Pharmacology - Treatment of Diabetes 3 Flashcards

1
Q

-gliflozin

A

SGLT2 inhibitors

inhibit glucose absorption by bocking sglt2 sodium glucose cotransporter

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2
Q

where is SGLT2 highly expressed

a.PCT
b.DCT
c.loop of henle

A

a.PCT

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3
Q

what effect do sglt 2 inhibitors have on the renal threshold for glucose

a. increase
b.decrease

A

a. increase

promote excretion of glucose in the urine

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4
Q

what line are sglt2 inhibitors in diabtetes treatment

a. 1
b.2
c.3

A

b.2
add on therapy
loss of calories and weight loss associated so good for cvd

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5
Q

what type of infection has increased risk when taking sglt2 inhibitors

a.chest infection
b. uti
c. sepsis

A

b. uti

due to polyuria

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6
Q

which of these drugs does sglt2 inhibitors NOT interact with

a. ACEi
b.ARBs
c.NSAIDS
d. B blockers

A

d. B blockers

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7
Q

what should patients be advised to do when starting an sglt2 inhibitor

A

ketoacidosis

advice patient of symptoms to check ketones and to stop if significant illness/ major surgery

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8
Q

when initiating insulin tretament it should be done as..

a.monotherapy
b.add on therapy

A

b.add on therapy

add onto metformin in particular as reduces weight gain and offers CV protection

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9
Q

patient has significant hyperglycaemia despite maximal doses of oral agents what should be done next

a.insulin therapy
b.insulin bolus
c.intermediate acting insulin bedtime / 2x daily

A

c.intermediate acting insulin bedtime / 2x daily - human NPH insulin

first line

2nd = long acting insulin analaogue eg insulin glargine 1x daily

eg if unable to self inject, lifestyle makes frequent injection innapropriate , target hba2 not reached because of hypoglycaemia or hypo with human nph insulin

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10
Q

what is hyperosmolar hyperglycaemic syndrome triggered by

a.acute illness, poor dietary and drug adherance

b.chronic illness, poor dietary and drug adherance

c. lack of excercise, poor dietary and drug adherance

A

a.acute illness, poor dietary and drug adherance

affects patients with type 2 diabetes

similar symptoms to DKA but still have some insulin so metabolism doesnt switch to fats and no acidosis

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11
Q

which of these are signs of HHS

a.v high blood glucose, low serum smolarity

b.low blood glucose, high serum osmolarity

c.v high blood glucose, high serum osmolarity

A

c.v high blood glucose, high serum osmolarity

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12
Q

what is the treatment for HHS

A

IV fluids, electrolytes and insulin

give LMWHeparin as high VTE risk state

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13
Q

which drug familiy are known as insulin resistance reducers

a.thiazolidinediones
b.sglt2 inhibitors
c.insulin
d.glp 1 analogue

A

a.thiazolidinediones

impact fatty acid metabolism

bind to PPARy receptors in adipose tissue , skeletal muscle and liver (insulin target tissues)

ligand activated transcription factors

target genes - enzymes involved in lipid metabolism so decreased FFAs

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14
Q

what is the mechanism of action of thiazolidinediones

A

impact fatty acid metabolism

bind to PPARy receptors in adipose tissue , skeletal muscle and liver (insulin target tissues)

ligand activated transcription factors

target genes - enzymes involved in lipid metabolism so decreased FFAs and glut 4 receptors so snesitivity to insulin incrased

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15
Q

thiazolidinediones are only effective in the prescence of which other substance ?

a.glucagon
b.insulin
c.LMWH
d.anticoagulants

A

b.insulin

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16
Q

what patients are thiazolidonediones used in

A

type 2 with inadequate control of hyperglycaemia and significant insulin resistance

17
Q

which drugs require LFTs prior to initiating therapy and to be monitored every 2-6 months

a.insulin
b.sglt2 inhibitors
c.thiazolidinediones

A

c.thiazolidinediones

18
Q

what is there an increased risk of when thiazolidine diones are combines with insulin

a.heart failure
b.MI
c.renal failure

A

a.heart failure

19
Q

t should be managed along side blood glucose in type 2 diabetes

A

VASCULAR RISKS

bp target below 130/80

use ace /arbS IF NOT CONTRAINDICATED

agressive lipid management