Cardiovascular Flashcards
1
Q
What is ischaemia?
A
result of impaired blood flow or perfusion of tissues depriving it of oxygen and nutrients
2
Q
What are the effects of ischaemia?
A
reversible
dependent of duration of ischaemia
dependent on tissue metabolic demands
3
Q
What is infarction?
A
death (necrosis) of tissue as a result of ischaemia
4
Q
What are the effects of infarction?
A
irreversible
tissues vary in ability to repair and regenerate
5
Q
What do infarctions illicit?
A
inflammatory response
6
Q
What determines whether ischaemia or infarction develops?
A
nature of blood supply (single or biphasic)
duration of occlusion
vulnerability of tissue to hypoxia
oxygen content of blood
7
Q
What are red infarcts?
A
venous occlusions
8
Q
Where do red infarcts occur?
A
loose tissues (like lung)
tissues with dual circulation
tissues which have been congested before and have referfusion damage
9
Q
Where do pale infarcts occur?
A
solid organs
single blood supply
10
Q
What causes ischaemia and infarction?
A
thrombosis embolism spasm atheroma compression vasculitis steal hyperviscosity
11
Q
What 3 areas cause ischaemia or infarction?
A
things in lumen
things in wall
things outside wall
12
Q
What 3 factors cause thrombosis?
A
Virchow's triad: changes in 1. intimal surface of vessel 2. pattern of blood flow 3. blood constituents
13
Q
Explain how a thrombus forms on an atheromatous plaque
A
turbulent blood flow around plaque (changes to flow)
changes in surface overlying atheromatous plaque (changes to intimal wall)
platelet activation due to these changes
activation of clotting cascade
deposition of thrombus
14
Q
What is propgation?
A
growth of thrombus in direction of flow
15
Q
What are the clinical effects of arterial thrombosis?
A
distal tissues become: oale cold painful infarcted
16
Q
What are the clinical effects of venous thrombosis?
A
usually happens in leg distal tissues become: red swollen tender
17
Q
What are the 4 fates of a thrombus?
A
- lysis and resolution
- organisation
- recanalisation
- embolism
18
Q
What is recanalisation?
A
blood flow restored with multiple small vessels but leaves behind scar and residual thrombus
19
Q
What is an embolism?
A
mass of material that can move within vascular system and become lodged in a vessel blocking its lumen
20
Q
What are emboli usually derived from?
A
thrombus
21
Q
What is the most common type of embolism?
A
thromboembolism
22
Q
What other types of embolus are there?
A
atheromatous emboli amniotic fluid (parturition) gas fat tumour (metastasis) foreign material infective agents
23
Q
Describe the structure of a normal artery from outside in
A
adventitiae external elastic lamina media internal elastic intima endothelium
24
Q
What is an atheroma?
A
deposition of tissue within intimal layers
25
What is deposited in atheromas?
fat macrophages
inflamatory cells
fibrovascular connective tissue
26
What do atheromas cause?
luminal narrowing and vascular insufficiency
27
What are the major risk factors for atheromas?
```
age
sex
hyperlipidaemia
smoking
hypertension
diabetes mellitus
sedentary lifestyle
```
28
What are the 3 types of atheromatous lesions?
fatty streak
fibrolipid plaque
comlicated lesion
29
WHat is a fatty streak?
linear elevations of lipid laden macrophages
30
What is a fibrolipid plaque?
bigger lesion that a fatty streak
fat
fibrosis
fibroblasts present
31
What is a complicated lesion?
narrowing
endothelial erosion with thrombosis
plaque rupture and fissuring
aneurysm formation
32
What sites are typically affected by atheroma?
```
high pressure vessels
lower abdominal arota/iliac
coronary
popliteal
descending thoracic aorta
internal carotid and circle of willis
```
33
What vesselsWhat are complications of an atheroma?
narrowing of vessel
thrombus on plaque
fissuring and cracking (bleeding onto plaque)
aneurysm
34
What is the s[ectrum of ischaemic heart disease?
angina
myocardial infarction
sudden death
35
What is the main cause of ischaemic heart disease?
atheroma
36
What are teh risk factors for ischaemic heart disease?
```
family Hx
smoking +++
diet
lifestyle
race (blackF)
obesity
diabetes mellitus
hypertension
hyperlipidaemia
stress
```
37
What is the pathogenesis of ischaemic heart disease?
when blood supply becomes inefficient through:
reduction in blood supply (atheroma)
increased demand (muscle hypertrophy)
reduced oxygen carriage (anaemia)
37
What is the pathogenesis of ischaemic heart disease?
when blood supply becomes inefficient through:
reduction in blood supply (atheroma)
increased demand (muscle hypertrophy)
reduced oxygen carriage (anaemia)
38
What does angina present with?
reversible chest pain
| can be stable (exertion related) or unstable (unpredictable)
39
What does MI present with?
central crushing chest pain
| left arm and neck radiation
40
What are the 3 commonest arteries to be affected in MI?
LAD
RCA
LCX
41
What happens the ventricles in acute MI?
necrosis of left ventricle
inflammatory infiltration
fibrous repair
necrotic muscle releases enzymes (troponin)
42
Explain the ECG changes depending on where the MI occurs?
LAD "artery of sudden death"
infarction of anterior aspect of myocardium
ECG changes in anterior chest leads
LCA
lateral infarction
ECG changes I, AVL, lateral chest leads
RCX
ECG changes II, III and AVF (inferior leads)
43
What changes within the first 24 hours of MI?
nothing to be seen
| within first 6 hours swollen mitochrondria microscopically
44
What can be seen 24 hours after MI?
infarction pale
inflammatory reaction
myocytes lose typical striations
45
What can be seen days to weeks after MI?
dead myocytes removed by macrophages
healing by repair, organisation and progressive fibrosis
formation of fibrous scar
46
WHat can be seen months after MI?
akinetic segment
47
What are the complications of MIs?
```
sudden death
arrhythmias
angina
cardiac failure
mitral incompetence
```
48
What causes sudden death in MI?
VF
49
What causes arrhythmias in MI?
damage to conducting system in first few days
50
What causes angina?
ischaemia
51
What causes cardiac failure?
muscle necrosis/arrhythmia
52
What causes mitral incompetence?
papillary muscle damage
53
What causes pericarditis to be a complication of MI and when does it occur?
transmural infarct with pericardial inflammation
| 2-4 days
54
What causes cardiac rupture in MI and when does it occur?
wall weakening following muscle necrosis and acute inflammation
3-5 days
55
Wjat causes mural thromosis in MI? When does it occur?
ischaemia and endothelial damage
| 7+ dyas
56
What causes ventricular aneurysm in MI?
muscle necrosis/arrhythmia
57
What causes Dressler's syndrome in MI?
autoimmune
58
What does Dressler's syndrome present with?
chest pain
fever
effusions
59
Compare and contrast myocardial rupture and ventricular aneurysm
60
What is arterial blood pressure?
measure of the force exerted on arterial walls by circulating blood
61
What is the diagnostic threshold of systolic and diastolic blood pressure?
systolic 140mmHg
| diastolic 90mmHg
62
What is hypertension a major risk factor for?
```
stroke
MI
HF
CKD
cognitive decline
premature death
```
63
What are risk factors for primary/essential hypertension?
```
age
FHx
african/caribbean origin
high salt
lack of excercise
overweight
smoking
alcohol
stress
```
64
What are 5 areas that can cause secondary hypertension?
```
renal
endocrine
coarctation of aorta
medications
pregnancy
```
65
What endocrine causes for hypertension are there?
pheochromocytoma
Cushing's
hyperaldosteronism
66
What medications can cause hypertension?
NSAIDs
oral contraceptive
steroids
67
What are renal parenchymal diseases?
```
diabetic nephropathy
chronic glomerulonephritis
polycystic kidney disease
chronic tubulointerstitial nephritis
hypertensive renal disease
```
68
What is renal artery stenosis?
decrease in blood flow through one/both main renal arteries or branches
69
What causes renal stenosis?
```
atherosclerosis
fibromuscular dysplasia (FMD)
```
70
How is renal stenosis diagnosed?
CT
angiography
MRI
71
What is FMD?
fibromuscular dysplasia
| pathogenic thickening of arterial wall
72
Who does FMD commonly affect?
younger adults
| mainly females 20-50s
73
What is produced in the adrenal cortex?
aldosterone
cortisol
testosterone precursor
74
What is produced in the adrenal edulla?
adrenaline
| noradrenaline
75
What is produced in the adrenal medulla?
adrenaline
| noradrenaline
76
What can cause elevated aldosterone?
aldosteronoma
77
What can cause elevated noradrenaline and adrenaline?
phaeochromocytoma
78
What can cause Cushing's syndrome/hypercortisolism?
ectopic ACTH due to lung cancer
pituitary adenoma
adrenal adenoma
corticosteroids
79
How does coarctation of the aorta cause hypertension?
reduced blood flow in lower half of body and lower BP
| higher BP in arms and upper body
80
What are the clinical manifestations of hypertension/what organs are affected?
cardiovascular system
kidneys
retina
81
What happens to the heart in hypertension?
left ventricular hypertrophy
82
What is hypertrophic cardiomyopathy?
asymmetrical left ventricular hypertrophy
often involves IV septum
genetic disease
can cause sudden death in young adults
83
What is the difference between atherosclerosis and arteriolosclerosis?
ATHERO - asymmetrical narrowing of lumen of LARGER vessels by LIPID accumulation within INTIMA
ARTERIOLO - symmetrical narrowing of lumen of SMALLER vessels by deposition of PROTEIN within the wall of blood vessels
84
What is haemorrhagic stroke?
rupture of small cerebral micro-aneurysms
85
What is hypertensive nephrosclerosis?
progressive renal impairment caused by chronic poorly controlled hypertension
86
What can results from hypertensive arteriolar nephrosclerosis?
CKD
87
What is hypertensive retinopathy?
thickened blood vessel walls reduces blood flow
causes ischaemia and infarction
damage to blood vessels then causes bleeding and loss of vision
88
Who is typically affected by rheumatic fever?
children with Group A haemolytic streptococci throat infection
89
When do symptoms of rheumatic fever generally present after Group A haemolytic streptococcal throat infections?
2-6 weeks
90
How is rheumatic fever diagnosed?
2 major or 1 major and 2 minor criteria and evidence of previous streptococcal infection
91
What is evidence of previous streptococcal infection?
rising antistreptolysin O titre
92
What are major criteria for rheumatic fever?
```
carditis
polyarthritis
erythema marginatum
Sydenham's chorea
subcutaneous nodules
```
93
What is erythema marginatum?
skin rash over trunk and limbs
| round, pale-pink centre surrounded by slightly raised red outline
94
What is Sydenham's chorea?
rare neurological disorder
sudden onset chorea
random-appearing, continuous, involuntary movements
often includes the face and tongue
95
What are the minor criteria for rheumatic fever?
```
fever
arthralgia
raised CRP (lab abnormalities)
ECG abnormalities (prolonged PR interval)
evidence of streptococcal infection
```
96
What is the hallmark of rheumatic fever?
pancarditis
97
What can patients present with in rheumatic fever?
pleural effusion and fibrinous pericarditis
man
manifests as audible rub
98
What is an Aschoff body?
when pericarditis develops into myocarditis and endocarditis
valves are swollen and infiltrated with inflammatory cells
small vegetations on valve leaflets
99
What causes the architectural disruption to the vales and the long term complications of rheumatic fever?
fibrotic healing response
100
What does an Aschoff body consist of and what is it surrounded by?
central core of collagen
| small Aschoff giant cells
101
What is seen by the arrow?
Anitschkow cells
| long bar of central chromatin
102
What are the 2 overarching areas causing valvular heart disease?
stenosis
| incompetence
103
What is stenosis of valves?
thickened and/or calcified causing obstruction to flow
104
What is incompetence of heart valves?
regurgitataion or insufficiency
| lose normal function and leak
105
What are causes of valve disease?
```
age - calcification
functional changes
rheumatic fever
floppy valves
congenital defects
infective endocarditis
```
106
What are 2 causes of aortic stenosis?
calcific degeneration
| rheumatic fever
107
What are complications of aortic stenosis?
```
left ventricular hypertrophy
angina
syncope
left ventricular failure
sudden death
```
108
What are causes of aortic incompetence?
aortic root dilatation
| rheumatic valve disease
109
What is the pathophysiology of left ventricular hypertrophy in aortic stenosis?
left ventricular chamber becomes pressure loaded
| compensatory hypertrophy
110
What is seen in the picture?
calcific aortic valve stenosis
111
What is seen in the picture?
congenital bicuspic aortic valve stenosis
112
What is seen in the picture?
aortic valve regurgitation due to dilatation of aortic root
113
What causes mitral stenosis?
rheumatic fever
114
What are the complications of mitral stenosis?
pulmonary hypertension
left atrial hypertrophy
right ventricular hypertrophy
115
What causes mitral incompetence?
floppy valves
rheumatic fever
dilated mitral valve annulus
papillary muscle dysfunction
116
What can be seen in the picture?
mitral valve leaflet expanded
| projecting back into left atrium
117
What is infective endocarditis
acute/chronic disease resulting from infection of focal area of endocardium (usually over valve)
118
What does infective endocarditis look like?
vegetations
| friable masses containing organisms, platelets, fibrin and inflammatory cells
119
What are predisposing factors to infective endocarditis?
structural cardiac abnormalities
prostheses and catheters
bacteraemias
altered immunity
120
What are local complications of infective endocarditis?
chordae/ cusp rupture
valvular incompetence
myocarditis
121
What are systemic complications of infective endocarditis?
fever
weight loss
malaise
122
What are systemic complications of infective endocarditis?
fever
weight loss
malaise
123
What is heart failure?
clinical syndrome characterised by typical symptoms accompanied by signs caused by structural/functional cardiac abnormality resulting in reduced cardiac output and/or elevated intracardiac pressures at rest or exertion
124
What is the equation for ejection fraction?
sttroke volume/ end diastolic volume
125
What is reduced LVEF?
<40%
126
How many classes are there in heart failure?
4
1 is no limitation
2 mild limitation - rest normal but exertion causes fatigue, dyspnoea or palpitations
3 marked limitation - comfortable at rest but gentle exertion is symptomatic
4 HF symptoms occur at rest and are exacerbated by exertion
127
What causes heart failure?
myocardial abnormality
128
What are the 3 Frank-Starling mechanisms in heart failure?
myocardial adaptations
endothelial function
antidiuretic hormone
129
What myocardial adaptations occur in heart failure?
```
myocyte hypertrophy
fibrosis
apoptosis
abnormal calcium homeostasis
gene expression
```
130
What happens to circulating levels of endothelin in heart failure?
increase
131
What happens sodium levels in HF?
decrease due to high levels of antidiuretic hormone
132
What happens the activity of NO in HF?
blunted
133
What are the 3 neurohumoral systems activated in heart failure?
1. RAAS
2. sympathetic nervous system
3. natriuretic peptides
134
How is the RAAS system activated in HF?
↓ cardiac output
↓ renal perfusion
RAAS activated
135
What does RAAS do?
salt and water retention
↑ venous pressure
toxic effects of myocardial cells
136
What medications are used if HF specifically for RAAS?
ACE inhibitors and ARBs
137
Why does the sympathetic nervous system get activated in HF?
CO = SV x HR
↓ SV due to myocardial impairment
↑ compensatory HR
138
What are ANP and BNP and what do they do?
natriuretic peptides
counter RAAS
reduces blood volume, arterial pressure and central venous pressure
139
What happens to lead to left-sided heart failure?
pulmonary congestion and oedema
pleural effusions
blood pools in the pulmonary circulation
140
What is the consequence of LSHF?
blood stasis in left chambers
| inadequate perfusion of downstream tissues
141
What increases in risk with left atrial dilatation?
atrial fibrilation and thrombus
142
What can be seen in the alveoli in LSHF?
haemosiderin-laden macrophages
143
Why can pulmonary effusions arise from LSHF?
elevated capillary pressure
144
What are the clinical symptoms of LSHF?
dyspnoea
orthopnoea
PND
145
What happens to the kidney in severe hypoperfusion?
impaired excretion of nitrogenous
| pre-renal azotaemia
146
What happens the brain in advanced heart failure?
hypoxic-ischaemic encephalopathy
irritability
progress to come
147
How does right sided heart failure commonly arise?
as a result of LSHF
148
What can also cause RSHF?
pulmonary hypertension
right ventricular infarction
right ventricular cardiomyopathy
adult congenital heart disease
149
In RSHF what is congested?
systemic and portal veins
| NOT lungs
150
What is the pathology of congestion of vessels in RSHF?
hepatomegaly (nutmeg liver)
splenomegaly (platelet sequestration)
congestion and oedema of bowel wall
151
What happens in systemic congestion in RSHF?
fluid accumulation in pleural, pericardial or peritoneal spaces
ankle and pre-tibial oedema
pre-sacral oedema
anasarca (generalised massive oedema)
152
What is an aneurysm?
localised, permanent abnormal dilatation of blood vessel
153
What is a false aneurysm?
haematoma which lies alongside vessel often enveloped by thin rim of adventitial tissue
communicates with vascular lumen via narrown defect in media
154
What is a true aneurysm?
weakness in vessel wall composed of intima, media and adventitia
155
What is the underlying pathology for false aneurysm and where is it normally found?
trauma
| femoral artery
156
What is the underlying pathology for saccular and diffuse aneurysm and where is it normally found?
atherosclerosis
abdominal aorta
thoracic aorta
cerebral artery
157
What is the underlying pathology for dissecting aneurysm and where is it normally found?
Marfan's (non-inflammatory medial disease)
| aorta and main branches
158
What is the underlying pathology for capillary micro aneurysm and where is it normally found?
hypertension
pericyte loss in diabetes
cerebral caps
retinal caps
159
What is the underlying pathology for myocytic aneurysm and where is it normally found?
infection and septic emboli
| any vessel
160
What are the consequences of aneurysms?
```
may be asymptomatic
can rupture causing life-threatening haemorrhage
compression of adjacent structures
tissue/organ ischaemia
thrombosis/embolism
```
161
What is seen on the picture?
atheromatous aneurysm in abdominal aorta
162
What is seen in the picture?
berry aneurysm in circle of willis
163
What is seen in the picture?
ruptured abdominal aortic aneurysm
| dark, porridge material lining aneurysm is thrombus
164
What is myocarditis?
inflammation of the myocardium
165
What are the 5 main causes of myocarditis?
```
viral
bacterial
parasitic
ionising radiation (inc therapy)
drugs
```
166
What viral causes are there for myocarditis?
caxsackie
ECHO
adenoviruses
167
What bacterial causes are there for myocarditis?
diphtheria
| meningococcus
168
What parasites cause myocarditis?
trypanosomiasis
| Chagas' disease
169
What drug can cause myocarditis?
adriamycin
170
What is pericarditis?
inflammatory reaction in visceral and/or parietal layers of pericardium
171
What are the causes of pericarditis?
```
viral
bacterial
TB
post MI
post surgery
Dressler's syndrome
carcinomatous
uraemic
```
172
What classifies a serous pericarditis?
clear, straw-coloured
high specific gravity
high protein content
173
What classifies a serofibrinous pericarditis?
clumps of fibrin mixed in fluid
174
What is a purulent or supprative pericarditis?
frank pus
175
What is a blood-stained pericarditis suspicious of?
mlignancy
176
What is caseous pericarditis?
fungal/mycobacterial infection
177
What can happen when a caseous pericarditis is healing?
fibrotic obliteration of pericardial space (constrictive pericarditis)
178
What must happen with any pericarditis?
aspirate submitted to cytological lab
179
What are end results of shock?
hypotension
impaired tissue perfusion
cellular hypoxia
180
What are the 3 categories of shock?
cardiogenic
hypovolaemic
septic
181
What happens the brain, heart, kidneys, lungs, liver and GI tract in shock?
1. neuronal damage
2. focal/widespread necrosis (sub-endocardial region)
3. acute tubular necrosis
4. diffuse alveolar damage
5. fatty change, zone 3 necrosis
6. haemorrhagic enteropathy
