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IPFC 3 - DM > DM Pharmacology > Flashcards

DM Pharmacology Flashcards

(47 cards)

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1
Q

What happens to blood sugar when fasting? Main sources of glucose

A

fasting—- blood sugar dropping

primary source: glycogenolysis (glycogen—- glucose) + gluconeogenesis

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2
Q

What is happening to glucose in prandial stage?

A
  • getting sugars from food — increase BS
  • stimulates insulin release + glucose uptake by tissues + storage of glucose
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3
Q

What are the counter-regulatory hormones

A

glucagon, E, cortisol + GH

E: increase glycogen — glucose, gluconeogenesis, promote lipolysis

C: gluconeogenesis

GH: decrease glucose use in periphery

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4
Q

Insulin production

A

beta cells- make pre-pro-insulin
- SP domain cleaved off to make pro-insulin
- disulphide bridges from bw A+B chains; C peptide cleaved off —— insulin now

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5
Q

What regulates insulin secretion

A

primarily - glucose

others: AA, ketones, incretin, autonomic activity

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6
Q

Mechanism of insulin secretion: glucose stimulated

A

Beta cells— normally hyperpolarized (K coming in)

  • glucose enter via glucose transporter—- metabolized + produces ATP
  • ATP binds to ATP-sensitive K channel + closes it (depolarization)
  • depolarization —- opening of voltage sensitive Ca channel —- Ca flow in
  • Ca cause exocytosis of granules with insulin
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7
Q

Insulin targets + impact

A

Skeletal muscle, liver, adipose

  • stop glucose production and glycogen breakdown, increase glucose storage
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8
Q

How does the insulin receptor work/cause its effects

A
  • kinase like receptor with 2 transmembrane subunits (alpha and beta)
  • alpha subunit: extracellular; insulin binds + causes the intracellular beta units to come together and phosphorylate each other
    —— beta subunit P —- causes intracellular cascade results in increase in glucose uptake in cell (increase glut4 glucose transport levels on cell surface)
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9
Q

T or F: insulin has a long t1/2 (4 hours)

A

F - very short; like less than 10 mins
- inactivated quickly by breaking disulphide bonds by insulinase
- metabolized by liver (no renal adjusting)

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10
Q

Difference bw natural insulin release + SC

A

Sc- rises + falls slower

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11
Q

Why is recombinat human insulin (regular insulin) slower than insulin made in body

A
  • when admin SC: insulin self-arranges in hexamers — which have to breakdown before they can absorbed

**slower

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12
Q

T or F: RA insulin is faster acting than regular insulin

A

T - made changes to AA to make it be absorbed faster

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13
Q

Examples of basal insulins

A
  • NPH (intermediate)
  • long-acting: determir, glargine, degludec
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14
Q

Examples of bolus insulins

A

aspart + lispro, glulisine

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15
Q

T or F: Regular insulin has the same structure as endogenous human insulin

A

T- just made with recombinant tech

  • short acting + given with meals (30-45 mins before)
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16
Q

When can you inject rapid acting insulin

A
  • 15 mins before meals, with meals or up to 15 mins after
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17
Q

Insulin lispro structure

A
  • swap lysine at P29 with proline at P28 to help hexamers break up faster
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18
Q

Insulin aspart structure

A

Proline at P28— aspartame

  • if with nicotinamide (Fiasp): faster onset + A
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19
Q

Insulin glulisine structure

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A

lysine at P29 replaced with glutamate + P3 asparagine replaced with lysine

20
Q

What is NPH

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A

Neutral protamine hagedorn
- regular human insulin + NPH and zinc

— slower action than human insulin because protease in body needs to degrade NPH before it get be absorbed

  • delayed peak + BID dosing (duration 12 hours)
21
Q

Insulin detemir structure

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A

deleted threonin at P30 + lysine at P29 myristolyated

—- helps it aggregate together + bind to albumin

22
Q

insulin glargine structure

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A

Add 2 arg residues to b chain + asparagine at P21 on A chain replaced with glycine

— changes solubility of insulin: soluble at acidic pH; once injected: precipitates

**can’t mix with other insulins

23
Q

insulin degludec structure

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A

Threonine deleted + added hexadecanedioic to lysine at B29

—- causes insulin molecules to bunch together + bind to albumin

Duration > 24hrs

24
Q

Insulin idodec structure

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A

Once weekly dosing
- binds strongly + reversible to albumin due to conjugation of lysine with C20

25
SEs of nocturnal hypo
sweating, nightmares, restless sleep —- giving hangover
26
Symptoms of hypo
sweating, blurred vision, dizzy, confusion, tingling
27
T or F: allergic reactions to insulin are rare but if do occur likely due to the specific insulin molecule used
F - they rare but normally due to protein contaminants not insulin itself
28
What cells secrete glucagon
Alpha cells during situations of hypoglycemia - from precursor: pre-glucagon — promotes glycogen breakdown, glucose production Receptor: GPCR
29
What are the 9 classes of meds used to treat T2DM
1) SU 2) Meglitinides 3) Biguanides 4) TZDs 5) Alpha glucosidase inhibitors 6) GLP-1 agonists 7) DPP-4 inhibitors 8) SGLT2 9) insulin
30
Mechanism of SUs
stimulate B cells to release insulin release - bind to SUR1 subunits of K channel (block it); depolarize cell Ex// glyburide, gliclazide, 1st gens (chlorpropamide)
31
Main SEs of SUs
Hypo + weight gain
32
Mechanisms of Meglitinides
Ex// Repaglinide - stimulates insulin release by B cells; binds to different area of K channel (blocking it)
33
Comparison of SUs vs M
M - faster onset + shorter duration - less hypo risk
34
MoA of biguanides
Ex// metformin - increase sensitivity to insulin (don’t fully know mechanism ; likely combo of shit) — not metabolized therefore duration depends on renal clearance (dose adjust)
35
T or F: metformin has hypo risk
F - doesn’t impact insulin secretion only changes S main SEs: GI + can impact B12
36
MoA TzDs
- binds to TF (PPAR gamma) nuclear receptor —— changes in transcription of genes that impact metabolism + insulin sensitivity in tissues ** only work if body makes enough insulin itself ; don’t use much due to receptor being found all over the body —- a lot SEs
37
Alpha glucosidase inhibitors MoA
Ex// Acarbose ——oligiosaccharide that works locally; i binds to enzyme alpha-glucosidase that metabolizes disaccharides (slow G A) * higher affinity to enzyme than disaccharides taken with meals
38
Ses of Alpha-glucosidase inhibitors
- low systemic A: GI, bloating etc SEs - if hypo: need to treat with monosaccharide (glucose, milk, honey)
39
What are incretins
- peptides released after eating that increase insulin release —- work alongside glucose induced insulin release
40
Why can’t we use IV GLP-1 as therapy for T2DM
super short t1/2 due to metabolism by DPP-4 (t1/2 of 1-2 mins) GLP-1: increase insulin release, slow down gastric emptying, decrease glucagon secretion + decrease appetite
41
GLP-1r A MoA
- binds to + activate G alpha coupled GLP-1 receptors on B cells to increase insulin secretion — binds to GPCR on cells + causes increase in cAMP — increase insulin Secretion —- mainly impacts glucose levels after you eat not FPG
42
Differences bw GLP-1 receptor agonists
Lixisenatide - SC, renally dose Liraglutide - SC, no renal adjusting (12 hour t1/2) Dulaglutide: t1/2 of 5 days, SC no renal dosing Semaglutide: oral + SC Tirzepatide: GLP + GIP (best in glycemic control + weight loss)
43
DPP 4 inhibitors
Enzyme normally: inactivate incretins by removing 2AAs - inhibit this to increase t1/2 of them + their fxns (insulin secretions, decrease glucagon secretion, + reduce hyperglycemia) **little impact on gastric emptying + satiety —- increase GLP + GIP levels by 2X
44
MoA of DPP4 i
- competitively inhibit DPP-4 —- saxagliptin: covalently binds though
45
Which DPP-4 is good for RF
lingatliptin : no renally dosing - sitagliptin + saxa + alo: renally dosed
46
SGLT2 MoA
inhibit SGLT2 — stop glucose reuptake in PCT of kidney (glucose peed out —- pulls out more fluid due to osmosis) ADRs: diuresis, UTI, infections, decrease in BP, weight loss, thirst, DKA ** renally protective but also works less as RF decreases
47

IPFC 3 - DM (9 decks)

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