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Cardiovascular System > Hypertension pharmacology > Flashcards

Hypertension pharmacology Flashcards

1
Q

3 key factors determining blood movement

A

Flow - determined by change in pressure and resistance to flow
Pressure - generated by heart
Reisstance

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2
Q

How to calculate flow

A

Change in P / R

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3
Q

What does resistance depend on?

A
  • Blood viscocity: thicker the blood, higher resistance to flow, e.g. increase in count (haematocrit), LDL - cholesterol or dehydrated
  • Vessel length (L): longer the vessel, higher the resistance to flow. Unlikely to change in adult
  • Vessel radius (r): narrow vessel = higher resistance to flow. Most important variable
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4
Q

How to calculate resistance

A

(viscosity x length) / (radius ^ 4)

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5
Q

What does cardiovascular system do?

A

Delivers oxygen and nutrients
Distributes hormones, fluids, electrolytes
Immune system
Thermoregulation

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6
Q

Characteristics of the pulmonary circuit

A

Relatively short, simple and operates at lower pressure than systemic

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7
Q

Where is blood regulation specialised?

A

Coronary, skeletal muscle, skin, cerebral, renal, GI, hepatic

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8
Q

What is the portal system?

A

From one capillary bed to another without passing through the heart

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9
Q

Why does pulmonary circuit have lower resistance?

A

Lower pressure too, fewer small vessels

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10
Q

Cardiac output, pulmonary vs systemic

A

Equal

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11
Q

Resistance, pulmonary vs systemic

A

Pulmonary is lower

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12
Q

Pressure in pulmonary vs systemic

A

Pulmonary is lower

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13
Q

How to diagnose hypertension

A
  • Measure BP in both arms - if the difference is more than 15mmHg repeat measurements
  • If difference remains higher, measure BPs in arm with higher reading
  • If BP is 140/90 mmHg or higher, take second measurement, if this is v
  • If BP is between 140/90 and 180/120 offer BP monitoring to confirm hypertension
  • Whilst waiting, carry out investigations for target organ damage and assessment of cardiovascular risk
  • When using ABPM to confirm hypertension ensure 2 measurements are taken per hour
  • When using HBPM to confirm hypertension, ensure that for each BP recording, 2 consecutive measurements are taken, at least 1 minute apart with the person seated, BP is recorded twice daily (morning and evening) and BP monitoring continues for 4 days
  • Confirm diagnosis with clinic BP of 140/90 or higher and ABPM daytime average or HBPM average of 135/85 or higher
  • If hypertension not diagnosed, measure BP every 5 years and measure more frequently if clinic BP is close to 140/90
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14
Q

What is the dicrotic notch?

A

After blood forced into aorta, increasing pressure closes aortic valve and increase pressure

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15
Q

What re the capacitance vessels?

A

Veins

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16
Q

How to calculate mean arterial blood pressure

A

Cardiac output x total peripheral resistance

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17
Q

Neurological regulation of BP

A
  • Autonomic NS
  • Short-term regulation
  • Influences cardiac output and vascular resistance
  • Signals to SAN
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18
Q

Humoral regulation of BO

A
  • Aldosterone, adrenaline, ADH, atrial natriuretic peptide, angiotensin ii
  • Short and long term regulation
  • Influences vascular resistance and blood volume
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19
Q

Arterial baroreceptors

A
  • Located in aortic arch and carotid sinus
  • Mechanoreceptors - stretch in wall
  • Aortic depressor nerve is branch of vagus nerve
  • Monitor arterial BP
  • Input to cardiovascular centre in medulla oblongata
  • Output is autonomic nervous system response
  • Rapid, short-term control of BP
  • Continually send nerve impulses to cardiovascular centre in medulla
  • Frequency at which they fire nerve impulses to CV centre is dependent on arterial BP
  • Always firing - always muscle tone
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20
Q

How do baroreceptors regulate BP?

A
  • Rapid response to short-term changes in MABP
  • Arterial baroreceptors sense changes in MABP according to stretch of artery walls in aortic arch and carotid sinus
  • Firing rate of APs along afferent glossopharyngeal and vagus nerves increases or decreases relative to arterial wall stretch
    • Sensory information received by medullary cardiovascular centre in medulla oblongata
  • Afferent AP frequency into CV centre from baroreceptors determines rate at which APs are sent along efferent neural pathways
  • Vagus nerve (parasympathetic, efferent) neurons to heart - altered heart rate and consequent CO, increases PS output to SAN
  • No parasympathetic to vascular smooth muscle
  • Sympathetic neurons to heart, arterioles and veins - altered HR, CO and vasoconstriction/dilation,
  • A1 interaction = vasodilation (SVR decreases) = vascular smooth muscle, sympathetic
  • Decrease B1 receptors = reduced CO
  • Carotid through glossopharyngeal
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21
Q

What does aldosterone do?

A

released from adrenal cortex in response to decreased blood volume, increases Na+ and water reabsorption from kidneys = higher BP

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22
Q

What does ADH do?§

A

released from posterior pituitary in response to increased blood osmolality, increases water reabsorption from kidneys and vasoconstriction, short term effector = higher BP

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23
Q

What does RAAS do?

A

long term response to decreased body fluid volume, loss of both water and salt resulting in no change in osmolality

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24
Q

What do type A and B natriuretic peptides do?

A

released in response to high volume load (stretch) on atria and ventricles, increases water and Na+ excreted from kidneys = decreased BP

25
Q

What does adrenaline do?

A

released from adrenal medulla in response to sympathetic nerve simulation (fight or flight response), actions on vascular smooth muscle depends on adrenergic receptors

26
Q

Examples of A1 receptors and what they do

A

GPCRs - G-alpha-Q, IP3, DAG, PKC increase Ca2+ in smooth muscle - vasoconstriction

27
Q

What do B2 receptors do and example

A

GPCRS - G-alpha-S, adenylate cyclase, cAMP

28
Q

Where does adrenaline normally act when does this change?

A

Normally B2 but when delivered in high amounts can do A1

29
Q

Characteristics of A1

A

Vasoconstriction
Higher density in body
++ adrenaline
+++ nor-adrenaline

30
Q

Characteristics of B2

A

Vasodilation
Higher density in skeletal and cardiac muscle
+++ adrenaline
+ nor adrenaline

31
Q

What does angiotensin ii do?

A

Vasoconstructor activated by angiotensin converting enzyme (ACE) within blood vessels

32
Q

Three layers of blood vessels and characteristics

A
  • Tunica intima/interna: innermost, endothelial cells, basement membrane, connective tissue
  • Tunica media: middle, internal and external elastic lamina, smooth muscle cells, elastin and collagen
  • Tunica externa/adventitia: outer, connective tissue, nerves, blood vessels, collagen and elastin, has sympathetic nerves for contraction
33
Q

What is the vast vasorum?

A

large nerves have own blood vessels in adventitia

34
Q

Variation between arteries, arterioles and veins

A
  • Arteries: thick elastic/muscular walls that release distention and maintain high pressure
  • Arterioles have thicker walls relative to lumen = good constrictors
  • Veins have thin walls and large, distensible lumens - good for holding blood = capacitance
35
Q

Characteristics of large elastic arteries

A

Buffer pressure change, convert intermittent to continuous flow and maintain pressure
Thick media = lots of elastin for rebound
Wide lumen
Low resistance but high pressure

36
Q

Characteristics of muscular arteries

A
  • Also called distributing or peripheral arteries
  • Distribute flow, resist collapse at joints and adjust blood flow to joints/organs
  • Thick smooth muscle media with less elastic fibres
  • Smooth muscle allows some degree of vasoconstriction/dilation to adjust flow
  • Thick tunica externa with loose structure and longitudinal collagen fibres prevents retraction when cut
  • Range from 1 cm to 0.5 mm
  • Distribution arteries - more smooth muscle but low resistance conduits and not able to generate MABP
37
Q

Characteristics of arterioles

A
  • Main site of resistance - lots of small vessels
  • Walls contain thick layer of smooth muscle
  • Lots of sympathetic nerve endings - vasoconstriction (a1) or vasodilation (b2)
  • Arteriolar vasoconstriction increases upstream arterial BP but reduces downstream flow to tissues
  • Active hyperaemia - adjust blood flow to tissues according to metabolic demand
38
Q

Characteristics of capillaries

A
  • Nutrients and gases are exchanged between blood and tissue fluids
  • 4-10 micrometre in diameter
  • Branched and extensive network
  • Large cross-sectional area
  • Thin walled - endothelial cell and basement membrane
  • More abundant in metabolically active tissue
  • Only about 25% perfused at rest due to presence of precapillary sphincters and metarterioles
  • Nailfold capillaries - single file flow at low velocity, RBCs have to deform to fit
39
Q

What are continuous capillaries?

A

muscle, skin, lung, fat, nerves

40
Q

What are fenestrated capillaries?

A

Fluid exchange, renal glomerulus, synovial

41
Q

Discontinuous/sinusoid capillaries

A

Spleen, liver, gaps allow RBC into bone marrow

42
Q

How to calculate velocity?

A

Blood Flow / cross sectional area

43
Q

What is hydrostatic pressure?

A

Flow and vessel resistance (BP), pushes water out of vessels

44
Q

What is osmotic pressure?

A

Colloid and oncotic pressure, determined by charged proteins that pull water into vessels

45
Q

Veins and venules

A
  • Venules communicate with arterioles to match capillary inflows and outflow
  • Veins have valves - permits one way flow back to the heart
  • Act as capacitance vessels - 65% of blood volume
  • Thin walled, large lumens
  • Skeletal muscle pump and respiratory pump aid venous return from lower body
  • Venoconstriction (a1) shunts blood from peripheral to central vessels to increase stroke volume (exercise)
  • Release of norepinephrine from sympathetic neurones induces venoconstriction increases blood flow into right atrium
46
Q

What can hypertension cause?

A 
Stroke (ischaemic and haemorrhage)
Left ventricular hypertrophy 
Heart failure
Angina
Organ damage
47
Q

Why are people hypertensive?

A

Stress - work, diet, fam history etc

48
Q

Essential hypertension

A

Obesity - 95% of cases

49
Q

Secondary hypertension

A
  • Young, difficult to treat
  • Rapid onset
  • Abnormal biochemistry
  • Abnormal urine dip
  • Headache/neuro
  • Abdominal pain
50
Q

Treatments for hypertension

A
  • Lifestyle factors very important
  • Weight loss
  • Low salt diet
  • Exercise
  • Smoking
  • Alcohol
  • For T2D recommend ARB/ACE inhibitor, under 55
  • Over 55 or BAME = calcium channel blocker
51
Q

What does amlodipine do?

A
  • Blocks L-type voltage gated calcium channels
  • Vasodilation in vascular tissue
  • Smooth muscle vasodilates due to blockers
52
Q

What do calcium channels do?

A

Dilate channels to increase radius

53
Q

How to calculate SV

A

Preload, afterload and contractility

54
Q

How to determine preload

A

venous blood volume and vascular compliance and ventricular compliance

55
Q

How to determine afterload

A

arterial resistance, arterial compliance and wall stress

56
Q

What do diuretics do?

A

ACEI and ARBs - reduce preload

57
Q

What do CCB, ACEI and ARBs do?

A

Reduce afterload

58
Q

What is spirolactone?

A

Weak antagonist of androgen receptor - males may exhibit gynaecomastia

59
Q

Angiotensin ii and renin

A
  • Angiotensin ii impacts arterial resistance
  • Renin production stimulated by reduced stretch in juxtoglomerular apparatus = causes renin production
  • Renin constricts blood vessels and retains sodium and water
  • For drug to reduce action of RAAS system, it should inhibit angiotensin converting enzymes
  • ACE inhibitors - angiotensin converting enzyme inhibitors - enalapril
  • ACE breaks down bradykinin
  • ACE inhibitors end in -pril
  • Bradykinin correlated with cough and angioedema. Side effects of ACE include cough and angioedema
  • RAAS blockade also targets AT1 angiotensin ii receptors
  • Angiotensin ii receptor blockers cause no increase in bradykinin
  • When aldosterone impaired, serum potassium will rise
  • Aldosterone holds onto sodium in exchange for potassium

Cardiovascular System (21 decks)

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