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Scientific Basis of Clinical Practice > Cardiology Pathology > Flashcards

Cardiology Pathology Flashcards

1
Q

what factors determines whether one has ischaemia or infarction?

A

the nature of the blood supply
the rate of development of the occlusion
vulnerability to the effects of hypoxia; neurones, myocardium vs CT, skeletal muscle
oxygen content of the blood; anaemia, hypoxic conditions

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2
Q

describe a red infarct

A

seen in the lung
because there are two blood supplies in the lung
bleeding into the tissues and it appears red
usually occur with venous occlusion; loose tissue
usually occur in dual circulation

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3
Q

describe a pale infarct

A 
seen in the spleen
because there is no blood there
a single vascular channel has been occluded
usually occur in solid organs
usually occur in a single blood supply
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4
Q

what are the most common causes of ischaemia and infarction?

A 
thrombosis
embolism
atheroma
hyper viscosity
vasculitis
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5
Q

describe the formation of a thrombus from an atheroma

A

atheromatous plaque causes turbulence in the blood flow
loss of endothelial cells
collagen exposure
platelet activation
clotting cascade activation
deposition of a thrombus
propagation; thrombus grows in the direction of flow

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6
Q

what are the clinical effects of an arterial thrombus?

A

limb; pale, cold, pulseless, ultimately undergoes infarction

coronary artery; MI

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7
Q

what are the clinical effects of a venous thrombosis?

A

leg; tissues become swollen, reddened, tender

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8
Q

what are the outcomes of thrombi?

A

full lysis and resolution
organisation; scar formation, vessel occlusion
slow recanalisation; leave a scar a residual thrombus
break off; embolism, may occlude another vascular system,

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9
Q

what are the types of emboli?

A 
thromboembolism; 90%
fragments of atheroma
amniotic fluid
gas embolism; trauma
fat embolism; trauma, particularly fracture of long bones
metastasis
foreign material
infective agents
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10
Q

define an atheroma

A

a deposition of material in the intimal layers of the tissues of the vascular tree

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11
Q

what are the components of atheroma?

A

fat macrophages
inflammatory cells
fibrovascular CT

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12
Q

what are the risk factors for developing atheroma?

A 
age; older
gender; male, frequent in women post-menopause
HTN
DM
hyperlipidaemia
smoking
sedentary lifestyle
obesity
soft water ingestion
high intake of complex carbohydrates
hyperuricaemia
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13
Q

name the types of atheromatous lesions

A

fatty streaks
fibrolipid plaque
complicated lesions

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14
Q

describe fatty streaks

A

linear elevation in the intima
composed of lipid-laden macrophages
younger patients

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15
Q

describe fibrolipid plaques

A

further deposition of fat, fibroblasts and collagen

fibrosis formation

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16
Q

describe complication atheromatous lesions

A 
narrow the lumen
causing vascular insufficiency
erosion of endothelium causing thrombosis
haemorrhage into the plaque
aneurysm formation
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17
Q

what sites are commonly affected by atheroma?

A 
lower abdominal vessels
aorta
iliac arteries
coronary arteries
popliteal vessels
descending thoracic aorta
internal carotid vessels
circle of willis
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18
Q

what are the complications of atheroma?

A 
narrowing
thrombus on a plaque
fissuring
cracking
bleeding in a plaque
aneurysm formation
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19
Q

what are the causes of ischaemic heart disease?

A

atheroma
vascular spasm
anaemia

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20
Q

what are the risk factors of ischaemic heart disease?

A 
smoking
race; black
age
men
obesity
DM; uncontrolled
HTN
hyperlipidaemia
stress
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21
Q

describe the pathogenesis of ischaemic heart disease

A

the blood supply is insufficient for the metabolic demands of the heart
due to reduced blood supply, muscle hypertrophy, reduced oxygen carriage

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22
Q

what are the most common arteries to be affected by a MI?

A

LCA anterior descending branch
RCA
LCA circumflex branch

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23
Q

describe the occlusion of the LAD artery

A

most common
“artery of sudden death”
anterior infarct

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24
Q

describe the occlusion of the circumflex branch of the LCA

A

lateral infarction

1/5 of cases

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25
Q

describe occlusion of the LCA proximal to bifurcation

A

occluded all territory supplied by the circumflex and LAD

devastating event

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26
Q

describe coronary artery obstruction in the right side

A

ECG changes in leads 2, 3 and aVF; inferior

can involve the posterior septum

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27
Q

describe the changing of features of transmural MI over time

A

6hrs; ECG changes, electron microscopy shows swollen mitochondria
after 24hrs; region of infarction is pale, myocytes lose their typical striations
days-weeks; dead myocytes removed by macrophages
weeks; healing by repair, organisation, progressive fibrosis
months; fibrous scar matures and akinetic segment formed

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28
Q

what are the complications of MI?

A 
sudden death; often due to VF
arrhythmias
angina
HF
mitral incompetence
pericarditis
cardiac rupture; 3-5 days post MI
ventricular aneurysm
autoimmune conditions; dresslers syndrome, rare
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29
Q

describe the pathogenesis of cardiac rupture

A

tissue weakening as damaged material is removed by macrophages
muscle necrosis and inflammation
rupture occurs at the point of weakest heart material; myomalacia cordis
ventricular septum; left to right ventricular shunt
papillary muscle damage; mitral incompetence

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30
Q

what are the symptoms and signs of Dressler’s syndrome?

A

chest pain
fever
pericardial effusion

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31
Q

describe the pathogenesis of ventricular aneurysm

A

dilatation of a fibrous scar

usually leads to dyskinetic segment, HF neural thrombosis

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32
Q

what does the prognosis of ischaemic heart disease depend on?

A 
age
extent of CAD
live of myocardial damage
symptom severity
pumping ability of the heart
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33
Q

what are the risk factors for primary hypertension?

A 
old age
FHx
african/caribbean origin
high salt diet
lack of exercise
overnight
smoking
excess alcohol
stress
urban dwelling
34
Q

what are the causes of secondary hypertension?

A

renal; parenchymal and renovascular disease
endocrine; pheochromocytoma, cushing’s, hyperaldosteronism
coarctation of the aorta
drugs; NSAIDs, OCP, steroids
pregnancy

35
Q

name some renal parenchymal diseases

A

diabetes
chronic glomerulonephritis
polycystic kidney disease
chronic tubulointerstitial nephritis

36
Q

what are the types of renovascular disease?

A 
atherosclerosis
fibromuscular dysplasia (FMD)
37
Q

describe atherosclerosis in renovascular disease

A

primarily in male patients >50yrs
usually affects the aortic orifice or proximal segment of the renal artery
after 30yrs, causes renal atrophy and CKD

38
Q

describe fibromuscular dysplasia in renovascular disease

A

primarily younger, female patients

pathologic thickening of the arterial wall. mostly the distal main renal artery or the intrarenal branches

39
Q

describe the endocrine causes of secondary hypertension

A

aldosteronoma; benign tumour of the adrenal gland
pheochromocytoma; secretes nor/adrenaline
Cushing’s syndrome

40
Q

describe the cardiovascular manifestations of hypertension

A

symmetrical LVH
atherosclerosis
arteriolosclerosis

41
Q

define atherosclerosis

A

asymmetrical narrowing the lumen of larger vessels by lipid accumulation within the intima

42
Q

define atheriolosclerosis

A

symmetrical narrowing of the lumen of the smaller vessels by deposition of protein within the walls of the blood vessels

43
Q

how does hypertension cause haemorrhagic stroke?

A

rupture of small micro aneurysms within the brain tissue which have been weakened by chronic hypertension

44
Q

describe hypertensive nephrosclerosis

A

progressive renal impairment caused by chronic, poorly controlled hypertension
this can damage small blood vessels, glomeruli and interstitial tissues causing benign hypertensive arteriolar nephrosclerosis

45
Q

describe hypertensive retinopathy

A

long history/severe hypertension
thickened blood vessel walls leads to a reduction in blood flow, resulting in ischaemia and infarction
bleeding
loss of vision

46
Q

what are the major and minor criteria required to rheumatic fever diagnosis?

A 
carditis
polyarthritis
syndenham's chorea
erythema marginatum
subcutaneous nodules
fever
arthralgia
lab abnormalities; raised CRP
ECG abnormalities; prolonged PR
evidence of streptococcal infection; rising antistreptolysin O titre
47
Q

what are the features of rheumatic fever?

A

pancarditis
pleural effusion
fibrinous pericarditis; audible rub
myocarditis; peculiar lesion known as the Aschoff body
swollen valves
small vegetations on the valve leaflets
valve disruption; fibrotic healing response

48
Q

describe Aschoff bodies

A

central core of collagen
surrounded by small Aschoff giant cells
bordered by anitschkow cells; long bar of central chromatin

49
Q

what are the causes and complications of aortic stenosis?

A

calcific degeneration
rheumatic fever

LVH
angina
syncope
LV failure
sudden death
50
Q

what are the causes of aortic incompetence?

A

aortic root dilatation
rheumatic valve disease
inflammatory diseases; aortitis

51
Q

what are the causes and complications of mitral stenosis?

A

rheumatic fever

pulmonary hypertension
LA and RV hypertrophy

52
Q

what are the causes and complications of mitral incompetence?

A

floppy valve
rheumatic fever
dilated mitral valve annulus
papillary muscle dysfunction; myxoid degeneration

AF

53
Q

describe infective endocarditis

A

a bacterium, fungi sor ricketsial organism invade the bloodstream and settles on a mass of thrombus on the valve leaflet
may occur on the endocardial surface of a chamber, intimal surface of the aorta
classified due to the nature of the causative organism

54
Q

describe the types of organisms in infective endocarditis and how they enter the blood

A

mouth; viridian’s group of streptococci
skin; coagulase negative staphylococci
GI/urogenital tract; gram negative organisms and enterococci
IV drug users; pseudomonas aeruginosa, fungi

55
Q

describe the histology of vegetations in infective endocarditis

A

a mass of fibrin, platelets, inflammatory cells and bacterial colonies
usually contain the relative organisms

56
Q

what are the risk factors for developing infective endocarditis?

A 
structural cardiac abnormalities; regurgitant flow
prosthetic valves
indwelling catheters
IV drug use
septic focus elsewhere
chronic gingivitis
immune suppression
diabetes
chronic alcoholism
57
Q

what are the complications of infective endocarditis?

A 
cusp/chordae rupture
valvular incompetence; acute HF
myocarditis
AV block; infection extends into neighbouring myocardial tissue
fever
weight loss
malaise
necrosis of cerebral circulation, kidneys, lungs
58
Q

what are the signs of infective endocarditis?

A 
finger clubbing
splinter haemorrhages
laneway lesions
roth spots
glomerulonephritis
59
Q

describe ejection fraction

A

SV/EDV
>50%; normal
<40%; reduced

60
Q

what are the causes of HF?

A 
myocardial abnormality
IHD; most common
valve disease
pericardial
endocardial
heart rhythm
conduction
61
Q

describe the pathophysiology of HF

A

increase in the volume of blood remaining after systole
increased diastolic volume
myocardial stretch; enhances contractility and SV
myocyte size increase
size and weight of the heart increases
supply and demand mismatch; vulnerable to ischaemia
remodelling continues after initial insult
this impairs the function of the heart as a pump
circulating level of endothelin increase
ADH is raised; precipitates hyponatraemia

62
Q

describe cardiac remodelling in HF

A

myocyte apoptosis
alteration of intracellular handling of calcium ions
reprogramming of gene expression

63
Q

what neurohumeral systems are activated in HF?

A

RAAS
sympathetic nervous system
natriuretic peptide release

64
Q

describe the sympathetic nervous system contribution in HF

A

reduction in stroke vuole causes an increase in heart rate
sinus tachycardia
chronic sympathetic activation; myocyte apoptosis

65
Q

describe the actions of natriuretic peptides in HF

A

counter-regulatory system for RAAS

reduction in blood volume, arterial pressure, central venous pressure

66
Q

describe LSHF

A

stasis of blood in the left chambers
inadequate perfusion of the downstream tissues; organ dysfunction
dilatation of the LA increases the risk of AF and thrombus; stroke risk
pulmonary congestion and oedema; haemosiderin -laden macrophages may be seen in the alveoli
elevated capillary pressure; pleural effusion
kidney hypo perfusion; impaired excretion of nitrogenous products, pre-renal azotaemia
cerebral hypo perfusion; hypoxic-ischaemic encephalopathy

67
Q

what are the causes of RSHF?

A 
commonly LSHF
pulmonary hypertension
RV infarction
RV cardiomyopathy
adult congenital heart disease

cor pulmonale; typically occurs in patients with a variety of lung disorders

68
Q

describe the pathologies of RSHF

A

minimal pulmonary congestion
congestion of the systemic and portal venous systems
hepatic necrosis; perfusion failure
portal venous HTN; splenomegaly, platelet sequestration, chronic congestion and oedema of the bowel wall
systemic venous congestion; pleural, pericardial or peritoneal fluid accumulation
anasarca
backward failure; kidney and brain

69
Q

describe false aneurysms

A

haematomas which lie alongside a blood vessel
often enveloped by a thin rim of adventitial tissue
communicate with the vascular lumen via a narrow defect in the media

70
Q

what are the causes and the typical locations of aneurysms?

A 
trauma
atherosclerosis
inflammatory disorders
marfan's syndrome
HTN
pericyte loss in diabetes
infection
septic emboli

femoral artery
abdominal/thoracic aorta
cerebral artery or capillaries
retinal capillaries

71
Q

what are the consequences of aneurysms?

A

rupture; haemorrhage
compress adjacent structures; ureter, causing hydronephrosis, cranial nerve
thrombus due to stasis
embolisation; ischaemia or infarction

72
Q

what are the causes of myocarditis?

A 
viral; coxsackie, ECHO, adenoviruses
bacterial; meningococcus, diphtheria
parasites; trypanosomiasis, chaga's disease
ionising radiation
drugs; adriamycin
73
Q

what are the histological features of myocarditis?

A

inflammatory cell infiltrate; mostly T lymphocytes in the interstitial spaces
myocyte death

dallas criteria

74
Q

what are the causes of pericarditis?

A 
viral
bacterial
TB
post-MI
post-surgical
autoimmune; dressler's syndrome
carcinomatous
uraemic
75
Q

describe serous pericarditis

A

clear
straw coloured
high specific gravity
high protein content

76
Q

describe serofibrinous pericarditis

A

clumps of fibrin within the fluid

77
Q

describe purulent/suppurative pericarditis

A

frank pus may form in the pericardial sac

78
Q

describe blood stained pericardial effusions

A

highly suspicious of malignancy

79
Q

describe caseous pericarditis

A

fungi and mycobacterial organisms invade the pericardial space
may lead to fibrotic obliteration
known as constrictive pericarditis

80
Q

what are the end results of shock?

A

hypotension
impaired tissue perfusion
cellular hypoxia

81
Q

what are the effects of shock?

A 
neuronal necrosis
focal/widespread necrosis of the heart
acute tubular necrosis
diffuse alveolar damage
fatty change of the liver, zone 3 necrosis
haemorrhagic enteropathy of the bowel

Scientific Basis of Clinical Practice (10 decks)

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