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ED Primary Exam > Week 4 Pharmacology - Endocrine > Flashcards

Week 4 Pharmacology - Endocrine Flashcards

1
Q

What does autocoid refer to?

A

Drug class consisting of serotonin, histamine, prostaglandins, leukotrienes

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2
Q

What is the proposed mechanism of action of triptans?

A

Activation of 5-HT receptors on presynaptic trigeminal nerve endings to inhibit release of vasodilation peptides (thought to be the cause of migraine)

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3
Q

Where are the different histamine receptors located?

A

H1 = smooth muscle, endothelium, brain
H2 = gastric mucosa, cardiac muscle, mast cells, brain
H3 = presynaptic autoreceptors, brain
H4 = granulocytes, CD4 T cells

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4
Q

What receptor is targeted in treating allergic/hypersensitivity induced histamine release?

A

H1 receptor antagonists

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5
Q

What is the difference between first generation and second generation antihistamines?

A

First generation are more likely to block autonomic receptors (prevent adrenergic activity) and have a stronger sedative response

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6
Q

PK of antihistamines?

A

Peak plasma concentration 1-2 hours, effective 4-6 hours.

Reversible antagonism of H1 receptors

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7
Q

Is insulin initially produced as a pro-hormone?

A

Yes! - Proinsulin

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8
Q

What occurs to pro-insulin when inside granules (within beta cell)?

A

Hydrolysed to Insulin and C-peptide (which are secreted in equimolar amounts in response to activation of insulin secretion)

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9
Q

Stimulates insulin secretion?

A

Glucose
Amino acids
GLP-1
Glucagon
CCK
Fatty acids
Beta adrenergic activity
Glucagon

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10
Q

What inhibits insulin secretion?

A

Insulin
Somatostatin
Alpha adrenergic activity
Leptin
Phenytoin
Colchicine

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11
Q

What are the steps that lead to release of insulin from islet cells?

A
  1. Increased intracellular glucose via GLUT 2 transport
  2. Increased ATP synthesis and presence within cell
  3. ATP binds and closes ATP dependent K+ cells, preventing K+ efflux
  4. Depolarisation and opening of voltage gated Ca2+ channels
  5. Calcium as cellular messenger acts to trigger exocytosis of preformed vesicles of insulin
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12
Q

What is the half life of circulating insulin?

A

3-5 minutes

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13
Q

What type of receptor is insulin receptor on peripheral cells?

A

Tyrosine kinase

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14
Q

What are the general metabolic effects of insulin on liver, adipose and muscle?

A

Liver:
- Reversal of catabolism
- Induction of anabolism

Muscle:
- Increased protein synthesis
- Increased glycogen production

Adipose:
- Increased triglyceride storage

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15
Q

Where is GLUT-1 found?

A

All tissues, all for one - and one for all! Basal uptake of glucose

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16
Q

Where is GLUT-2 found?

A

Beta cells pancreas
Liver
Kidney
GIT

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17
Q

Where is GLUT-3 found? (Three is an odd number)

A

Brain, placenta

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18
Q

Where is GLUT 4 found? (May the four be with you)

A

Muscle, adipose (this is insulin mediated uptake)

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19
Q

Where is GLUT-5 found? (Five, ffff)

A

Gut, Kidney - absorption of fructose

20
Q

What effect does insulin binding have on insulin sensitive cells?

A

Translocation of GLUT-4 transporters to cell membrane

21
Q

Where is insulin metabolised?

A

65% liver, 35 kidney (reversed for exogenous insulin)

22
Q

What are the rapid effects of insulin administration?

A

Increased glucose and amino acid transport
Potassium uptake into insulin sensitive cells

23
Q

What the intermediate effects of insulin administration (minutes)?

A

Stimulation of protein synthesis/inhibition of degradation
Activation of glycolytic enzymes and glycogen synthase
Inhibition of gluconeogenesis

24
Q

What are the delayed effects of insulin administration (hours)?

A

Increase in mRNAs for lipogenic / other enzymes

25
Q

What medications antagonise the effect of insulin?

A

Steroids
Thyroxine
Sympathomimetics
Thiazides

26
Q

Where is glucagon synthesised?

A

Pancreatic islet alpha cells

27
Q

Where are the target cells for glucagon metabolically? Effects?

A

Liver - GPCR binding that causes increased gluconeogenesis and ketogenesis and glycogenolysis

28
Q

What are the cardiac effects of glucagon?

A

Potent inotropy and chronotropy (not requiring functioning beta receptors, reason why useful in beta blocker poisoning)

29
Q

What is the half life of glucagon?

A

3-5 minutes

30
Q

Compare onset and duration of novorapid with glargine?

A

Novorapid: Onset 5-15 mins, peak 1.5 hrs, duration 5 hrs

Glargine: Onset 30mins-1hr, peak is flat, duration 24 hours

31
Q

What are the two main categories of oral hypoglycaemic?

A

Insulin secretagogues vs non secretagogues

32
Q

What are the different types of insulin secretagogues?

A
  • Sulphonylureas
  • Incretins
  • DPP-4 Inhibitors
33
Q

What is the mechanism of sulphonylureas?

A

Act directly on ATP sensitive K+ channels in pancreatic beta cells to close –> depolarisation and insulin release in the same manner as physiological insulin release

34
Q

What are examples of sulphonylureas?

A

Gliclazide

35
Q

What are adverse effects of sulphonylureas?

A

Weight gain, hypoglycaemia

36
Q

What are incretins?

A

Hormones released by GIT following meal that leads to increased insulin release, i.e. GLP-1

37
Q

What two medication classes mimic the action of incretins?

A
  1. Glucagon-Like-Peptide-1 Agonists, i.e. semaglutide, liraglutide, exendatide
  2. DPP4 Inhibitors: Sitagliptin, Linagliptin
38
Q

What is the mechanism of action of DPP4 inhibitors?

A

Act to inhibit the enzymes that break down GLP-1, which has the effect of facilitating its function –> which is binding to beta cells and increasing insulin release

39
Q

What are the extra-pancreatic effects of GLP-1 agonists?

A

Increased satiety, decreased gastric emptying rate, lower glucagon levels

40
Q

What is the mechanism of metformin/biguanide?

A

Activation of AMP Kinase (liver enzyme) which acts to inhibit hepatic gluconeogenesis, as well as intestinal absorption of glucose.

41
Q

What are adverse effects of metformin?

A

GI upset
Lactic acidosis

42
Q

What is the mechanism of SGLT-2 inhibitors?

A

Direct inhibition of transporters in PCT of nephron to reduce glucose absorption

43
Q

What are adverse effects of SGLT-2 inhibitors?

A

UTI
Euglycaemic ketoacidosis
Osmotic diuresis

44
Q

Is carbimazole a pro-drug?

A

Yes! Converted to methimazole, which accumulates in thyroid gland

45
Q

How does carbimazole act?

A

Major mechanism = inhibition of thyroid peroxidase reactions, as well as coupling of iodotyrosines

46
Q

How long after commencing carbimazole does it take for effect?

A

3-4 weeks (as it only interferes with synthesis of thyroid hormone, NOT release)

47
Q

What role does propranolol have in management of hyperthyroidism?

A

Inhibition of beta adrenoceptors manages symptoms, as well as decreased peripheral conversion of T4 –> T3

ED Primary Exam (46 decks)

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