CPTP 4.6-8 Flashcards

1
Q

What is tolbutamide

A

A sulphonylurea

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2
Q

how do sulphonylureas work

A

close K channels, depolarise beta bell, calcium channels then open, insulin vesicle can fuse with csm and insulin released

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3
Q

TZDs aka

A

PPARy agonists

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4
Q

Endogenous ligands for PPARy receptors

A

free fatty acids

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5
Q

TZDs mechanisms of action

A

increase lipogenesis and decrease lipolysis and free fatty acids

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6
Q

adverse effects of TZDs

A

bladder cancer, fractures, fluid retention, weight gain

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7
Q

Two drugs that act affect incretins to promote glucose dependent insulin secretion

A

DPP-IV inhibitors (e.g. sitagliptin) GLP-1 mimetics (exenatide)

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8
Q

A diabetes treatment that doesn’t directly affect insulin levels

A

SGT2 inhibitors - prevent glucose reabsorption in proximal tubule

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9
Q

advantages of insulin analogues e.g. novorapid, Humalog, glargine, detemir

A

less nocturnal hypos, reduced fasting glucose. smoother metabolic profile - less overlapping

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10
Q

statins mechanism of action

A

decrease cholesterol biosynthesis, increase cholesterol uptake into liver, reduce inflammation and thrombus formation

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11
Q

How do you calculate anion gap

A

Na + K - (HCO3 + Cl)

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12
Q

what is a normal anion gap

A

16 +/- 4

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13
Q

causes of a high anion gap metabolic acidosis

A
methanol, metformin 
uremia 
dka
paracetamol 
iron, isoniazid  
lactic acidosis 
ethanol
salicylate
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14
Q

why are serum K levels high in DKA

A

body trying to get rid of H+ ions in urine therefore retaining potassium instead

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15
Q

is the administration of sodium bicarbonate needed in DKA

A

no. adequate fluid and insulin tx will resolve the acidosis, administering HCO3 may increase risk of cerebral oedema as rise in CSF CO2 and acidosis

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16
Q

can you rely on urine ketone clearance to indicate DKA resolution

A

no, will lag behind and still be present once resolved

17
Q

reaction between which statin and which antibiotic?

A

simvastatin and clarithromycin (rhabdomyolysis)