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IPFC 3 Midterm 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are the steps of insulin synthesis? (3)

A
  1. Pancreatic B-cells make pre-pro-insulin
  2. SP domain is removed to result in pro-insulin
  3. 3 disulfide bridges are formed and the C peptide is removed = insulin
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2
Q

Main MOA of action of the counterregulatory hormones
Epinephrine
Cortisol
Growth hormone

A

Epinephrine
- glycogenolysis
- gluconeogenesis

Cortisol
- promotes gluconeogenesis
- impairs insulin secretion

Growth hormone
- decreases glucose utilization/transport

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3
Q

What is the structure of insulin?

A

51 amino acids with A and B chains linked by 3 disulfide bonds

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4
Q

What is the primary regulator of insulin secretion?

A

Glucose

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5
Q

What are the steps for insulin secretion? (6)

A
  1. B-cells are hyperpolarized in resting state (insulin stored in vesivles)
  2. Glucose enters the cell through GLUT4 (glucose transporters)
    - hexokinase converts glucose to G6P
  3. Glucose is metabolized to inc ATP production
  4. inc ATP and depolarization closes the K+ channel
  5. Depolarization leads to opening voltage Ca2+ channels
  6. Calcium enters the cell leading to exocytosis of insulin vesicles into bloodstream
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6
Q

What are the physiological effects when insulin is released? (3)

A
  1. Inc glucose in muscle, liver, and adipose tissue
  2. Suppresses gluconeogenesis and FFA release
  3. Anabolic actions: glycogenesis, lipogenesis, protein synthesis
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7
Q

How does the insulin receptor work?

A

Insulin receptor 2 subunits A and B
1. Insulin binds A subunits –> brings B subunits close together
2. B subunits (contain tyrosine kinase) phosphorylate each other –> activate other proteins

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8
Q

What is the structure of amino acids for the following insulin
Lispro
glulisine
aspart
detemir
degludec
glargine

A

Lispro Lys Pro
glulisine Lys Glu
aspart Asp
detemir Lys
degludec Asp Pro Lys A-chain
glargine Gly Arg Arg

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9
Q

Which insulins bind to albumin

A

Detemir and degludec

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10
Q

Rank the insulin from quickest to longest acting.

A

Aspart (Fiasp)

Pre-mixed rapid acting

Fast-acting
- Aspart Novorapid
- Glusline/lispro

Short-acting
- Regular human insulin (humulin)

pre-mixed NPH

intermediate-acting NPH

Long acting
Detemir
glargine U-100
glargine U-300
glargine biosimilar
Degludec

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11
Q

Which insulin can you not mix with other insulins

A

insulin glargine because it will precipitate with the other insulins

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12
Q

Where does glucagon come from?

A

Secreted by A cells of the pancreas in response to hypoglycemia
- derived from a larger precursor protein, proglucagon

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13
Q

What is the glucagon receptor structure?

A

GPCR and coupled G-alpha subunits

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14
Q

What is the MOA of glucagon (2)

A
  1. Promotes breakdown of glycogen to glucose
  2. Increases gluconeogenesis and ketogenesis
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15
Q

What are other uses for glucagon

A
  • reverse B-blocker overdose
  • bowel radiology (antiperistaltic - promotes bowel distension)
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16
Q

What is the primary MOA of sulfonylureas? How does it work

A

Primary MOA: stimulate the release of insulin from B cells
- act directly on the ATP driven potassium channel to close it
- depolarization of the cell (without glucose intake) to open Ca2+ channel
- Ca2+ influx to release insulin via exocytosis

17
Q

What are ADRs of sulfonylureas? is it safe in renal-failure

A

Hypoglycemia
Weight gain

safe in renal-failure

18
Q

Which drug class is the most similar to sulfonylureas? whats the difference

A

Meglitinides (repaglinide)

Difference
- less risk of hypoglycemia
- better postprandial control
and usually dosed around meals (no meal = no drug)

19
Q

What is the MOA of biguanides? metformin

A

Increased insulin sensitivity in target tissues
- antihyperglycemic drug
- NO HYPO

20
Q

What are ADRs of metformin/biguanides? is it safe in renal-failure?

A

GI N/V/D
Anorexia

Completely cleared by kidneys
- not safe in eGFR under 30

21
Q

What are long-term effects of taking metformin?

A

Reduced vitamin B12 levels

22
Q

What is the primary MOA of thiazolidinediones TZDs

A

Changes in the transcription of genes
- indirectly inc insulin sensitivity

23
Q

What are the ADRs for TZDs

A

CV disease mimic Heart failure such as fluid retention and edema

Weight gain

24
Q

What is the MOA of alpha-glucosidase inhibitors

A

oligosaccharide competitively binds to alpha-glucosidase to prevent breakdown of disaccharides to monosaccharides

Acarbose

25
Q

What are the ADRs of alpha-glucosidase inhibitor

A

Limited systemic absorption, act locally in the GI tract

Lots of diarrhea

26
Q

What is the MOA of GLP-1 receptors agonists? Which lab value does it effect more?

A

Bind to G alpha/s coupled receptor –> promote insulin secretion
- reduced glucagon secretion
- slower gastric emptying

as soon as you have food in the stomach insulin is released BEFORE glucose levels start to rise
Problem: GLP-1 is broken down in 1-2 mins by DPP-IV
Solution: GLP-1 agonists and DPP-IV inhibitors
- therefore, best for PPG (less effect on fasting glucose)

27
Q

What are some ADRs of GLP-1 receptor agonists?

A

N/V (up to 50%) due to delayed gastric emptying
Weight loss
Acute pancreatitis
Risk of cancer thyroid

28
Q

What is the newest GLP-1 receptor agonist that has more efficacy for glycemic control and weight loss

A

Tirzepatide
dual GIP and GLP-1 receptor agonist

29
Q

Which GLP-1 receptor agonist are clearned by the kidney? (2)

A

Exenatide
Lixisenatide

30
Q

What is the MOA of DPP-IV inhibitor

A

Increases half-life of GLP-1 and GIP

problem: DPP-IV usually removes 2 AA off incretins (GLP-1,GIP) which results in their inactivation

improves insulin secretion in response to food
- reduces glucagon release
- reduces hyperglycemia
- little effect on gastric emptying or satiety

no weight loss

31
Q

Which DPP-IV inhibitors are renally cleared? Which are not

A

Renaly cleared
- sitagliptin (januvia)
- saxagliptin

Not renally cleared
- Linagliptin (trajenta)

32
Q

What is the MOA of SGLT-2 inhibitors

A

prevents/decrease glucose reabsorption in the kidneys
- glucose remains in urine
- results in glycosuria (sugar in pee) + osmotic diuresis (pee more)

33
Q

What are the benefits of SGLT-2 inhibitors

A

Loss of calories in excreted glucose –> weight loss
Lower BP through water loss
low hypo risk

34
Q

What are the ADRs of SGLT-2 inhibitors

A
  • Glucose in urine –> yeast infection -> UTI
  • Thirst, inc urination, nausea
  • hypovolemic
  • risk of DKA
  • postural hypotension, lightheadedness
35
Q

T/F SGLT-2 inhibitors have reduced efficacy in renal patient but still have renal protective effects?

A

True

IPFC 3 Midterm 1 (8 decks)

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