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Pharmaco Ca2 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

How is proinsulin converted to active insulin

A

C peptide is cleaved off (hence presence of c peptide indicates endogenous synthesis of insulin)

Active insulin is a and b peptide chains connected by disulphide bond

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2
Q

How are insulin receptors downregulated

A

Internalization of insulin receptor complex. Metabolised at lysosome and recycled to plasma membrane

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3
Q

What is type 1 diabetes

A

Immune mediated B cell destruction, absolute insulin deficiency

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4
Q

What is type 2 diabetes

A

Insulin resistance with relative insulin deficiency or predominant secretory defect with resistance

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5
Q

How is type 2 diabetes treated

A

Start from lifestyle modification, then hypoglycemia agents, then insulin therapy

Insulin therapy used when glycemic target not reached with 2 or more oral hypogycemic agents

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6
Q

How to test for type 2 diabetes

A

Casual non fasting plasma glucose ≥ 11.1mmol/L

Fasting glucose ≥ 7mmol/L

6.1-6.9mmol/L means prediabetic. Undergo glucose tolerance test to see if 2 hour post challenge plasma glucose ≥11.1mmol/L

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7
Q

How can insulin be administered

A

Subcutaneously

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8
Q

What is prandial insulin

A

Insulin replacement to get rid of glucose post meal

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9
Q

What is basic insulin

A

Background insulin to suppress hepatic glucose production overnight and in between meals

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10
Q

How is rapid acting insulin made

A

Substitute or add amino acids to change charge/conformation of insulin at physiological pH. This weakens propensity to self associate/dimerise via charge repulsion, allowing for rapid absorption

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11
Q

Examples fo rapid acting insulin

A

Lispro, glulisine, aspartame’s

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12
Q

When should rapid acting insulin be administered

A

Right before meal to reduce risk of hypoglycemia

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13
Q

What is the duration of action of rapid acting insulin

A

2-4h

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14
Q

Why is rapid acting insulin more able to reduce post prandial glucose to a greater extent than human insulin

A

Higher concentration after subcutaneous injection

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15
Q

Appearance of lispro

A

Rapid acting insulin, clear appearance

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16
Q

What is the appearance of short acting/regular insulin

A

Clear appearance

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17
Q

Why does short acting insulin have delayed onset

A

Self aggregate in subcutaneous tissue hence should inject 20-30min before meal

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18
Q

When is short acting insulin given intravenously

A

During hyperglycemia crisis in the hospital

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19
Q

What kind of insulin is neutral protamine hagedorn insulin

A

Intermediate acting insulin (human insulin + protamine)

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20
Q

What is the appearance of NPH insulin

A

Cloudy

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21
Q

Risk of taking NPH insulin

A

High risk of hypoglycemia due to high intra and inter patient variability and long peak effect (patient must eat meal when insulin is peaking)

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22
Q

Name some long acting insulin

A

Glargine and determir

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23
Q

Duration of action of glargine

A

18-24h, virtually no plasma peak

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24
Q

What is long acting insulin used for

A

Basal glucose levels, background insulin

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25
Q

What is the hypoglycemia risk of long acting insulin

A

Low because lower intra subject variation

26
Q

How do glargine and detemir have long action

A

Glargine has acidic ph of 4, aggregate and slowly release over time

Determir has fatty acid side chain that increases a self association or aggregation into hexamer and has reversible albumin binding

27
Q

How can NPH be combine with other insulin’s

A

Can combine with rapid acting, regular

28
Q

Why is degludec ultra long acting

A

Forms large multi hexamer at physiological pH

Large molecular size allow for continued slow release doa>42j

29
Q

What can degludec be mixed with

A

Aspart

30
Q

Why might you not want to give degludec to pt with renal or hepatic impairment

A

Decreased ability to make day to day adjustments due to long doa. This risk is more pronounced in patients with hepatitic or renal impairment

31
Q

Factors affecting absorption of insulin

A

Site of injection. Abdomen faster due to increased blood flow

Depth of injection. Directly into muscles = greater absorption as there is greater vascularisation

Increased volume delays absorption

Exercising muscle group before injection increases absorption rate

Heat/massage of the injection site increases absorption rate

32
Q

Adverse effects of insulin injection

A

Hypoglycemia — dizziness, tremor, shaky hands

Lipodystrphy at side of injection due to accumulation of fate (insulin lipogenesis action

33
Q

Name the insulin snesitisers

A

Biguanide (metformin)

Thiazoldinedione (pioglitazone, rosiglitazone)

34
Q

What is first line oral hypoglycemia agent

A

Metformin

35
Q

Action of metformin

A

Insulin sensitiser, does not affect insulin secretion

Decrease hepatic glucose production
Increase density of insulin receptors
Decrease intestinal glucose absorption
Increase muscular glucose absorption

36
Q

Side effects of metformin

A

Git issues eg flatulence, diarrhea (take with or after meals to reduce side effects)

Increase risk of vitamin b12 malabsorption hence b12 deficiency

Use with caution in patients with renal problems or lactic acidosis

No hyperinsulinemia or hypoglycemia

Weight loss

37
Q

Mechanism of action of thiazoldinedione

A

Activate nuclear transcription factor PPAR-gamma whose ligands regulate glucose metabolism, adipogenesis to increase insulin dependent glucose disposal

Improve insulin sensitivity at tissue

38
Q

Side effects of thiazoldinedione

A

PCHEFB

Pioglitazone induces CYP450 enzyme activity —> reduce serum concentration of drugs
Increased risk of heart failure due to fluid retention
Peripheral edema
Fat/weight gain
Bone fracture

39
Q

What is sulfonylurea

A

Insulin secretagogue, second line oha

First gen tolbutamide
Second gen glibenclamide, glipizide, glicazide, glimepiride [more potent]

40
Q

Which sulfonylureas have lower ris of hypoglycemia

A

Glipizide and glicazide

41
Q

Mechanism of action of glibenclamide

A

Sulfonylurea urea, insulin secretagogie

Stimulate release of insulin from pancreas by beta cells in pancreatic islets
Target pancreatic B cell atp sensitive potassium channel —> bind to Su receptor protein at k-atp channel
Inhibit k-atp channel mediated K+ efflux
Depolarisation
Voltage sensitive ca2+ channel opens and ca2+ influx
Calcium dependent exocytosis of insulin granules from pancreatic B cells

42
Q

Which sulfonylurea has high risk of hypoglycemia

A

Gibenclamide

43
Q

Side effects of sulfonylureas

A 
Weight gain (1-4kg)
Hypoglycemia risk esp elderly, those with renal/hepatic impairment
44
Q

Meglitinide mechanism of action

A

Bind and close atp dependent potassium channel in glucose dependent manner. Similar to sulfonyl urea —> less k+ efflux —> depolarisation —> ca2+ —> calcium dependent exocytosis of insulin

Difference being it binds to SUR1 site instead of SU receptor protein

And also glucose dependent manner hence only augmenting action of glucose dependent insulin release, reducing risk of hypoglycemia

45
Q

Name egs of meglitinide

A

Repaglinide, netaglinide

46
Q

Name examples of alpha glucosidase inhibitor

A

Acarbose, miglitol

47
Q

Mechanism of action og miglitol

A

Alpha glucosidase inhibitor. Irreversibly inhibits membrane bound alpha glucosidase at intestinal brush borders, slowing down hydrolysis of oligosaccharide to glucose and other sugars (carb digestion). This slows down rise in glucose levels after meal, inhibiting post prandial hyperglycemia

Inhibitor has strong affinity to alpha glucosidase than dietary carbohydrates

48
Q

How much acarbose be administered

A

Alpha glucosidase inhibitor administer with food

49
Q

Why may alpha glucosidase inhibitors be poor tolerated by patients

A

Carbohydrates remain at gut and broken down by bacteria, leading to flatulence, gastric distension

50
Q

A glucosidase inhibitors contraindicated in

A

Patients with GI diseases, patients with severe renal or hepatic disease (not related to excretion)

51
Q

What o dipeptidyl peptidase 4 inhibitors do

A

Bind and inhibit dpp4 which breaks down incretin
Prolongs action of endogenous incretin which stimulate B cell to secrete insulin in glucose dependent manner, and suppress a-cell mediated glucagon release and hepatic glucose production

52
Q

Vildagliptin cannot be used in

A

Patients with hepatic impairment

53
Q

Can patient with chronic kidney disease take linagliptin

A

Yes, no dose adjustment needed

54
Q

Side effects of linagliptin

A

Dpp4 inhibitor

GI problems eg diarrhea, flue like symptoms eg headache, runny nose

Use with caution in patients with pancreatitis history

Expensive

55
Q

What are exenatide, liraglutide

A

Glucagon like peptide 1 receptor agonist

56
Q

How are glp 1 receptor agonists administered

A

Subcutaneous injection

57
Q

Mechanism of action of liraglutide

A

Active glp-1 receptor in beta cells, resulting in initial rapid release of endogenous insulin in presence of elevated glucose.

Suppress glucagon release by pancreas

Delay gastric emptying and reduce appetite hence weight loss `

58
Q

Side effects of glp 1 receptor agonist

A 
GI problems
Cannot use inpatient with pancreatitis
Expensive
Low risk of hypoglycemia 
Weight loss
Reduce major adverse cardiovascular events
59
Q

Name sodium glucose co transporter 2 inhibitors

A

Empagliflozin, canagliflozin, dapagliflozin

60
Q

Mechanism of sglt2 inhibitors

A

Reduce reabsorption of filtered glucose at pct, increase urinary glucose excretion

61
Q

Effects of sglt2 inhibitors

A 
Reduce risk for major cardiac event in patient with atherosclerotic cvs
Reduce hospitalisation for heart failure
Reduce progression of renal disease
UTI
Increased urination 
Yeast infection 
Canagliflozin increases risk of lower limb amputation 
Diabetic ketoacidosis

Pharmaco Ca2 (11 decks)

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