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Pharmacology > Pharmacology of hypertension > Flashcards

Pharmacology of hypertension Flashcards

1
Q

What are the core drugs of hypertension?

A

Ramipril, Lisinopril, Perindopril (ACE-i)
Amlodipine, Felodipine (Ca2+ channel blockers)
Bendro-flumethiazide (thiazide), Indapamide (thiazide-like) (Thiazide or thiazide-like diuretics)
Losartan, Irbesartan, Candesartan (Angiotensin receptor blockers)

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2
Q

What is the drug class of Ramipril/ Lisinopril/ Perindopril?

A

There are Angiotensin converting enzyme inhibitors

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3
Q

What is the primary mechanism of action of Ramipril, Lisinopril, Perindopril

A

Inhibit the angiotensin converting enzyme.
Prevent the conversion of angiotensin I to angiotensin II by ACE.

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4
Q

What is the drug target of Ramipril, Lisinopril, Perindopril

A

Angiotensin converting enzyme

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5
Q

What are the main side effects of Ramipril, Lisinopril, Perindopril

A

Cough
Hypotension
Hyperkalaemia (care with K+ supplements or K+-sparing diuretics)
Foetal Injury (AVOID IN PREGNANT WOMEN)
Renal failure (in patients with renal artery stenosis)-
Urticaria/Angioedem

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6
Q

Why is hepatic activation required with the use of Ramipril, Lisinopril, Perindopril

A

Most ACE inhibitors (not lisinopril) are pro-drugs. They require hepatic activation to generate the active metabolites required for therapeutic effects.

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7
Q

What must be monitored when prescribing Ramipril, Lisinopril or Perindopril?

A

eGFR and serum potassium must be regularly monitored when prescribing ACE inhibitors.

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8
Q

What is the drug class of Amoldipine and Felodipine?

A

Calcium channel blockers

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9
Q

What is the primary mechanism of action of Amoldipine and Felodipine?

A

Block L-type calcium channels – predominantly on vascular smooth muscle. This results in a decrease in calcium influx, with downstream inhibition of myosin light chain kinase and prevention of cross-bridge formation. The resultant vasodilation reduces peripheral resistance.

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10
Q

What are the drug targets of Amoldipine and Felodipine?

A

L-type calcium channel

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11
Q

What are the main side effects of Amoldipine and Felodipine?

A

Ankle oedema
Constipation
Palpitations
Flushing/Headaches

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12
Q

Dihydropyridine type calcium channel blockers demonstrate a higher degree of vascular selectivity, true or false?

A

TRUE

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13
Q

What is the drug class of Bendro-flumethiazide (thiazide) and Indapamide (thiazide-like)

A

Thiazide or thiazide-like diuretics

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14
Q

What is the primary mechanism of action of Bendro-flumethiazide (thiazide) and Indapamide (thiazide-like)

A

They block the Na+, Cl- co-transporter in the early DCT. Therefore Na+ and Cl- reabsorption is inhibited.
As a result the osmolarity of the tubular fluid increases, decreasing the osmotic gradient for water reabsorption in the collecting duct.
- decreases blood volume
- decreases venous return/ cardiac output
- decreases b.p

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15
Q

What are the drug targets of Bendro-flumethiazide (thiazide) and Indapamide (thiazide-like)?

A

Sodium/chloride cotransporter

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16
Q

What are the main side effects of Bendro-flumethiazide (thiazide) and Indapamide (thiazide-like)?

A

Hypokalemia
Hyponatremia.
Metabolic alkalosis (increased hydrogen ion excretion)
Hypercalcemia.
Hyperglycemia (hyperpolarised pancreatic beta cells).
Hyperuricemia.

17
Q

How long can you use the diuretics Bendro-flumethiazide (thiazide) and Indapamide (thiazide-like)

A

Thiazide and thiazide-like diuretics both lose their diuretic effects within 1-2 weeks of treatment. Continuing anti-hypertensive action appears to be due to vasodilating properties (these are more pronounced for the thiazide-like diuretics)

18
Q

What is the drug class of Losartan, Irbesartan and Candesartan?

A

Angiotensin receptor blockers

19
Q

What is the primary mechanism of action of Losartan, Irbesartan and Candesartan?

A

These agents act as insurmountable (i.e. non-competitive) antagonists at AT1 receptor (found on kidneys and on the vasculature)

20
Q

What is the drug target of Losartan, Irbesartan and Candesartan?

A

Angiotensin receptor

21
Q

What are the main side effects of Losartan, Irbesartan and Candesartan?

A

Hypotension
Hyperkalaemia (care with K+ supplements or K+-sparing diuretics)
Foetal Injury (AVOID IN PREGNANT WOMEN)
Renal failure (in patients with renal artery stenosis)

22
Q

What is more effective for hypertension, angiotensin receptor blockers or ACEi?

A

Most trials indicate that angiotensin receptor blockers are not as effective anti-hypertensive agents as ACE inhibitors.

23
Q

What drugs require hepatic activation before use?

A

Losartan and candesartan are pro-drugs. They require hepatic activation to generate the active metabolites required for therapeutic effects.

24
Q

What are the “seven steps” taken when prescribing drugs?

A
  1. Identify the patient’s problem
  2. Specify the therapeutic objective
  3. Select a drug on the basis of comparative efficacy, safety, cost and suitability
  4. Discuss choice of medication with patient (and carer) and make a shared decision about treatment
  5. Write a correct prescription
  6. Counsel the patient on appropriate use of the medicine
  7. Make appropriate arrangements for follow up (Monitor/stop the treatment)
25
Q

What is the mechanism of action of calcium channel blockers in the treatment of hypertension?

A
  1. Reduced vascular smooth muscle contractions=
  2. Reduced cardiac contraction= reduced cardiac output= reduced b.p
  3. Reduced vasoconstriction of blood vessels= reduced peripheral resistance= reduced b.p
26
Q

What is the mechanism of action of ACE inhibitors in the treatment of hypertension?

A
  • ACE enzyme catalyses the conversion of angiotensin I into angiotensin II
  • Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion (causes water to be reabsorbed along with sodium; this blood pressure)
  • Inhibition decreases vasoconstrictor, decreasing blood pressure
27
Q

Why are ACEi associated with the side effects of cough whereas angiontensin receptor blockers are not?

A
  • ACE enzyme also converts bradykinin ( causes contraction of smooth muscle and dilation of blood vessels) into inactive metabolites
  • ACEi cause a build up of bradykinin- too much becomes irritative=
    COUGH
28
Q

What is more ideal to use ACEi or ARBs for the treatment of hypertension

A

DEPENDS:
- generally ACEi are used ahead of angiotensin 2 receptor blockers (ARBs) partly due to cost
- Evidence also shows the ACEi’s are more effective

BUT:
- ARBs are more suitable for patients of African or Caribbean descent

29
Q

Why might ACEi’s have a negative effect on eGFR and serum potassium?

A
  • ACE enzyme catalyses the conversion of angiotensin I into angiotensin II
  • Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion

DECREASED VASOCONSTRICTION=
* Increased dilation of efferent arterioles
* Glomerular pressure decreases
* eGFR regulation is lost
* Ability to filter decreases
* Causes build up of toxins in the blood= acute renal failure

DECREASED ALDOSTERONE=
* No sodium retention & reduced potassium lose
* High K+ in the cell
* leads to cardiac rhythm abnormality

30
Q

Two of the most commonly prescribed ACE inhibitors are ramipril and lisinopril. Ramipril (like most ACE inhibitors) is a pro-drug whereas lisinopril is not. What does this mean?

A

“Pro-drug”= the drug is inactive before metabolism
- requires metabolism via liver
- if liver function decreases and you take a pro drug, you won’t get any active drug
- Whereas lisinopril is an “active drug”= drug takes effect directly

31
Q

Indapamide (and other thiazide-like diuretics) are excreted unchanged in the urine.

Why is this a vital part of the therapeutic action of thiazide-like diuretics?

A

The diuretics need to move from the blood -> transported on basolateral side, and only then can it access the sodium chloride transporter on the apical side of distal tubule

32
Q

Why do the diuretic effect of thiazides only last 1-2 weeks?

A

The kidney becomes tolerant to the diuretics because there is a rebound activation of the renin angiotensin system which counteracts the diuretic effect due to increasing sodium reabsorption.

33
Q

Why do thiazides continue to have an anit-hypertensive effect, when their diuretic effect only lasts 1-2 weeks?

A

The continuing anti-hypertensive effect of thiazides is due to a further (less well understood) vaso-dilating action.

Pharmacology (7 decks)

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