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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
describe the pharmacokinetics of NPH insulin
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
what is the mechanism of glargine?
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
what is the mechanism of detemir?
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
besides vitals, you should always check what in unconscious patients?
always check blood sugar in unconscious patients !! could be due to hypoglycemia, which is easily reversible !
29
what is the half life of circulating pancreatic insulin and how is it cleared from the body?
t1/2 = 3-5 mins liver clears ~60%, kidney ~40% compared to exogenous insulin which is cleared 60% by kidney, 40% by liver
30
what is the difference between SC (subcutaneous) and IV prep regular (short-acting) insulin?
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
what is the difference between *lispro*, *aspart*, and *glulisine* insulin analogs?
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
degludec
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
what are 4 adverse effects of insulin preparations?
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
metformin decreases absorption of which vitamin?
decreases vitamin B12 absorption - annual screening for deficiency is recommended
35
what kind of drugs are *gliflozins*? (canagliflozin, dapagliflozin, bexagliflozin, etc)
renal SGLT2 inhibits - reduce reabsorption of glucose used to treat type 2 diabetes
36
what kind of drugs are exenatide, liraglutide, lixisenatide, dulaglutide, semaglutide, and albiglutide?
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
what kind of drugs are sitagliptin, saxagliptin, linagliptin, and alogliptin?
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
what kind of drug is tirzepatide?
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
what kind of drugs are *chlorpropamide* and *tolbutamide*?
first generation sulfonylureas (insulin secretogogues) stimulate release of insulin from beta cells, chronically lower circulating glucagon
40
what kind of drugs are *glyburide*, *glipizide*, and *glimepiride*?
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
what kind of drug is *repaglinide*?
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
what kind of drug is *nateglinide*?
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
what kind of drugs are *pioglitazone* and *rosiglitazone*?
thiazolidinediones (TZDs), aka “gliTaZones”: primarily target adipose, reduce insulin resistance via agonism of PPARy (nuclear TF)
44
what kind of drugs are *acarbose* and *miglitol*?
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
what kind of drug is *pramlintide*?
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
what do the following suffixes indicate about the diabetic drug type? a. “-natide” b. “-glutide” c. “-liptin” d. “-gliflozin” e. “-glinide” f. “-glitazone”
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
which of the following does NOT depend on functional pancreatic beta cells? a. chlorpropamide b. glyburide c. netaglinide d. acarbose e. tolbutamide
d. acarbose: alpha-glucosidase inhibitor —> decreases dietary glucose absorption insulin secretogogues (increase beta cell insulin secretion) - chlorpropamide, glyburide, netaglinide, tolbutamide
48
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
*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
which of the followings poses a risk of vaginal yeast infections or UTIs? a. chlorpropamide b. canagliflozin c. pioglitazone d. miglitol e. alogliptin
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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