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Systemic Pathology > CVS > Flashcards

CVS Flashcards

1
Q

What is the average weight of a heart?

A

Male: 300-350gm
Female: 250-300gm

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2
Q

What is the average ventricle wall thickness of the heart?

A

Left: 1.3-1.5cm
Right: 0.3-0.5cm

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3
Q

What is hypertrophy of the heart?

A

Increase weight or ventricle thickness

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4
Q

What is Dilation of the heart?

A

Enlarged chamber size

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5
Q

What are the possible anatomical components and the relative heart diseases?

A
  1. Vessels (coronary arteries, large vessels) - Atherosclerosis, Ischaemic Heart Disease, Hypertension
  2. Pericardium - Pericarditis (Acute, Chronic)
  3. Myocardium - Myocarditis, Cardiomyopathies
  4. Endocardium/Valves
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6
Q

What are the possible aetiology (causes) of heart diseases?

A
  1. Congenital - Shunts, obstruction, metabolic etc.
  2. Acquired
  3. Multifactorial - Heart Failure
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7
Q

What is atherosclerosis?

A

A degenerative and inflammatory disease affecting large and medium sized arteries causing thickening and loss of elasticity.

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8
Q

What are the arteries that atherosclerosis can happen in?

A

Aorta, Coronary, Carotid, Mesenteric, Iliac, Femoral and Cerebral.

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9
Q

What are lesions in the tunica intima called?

A

Atheromas

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10
Q

What are the 3 layers of an artery?

A
  1. Tunica Intima
  2. Tunica Media
  3. Tunica Externa
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11
Q

What is an Atheromas?

A

A plague consisting of a raised lesion with soft, yellow core of lipid covered by a white fibrous cap

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12
Q

What is the pathogenesis of Atheroma?

A
  1. Chronic endothelial injury (Causes: Hyperlipidemia, Hypertension, Smoking, Homocysteine, Haemodynamic Functions, Toxins, Viruses, Immune reactions)
  2. Endothelial dysfunction - Increased permeability, leukocyte adhesion, monocyte adhesion and emigration
  3. Smooth Muscle recruitment to the intima + Macrophage activation
  4. Macrophages and smooth muscle cells engulf lipid to form a fatty streak
  5. Smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid. Results in lipid debris covered in fibrofatty atheroma
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13
Q

Types of atherosclerosis lesions?

A

Early: Fatty streak
Established: Atheromatous plague
Complication

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14
Q

Causes of Atherosclerosis?

A 
Consitutional (Nonmodifiable) Risk factors:
1. Age
2. Male gender
3. Family history
4. Genetics
Modifiable Risk Factors
1. Hyperlipidemia
2. Hypertension
3. Diabetes
4. Cigarette smoking
Inflammation - C reactive protein
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15
Q

Consequences of Atherosclerosis?

A
  1. Vessel thickening –> Narrowed Lumen –> Poor tissue perfusion –> Ischaemia
  2. Loss of elasticity –> Predisposition to aneurysm formation, rupture and haemorrhage
  3. Endothelial changes –> Predisposition to thrombosis
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16
Q

Where and what are the clinical effects of Atherosclerosis?

A
  1. Aorta = Aneurysm (rupture and bleed)
  2. Coronary Arteries = Ischaemic Heart Disease
  3. Cerebral Arteries = Cerebrovascular Disease (occlude vessels, haemorrhage into brain)
  4. Common iliac/femoral arteries
  5. Peripheral Vessels = Peripheral Vascular Disease (Painful and Ischaemic lower limbs)
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17
Q

What is Ischaemic Heart Disease?

A

A Spectrum of disorders due to imbalance between myocardial metabolic demands and coronary blood flow.

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18
Q

What are the Causes of Ischaemic Heart Disease?

Mainly need to know most impt cause

A
  1. Atherosclerosis (90-95%)
  2. Embolism
  3. Ostial Stenosis in syphilitic aortitis
  4. Dissecting Aneurysms
  5. Direct trauma
  6. Arteritis
  7. Anomalous origin of left coronary artery
  8. Hypoxaemia - Anaemia, Carbon monoxide posioning, hypotensive crises
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19
Q

What is the pathogenesis of Ischaemic Heart Disease?

A 
1, Reduced coronary flow
75% occlusion of coronary arterial lumen
(Degree of occlusion does not parallel the severity or nature of the myocardial lesions)
2. Increased myocardial demand
Exercise
Infection
Pregnancy
Hyperthyroidism
Myocardial hypertrophy
3. Availability of Oxygen in the blood
Anaemia
CO poisoning
pulmonary disease
left to right shunts
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20
Q

What are vulnerable (unstable) plagues?

A
  • Most clinically dangerous
  • Vary in size but are often smaller
  • Relatively large lipid core with a thin fibrous cap
  • More likely to fissure, rupture, ulcerate and plague haemorrhage

Less stable than a larger and more occlusive plague (smaller lipid core and more fibrous tissue)

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21
Q

What are the 4 Classical Patterns of Ischaemic Heart Disease?

A
  1. Angina Pectoris
  2. Myocardial Infarction
  3. Chronic Ischaemic heart disease with heart failure (progressive heart failure consequent to previous myocardial infarction)
  4. Sudden Cardiac Death
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22
Q

What is Angina Pectoris?

A

Episodic chest pain on exertion caused by transient ischaemia of the myocardium (usually a result of stenosis of the coronary arteries)

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23
Q

How is angina pectoris relieved?

A

Rest or vasodilators (eg. Glyceryl Trinitrate)

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24
Q

What are the 3 symptoms of patterns of Angina Pectoris?

A
  1. Stable angina (pain with fixed level of exercise)
  2. Prinzmental angina (unpredicted: at rest, coronary artery spasm)
  3. Unstable angina (increased frequency of pain, longer duration, less effort, may occur at rest, due to acute plague changes and/or artery spasm)
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25
Q

What is myocardial infarction?

A

Heart attack
Death of cardiac muscle following impaired blood flow
1. Regional myocardial infarction (90%)
- thrombus on complicated atheroma
- full thickness (regional transmural MI)
- partial thickness (regional subendocardial MI)
2. Circumferential subendocardial infarction (10%)
- general hypoperfusion caused by hypotension

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26
Q

Where does occlusion of the coronary arteries causing myocardial infarction usually occur? What areas does this affect?

A

Left Anterior Descending (LAD): 40-50%
Affects: Anterior wall of LV near apex, Anterior 2/3 of interventricular septum

Right Coronary Artery (RCA): 30-40%
Affects: Inferior/posterior wall of LV, Posterior 1/3 of interventricular septum, Posterior wall of RV

Circumflex Coronary Artery (LCX): 15-20%
Affects: Lateral wall of LV

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27
Q

What is the typical case of coronary artery occlusion?

A
  1. Acute plague event
  2. Thrombus formation
  3. complete occlusion of lumen
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28
Q

What is the pathogenesis causing less than 10% of transmural MI

A
  • Vasospasm
  • Emboli
  • Ischemia without atherosclerosis/thrombi (vasculitis, shock, vascular dissection, amyloidosis)
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29
Q

What are the clinical diagnosis of MI?

A
  1. Symptoms: severe, crushing central chest pain
  2. ECG changes
  3. Elevated cardiac enzymes
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30
Q

What is the mortality rate of MI

A

30% in 1st yr post-infarction

3-4% every succeeding year

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31
Q

What are the complications of myocardial infarction?

A 
1. Ventricles
LV failure --> congestive heart failure
Rupture myocardium --> cardiac tamponade (blood fills the space between the sac and the heart, increasing pressure on the heart, preventing it from pumping properly)
Fibrosis and Aneurysm
Thrombosis
  1. Conduction system
    Arrhythmias –> sudden cardiac death
  2. Pericarditis
    Dressler’s syndrome
  3. Valves
    Ruptured papillary muscle
32
Q

What is the pathogenesis of chronic ischaemic heart disease?

A
  1. Chronic atherosclerotic narrowing of coronary arteries
  2. Slow loss of myocardial fibres
  3. Generalised myocardial fibrosis
  4. Insidious cardiac failure –> Death
33
Q

What is sudden cardiac death?

A

Lethal arrhythmias - Ventricular Fibrillation (no time to develop infarction)

34
Q

What are the causes of sudden cardiac death?

A
  1. pronounce stenosis of 1 or more major arteries

2. acute plague changes

35
Q

What is heart failure?

A

A clinical condition where impaired cardiac function renders the heart unable to maintain an output enough for the metabolic requirements of the body.
It is a common endpoint of many heart diseases

36
Q

What is congestive cardiac failure?

A

Heart failure involving the right and left ventricles
Fluid accumulates in the lungs, legs, abdominal cavity
Reduced flow of arterial blood from the heart, which in extreme cases results in peripheral circulatory failure (cardiogenic shock)

37
Q

What determines normal cardiac function?

A
  1. Pump
  2. Flow
  3. Conduction
38
Q

What side is deoxygenated blood pumped in?

A

Right side

39
Q

What are some cardiac adaptive (compensatory) measures?

A
  1. Increased heart rate
  2. Blood volume expansion - salt and water retention
  3. Myocardial hypertrophy - caused by hypertension (pressure or volume stress)
  4. Cardiac dilation (Frank-Starling mechanism) - increased contraction by stretching of myofibres

When these are exceeded, cardiac failure results

40
Q

What are the classifications of heart failure?

A
  1. Right sided vs Left sided
  2. High output vs Low output
  3. Systolic vs Diastolic
  4. Acute vs Chronic
41
Q

What are some causes of Left Ventricular Failure (Oxygenated Blood)?

A
  1. Volume Overload
    - Mitral and aortic valvular disease eg. Regurgitation
    - High-output states eg. Anaemia
  2. Pressure overload
    - Systemic Hypertension
  3. Loss of Muscle (Pump failure)
    - Myocardial Infarction
  4. Loss of Contractility
    - Poisons
    - Myocarditis
    - Infiltrative Diseases eg. Amyloidosis
  5. Restricted filling
    - Pericardial effusion
  6. Conduction Problems
    - Arrhythmias eg. Atrial Fibrillation
42
Q

What are some causes of Right Ventricular Failure (Deoxygenated Blood)?

A

Most common: Left-sided Failure (Congestive cardiac failure)
Pure right heart failure:
- Right heart valvular disease (pulmonary stenosis, tricuspid regurgitation)
- Lung disease - lung parenchymal disease eg. COPD (emphysema), pulmonary embolism, interstitial lung disease –> altered lung vasculature –> pulmonary hypertension –> pressure overload (corpulmonale)

43
Q

What are the clinical effects of Left Heart Failure?

A
  1. Exertional Dyspnoea - shortness of breath on exertion
  2. Orthopnoea - Increasing breathlessness on lying flat
  3. Paroxysmal nocturnal dyspnoea: sudden nighttime attack of severe breathlessness
  4. Restlessness
  5. Confusion
  6. Tachycardia
  7. Fatigue
  8. Cyanosis
  9. Elevated Pulmonary Capillary Wedge Pressure
  10. Pulmonary Congestion –> Cough, Crackles, Wheezes, Blood-Tinged Sputum, Tachypnea
44
Q

What is the backward failure effects of Left Heart Failure?

A

Left Atrium Dilation –> Pulmonary Hypertension –> Pulmonary Congestion and Oedema

45
Q

What is the forward failure effects of Left Heart Failure

A

Hypotension –> Poor Tissue Perfusion –> Poor Tissue Oxygenation –> Kidney (activation of Renin Angiotensin Aldosterone system + Impaired excretion of nitrogenous products) + Brain (cerebral hypoxia)

46
Q

How is pulmonary oedema seen in xrays?

A

Hazy opacification chiefly in central lung area in a butterfly pattern
Advanced: lower parts of both lungs

47
Q

What are the clinical effects of Right Heart Failure?

A

Systemic and Portal Venous Congestion:

  1. Congestive hepatomegaly (Hepatic venous congestion causing nutmeg liver, Centrilobularatrophy and Necrosis, Cardiac Cirrhosis)
  2. Congestive splenomegaly
  3. Effusions in body cavities eg. Ascites - Peritoneal effusion
  4. Peripheral subcutaneous oedema - Swelling of dependent parts of the body, eg. lower limbs
  5. Nocturia: Frequent nighttime urination. Cause fluid from legs is returned to the bloodstream while lying down at night
  6. Fatigue
  7. Anorexia and complaints of GI distress
  8. Weight gain
48
Q

Why is hypertension?

A

Hypertension is a sustained blood pressure of 140/90mm Hg or above
1. Primary or Essential Hypertension (90-95%)
2. Secondary Hypertension (5-10%)
R: Renal - Renal Artery Stenosis
E: Endocrine - Hypercortisolism, Pheochromocytoma
N: Neurologic - Increased Intracranial pressure
A: Aortic - Coarctation, Atherosclerotic Rigidity or Aorta
L: Labile - Psychogenic, Stress-related

49
Q

What is Accelerated Hypertension?

A

Malignant Hypertension (5%)
Systolic pressure > 200mmHg
Diastolic Pressure > 120mmHg

50
Q

What are the pathological effects of hypertension?

A
  1. Blood vessels
    - Atherosclerosis (modifiable risk factor)
    - Arteriolosclerosis
    Small arteries/arterioles - hyaline or proliferative thickening:
    Hyaline arteriolosclerosis (benign HT) - hyaline thickening –> narrowing, Eg. Renal Nephrosclerosis
    Hyperplastic Arteriosclerosis (malignant HT) - “Onion-skin” concentric laminated thickening –> fibrinoid necrosis of vessel wall
    - Aneurysms
  2. Heart
    - Hypertensive Heart Diseases:
    LV pressure overload –> LV hypertrophy (wall thicker, stiffer)
    Impaired LV diastolic filling –> Left Atrial Dilation (increased LA pressure) –> LV failure
  3. Kidneys
    - Nephrosclerosis
  4. CNS
    - Cerebral Hemorrhage
    - Cerebral Thrombosis
    - Hypertensive encephalopathy (Malignant HT)
51
Q

What is Valvular Heart Disease?

A

Stenosis
- Failure of valve to open completely –> prevents forward flow

Insufficiency/ Regurgitation/ Incompetence
- Failure of valve to close completely –> allow reverse flow

Both

52
Q

What are the causes of valvular heart disease?

A
  1. Developmental eg. Mitral Valve Prolapse (association with Marfan Syndrome, Fibrillin-1 mutation)
  2. Degenerative eg. Mitral Valve prolapse, calcific aortic stenosis
  3. Inflammatory/immune mediated eg. Infective endocarditis, Rheumatic heart disease
53
Q

What valves are usually affected by valvular heart disease?

A

Left sided valves eg. mitral and aortic

Structurally abnormal valves - more prone to colonisation (infective)

54
Q

What is Stenosis?

A

Narrowing of the valvular aperture at the fully open position
Failure of the valve to open completely
Prevents the forward flow of blood
Usually due to the pathology of the valve cusps

55
Q

What is Mitral Stenosis caused by?

A
  1. Rheumatic Heart Disease

2. Post inflammatory scarring

56
Q

What are the effects of Mitral Stenosis?

A
  1. Heart
    - Elevated LA pressure –> LA dilation
    - Atrial fibrillation
    - Mural thrombosis in LA
    - Right ventricular hypertrophy and failure (congestive changes in the lungs)
  2. Lung
    - Pulmonary hypertension
    - Pulmonary oedema
57
Q

What is Aortic Stenosis caused by?

A
  1. Calcific aortic stenosis
  2. Rheumatic Heart Disease
  3. Infective endocarditis
  4. Congenital bicuspid valve
58
Q

What are the effects of Aortic Stenosis?

A
  1. Left ventricular hypertrophy and failure
  2. Predisposition to myocardial ischemia
  3. Sudden death
59
Q

What is regurgitation or insufficiency?

A

Backflow of blood through the valve in the fully closed position
Failure of the valve to close completely
Allows blood to flow in the wrong direction across the valve

Causes: 
valve cusps
valve ring
chordae tendinae
papillary muscles
60
Q

What is Mitral Insufficiency caused by?

A
  1. Floppy valve syndrome (mitral valve prolapse)

2. Rheumatic Heart Disease

61
Q

What are the effects of Mitral Insufficiency?

A
  1. Atrial Fibrillation
  2. Left ventricular failure

If acute mitral incompetence, severe pulmonary congestion and oedema

62
Q

What is Aortic Insufficiency caused by?

A
  1. Dilation of ascending aorta (hypertension, aging)
  2. Rheumatic heart disease
  3. Infective endocarditis
  4. Dilation of valve ring eg. syphilis
63
Q

What are the effects of Aortic Insufficiency?

A
  1. Left ventricular hypertrophy and failure

2. Predisposition to myocardial ischemia

64
Q

Is right side heart valve (pulmonary and tricuspid) diseases common?

A

No. But it can be caused by rheumatic heart disease and Intravenous drug abuse

65
Q

What is Rheumatic Heart Disease?

A

An abnormal immune response to Group A Streptococcal Pharyngitis.
Immune mediated/inflammatory valve disease

66
Q

What is the pathogenesis of rheumatic heart disease?

A

Cross-reactivity between the immune response to cell surface antigens of the strep and antigens on cardiac myocytes and with heart valve glycoprotein
Causes Stenosis/Regurgitaion of Mitral/Aortic valves

67
Q

How do Rheumatic Valvulitis look like?

A

Small vegetations (verrucae) are visible along the line of closure of the mitral valve leaflet, causing fibrous thickening and fusion of chordae tendinae

68
Q

What is infective endocarditis?

A

A disease caused by microbial infection of the cardiac valves or endocardium causing formation of vegetation leading to tissue destruction

69
Q

What is the incidence of infective endocarditis?

A

Approximately 6-7 cases/100,000/year

70
Q

What is the frequency of valve involvement in infective endocarditis?

A 
25-30% Mitral valve
25-30% aortic valve
10% mitral and aortic valves
10% tricuspid valve (IV drug abusers)
10% Prosthesis
10% congenital heart disease
71
Q

What kind of valves can infective endocarditis affect?

A

Native Valves:

  1. Underlying abnormalty eg. Mitral Valve Prolapse, degenerative calcific valvular stenosis, bicuspid aortic valve
  2. normal valves

Prosthetic Valves

72
Q

What type of microorganisms can cause infective endocarditis?

A
  1. Subacute endocarditis - Streptococcus viridans (75%) - found in the oral cavity
  2. Acute endocarditis - Staph Aureus (IV drug users)
  3. Prosthetic valve endocarditis - S. epidermmis
  4. Enterococci
  5. HACEK group
  6. Fungi
73
Q

What are some predisposing factors of Infective Endocarditis?

A
  1. Dental or surgical procedures
  2. Contaminated needle sharing by IV drug users
  3. Breaks in epithelial barriers of the gut, oral cavity, skin
74
Q

When should prophylactic antibiotics be given for infective endocarditis?

A

Before dental procedures for patients with:

  • Cyanotic heart disease (right to left shunts)
  • Valvular disease/replacement
75
Q

Why should prophylactic antibiotics be given for infective endocarditis?

A

To prevent infective (bacterial) endocarditis)

76
Q

What are some possible complications caused by infective endocarditis?

A
  1. Local
    - Valve rupture
    - Myocardial ring abscess
    - Suppurative pericarditis
  2. Distant
    - Embolic - organ infarction and abscess formation
    - Immune complex mediated - vasculitis, glomerulonephritis
    - Anaemia of chronic diseases
    - Splenomegaly

Systemic Pathology (2 decks)

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