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Pharmacology Flashcards

1
Q

What is the general mechanism of action of diuretics?

A

Increase urine flow by inhibiting the reabsorption of electrolytes and enhance salt/water excretion where increased ECF causes tissue swelling

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2
Q

In what circumstance does oedema occur?

A

When formation does not equal absorption of interstitial fluid

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3
Q

Which forces move fluid out of the capillary?

A

Pc - capillary hydrostatic

Pi i - interstitial oncotic

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4
Q

Which forces move fluid into the capillary?

A

Interstitial hydrostatic

Plasma oncotic

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5
Q

What changes to the forces result in oedema?

A

Increase in capillary hydrostatic or decrease in plasma oncotic

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6
Q

Name three disease that can cause oedema

A
  • heart failure
  • cirrhosis
  • nephrotic syndrome
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7
Q

How does decreased plasma oncotic pressure lead to oedema?

A

Increased interstitial fluid
Decreased blood volume, activates RAAS which leads to salt/water retention increasing capillary hydrostatic and reducing plasma oncotic

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8
Q

How does congestive heart failure lead to oedema?

A

Reduced cardiac output leads to renal hypoperfusion activating RAAS causing increased blood volume and increasing venous/capillary pressures

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9
Q

Describe how cirrhosis causes oedema

A

Increased pressure in portal vein and decreased albumin leads to loss of fluid in the peritoneal cavity (ascites)

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10
Q

Which part of the cell do diuretics usually work?

A

Apical membrane

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11
Q

What happens to most salt and water that enters the filtrate?

A

It is reabsorbed

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12
Q

How can diuretics enter the filtrate?

A
  • glomerular filtration

- secretion in proximal tubule (organic anion/cation)

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13
Q

Give examples of drugs that move via organic anion transport

A

Simvastatin
Furosemide
NSAIDs
Penicillin

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14
Q

Describe what happens at the basolateral membrane in organic anion transport

A

OA- enters against the gradient in exchange for alpha ketogluterate which moves against its own gradient by a sodium transporter

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15
Q

Describe what happens at the apical membrane in organic anion transport

A

OA- crosses via multidrug resistance proteins and breast cancer resistance protein and comes from the lumen via OAT 4 in exchange for alpha ketogluterate

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16
Q

Give examples of drugs that move by organic cation transport

A

Triamterene

Amiloride

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17
Q

What happens in the cation transport at the basolateral membrane?

A

Enters by OCT2 which is driven by electrical potentials

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18
Q

What happens in cation transport at the apical membrane?

A

Enters lumen via MATE and MDR1 in a rate limiting manner

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19
Q

Name two loop diuretics

A

Furosemide and bumetanide

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20
Q

Describe the mechanism of action of loop diuretics

A

Inhibits sodium/potassium/chlorine triple transporter by binding to the chloride site

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21
Q

What is the effect of loop diuretics binding to the chloride site?

A

Decrease tonicity of the interstitial and prevents dilution of filtrate in ascending limb
Increased sodium delivered to distal regions, increased calcium and magnesium excretion

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22
Q

State the indications for loop diuretics

A

Reduce salt/water overload (HF/ascites/nephrotic syndrome)
Increases urine volume in AKI
Resistant hypertension
Reduce hypercalcaemia

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23
Q

When are loop diuretics contraindicated?

A

Severe hypovolaemia

Dehydration

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24
Q

Name the side effects of loop diuretics

A
  • hypokalaemia
  • metabolic alkalosis
  • hypocalcaemia
  • hypomagnesaemia
  • hypovolaemia
  • hypotension
  • hyperuricaemia (gout)
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25
Name two thiazide/thiazide like diuretics
Bendroflumathiazide | Indapamide
26
Describe the mechanism of action of thiazide diuretics
Inhibit the sodium/chloride carrier by binding to the chloride site - this prevents dilution of filtrate and increases sodium delivery to the collecting duct and increases calcium reabsorption
27
Where are most diuretics absorbed?
GI tract
28
What are the indications for thiazide diuretics?
``` Mild heart failure Hypertension Resistent oedema Renal stones Nephrogenic diabetes insipidus ```
29
What are the contraindications of thiazide diuretics?
Hypokalaemia Gout Hyponatraemia
30
State the side effects of thiazide diuretics
- hypokalaemia - metabolic acidosis - hypovolaemia/hypotension - hypomagnaesmia - hyperuricaemia - erectile dysfunction - impaired glucose tolerance
31
How do diuretics cause potassium loss?
Increased sodium enhances sodium reabsorption and the charge separation leads to a gradient across the lumen and an increased driving force of potassium secretion
32
Name four potassium sparing diuretics
- amiloride - triamterene - spironolactone - eplerenone
33
Describe the mechanism of action of amiloride and triamterene
Block the apical sodium channel and reduce sodium reabsorption by blocking sodium channels in the collecting tubules
34
Describe the mechanism of action of spironolactone and eplerenone
Compete with aldosterone for intracellular receipts preventing the action of steroid. Increase sodium excretion and decrease potassium excretion
35
What are the clinical indications fro potassium sparing diuretics?
Heart failure Hyperaldosteronism Resistant essential hypertension
36
Why are potassium sparing diuretics usually used in conjunction with thiazide/loop diuretics?
Alone they can cause hyperkalaemia
37
State the contraindications of potassium sparing diuretics
Severe renal impairment Addison's Hyperkalaemia
38
Give an example of an osmotic diuretic
Mannitol
39
Describe the mechanism of action of osmotic diuretics
Enter the nephron by glomerular filtration but are not reabsorbed - they increase the osmolality of filtrate opposing water and sodium reabsorption
40
State the indications for osmotic diuretics
- prevention of acute pre-renal failure | - increased ICP/intraocular pressure
41
What are the side effect of osmotic diuretics?
Transient expansion of blood volume and hyponatraemia
42
What can cause osmotic diuresis?
hyperglycaemia, iodine contrast
43
Name a carbonic anhydrase inhibitor
Acetazolamide
44
What can carbonic anhydrase inhibitors cause?
Alkaline diuresis | Metabolic acidosis
45
When are carbonic anhydrase inhibitors?
Glaucoma Altitude sickness Infantile epilepsy
46
When is it useful to alkalise urine?
Can help with dyuria, decrease stone formation and enhance acid excretion (useful in aspirin overdose)
47
State three things that inhibit vasopressin
- lithium - demedocycline - vaptans
48
When can synthetic vasopressin be used?
To treat neurogenic diabetes insipidus - replaces lack of secretion from the posterior pituitary Can also be used in bed wetting
49
Can nephrogenic diabetes insipidus be treated?
No - it is genetic X linked
50
How do vaptans work?
Act as competitive antagonists of vasopressin receptors
51
Name the two types of vasopressin receptor and what they do
V1A - vasoconstriction | V2 - water reabsorption by aquaporins
52
Give an example of a vaptan that treats SIADH and explain its mechanism
Tolvaptan | Blocking of V2 leads to water excretion and increased plasma sodium
53
Give an example of a vaptan that treats heart failure
Conivaptan | Blocks both receptors used in hypervolaemic hyponatraemia
54
Name an SGLT2 inhibitor
Canagliflozin
55
Where is SGLT2 found?
Proximal tubule and reabsorbs glucose by secondary active transport and facilitated diffusion at the basolateral membrane. Glucose is transported by coupling with sodium influx
56
What does inhibition of SGLT2 cause?
Glucosuria - used in T2DM
57
State two types of prostaglandins
PGE2 - medulla | PGI2 - glomeruli
58
What is needed for prostaglandins to be produced?
COX1/2
59
What are the effects of prostaglandins on the kidneys?
They cause vasodilation in the afferent arteriole, releasing renin and causing efferent constriction to increase GFR
60
What drugs inhibit COX?
NSAIDs
61
In what cases are NSAIDs detrimental?
Conditions that rely on prostaglandins to maintain renal blood flow e.g HF and cirrhosis
62
What drugs act on the kidneys and are useful in gout?
Probenecid and sulfinpyrazole - block rate reabsorption in the proximal tubule

Renal (20 decks)

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