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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
What is the hypoglycemia risk of long acting insulin
Low because lower intra subject variation
26
How do glargine and detemir have long action
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
How can NPH be combine with other insulin’s
Can combine with rapid acting, regular
28
Why is degludec ultra long acting
Forms large multi hexamer at physiological pH Large molecular size allow for continued slow release doa>42j
29
What can degludec be mixed with
Aspart
30
Why might you not want to give degludec to pt with renal or hepatic impairment
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
Factors affecting absorption of insulin
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
Adverse effects of insulin injection
Hypoglycemia — dizziness, tremor, shaky hands Lipodystrphy at side of injection due to accumulation of fate (insulin lipogenesis action
33
Name the insulin snesitisers
Biguanide (metformin) Thiazoldinedione (pioglitazone, rosiglitazone)
34
What is first line oral hypoglycemia agent
Metformin
35
Action of metformin
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
Side effects of metformin
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
Mechanism of action of thiazoldinedione
Activate nuclear transcription factor PPAR-gamma whose ligands regulate glucose metabolism, adipogenesis to increase insulin dependent glucose disposal Improve insulin sensitivity at tissue
38
Side effects of thiazoldinedione
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
What is sulfonylurea
Insulin secretagogue, second line oha First gen tolbutamide Second gen glibenclamide, glipizide, glicazide, glimepiride [more potent]
40
Which sulfonylureas have lower ris of hypoglycemia
Glipizide and glicazide
41
Mechanism of action of glibenclamide
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
Which sulfonylurea has high risk of hypoglycemia
Gibenclamide
43
Side effects of sulfonylureas
``` Weight gain (1-4kg) Hypoglycemia risk esp elderly, those with renal/hepatic impairment ```
44
Meglitinide mechanism of action
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
Name egs of meglitinide
Repaglinide, netaglinide
46
Name examples of alpha glucosidase inhibitor
Acarbose, miglitol
47
Mechanism of action og miglitol
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
How much acarbose be administered
Alpha glucosidase inhibitor administer with food
49
Why may alpha glucosidase inhibitors be poor tolerated by patients
Carbohydrates remain at gut and broken down by bacteria, leading to flatulence, gastric distension
50
A glucosidase inhibitors contraindicated in
Patients with GI diseases, patients with severe renal or hepatic disease (not related to excretion)
51
What o dipeptidyl peptidase 4 inhibitors do
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
Vildagliptin cannot be used in
Patients with hepatic impairment
53
Can patient with chronic kidney disease take linagliptin
Yes, no dose adjustment needed
54
Side effects of linagliptin
Dpp4 inhibitor GI problems eg diarrhea, flue like symptoms eg headache, runny nose Use with caution in patients with pancreatitis history Expensive
55
What are exenatide, liraglutide
Glucagon like peptide 1 receptor agonist
56
How are glp 1 receptor agonists administered
Subcutaneous injection
57
Mechanism of action of liraglutide
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
Side effects of glp 1 receptor agonist
``` GI problems Cannot use inpatient with pancreatitis Expensive Low risk of hypoglycemia Weight loss Reduce major adverse cardiovascular events ```
59
Name sodium glucose co transporter 2 inhibitors
Empagliflozin, canagliflozin, dapagliflozin
60
Mechanism of sglt2 inhibitors
Reduce reabsorption of filtered glucose at pct, increase urinary glucose excretion
61
Effects of sglt2 inhibitors
``` 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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