Pathology Flashcards

1
Q

Acute rheumatic fever cause

A

Group A streptococcus bacteria infects upper respiratory tract causing sore throat and later auto-immune response

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2
Q

Latency period between GAS infection and ARF symtoms

A

3 weeks

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3
Q

Rheumatic heart disease

A

Damage to mitral or aortic valves that remains after ARF has resolved

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4
Q

Populations most likely to get ARF

A

Children between 5 and 15
North island
Maori (20 x higher) and Pacific (40 x higher)

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5
Q

Link between ARF and socio-economic status

A

Crowded housing conditions
Barriers to primary healthcare
Untreated strep throat infections

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6
Q

Symptoms of ARF

A
Sore knee, elbow, ankle, wrist joints due to moving inflammation
Skin rash
Fever
Fatigue
Breathlessness
Fidgety, jerky movements
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7
Q

Primary prevention of ARF

A

Appropriate treatment of sore throats in high risk populations
Intramuscular penicillin or 10 day course oral penicillin

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8
Q

Secondary prevention of ARF

A

Continuous administration of antibiotics in those with recurrent ARF or RHD to prevent infection with GAS again

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9
Q

Primordial prevention of ARF

A

Social and environmental risk factors

Overcrowding, poor living conditions and other effects of poverty

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10
Q

RHD

A

Most often the mitral valve with mitral regurgitation
Fibrosis of leaflets and subvalvular structures
Valve leaflets become immobile
Eventually dilation of left ventricle leading to myocardial fibrosis and eventually ventricular dysfunction and cardiac failure
Mitral stenosis leads to atrial dilatation which can cause atrial fibrillation and thromboembolism

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11
Q

Main causes of CHD and stroke

A
High LDL
High saturated fat diet
High blood pressure
High BMI
HIgh salt and alcohol intake
High blood sugar
Smoking
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12
Q

Atherosclerosis

A

Disease affecting the inenrmost layer of large and medium sized arteries

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13
Q

Plaques

A

Deposits of fibrous tissue and lipids

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14
Q

Arteriosclerosis

A

General term for hardening or arteries of which atherosclerosis is a type

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15
Q

Four major positive risk factors for atherosclerosis

A

Hyperlipidaemia
Smoking
Hypertension
Diabetes mellitus

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16
Q

Four additional positive risk factors for atherosclerosis

A

Age
Family history
Obesity
Alcohol intake

17
Q

Three major negative risk factors for atherosclerosis

A

High HDL
Moderate alcohol consumption
Cardiovascular fitness

18
Q

4 stages of atherosclerosis

A

Endothelial cell injury
Leukocyte migration
Smooth muscle cell activation and migration
Lipoprotein infiltration

19
Q

Endothelial cell injury in atherosclerosis

A

Initiator of atherosclerosis

Caused by a comibination of hypertension, chemical insult and cytokines

20
Q

3 things endothelial cell injury leads to

A

Altered permeability
Adhesion of leukocytes
Activation of thrombosis

21
Q

Leukocyte migration in atherosclerosis

A

Acute inflammation - neutrophil invasion
Monocytes enter atherosclerotic lesion and mature into macrophages
Macrophages eat oxidised lipoproteins and turn into foam cells
Dead foam cells in the centre form a necrotic core, cholesterol crystals and calcifications

22
Q

Role of mast cells in atherosclerosis

A

Degrade protective HDL and promote smooth muscle cell and leukocyte migration into the plaque

23
Q

Smooth muscle cell activation and migration in atherosclerosis

A

Growth factors activate vascular smooth muscle cells
SMCs proliferate and migrate into the TI from the TM
Cytokines produced, leukocytes activated
Leukocytes take up lipids and produce specialised ECM proteins

24
Q

Lipoprotein infiltration in atherosclerosis

A

Become oxidised in plaques
Attract monocytes
Stimulate cells to release growth factors and cytokines
Cause dysfunction and apoptosis in SMCs, macrophages and endothelial cells

25
Q

3 consequences of atherosclerosis

A

MI
Peripheral vascular disease
Cerebrovascular disease

26
Q

Haemostasis

A

Physiological response of blood vessels to injury

Plugs leaks in injured vessels and sets them up for repair

27
Q

Endothelial cells in haemostasis

A

ECs normally inhibit haemostasis in healthy vessels and activate haemostais in injured vessels

28
Q

3 key substances endothelial cells secrete in healthy vessels

A

NO and prostacyclin to inhibit platelet activation

Antithrombin to bind and inactivate thrombin

29
Q

3 key substances endothelial cells secrete in damaged vessels

A

Endothelin for vasoconstriction
von Willebrand factor to promote platelet adhesion
Tissue factor which activates the coagulation cascade

30
Q

Activation of platelets

A

Extracellular matrix proteins, mostly collagen but also other connective tissue proteins

31
Q

Cooperation of haemostasis

A

Endothelial cells
Platelets
Clotting cascade

32
Q

3 chemical signals platelets secrete

A

Thromoxane A, vasoactive amines and ADP

All promote vasoconstriction and platelet aggregation

33
Q

Purpura

A

Bleeding from skin capillaries

34
Q

Coagulation

A

Cascade of proteolytic reactions through which inert circulation zymogens are sequentially activated

35
Q

Thrombin

A

Penultimate step in clotting cascade
Catalyses conversion of fibrinogen to fibrin
Activates platelets and catalyses several earlier steps in coagulation cascade (positive feedback loop)

36
Q

Fibrin

A

Strands form meshwork with fused platelets to form stable haemostatic plug

37
Q

Fibrinolytic system

A

Disassembles haemostatic plug when no longer needed