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M103 T3 > M103 T3 L11 > Flashcards

M103 T3 L11 Flashcards

1
Q

What three drugs can be administered for the 1LoT for hypertension depending on age and race?

A 
ARBs, ACE inhibitors & CCBs
--
angiotensin receptor blocker 
ACE inhibitor 
calcium channel blocker
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2
Q

What are the different LoTs for hypertension?

A

2nd line = a combination of all 1st line drugs
3rd line = 2nd line + a diabetic
4th line = 3rd line + another diuretic (an a/b-blocker)

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3
Q

What are the different LoTs for hypertension?

A

2nd line = a combination of all 1st line drugs
3rd line = 2nd line + a diabetic
4th line = 3rd line + another diuretic (an a/b-blocker)

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4
Q

What are the side effects of ACE inhibitors?

A

dry cough (main - around 20 - 25 % of patients)
hypotension
renal impairment
hyperkalaemia

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5
Q

What drug blocks the action of kininase II?

A

ACE inhibitors

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6
Q

What is the function of kininase II?

A

breaks down substance P and badikinin into inactive peptides

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7
Q

How do ACE inhibitors cause a dry cough?

A

their aim is to block ACE
They accidentally also block kininase II - an enzyme related to ACE
Not enough kininase II leads to a build up of substance P and badikinin in the body
These are both irritants
can cause respiratory tract sensitivity
leads to a dry cough

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8
Q

What is the most common reason for the intolerance of ACE inhibitors by patients?

A

bc it can stop patients and their partners from sleeping

in these cases, the ACE inhibitors should be removed

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9
Q

How do ACE inhibitors cause hypotension?

A

angiotensin II can have effects on a whole range of systems which are all designed to keep bp high
so when the amount of angiotensin in the system is suddenly reduced, bp plummets quite dramatically

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10
Q

What are some consequences of hypotension caused by ACE inhibitors if taken during the day?

A

if the patient changes position or stands up very suddenly, they can feel very faint bc their bp is quite low
can cause collapse and a potential head injury

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11
Q

How are some of the side effects of hypotension caused by ACE inhibitors reduced?

A

prescribe the initial dose of the ACE inhibitor to be taken at night time
if the patient takes it just before they go to bed when they’re lying down, they won’t fall down
so if bp is low, it’s not going to cause them any injury
usually, as the dose wears off by the morning, the patients’ bp is at a high enough level
so when they get out of bed, they’re not at risk of fainting

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12
Q

Are the side effects of hypotension caused by ACE inhibitors long term problems and why?

A

no
usually the body gets used to the dose of the ACE inhibitors over time
eventually it is no longer a problem

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13
Q

Why is it important to measure the patients’ renal functioning before giving them ACE inhibitors?
How and why this done?

A

ACE inhibitors can cause renal impairment
how - by measuring creatinine levels in the blood
why - elevation in blood creatinine levels indicate faulty renal functioning

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14
Q

How is low blood flow in the kidneys brought to normal levels?

A

renin is synthesised, creates angiotensin II, a vasoconstrictor
glomerular pressure increases, so blood flow does as well

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15
Q

How do ACE inhibitors cause renal impairment?

A

reduce levels of angiotensin II

reduce the ability of this efferent vessel to constrict

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16
Q

What are the effects of hyperkalaemia?

A

increased cardiac & NS excitability
arrhythmias
epileptic attacks

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17
Q

What are the normal K+ levels in the blood compared to that for hyeprkalaemia?

A

3 - 5 mM

above 5 mM

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18
Q

When are the patients’ serum K+ levels monitored?

A

before the ACE inhibitor is administered

before increasing in the dose of ACE inhibitor

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19
Q

Why are ACE inhibitors useful for patients with diabetes and hypertension?

A

they protect the kidneys from diabetic nephropathy
they don’t have any effects on blood lipids
so the fact that these drugs don’t affect serum glucose or serum lipids in a negative way means that they are very good drugs for the treatment of diabetes and hypertension

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20
Q

What is the suffix for all ACE inhibitor drugs?

A

-pril

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21
Q

What are the effects of Angiotensin receptor antagonists?

A

hyperkalemia
renal impairment
side effects are minimal

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22
Q

What are aldosterone antagonists used for?

A

can also be front line hypertension treatment for patients with primary aldosteronism

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23
Q

What are the three main classes of calcium channel blockers?

A

dihydropyridines
phenylalkylamines
benzothiazepines

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24
Q

How do dihydropyridines work?

A

blocks a portion of L-type Ca2+ channels on smooth muscle of arterioles
calcium entry into the smooth muscle cells will be reduced
AAR the smooth muscle will relax, arterioles will dilate
peripheral resistance will dcs, bp will dcs

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25
Q

How do phenylalkylamines and benzothiazepines work?

A

they preferentially target L-type channels in the heart

they d thcse frequency and force of contraction

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26
Q

What is an example of each of the main classes of clacium channel blockers?

A

dihydropyridine - amlopidine
phenylalkylamines - verapamil
benzothiazepines - diltiazem

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27
Q

When are phenylalkylamines and benzothiazepines used?

A

less used to treat hypertension

only in those patients whose hypertension is due to a tachycardia faster than normal heartbeat

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28
Q

Whaet is the mechanism by which calcium leads to muscle contraction?

A

in smooth muscle cells there are L-type calcium channels
calcium entry in a smooth muscle cell
leads to an increase in intracellular calcium
binds to calmodulin protein which activates the Myosin light chain kinase enzyme
MLCK phosphorylates MLC
allows myosin and actin to interact and muscle contraction

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29
Q

What is the main side effect of taking a calcium channel blocker and why?

A

peripheral oedema - swelling in the ankles
Preferential dilation of precapillary arteriole and impairment of the function of the pre-capillary sphincter increases hydrostatic pressure across the capillary and reducing fluid reabsorption

30
Q

What is the function of precapillary sphincters?

A

to regulate the flow of blood into capillary beds

31
Q

What happens to precapillary sphincters when you sit down?

A

they contract to reduce blood flow into the capillaries because they’re under much higher pressure than they would be normally due to increased gravital force

32
Q

How do precapillary sphincters react to calcium channel blockers and why?

A

they have L-type calcium channels on the
calcium channel blockers prevent precapillary sphincters from contracting
leads to elevated bp at the arterial end of the capillary on standing
this drives more fluid out of the capillary
the same increase in pressure will be seen at the venous end

33
Q

What is the main side effect of taking a calcium channel blocker and why?

A

peripheral oedema

flushing, headaches

34
Q

Why does taking calcium channel blockers lead to flushing?

A

it dilates blood vessels in our skin

skin becomes more red bc more blood is flowing near the surface

35
Q

Why does taking calcium channel blockers lead to headaches?

A

the blood vessels that perfuse the meninges that surround the brain become dilated

36
Q

Why are combinations of Ca2+ channel antagonists not recommended?

A

bc both cause a big reduction in bp

37
Q

What does CYP3A4 do?

A

metabolise calcium channel blockers to their inactive metabolites

38
Q

What inhibits CYP3A4? What happens if you drink too much?

A

grapefruit juice
any calcium channel blocker drugs being taken will not be metabolised as well
so the levels of the active compound will increase in the bloodstream
so patients should not to drink excessive levels of or change their consumption of grapefruit juice

39
Q

What part of the nephron do drugs treating hypertension work on and how?

A

DCT - works by blocking the nacl co transporter present in the cells lining the DCT
so na and cl ions and water will remain in the tubular lumen
diuresis will start to produce more urine and less water will appear in the blood system
therefore bc there’s less water and less blood returning to the heart, there’s less cardiac output
so bp is reduced

40
Q

What do thiazide and thiazide like dieuretics do?

A

act in the same way as dihydropyridines

act in the same way as all drugs that treat hypertension

41
Q

How does indapamide hyperpolarise smooth muscle cells?

A

it stimulates KATP channels to allow more K+ to leave
the cells become more negative
this inhibits the opening of a voltage gated ca channel,

42
Q

What are the symptoms of thiazide diuretics?

A

hypokalaemia
Increase in urate
Increase in glucose & blood lipids

43
Q

How can thiazide diuretics cause hypokalaemia?

A

indapamides cause diuresis
loss of na and k ions
when k levels drop below three mM can cause problems in excitable tissue like the heart and the CNS
bc they will become less excitable due to the low levels of k

44
Q

Why aren’t thiazide diuretics typically used for patients with high ureate levels?

A

indapamides cause diuresis
diuresis ics’es uric acid retention
would make the problem worse for patients who already have this problem

45
Q

Why are thiazide diuretics no longer used as front line treatment for over 55s against hypertension?

A

they reduced bp very well but they didn’t protect against cardiovascular complications such as heart attacks and strokes

46
Q

Why don’t thiazide diuretics protect against cardiovascular complications?

A

thiazide diuretics ics blood glucose and blood lipids which are risk factors for cardiovascular disease

47
Q

How do beta cells produce insulin?

A

blood glucose levels are elevated
glucose enters beta cells, become metabolised, generate ATP
ATP closes the Katp channel
it then depolarises the beta cell
which allows ca to enter through voltage dependent ca channels
ca acts as a stimulus for the release of insulin
insulin will then increase the permeability of cells to glucose to reduce extra glucose

48
Q

How do thiazide diuretics increase the blood glucose levels?

A

they stimulate and open the K ATP channel
AAR the voltage dependent ca channels can’t open
less ca will come in
less insulin release
blood glucose levels rise

49
Q

What is the effect of beta blockers?

A

they reduce the heart rate & the force of contraction

they block b1 receptors

50
Q

What is the main side effect of beta blockers? How is this caused?

A

fatigue - when we do exercise, the blood maintains perfusion via increased cardiac output
beta blockers lower the heart rate
so the blood can’t keep up with the increased perfusion levels demanded by the muscle tissue even for simple things bc of lower cardiac output

51
Q

Which receptor will beta blockers show a preference for binding to?

A

b-1 receptors

52
Q

Where are beta receptors located in the body?

A

the heart - b1
smooth muscle cells of the airways - b2
blood vessels that perfuse the skeletal muscles - b2

53
Q

What is the function of beta blockers?

A

to drive relaxation in the muscle cells

54
Q

What effect does adr have on skeletal and smooth muscle arterials?

A

adrenaline dilates the arterials that perfuse skeletal muscle - increased blood flow when exercising

55
Q

How do beta blockers cause muscle relaxation?

A 
b-2 receptors are activated
cyclic AMP is produced
phosphorylates myosin light chain kinase
this MLCK enzyme is inhibited
causes smooth muscle relaxation
56
Q

Why can beta blockers be dangerous?

A

can cause asthma attacks

57
Q

How can beta blockers cause asthma attacks in certain patients?

A

while beta blockers show a preference for binding to b-1 receptors, it can block some b-2 receptors
b-2 receptors are mainly present in the smooth muscles of the airway
in patients sensitive to bronchoconstriction (asthma), their bronchioles are more likely to to constrict
this can cause further broncho constriction

58
Q

How can beta blockers cause vasoconstriction in certain patients?

A

in patients with Raynaud’s disease, their peripheral arteries are more likely to to constrict
beta blockers might block b2 receptors which are normally trying to dilate those blood vessels

59
Q

How can beta blockers cause hypoglycaemia in certain patients?

A

in a diabetic patient, their insulin injections cause the blood glucose level to become very low
in response, adrenaline is released - used to mobilise glucose release from the liver
patient might start to feel a little bit shaky and light-headed, can cause palpitations and sweats
beta blockers will block the ability of adr to cause a tremor, palpitations to increase bpm and sweat
so all of those symptoms are removed and the patient won’t know that they potentially got low blood glucose

60
Q

What combinations of drugs are NOT given to diabetics to treat hypertension?

A

certain combinations of beta blockers and thiazides should not be used at all - contraindicated in diabetics

61
Q

What types of beta-blockers are there?

A

Non-selective - useful for treating anxiety

Selective - useful for treating a range of cvs conditions including hypertension

62
Q

What are the add on vasodilator drugs in stage four of hypertension treatment?

A

a1-antagonists

minoxidil

63
Q

How does minoxidil reduce bp?

A

it opens k channels in vascular smooth muscle
it hypolerises the cell, reduces calcium entry
AAR decreases peripheral resistance and bp

64
Q

How do a1-antagonists cause contraction?

A

normally when they’re activated by noradrenalin, they will produce iP3, increase intracellular ca
leads to smooth muscle contraction

65
Q

Which group of patients are prescribed vasodilator drugs in stage for of hypertension treatment?

A

older males who might have benign prostatic hypertrophy

66
Q

What are the effects of benign prostatic hypertrophy?

A

they take longer to urinate / sometimes won’t urinate
bc an enlarged prostate gland will push in on the urethra
AAR, will restrict the flow of urine

67
Q

What is the effect of vasodilator drugs on benign prostatic hypertrophy?

A

this prostate gland is surrounded by a muscular sheath which has a1 receptors on it
so if a patient who has benign prostatic hypertrophy amd high bp is prescribed an alpha one antagonist like toxins is and will not only relax the muscular sheath around the prostate (allowing the prostate to move away from the Ureta urethra)
but also dilates the blood vessels and reduces bp

68
Q

What should be done if patients aren’t tolerating ACE inhibitors due to lack of sleep?

A

they should be offered an angiotensin receptor blocker instead

69
Q

What are other terms for primary aldosteronism?

A

primary hyperaldosteronism

Conn’s syndrome

70
Q

What is Doxazosin used to treat?

A

benign prostatic hypertrophy

high bp

71
Q

What receptor does angiotensin II act on?

A

AT1 receptors in the efferent vessel

M103 T3 (21 decks)

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