Mer Scott
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PHCY310 Quiz on L32 Clinical Pharmacology of T2DM, created by Mer Scott on 16/04/2019.

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L32 Clinical Pharmacology of T2DM

Question 1 of 9

1

Insulin homeostasis:
- Under fasting conditions, insulin is released in a manner every mins​.
- In response to increased glucose:​
Phase 1:​ insulin release within ​, peak at mins​
Phase 2: more release with a peak​

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    pulsatile
    10-14
    seconds
    3-5
    gradual
    lower

Explanation

Question 2 of 9

1

Choose the incorrect statement about insulin.

Select one of the following:

  • Insulin acts on a plasma membrane receptor which activates a cascade of signalling events.

  • Insulin has anabolic effects resulting in uptake, use, and storage of glucose, lipids, and amino acids.​

  • Insulin inhbits glycogenesis, lipogenesis, and protein synthesis.

  • Insulin controls gene transcription and mRNA translation.​

Explanation

Question 3 of 9

1

Which of these is not a diabetic medication used in NZ?

Select one of the following:

  • Exogenous insulin

  • Sulphonyureas

  • DPP-4 inhibitors

  • Alpha glucosidase inhibitors

  • Biguanides

  • 1,4-DDPs

  • Thiazolidinediones

Explanation

Question 4 of 9

1

Sulphonylureas stimulate insulin release by binding to a specific site on the beta islet cell's complex (SUR) and its activity. Inhibition causes cell membrane and insulin .
Their effect declines over because of down-regulation of cell surface and​ progression of beta islet cell failure​.
Side effects are hypoglycaemia and initial gain​, less-common side effects include nausea, vomiting, cholestatic jaundice, and agranulocytosis.​

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    KATP channel
    inhibiting
    depolarisation
    secretion
    time
    receptors
    weight

Explanation

Question 5 of 9

1

DPP-4 is dipeptidyl peptidase 4, a serine protease that is widely distributed throughout the body​. It GLP-1​. Inhibiting cause increase in plasma , resulting in higher insulin secretion.​

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    inactivates
    DPP-4
    GLP-1

Explanation

Question 6 of 9

1

Alpha glucosidase inhibitors reduce the intestinal of starch, dextrin, and disaccharides ​by inhibiting the action of in the intestinal brush border​.
They are taken each meal and not absorbed​. They are often used in with other meds.
Side effects are malabsorption, flatulence, diarrhoea, and abdominal bloating​.

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    absorption
    α-glucosidase
    before
    combination

Explanation

Question 7 of 9

1

Biguanides include metformin. Metformin reduces glucose production by gluconeogenesis.​
It activates (AMPK), leading to stimulation of:​
- hepatic oxidation
- uptake
- non-oxidative glucose
- of lipogenesis and gluconeogenesis. ​
Side effects are GI: nausea, indigestion, abdominal cramps, bloating, diarrhoea​.

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    hepatic
    reducing
    AMP-dependent protein kinase
    fatty acid
    glucose
    metabolism
    reduction

Explanation

Question 8 of 9

1

Thiazolidinediones are PPAR-gamma inhibitors that cause insulin sensitisation.
The PPARγ receptor is a involved in the regulation of genes related to .​ PPARγ receptors are expressed primarily in adipose tissue. They promote uptake of circulating fatty acids into cells, and glucose uptake into tissue.​ They insulin resistance.
Side effects are weight and oedema​.

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    nuclear hormone receptor
    glucose and lipid metabolism
    fat
    muscle and adipose
    reduce
    gain

Explanation

Question 9 of 9

1

SGLT2 is a Na+-glucose cotransporter located in the proximal portion of the tubule. It reabsorbs . SGLT2 inhibitors glucose transport thus blood glucose.​
Side effects:
- A 1%-2% increase in lower infections.​
- A 3%-5% increase in mycotic infections. ​
- Mild , which can lead to hypotension. ​
- Effectiveness decreases by 40%–80% in kidney disease (GFR 60–30 mL/min). ​

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    renal
    glucose
    block
    lowering
    urinary tract
    genital
    diuresis

Explanation