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Medicine 1 > Anatomy - Hypertension > Flashcards

Anatomy - Hypertension Flashcards

1
Q

What are the different things to remember in Darcy’s law of flow?

A
  • Flow = ‘delta’ pressure / resistance
  • ‘delta’ p = pressure gradient between arteries and veins, created by heart pumping
  • Resistance = measure of degree which blood vessel resists blood flow
  • Flow = directly related to pressure difference
  • Flow = inversely related to resistance
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2
Q

What is the equation for Poiseuille’s law of flow?

A
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3
Q

What effects does longer vessel, + viscosity and + radius have on flow?

A

Lower flow

Lower flow

Greater flow

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4
Q

What does the graph for relative flow against relative radius look like?

A
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5
Q

What is the resistance equation?

A
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6
Q

What are the properties of small arteries and arterioles?

A
    • ability to change radius
    • pressure change
  • Must decrease pressure before capillay entry
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7
Q

How do you calculate total peripheral resistance?

A

Arterial - venous pressure / cardiac output

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8
Q

What is laminar blood flow?

A

Largest velocity in the centre of blood vessel

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9
Q

What is the function of arterial compliance?

A

Provides filtering / smoothing

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10
Q

What is the function of venous compliance?

A

Provides capacity for storage (reservoir blood), which is reduced by constricting veins

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11
Q

What 4 things is venous return affected by?

A
  • Affected by venomotor tone (constriction)
  • Affected by venous valve competence
  • Affected by skeletal muscle pump –> leg muscle contraction squeezes blood from superficial vein to deep vein to heart
  • Affected by respiration –> inspiration decreases intra-thoracic pressure & increases intra-abdominal pressure hence provides a pressure gradient to assist blood flow to the heart
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12
Q

What are the 3 determinants of blood vessel radius?

A
  • Active tension exerted by smooth muscle
  • Passive elastic wall properties
  • Blood pressure inside of vessel
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13
Q

What does an increase in vessel radius lead to?

A
    • wall tensions
  • Aneurysm
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14
Q

What things does active control of vessel calibre allow?

A
  • Allows redistribution of blood flow
  • Allows control of pre/post capillary sphincters
  • Allows regulation of vascular tone and control of blood pressure
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15
Q

What is vascular tone?

A

Degree of constriction / dilatation

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16
Q

What does vasomotor tone refer to?

A

Arteries and arterioles

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17
Q

What does venomotor tone refer to?

A

Veins and venules

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18
Q

What factor causes vasoconstriction?

A

Noradrenaline:

  • Released from sympathetic
  • Binds to alpha receptors
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19
Q

What factor causes vasodilatation?

A

Noradrenaline:

  • Released by sympathetic
  • Binds to beta receptors in skeletal muscle
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20
Q

What effect do certain hormoenes have on smooth muscle vessel contraction?

A

Catecholamines:

  • Noradrenaline / adrenaline
  • Constrict / dilate

Peptides:

  • Vasopressin, angiotensin = constrict
  • Bradykinin = dilate
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21
Q

What intrinsic mechanisms affect vessel contraction/dilatation?

A
  • Endothelium-derived vasorelaxants (PGI2, NO, EDHF)
  • Endothelium-derived vasoconstrictors (endothelin)
  • Metabolites
  • Myogenic (autoregulation of blood-flow)
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22
Q

What effects do certain metabolites have on vessels?

A
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23
Q

What factors contribute to extrinsic control?

A
  • Nerves
  • Hormones
  • Regulate arterial bp
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24
Q

How is cerebral blood flow regulated?

A
  • 14% cardiac output at rest
  • Neural control = alpha vasoconstriction
  • Autoregulation resets during hypertension and abloshed by hypercapnia
  • H+, K+, adenosine, hypercapnia, hypoxia = vasodilatation
  • Mechanical = constrained in rigid cranium, influenced by VSF pressure
  • Medullary ischaemic reflex = special feature
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25
Q

How is coronary blood flow regulated?

A
  • 4% of cardiac output
  • Neural = secondary effect on flow due to cardiac function and metabolism changes
  • Sympathetic stimulation = B-mediated increase in HR and stroke volume, increasing oxygen consumption
  • Local = Hypoxia, hypercapnia, adenosine = vasodilation
  • Hormones = adrenaline
  • Mechanical = major influence on flow during cardiac cycle – peak flow = early diastole, 0/- at onset of systole
  • Special features = parallelism between metabolism and flow
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26
Q

How is skin blood flow regulated?

A
  • 4% cardiac output at rest in thermoneutral environment
  • Neural = arterioles = weak innervation, A-V anastomoses = dense innervation
  • Local = arterioles = myogenic autoregulation, AV anastomoses = no autoregulation and no reactive hyperaemia, endothelin = may be involved in pathological states, i.e. Raynauds
  • Hormones = angiotensin, vasopressin, noradrenaline, adrenaline = vasoconstriction
  • Special features = thermoregulation is primary function, sweat glands = sympathetic cholinergic innervation, causes vasodilation vie bradykinin release, i.e.
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27
Q

How is skeletal blood flow regulated?

A
  • 15% cardiac output at rest
  • Neural = rest – important alpha vasoconstriction, some beta vasodilatation, some sympathetic cholinergic vasodilatation – exercise – little neural influence, some beta vasodilation
  • Local = rest – neural control override autoregulatory mechanisms – exercise – local metabolites = major influence
  • Hormones = adrenaline at low concentrations = beta vasodilatation
  • Mechanical = muscle pumping
  • Special features = capacity to increase flow in exercise 20-fold, active hyperaemia, large increase in flow post-occlusion- reactive hyperaemia (increased blood flow)
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28
Q

How is splanchnic blood flow regulated?

A
  • Superior mesenteric = 10% cardiac output, hepatic = 25% cardiac output
  • Neural = intestinal: moderate a vasoconstriction, hepatic: important a venoconstriction
  • Local = intestinal: importantly influenced by local peptides, hepatic: portal vein - no autoregulation, hepatic artery - good autoregulation
  • Hormones = G-I hormones (gastrin, cholecystokinin) vasodilate; vasopressin, angiotensin constrict potently
  • Special features = intestinal circulation exhibits functional hyperaemia following feeding. Intense vasoconstriction can lead to damage and release of toxins à Vasoconstriction (neurohumoral) beneficial in baroreflex but can be detrimental in haemorrhage/septic shock
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29
Q

How is renal blood flow regulated?

A
  • 25% cardiac output
  • Neural = important a vasoconstriction; some b vasodilatation. Renin secreting cells have a sympathetic innervation (b adrenoceptors)
  • Local = good autoregulation of flow over a wide pressure range
  • Hormones = noradrenaline, adrenaline, angiotensin = constriction. Vasopressin = vasodilatation via prostaglandin/NO release. Dopamine = vasodilatation
  • Mechanical = renal capsule may restrict flow in pathological states
  • Special features = excretory function of kidney depends on (autoregulation). Vascular connections provide for capacity to regulate afferent/efferent resistances
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30
Q

How is pulmonary blood flow regulated?

A
  • 100% cardiac output
  • Neural = a vasoconstriction
  • Local = hypoxia causes vasoconstriction = augmented by hypercapnia - possibly mediated by endothelin. NO = dilatation - may be used therapeutically - Pulmonary hypertension: - possible therapeutic strategies include endothelin receptor antagonism and NO inhalation
  • Mechanical = flow is affected by changes in alveolar pressure and lung volume. Increase in flow = recruitment and distension of micro vessels = decrease in vascular resistance - If alveolar pressure > intravascular pressure, flow reduced. Lung inflation reduces resistance in extra-alveolar vessels (traction) and increases resistance in intra-alveolar vessels (compression)
  • Special features = thin walled vessels with low resistance, low vasoconstrictor capacity. Hydrostatic pressure (10mmHg) < colloid osmotic pressure (25mmHg) which favours reabsorption
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31
Q

How do you calculate mean blood pressure?

What is the reason for this?

A

diastolic bp + 1/3 pulse pressure

Spoends more time in diastole than systole

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32
Q

What are the 2 systolic bp determinants?

A
  • Stroke volume
  • Aortic elasticity (elastic absorbs energy from systole, so less elkastic = + bp)
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33
Q

What are the 3 diastolic bp determinants?

A
  • Peripheral resistance (+ = + bp)
  • Aortic elasticity (- = - bp as less energy to give back during diastole)
  • Heart rate (- = - bp because greater run-off time)
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34
Q

How do you calculate mean arterial bp?

A

Cardiac output X total peripheral resistance

35
Q

How is arterial blood pressure controlled?

A
  • Pressure sensors in circulation (baroreceptors in carotid sinus and aortic arch) –> afferent input
  • Integration systems in CNS –> efferent output
  • Effector mechanisms via ANS –> PNS and SNS activation supplying heart (NA on alpha 1/2 = vasoconstriction = + TPR)
36
Q

What are the order of events for the medulla integration systems in controlling arterial bp?

A
37
Q

What are the properties of the pressor area in arterial bp control?

A

Tonically active

Tonically inhibited by baroreceptors

38
Q

What are the properties of the depressor area in arterial bp control?

A

Not tonically active

Activated by increase in baroreceptor afferent nerve discharge

39
Q

What are the order of events when arterial bp decreases?

A
40
Q

What are the order of events when arterial bp increases?

A
41
Q

What happens to dbp and sbp upon standing from lying down?

A

DBP = increases

SBP = decreases

42
Q

What 3 things determine solvent movement across capillaries?

A

Diffusion

Filtration

Pinocytosis

43
Q

What are the 2 components of bulk flow?

A

Filtration

Reabsorption

44
Q

What is filtration favoured by?

A

Capillary hydrostatic pressure (Pc)

Interstitial fluid colloid osmotic pressure (πi)

45
Q

What is reabsorption favoured by?

A

Capillary colloid osmotic pressure (πc)

Interstitial fluid hydrostatic pressure (Pi)

46
Q

What are the properties of capillary hydrostatic pressure (Pc)?

A
  • Major determinant of fluid movement
  • Depends on:
    • pre/post capillary resistances
    • venous pressure
    • (arterial pressure)
  • If an arteriole constricts
    • increase pressure upstream
    • decrease pressure downstream
  • Precapillary constriction reduces Pc
47
Q

What are the properties of interstitial fluid colloid osmotic pressure (Pi)?

A
  • Normally minor determinant of fluid movement
  • Depends on the presence of protein in interstitium hence capillary permeability to protein - normally very low
48
Q

What are the properties of capillary colloid osmotic pressure (Pc)?

A
  • Major determinant of fluid movement
  • Depends upon:
    • synthesis/breakdown of protein (liver)
    • capillary permeability to protein
    • abnormal protein loss (kidney damage)
49
Q

What are the properties of interstitial fluid hydrostatic pressure (Pi)?

A
  • Normally minor determinant of fluid movement
  • Depends upon:
    • interstitial fluid volume
    • compliance of organ
    • effective drainage
  • Lymphatic system provides drainage
  • Lymphatic vessels are valved & highly permeable to protein
  • Lymph flow rate ~ 2-4 litres/day - returns excess filtered fluid and 95% of protein lost from vascular system back to the circulation (subclavian vein)
50
Q

What does right sided heart failure lead to?

A

Peripheral oedema

51
Q

What does left sided heart failure lead to?

A

Pulmonary oedema

52
Q

What factors affect capillary fluid transfer?

A

Capillary hydrostatic pressure (+Pc = + filtration)

Plasma colloid osmotic pressure (+πc = + reabsorption)

53
Q

What are some causes of secondary hypertension?

A
  • Renal disease
  • Renovascular disease
  • Conn’s syndrome
  • Cushing’s syndrome
  • Hyperthyroidism
  • Phaeochromocytoma
  • Pregnancy
  • Drugs (e.g. NSAIDs, corticosteroids, sympathomimetics)
54
Q

What are the goals of hypertension treatment?

A
  • Reduction in cardiovascular damage.
  • Preservation of renal function.
  • Limitation or reversal of left ventricular hypertrophy.
  • Prevention of Ischaemic Heart Disease.
  • Reduction in mortality due to stroke and myocardial infarction
  • Get systolic < 140 mmHg
  • Get diastolic < 90 mmHg
55
Q

How do you calculate blood pressure?

A

Cardiac output X total peripheral resistance

56
Q

How do ACEIs work and their contraindications?

A

Aldosterone = water retaining and sodium retaining (cough from + bradykinin)

ACEIs = prevent aldosterone production by inhibiting angiotensin ii

Contraindication = renal artery stenosis as + decrease in BP, can be fatal

57
Q

How do AT1 receptor antagonists work?

A

Block angiotensin 2 at angiotensin 1 receptor

Less likely to give rise to a cough

58
Q

How do calcium channel inhibitors work and their contraindications?

A

Reduce bp and cause vasodilatation

Rate-limiting = + cardiac tissue effect

Contraindication with heart failure as they worsen it - DHPs = + favourable, + action on vascular smooth muscle

59
Q

How do diuretics work and their side effects?

A

Inhibit na+/cl- transporter, prevent reabsorption so ions excreted, followed by water

Circulating volume reduced

Side effects = hypokalaemia, postural hypotension, impaired glucose control

60
Q

What are the properties of alpha blockers?

A

Block alpha adrenoceptors

Reduce bp

Used as last resort as side effects poorly tolerated

61
Q

How do beta-blockers work and their contraindications?

A

Reduce renin release

Reduce sympathetic drive to heart and reduce cardiac output

Contraindicated = asthma, used with caution in COPD

62
Q

What is apoptosis?

A

Intracellular mechanism

63
Q

What are the treatment guidelines for hypertension + type 2 diabetes, <55 + non-black and >55 or black?

A
64
Q

What is necrosis and the different types?

A

Extracellular mechanism

Coagulative, liquefactive, caseous, fat and fibrinoid necrosis - infarction (ischaemic necrosis), gangrene (ischaemic necrosis with some putrefaction)

65
Q

What is infarction?

A

An area of ischemic necrosis due to abrupt cessation of the arterial supply (‘arterial infarction’) or venous drainage (‘venous infarction’)

66
Q

What factors affect infarction development?

A
  • Vascular occlusion
  • Nature of vascular supply
  • Rate of occlusion development
  • Type of tissue (have different vulnerabilities to hypoxia à neurons = 2-3mins, myocardium = 20-40 mins, fibroblast = many hours)
67
Q

How do you characterise infarctions based on their colour?

A
  • Based on amount of haemorrhage
  • Pale or white infarct (A): solid organs such as heart & spleen
  • Red or haemorrhagic infarct (V): in loose spongy tissue rich in blood supply or has dual blood supply such as lung
68
Q

What are the 2 origins of causes of infarction?

A

Arterial

Venous

69
Q

What are the two types of infarction infection?

A
  • Septic: causes by septic emboli such as vegetation of SBE
  • Bland: caused by aseptic emboli or thrombi. Most common
70
Q

What is the morphology of infarction?

A
  • Infarct is usually wedge shaped with occluded artery at apex and base at periphery (if serosa- fibrinous exudate)
  • Margins: early poorly defined slightly haemorrhagic but later well defined
  • Inflammatory response followed by reparative response - finally scar tissue
71
Q

What are the causes of arterial infaction?

A
  • Occlusion by EMBOLUS
  • Occlusion by ATHEROMA + THROMBOSIS
  • Occlusion by ATHEROMA WITH PLAQUE FISSURE
  • Occlusion by ATHEROMA ALONE
  • Other cases: arterial spasm or arterial trauma
72
Q

What are the stages of infarction (timeline)?

A
  • 0-12 hours - early stages of cell death
  • 12 - 24 hours - necrotic muscle fibres apparent microscopically
  • 24 - 72 hours - acute inflammatory reaction to dead muscle
  • 3 - 14 days - macrophagic removal of debris and vascular granulation tissue formation
  • 14 - 21 days - fibrous granulation tissue formation
  • 21 - 56 days - scar formation and cicatrisation
73
Q

What are the early complications of arterial infarction?

A
  • Sudden death due to cardiac dysrhythmia
  • Sudden death due to acute left ventricular failure
  • Rupture of myocardium -> haemopericardium
  • Rupture of papillary muscle -> acute valve failure->LVF
  • Mural thrombus on infarct -> embolism -> stroke & others
  • Fibrinous Pericarditis & extension of MI
74
Q

What are the late complications of arterial infarction?

A
  • Chronic LVF
  • Ventricular aneurysm
75
Q

What are the properties of a renal infarct?

A
  • Usually due to emboli from L side of heart
  • Wedge-shaped
  • Pale area with hyperaemia around
  • Heals by scar formation
76
Q

What are the properties of cerebral infarct?

A

Causes are:

  • Atherothrombotic in extra-cerebral arteries
  • Embolic
  • Watershed (Border zone) infarct: hypoperfusion & microembolisms
77
Q

What is this and how does it heal?

A

Liquefaction necrosis

Heals by astrocytic gliosis

78
Q

What are the properties of gangrene?

A
  • Type of necrosis caused by vascular insufficiency following injury or infection
  • Infarction of extremities or bowel
  • Foot and leg most common. Often in diabetics
  • Only solution is amputation
  • Types = dry, wet or gas
79
Q

What are the 2 causes of gangrene?

A
  • Thrombus occluding atheromatous ilio-femoral artery
  • Thromboembolism from left side of heart
80
Q

What are the properties of venous infarction?

A
  • Can occur when the entire venous drainage from an organ or tissue is, and remains, completely obstructed.
  • Three common examples:
    • Bowel infarction e.g. volvulus, hernial strangulation.
    • Testis infarction, due to torsion.
    • Ovarian infarction, due to torsion.
81
Q

What are the events of venous infarction?

A
  • Veins become obstructed, usually by extrinsic pressure
  • Tissues become congested with blood, venules and capillaries being engorged with blood which cannot escape
  • Pressure in capillaries and venules rises so high that:
    • Many of them rupture, with leakage of blood
    • Arterial blood cannot enter, so hypoxia ensues
  • Tissues become congested, hypoxic and necrotic
82
Q

What is this?

A

Volvulus

  • Colon has twisted on its vascular pedicel
  • Venous outflow obstructed
  • Venous infarction ensued
83
Q

What is this?

A

Venous infarction - torsion of testes

  • Twisted spermatic cord
  • Plexus of veins are compressed
  • Blood cannot drain out of tested or epididymis
  • Venous infarction occurs

Medicine 1 (28 decks)

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