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Renal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Where is most Na reabsorbed?

A

PCT (67%)

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2
Q

SGLT2 inhibitors inhibit reabsorption of what and where?

A

Glucose in PCT = glucose in urine

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3
Q

Uricosuric drugs

A

Promote excretion of uric acid into urine or prevent reabsorption of uric acid
Treat gout

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4
Q

4 Starling forces

A

Capillary hydrostatic pressure
Capilary oncotic pressure
IF hydrostatic pressure
IF oncotic pressure

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5
Q

Disease states that increase _____ or decrease ______ cause oedema

A

Increase capillary hydrostatic pressure

Decrease capillary oncotic pressure

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6
Q

Causes of oedema

A

Nephrotic syndrome
Congestive HF
Hepatic cirrhosis with ascites

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7
Q

Sign of proteinuria

A

Frothy urine

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8
Q

Congestive HF arises from:

A

Reduced CO = hypovolaemia = activates RAAS

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9
Q

Ascites arises from:

A

Increased HPV pressure, decreased albumin (oncotic pressure) = oedema and activates RAAS

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10
Q

Which diuretics act on PCT?

A

CA inhibitors

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11
Q

Where is next 25% of Na reabsorbed?

A

Thick ascending LOH

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12
Q

Where is last 10% of Na reabsorbed?

A

DCT

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13
Q

Is thick ascending LOH permeable or impermeable to water?

A

Impermeable

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14
Q

What do CA inhibitors block?

A

Na/H exchange in PCT and DCT

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15
Q

Which diuretics act on thick ascending LOH?

A

Loop diuretics

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16
Q

What do loop diuretics block?

A

Na/K/2Cl in thick ascending LOH

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17
Q

What diuretics act on DCT?

A

CA inhibitors

Thiazide diuretics

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18
Q

What do thiazide diuretics block?

A

Na/Cl in DCT (mild diuresis)

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19
Q

What diuretics act on CD?

A

K sparing diuretics

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20
Q

What do K sparing agents block?

A

Na/K in CD

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21
Q

Where on the membrane is the site of action of thiazide, loop and K sparing diuretics?

A

Apical membrane

= enter from filtrate (apart from spironolactone which enters at basolateral membrane)

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22
Q

Marker for renal plasma flow

A

PAH (enters at PCT)

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23
Q

OATs

A

Organic Anion Transporters
Transport acidic drugs (negative), e.g. PAH, thiazides, loop
At PCT

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24
Q

OCTs

A

Organic Cation Transporters
Transport basic drugs (positive), e.g. triamterene, amiloride
At CD

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25
Q

Na/K/ATPase is always at what membrane:

A

Basolateral

Maintains low IC Na

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26
Q

Side effects of loop diuretics

A 
Hypokalaemia
Hypocalcaemia
Hypomagnaesaemia
Metabolic alkalosis
Hypovolaemia
Hyperuricaemia = gout
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27
Q

Additional effect of loop diuretics

A

Venodilator = good in pulmonary oedema

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28
Q

Indications for loop diuretics

A 
Acute pulmonary oedema
Chronic HF
Chronic kidney failure
Nephrotic syndrome
Hepatic cirrhosis
AKI
Ant-HT
Hypercalcaemia (lowers Ca)
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29
Q

Indications for thiazide diuretics

A 
Mild HF
HT
Severe resistant oedema
Kidney stones (reduced urinary Ca excretion)
Nephrogenic DI
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30
Q

Side effects of thiazide diuretic

A 
Hypokalaemia
Hypomagnaesaemia
NOT Ca
Hyperuricaemia = gout
Metabolic alkalosis
Hypovolaemia
Male ED
Glucose intolerance
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31
Q

How is Na reabsorbed?

A

At apical membrane by ENaC channel - depends on aldosterone

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32
Q

How does aldosterone help Na reabsorption?

A

Released in response to AT II

Acts on basolateral membrane to increase synthesis of Na/K channels and ENaC channels

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33
Q

ADH acts via G coupled receptors to:

A

Increase aquaporins in apical membrane of DCT and CD

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34
Q

How do Amiloride and Triamterene (K sparing) work?

A

Block ENaC = decreased Na reabsorption in CD, decreased K efflux

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35
Q

How does spironolactone work?

A

Competes with aldosterone for binding sites = reduced ENaC at apical and reduced Na/K at basolateral = less Na reabsorption and less K efflux

36
Q

Indications for spironolactone

A

HF
Conn’s (primary hyperaldosteronism)
Resistant essential HT
Secondary hyperaldosteronism (liver cirrhosis with ascites)

37
Q

Is spironolactone used on its own?

A

Used with other agents that cause K loss (given alone cause hyperkalaemia)

38
Q

Example of an osmotic diuretic

A

Mannitol

39
Q

How do osmotic diuretics work?

A

Opposes absorption of water in parts of nephron that are water permeable
Decreases Na reabsorption in PCT

40
Q

Indications for osmotic diuretics

A

Acute hypovolaemic renal failure (haemorrhage)
Raised ICP and IOP
Hyperglycaemia - glucose in filtrate retains fluid

41
Q

Indications for CA inhibitors

A

Glaucoma
Altitude sickness
Infantile epilepsy
Alkalinising the urine

42
Q

Where does aldosterone act on?

A

DCT and CD to enhance water and Na reabsorption
Prevents ENaC being internalised on apical
Na/K on basolateral membrane

43
Q

Difference between diuretic and aquaretic

A

Diuretic: loss of water and Na
Aquaretic: water loss without Na = increased plasma osmolarity

44
Q

How do aquaretics work?

A

Competitive antagonist of ADH receptors

Vasodilation and water not reabsorbed

45
Q

Example of an aquaretic

A

Tolvaptan

46
Q

Indications for aquaretics

A

SIADH to correct hyponatraemia

47
Q

Does SGLT1 have a high/low affinity and high/low capacity?

SLT2?

A

SGLT1: high affinity, low capacity
SGLT2: low affinity, high capacity

48
Q

SGLT2 inhibitors cause:

A

Glucose excretion
Decreased HbA1c
Weight loss

49
Q

Example of SGLT2 inhibitor

A

Dapagliflozin

Canagliflozin

50
Q

PG produced by the kidney act as:

A

Vasodilators

Natriuretic (promote Na loss)

51
Q

PGs are synthesised by kidney in response to:

A 
Ischaemia
Trauma
AT II
ADH
Bradykinin
52
Q

PGs affect GFR by:

A

Vasodilating afferent arteriole

Releasing renin = more AT II = vasoconstricts efferent arteriole = increases filtration pressure

53
Q

PGs are produced in the kidney by what enzyme?

A

COX

54
Q

What drug inhibits COX?

A

NSAIDs = inhibits PG = may cause renal failure

55
Q

Triple whammy

A

NSAID + ACEI + Diuretic

56
Q

Example of uricosuric agents

A

Probenecid

Sulfinpyrazole

57
Q

How do uricosuric agents work?

A

Block reabsorption of urate in PCT

Treats gout

58
Q

Define pharamcokinetics

A

Behaviour of drug in regard to reabsorption/distribution/metabolism/elimination

59
Q

How can drugs be eliminated?

A

Renal

Biliary

60
Q

Azotemia

A

High levels of urea in blood

61
Q

ACEI can cause ________ as side effect

A

Hyperkalaemia

62
Q

Treatment of hyperkalaemia

A

Ca gluconate 10% 10ml 10 mins (to protect myocardium)
Insulin and dextrose (internalises K)
Salbutamol neb (internalises K)
Na bicarbonate (treats metabolic acidosis)
Ca resonium (removes K by swapping it for Ca)
Emergency dialysis

63
Q

Where do osmotic agents (Mannitol) work?

A

PCT, thick ascending LOH, DCT

64
Q

Many drugs contain

A

salt

65
Q

7 factors influencing prescribing

A 
Indication/diagnosis
Recommended drug/regime
Contraindications
Product licence
Patient expectations
Cost
Follow up
66
Q

Treatment of pyelonephritis (in community)

A

Co-trimoxazole or Co-amoxiclav

67
Q

ACEI is never used in:

A

Bilateral renal artery stenosis
Pregnancy
Caution in hepatic impairment

68
Q

Warfarin is never used in:

A

Pregnancy

69
Q

Furosemide should be avoided in:

A

Gout

70
Q

NSAID should be avoided in:

A

HT

Warfarin

71
Q

What UTI antibiotics avoided in pregnancy?

A

Ciprofloxacin
trimethoprim 1st trimester
nitrofurantoin 3rd trimester

72
Q

1st choice ACEI in hepatic impairment

A

Lisinopril

73
Q

Safety net for OCP

A

headaches

leg pain

74
Q

Safety net for carbimazole

A

Sore throat, mouth ulcers, bruising,f ever

75
Q

Safety net in champix/varenicline

A

Depression/suicidal thoughts

76
Q

Side effect of CCB

A

ankle oedema

77
Q

Type A drug reaction

A

Augmented - dose dependent and predictable

78
Q

Type B drug reaction

A

Bizarre - dose independent and unpredictable

79
Q

Type C drug reaction

A

Chronic effects (steroids)

80
Q

Type D drug reaction

A

Delayed effects (years after stopping)

81
Q

Type E drug reaction

A

End of treatment effects (abrupt end)

82
Q

Type F drug reaction

A

Failure of therapy

83
Q

Mechanisms of type A drug reaction

A

Pre renal
Renal
Post renal
Drug interactions (drug-drug, drug-otc, drug-disease, drug-food)

84
Q

Examples of Type B drug reactions

A

Drug rashes
Bone marrow aplasia
Hepatic necrosis
High mortality

85
Q

Examples of type C drug reactions

A

Steroids, B blockers and diaebtes, NSAIDs and HT

86
Q

Examples of type D drug reactions

A

Teratogenic/carcinogenic, years after stopping
Secondary malignancy post chemo
Craniofacial abnormaltieis in babies after isotretinoin

87
Q

Examples of type E drug reactions

A

Rebound effects e.g. B blocker -angina
Loss of physiolgoical coping, e.g. steroid - addisonian crisis
Anticonvulsants and epilepsy frequency

Renal (19 decks)

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