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cardiac pathology Flashcards

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1
Q

what is pericarditis

A

inflammation of the pericardium (membrane surrounding heart)

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2
Q

classic features of pericarditis?

A

-pericardial friction rub (scraping sound on auscultation) relieved when leaning forward
-pleuritic chest pain (often recent viral infection)
-diffuse concave ST elevation and PR depression on ECG

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3
Q

ECG finding - pericarditis?

A

diffuse concave ST elevation & PR depression

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4
Q

causes of pericarditis?

A

-viral and idioapthic
-uraemia (CKD) (toxins irritate pericardium)
-post MI (dresslers syndrome)
-granulomatous (TB)
-fibrous (restrictive - can arise from any)

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5
Q

most common cause of pericarditis

A

viral & idiopathic

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6
Q

what is pericardial effusion?

A

Accumulation of fluid in the pericardial sac

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7
Q

different types of pericardial effusion + causes?

A

-serous: lighter inflammation - chronic heart failure
-exudative (higher protein content): (due to increased vascular permeability - inflammation, infection, malignancy or auto-immune

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8
Q

what is cardiac tamponade?

A

A medical emergency where excess fluid in the pericardial sac puts pressure on the heart, impairing its ability to pump blood.

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9
Q

classic signs of tamponade?

A

Becks triad
1) Muffled Heart Sounds
2) Elevated Jugular Venous Pressure (JVP)
3) Hypotension

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10
Q

sign during breathing in cardiac tamponade?

A

pulsus paradoxus - abnormal drop in systolic blood pressure of more than 10 mmHg during inspiration.

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11
Q

what is Haemopericardium?

A

Blood in the pericardial sac, which can arise following myocardial rupture from myocardial infarction or traumatic injury.

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12
Q

what is atherosclerosis?

A

Atherosclerosis is the chronic inflammation of the intima (innermost layer) of large arteries. It’s marked by lipid accumulation and intimal thickening, leading to narrowing of the arteries.

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13
Q

what does atherosclerosis depend on and what diseases can arise from it?

A

-Disease depends on which vessel is affected and includes:
-Stroke
- Ischaemic heart disease
- Peripheral arterial disease
- Chronic mesenteric ischaemia

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14
Q

what are the steps of atherogenesis?

A
  1. Endothelial injury causes accumulation of LDL.
  2. LDL enters intima and is trapped in sub-intimal space.
  3. LDL is converted into modified and oxidized LDL causing inflammation.
  4. Macrophages take up ox/modLDL via scavenger receptors and become foam cells.
  5. Apoptosis of foam cells causes inflammation and cholesterol core of plaque.
  6. Increase in adhesion molecules on endothelium due to inflammation results in more macrophages and T cells entering the plaque.
  7. Vascular smooth muscle cells form the fibrous cap, segregating thrombogenic core from
    lumen.
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15
Q

components of atherosclerotic plaque?

A

1) Cells - including smooth muscle cells, macrophages and other leukocytes
2. Extracellular matrix proteins including collagen
3. Intracellular and extracellular lipid

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16
Q

difference between stable plaque and vulnerable plaque?

A

1) stable plaque
-small lipid pool
-thick fibrous cap
-preserved lumen

2) vulnerable plaque
-thin fibrous cap
-large lipid pool
-many inflammatory cells
(this can lead to thrombosis or ruptured plaque)

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17
Q

which part of the aorta is more affected and what can this lead to?

A

-Abdominal aorta affected more than thoracic aorta
-can lead to an AAA (due to weakening and dilation of vessel wall) -typically presents as an older man who is a long-term smoker who has presented with back pain and
LOC.

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18
Q

why is atherosclerosis more prominent around the ostia (origins) of major branches?

A

-turbulent blood flow has
low/oscillatory shear stress, which is atherogenic.
-High laminar flow is protective.
-Increased cap thickness confers greater stability and lower rupture risk.

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19
Q

modifiable risk factors for atherosclerosis?

A

-Type 2 Diabetes Mellitus
-Hypertension
-Hypercholesterolaemia
- Smoking

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20
Q

non-modifiable risk factors for atherosclerosis?

A

-Gender (Males>Females)
- increasing age
- Family History

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21
Q

what is ischaemic heart disease?

A

Group of conditions that occur when oxygen supply < demands of the myocardium due to narrowed
coronary vessels.
-includes: stable/unstable/prinzmetal angina

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22
Q

Features of different types of IHD?

A

stable angina: ~70% vessel occlusion – pain on exertion.

Unstable angina: ~>90% vessel occlusion – pain at rest also, and usually normal troponins, which
distinguishes it from NSTEMI. High likelihood of impending infarction.

Prinzmetal angina: Rare, due to coronary artery spasm rather than atherosclerosis.

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23
Q

is there muscle death in angina

A

no

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24
Q

pathogenesis of myocardial infarction?

A

1) Coronary Atherosclerosis → Plaque rupture.
2)Platelet aggregation → Thrombus formation.
3) Vasospasm → Occlusion of coronary artery.
4) Myocardial Necrosis.

Severe ischaemia lasting >20-40mins
results in irreversible injury and myocyte death.

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25
what does severe ischaemia lasting >20-40 minutes result in?
irreversible injury and myocyte death.
26
mechanical complications of MI?
1) cardiogenic shock: due to contractile dysfunction & loss of muscle 2) congestive heart failure: due to ventricular dysfunction + inability to pump 3) mitral regurgitation: papillary muscles which anchor can be damaged during an MI leading to mitral valve insufficiency and regurgitation. 4) ventricular septal rupture & rupture of ventricular wall 5) ventricular aneurysm; The left ventricular wall may thin out and form a ventricular aneurysm. develops >4 wks post MI
27
mechanism of ventricular free wall rupture
-tear occurs in the free wall of the left ventricle, usually within a few days to a week after a large MI. Mechanism: The infarcted tissue becomes weakened and may rupture due to the increased pressure inside the heart.
28
what does ventricular aneurysm post - MI present with
develops >4 weeks post-MI (persistent ST elevation)
29
arrythmic complications post-MI
VF – usually occurs in the first 24hrs, common cause of sudden death 90% of patients develop an arrhythmia following MI
30
common cause of sudden death post-MI
VF (usually in first 24hrs)
31
pericardial complications of MI
early pericarditis: dusky haemorrhagic tissue pericardial effusion (+/- tamponade) dresselers syndrome: pericarditis weeks/months post-MI - inflammation during healing process Fibrinous Pericarditis – occurs if infarct extends to epicardium
32
thrombotic complications of MI
increased risk of blood clot formation in the heart (especially in the left ventricle) due to stasis of blood in areas of infarction. -leads to embolisation of thrombus
33
mnemonic of post-MI complications
DREAD 1. Death 2. Rupture of the ventricle 3. Edema (congestive cardiac failure) 4. Arrhythmia/Aneurysm 5. Dressler’s syndrome – pericarditis signs 4 weeks after MI
34
Histological findings at different stages of MI?
Under 6 hours - normal by histology (CK-MB also normal) 6–24 hrs - loss of nuclei, homogenous cytoplasm, necrotic cell death 1-4 days - infiltration of polymorphs then macrophages (clear up debris) 5-10 days - removal of debris 1-2 weeks - granulation tissue, new blood vessels, myofibroblasts, collagen synthesis Weeks to months - strengthening, decellularising scar tissue.
35
what happens in heart failure?
The heart is unable to pump sufficient blood to supply the demand of the body
36
what is preload?
Initial stretch of cardiomyocytes before contraction due to ventricular filling → increase will increase stroke volume (volume of blood ejected w each beat)
37
what is afterload?
Pressure of vessels (aortic or pulmonary artery pressures) against which heart must contract to eject blood → increase in afterload will decrease stroke volume (makes it harder for heart to pump effectively)
38
common causes of heart failure?
CHAVI heart -Cardiomyopathy (dilated) -Hypertension -Arrhythmias -Valve disease -Ischaemic heart disease -Myocarditis
39
complications of heart failure?
-Sudden Death (largely arrythmia) -Systemic emboli (clots forming in heart) -Arrhythmias
40
pathophysiology in heart failure
1) Pulmonary Oedema with Superimposed Infection -Fluid accumulation in the lungs, increasing the risk of infection. 2) Haemosiderin-Laden Macrophages ("Heart Failure Cells") -Macrophages in the lungs engulf iron from red blood cells that leak due to congestion. 3) Hepatic Cirrhosis ("Nutmeg Liver") -Congestion in the liver due to right heart failure, leading to a mottled appearance
41
how does chronic preload activation lead to heart failure?
Heart damage → low cardiac output (cos low perfusion)→ Renin-Angiotensin System (RAS) activation → salt and water retention (to compensate for low perfusion) Over time, this leads to fluid overload and worsening heart failure.
42
how does chronic afterload activation worsen heart failure?
-Heart damage → low stroke volume → baroreceptors activate the sympathetic nervous system → increased total peripheral resistance → higher afterload. -Left ventricular hypertrophy (LVH) develops to cope, but this eventually leads to ventricular dilation and poor contractility.
43
what is LV failure? features?
The left side of the heart fails to pump against high pressures, leading to blood pooling in the lungs features: -Dyspnoea (shortness of breath) -Orthopnoea (worse when lying flat) -Paroxysmal nocturnal dyspnoea (waking up gasping for air) -Fatigue -Pulmonary oedema (fluid in the lungs).
44
what is RV failure? features?
-Most commonly secondary to LVF (i.e., when left heart failure progresses). -Primary cause: chronic severe pulmonary hypertension. Symptoms: -Peripheral oedema (swelling in the legs). -Ascites (fluid buildup in the abdomen). -Facial engorgement (swollen face). -Congestion of venous blood in the liver ("nutmeg liver").
45
investigations + findings in heart failure?
-BNP/ NT-proBNP – elevated -CXR – pulmonary oedema (batwing appearance) -ECG, Echo
46
mechanism of heart failure in dilated cardiomyopathy?
systolic dysfunction
47
causes of dilated cardiomyopathy?
-Idiopathic - alcohol ! - thyroid disease - viral myocarditis.
48
hypertrophic cardiomyopathy mechanism of heart failure
diastolic dysfunction
49
hypertrophic cardiomyopathy causes
Genetic storage diseases
50
restrictive cardiomyopathy mechanisms of heart failure
diastolic dysfunction
51
restrictive cardiomyopathy: causes?
Sarcoidosis, amyloidosis radiation-induced fibrosis
52
phenotype of hypertrophic cardiomyopathic myopathy?
myocardial hypertrophy (especially within the septum and left ventricle) without ventricular dilation.
53
histology of hypertrophic cardiomyopathic myopathy
myocyte disarray. (Myocyte disarray is arrhythmogenic.)
54
hypertrophic cardiomyopathic myopathy: inheritance
autosomal dominant
55
hypertrophic cardiomyopathic myopathy: mutation
genes encoding sarcomeric proteins -Mutations in the βMHC (β-myosin) gene most common (βMHC mutation is Arg-403 → Gln). ● MYBP-C and Trop-T gene mutations also common.
56
hypertrophic cardiomyopathic myopathy: complication
-May cause sudden cardiac death in young people. -Troponin T mutations have a high risk of sudden cardiac death (likely due to arrhythmia)
57
hypertrophic obstructive cardiomyopathy: pathophysiology
asymmetrical septal hypertrophy resulting in an outflow tract obstruction (so less blood being pumped out of LV)
58
arrythmogenic Right Ventricular Cardiomyopathy (ARVC): histology/pathophysiology
Myocyte loss with fibrofatty replacement, typically affecting the right ventricle.
59
what is acute rheumatic fever?
-A multisystem illness affecting: * Heart: pancarditis i.e. endocarditis, myocarditis, pericarditis; * Joints: arthritis and synovitis; * Skin: erythema marginatum, subcutaneous nodules * CNS: encephalopathy, Sydenham’s chorea.
60
peak age of acute rheumatic fever?
5-15 years
61
major criteria for rheumatic fever?
CASES carditis arthritis syndenhams chorea erythema marginatum subcutaneous nodules
62
minor criteria for rheumatic fever?
fever raised CRP migratory arthalgia prolonged PR previous rheumatic fever malaise tachycardia
63
what counts as evidence of group A strep infection?
positive throat culture elevated AsO titre recent scarlet fever
64
diagnosis of rheumatic fever?
group A strep infection + 2 major criteria or 1 major + 2 minor criteria
65
what are the criteria for rheumatic fever called?
jones criteria
66
when does rheumatic fever develop?
Develop 2-4 weeks after strep throat infection.
67
which valve is commonly affected in rheumatic fever?
Commonly affects mitral valve only (70%) but can affect both mitral and aortic (25%).
68
rheumatic fever pathogen?
Group A streptococcus (Streptococcus pyogenes)
69
pathophysiology of rheumatic fever?
Antigenic mimicry: cell-mediated immunity and antibodies to streptococcal antigen cross-react with myocardial antigens
70
rheumatic fever histology?
-Beady fibrous vegetations (verrucae), -Aschoff bodies (small giant cell granulomas) -Anitschkov myocytes (regenerating myocytes).
71
rheumatic fever treatment?
Benzylpenicillin Erythromycin if penicillin-allergic
72

histopath (5 decks)

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