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103: Theme 3 > How the CVS fails > Flashcards

How the CVS fails Flashcards

1
Q

Stroke

A

Rapid loss of brain function due to loss of perfusion to parts of the brain

Cerebrovascular accident

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2
Q

Haemorrhagic stroke

A

Cerebral blood vessel rupture

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3
Q

Ischaemic stroke

A

Cerbebral blood vessel blockage

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4
Q

Causes of BV burst

A

Stresses

  • high pressure
  • large diameter/ high wall tension
  • low elasticity/ low compliance
  • turbulent flow

Damage

  • trauma
  • atherosclerosis
  • diabetes
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5
Q

Vessel wall tension

A

Tension in a cylinder is the force trying to rip the wall apart
Proportional to P x radius
Larger the vessel, greater the wall tension

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6
Q

Compliance

A

The change in volume caused by a change in pressure

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7
Q

Causes of turbulent flow

A 
Junctions
Mixing
Obstacles 
- atherosclerosis
- endothelial damage
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8
Q

Endothelium activities (6)

A

Blood vessel tone: local control of perfusion, vasodilation
Fluid filtration: blood brain barrier, CSF, kidney, GI secretions
Haemostasis: esp fibrinolysis
White cell recruitment: atherosclerosis
Angiogenesis
Hormone trafficking

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9
Q

Transcytosis

A

The transport of molecules across the cytoplasm, especially the epithelium

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10
Q

Acute myocardial infacrtion

A

Region of heart tissue is dead or dying
Usually caused by blocked coronary artery
Reduces the capacity of the heart to pump

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11
Q

Atherosclerosis

A

A disease process resulting in furring of the arteries

Asymptomatic but can lead to other disorders

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12
Q

Coronary artery disease

A

A disease process resulting in obstruction of the arteries supplying heart tissue

Angina or asymptomatic

Primary causes is atherosclerosis

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13
Q

Treatment for coronary artery disease

A

Drugs for hyperlipidaemia, angina or hypertension

Stenting or surgically replacing clogged vessels

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14
Q

Plaque rupture

A

When the fibrous cap of a plaque bursts open

Can cause a thrombus or and embolism

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15
Q

MI: sympathetic activity

A

Sympathetic nervous system releases adrenaline and noradrenaline
- response to pain and haemodynamic abnormalities

In heart failure leads to:

  • increased HR
  • increased contractility
  • increased PR
  • increased risk of arrhythmia
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16
Q

Forces on H2O in capillaries

A

Arterial end:

  • low osmotic pressure
  • high hydrostatic pressure
  • net movement into lymphatic system

Venous end

  • high osmotic pressure
  • low hydrostatic pressure
  • net movement into capillaries
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17
Q

Pulmonary oedema

A

Fluid accumulation in lungs so impaired gas exchange as O2 diffusion is lengthened

Caused by left heart failure

Symptoms:

  • dyspnoea, orthopnoea
  • hypoxia
18
Q

Ascites

A

Accumulation of fluid in the peritoneal cavity

Many causes including heart failure

19
Q

Peripheral oedema

A

Swelling of tissues, esp ankles

Many causes, esp chronic low output heart failure

20
Q

Compensation

A

Maintaining homeostasis of a physiological function despite stresses or malfunctions

21
Q

Decompensated heart failure

A

Medical emergency
The failure of the heart to maintain adequate blood circulation after long standing vascular disease
Respiratory distress
Kidneys increase plasma volume to compensate for poor perfusion of renal tissue, leads to fluid overload

22
Q

Cardiac remodelling

A

Growth of cardiac muscle

Caused by injury:

  • MI
  • hypertension
  • valve disease

Results in hypertrophy or dilation

23
Q

Ventricular hypertrophy

A

Response to work
Athlete’s heart
Eccentric: dilate due too volume overload
Concentric: thicken due to pressure overload

24
Q

Antidiuretic hormone

A 
Also called vasopressin
Causes kidneys to reabsorb more water
Decreases diuresis
From posterior pituitary
Peptide
25
Q

Aldosterone

A

Causes kidneys to reabsorb more NaCl
Directly decreases natriuresis which decreases diuresis
From adrenal cortex
Steroid

26
Q

Natriuresis

A

Loss of sodium to the urin

27
Q

Diuresis

A

Loss of water to the urine

28
Q

Angiotensin II

A

Increases pressure
Vasoconstriction
Increased fluid retention
- increases aldosterone secretion by adrenal cortex
- increases ADH secretion by posterior pituitary

Contributes to ventricular hypertrophy and remodelling

29
Q

Angiotensin I

A

Precursor of angiotensin II

Decapeptide

30
Q

Angiotensin converting enzyme

A

The enzyme that converts inactive Ang I into vasoactive Ang II
Secreted by the kidneys and lungs

31
Q

Renin- angiotensin- aldosterone system

A

Angiotensinogen converted to Ang I with renin enzyme
Ang I converted to Ang II with ACE
ACE causes an increase in aldosterone secretion by adrenal cortex

32
Q

Thiazide and thiazide like diuretics

A

E.g. indapamide

Blocks reabsorption at the distal convoluted tube

33
Q

Loop diuretics

A

E.g. furosemide

Blocks reabsorption in the thick loop

34
Q

K+ sparing diuretics

A

E.g. spironolactone

Inhibits aldosterone receptors in cortical collecting duct

35
Q

Chronic low output heart failure

A

Cardiac output is low, usually due to accumulated damage to the heart
Chronic condition with poor 5 year survival rate

36
Q

Left heart failure

A

Respiratory symptoms

Right heart pumps into lungs but left atrium is too full
Increased hydrostatic pressure in pulmonary circulation

37
Q

Right heart failure

A

Systemic symptoms

Increased central venous pressure
Can lead to peripheral oedema

38
Q

Heart failure symptoms and signs

A 
Fatigue especially during exertion
Peripheral oedema
Dyspnoea
- orthopnoea
- paroxysmal nocturnal dyspnoea
39
Q

Cardiogenic shock

A

Critically low perfusion due to low cardiac output
Medical emergency
Progresses by positive feeback

40
Q

Chronic heart failure treatments

A

ACE inhibitors
Diuretics
Beta blockers

41
Q

Fluid overload

A 
Pathological state where there is too much fluid in the blood 
Symptoms:
- peripheral oedema
- ascites
- pulmonary dyspnoea
- increased central venous pressure

103: Theme 3 (17 decks)

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