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Charis & Ellie vs Renal > Pharmacology and Kidneys > Flashcards

Pharmacology and Kidneys Flashcards

1
Q

2 names of loop diuretics?

A

Furosemide

Bumetanide

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2
Q

Indication for loop diuretics?

A
  • Pulmonary oedema
  • CHF
  • CKD
  • Hepatic cirrhosis with ascites
  • Diuretic-resistant oedema (in combo with thiazide)
  • Add on for HT
  • Reduce acute hypercalcaemia
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3
Q

Mode of action for loop diuretics?

A 
-Absorbed in GI tract 
|
-Bind to Plasma proteins 
|
Enter nephron by OAT 
|
Targets Cl- site & blocks the NKCC2 triple transporter on the apical surface of the tubular epithelium (thick ascending loop of henle TAL) 
|
Decrease tonicity of the medullary interstitium 
-Prevent dilution of filtrate in TAL 
-Increase Na+ load delivered to distal nephron (causing K+ loss_
-Increase Ca2+ and Mg2+ excretion 
-Additional venodilator action
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4
Q

What is an OAT?

A

Organic anion transporter

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5
Q

What site do loop diuretics target?

A

Cl-

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6
Q

What is result of Loop diuretics blocking NKCC2 triple transporter?

A

Prevents dilution of filtrate in TAL

-Increasing Na+ load delivered to distal nephron

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7
Q

Contraindications for loop diuretic?

A

Hypovolaemia/dehydration

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8
Q

Be cautious of what with loop diuretics?

A

Hypokalaemia
Hyponatraemia
Hepatic encephalopathy
Gout

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9
Q

Side effects of loop diuretic?

A
  • Hypokalaemia
  • Metabolic acidosis (increased H+ secretion)
  • Hypocalcaemia
  • Hypomagnesaemia
  • Hypovolaemia & hypotension
  • Hyperuricaemia (can precipitate acute gout)
  • Dose related hearing loss
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10
Q

Example of thiazide diuretic?

A

Bendroflumethiazide

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11
Q

Indications for thiazide diuretic?

A 
HT 
Mild heart failure 
Severe resistant oedema (combo with loop)
Renal stone disease 
Nephrogenic diabetes insipidus
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12
Q

Mechanism of thiazide diuretic?

A
  • Absorbed from GI Tract to enter nephron by OAT
  • Target CL- site and Block Na+/Cl- co-transporter
  • Prevents dilation of urine in early DCT
  • Increases Na+ load going to Collecting tubule (K+ loss)
  • Increases reabsorption of Ca2+
  • Additional vasodilator action
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13
Q

Where is the Cl-/Na+ cotransporter?

A

Tubular epithelium of early distal convoluted tubule

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14
Q

Main mechanism of thiazide/thiazide-like diuretic?

A

Increases reabsorption of Ca2+

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15
Q

Contraindications of thiazide/thiazide-like diuretic?

A

Hypokalaemia

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16
Q

Be cautious using thiazide/TL diuretics if patient has?

A

Hyponatraemia

Gout

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17
Q

Side effects of thiazide/TL diuretics?

A
  • Hypokalaemia
  • Metabolic alkalosis
  • Hypovolaemia & hypotension
  • Hypomagnesaemia
  • Hyperuricaemia (poss lead to gout)
  • Erectile dysfunction
  • Impaired glucose tolerance in diabetics
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18
Q

Examples of thiazide-like diuretics?

A
  • Chlortalidone
  • Indapamide
  • metolazone
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19
Q

Indications for thiazide like diuretics?

A 
HT 
Mild heart failure 
Severe resistant oedema (combo with loop)
Renal stone disease 
Nephrogenic diabetes insipidus
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20
Q

Mechanism of thiazide like diuretics?

A
  • Absorbed from GI Tract to enter nephron by OAT
  • Target CL- site and Block Na+/Cl- co-transporter
  • Prevents dilation of urine in early DCT
  • Increases Na+ load going to Collecting tubule (K+ loss)
  • Increases reabsorption of Ca2+
  • Additional vasodilator action
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21
Q

Example of potassium sparing diuretics?

A

Spironolactone
Eplerenone
Amiloride hydrochloride
Triamterene

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22
Q

Indications for potassium sparing diuretics?

A
  • Heart failure
  • Primary
  • Hyperaldosteronism (Conns)
  • Resistant HT
  • Secondary hyperaldosteronism

Used in combo with thiazides and loops to prevent hyperkalaemia

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23
Q

Mechanism of potassium sparing diuretics?

A

Limited diuretic action

  • Competitive antagonists of aldosterone at cytoplasmic aldosterone receptors
  • increase Na+ excretion
  • Decrease K+ excretion
  • Block luminal Na channels in collecting tubules
  • Increase Na+ excretion
  • Decrease K+ excretion
  • Enter nephron via OCT in proximal tubule
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24
Q

What is spironolactone metabolised to?

A

Rapidly spironolactone metabolised to canernone

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25
Q

Contraindications of potassium sparing diuretic?

A
  • Severe renal impairment
  • Anuria
  • Hyperkalaemia
  • Addison’s disease
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26
Q

Cautions for potassium sparing diuretic?

A

Acute porphyria’s

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27
Q

Side effects of potassium sparing diuretic?

A

Metabolic acidosis
AKI
Other random stuff

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28
Q

Triamterene has what type of GI absorption?

A

Good GI absorption

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29
Q

Amiloride has poor GI absorption. True or False?

A

True

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30
Q

Cautions using triamterene?

A

DM
Gout
Can cause blue fluorescence of urine

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31
Q

Side effects of triamterene?

A

Diarrhoea
Hyperkalaemia
Uncommon- hyperuricaemia, reversible renal failure

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32
Q

Example of osmotic diuretics?

A

Mannitol (IV)

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33
Q

Indications for osmotic diuretics?

A

Prevention of acute hypovolaemic renal failure: maintains urine flow

-Emergency treatment of acutely raised intracranial pressure/intraocular (increases plasma osmolarity which extracts water from these compartments)

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34
Q

Mechanism of osmotic diuretic?

A

IV infusion enters nephron via simple glomerular filtration

  • Remains in filtrate (too polar for reabsorption)
  • Creates osmotic potential for water
  • Dilutes solute in proximal tubule (decreases force for sodium to move from tubular fluid into interstitium)
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35
Q

Contraindications for osmotic diuretic?

A 
Anuria 
Intracranial bleeding 
Severe cardiac failure 
Severe dehydration 
Severe pulmonary oedema
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36
Q

Caution using osmotic diuretics if?

A

Extravasation causes inflammation and thrombophlebitis

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37
Q

Side effects of osmotic diuretic?

A

Pretty generic (wow specific)

38
Q

Example of carbonic anhydrase inhibitors?

A

Acetazolamide

39
Q

Indications for carbonic anhydrase inhibitors?

A

NOT USED AS DIURETIC ANYMORE

  • Glaucoma
  • Altitude sickness prophylaxis
40
Q

Mechanism of carbonic anhydrase inhibitors?

A

Increase HCO3- excretion with Na+, K+, H20

41
Q

Contraindications of carbonic anhydrase inhibitors?

A
  • Adrenocortical insufficiency
  • Metabolic acidosis
  • Hypokalaemia
  • Hyponatraemia
42
Q

Caution if using carbonic anhydrase inhibitors if?

A

DM
Elderly
Renal calculi (stones)

43
Q

Side effects of carbonic anhydrase inhibitors?

A

Metabolic acidosis
Haemorrhage
Nephrolithiasis

44
Q

Indications for citric acid with potassium citrate?

A

Relief or discomfort i mild UTIs
-Alkalises urine

-May help prevent renal stone formation (ionised form is preferred- rather than crystal)

45
Q

Contraindications for citric acid with potassium citrate?

A

Avoid in severe renal impairment

46
Q

Side effects of citric acid with potassium citrate?

A

Hyperkalaemia
Nausea
Vomiting

47
Q

Name for synthetic ADH analogue?

A

Desmopressin

48
Q

Indications for synthetic ADH analogue?

A

Treatment for neurogenic diabetes insipidus
-Primary nocturnal enuresis
-Post-operative polyuria/polydipsia
(also an investigation)

49
Q

Mechanism of Synthetic ADH analogue?

A

Specific to V2 receptor (found only in kidneys)

Acts to replace ADH that is otherwise not being secreted from the pituitary gland

50
Q

Contraindications for synthetic ADH analogue?

A
  • Cardiac insufficiency
  • Conditions treated with diuretics
  • History of hyponatraemia
  • Polydipsia in alcohol dependence
  • SIADH
51
Q

Cautions with synthetic ADH analogue?

A

Conditions aggravated by water retention, CF

52
Q

Side effects of synthetic ADH analogue?

A

HYPONATRAEMIA

53
Q

Example of aquaretic/Vapten?

A

Tolvaptan

54
Q

Indications for aquaretic?

A

-Hyponatraemia secondary to syndrome of inappropriate ADH secretion

55
Q

Mechanism of aquaretic?

A

-Competitive antagonists to V1 or V2 receptor (target the Hs protein specifically)
Blocks ADH effect
-Reduced permeability at apical membranes & enhanced water excretion via aquaporins (Na not removed with water)

56
Q

Contraindications for aquaretics?

A

Anuria
Hypernatremia
Hypovolemic
Volume depletion

57
Q

Cautions when using aquaretics?

A

Abnormal LFTs
Diabetes mellitius
Risk of dehydration
Urinary outflow obstruction

58
Q

How thiazide and loop diuretics cause K+ loss?

A
  1. Increase Na+ load (loop/thiazide diuretics) produces enhanced Na+ reabsorption
  2. Results in charge separation= lumen more -ve causing DEpolarization of luminal vs basolateral membrane
  3. Increased driving force of K+ across luminal membrane enhanced K+ secretion (number of ROMK channels increase)
  4. Secreted K+ is washed away by increased urinary flow rate
59
Q

Syndromes that mimic diuretic effects?

A

Gitelman Syndrome

Bartter syndrome

60
Q

Major sites of diuretic action in the nephron?

A

PCT
Thick ascending loop of Henle
Early distal convoluted tubule
Collecting tubule and duct

61
Q

What exchanges happen in PCT?

A
  • Na+ (passive Cl- reabsorption)

- Na+/H exchange

62
Q

Exchange in the thick ascending limb of loop of henle?

A

Na+/K+/Cl- co-transport

63
Q

What is transport in thick ascending limb of loop of Henle blocked by?

A

Loop diuretics- significant diuresis

64
Q

What is transport in PCT blocked by?

A

Carbonic anhydrase inhibitors
-Mild diuresis
Inhibit production of H2CO3 H+ and HCO3-

65
Q

Transport in early distal convoluted tubule?

A

Na+/H+ exchange

Na+/Cl- co-transport

66
Q

What is Na+/H+ exchange blocked by?

A

Carbonic anhydrase inhibitors (mild diuresis)

67
Q

What is Na+/Cl- co-transport blocked by?

A

Thiazide diuretics: modest diuresis

68
Q

What occurs in collecting tubule and duct?

A

Na+/K+ exchanged

69
Q

What blocks Na+/K+ exchange in Collecting tubule and duct?

A

Potassium sparing diuretics

70
Q

Site of diuretic action in nephron?

A

Apical membrane

71
Q

OATs secrete what into PCT?

A

Acidic drugs: thiazides, loop agents

72
Q

OCTs secrete what into PCT?

A

Basic drugs: triamterene, amiloride

73
Q

Where do loop diuretics work on?

A

Thick ascending loop of Henle

74
Q

If you use loop diuretics what will build up in the tubule?

A

Na
2Cl
K+

75
Q

What does both loop and thiazide diuretics cause?

A

Hypokalaemia

76
Q

What can loop diuretics cause?

A

Hypocalcaemia

77
Q

What don’t thiazide diuretics cause?

A

Hypocalcaemia

THEY = ORMOCALCAEMIA

78
Q

If an old person with osteoporosis needs diuretics which should you give them?

A

THIAZIDE DIURETICS

79
Q

What are prostaglandins synthesized in response to?

A 
Ischaemia 
Mechanical trauma 
Angiotensin II 
ADH 
Bradykinin
80
Q

What would a NSAID and ACI combo be?

A

DETRIMENTAL

81
Q

Effects of prostglandins?

A

Vasodilators

Natriuretic

82
Q

What do NSAIDs inhibit?

A

Enzyme cyclo-oxygenase 1 and cyclo-oxygenase 2

83
Q

What is cyclo-oxygenase 1 & 2 required for?

A

Prostaglandin and thromboxane synthesis

84
Q

What effect do prostaglandins have?

A

Vasodilatory effect on renal afferent arteriole, thereby increasing GFR

85
Q

How heavy is role of prostaglandins in a healthy individual?

A

Minimal

86
Q

In states of volume depletion how effective are prostaglandins?

A

Prostaglandin induced vasodilation is vital compensatory mechanism (Heat fauilure, dehydration)

87
Q

Why avoid NSAIDs in patients with renal impairment?

A

Inhibition of renal prostaglandin synthesis can result in vasoconstriction of afferent arteriole and decreased GFR

88
Q

Angiotensin induces what?

A

Vasoconstriction of efferent arteriole, therefore increasing intraglomerular perfusion pressure and GFR

89
Q

What happens to GFR when angiotensin is blocked by ACEis/ARBs?

A

Reduced

90
Q

What can ACEis/ARBs cause?

A

Hyperkalemia

Charis & Ellie vs Renal (40 decks)

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