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DRUGS > Hypertension drugs > Flashcards

Hypertension drugs Flashcards

1
Q

how is pressure produced in the systemic circulation

A

by the left ventricle pushing blood out into the vessels

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2
Q

what is blood pressure

A

cardiac output x total peripheral resistance

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3
Q

what are the heart and blood vessels innervated by

A

sympathetic nervous system

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4
Q

where do diuretics work

A

on the kidney

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5
Q

what are the two vasodilator drugs

A

calcium antagonists and alpha1 adrenoceptor blockers

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6
Q

types of drugs that inhibit the RAAS system

A

ACE inhibitors
ARBs
Renin inhibitors

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7
Q

what do beta blockers compete with

A

noradrenaline released from sympathetic nerves and adrenaline

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8
Q

where is adrenaline released from

A

chromaffin cells in the adrenal gland

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9
Q

what are the beta receptors in the heart and kidney

A
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9
Q

what are the beta receptors in the heart and kidney

A

beta 1 subtype

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10
Q

what are the beta1 blocker drugs

A

atenolol - x1 daily
metoprolol - x1 daily
bisoprolol - x1 daily

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11
Q

what is propranolol

A

a non-selective beta blocker - inhibiting both beta1 and beta2 receptors

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12
Q

what is carvedilol

A

an antagonists at the alpha-adrenergic receptors

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13
Q

what are the unwanted effects of beta blockers

A

cold hands - due to the loss of beta2 receptor mediated vasodilation in the skin
fatigue due to the fall in cardiac output and impaired beta2 receptor mediation of vasodilation in skeletal muscle

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14
Q

what is a less common effect of beta blockers

A

Bradycardia - cardiac depression which is loss of response to the sympathetic drive to the heart which ca progress to heart block and heart failure.

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15
Q

when is cardiac depression likely

A

mainly in elderly patients and more likely if given with a calcium channel antagonist

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16
Q

where do diuretics work in the kidney

A

on the nephron

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17
Q

what is the pathway of blood through the kidney’s nephron

A

passes through the Bowman’s capsule which contains the glomerulus - fluid entering the tubule passes through the loop of Henle and the distal convoluted tubule on its way to the collecting ducts and eventually to the bladder where it is stored as urine

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18
Q

diagram for the sites of action of diuretics

A
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19
Q

where in the kidney is impermeable to water but remains permeable to ions

A

the loop of Henle

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20
Q

what is the co-transporter found in the loop of Henle

A

the NaK2Cl co transporter

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21
Q

what is the NaK2Cl transporter blocked by

A

a group of diuretics known as loop diuretics

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22
Q

what do loop diuretics do

A

they inhibit removal of ions form the tubular fluid in the thick ascending loop of Henle so that the renal fluid is more concentrated as it travels through the rest of the nephron. as it reaches the vital convoluted tubule, which is permeable to water, osmotic forces draw water out from the epithelial cells into the tubular lumen. the result is increased loss of salt and water from the body.

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23
Q

what is the transporter in the distal convoluted tube called

A

NaCl cotransporter

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24
Q

what does the transporter in the distal convoluted tubule not transport

A

it doesn’t transport K+. The K+ entering through this pump is removed again in exchange for Ccl- this maintains the ionic composition and charge in the cell

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25
Q

what drug combats the NaCl transporter in the distal convoluted tubule

A

thiazide diuretics

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26
Q

what do thiazide diuretics do

A

they inhibit the transporter and prevent the removal of Na+ and Cl- from the tubular fluid along with the water that would have travelled with the ions to maintain osmolarity. there is therefore increased loss of salt and water from the body

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27
Q

the epithelial cells express what receptor

A

receptor for a steroid hormone known as a mineralocorticoid

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28
Q

what does the main endogenous activate for the mineralocorticoid recerpoe do

A

aldosterone, produced in the cortex of the adrenal gland. by activating the receptor, aldosterone increases the expression of basolateral Na/K pumps therefore increasing pump activity. thus increases the reabsoportion of Na+ ions and its accompanying water, while decreasing the reabsorption of K+ ions which are lost in the unrine

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29
Q

what is the mineralocorticoid receptor blocker called

A

spironolactone

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30
Q

what is the mechanism of spironolactone

A

it prevents the action of aldosterone thereby causing increased excretion of Na+ and water, while preserving K+ ions in the circulation. this drug is therefore known as a potassium sparing diuretic

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31
Q

how potent are loop diuretics

A

high - loss of fluid can be dramatic

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32
Q

how potent are thizide diuretics

A

moderate

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33
Q

how potent are aldosterone antagonists

A

weak

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34
Q

what is the anti-hypertensive effect of thiazide diuretics

A

reduce systolic and diastolic pressure in hypertensive patients, and the risk of cardiovascular complications

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35
Q

what is the clinical use of loop directs

A

reserved for patients with pulmonary oedema, heart failure, renal insufficient or resistant hypertension. reduce oedema

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36
Q

when are thiazide diuretics given

A

as an add on if other drugs are not sufficiently effective on their own

37
Q

what does aldosterone antagonist do if given with a loop or thiazide diuretic

A

prevents hypokalaemia

38
Q

examples of loop diuretics

A

furosemide

39
Q

examples of original thiazide drugs

A

chlorothiazide
hydroclothiazide
bendroglumethiazide

40
Q

what are examples of new thiazide like drugs that have the sam action

A

indapamide
chlorthalidone
metolazone

41
Q

what are examples of aldosterone antagonist

A

spironolactone

eplernone

42
Q

the key mediator of contraction and explanation

A

the interaction between actin and myosin to form a cross bridge. in smooth ,muscle this interaction depends on the phosphorylation of the light chain of myosin. the degree of phosphorylation depends on the relative actions of two enzymes

43
Q

what are the two enzymes that the degree phosphorylation depends on

A

myosin light chain kinase promotes myosin phosphorylation by transferring a phosphate group from ATP. the removal of phosphate from myosin is mediated by the enzyme myosin phosphatase

44
Q

what determines the effects of MLCK

A

contraction begins when there is a rise in free Ca2+ Ions in the cytoplasm. the Ca2+ binds with calmodulin and forms a complex. this in turn activates myosin light chain kinase to phosphorylate myosin.

45
Q

what signalling pathways can interfere with the reaction between Ca-modulin and myosin light chain kinase

A

cAMP and cGMP both inhibit the reaction and cause relaxation of the muscle. many vasodilators act via these second messengers.

46
Q

what is cGMP produced by

A

nitrovasodilators like glyveryltrinitrate.

47
Q

what is myosin phosphatase activity inhibited by

A

Rho kinase and protein kinase C. they prevent dephosphorylation of myosin so that contraction remains even after the calcium concentration has fallen

48
Q

what is the contraction remains after Ca+ conc falls called

A

calcium sensitisation - calcium is not needed to maintain contraction

49
Q

how can the calcium ion concentration in smooth muscle be increased

A

by activating G-protein coupled receptors that emplynthe Gq/G11 family.

50
Q

what happens when the G protein is activated

A

the Ga subunit stimulates the activity of the enzyme phospholipase C, which results in the cleavage of phosphatidylinositol to IP3 and diacylglycerol

51
Q

what does IP3 do

A

It diffuses to the sarcoplasmic reticulum which acts as an intracellular store of calcium. it binds to and activates the IP3 receptor which is the Ca2+ permeable ion channel in the sarcoplasmic reticulum. Ca2+ ions flow out of the SR down the gradient to stimulate contraction.

52
Q

how Does the diacyglycerol that is generated alongside IP3 act

A

causes Ca2+ sensitisation due to the inhibition of myosin phosphatase.

53
Q

n example of the GCPRs that mediate contraction

A

the alpha q andrenoceptor and angiotensin,

54
Q

what is the Ca reuptake into the SR mediated by

A

the SERCA pump

55
Q

what is the pump that takes Ca out of the cell

A

PMCA pump

56
Q

what is the key channel for contraction

A

the L type voltage operated Ca channel.

57
Q

what happens when the L type voltage channels are opened

A

the Ca2+ enters the cell and directly triggers contraction.

58
Q

what do the alpha adrenoceptor blockers do

A

they are selective antagonists at the alpha 1 subtype of adrenergic receptor. these receptors are widely expressed in arterial smooth muscle and mediate the vasoconstriction actions of noradrenaline and adrenaline from the adrenal medulla.

59
Q

what are examples of alpha adrenoceptor blockers

A

dozazosin

terazosin

60
Q

calcium antagonist drug groups

A

dihydroprydines
phenylalkylamines
benzothiazepines

61
Q

examples of dihydropyridines

A

amlodipine
felodipine
nimodipine

62
Q

cardiovascular selectively of dihydropyidines

A

smooth muscle selective. inhibit calcium channels in vascular smooth muscle with little effect on the heart.

63
Q

where does nimodipine preferentially act

A

cerebral arteries

64
Q

therapeutic use of dihydropyridines

A

first line anti hypertensive drugs

65
Q

example of phenylkylamines

A

verapamil

66
Q

what is the cardiovascular selectivity of phenylalkylamines

A

cardiac selective. at doses inhibiting cardiac channels, there is little effect on smooth muscle

67
Q

what is verapamil used to treat

A

cardiac arrhythmias and angina

68
Q

example of benxothiazepines

A

diltiazem

69
Q

what is the cardiovascular selectivity of benzothiazepines

A

discriminate poorly between cardiac and smooth muscle channels

70
Q

therapeutic use of benzothiazepines

A

used for angina that is resistant to beta blockers

71
Q

who are calcium antagonists the choice of drug for

A

patients at least 55 years and blaxck African origin

72
Q

what are the main side effects of calcium antagonists

A

peripheral oedema, flushing, headache, and constipation which all result from calcium channel inhibition in smooth muscle

73
Q

where is angiotensin made

A

in the liver

74
Q

what does angiotensin encounter in the blood

A

renin made in the kidneys. it is a hormone

75
Q

what does renin do to angiotensinogen

A

cleaves it into smaller peptide known as angiotensin 1

76
Q

where does angiotensin 1 encounter ACE

A

in the lungs

77
Q

what does ACE do to angiotensin 1

A

it cleaves it further to angiotensin 2

78
Q

what does angiotensin 2 then do

A

interacts with the angiotensin receptor 1 AT1 receptor and results in several effects

79
Q

what is the key effect of the AT1and AT2 complex

A

causes vasoconstriction. AT2 is one of the most potent natural vasocvontrictors. it directly contracts vascular smooth muscle via AT1 receptors on the muscle but it also acts on the AT1 receptors located on the sympathetic nerve endings

80
Q

what happens when AT2 acts on the AT1 receptors in the cortex of the adrenal gland

A

it stimulates the release of the hormone aldosterone. aldosterone plats a central role in the homeostatic control of plasma volume. it acts on the nearby kidney to promote the retention of Na and H2O which increases blood volume and consequently cardiac output. that in turn raises flow throughout the circulation and increases blood pressure

81
Q

what can the effect of angiotensin on blood vesslesnand kidney be inhibited by

A

preventing the production of AT2 or by blocking its actions. production can be prevented by inhibiting the conversion of AT1 -AT2 by ACE inhibtitors

82
Q

what are the actions of angiotensin 2 prevented by

A

drugs that compete with angiotensin for binding to the AT1 receptor and they are known as angiotensin receptor blockers

83
Q

renin-angiotensin-aldosterone system diagram

A
84
Q

diagram of RAAS system drug action

A
85
Q

how do ACE inhibitors produce a side effect of a dry cough

A

ACE beaks down other bioactive peptides Like bradykinin and substance P which are included in the cough reflex. when ACE is inhibited the levels of these peptides increase and give rise to a dry persistent cough which may not be tolerated. if not, an ARB can be prescribed instead

86
Q

examples of ACE inhibitors

A 
ramipril 
lisinopril 
enalapril 
perindopril 
quinapril 
trandolapril 
imidapril
87
Q

ARB examples

A 
candesartan 
losartan 
eprosartan 
irbesartan 
olmesartan 
telmisartan 
valsartan
88
Q

what is a renin inhibitor example

A

aliskkiren

89
Q

adverse effects caused by inhibiton of angiotensin 2 production or action

A

all of the drugs that interfere with the RAAS system can cause hypotension when the first dose is given. the effect wears off with time but leaves a lower BP. can also cause hyperkalemia due to inhibition of aldosterone secretion. drop in renal auction also which is monitored by measuring serum creatine levels

90
Q

which drugs when

A
91
Q

diagram from G protein to Ca influx

A

DRUGS (4 decks)

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