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BRS Y2 > Pharmacology of Hypertension > Flashcards

Pharmacology of Hypertension Flashcards

1
Q

What is Q risk?

A

Cardiovascular risk= risk of having a stroke or heart attack in the next 10 years

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2
Q

What are the 2 main calcium channel blockers (CCBs)?

A

Amlodipine

Felodipine

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3
Q

What hypertensive patients are CCBs prescribed to?

A

Those who aren’t black or diabetic

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4
Q

What is the target site of CCBs?

A

L type calcium channel

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5
Q

What is the location where CCBs work?

A

Vascular smooth muscle

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6
Q

What is the effect of CCBs?

A

Relaxes smooth muscle by blocking calcium influx

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7
Q

How do CCBs affect cardiac output?

A

Slightly reduce it

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8
Q

At what time of day is blood pressure highest?

A

In the morning

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9
Q

Define clearance

A

The measure of the ability of the body to eliminate a drug

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10
Q

Define elimination half life

A

The length of time required for the concentration of a particular drug to decrease to half of its starting dose in the body

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11
Q

Define time to peak plasma levels and explain how absorption rate effects it

A

Time required for a drug to reach peak concentration in plasma. The faster the absorption rate, the lower is the time to peak plasma concentration.

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12
Q

What do swollen ankles in hypertension indicate?

A

Decreased cardiac output and heart failure

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13
Q

What is the target site for ACE inhibitors?

A

Angiotensin converting enzyme

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14
Q

Where is the location where ACE inhibitors work?

A

Lungs and kidneys

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15
Q

What is the effect of ACE inhibitors?

A

Less angiotensin II production so less vasoconstriction, salt/water retention and aldosterone secretion

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16
Q

Why do ACE inhibitors cause a cough as a side effect?

A

They stop the conversion of bradykinin into inactive metabolites causing a cough

17
Q

How does losartan work and why doesn’t it cause a cough?

A

It blocks angiotensin receptors not ACE so bradykinin can still be converted into inactive metabolites

18
Q

How do ACE inhibitors effect eGFR?

A

Reduce it because less angiotensin II is produced, leading to less vasconstriction of the efferent arteriole

19
Q

How do ACE inhibitors increase risk of renal failure?

A

They reduce eGFR which means things that should be filtered out of the blood and be excreted remain in the blood, this is renal failure

20
Q

Why do ACE inhibitors increase serum potassium?

A

Less aldosterone will be produced so less potassium is excreted

21
Q

What is a pro drug?

A

A drug that is only active after being metabolised in the liver

22
Q

What is the target of thiazide like diuretics?

A

Sodium chloride co transporter

23
Q

What is the location where thiazide like diuretics work?

A

Distal tubule cells in nephrons

24
Q

What is the effect of thiazide like diuretics?

A

Sodium chloride reuptake is blocked, osmolarity of tubular fluid increases, more water is retained in the urine, reducing blood pressure

25
Q

How do thiazide like diuretics affect potassium levels and why?

A

They cause hypokalaemia because the sodium chloride reuptake transporter is inhibited and sodium levels in the urine rise.
This causes activation of a cotransporter which reabsorbs sodium and while doing so, excretes potassium into the urine

26
Q

How long does the diuretic effect of thiazide like diuretics last and why?

A

1-2 weeks, the kidney becomes resistant

27
Q

What must be given with thiazide like diuretics? Why?

A

ACE inhibitor, they reverse the hypokalemic effect of thiazide like diuretics

28
Q

What are the main side effects of CCBs?

A

Ankle oedema, constipation, palpitations and headaches/flushing

29
Q

What type of CCBs have a higher degree of vascular selectivity?

A

Dihydropyridine

30
Q

What conversion do ACE inhibitors stop?

A

Conversion of angiotensin I to angiotensin II

31
Q

Are angiotensin receptor blockers as effective as ACE inhibitors?

A

No, they are less effective

32
Q

What type of drug are most ACE inhibitors and angiotensin receptor blockers like losartan?

A

Pro drugs

33
Q

Describe how ACE inhibitors increase serum potassium

A

ACE inhibitors result in less angiotensin II production
Less angiotensin II means less aldosterone is produced
Aldosterone increases the secretion of potassium so if there is less, more potassium will be retained in the kidney

34
Q

What is the target site of angiotensin receptor blockers?

A

AT1 receptor

35
Q

Where is the location at which angiotensin receptor blockers work?

A

Kidneys and vasculature

36
Q

What are the main side effects of angiotensin receptor blockers?

A

Hypotension
Hypercalcaemia
Foetal injury
Renal failure (in patients with renal artery stenosis)

37
Q

What group of anti hypertensive drugs cannot be given to pregnant women? Why?

A

Angiotensin receptor blockers, they can cause foetal injury

38
Q

What are the other main side effects of thiazide like diuretics?

A

Hyponatremia
Metabolic alkalosis (due to increased hydrogen ion secretion)
Hypercalcaemia
Hyperglycaemia (due to hyperpolarized pancreatic beta cells)
Hyperuricaemia

BRS Y2 (85 decks)

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