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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
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

Renal (19 decks)

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