • Caused by anterosuperior displacement of the infundibular septum.
    • Most common cause of early childhood cyanosis.
    • Tetralogy: PROVe
      1. Pulmonary infundibular stenosis (most important determinant for prognosis)
      2. RVH—boot-shaped heart on CXR
      3. Overriding aorta
      4. VSD
    • Pulmonary stenosis forces right-to-left flow across VSD –>Ž early cyanotic “tet spells,” RVH.
    • Squatting: increased SVR, decreased right-to-left shunt, improves cyanosis.
    • Treatment: early surgical correction.
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6
Q

Total anomalous pulmonary venous return (TAPVR)

  • Type of disease
  • Characteristics
A
  • Type of disease
    • Right-to-left shunt congenital heart disease
  • Characteristics
    • Pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc.)
    • Associated with ASD and sometimes PDA to allow for right-to-left shunting to maintain CO.
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7
Q

Congenital heart diseases:
Left-to-right shunts

  • Characteristic findings
  • Diseases
A
  • Characteristic findings
    • Late cyanosis
    • “Blue kids.”
  • Diseases
    • Frequency: VSD > ASD > PDA
      • Ventricular septal defect (VSD)
      • Atrial septal defect (ASD)
      • Patent ductus arteriosus (PDA)
    • Eisenmenter syndrome
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8
Q

Ventricular septal defect

  • Type of disease
  • Characteristics
A
  • Type of disease
    • Left-to-right shunt congenital heart disease
  • Characteristics
    • Most common congenital cardiac defect.
    • Asymptomatic at birth, may manifest weeks later or remain asymptomatic throughout life.
    • Most self resolve
    • Larger lesions may lead to LV overload and heart failure.
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9
Q

Atrial septal defect

  • Type of disease
  • Characteristics
A
  • Type of disease
    • Left-to-right shunt congenital heart disease
  • Characteristics
    • Defect in interatrial septum
      • Loud S1
      • Wide, fixed split S2.
    • Usually occurs in septum secundum
      • Septum primum defects usually occur with other anomalies.
    • Symptoms range from none to heart failure.
    • Distinct from patent foramen ovale in that septa are missing tissue rather than unfused.
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10
Q

Patent ductus arteriosus

  • Type of disease
  • Characteristic findings
A
  • Type of disease
    • Left-to-right shunt congenital heart disease
  • Characteristic findings
    • In fetal period, shunt is right to left (normal).
    • In neonatal period, decreased lung resistance –>Ž shunt becomes left to right –> progressive RVH and/or LVH and heart failure.
    • Associated with a continuous, “machine-like” murmur.
    • Patency is maintained by PGE synthesis and low O2 tension.
      • “Endomethacin” (indomethacin) ends patency of PDA
      • PGE** kEEps it open (may be necessary to sustain life in conditions such as transposition of the great vessels).**
    • Uncorrected PDA can eventually result in late cyanosis in the lower extremities (differential cyanosis).
    • PDA is normal in utero and normally closes only after birth.
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11
Q

Eisenmenger syndrome

  • Type of disease
  • Characteristics
A
  • Type of disease
    • Left-to-right shunt congenital heart disease
  • Characteristics
    • Uncorrected left-to-right shunt (VSD, ASD, PDA)
      • –>Ž increased pulmonary blood flow
      • –>Ž pathologic remodeling of vasculature
      • –> pulmonary arteriolar hypertension.
    • RVH occurs to compensate –>Ž shunt becomes right to left.
    • Causes late cyanosis, clubbing, and polycythemia.
    • Age of onset varies.
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12
Q

Coarctation of the aorta

  • Associated with…
  • Infantile type
  • Adult type
A
  • Associated with bicuspid aortic valve, other heart defects.
  • Infantile type
    • Aorta narrowing is proximal to insertion of ductus arteriosus (preductal).
      • Infantile: in close to the heart.
    • Associated with Turner syndrome.
    • Can present with closure of the ductus arteriosus (reverse with PGE2).
  • ​Adult type
    • Aorta narrowing is distal to ligamentum arteriosum (postductal).
      • Adult: distal to ductus.
    • Associated with notching of the ribs (collateral circulation), hypertension in upper extremities, and weak, delayed pulses in lower extremities (radiofemoral delay).
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13
Q

Defects associated with these congenital cardiac disorders

  • 22q11 syndromes
  • Down syndrome
  • Congenital rubella
  • Turner syndrome
  • Marfan syndrome
  • Infant of diabetic mother
A
  • 22q11 syndromes
    • Truncus arteriosus
    • Tetralogy of Fallot
  • Down syndrome
    • ASD
    • VSD
    • AV septal defect (endocardial cushion defect)
  • Congenital rubella
    • Septal defects
    • PDA
    • Pulmonary artery stenosis
  • Turner syndrome
    • Bicuspid aortic valve
    • Coarctation of aorta (preductal)
  • Marfan syndrome
    • MVP
    • Thoracic aortic aneurysm and dissection
    • Aortic regurgitation
  • Infant of diabetic mother
    • Transposition of great vessel
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14
Q

Hypertension

  • Definition
  • Risk factors
  • Features
  • Predisposes to…
A
  • Definition
    • A systolic BP ≥ 140 mmHg and/or diastolic BP ≥ 90 mmHg
  • Risk factors
    • Increased age
    • Obesity
    • Diabetes
    • Smoking
    • Genetics
    • Black > white > Asian.
  • Features
    • 90% of hypertension is 1° (essential) and related to increased CO or increased TPR
    • Remaining 10% mostly 2° to renal disease, including fibromuscular dysplasia in young patients [A].
    • Hypertensive emergency—severe hypertension (≥ 180/120 mmHg) with evidence of acute, ongoing target organ damage (e.g., papilledema, mental status changes).
  • Predisposes to…
    • Atherosclerosis
    • LVH
    • Stroke
    • CHF
    • Renal failure [B]
    • Retinopathy
    • Aortic dissection.
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15
Q

Hyperlipidemia signs

A
  • Xanthomas
    • Plaques or nodules composed of lipid-laden histiocytes in the skin [A], especially the eyelids (xanthelasma [B]).
  • Tendinous xanthoma
    • Lipid deposit in tendon [C], especially Achilles.
  • Corneal arcus
    • Lipid deposit in cornea, appears early in life with hypercholesterolemia.
    • Common in elderly (arcus senilis [D]).
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16
Q

Arteriosclerosis

  • Mönckeberg (medial calcific sclerosis)
  • Arteriolosclerosis
A
  • Mönckeberg (medial calcific sclerosis)
    • Uncommon.
    • Calcification in the media of the arteries, especially radial or ulnar.
    • Usually benign
    • “Pipestem” arteries on x-ray [A].
    • Does not obstruct blood flow
    • Intima not involved.
  • Arteriolosclerosis
    • Common.
    • Two types:
      • Hyaline (thickening of small arteries in essential hypertension or diabetes mellitus [B])
      • Hyperplastic (“onion skinning” as seen in severe hypertension [C]).
17
Q

Atherosclerosis

  • Definition
  • Risk factors
    • Modifiable
    • Non-modifiable
  • Progression
  • Complications
  • Location
  • Symptoms
A
  • Definition
    • Disease of elastic arteries and large- and medium-sized muscular arteries.
  • Risk factors
    • Modifiable: smoking, hypertension, hyperlipidemia, diabetes.
    • Non-modifiable: age, sex (increased in men and postmenopausal women), and family history.
  • Progression
    • Inflammation important in pathogenesis.
    • Endothelial cell dysfunction Ž–> macrophage and LDL accumulation –>Ž foam cell formation –>Ž fatty streaks Ž–> smooth muscle cell migration (involves PDGF and FGF), proliferation, and extracellular matrix deposition –>Ž fibrous plaque –>Ž complex atheromas [A].
  • Complications
    • Aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli.
  • Location
    • Abdominal aorta > coronary artery > popliteal artery > carotid artery [B].
  • Symptoms
    • Angina, claudication, but can be asymptomatic.
18
Q

Aortic aneurysms

  • Definition
  • Abdominal aortic aneurysm
  • Thoracic aortic aneurysm
A
  • Definition
    • Localized pathologic dilation of the aorta.
    • May cause pain, which is a sign of leaking, dissection, or imminent rupture.
  • Abdominal aortic aneurysm
    • Associated with atherosclerosis.
    • Occurs more frequently in hypertensive male smokers > 50 years old [A].
  • Thoracic aortic aneurysm
    • Associated with cystic medial degeneration due to hypertension (older patients) or Marfan syndrome (younger patients).
    • Also historically associated with 3° syphilis (obliterative endarteritis of the vasa vasorum) [B].
19
Q

Aortic dissection

A
  • Longitudinal intraluminal tear forming a false lumen [A].
  • Associated with hypertension, bicuspid aortic valve, and inherited connective tissue disorders (e.g., Marfan syndrome).
  • Can present with tearing chest pain, of sudden onset, radiating to the back +/- markedly unequal BP in arms.
  • CXR shows mediastinal widening.
  • The false lumen can be limited to the ascending aorta, propagate from the ascending aorta, or propagate from the descending aorta.
  • Can result in pericardial tamponade, aortic rupture, and death.
20
Q

Ischemic heart disease manifestations:
Angina

  • Definition
  • Stable
  • Variant angina (Prinzmetal)
  • Unstable/crescendo
A
  • Definition
    • Chest pain due to ischemic myocardium 2° to coronary artery narrowing or spasm
    • No myocyte necrosis.
  • Stable
    • Usually 2° to atherosclerosis
    • Exertional chest pain in classic distribution (usually with ST depression on ECG), resolving with rest.
  • Variant angina (Prinzmetal)
    • Occurs at rest 2° to coronary artery spasm
    • Transient ST elevation on ECG.
    • Known triggers include tobacco, cocaine, and triptans, but trigger is often unknown.
    • Treat with calcium channel blockers, nitrates, and smoking cessation (if applicable).
  • Unstable/crescendo
    • Thrombosis with incomplete coronary artery occlusion
    • ST depression on ECG (increases in frequency or intensity of chest pain; any chest pain at rest).
21
Q

Ischemic heart disease manifestations:
Coronary steal syndrome

A
  • Distal to coronary stenosis, vessels are maximally dilated at baseline.
  • Administration of vasodilators (e.g., dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well-perfused areas –>Ž decreased flow and ischemia in the poststenotic region.
  • Principle behind pharmacologic stress tests
22
Q

Ischemic heart disease manifestations:
Myocardial infarction

A
  • Most often acute thrombosis due to coronary artery atherosclerosis with complete occlusion of coronary artery and myocyte necrosis.
  • If transmural, ECG will show ST elevations
  • If subendocardial, ECG may show ST depressions.
  • Cardiac biomarkers are diagnostic.
23
Q

Ischemic heart disease manifestations:
Sudden cardiac death

A
  • Death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrhythmia (e.g., ventricular fibrillation).
  • Associated with CAD (up to 70% of cases), cardiomyopathy (hypertrophic, dilated), and hereditary ion channelopathies (e.g., long QT syndrome).
24
Q

Ischemic heart disease manifestations:
Chronic ischemic heart disease

A
  • Progressive onset of CHF over many years due to chronic ischemic myocardial damage.
25
Q

Evolution of MI

  • Commonly occluded coronary arteries
  • Symptoms
  • 0-4 hr
    • Gross
    • Light microscope
    • Complications
A
  • Commonly occluded coronary arteries
    • LAD > RCA > circumflex.
  • Symptoms
    • Diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw, shortness of breath, fatigue.
  • 0-4 hr
    • Gross
      • None
    • Light microscope
      • None
    • Complications
      • Arrhythmia, HF, cardiogenic shock, death.
26
Q

Evolution of MI:
4-12 hr

  • Gross
  • Light microscope
  • Complications
A
  • Gross
    • Occluded artery
    • Infarct
    • Dark mottling
    • Pale with tetrazolium stain
  • Light microscope
    • Early coagulative necrosis, release of necrotic cell contents into blood
    • Edema, hemorrhage, wavy fibers.
  • Complications
    • Arrhythmia, HF, cardiogenic shock, death.
27
Q

Evolution of MI:
12–24 hr

  • Gross
  • Light microscope
  • Complications
A
  • Gross
    • Occluded artery
    • Infarct
    • Dark mottling
    • Pale with tetrazolium stain
  • Light microscope
    • Neutrophil migration starts.
    • Reperfusion injury may cause contraction bands (due to free radical damage).
  • Complications
    • Arrhythmia, HF, cardiogenic shock, death.
28
Q

Evolution of MI:
1–3 days

  • Gross
  • Light microscope
  • Complications
A
  • Gross
    • Hyperemia
  • Light microscope
    • Extensive coagulative necrosis.
    • Tissue surrounding infarct shows acute inflammation with neutrophils.
  • Complications
    • Fibrinous pericarditis.
29
Q

Evolution of MI:
3–14 days

  • Gross
  • Light microscope
  • Complications
A
  • Gross
    • Hyperemic border
    • Central yellow-brown softening
      • Maximally yellow and soft by 10 days
  • Light microscope
    • Macrophages, then granulation tissue at margins.
  • Complications
    • Free wall rupture –>Ž tamponade
    • Papillary muscle rupture –>Ž mitral regurgitation
    • Interventricular septal rupture due to macrophage-mediated structural degradation.
    • LV pseudoaneurysm (mural thrombus “plugs” hole in myocardium –>Ž “time bomb”).
30
Q

Evolution of MI:
2 weeks to several months

  • Gross
  • Light microscope
  • Complications
A
  • Gross
    • Recanalized artery
    • Gray-white
  • Light microscope
    • Contracted scar complete.
  • Complications
    • Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (outward bulge during contraction, “dyskinesia”).
31
Q

Diagnosis of MI

  • Gold standard
  • Cardiac troponin I
  • CK-MB
  • ECG changes
A
  • In the first 6 hours, ECG is the gold standard.
  • Cardiac troponin I
    • Rises after 4 hours
    • Increased for 7–10 days
    • More specific than other protein markers.
  • CK-MB
    • Predominantly found in myocardium but can also be released from skeletal muscle.
    • Useful in diagnosing reinfarction following acute MI because levels return to normal after 48 hours.
  • ECG changes
    • ST elevation (STEMI, acute transmural infarct)
    • ST depression (subendocardial infarct)
    • Pathologic Q waves (evolving or old transmural infarct).
32
Q

Types of infarcts

  • Transmural infarcts
  • Subendocardial infarcts
A
  • Transmural infarcts
    • Increased necrosis
    • Affects entire wall
    • ST elevation on ECG, Q waves
  • Subendocardial infarcts
    • Due to ischemic necrosis of < 50% of ventricle wall
    • Subendocardium especially vulnerable to ischemia
    • ST depression on ECG
33
Q

ECG diagnosis of MI:
Leads with Q waves for these infarct locations

  • Anterior wall
  • Anteroseptal
  • Anterolateral
  • Lateral wall
  • Inferior wall
A
  • Anterior wall (LAD)
    • V1–V4
  • Anteroseptal (LAD)
    • V1–V2
  • Anterolateral (LAD or LCX)
    • V4–V6
  • Lateral wall (LCX)
    • I, aVL
  • InFerior wall (RCA)
    • II, III, aVF
34
Q

MI complications

  • Cardiac arrhythmia
  • Cardiogenic shock
  • Greatest risk 6–14 days postinfarct
  • Ventricular pseudoaneurysm formation
  • Postinfarction fibrinous pericarditis
  • Dressler syndrome
  • Other
A
  • Cardiac arrhythmia
    • Important cause of death before reaching hospital
    • Common in first few days.
  • Cardiogenic shock
    • Large infarct
    • High risk of mortality.
  • Greatest risk 6–14 days postinfarct
    • Ventricular free wall rupture Ž–> cardiac tamponade
    • Papillary muscle rupture –>Ž severe mitral regurgitation
    • Interventricular septum rupture Ž–> VSD
  • Ventricular pseudoaneurysm formation
    • Decreased CO, risk of arrhythmia, embolus from mural thrombus
    • Greatest risk approximately 1 week post-MI.
  • Postinfarction fibrinous pericarditis
    • Friction rub (1–3 days post-MI).
  • Dressler syndrome
    • Autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post-MI).
  • Other
    • LV failure
    • Pulmonary edema

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