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Flashcards in Pharmacology Deck (87):
1

Where is most Na reabsorbed?

PCT (67%)

2

SGLT2 inhibitors inhibit reabsorption of what and where?

Glucose in PCT = glucose in urine

3

Uricosuric drugs

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

4

4 Starling forces

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

5

Disease states that increase _____ or decrease ______ cause oedema

Increase capillary hydrostatic pressure
Decrease capillary oncotic pressure

6

Causes of oedema

Nephrotic syndrome
Congestive HF
Hepatic cirrhosis with ascites

7

Sign of proteinuria

Frothy urine

8

Congestive HF arises from:

Reduced CO = hypovolaemia = activates RAAS

9

Ascites arises from:

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

10

Which diuretics act on PCT?

CA inhibitors

11

Where is next 25% of Na reabsorbed?

Thick ascending LOH

12

Where is last 10% of Na reabsorbed?

DCT

13

Is thick ascending LOH permeable or impermeable to water?

Impermeable

14

What do CA inhibitors block?

Na/H exchange in PCT and DCT

15

Which diuretics act on thick ascending LOH?

Loop diuretics

16

What do loop diuretics block?

Na/K/2Cl in thick ascending LOH

17

What diuretics act on DCT?

CA inhibitors
Thiazide diuretics

18

What do thiazide diuretics block?

Na/Cl in DCT (mild diuresis)

19

What diuretics act on CD?

K sparing diuretics

20

What do K sparing agents block?

Na/K in CD

21

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

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

22

Marker for renal plasma flow

PAH (enters at PCT)

23

OATs

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

24

OCTs

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

25

Na/K/ATPase is always at what membrane:

Basolateral
Maintains low IC Na

26

Side effects of loop diuretics

Hypokalaemia
Hypocalcaemia
Hypomagnaesaemia
Metabolic alkalosis
Hypovolaemia
Hyperuricaemia = gout

27

Additional effect of loop diuretics

Venodilator = good in pulmonary oedema

28

Indications for loop diuretics

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

29

Indications for thiazide diuretics

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

30

Side effects of thiazide diuretic

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

31

How is Na reabsorbed?

At apical membrane by ENaC channel - depends on aldosterone

32

How does aldosterone help Na reabsorption?

Released in response to AT II
Acts on basolateral membrane to increase synthesis of Na/K channels and ENaC channels

33

ADH acts via G coupled receptors to:

Increase aquaporins in apical membrane of DCT and CD

34

How do Amiloride and Triamterene (K sparing) work?

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

35

How does spironolactone work?

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

36

Indications for spironolactone

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

37

Is spironolactone used on its own?

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

38

Example of an osmotic diuretic

Mannitol

39

How do osmotic diuretics work?

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

40

Indications for osmotic diuretics

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

41

Indications for CA inhibitors

Glaucoma
Altitude sickness
Infantile epilepsy
Alkalinising the urine

42

Where does aldosterone act on?

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

43

Difference between diuretic and aquaretic

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

44

How do aquaretics work?

Competitive antagonist of ADH receptors
Vasodilation and water not reabsorbed

45

Example of an aquaretic

Tolvaptan

46

Indications for aquaretics

SIADH to correct hyponatraemia

47

Does SGLT1 have a high/low affinity and high/low capacity?
SLT2?

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

48

SGLT2 inhibitors cause:

Glucose excretion
Decreased HbA1c
Weight loss

49

Example of SGLT2 inhibitor

Dapagliflozin
Canagliflozin

50

PG produced by the kidney act as:

Vasodilators
Natriuretic (promote Na loss)

51

PGs are synthesised by kidney in response to:

Ischaemia
Trauma
AT II
ADH
Bradykinin

52

PGs affect GFR by:

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

53

PGs are produced in the kidney by what enzyme?

COX

54

What drug inhibits COX?

NSAIDs = inhibits PG = may cause renal failure

55

Triple whammy

NSAID + ACEI + Diuretic

56

Example of uricosuric agents

Probenecid
Sulfinpyrazole

57

How do uricosuric agents work?

Block reabsorption of urate in PCT
Treats gout

58

Define pharamcokinetics

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

59

How can drugs be eliminated?

Renal
Biliary

60

Azotemia

High levels of urea in blood

61

ACEI can cause ________ as side effect

Hyperkalaemia

62

Treatment of hyperkalaemia

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

Where do osmotic agents (Mannitol) work?

PCT, thick ascending LOH, DCT

64

Many drugs contain

salt

65

7 factors influencing prescribing

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

66

Treatment of pyelonephritis (in community)

Co-trimoxazole or Co-amoxiclav

67

ACEI is never used in:

Bilateral renal artery stenosis
Pregnancy
Caution in hepatic impairment

68

Warfarin is never used in:

Pregnancy

69

Furosemide should be avoided in:

Gout

70

NSAID should be avoided in:

HT
Warfarin

71

What UTI antibiotics avoided in pregnancy?

Ciprofloxacin
trimethoprim 1st trimester
nitrofurantoin 3rd trimester

72

1st choice ACEI in hepatic impairment

Lisinopril

73

Safety net for OCP

headaches
leg pain

74

Safety net for carbimazole

Sore throat, mouth ulcers, bruising,f ever

75

Safety net in champix/varenicline

Depression/suicidal thoughts

76

Side effect of CCB

ankle oedema

77

Type A drug reaction

Augmented - dose dependent and predictable

78

Type B drug reaction

Bizarre - dose independent and unpredictable

79

Type C drug reaction

Chronic effects (steroids)

80

Type D drug reaction

Delayed effects (years after stopping)

81

Type E drug reaction

End of treatment effects (abrupt end)

82

Type F drug reaction

Failure of therapy

83

Mechanisms of type A drug reaction

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

84

Examples of Type B drug reactions

Drug rashes
Bone marrow aplasia
Hepatic necrosis
High mortality

85

Examples of type C drug reactions

Steroids, B blockers and diaebtes, NSAIDs and HT

86

Examples of type D drug reactions

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

87

Examples of type E drug reactions

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