P12- Hypertension, thrombosis, embolism , Infarction Flashcards

1
Q

what is systole?

A

left ventricular contraction

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2
Q

what is diastole?

A

left ventricular relaxation

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3
Q

what is blood pressure?

A

cardiac output x peripheral resistance

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4
Q

what contributes to cardiac output?

A
  • heart rate
  • contractility
  • blood volume
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5
Q

Name peripheral resistance constrictors.

A

Angiotensin II , Catecholamines

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6
Q

Name peripheral resistance dilators.

A

Nitric oxide,

Prostaglandins

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7
Q

what is hypertension?

A

‘a disorder in which the level of sustained arterial pressure is higher than expected for the age, sex, and race of the individual’

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8
Q

what is hypertension synonymous with?

A

systemic arterial hypertension

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9
Q

what is high blood pressure ?

A

blood pressure of >140/90 mmHg consistently

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10
Q

Does hypertension affect ages specifically?

A
  • NB age

- Children, adolescent, adult, 3rd decade

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11
Q

what is normal variation of hypertension?

A

Normal variation in individuals at different times of day- lowest levels during sleep

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12
Q

when does BP increase?

A

BP increases on standing up, on exercise and on exposure to cold and emotion

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13
Q

who is at risk of permanent hypertension -labile hypertension?

A

Individuals with a larger than normal pressure rise in response to these stimuli

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14
Q

How is hypertension monitored?

A

24 hr

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15
Q

what are the 2 types of classifications of hypertension?

A
  • according to cause (Aetiological)

- according to consequences (Clinicopathological)

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16
Q

what are the 2 types of “according to cause” hypertension?

A
  • primary

- secondary

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17
Q

what are the 2 types of “according to consequences” hypertension?

A
  • benign

- malignant

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18
Q

what are 95% of cases?

A

no detectable cause- “primary” or “essential” hypertension

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19
Q

Give some causes of primary hypertension?

A
  • Interplay of genetic and environmental factors

* Race, Stress, diet (salt, animal fats), alocohol intake, intrauterine life, exercise

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20
Q

what is secondary hypertension?

A

renal disease, endocrine disorders, aortic disease (Coarcta(on of the aorta ‐ congenital narrowing of segments of the aorta)

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21
Q

what are endocrine causes of hypertension?

A
  • Adrenal gland hyperfunction / tumours
  • Conn’s syndrome - excess Aldosterone
  • Cushing’s syndrome - excess corticosteroid
  • Phaeochromocytoma - excess noradrenaline
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22
Q

what is prognosis of patients with hypertension is related to?

A

height and rate of pressure rise

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23
Q

what is benign hypertension?

A

prognosis is measured in decades

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24
Q

what is malignant hypertension?

A

accelerated form fatal within 2 yrs if untreated

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25
Q

what can benign hypertension cause?

A
  • Iscahemic Heart disease
  • Heart Failure
  • Stroke
  • Acceleration of Renal Disease
  • Malignant Hypertension
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26
Q

what are the symptoms of hypertension?

A

usually asymptomatic

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27
Q

How is bonging hypertension often detected ?

A
  • Often detected in middle age during routine checkup

* BP rises slowly over many years

28
Q

what does benign hypertension affect?

A
  • Affects heart and arteries of all sizes

* Main target organs are heart, brain and kidneys

29
Q

what is the most common complication of benign hypertension?

A

Ischaemic heart disease is most common complication (insufficient blood supply to the myocardium to meet functional demand)

30
Q

what effect does benign hypertension have on the cardiovascular system?

A
  • Increased pressure causes hypertrophy of the arteries and heart
  • Resistance arteries have thicker walls and more narrow lumina
  • Longstanding hypertension aggravates atherosclerosis and contributes to development and rupture of aneurysms and dissections
31
Q

what effect does benign hypertension have on the heart?

A
  • Left ventricular hypertrophy impairs diastolic function
  • Increased muscle mass and interstitial fibrosis
  • Poorer coronary artery perfusion
  • If coronary atherosclerosis, increased oxygen demand of hypertrophied ventricle contributes to ischaemia, even at rest
  • Leads to cardiac arrhythmias and myocardial infarct
32
Q

what effect does benign hypertension have on the brain?

A
  • Hypertension cause microaneurysms in arteries supplying basal ganglia, pons, cerebellum
  • Rupture leads to hypertensive cerebral haemorrhages
  • Also predisposes to cerebral infarction
33
Q

what can occur in a subarachnoid haemorrhage?

A

rupture of berry aneurysm

34
Q

what effect does benign hypertension have on the kidney?

A

Hypertension aggravates many renal diseases but only in severe cases does it cause renal failure

35
Q

what are the values for benign hypertension?

A
  • Every 10mmHg of diastolic pressure above 85 doubles risk of MI
  • Every 8mmHg of diastolic pressure above 85 doubles risk of stroke
36
Q

what is malignant hypertension?

A
  • Serious life-threatening condition
  • Diastolic pressure >130 mmHg
    • Retinal changes of bilateral flame-shaped haemorrhages and /or papilloedema (swelling of optic nerve)
  • Can develop from either benign primary or secondary hypertension (most common), or arise de-novo
  • Usually younger people with hypertension 30-40yrs
  • Needs urgent treatment to prevent death
37
Q

what can malignant hypertensions cause?

A
  • Causes cerebral oedema - seen as papilloedema (swelling of optic disc)
  • Acute heart failure
  • Stroke
  • Acute renal failure
  • Blood vessels show fibrinoid necrosis and endarteritis proliferans of their walls
38
Q

what are the conclusions of hypertension?

A
  • Hypertension is very common
  • It is usually asymptomatic
  • It may be due to an underlying disease
  • It requires treatment to prevent complications and death
  • It affects the physiology of several organs
39
Q

what is blood clotting?

A

Solid mass of blood constituents EXTERNAL to the blood vessel

40
Q

what is blood clotting a defence mechanisms against?

A

haemorrhage

41
Q

what is blood clotting important in?

A

trauma and surgery /anaesthetics

42
Q

what is a thrombus?

A

Solid mass of blood constituents formed WITHIN the blood vessel

43
Q

where does thrombus occur?

A

Thrombosis occurs most commonly in veins but can occur in arteries

44
Q

what is the risk of thrombosis increased by?

A

‘Virchows triad”

45
Q

what is the Virchows triad?

A
  1. Injury to the VESSEL WALL
  2. Alterations in BLOOD FLOW
  3. Alterations in blood constituents that increase coagulability
46
Q

what effect does Virchows triad have on vessels?

A
  • loss of endothelial surface

- inflammation

47
Q

what effect does Virchows triad have on flow?

A
  • stasis

- turbulence

48
Q

what effect does Virchows triad have on constituents?

A
  • platelets
  • coagulation proteins
  • viscosity
49
Q

what is involved in thrombus formation?

A
  • platelets
  • coagulation cascade
  • fibrinolytic cascade
50
Q

Describe the formation of a platelet rich thrombus?

A
  • In rapidly flowing blood, vascular injury results in formation of platelet-rich thrombus which grows by gradual build up of activated platelets and fibrin (white/pale thrombus)
  • Platelets stick to endothelium and become activated
  • Coagulation cascade generates fibrin strands
  • Thrombus occludes the vessel, blood flow slows and red blood cells can adhere to the surface of the thrombus (red thrombus)
  • Further thrombosis both sides of blockage due to altered flow -propagation
51
Q

what is the fate of thrombus?

A
  • Can be lysed by anticlotting factors
  • Larger thrombi on vessel wall can reorganise- infiltartion of macrophages and endothelial cells, recanalise, restore blood flow
  • Some may become detached from vessel wall and move in blood flow to impact downstream (embolism)
52
Q

what is an embolus?

A

Abnormal material carried in the blood which may block downstream vessels, depending on the size and nature of the material

53
Q

what do large emboli result in?

A

infarction of the tissue in which the material impacts, eg brain‐stroke

54
Q

Name the major types of embolism.

A
  • THROMBOEMBOLISM
  • Arterial side , heart to brain and kidney
  • Venous side, pulmonary circulation
  • ATHEROEMBOLISM (cholesterol crystals)
  • FAT EMBOLISM
  • AIR EMBOLISM
  • TUMOUR EMBOLISM
  • SEPTIC EMBOLISM
  • AMNIOTIC FLUID
55
Q

what happens in deep vein thrombosis?

A
  • post op
  • bed bound
  • travel
  • unilateral leg swelling
  • oedema
  • pain
56
Q

what happens in pulmonary thromboembolism?

A
  • sudden onset
  • potentially life threatening
  • haemoptysis
  • breathlessness
  • cardiovascular collapse and shock
  • cardiac arrest
57
Q

what is infarction?

A

Zonal necrosis due to sudden occlusion of blood supply:

  • anatomy of blood supply is important
  • atheroma
  • embolism
58
Q

what is necrosis due to?

A

lack of oxygen and nutrient

59
Q

How is susceptibility to necrosis varied?

A

different tissues have different susceptibility

60
Q

what can an infarction be?

A

fatal

61
Q

what is a myocardial infarct?

A

Death of myocardial tissue caused by ischaemia (reduction or cessation of blood flow), such that oxygen delivery is not adequate to meet metabolic demands of cells

62
Q

Is ischaemia reversible?

A

initially reversible - stable angina

63
Q

what does persistent ischaemia lead to?

A

structural changes then death of myocytes

64
Q

what are most infarcts due to?

A

thrombosis over atherosclerotic plaque

65
Q

what do complications of myocardial infarct include?

A
  • Arrhythmias
  • Cardiogenic Shock
  • Cardiac rupture
  • Ventricular septal defects
  • Heart Failure
66
Q

what can re-perfusion result in?

A

injury to cells not previously affected

67
Q

What is re-perfusion injuring due to?

A

Due to toxic oxygen species that are over-produced on restoration of blood supply