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BOK280 > Kidneys (pharmacology) > Flashcards

Kidneys (pharmacology) Flashcards

1
Q

List two ways in which blood pressure is normalised.

A

-Baroreceptor reflex system
-Renin-Angiotensin-Aldosterone system (RAAS)

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2
Q

What does the RAAS function to control? (4)

A

-Blood volume
-Vascular tone
-Potassium excretion
-Sodium and water reabsorption

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3
Q

Organs systems involved in RAAS (4)

A

Kidney, lungs, systemic vasculature, brain.

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4
Q

Explain the RAAS mechanism, eg when there is a drop in BP. (4)

A

•Drop in BP stimulates the release of renin from the kidneys.
•Renin cleaves angiotensinogen to angiotensin 1.
•Angiotensin 1 is cleaved into angiotensin 2 by the angiotensin converting enzyme in the lungs.
•Angiotensin 2 acts on various systems, which then increases the BP.

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5
Q

What are the effects of angiotensin 2 (4)

A

•Vascular effects: Causes vasoconstriction to increase bloop pressure.
•Renal: Stimulates reabsorption of sodium and water in the proximal convoluted tubules.
•Neural: Stimulates thirst and the release of ADH
:Activates the sympathetic nervous system.
•Adrenal glands: Causes release of aldosterone from the zona glomerulosa of the adrenal cortex.

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6
Q

What is the role of aldosterone in RAAS? (3)

A

•Aldosterone upregulates the sodium/potassium pumps in the distal tubule and collecting ducts.
•Also upregulates the channels in collecting ducts.
•This increases the reabsorption of sodium and water and increases the excretion of potassium.

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7
Q

What effects does ADH have on RAAS? (4)

A

•Inserts aquaporin-2 channels on the membranes of distal tubule and collecting ducts.
•This increases water reabsorption.
•Also increases Na+ reabsorption in the loop of henle.
•Causes vasoconstriction, which increases BP.

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8
Q

Which diseases/disorders does hypertension leads to risk of? (4)

A

-Myocardial infarction
-Kidney failure/ decrease in function
-Congestive heart failure
-Chronic venous insufficiency

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9
Q

What are the two targets that drugs affecting RAAS act on?

A

ACE - ace inhibitors inhibits production of ACE.
AT 1 receotor- Angiotensin 2 receptor blockers

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10
Q

Mechanism of action for ace inhibitors.

A

Block conversion of Angiotensin 1 to Angiotensin 2.

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11
Q

Suffix for ace inhibitors

A

-pril

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12
Q

Name the types of ace inhibitors

A

Class 1(captopril like): Captopril
Class 2: enalapril, ramipril, trandopril etc.
Class 3: Lisinopril

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13
Q

What are the side effects of ace inhibitors?

A

Dry, persistent cough; Hypotension; Taste disturbances.
Hyponatraemia; Hyperkalaemia.
Nephrotoxicity
Photosensitivity

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14
Q

Contraindications for ace inhibitors

A

Pregnancy, renal stenosis

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15
Q

Mechanism of action for AT 2 receptor blockers

A

Reversible competitive antagonists of AT 2 receptor.

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16
Q

Suffix for AT 2 receptor blockers

A

-tan

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17
Q

Some of the examples of AT 2 receptor blockers

A

Losartan, Telmisartan, Valsartan etc

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18
Q

Side effects of AT2 receptor blockers

A

Dizziness, hyperkalaemia, hypotension.

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19
Q

Contraindications for AT2 receptor blockers

A

Renal stenosis, pregnancy

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20
Q

What causes oedema?

A
  • High reabsorption of sodium chloride .
    -Causes water retention.
    -Expansion of extravascular fluid compartments.
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21
Q

What are some of the oedematous states?

A

Congestive heart failure, Premenstrual oedema, Nephrotic syndrome, Hepatic cirrhosis.

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22
Q

Which part of the nephron is responsible for the active reabsorption of 60-70% of Na+?

A

Proximal convoluted tubule

23
Q

Explain briefly the reabsorption process that takes place in the proximal convoluted tubule.

A
  • Exchange of Na+ for H+ via the Na+/H+ transporters.
    -H+ provided by dissociation of carbonic acid via carbonic anhydrase.
    -Na+/K+ pumps which kicks out sodium and pump in potassium.
    -Water follows sodium, hence blood volume increases.
24
Q

Regulation of the reabsorption in proximal convoluted tubule is through which drugs?

A

Carbonic anhydrase ihibitors (acetazolamide)
Osmotic diuretics (mannitol)

25
Q

How do the carbonic anhydrase inhibitors regulate reabsorption (mechanism of action)? (3)

A

-They block the formation of carbonic acid which dissociates to form H+.
-They will be no H+ available for the sodium/hydrogen antiporter.
-Sodium remains in the lumen and hence water.

26
Q

What is the clinical indication and side effect of the carbonic anhydrase inhibitors?

A

Clinical indication- Used to treat glaucoma.
Side effect- Metabolic acidosis, due to bicarbonate ion loss.

27
Q

What are osmotic diuretics?

A

Pharmacologically inactive compounds that retain water.

28
Q

What is the mechanism of action for mannitol?

A

Increases the osmolarity inside the tubules, ‘holding back’ water.

29
Q

Clinical indication of mannitol

A

Acute elevated intracranial and intraocular pressure.

30
Q

What are the side effects of mannitol? (3)

A

Systemic acidosis
Left ventricular failure due to increased ECF.
Hyponatraemia

31
Q

Briefly explain the reabsorption process that takes place in the loop of henle. (5)

A

•Reabsorption of Na+ in the ascending limb.
-Permeable to Na+ but impermeable to water.
-Na+ enter the cells via the Na+/H+/2Cl- symporter.
-It is then reabsorbed via the Na+/K+ antiporter.

•Reabsorption of water in the descending limb
-Permeable to water, but impermeable to Na+.
-This increases osmolarity from cortex to medulla.

32
Q

Which drugs are active in the loop of henle?

A

Loop diuretics

33
Q

What is the mechanism of action for loop diuretics?

A

Inhibition of Na+/K+/Cl- symporter.
Less Na+ reabsorption

34
Q

Two examples of loop diuretics

A

Furosemide, Bumetanide

35
Q

Clinical indications for furosemide and bumetanide? (4)

A

Heart failure and hypertension.
Pulmonary oedema and hypercalcaemia.

36
Q

Side effects of loop diuretics (5)

A

-Hypokalaemia, hypocalcaemia, hypomagnesaemia, hypovolaemia, hyperuricaemia.

37
Q

Explain the reabsorption process in the distal convoluted tubule. (2)

A

-Na+ reabsorption into tubular cell by Na+/Cl- carrier.
-Na+ is transported to interstitium by Na+/K+ ATPase.

38
Q

Drugs present in the distal convoluted tubule (3)

A

Thiazides
Indapamide
Chlortalidone

39
Q

Another name for loop diuretics

A

High-ceiling diuretics

40
Q

What is the mechanism of action for low ceiling diuretics?

A

Blocks the Na+/Cl- symporter.
Less Na+ for reabsorption.

41
Q

An example of low ceiling diuretic

A

Hydrochlorothiazide

42
Q

Clinical indications for indapamide and hydrochlorothiazide

A

-Hypertension, Mild heart failure and Nephrogenic diabetes insipidus.

43
Q

Side effects of the low ceiling diuretics

A

Hyponatraemia, hypokalaemia, hypocalcuria.
Hyperglycaemia, erectile dysfunction.
Accumulation in renal failure.

44
Q

Briefly explain the reabsorption process in the collecting ducts.

A

•Reabsorption of sodium
-Sodium enters the cells via Na+ channels and is transported to the medullar interstitium via Na+/K+ ATPase.
-Expression is modulated by aldosterone.

•Passive reabsorption of water
-Aquaporins allow for water reabsorption
-Expression is modulated by vasopressin.

45
Q

Which drugs are active in the collecting duct (3)

A

-Mineralocorticoids receptor antagonist
-ADH antagonist
-Na+ channel blockers

46
Q

Mechanism of action for sodium channel blockers.

A

They block the Na+ channel on the luminal side.

47
Q

Examples of sodium channel blockers

A

Amiloride and triamterene

48
Q

Clinical indicators for amiloride and triamterene (3)

A

Hypertension, congestive heart failure and oedema

49
Q

Side effect of triamterene

A

Deplets folic acid

50
Q

Mechanism of action for aldosterone antagonists

A

Competitive antagonist for moneralocorticoid receptor.
Prevents aldosterone from binding.

51
Q

Examples of aldosterone antagonists

A

Spironolactone and eplerenone

52
Q

Clinical indications for spironolactone and eplerenone (3)

A

Hypertension
Heart failure
Hyperaldosteronism

53
Q

Side effects of spironolactone and eplerenone (2)

A

Hyperkalaemia and Gynecomastia

54
Q

Relationship btwn dose and low ceiling as well as high ceiling diuretics.

A

Increase in dose:
-Increases the diuretic capability of high ceiling diuretics.
-Does not promote further diuretic response in low ceiling diuretics.

BOK280 (66 decks)

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