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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
what does the transporter in the distal convoluted tubule not transport
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
25
what drug combats the NaCl transporter in the distal convoluted tubule
thiazide diuretics
26
what do thiazide diuretics do
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
27
the epithelial cells express what receptor
receptor for a steroid hormone known as a mineralocorticoid
28
what does the main endogenous activate for the mineralocorticoid recerpoe do
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
29
what is the mineralocorticoid receptor blocker called
spironolactone
30
what is the mechanism of spironolactone
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
31
how potent are loop diuretics
high - loss of fluid can be dramatic
32
how potent are thizide diuretics
moderate
33
how potent are aldosterone antagonists
weak
34
what is the anti-hypertensive effect of thiazide diuretics
reduce systolic and diastolic pressure in hypertensive patients, and the risk of cardiovascular complications
35
what is the clinical use of loop directs
reserved for patients with pulmonary oedema, heart failure, renal insufficient or resistant hypertension. reduce oedema
36
when are thiazide diuretics given
as an add on if other drugs are not sufficiently effective on their own
37
what does aldosterone antagonist do if given with a loop or thiazide diuretic
prevents hypokalaemia
38
examples of loop diuretics
furosemide
39
examples of original thiazide drugs
chlorothiazide hydroclothiazide bendroglumethiazide
40
what are examples of new thiazide like drugs that have the sam action
indapamide chlorthalidone metolazone
41
what are examples of aldosterone antagonist
spironolactone | eplernone
42
the key mediator of contraction and explanation
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
what are the two enzymes that the degree phosphorylation depends on
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
what determines the effects of MLCK
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
what signalling pathways can interfere with the reaction between Ca-modulin and myosin light chain kinase
cAMP and cGMP both inhibit the reaction and cause relaxation of the muscle. many vasodilators act via these second messengers.
46
what is cGMP produced by
nitrovasodilators like glyveryltrinitrate.
47
what is myosin phosphatase activity inhibited by
Rho kinase and protein kinase C. they prevent dephosphorylation of myosin so that contraction remains even after the calcium concentration has fallen
48
what is the contraction remains after Ca+ conc falls called
calcium sensitisation - calcium is not needed to maintain contraction
49
how can the calcium ion concentration in smooth muscle be increased
by activating G-protein coupled receptors that emplynthe Gq/G11 family.
50
what happens when the G protein is activated
the Ga subunit stimulates the activity of the enzyme phospholipase C, which results in the cleavage of phosphatidylinositol to IP3 and diacylglycerol
51
what does IP3 do
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
how Does the diacyglycerol that is generated alongside IP3 act
causes Ca2+ sensitisation due to the inhibition of myosin phosphatase.
53
n example of the GCPRs that mediate contraction
the alpha q andrenoceptor and angiotensin,
54
what is the Ca reuptake into the SR mediated by
the SERCA pump
55
what is the pump that takes Ca out of the cell
PMCA pump
56
what is the key channel for contraction
the L type voltage operated Ca channel.
57
what happens when the L type voltage channels are opened
the Ca2+ enters the cell and directly triggers contraction.
58
what do the alpha adrenoceptor blockers do
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
what are examples of alpha adrenoceptor blockers
dozazosin | terazosin
60
calcium antagonist drug groups
dihydroprydines phenylalkylamines benzothiazepines
61
examples of dihydropyridines
amlodipine felodipine nimodipine
62
cardiovascular selectively of dihydropyidines
smooth muscle selective. inhibit calcium channels in vascular smooth muscle with little effect on the heart.
63
where does nimodipine preferentially act
cerebral arteries
64
therapeutic use of dihydropyridines
first line anti hypertensive drugs
65
example of phenylkylamines
verapamil
66
what is the cardiovascular selectivity of phenylalkylamines
cardiac selective. at doses inhibiting cardiac channels, there is little effect on smooth muscle
67
what is verapamil used to treat
cardiac arrhythmias and angina
68
example of benxothiazepines
diltiazem
69
what is the cardiovascular selectivity of benzothiazepines
discriminate poorly between cardiac and smooth muscle channels
70
therapeutic use of benzothiazepines
used for angina that is resistant to beta blockers
71
who are calcium antagonists the choice of drug for
patients at least 55 years and blaxck African origin
72
what are the main side effects of calcium antagonists
peripheral oedema, flushing, headache, and constipation which all result from calcium channel inhibition in smooth muscle
73
where is angiotensin made
in the liver
74
what does angiotensin encounter in the blood
renin made in the kidneys. it is a hormone
75
what does renin do to angiotensinogen
cleaves it into smaller peptide known as angiotensin 1
76
where does angiotensin 1 encounter ACE
in the lungs
77
what does ACE do to angiotensin 1
it cleaves it further to angiotensin 2
78
what does angiotensin 2 then do
interacts with the angiotensin receptor 1 AT1 receptor and results in several effects
79
what is the key effect of the AT1and AT2 complex
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
what happens when AT2 acts on the AT1 receptors in the cortex of the adrenal gland
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
what can the effect of angiotensin on blood vesslesnand kidney be inhibited by
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
what are the actions of angiotensin 2 prevented by
drugs that compete with angiotensin for binding to the AT1 receptor and they are known as angiotensin receptor blockers
83
renin-angiotensin-aldosterone system diagram
84
diagram of RAAS system drug action
85
how do ACE inhibitors produce a side effect of a dry cough
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
examples of ACE inhibitors
``` ramipril lisinopril enalapril perindopril quinapril trandolapril imidapril ```
87
ARB examples
``` candesartan losartan eprosartan irbesartan olmesartan telmisartan valsartan ```
88
what is a renin inhibitor example
aliskkiren
89
adverse effects caused by inhibiton of angiotensin 2 production or action
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
which drugs when
91
diagram from G protein to Ca influx

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