Pathology Flashcards
(80 cards)
1
Q
What is an atheroma?
A
Focal accumulation of lipid in the intima of arteries
2
Q
What is the aetiology of atheroma?
A
Smoking Family History Hypertension Hyperlipidaemia Male gender Diabetes Mellitus Increased age
3
Q
Where does atheroma commonly occur?
A
Circle of Willis
Branches of major arteries - iliac/femoral vessels
Coronary arteries
Abdominal aorta
4
Q
What is atherosclerosis?
A
Asymmetrical thickening of large and medium sized arteries
5
Q
What is arteriolosclerosis?
A
Symmetrical thickening of small arteries or arterioles
6
Q
What is arteriosclerosis?
A
Hardening of the arteries.
Consists of atherosclerosis and arteriolosclerosis
7
Q
Pathogenesis of atherosclerosis
A
- Damage to endothelium
- LDLs enter the tunica media of arteries and become oxidised
- Monocytes bind to endothelial cells and then enter the intima
- Monocytes become macrophages and initiate an inflammatory reaction
- Macrophages accumulate lipid in their cytoplasm, becoming foamy macrophages (foam cells)
- Lipid-laden macrophages die, spilling lipid into the core of the plaque
- Cytokines promote smooth muscle cell proliferation
- Smooth muscle cells migrate into the intima and synthesise collagen, forming a fibrous cap
- Neovascularisation at the plaque periphery is induced by cytokines
- Plaque size can increase due to micro thrombi formation on the surface
- Dystrophic calcification might occur
8
Q
Name and define the 3 types of atheromatous lesion
A
- Fatty streaks: linear elevations of lipid-laden (foamy) macrophages
- Fibrolipid plaque: bigger lesions with fat and fibrosis and fibroblasts
- Complicated lesion: narrowing, endothelial erosion with thrombosis, plaque rupture and fissuring, aneurysm formation, also embolic phenomena
9
Q
What are the complications of atheroma?
A
- Plaque rupture and thrombosis = acute arterial occlusion
- Progressive luminal narrowing = organ ischaemia
- Erosion of media by the plaque = aneurysm
- Dislodgement of plaque thrombus = emboli
10
Q
What is the evolution of a plaque?
A
fatty streak –> atherosclerotic plaque –> lumen narrowing, atherothrombotic occlusion, embolisation
11
Q
What are the layers of the artery?
A
Intima = single layer of endothelium with thin layer of CT Internal elastic lamina Media External elastic lamina Adventitia
12
Q
What is ischaemia?
A
Impaired blood flow/perfusion of a tissue so that it is deprived of vital nutrients, especially oxygen. Effects are reversible and depend on duration and metabolic demand of the tissue.
13
Q
What is infarction?
A
Tissue necrosis due to ischaemia. The effects are irreversible. Tissue varies depending on repair and regeneration
14
Q
Factors of ischaemia and infarction?
A
- Nature of blood supply
- Rate of development of occlusion
- Vulnerability of the tissue to hypoxia
- Oxygen content of the blood
15
Q
What is ischaemic heart disease (IHD)
A
spectrum of clinico-pathological entities including angina, myocardial infarction, and sudden death mainly due to atheroma & its complications; or vascular spasm & anaemia.
16
Q
What 3 things cause coronary artery occlusion?
A
- Plaque rupture
- Plaque erosion
- Calcified nodules: eruptive dense calcified bodies protruding into luminal space
17
Q
Gross changes that occur within a few hours 1-3 days 5-10 days several weeks of a myocardial infarction
A
a few hours: Normal
1-3 days: pale, soft
5-10 days: yellow centre with hyperaemic border
several weeks: white scar
18
Q
Microscopic changes that occur within a few hours 1-3 days 5-10 days several weeks of a myocardial infarction
A
a few hours: normal
1-3 days: neutrophils
5-10 days: macrophages, granulation tissue
several weeks: scar (collagen)
19
Q
Complications of a myocardial infarction
A
Death Another MI Rupture free wall ventricle/ventricular septum Thrombus Heart failure Ventricular aneurysm Arrhythmia Dressler's syndrome (pericarditis) Emboli Regurgitation (mitral)
DARTH VADER
20
Q
What organs have a dual blood supply and what are the blood vessels called?
A
lungs (pulmonary and bronchial arteries)
liver (hepatic artery and portal vein)
21
Q
Will organs with a dual blood supply suffer from ischaemia or infarction?
A
Ischaemia: if one of the blood supplies is affected, they can still receive blood from the other one, so they are less likely to be infarcted
22
Q
Which organs have a single blood supply?
A
Spleen and kidney
23
Q
How does the rate of development of arterial occlusion affect whether or not an organ will suffer from ischaemia or infarction?
A
If an arterial occlusion develops slowly, the blood vessel will have time to develop an alternative pathway for the blood to ‘get around’ the blockage. This is called collateral circulations and functions like roadworks directing traffic around a RTC
24
Q
What is ischaemia of the brain called?
A
Transient ischaemic attack (TIA)
25
If ischaemia develops to infarction in the brain what is it called?
Stroke
26
What is stable angina?
Ischaemia of the heart causing chest pain that occur on exertion and stop at rest due to stable atheroma plaques in the coronary arteries.
27
What is unstable angina?
Severe ischaemia that occurs when an atheroma plaque ruptures or develops a thrombus, partially occluding the coronary vessel
28
What occurs if unstable angina isn't treated in time?
Full occlusion of the artery resulting in myocardial infarction
29
If you develop an atheromatous plaque in your lower limbs what is it called clinically?
```
Intermittent claudication (or peripheral vascular disease)
which means pain in the legs when walking but stops when you rest.
```
30
If intermittent claudication progresses to infarction, what is it called?
Acute limb ischaemia
31
What are the symptoms of acute limb ischaemia
```
The 6 Ps:
Pain
Pallor
Paraesthesia
Pulselessness
Paralysis
Poikilothermia (perishingly cold)
```
32
What is the name that encompasses unstable angina and myocardial infarction?
Acute Coronary Syndrome (ACS)
33
How might coronary artery occlusion occur?
1. Plaque rupture
2. Plaque erosion, forming a thrombus on top
3. Calcified nodules/bodies that protrude into the lumen
34
What is an aneurysm?
A localised, permanent abnormal dilation of blood vessels
35
What are the different types of aneurysm?
```
Atherosclerotic
Dissecting
Berry
Capillary micro-aneurysms (Charcot-Bouchard Aneurysms)
Syphilitic
False
```
36
What is a false aneurysm?
Blood-filled space that forms around a blood vessel, usually after traumatic rupture/perforating injury. A haematoma forms and is contained by the adventitial fibrous tissue
37
What are atherosclerotic abdominal aortic aneurysms (AAA)?
Most common and clinically significant type of atherosclerotic aneurysm
38
How do AAAs form?
Erosion and placement of the media by an adjacent, complicated atheroma.
39
What are the consequences of an AAA?
1. If the size is greater than 5.5cm it can rupture into the retroperitoneal space
2. Form a thrombus, which could become an emboli if it breaks off
3. Extend into the iliac arteries causing thickening of the wall, decreased lumen, peripheral vascular disease
40
What is the triad of symptoms for AAA?
Pain in the flank/back
Hypotension
Pulsatile abdominal mass
41
What happens in dissecting aortic aneurysms?
Blood is forced through a tear int he aortic intima, creating a blood-filled space (haematoma) int he media which can be propagated along the blood vessel
42
Outcomes of a dissecting aortic aneurysm are....
1. Blood can rupture through the adventitia = massive haemorrhage into the pericardium, pleura or other structures
2. Blood can re-enter aortic lumen = 'double-barrelled' aorta
3. Blood may extend down tributary arteries = compression of the lumen, and end-organ infarction.
43
What are the risk factors for dissecting aortic aneurysm?
Systemic Hypertension
Bicuspid Aortic Valve
Marfan Syndrome
44
What is the pathogenesis of a berry aneurysm?
Occurs in the circle of Willis
Normal muscular arterial wall is replaced by fibrous tissue = lesions at the points of branching in the circle of willis
Rupture = subarachnoid haemorrhage
45
What are the symptoms of a berry aneurysm?
```
Thunderclap headache
Stiff neck
Nausea and vomiting
Loss of consciousness/convulsions
Stroke-like symptoms - slurred speech, weakness on one side
```
46
What is Charcot-Bouchard aneurysm associated with?
hypertension
| diabetic vascular disease
47
Where do capillary-microaneurysms in hypertension occur?
Commonly occur in the branches of the middle cerebral artery
48
What is oedema?
Build up of fluid in the interstitial tissue
49
What are the different categories of pathogenesis in oedema and why do they occur?
1. Inflammation - increased vascular permeability
2. Venous - increased intravenous pressure
3. Lymphatic - obstruction of lymphatic drainage
4. Hypoalbuminaemic - reduced plasma oncotic pressure
50
What are the 3 different types of oedema?
Subcutaneous
Pulmonary
Cerebral
51
How can you identify if subcutaneous oedema is present?
Affected area shows pitting.
Ident skin firmly with finger.
If oedema is present an indentation will be left due to redistribution of some of the excess fluid.
52
What causes pulmonary oedema?
Abnormal accumulation of fluid in the intra-alveolar spaces of the lungs
53
What are the consequences of pulmonary oedema?
Reduction in effective lung volume = breathlessness
54
What are the causes of pulmonary oedema?
```
Left ventricular failure
Renal failure
Acute respiratory distress syndrome
Pulmonary inflammation/infection
Iatrogenic (due to IV fluid prescription)
```
55
What is cerebral oedema?
Abnormal accumulation of fluid in the brain parenchyma = increased brain volume
56
Where does cerebral oedema occur?
Rigid confines of the cranial cavity
= compression of the brain which
= herniation of brain tissue
= irreversible and fatal damage
57
What is shock?
inadequate blood flow, resulting in lack of oxygen and nutrients (hypo perfusion) to vital organs
58
What are the causes of shock?
Cariogenic
| Hypovolaemic
59
What causes cariogenic shock?
Most commonly acute myocardial infarction
60
What is Hypovolaemic shock?
Loss of effective circulating blood volume due to:
internal/external haemorrhage
Increased vascular permeability and/or dilation
61
What causes internal/external haemorrhage?
Traumatic rupture of an internal organ
| Accidental severing of a major vessel
62
What causes increased vascular permeability/dilation?
Neurogenic mechanisms - spinal cord injury
Anaphylactic reactions
Extensive burns
Bacterial toxaemia (septic shock)
63
What are the phases of shock & what occurs in each phase?
Compensatory
- dilation of cerebral arteries = normal blood flow rate
- Vasoconstriction in non-vital organs
- Increased HR and contraction
Progressive
- Hypotension = tissues vulnerable to ischaemic injury
Irreversible
- Multi-organ failure
- If 3+ organs fail = death
64
What are the consequences of shock?
Renal failure - due to necrosis of renal tubules
Acute Respiratory Distress Syndrome - due to severe inflammation of alveolar walls
Acute pancreatitis
Cerebral infarction
Infarction - due to hypoperfusion
65
What is hypertension?
BP 140/90mmHg or higher on separate occasions
66
Explain the renin-angiotensin-aldosterone system
Serious of reactions designed to help regulate BP
1. when BP falls, kidneys release renin enzyme into blood
2. Renin splits angiotensinogen into pieces. One piece = angiotensin I
3. Angiotensin I split into pieces by angiotensin-converting enzyme (ACE). One piece is angiotensin II
4. Angiotensin II causes muscular walls of arterioles to constrict, increasing BP
Angiotensin II releases aldosterone and antidiuretic hormones
5. aldosterone causes kidneys to retain sodium and exert potassium
sodium = water retention, increasing BP and BV
67
What are the causes of primary hypertension?
```
Unknown cause, probably multifactorial:
genetic predisposition
excessive sympathetic system activity
Na/K membrane transport abnormalities
renin-angiotensin-aldosterone system abnormalities
age
high salt in diet
lack of exercise
obesity
smoking
excessive alcohol intake
stress
african/caribbean origin
```
68
What are the causes of secondary hypertension?
Renal - parenchymal or renovascular disease
Endocrine - cushion's, pheochromocytoma, hyperaldosteronism
Medications - NSAIDs, oral contraceptive, steroids
Coarctation/congential narrowing of the aorta
pregnancy-induced
69
What is renovascular disease?
renal artery stenosis
| decreased blood flow through one/both renal retires or their branches due to atherosclerosis or fibromuscular dysplasia
70
What hormones are produced by the adrenal cortex?
aldosterone
cortisol
testosterone precursor
71
What hormones are produced by the adrenal medulla?
noradrenaline
| adrenaline
72
What is aldosteroma?
benign tumour of the adrenal gland
73
What is pheochromocytoma?
Tumour of the adrenal medulla. Usually benign but can be malignant
74
What is cashing's syndrome?
```
Hypercortisolism
Rare condition caused by:
pituitary microadenoma (benign tumour)
iatrogenic (steroid use)
ectopic ACTH due to lung cancer
adrenal adenoma (benign tumour)
```
75
What is coarctation of the aorta?
Narrowing of the aorta
| causes decreased blood flow to the lower half of the body
76
What are the effects of hypertension on the blood vessels
atheroma
| atherosclerosis
77
What are the effects of hypertension on the myocardium
ischaemic heart disease - angina, MI, sudden death
| left ventricular hypertrophy - cardiomegaly
78
What are the effects of hypertension on the brain
Transient ischaemic attack (stroke) - atheroma/emboli
| haemorrhage stroke - rupture of charcot-bouchard micro aneurysm
79
What are the effects of hypertension on the kidneys
renal failure
| hypertension damages small BVs, glomeruli, renal tubules, & interstitial tissues
80
What are the effects of hypertension on the eyes
retinal vascular damage (hypertensive retinopathy)
- arteriolar constriction and arteriovenous nicking
- flame shaped haemorrhages
- cotton-wool spots
- yellow hard exudates
- papilloaedema
