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Year 1 - Cardiovascular (DP) > Cardiovascular Risk Factors > Flashcards

Cardiovascular Risk Factors Flashcards

0
Q

Which is more common, primary or secondary hypertension?

A

Primary (~90% of cases)

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1
Q

How is hypertension diagnosed?

A

Clinic BP is 140/90 or higher
- Take a second measurement
Ambulatory BP is 135/85 or higher
- Hypertension confirmed

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2
Q

What are some secondary causes of hypertension?

A

Renal/Endocrine/Aortic disease
Renal artery stenosis
Drug therapy

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3
Q

How does renal artery stenosis cause hypertension?

A

Decreased renal blood flow
Excess renin secretion
Huge sodium and water retention - plasma volume increases

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4
Q

What is Conn’s syndrome?

A

Excess aldosterone

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5
Q

What is Cushing’s syndrome and how does it present?

A

Excess corticosteroid

Weight gain, rounded face etc

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6
Q

What can hypertension lead to?

A

LVH
CCF
Atheroma
Aneurysm rupture (Berry aneurysm - subarachnoid haemorrhage - thunderclap headache)

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7
Q

What is pre-eclampsia?

A

Hypertension and proteinuria in pregnancy

Resolves after birth

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8
Q

What can result due to cardiac Ischaemia?

A

Angina
Infarct
Cardiac failure

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9
Q

How is the heart affected when fibrosis occurs?

A

Loses elasticity

Decreased EDV and hence decreased SV

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10
Q

What can occur if the carotid arteries become stenosed?

A

TIAs
CVAs
Vascular dementia

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11
Q

What can cause an aneurysm can form?

A 
Congenital causes
Syphilis
Mycotic - bacterial infection of artery wall
Iatrogenic
Copper deficiency
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12
Q

What is the difference between a true aneurysm and a pseudoaneurysm?

A

True aneurysm
- Involves all three layers of arterial wall
Pseudo
- Blood leaking completely out of artery into surrounding tissues

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13
Q

What is an arterial dissection?

A

Tunica media split by blood

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14
Q

What colour is an arterial thrombus?

A

White - mainly platelets in fibrin mesh

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15
Q

What colour is a venous thrombus?

A

Red

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16
Q

What happens in the coagulation cascade?

A

Factor X — Factor Xa

Factor Xa stimulates Prothrombin (II) — Thrombin (IIa)

Thrombin stimulates Fibrinogen (soluble) — Fibrin (insoluble)

Fibrinogen and Thrombin cause platelet aggregation

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17
Q

Why is and what form is vitamin K required for coagulation?

A 
Used in production of carboxylase enzyme
Reduced form (Hydroquinone)
18
Q

What reaction does carboxylase enzyme mediate?

A

Activation of precursors (II, VII, IX and X) to gamma-carboxyglutamic acid residues (serine proteases)

19
Q

How does warfarin work?

A

Prevents reduction of Vitamin K back to hydroquinone by competing for vitamin k reductase

20
Q

What does Antithrombin III do?

A

Neutralises serine proteases

21
Q

How does heparin work?

A

Binds to ATIII

Increases its affinity for serine proteases (esp IIa and Xa)

22
Q

How do low molecular weight heparins work?

A

Inhibit factor Xa

23
Q

Heparin or LMWH; when is each preferred?

A

Heparin
- Renal failure since LMWH is excreted by the kidneys
LMWH
- In outpatient treatment as it can be given subcutaneously
- Huge PE due to more predictable pharmacokinetics

24
Q

What chemicals cause platelet aggregation and how?

A 
ADP
5-hydroxytryptamine (5-HT)
Thromboxane A2 (TXA2)

Cause expression of GPIIb/IIIa receptors - cross link platelets via fibrinogen

25
Q

How does aspirin work?

A

Blocks COX-1 irreversibly
Prevents TXA2 synthesis
Less GPIIb/IIIa expression
Less cross linking

26
Q

How does tirofiban work?

A

Blocks the GPIIb/IIIa receptors

Prevents fibrinogen cross-linking of platelets

27
Q

How does clopidogrel work?

A

Blocks P2Y12 receptor irreversibly
ADP cannot bind to and activate receptor
Decreased GPIIb/IIIa expression
Less cross linking

28
Q

How does plasminogen work?

A

Converted to plasmin
Promotes conversion of fibrin to fibrin fragments
Clot lysis

29
Q

What does streptokinase act as and how?

A

A fibrinolytic extracted from streptococci

Stimulates conversion of plasminogen to plasmin

30
Q

What patients is streptokinase not suitable in?

A

Patients with strep infection

Patients who have received it for longer than 4 days - antibodies produced

31
Q

Give examples of tPAs and explain how they work?

A

Alteplase and Duteplase
Convert fibrin-bound plasminogen to plasmin
- Selective for clots

32
Q

How can fibrinolytic drug overdose be treated?

A

Tranexamic acid

Inhibits plasmin production

33
Q

What are some special adaptations of the coronary circulation?

A

High capillary density
High basal blood flow
High oxygen extraction into tissues

34
Q

What effect does decreased PaO2 have on coronary arteries?

A

Vasodilation

35
Q

What effect does adenosine have on coronary arteries?

A

Vasodilation

36
Q

The coronary arteries are supplied by sympathetic nerves, why don’t they vasoconstrict?

A

Over-ridden by metabolic hyperaemia - functional sympatholysis
Adrenaline activates Beta2 receptors - vasodilation

37
Q

What happens to coronary flow if diastole is shortened?

A

Decreased coronary flow

38
Q

What do the internal carotids and vertebral arteries combine to form?

A

Basilar artery

39
Q

What is the circle of Willis?

A

An anastomosis of the basilar artery and internal carotid arteries
- Maintains perfusion if one carotid occluded

40
Q

Between what BPs can autoregulation protect the brain against MAP changes?

A

60-160

41
Q

What happens if intracranial pressure increases?

A

Decreased cerebral perfusion pressure

Decreased blood flow

42
Q

Why, in hypoxia, do pulmonary arteries vasoconstrict instead of dilate like everywhere else in the body?

A

To divert blood away from poorly oxygenated alveoli

- Blood taken to areas rich in oxygen to maintain gas exchange

43
Q

Why does skeletal muscle blood flow increase during exercise?

A

Local hyperaemia overcomes SNS vasoconstrictor tone
Adrenaline - Beta2 receptors - Vasodilation
Increased cardiac output - increased blood flow

Year 1 - Cardiovascular (DP) (6 decks)

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