6.1 Diabetes Flashcards

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1
Q

what stimulates insulin secretion from B cells?

A

-increased glucose
-incretins (GLP-1, GiP)
-parasymp activity M3

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2
Q

insulin half life

A

5 mins

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3
Q

what inhibits insulin secretion?

A

decrease glucose
cortisol
sympathetic activity
exogenous steroids

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4
Q

why is insulin secreted even during fasting?

A

prevents receptor down regulation

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5
Q

DKA triad

A

hyperlgycaemia
ketonaemia
acidosis

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6
Q

when to suspect DKA

A

blood glucose >11 ANDA
polydipsia
polyuria
abdo pain
V+D
lethargy
confusion
acetonic breath
shock

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7
Q

precipitating factors to DKA

A

infection
trauma
non adherence to insulin treatment drug drug interactions

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8
Q

treatment pathway for DKA

A

iv fluids
iv insulin
k+ correction

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9
Q

different ways to slow insulin absorption:

A
  1. soluble insulin forms hexamers (takes longer so get to monomers)
  2. analogues, change a few AAs (changes PK, not PD)
  3. complex with zinc/protamine
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10
Q

important drug drug interactions for diabetes treatments

A

-other hypoglycaemic agents
-exogenous steroids
-NSAIDS, ACEi (impair renal function)
-loop/thiazide diuretics (increase glucose)

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11
Q

basal bolus dosing

A

3 meals per day: rapid acting insulin

long acting each day

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12
Q

diabulimia

A

type 1 diabetic stops/reduces insulin to control weight

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13
Q

why can sulfonylureas cause weight gain?

A

anabolic effects of insulin

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14
Q

MOA for SGLT-2 inhibitors

A

competitively reversibly inhibit SGLT-2 in PCT, so decrease glucose reabsorption from filtrate and increase urinary glucose excretion

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15
Q

aside from diabetes, what else can SGLT-2 inhibitors be used for?

A

HFrEF, HFpEF

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16
Q

DPP-4 inhibitors have a lower hypoglycaemic risk, why?

A

don’t stimulate insulin secretion at normal blood glucose levels

17
Q

why are GLP-1 receptor agonists resistant to degradation by DDP-4?

A

they’re mimetic i.e. modified