Flashcards in Pharmacology Deck (87):
Where is most Na reabsorbed?
SGLT2 inhibitors inhibit reabsorption of what and where?
Glucose in PCT = glucose in urine
Promote excretion of uric acid into urine or prevent reabsorption of uric acid
4 Starling forces
Capillary hydrostatic pressure
Capilary oncotic pressure
IF hydrostatic pressure
IF oncotic pressure
Disease states that increase _____ or decrease ______ cause oedema
Increase capillary hydrostatic pressure
Decrease capillary oncotic pressure
Causes of oedema
Hepatic cirrhosis with ascites
Sign of proteinuria
Congestive HF arises from:
Reduced CO = hypovolaemia = activates RAAS
Ascites arises from:
Increased HPV pressure, decreased albumin (oncotic pressure) = oedema and activates RAAS
Which diuretics act on PCT?
Where is next 25% of Na reabsorbed?
Thick ascending LOH
Where is last 10% of Na reabsorbed?
Is thick ascending LOH permeable or impermeable to water?
What do CA inhibitors block?
Na/H exchange in PCT and DCT
Which diuretics act on thick ascending LOH?
What do loop diuretics block?
Na/K/2Cl in thick ascending LOH
What diuretics act on DCT?
What do thiazide diuretics block?
Na/Cl in DCT (mild diuresis)
What diuretics act on CD?
K sparing diuretics
What do K sparing agents block?
Na/K in CD
Where on the membrane is the site of action of thiazide, loop and K sparing diuretics?
= enter from filtrate (apart from spironolactone which enters at basolateral membrane)
Marker for renal plasma flow
PAH (enters at PCT)
Organic Anion Transporters
Transport acidic drugs (negative), e.g. PAH, thiazides, loop
Organic Cation Transporters
Transport basic drugs (positive), e.g. triamterene, amiloride
Na/K/ATPase is always at what membrane:
Maintains low IC Na
Side effects of loop diuretics
Hyperuricaemia = gout
Additional effect of loop diuretics
Venodilator = good in pulmonary oedema
Indications for loop diuretics
Acute pulmonary oedema
Chronic kidney failure
Hypercalcaemia (lowers Ca)
Indications for thiazide diuretics
Severe resistant oedema
Kidney stones (reduced urinary Ca excretion)
Side effects of thiazide diuretic
Hyperuricaemia = gout
How is Na reabsorbed?
At apical membrane by ENaC channel - depends on aldosterone
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
ADH acts via G coupled receptors to:
Increase aquaporins in apical membrane of DCT and CD
How do Amiloride and Triamterene (K sparing) work?
Block ENaC = decreased Na reabsorption in CD, decreased K efflux
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
Indications for spironolactone
Conn's (primary hyperaldosteronism)
Resistant essential HT
Secondary hyperaldosteronism (liver cirrhosis with ascites)
Is spironolactone used on its own?
Used with other agents that cause K loss (given alone cause hyperkalaemia)
Example of an osmotic diuretic
How do osmotic diuretics work?
Opposes absorption of water in parts of nephron that are water permeable
Decreases Na reabsorption in PCT
Indications for osmotic diuretics
Acute hypovolaemic renal failure (haemorrhage)
Raised ICP and IOP
Hyperglycaemia - glucose in filtrate retains fluid
Indications for CA inhibitors
Alkalinising the urine
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
Difference between diuretic and aquaretic
Diuretic: loss of water and Na
Aquaretic: water loss without Na = increased plasma osmolarity
How do aquaretics work?
Competitive antagonist of ADH receptors
Vasodilation and water not reabsorbed
Example of an aquaretic
Indications for aquaretics
SIADH to correct hyponatraemia
Does SGLT1 have a high/low affinity and high/low capacity?
SGLT1: high affinity, low capacity
SGLT2: low affinity, high capacity
SGLT2 inhibitors cause:
Example of SGLT2 inhibitor
PG produced by the kidney act as:
Natriuretic (promote Na loss)
PGs are synthesised by kidney in response to:
PGs affect GFR by:
Vasodilating afferent arteriole
Releasing renin = more AT II = vasoconstricts efferent arteriole = increases filtration pressure
PGs are produced in the kidney by what enzyme?
What drug inhibits COX?
NSAIDs = inhibits PG = may cause renal failure
NSAID + ACEI + Diuretic
Example of uricosuric agents
How do uricosuric agents work?
Block reabsorption of urate in PCT
Behaviour of drug in regard to reabsorption/distribution/metabolism/elimination
How can drugs be eliminated?
High levels of urea in blood
ACEI can cause ________ as side effect
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)
Where do osmotic agents (Mannitol) work?
PCT, thick ascending LOH, DCT
Many drugs contain
7 factors influencing prescribing
Treatment of pyelonephritis (in community)
Co-trimoxazole or Co-amoxiclav
ACEI is never used in:
Bilateral renal artery stenosis
Caution in hepatic impairment
Warfarin is never used in:
Furosemide should be avoided in:
NSAID should be avoided in:
What UTI antibiotics avoided in pregnancy?
trimethoprim 1st trimester
nitrofurantoin 3rd trimester
1st choice ACEI in hepatic impairment
Safety net for OCP
Safety net for carbimazole
Sore throat, mouth ulcers, bruising,f ever
Safety net in champix/varenicline
Side effect of CCB
Type A drug reaction
Augmented - dose dependent and predictable
Type B drug reaction
Bizarre - dose independent and unpredictable
Type C drug reaction
Chronic effects (steroids)
Type D drug reaction
Delayed effects (years after stopping)
Type E drug reaction
End of treatment effects (abrupt end)
Type F drug reaction
Failure of therapy
Mechanisms of type A drug reaction
Drug interactions (drug-drug, drug-otc, drug-disease, drug-food)
Examples of Type B drug reactions
Bone marrow aplasia
Examples of type C drug reactions
Steroids, B blockers and diaebtes, NSAIDs and HT
Examples of type D drug reactions
Teratogenic/carcinogenic, years after stopping
Secondary malignancy post chemo
Craniofacial abnormaltieis in babies after isotretinoin