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Pharm 2 > Diabetes P2 > Flashcards

Diabetes P2 Flashcards

1
Q

What does intake of carbohydrates tell the liver?

A

-inh glycogenolysis
-inh gluconeogenesis
-stim glycogen synth
-stim GLC uptake
-stim glycolysis

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2
Q

What does protein intake tell the liver?

A

-stim AA transport in liver and muscles
-stim protein synth
-inhibit release of AA from muscles

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3
Q

What ion is affected by insulin?

A

-potassium
-favors movements of K into cells
-lots of insulin treatment causes hypokalemia (K+ leaves blood for cells)
-also promotes growth and development

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4
Q

What is IGF?

A

-insulin-growth factor
-backup system for insulin
-IGF1 and IGF2
-secreted by liver, cartilage and tissue in response to growth hormone
-its receptor is very similar to insulin receptor

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5
Q

What is another name for IGFs?

A

-somatomedins

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6
Q

What are glucose transporters?

A

-helps glucose enter cell
-1-7
-GLUT1 in brain = insulin insensitive
-GLUT2 in beta cells
-GLUT4 in muscle and adipose

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7
Q

How are insulin secretions regulated?

A

-direct feedback of plasma glucose levels on beta cells or alpha cells
-tells the pancreas to secrete either glucagon or insulin to raise or lower blood glucose

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8
Q

What are three major drug groups that regulate insulin secretions?

A

-sulfonylurea
-biguanides
-thiazolidinediones

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9
Q

how does the sympathetic and parasympathetic NS affect the pancreas?

A

-symp: inhibits insulin secretion
-parasymp: increases insulin secretion

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10
Q

What GI secretions regulate insulin secretions?

A

-glucagon
-glucagon derivatives
-secretin
-cholecystokinin
-gastric inhibitory peptide

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11
Q

What is the incretin effect?

A

-when glucose is given orally it better stimulates insulin production than IV

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12
Q

What are two important incretin hormones?

A

-Glucose-dependent insulinotropic polypeptide (GIP)
-glucagon-like peptide 1

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13
Q

What are some characteristics of glucagon-like polypeptide 1?

A

-synth in L cells in ileum and colon
-stimulates insulin, suppresses glucagon
-slows gastric emptying
-increase beta cell mass
-increases insulin sensitivity
-long-term effects not fully known
-for type 2 diabetes
-30-31aa, derived from proglucagon

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14
Q

What are some characteristics of glucose-dependent insulinotropic peptide?

A

-42aa
-derived from proGIP
-secreted by K cells in duodenum and jejunum

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15
Q

What is GLP-1 degraded by?

A

-dipeptidyl peptidase 4 (DPP-4)
-after parenteral admin

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16
Q

What are two drug types that avoid DPP4?

A

-GLP-1 receptor agonists
-DPP4 inhibitors

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17
Q

What is the mechanism of action of insulin?

A

-binds to tyrosine kinase receptors
-phosphorylation cascade = translocate GLUT4 to PM
-induces transcription of genes for catabolism
-promotes the uptake of K+ into cells

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18
Q

What does insulin tell the muscle?

A

increase:
-glc transport
-glycolysis
-glycogen
-protein synth

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19
Q

What does insulin tell the adipose tissue?

A

increase
-glc transport
-increase lipogenesis
-decrease intracellular lipolysis

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20
Q

How is insulin given to best mimic regular non-diabetic insulin?

A

-combinations of short-acting and long/intermediate-acting
-short-acting gives the peak
-intermediate-acting gives the basal level

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21
Q

Difference between lispro and regular insulin and glulisine?

A

-lispro given 15min before meal and peak effect at 30-90min after
-regular insulin peak effect 50-120 min later
-glulisine can be taken 15 min before to 20 min after meal

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22
Q

What is lente insulin?

A

-amorphous insulin
-zinc ion
-slow onset but better sustained
-cannot be given IV

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23
Q

What is isophane NHP insulin?

A

-neutral protamine Hagedorn insulin
-crystalline zinc
-protamine: delays onset and prolongs effectiveness

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24
Q

Where in the body is the insulin pump?

A

-the fatty layer under the skin

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25
Q

What is ultralente insulin?

A

-zinc insulin suspension
-large particles that dissolve
-delayed onset

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26
Q

what is insulin glargine?

A

-precipitation at the injection site
-prolonged action
-no peak gives baseline insulin

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27
Q

What is detemir insulin?

A

-insulin with a FA complex
-slow dissolution

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28
Q

What are the adverse effects of insulin?

A

-hypoglycemia (insulin overdose, alcohol)
-hypokalemia
-lipodystrophy
-weight gain
-injection complications

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29
Q

What are the signs and symptoms of hypoglycemia?

A

-tachycardia
-confusion
-sweating
-drowsiness
-coma
-death

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30
Q

How is type 2 diabetes mellitus treated?

A

-lifestyle changes
-oral hypoglycemic drugs (lower glucose levels, may cause hypoglycemia)

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31
Q

What are oral hypoglycemics?

A

-agents useful in type 2 diabetes treatment
-newly diagnosed pt respond well
-never indicated for T1D

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32
Q

What are the drug classes for T2D?

A

-sulfonylureas
-biguanides
-thiazolidinediones
-alpha-glucosidase inhibitors
-meglitinides

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33
Q

What are sulphonylureas?

A

-work on ppancreas
-stimulates the release of insulin from islet cells
-increase receptor sensitivity
-adverse effect: hypoglycemia from not enough food or too much meds

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34
Q

What is a common issue of insulin?

A

hypoglycemia is the number one problem with drugs that promote insulin release

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35
Q

MOA of sulfonylureas

A

-release insulin from beta cells
-binds to SUR1 subunit and block the ATP-sensitive K+ channel in b-cell -> depolarization causes Ca influx -> insulin secretion
-also reduce glucagon

36
Q

What is the pharmacokinetics of sulfonylureas?

A

-binds to plasma proteins
-met and exc in liver

37
Q

tolbutamide

A

-sulfonylureas
-short-acting
-associated with 2.5x increase in cardiovascular mortality
-banned in canada

38
Q

glyburide

A

-sulfonylureas
-intermediate-acting

39
Q

glipizide

A

-sulfonylureas
-intermediate-acting

40
Q

glimepiride

A

-sulfonylureas
-long-acting

41
Q

What are the adverse effects of sulfonylureas?

A

-weight gain
-hyperinsulinemia
-hypoglycemia
-hepatic or renal insufficiency would make risks worse
-may increase cardiovascular events

42
Q

Which organelle is important in diabetes?

A

-mitochondria
-we inherit only mothers mitochondria
-if mother has type 2 diabetes, then you will probably have type 2 diabetes

43
Q

slide 60 drug interactions

A

remember any two in each box

44
Q

Which drugs reduce the effects of sulfonylureas?

A

-diuretics
-corticosteroids
-niacin

45
Q

Which drugs increase the effects of sulfonylureas?

A

-beta-blockers
-monoamine oxide inhibitors
-salicylates

46
Q

Metformin

A

-biguanide
-insulin sensitizer

47
Q

What are biguanides?

A

-works on the liver and occasionally muscle/adipose
-decrease hepatic gluconeogen

48
Q

What is the MOA of metformin?

A

-reduces plasma glucose
-inh hepatic gluconeogen
-slows abs of sugars
-reduces hyperlipidemia
-decreases appetite
-reduces cardiovascular mortality

49
Q

What are the adverse effects of metformin?

A

-hypoglycemia in combination medication
-rarely lactic acidosis

50
Q

Why can you not have hypoglycemia when on metformin?

A

-does not promote insulin secretion

51
Q

What is AMP Kinase?

A

-regulator for metabolism

52
Q

What is the inhibitory pathway of AMPK?

A

decreases in ATP:AMP -> activates AMP kinase -> inhibits ATP consuming pathways (protein, glycogen, FA synthesis) -> consumes less ATP -> brings ATP:AMP ratio back

53
Q

What is the activating pathway from AMPK?

A

stimulates ATP producing pathways
-glycolysis, beta-ox, glc uptake
-produces more ATP
-brings ATP:AMP back up

54
Q

How does metformin work in a hepatocyte?

A

-enters cell via SLC22A1 transporter -> inhibits mito complex 1 -> less ATP -> high AMP -> gluconeogenesis suppressed -> reduced glucogenic enzymes -> reduced gene expression
-also suppresses fat metabolism and improves insulin receptor function

55
Q

What are a-glucosidase inhibitors?

A

-for type 2 diabetes
-work on GI tract
-oligosaccharide derivatives
-inhibits an enzyme of the intestinal brush border

56
Q

Acarbose

A

-a-glucosidase inhibitor
-poorly absorbed
-stays in intestinal lumen

57
Q

miglitol

A

-a-glucosidase inhibitor
-absorbed and excreted by kidney
-effects intestinal lumen

58
Q

MOA of a-glucosidase inhibitors

A

-taken beginning of a meal
-inhibits a-glucosidase = membrane-bound enzyme in the intestine
-hydrolyses oligosach to monosach -> absorbed -> blunts post-prandial glucose rise -> rises modestly and stays slightly elevated

59
Q

What are thiazolidinediones?

A

-work on the liver and peripheral tissue
-insulin sensitizers
-increase insulin sensitivity of PPARy receptors in cell nucleus
-does not promote insulin secretion
-insulin required for function
-decreases insulin resistance by inhibiting gluconeogen

60
Q

What are the adverse effects of thiazolidinediones?

A

-fluid retention
-headache
-weight gain
-NOT hypoglycemia

61
Q

pioglitazone

A

-thiazolidinedione
-can be taken with insulin

62
Q

rosiglitazone

A

-thiazolidinedione

63
Q

What is the MOA of thiazolidinediones?

A

-activate peroxisome proliferator-activated receptor-gamma
-when ligand binds -> increases insulin sensitivity in adipocytes, hepatocytes and muscle
-elevates HDL levels

64
Q

What is PPAR-y?

A

-when ligand is bound, it regulates adipocyte production, FA secretion, and glucose met
-liver: decreases FA and gluconeogen, increases insulin action
-muscle: increases insulin action
-liver: increases b-cell mass and insulin secretion
-pancreas: increases FA uptake, decreases lipolysis

65
Q

Which drug can you not take with rosiglitazone?

A

-insulin
-causes severe edema

66
Q

What are meglitinides?

A

-work on pancreas
-new class of oral hypoglycemics
-work similar to sulfonylureas
-stimulate release of insulin from islet cells
-short-acting

67
Q

What does secretagogue mean?

A

-a substance that causes another substance to be secreted

68
Q

repaglinide

A

-meglitinide analog
-secretagogue

69
Q

nateglinide

A

-meglitinide analogs
-secretagogue

70
Q

MOA of meglitinide analogs?

A

-bind to ATP sensitive K channels -> mimick prandial and post-prandial insulin release -> very short acting

71
Q

What are the adverse effects of meglitinide analogs?

A

-hyopglycemia (but less than sulfonylureas
-drugs that inhibit CYP3A4 prolong effects
-interactions with other drugs

72
Q

What is incretin therapy?

A

-naturally occurring hormones secreted by the gut
-increases when food is digested

73
Q

what two drugs block cyp3a4?

A

-fluconazole
-erythromycin

74
Q

What does DPP-4 enzymes do?

A

rapidly degrades active incretins when released

75
Q

How does januvia (sitagliptin) work?

A

-food ingested -> incretins released -> januvia inhibits DPP-4 -> less incretins degraded -> increases insulin and reduces glucagon

76
Q

What is SGLT 1 and 2?

A

-both: responsible for renal glucose reabsorption
-1: minor; in intestinal mucosa and proximal straight tubule in nephron
-2: major; in proximal convoluted tubule in nephron

77
Q

How do sodium-glucose cotransporters work?

A

-let in sodium and glucose into cell

78
Q

What is the difference between the three types of SGLTs?

A

-SGLT1:in GI and kidney; high affinity cotransporter
-SGLT2: in kidney; low affinity cotransporter
-SGLT3: throughout body; not glucose transporter

79
Q

What are some SGLT2 inhibitors?

A

-dapagliflozin
-canagliflozin
-empagliflozin
-ipragliflozin

80
Q

dapagliflozin

A

-SLGT2 inhibitor

81
Q

canagliflozin

A

-SLGT2 inhibitor

82
Q

empagliflozin

A

-SLGT2 inhibitor

83
Q

What are the adverse effects of SLGT2 inhibitors?

A

-increase in genital infections (high glucose environment = bacteria grow)
-decrease in BP and weight
-increase in cancer: but not rly anymore?

84
Q

What is the difference between standard and intensive treatment of diabetes?

A

more frequent hypoglycemic events

85
Q

What is HbA1c used for?

A

-hemoglobin A1c
-good measure of glucose control

Pharm 2 (11 decks)

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