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Unit 12 Week 1 (Sam) > Pharmacology of hypertension > Flashcards

Pharmacology of hypertension Flashcards

1
Q

What is hypertension

A

persistently raised arterial blood pressure

140/90

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2
Q

normal blood pressure

A

120/80

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3
Q

elevated blood rpessure

A

120-129/ <80

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4
Q

hypertension stage 1

A

130-139/ 80-89

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5
Q

hypertension stage 2

A

140+/ 90+

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6
Q

hypertension stage 3

A

180+/ 120+

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7
Q

What does clinical management depend on

A

severity and cause

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8
Q

2 typoes pf hypertension cause

A

essential (>90%)

secondary

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9
Q

essential hypertension

A

cause is unknown (idiopathic)

no clear causative factor

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10
Q

secondary hypertension

A
  • renal disorders (role of kidneys in regulating long term BV and therefore BP)
  • Endocrine: 1* hyperaldosteronism (fluid regulation)

phaeochromocytoma (sympathetic NS)

Cushing’s syndrome (cortisol)

  • Drug induced- abuse- e.g., cocaine (SNS)
  • iatrogenic e.g., combined oral contraceptive
  • pregnancy- pre-eclampsia
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11
Q

exogenous causes of hypertension

A

smoking

diet

stress

drugs

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12
Q

endogenous (genetic) causes of hypertensino

A

obesity

ethnicity

metabolic/ hormonal

renal (RAAS)

CNS

arterial

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13
Q

Consequences of hypertension

A

inc reased risk of cardiovacular disorder

coronary artery disease

stroke

heart failure

peripheral arterial disease

vascualr dementia

chronic kidney failure

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14
Q

pathophysiology mechanisms involved

A
  • Cardiac output
  • Peripheral resistance
  • Autonomic nervous system
  • Endothelium
  • Vasoactive peptides
  • Renin-angiotensinogen-aldosterone system
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15
Q

lowering ypertension affects health how?

A

health benefits

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16
Q

ABP=

A

CO x TPR

ABP = force on walls

CO= flow of blood

TPR= resistance of vessels to flow

force = flow x resistance

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17
Q

to reduce ABP you

A

decrease either CO or TPR or both

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18
Q

Cardiac output =

A

stroke volume x HR

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19
Q

stroke volume is directly proportional to

A

central venous pressure

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20
Q

paheachromocytoma

A

benign tumour in adrenal gland

increase adrenaline

increase CVP

responsive vasoconstriction

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21
Q

in most eddential hypertension which of CO and TPR is raised

A

TPR

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22
Q

chronic adaptive response in blood vessels may lead to

A

irreversible rise in TPR

23
Q

Role of autonomic NS in hypertension

A

heart function (CO)

vessel function (TPR)

SR regulation of pressure and flow: baroreceptor reflex and myogenic response

sympatholytic (antag or inhib SNS transmission) drugs lower ABP

24
Q

Which receptors does adrenaline act upon to cause vessel smooth muscle constriction- vasoconstriction

A

A2 adrenoreceptor

25
ANS heart function
**B1 receptors-activation** by catecholamines increases sinoatrial (SA) nodal, atrioventricular (AV) nodal, and ventricular muscular firing, thus increasing heart rate and contractility. **incvreases CO** **vessel function**- arteriolar tone regulates TPR and venous tone CVP a1- vasoconstriction B2- vasodilation
26
endothelium
* Endothelial cells produce vasoactive agents * EDRF (endothelium-derived relaxing fibre) = Nitric oxide (NO) -vasodilator * prostacyclin - vasodilator andelyl cyclase- increase cGMP- increase PKG sm. muscle relaxation endothelin- vasoconstrictor atheroma (plaque) decreases NO production- constrict
27
vasoactive peptides
bradykinin- vasodilator (ACE inhibs stop bradykin inactivation- keeping dilated) Natriuretic peptides-direct vasodilators -----NPR1 (receptor) = guanylyl cyclase = increased cGMP = sm muscle relaxation + increase sodium and water excretion- secreasing blood volume ADH= vasoconstrictor, increases BP and H20 reabsorption
28
natriuretic peptides
ANP-atrial: secreted by atrium BNP- brain: secreted by ventricles CNP- C-type secreted in response to low BP
29
link between vasodilation and BP
vasodilation increase venous capacitance decrease central venous oressure decreases ventricular preload decreases CO
30
Renin-angiotensin-aldosterone system in BP
longer term regulation of BV (ECF) and systemic vascular resistance RAAS is a target for many important and effective drugs used in hypertension
31
ABp and renin
decrease in BP→ increase Symp. activity and decrease GFR a) increase symp- activates B1 receptors on granular cells of JGA- release of renin b) macula densa cells detect Na+/Cl- in DCT-- decrease GFR -- decrease NaCl filtered load-- release renin-- dailtion of AFF and constriction of EFF-- less water is lost through filtration-- more in vessels
32
angiotensinogen
plasma protein produced by liver and secreted into blood the substrate for renin gtes converted into ang1
33
angiotensin 1
endogenous peptide decapeptide cleaved from N-terminal of ang by renin converted to ang II by ACE. ACE is widely expressed e.g., lung
34
angiotensin II
octapeptide produced by cleavahe of C terminal dipeptide by ACE full agonist at AT1 receptor (GCPR) causing the release of aldosterone (mineralocorticoid) from adrenal cortex- increasinf ECF arteriolar vasoconstrictor causes ADH release from posterior pituituary
35
how many ACE enzymes are there
2 ACE 1 ACE 2
36
ACE 1
widely expressed in endothelium of lungs and kidneys has 2 catalytic ZN metalloproteinase domains cleaves AT-1 - AT-2 also cleaves bradykinin, stopping its vasodilatory effects
37
ACE 2
1 catalytic domain cleaves ANG-II antagonising it
38
AT1 (angiotensin II type 1 receptor)
PGCR (Gi and Gq signalling) activated by anG ii Causes: sm. muscle contraction and vasoconstriction C and SNS stimulation aldosterone release ADH release tubular Na+ reabsorption in the PCT endothelin release (vasoconstictor)
39
Aldosterone
steroid (mineralocorticoid) full agonist at intracellular mineralocorticoid receptors in tubular cells of the DCT activation causes na+reuptake
40
mineralocorticoid receptor
nuclear hormone receptor ## Footnote Expressed in epithelia with high electrical resistance, e.g. distal kidney tubular cells selectively changes transcription of cell-- increasing production of ENaCs and Na+/ K+-ATPase pump
41
spirinalactone
competitive antagonist of mineralocorticoid receptor
42
epithelial soidium channels )ENaCs
widely expressed esp in kidney tubules (late DCT and CD) , lung and resp tract increased ENaC expression on apical membrane due to activation of mineralocorticoid receptor increases Na+ permeability and Na+ reabsorption from tubule lumen into the cell rate limiting step in salt reabsorption in this part of the nephron these are NOT voltage gated
43
amiloride is a what
ENaC blocker potassium sparing
44
Na+Cl- ATPase (Na+ pump)
tansmembrane ATP-dependant active transporter ubiquitously expressed for each ATP, 3 Na+ out and 2k+ in pumps Na+ out of cell into interstitium, keeping intracellular conc low so the NaKATPase pump can keep working
45
what drugs inhibit Na+Cl-ATPase pumps
cardiac glycosides e.g., digoxin
46
Liddle syndrome
rare genetic (autosomal dominant) disorder causes severe hypertension from a young age mutations prevent channel internalization and degradation overexpression of ENaCs causes excess Na+ reabsorption treat with ENaC blockers e.g., amiloride
47
Master slide
48
antihypertensive drugs
diURETICS (thiazides, loops, K sparing) renin inhibitor ACE inhibitos -pril Angiotensin recptor blocker -sartan B blockers -lol calcium channel blockers -dipine centrally acting a2 agonists e.g., clonidine vasodilators
49
aliskiren
renin inhibitor essential hypertension target= renin action= competitive inhibitor physiology: decrease production of AngI
50
enalapril
ACE inhibitor (most ACE inhibitors are pro drugs) Prodrug essential hypertension and heart failure target: ACE Activity: competitive inhibitor Physiology: decrease prod of AT-II and decrease breakdown of the vasodilator bradykinin
51
valsartan
angiotensin receptor blocker essential hypertension + heart failure target: AT1. activity: competitive antagonist Physiology: decreases effects of AT-II...... no effect on bradykinin so no cough
52
atenolol
selective B1 blocker essential hypertension - angina -arrthmias target: B1 receptor as higher affinity than B2. activity: competitive antagonist Gs coupled therefore antagonism of their activation reduces activity of adenylyl cyclase and its downstream signalling via cyclic adenosime monophosphate and protein kinase A (PKA) not understood but decreases CO, alters baroreceptor reflexes and decreases renin secretion
53
amlodipine
calcium channel blocker essential hypertension angina target= L-type voltage gated calcium channel activity- gating inhibitor greater specificity fpr sm over cardiac msucle decreased calcium mobilisation in smooth muscle means vasodilation
54
voltage gated calcium channels
all open in response to depolarisation L-type: once open stay open for a Long time, inactivate slowly phosphorylated by action of adrenaline/ NA amlodipine does not block but stabillises it in either 1) an unresponsive state 2) a hyper-responsive state

Unit 12 Week 1 (Sam) (6 decks)

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