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Endocrine > Treatment of Diabetes + Insulin B&B > Flashcards

Treatment of Diabetes + Insulin B&B Flashcards

1
Q

how do the following drugs treat type 2 diabetes?
a. sulfonylureas
b. incretins
c. biguanides (metformin)
d. acarbose
e. SGLT-2 inhibitors

A

a. sulfonylureas: stimulate insulin release
b. incretins: stimulate insulin release
c. biguanides (metformin): inhibit gluconeogenesis
d. acarbose: inhibit alpha-glucosidase
e. SGLT-2 inhibitors: decrease reabsorption of glucose from kidneys

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2
Q

what is the mechanism and use of sulfonylureas (glyburide)?

A

inhibit pancreatic beta cell K+ channels, causing depolarization independent of glucose concentration —> rise in intracellular Ca2+ stimulates insulin secretion

used to treat Type 2 diabetes

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3
Q

what is the mechanism and use of DPP-4 inhibitors (“gliptins” -
sitagliptin, saxagliptin, alogliptin)?

A

enhance active incretin levels by inhibiting degradative enzyme DPP-4

incretins stimulate insulin release from beta cells

work in glucose dependent manner, used to treat type 2 diabetes

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4
Q

what is the mechanism and use of GLP-1/GIP receptor agonists (“-natide” or “-glutide”)?

A

GLP-1 and GIP are incretins - secreted from enteroendocrine cells, stimulate insulin release after eating, before glucose levels rise

agonists used to treat type 2 diabetes

ex - exenatide, liraglutide, dulaglutide, lixisenatide

[GLP1 = glucagon like peptide 1, GIP = glucose dependent insulinotropic protein]

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5
Q

what is the mechanism and use of biguanides, such as metformin (glucophage)?

A

first line therapy for type 2 diabetes mellitus

inhibits gluconeogenesis in liver —> decreases hepatic glucose production and increases peripheral glucose uptake by muscle

inhibits complex I of ETC, decreasing ATP production —> AMP allosterically inhibits gluconeogenesis enzymes

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6
Q

what is the mechanism and use of alpha-glucosidase inhibitors, such as acarbose?

A

alpha-glucosidase causes breakdown of polysaccharides (hydrolyzes 1,4 linkages)

therefore, acarbose inhibits breakdown of polysaccharides —> reduced absorption of carbohydrates, reduced postprandial elevations in plasma glucose

used to treat type 2 diabetes

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7
Q

what is the mechanism and use of SGLT-2 inhibitors (canagliflozin, invokana)?

A

block reabsorption of glucose in the proximal tubule of kidneys —> increased glucose excretion, lowering blood glucose levels

used to treat type 2 diabetes

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8
Q

which patients should not receive metformin?

A

metformin: first line for type 2 diabetes, inhibits hepatic gluconeogenesis

rare but life-threatening side effect is lactic acidosis

CANNOT be given to patients with renal insufficiency as they are at greater risk for developing lactic acidosis

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9
Q

which of the following diabetic drugs may cause hypoglycemia as an adverse effect?
a. metformin
b. sulfonylureas

A

b. sulfonylureas - glucagon levels fall, occurs with exercise or skipping meals

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10
Q

what 2 adverse effects are associated with sulfonylureas?

A
  1. hypoglycemia - via reduced glucagon signaling
  2. weight gain - via increased insulin signaling

used to treat Type 2 diabetes, increase insulin secretion from pancreatic beta cells (via blocking K+ channels, causing depolarization)

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11
Q

which of the following must be taken right before eating?
a. sulfonylureas
b. biguanides (metformin)
c. acarbose
d. SGLT-2 inhibitors

A

c. acarbose (glucosidase inhibitor)

recall alpha-glucosidase causes breakdown of polysaccharides (hydrolyzes 1,4 linkages)

alpha-glucosidase causes breakdown of polysaccharides (hydrolyzes 1,4 linkages)

therefore, acarbose reduces absorption of carbohydrates, reducing postprandial elevations in plasma glucose

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12
Q

what is the mechanism and use of meglitinides (repaglinide)?

A

short acting oral therapy for diabetes

similar mechanism to sulfonylureas - close K+ channels in beta cells to trigger depolarization and insulin secretion

however, don’t contain sulfur - safe for sulfa allergy

given prior to meals

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13
Q

what drug is first line for type 2 diabetes and how does it work?

A

metformin (biguanide): inhibits gluconeogenesis in liver —> decreases hepatic glucose production and increases peripheral glucose uptake by muscle

inhibits complex I of ETC, decreasing ATP production —> AMP allosterically inhibits gluconeogenesis enzymes

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14
Q

what is the mechanism and use of thiazolidinediones (TZDs), such as pioglitazone and rosiglitazone?

A

TZDs (“glitazones”): oral therapy for diabetes, decrease insulin resistance

act on PPAR-gamma receptors in nucleus, causing it to bind retinoid X receptors (RXR)

—> upregulated GLUT4, antagonism of TNF-alpha, adiponectin secretion (from adipocytes, increase insulin sensitivity)

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15
Q

which patients cannot receive TZDs (thiazolidinediones) for diabetes?

A

TZDs (“glitazones”): act on PPAR-gamma receptors in nucleus to decrease insulin resistance

PPAR-y receptors also cause increased Na+ retention —> edema

risk of pulmonary edema, not used in patients with advanced heart failure

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16
Q

what type of receptor is acted on by TZDs vs fibrates?

A

TZDs: act on PPAR-gamma receptors to decrease insulin resistance

fibrates: act on PPAR-alpha receptors to lower triglycerides

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17
Q

what is the therapeutic use of amylin analogs such as pramlintide?

A

amylin (IAPP): hormone secreted by beta cells and released with insulin —> suppresses glucagon release, delays gastric emptying, reduces appetite

amylin analogs are given with meals (SC injection) alongside insulin and enhance effects of insulin

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18
Q

what 3 adverse effects are associated with SGLT2 inhibitors (gliflozins)?

A

block reabsorption of glucose in the proximal tubule of kidneys —> increased glucose excretion

however increased glucose in urine is favorable environment for infections:
1. vulvovaginal candidiasis
2. UTIs

  1. increase DKA risk
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19
Q

which 2 diabetic drugs must be avoided in patients with advanced heart failure, and why?

A
  1. TZDs: act on PPAR-y receptors, cause fluid retention
  2. metformin: decrease hepatic gluconeogenesis, risk of lactic acidosis
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20
Q

how do Lispro, Aspart, and Glulisine function as rapid-acting insulin?

A

insulin typically forms hexamers in the body, causing slower onset of action

rapid-acting insulin analogs have modified amino acids to reduce polymer formation —> rapid absorption, onset, and duration

onset 5-15 mins, peak 1 hour, duration 2-4 hours, taken pre-meal

21
Q

describe the onset, peak, and duration of action of Lispro, Aspart, and Glulisine

A

rapid acting insulin analogs (modified amino acids prevent polymerization)

onset: 5-15 mins
peak: 1 hour
duration: 2-4 hours

taken pre-meal

22
Q

describe the onset, peak, and duration of action of “regular” insulin (short-acting)

A

regular insulin = synthetic analog of human insulin made via recombinant DNA

onset: 30 mins
peak: 2-3 hours
duration: 3-6 hours

23
Q

what is the only type of insulin that is given IV?

A

“regular” (short-acting) insulin: synthetic analog of human insulin, commonly used in hospitalized patients (blood sugar elevations common with infection/injury)

used to treat DKA, HHS, hyperkalemia

24
Q

what is NPH insulin?

A

NPH insulin = neutral protamine hagedorn, aka Isophane insulin

regular insulin (neg charge) combined with neutral protamine (pos charge), which slows absorption

onset 2-5 hours, peak is 4-8 hours, duration 12-16 hours

25
Q

describe the pharmacokinetics of NPH insulin

A

NPH insulin = neutral protamine hagedorn, aka Isophane insulin

onset 2-5 hours
peak: 4-8 hours
duration: 12-16 hours

action of NPH is highly unpredictable, clinical use is waning

26
Q

what is the mechanism of glargine?

A

modified insulin that precipitates at body pH after SQ injection and slowly dissolves from crystals

provides low/ continuous levels of insulin, once daily injection

onset: 1-1.5 hours
duration: 11-24 hours

27
Q

what is the mechanism of detemir?

A

insulin with fatty acid side chain which slows rate of absorption via aggregation in subcutaneous tissue and reversible binding to albumin

onset: 1-2 hours
duration: >12 hours

can be given once/twice daily, may cause less weight gain that other forms of insulin

28
Q

besides vitals, you should always check what in unconscious patients?

A

always check blood sugar in unconscious patients !!

could be due to hypoglycemia, which is easily reversible !

29
Q

what is the half life of circulating pancreatic insulin and how is it cleared from the body?

A

t1/2 = 3-5 mins

liver clears ~60%, kidney ~40%

compared to exogenous insulin which is cleared 60% by kidney, 40% by liver

30
Q

what is the difference between SC (subcutaneous) and IV prep regular (short-acting) insulin?

A

SC prep: soluble crystalline Zn2+ formulation of recombinant human insulin, tends to hexamerize at injection site, onset ~30mins, peak 2-3hours, duration 5-8hours

IV prep: diluted phosphate-buffered (no Zn2+) formulation of recombinant human insulin, forms monomers

31
Q

what is the difference between lispro, aspart, and glulisine insulin analogs?

A

all forms of rapid-acting insulin analogs, injected right before meals

lispro: reversed proline and lysine residues on beta chain (LYS then PRO)

aspart: ASPARTate residue added on beta chain

glulisine: lysine and glutamate added on beta chain (GLU LYSINE)

32
Q

degludec

A

human insulin analog, modified with conjugation to hexadecanedioic acid

ultra-long lasting basal insulin - onset 1-1.5 hours, duration up to 42 hours

injected once daily

33
Q

what are 4 adverse effects of insulin preparations?

A
  1. hypoglycemia - more common in type 1 (tachycardia, sweating, trembling, confusion, convulsions)
  2. weight gain - more common in type 2
  3. lipodystrophy at injection site
  4. human insulin generates some Abs, but insulin allergy very rare
34
Q

metformin decreases absorption of which vitamin?

A

decreases vitamin B12 absorption - annual screening for deficiency is recommended

35
Q

what kind of drugs are gliflozins? (canagliflozin, dapagliflozin, bexagliflozin, etc)

A

renal SGLT2 inhibits - reduce reabsorption of glucose

used to treat type 2 diabetes

36
Q

what kind of drugs are exenatide, liraglutide, lixisenatide, dulaglutide, semaglutide, and albiglutide?

A

GLP-1 (incretin) receptor agonists - subcutaneous injection

stimulates glucose-dependent insulin secretion, inhibits glucagon release, delays gastric emptying, reduces food intake

may cause weight loss, reduce risk of atherosclerosis/ heart failure/ CKD

[“-natide” or “-glutide” = GLP-1 receptor agonist]

37
Q

what kind of drugs are sitagliptin, saxagliptin, linagliptin, and alogliptin?

A

DPP-4 inhibitors (which breaks down incretins) - cause increase in GLP-1 and GIP, which stimulate insulin secretion

note saxagliptin is CYP3A4/5 metabolized

[“-gliptin” = DPP-4 inhibitor]

38
Q

what kind of drug is tirzepatide?

A

GLP-1 and GIP (incretins) receptor dual agonist

once weekly subcutaneous injection, causes significant weight loss

being used to treat type 2 diabetes and obesity

39
Q

what kind of drugs are chlorpropamide and tolbutamide?

A

first generation sulfonylureas (insulin secretogogues)

stimulate release of insulin from beta cells, chronically lower circulating glucagon

40
Q

what kind of drugs are glyburide, glipizide, and glimepiride?

A

second generation sulfonylureas (insulin secretogogues)

stimulate release of insulin from beta cells, chronically lower circulating glucagon

glipizide - short half life (less risk for hypoglycemia)
glimepiride - longest half life (once daily use)

41
Q

what kind of drug is repaglinide?

A

meglitinide - insulin secretogogue similar to sulfonylureas

rapid absorption/ short half life - produces fast and brief stimulation of insulin secretion, indicated to reduce postprandial hyperglycemia (take prior to eating)

42
Q

what kind of drug is nateglinide?

A

D-phenylalanine derivative (insulin secretogogue), VERY quick onset/ short duration

safe for patients with very reduced renal function, but caution in patients with liver disease (hepatic clearance)

43
Q

what kind of drugs are pioglitazone and rosiglitazone?

A

thiazolidinediones (TZDs), aka “gliTaZones”: primarily target adipose, reduce insulin resistance via agonism of PPARy (nuclear TF)

44
Q

what kind of drugs are acarbose and miglitol?

A

alpha-glucosidase inhibitors

(alpha-glucosidase breaks down polysaccharides)

—> reduced absorption of carbohydrates, reduced postprandial elevations in plasma glucose

used to treat type 2 diabetes

45
Q

what kind of drug is pramlintide?

A

amylin (IAPP) agonist: hormone secreted by beta cells and released with insulin —> suppresses glucagon release, delays gastric emptying, reduces appetite

amylin analogs are given with meals (SC injection) alongside insulin and enhance effects of insulin

prAMLINtide = AMYLIN

46
Q

what do the following suffixes indicate about the diabetic drug type?
a. “-natide”
b. “-glutide”
c. “-liptin”
d. “-gliflozin”
e. “-glinide”
f. “-glitazone”

A

a. “-natide” and b. “-glutide” = GLP-1 receptor agonist (ex, exenatide, liraglutide)

c. “-liptin” = DPP-4 inhibitor (ex, sitagliptin)

d. “-gliflozin” = SGLT-2 inhibitor (ex, dapagliflozin)

e. “-glinide” = insulin secretogogues (ex, repaglinide, netaglinide)

f. “-glitazone” = TZDs (ex, pioglitazone, rosiglitazone)

47
Q

which of the following does NOT depend on functional pancreatic beta cells?
a. chlorpropamide
b. glyburide
c. netaglinide
d. acarbose
e. tolbutamide

A

d. acarbose: alpha-glucosidase inhibitor —> decreases dietary glucose absorption

insulin secretogogues (increase beta cell insulin secretion) - chlorpropamide, glyburide, netaglinide, tolbutamide

48
Q

which of the following causes significant weight loss, and can be used to treat obesity?
a. tirzepatide
b. sitagliptin
c. repaglinide
d. pramlintide
e. bexagliflozin

A

tirzepatide: GLP-1 and GIP receptor dual agonist

b. sitagliptin: DPP-4 inhibitor
c. repaglinide: insulin secretogogue
d. pramlintide: amylin agonist
e. bexagliflozin: SGLT-2 inhibitor

49
Q

which of the followings poses a risk of vaginal yeast infections or UTIs?
a. chlorpropamide
b. canagliflozin
c. pioglitazone
d. miglitol
e. alogliptin

A

b. canagliflozin: renal SGLT-2 inhibitor (“gliflozins”) - remember this makes sense because they cause more glucose excretion in the urine, which is favorable for bacteria

a. chlorpropamide: sulfonylurea
c. pioglitazone: TZD (“glitazone”)
d. miglitol: alpha-glucosidase inhibitor
e. alogliptin: DPP-4 inhibitor

Endocrine (29 decks)

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