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Endocrine > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What’s the MoA for metformin / biguanides? (2)

A

Reduce hepatic gluconeogenesis, increase peripheral blood glucose uptake.

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2
Q

What affect does metformin have on weight?

A

Weight neutral / may promote weight loss

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3
Q

Does metformin risk hypoglycaemia?

A

Not as a monotherapy

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4
Q

What are the adverse effects of metformin? (3)

A

GI upset, lactic acidosis, obstruction of B12/folate metabolism

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5
Q

What’s the MoA of SUR drugs? (3)

A

Binds to SUR1 subunit of Katp channel, closing it (depolarising), leading to opening of voltage-gated calcium channels and insulin release.

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6
Q

Do SUR drugs risk hypoglycaemia?

A

Yes

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7
Q

What effect do SUR drugs have on weight?

A

Weight gain

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8
Q

Side effects of SUR drugs?

A

Abnormal LFTs, renal failure, CHD risk

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9
Q

GLP-1 drugs are given orally or by injection?

A

Injection

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10
Q

What effect do GLP-1 drugs have on weight?

A

Weight loss

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11
Q

Are biguanides safe in pregnancy?

A

Yes

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12
Q

Maximum daily dose of metformin

A

2g (1g BD)

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13
Q

Example SUR drug

A

Gliclazide

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14
Q

Do SUR drugs prevent microvascular / macrovascular complications? (2)

A

Microvascular - Yes

Macrovascular - No

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15
Q

Side-effects of GLP-1 includes

A

Nausea, pancreatitis

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16
Q

Examples of GLP1 drugs

A

Exenatide, Liraglutide

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17
Q

DPP-4 drug example

A

Any -gliptin drugs (e.g. vildagliptin)

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18
Q

How do DPP-4 drugs work?

A

Reduce breakdown of GLP-1 (which itself promotes insulin secretion, lowers glucose absorption)

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19
Q

How do GLP-1 agonist drugs work? (4)

A

1) Promotes insulin secretion from pancreas
2) Lower glucose absorption in the gut
3) Suppress glucagon release
4) Delay gastric emptying & lower hunger

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20
Q

Are DPP-4 inhibitors weight-neutral?

A

Yes

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21
Q

Do DPP-4 inhibitors risk hypoglycaemia?

A

No

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22
Q

Do GLP-1 agonists protect against micro and macrovascular complications? (2)

A

Micro- assumed

Macro - unknown (but decreases SBP)

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23
Q

Do DPP-4 inhibitors protect against macrovascular progression?

A

No

24
Q

Are DPP-4 inhibitors oral?

A

Yes (they block GLP-1 which is produced in the GI tract)

25
Q

Glitazone/TZD drugs act how? Are they insulin dependent?

A

Through PPAR-gamma (induction of peripheral glucose uptake & fatty acid synthesis in adipocytes). No

26
Q

Are glitazone/TZD drugs weight neutral?

A

No, they encourage production of fat.

27
Q

What are the side-effects of glitazone drugs?

A

Fracture, hepatotoxic, fluid retention (can lead to heart failure)

28
Q

SIGN 154 guidance of glycaemic control in T2DM: give the 1st line therapy (and alternative)

A

1st line = metformin
Alternative* = SUR

*if intolerant OR osmotic symptoms present.
Both are in addition to lifestyle measures.

29
Q

SIGN 154 guidance of glycaemic control in T2DM: give the 2nd line therapy

A

Metformin / SUR + (one of) SUR / SGLT2/ DPP-4 / TZD

30
Q

SIGN 154 guidance of glycaemic control in T2DM: give the third line therapy

A

Metformin / SUR + 2nd line therapy + addition of agent from another class (not used). If patient’s BMI is >30 substitute this new drug for GLP-1 injections (weight loss) OR insulin (if <30).

31
Q

If patient’s have a history of CVD, what’s the standard 2 drugs used in T2DM control?

A

Metformin + SGLT2

32
Q

DPP-4 drug naming convention….

A

-Gliptin

33
Q

In T2DM, insulin therapy tends to be basal/bolus focused?

A

Basal (T1DM tends to be basal and bolus)

34
Q

In T2DM, is the initial insulin therapy used as a monotherapy?

A

No, combined with metformin

35
Q

Which tricyclic antidepressant is useful in neuropathic pain?

A

Amitriptyline (off-label)

36
Q

If the patient cannot tolerate oral medication for neuropathic pain, which topical alternative is available?

A

Capsaicin cream

37
Q

Metoclopramide and domiperidone are examples of what kind of drug?

A

Promotility agents

38
Q

Ondansetron is an example of which type of drug?

A

Anti-emetic

39
Q

What’s the standard therapy for hypothyroidism & starting dose for young patients?

A

Levothyroxine (T4) 50-100micrograms per day

40
Q

In elderly, the dosage of levothyroxine is higher/lower than youth?

A

Lower (25-50micrograms per day versus 50-100 in youth)

41
Q

In pregnancy, how should levothyroxine dose be adjusted in hypothyroidism?

A

Increase by 25-50%

42
Q

How often should TSH be checked in hypothyroidism if the dosage is changed?

A

Every 2 months (versus 12-18 months once stabilised)

43
Q

In secondary hypothyroidism, TSH is unreliable and treatment should be titrated to what?

A

Free T4 level

44
Q

Levothyroxine should be taken at what time & how?

A

Before breakfast without other tablets

45
Q

T4 is much more potent than T3, true or false?

A

False - T3 is more potent

46
Q

Carbimazole represents the 1st/2nd line therapy in hyper/hypothyroidism?

A

1st in hyperthyroidism

47
Q

Why is carbimazole not used in the 1st trimester of pregnancy?

A

Risk of aplasia cutis

48
Q

What drug is used in the 1st trimester of pregnancy in hyperthyroidism?

A

PTU

49
Q

PTU is how much less potent than carbimazole?

A

10x

50
Q

How does PTU work?

A

Inhibits DIO1 (conversion of T4 to T3) rather than production of T4

51
Q

What’s the major risk associated with ATDs?

A

Agranulocytosis

52
Q

Once agranulocytosis has been treated, ATDs can be resumed. True/false?

A

False

53
Q

How should suspected agranulocytosis be managed in hyperthyroid patients? (2)

A

1) Cease ATD immediately

2) Refer for immediate FBC

54
Q

How do beta-blockers work in hyperthyroid disease?

A

These work on beta-adrenoceptors which reduce sympathetic nervous activity (excessive in hyperthyroid disease)

55
Q

What’s the beta-blocker of choice in hyperthyroidism?

A

Propanolol

56
Q

The immediate symptoms of thyrotoxicosis can be managed with which drug?

A

Beta-blocker

57
Q

If a hyperthyroid patient is also asthmatic, how are cardiac symptoms managed?

A

Use calcium-channel blocker instead

Endocrine (17 decks)

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