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Pharmacology Exam 4 > Diabetes Meds > Flashcards

Diabetes Meds Flashcards

1
Q

What cells create glucagon?

A

alpha cells in pancreas

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2
Q

Where is insulin created and stored?

A

in granules in the beta islet cells of pancreas

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3
Q

What is the normal insulin secretion per day?

A

60 units/day, 25% of total content

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4
Q

True/False. Insulin is released continuously?

A

true, also additional increases following carbohydrate ingestion

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5
Q

Where does insulin go from the pancreas?

A

enters the portal vein into liver where half is taken up to turn glucose into glycogen or fatty acids for storage in liver, muscle, and fat.

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6
Q

How does high blood glucose stimulate insulin release?

A

glucose enters beta cell via glut-2 transporter and is converted to ATP through oxidation. closes ATP sensitive K channel stopping K from leaving, causing depolarization and Ca enters cell–>insulin secretion

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7
Q

Does oral admin or IV admin of carbohydrates stimulate higher secretion of insulin?

A

oral admin

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8
Q

What is the stim of insulin by carb intake called?

A

Incretin Effect

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9
Q

Describe the Incretin effect.

A

GLP-1 and GIP released from specialized neuroendocrine cells of SI.

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10
Q

How is the incretin effect altered in DM II?

A

blunted incretin response and GIP becomes ineffective

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11
Q

Other than incretin effect and high glucose, what stimulates insulin release?

A

vagus nerve stim “cephalic phase,” pituitary adenylate cyclase activating polypeptide (PACAP), vasoactive intestinal peptide (VIP), beta agonists, hormones (cortisol, catecholamines, glucagon, growth hormone

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12
Q

What does insulin stimulate in carbohydrate metabolism?

A

Glucose transport in adipose tissue and muscle
Rate of glycolysis in muscle and adipose tissue
Glycogen synthesis in adipose tissue, muscle, liver

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13
Q

What does insulin inhibit in carbohydrate metabolism?

A

Glycogen breakdown in muscle/liver

Rate of glycogenolysis and gluconeogenesis in liver

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14
Q

What does insulin stimulate in lipid metabolism?

A

Fatty acid and triacylglycerol synthesis in tissues
Uptake of TG from blood into adipose tissue/muscle
Rate of cholesterol synthesis in liver

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15
Q

What does insulin inhibit in lipid metabolism?

A

Lipolysis in adipose tissue/lower plasma fatty acid level
Fatty acid oxidation in muscle/liver
Ketogenesis

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16
Q

What does insulin stimulate in protein metabolism?

A

Amino acid transport into tissues

Protein synthesis in muscle/adipose/liver/other tissues

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17
Q

What does insulin inhibit in protein metabolism?

A

Protein degradation in muscle

Urea formation

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18
Q

What role does muscle play in the transportation and storage of insulin?

A

anabolic hormone enhancing protein synthesis and decreasing protein breakdown, glucose transport into muscle using Glut-4 transporter, glycogen synthesis/storage

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19
Q

What role does fat have in transportation and storage of insulin?

A

insulin increases fatty acid and TG uptake into fatty tissues and lowers plasma fatty acid level, increased glucose transport into fat cells using GLUT-4 transporter, inhibits breakdown of fat and increases clearance of ketone bodies

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20
Q

Where is insulin NOT required to transport glucose to?

A

brain, liver, kidneys

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21
Q

What role does insulin have in the liver?

A

increased synthesis of glycogen in liver (glycogenesis), inhibits gluconeogenesis, glycogenolysis, and ketogenesis, excess glucose converted to free fatty acids, synthesis of free fatty acids and glycerol into TG for fat storage, increased protein synthesis from amino acids

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22
Q

What effect does insulin have on electrolytes?

A

potassium uptake into cells-hyperkalemia, renal sodium retention

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23
Q

What effect does insulin have on the brain?

A

stimulates memory, controls appetite–feel full

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24
Q

What effect does insulin have on CV system?

A

vasodilatory properties

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25
Q

What does pancreatic beta islet cells secrete insulin along with?

A

Glut-2 transporter

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26
Q

What rapidly deactivates GLP-1 and GIP?

A

DPP-4

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27
Q

What does insulin do?

A

stim body to store glucose in liver/fat/muscle, inhibit liver from making glucose, stim liver to make and store glycogen and fatty acids, transport glycogen/fatty acids to muscle/fat with glut-4 transporter, inhibit fat to release fatty acids, promote protein synthesis, inhibit pancreas from secreting glucagon=LOWER BLOOD SUGAR

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28
Q

What’s A1C for type II DM diagnosis?

A

> 6.5%

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29
Q

What’s fasting BS for type II DM?

A

> 126

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30
Q

What’s the glucose tolerance test for type II DM?

A

> 200

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31
Q

What’s normal A1C?

A

<5.7

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32
Q

What’s normal fasting BS?

A

<99

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33
Q

What’s normal glucose tolerance test?

A

<140

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34
Q

What are type II DM lifestyle risk factors?

A

increased carb intake, metabolic syndrome, inactivity, obesity, HTN, HLD

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35
Q

What are genetic type II DM risk factors?

A

black, alaska natives, indians, asian, latino, hawaiian, PI, obese tencency

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36
Q

What happens in type II DM?

A

stimulates an abnormal amount of insulin release and over time may cause increases resistance to insulin in muscles, fat, liver and pancreas does not produce enough to compensate

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37
Q

What’s the classic triad of type II DM?

A

polyuria, dehydration, polydipsia

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38
Q

What are some complications of diabetes?

A

alzheimers, nerve damage, eye damage, hearing impairment, dental problems, cardio/cerebral/vascular disease, kidney damage, extremity damage, skin conditions

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39
Q

Does glucose intolerance progress over time in type II DM?

A

yes, may need to evolve therapy as disease worsens

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40
Q

What’s the hierarchy of therapies for type II DM?

A

diet/lifestyle
monotherapy with oral agents
combinations of oral therapies
insulin/injection therapy alone or in combination

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41
Q

What are the categories of glucose lowering medications?

A

Secretagogues, Insulin Sensitizers, Dopamine agonists, Glucose absorption inhibitors, glucagon secretion inhibitors

42
Q

What types of meds are secretagogues?

A

sulfonylureas, meglitinides, GLP-1 agonists, DPP-4 inhibitors

43
Q

What types of meds are insulin sensitizers?

A

biguanides (metformin), thiazolidinediones

44
Q

What types of meds are dopamine agonists?

A

bromocriptine mesylate (give in morning)

45
Q

What types of meds are glucose absorption inhibitors?

A

sodium-glucose CO-transporter-2 (SGLT2) inhibitors, alpha-glucosidase inhibitors, fiber

46
Q

What types of meds are glucagon secretion inhibitors?

A

amylinomimetic

47
Q

How does secretagogue therapy lower glucose?

A

increase endogenous insulin release in the pancreas. Needs 30% normal beta cell function.

48
Q

How does insulin sensitizers lower glucose?

A

reduce insulin resistance

49
Q

How does dopamine agonists lower glucose?

A

increase early morning dopamine levels, decrease SNS to make glucose agents to reduce glucose absorption within small bowel and kidneys

50
Q

What’s the suffix for sulfonylureas?

A

-ides

51
Q

How effective are sulfonylureas at reducing A1C?

A

lowers 1-2%

52
Q

Who are good candidates for sulfonylureas?

A

not overweight, may have intolerance to metformin

53
Q

What’s the MOA of sulfonylureas?

A

bind to ATP-dependent K channel of pancreatic beta cells causing depolarization, calcium channels open increasing secretion of insulin

54
Q

What are the actions of sulfonylureas?

A

increase sensitivity of beta cells to glucose, limit glucose production in liver, decrease lipolysis, decrease liver clearance of insulin

55
Q

What are the adverse effects of sulfonylureas?

A

hypoglycemia, weight gain, GI symptoms, higher incidence of increased CV morbidity/mortality vs metformin

56
Q

What are the contraindications of sulfonylureas?

A

sulfa allergy potentially, liver/kidney dysfunction (50-80% renal elimination, also liver, fecal)

57
Q

What is the suffix for meglitinides?

A

-nides

58
Q

Do meglitinides have a stronger or weaker binding affinity than sulfonylureas?

A

weaker binding affinity, don’t last as long

59
Q

What are the adverse effects of meglitinides?

A

hypoglycemia, weight gain

60
Q

What are some considerations of giving meglitinides?

A

give 30 min before each meal, short 1/2 life, skip if meal is held.

61
Q

What is the suffix for GLP-1 Agonists?

A

-tides

62
Q

What is different about administration of GLP-1 agonists?

A

injections mostly, 1-2x/day or week

63
Q

How do GLP-1 agonists work?

A

amplifies secretion of insulin, decrease stim of glucagon

64
Q

What are some side effects of GLP-1 agonists?

A

slow gastric emptying, slowed absorption of glucose following meals, reduce appetite, weight loss, nausea, diarrhea. lower incidence of hypoglycemia, pancreatitis, renal issues–only one not recommended with renal insufficiency

65
Q

How effective are GLP-1 agonists at reducing A1C?

A

1-2%

66
Q

What is the black box warning from GLP-1 agonists?

A

thyroid CA

67
Q

What is the suffix for DPP-4 inhibitors?

A

-gliptins

68
Q

How do DPP-4 inhibitors work?

A

alternative strategy for targeting GLP-1 pathway, prevents inactivation of GLP-1 and inhibits activity of enzyme DPP-4

69
Q

What are some considerations with DPP-4 inhibitors?

A

well tolerated, may increase hypoglycemia if combined with another agent, dose adjustment with renal impairment, taken with meals

70
Q

How effective at reducing A1C is DPP-4 inhibitors?

A

1%

71
Q

What is the first line med for obese patients?

A

metformin

72
Q

What is the MOA of metformin?

A

metformin targets the enzyme adenosine monophosphate-activated protein kinase (AMPK) system to decrease liver glucose production (decreased gluconeogenesis), decrease hepatic glucose output, improves insulin-sensitizing effect in peripheral tissue (increase GLUT-4 activity), decreased glucose absorption for the GI tract

73
Q

What is AMPK?

A

central regulator for energy homeostasis in every cell in our body. AMP/ATP ratio increases with exercise b/c of hydrolysis of ATP to ADP leading to the generation and storage of ATP. Diabetes is a disorder of this energy balance where the AMP/ATP balance is low causing excessive free glucose

74
Q

What are adverse effects of metformin?

A

anorexia, diarrhea, nausea, low risk of hypoglycemia

75
Q

What is the contraindication of metformin?

A

renal impairment–virtually all excreted unchanged in urine

76
Q

What is the black box warning for metformin?

A

risk of lactic acidosis

77
Q

How effective is metformin at reducing A1C?

A

1.5-3%

78
Q

What is the suffix of thiazolidinediones?

A

-glitazones

79
Q

What is the mechanism of action of glitazone?

A

Peroxisome proliferator-activated receptor (PPAR) and alpha. found in all tissue types: mainly adipose increasing free fatty acid storage.

80
Q

What does glitazone do?

A

Increase the transcription of certain insulin-sensitive genes in adipose, muscle, and liver. Facilitates glucose transport activity and metabolism: glycogen synthesis, promote lipid storage, hepatic insulin sensitivity, lipid/glycogen store in heart.
Requires the presence of sufficient amount of insulin, doesn’t increase insulin secretion but decreases insulin resistance

81
Q

How effective is glitazone at decreasing A1C?

A

0.5-1.4%

82
Q

What is glitazone used in combination with?

A

metformin or sulfonylureas.

83
Q

What are the negative effects of glitazone?

A

weight gain increases, worsening CHF, increased CAD risk, bladder CA, hepatitis, liver failure

84
Q

How do dopamine levels affect blood sugar?

A

dopamine levels are low during insulin-resistant state and increase to normal following a return to insulin-sensitive state.

85
Q

What does bromocriptine mesylate do?

A

oral dopamine receptor agonists reduce plasma glucose, TG, and free fatty acid levels.

86
Q

What’s the MOA of bromocriptine mesylate (cycloset)?

A

augment low hypothalamic dopamine levels and inhibit excessive SNS tone within CNS causing reduction in post meal plasma glucose levels d/t enhanced suppression of hepatic glucose production

87
Q

What are the s/e of cycloset?

A

hypotension, dizziness, nausea, diaphoresis

88
Q

How effective is cycloset at reducing A1C?

A

0.4-0.8%

89
Q

How do alpha glucosidase inhibitors work?

A

reduce the digestion of complex carbs and slow their absorption from the gut thus reducing postprandial glycemia

90
Q

What are the adverse effects of alpha glucosidase inhibitors?

A

flatulence, diarrhea

91
Q

What is the MOA of SGLT2 inhibitors?

A

SGLT2 protein facilitates 90% of glucose reabsorption: allowing for more glucose to remain in urine without reabsorption. Increases insulin sensitivity: increase glucose uptake in muscle, decrease gluconeogenesis

92
Q

What’s the suffix of SGLT2 inhibitors?

A

-gliflozin

93
Q

What are the considerations of SGLT2 inhibitors?

A

give in morning–diuretic effect

94
Q

What are the advantages of SGLT2 inhibitors?

A

lower weight, lower BP, low risk of hypoglycemia, cardiac protective

95
Q

What are the adverse effects of SGLT2 inhibitors?

A

hypotension, UTI, yeast infection cholesterol increase, hyperkalemia, bladder CA

96
Q

What are the contraindications of SGLT2 inhibitors?

A

renal dysfunction, risk of ketoacidosis

97
Q

How effective are SGLT2 inhibitors on A1C?

A

> 1% reduction in A1C

98
Q

How do dietary fibers work on blood sugar?

A

gel-forming fiber, inabsorbable, reduces carb absorption, reduces need for insulin and oral agents, poor compliance

99
Q

When should oral diabetic meds be stopped preop?

A

day of surgery

100
Q

What do amylinomimetics do?

A

inhibit glucagon secretion. Amylin is co-secreted with insulin from beta cells so slow gastric emptying, suppress postprandial glucagon secretion, decrease food intake, weight loss

101
Q

What’s the suffix for amylinomimetics?

A

-tide

102
Q

What’s the considerations of amylinomimetics?

A

given with insulin during meal time, reduces insulin dose by 50%, SQ injection

Pharmacology Exam 4 (7 decks)

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