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Pharm > Diabetes- Exam 4 > Flashcards

Diabetes- Exam 4 Flashcards

1
Q

What islets are in the endocrine?

A

islets of langerhans

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2
Q

What does the pancreas consist of?

A

exocrine and endocrine gland

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3
Q

What enzymes are involved with exocrine?

A

digestive enzymes

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4
Q

what control centers are involved in the pancreatic islets?

A

blood glucose control center

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5
Q

what cells release insulin

A

beta

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6
Q

what cells release glucagon

A

alpha cells

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7
Q

how many types of DM

A

4

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8
Q

what type is insulin dep

A

type 1

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9
Q

what type is noninsulin dependent?

A

type 2

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10
Q

typer 4 is what?

A

gestational

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11
Q

what does amylin suppress?

A

glucagon

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12
Q

DM 1 has destruction of what cell?

A

beta

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13
Q

is the insulin severe deficiency or enough insulin in DM1?

A

severe deficiency

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14
Q

what are clinical manifestations with Type 1?

A

hyperglycemia, polydipsia, polyuria, weight loss, fatigue, DKA

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15
Q

what type is adult onset?

A

type 2

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16
Q

what type is ametabolic syndrome?

A

type 2

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17
Q

insulin and glucagon are ____ proportional

A

inversely

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18
Q

Type 2 is a combination _____ of insulin secretion with tissue _____ resistance

A

relative deficiency, insulin

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19
Q

Treatment of type2

A

exercise, treatment of obesity, medication

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20
Q

clinical manifestation of type 2

A

recurrent infections, vision problems, neuropathy, dehydration

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21
Q

chronic complications of DM

A

hyperglycemia, nonenzymatic glycosylation, more protein kinase C, retinopathy and diabetic neuropathy

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22
Q

% of pregnancies for type 4

A

7

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23
Q

how does type 4 work

A

hormones blocked, insulin resistance

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24
Q

do we see a higher birth weight

A

yes

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25
Q

does pancreatits cause type 3?

A

yes

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26
Q

is type 3 temporary?

A

yes

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27
Q

do we see increased risk for 2nd pregnancy w type 4?

A

yes

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28
Q

whats the risk for DM2 with type 4?

A

increased

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29
Q

how do we test for DM?

A

fasting blood glucose, glucose tolerance test

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30
Q

self monitoring includes

A

glucose POC

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31
Q

what test to determine DM

A

HBA1C

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32
Q

Where are beta cells activated?

A

granules

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33
Q

Insulin secretagogoues include?

A

glucose, amino acids, hormones, fatty acids, incretins, drugs (sulfonureas, isoproterenol)

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34
Q

smell of DKA

A

fruity breath

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35
Q

what is the insulin receptor?

A

tyrosine kinase

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36
Q

effects of tyrosine kinase receptor

A

membrane translocation of GLUT, increased glycogen formation, activated transcription factors

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37
Q

can type 2 convert to type 1

A

yes

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38
Q

reversal of catabolic features of insulin deficiency on liver?

A

inhibits glycogenolysis, inhibt conversion of fatty acids and amino acids to keto acids

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39
Q

anabolic action of insulin on liver

A

promotes glucose storage, glucose stored as glycogen

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40
Q

what type is metformin used for?

A

type 2

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41
Q

what inhibits insulin secretion?

A

insulin, leptin, SNS, chronically high glucose, drugs

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42
Q

what drugs inhibit insulin secretion

A

diazoxide, phenytoin, vinblastine, colchicine

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43
Q

what does high glucose get converted to?

A

sorbitol and fructose

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44
Q

do sorbitol and fructose increase intracellular osmotic pressure?

A

yes

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45
Q

where does sorbitol and fructose work?

A

eye lens, nerves, RBC

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46
Q

rapid acting insulin

A

lispro, aspart, glulisine

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47
Q

short acting (regular)

A

novolin, humulin

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48
Q

intermediate acting

A

neutral protamine hagedorn

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49
Q

long acting insulin

A

glargine, detemir

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50
Q

How often to sterile change CSIID?

A

2-3 days

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51
Q

you take 1 unit of RA insulin for how many carbs?

A

12-15 g of carbs

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52
Q

a basal dose is how many injections?

A

1 and its long acting

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53
Q

correction of a high glucose is 1 unit of RA insulin to drop ___ mg/dL

A

50

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54
Q

intensive insulin regiment

A

IDDM: tight control, basal and bolus (calculated)

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55
Q

conventional insulin regiment

A

70:30 premixed

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56
Q

insulin is what kind of molecule?

A

peptide

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57
Q

why peptide instead of protein?

A

not 3D

58
Q

what holds the alpha and beta chains together?

A

sulfide linkages

59
Q

is C peptide cleaved before release of insulin?

A

yes

60
Q

illness insulin regiment

A

metabolic rate increases, insulin requirement increases

61
Q

what is a complication of insulin treatment?

A

hypoglycemia

62
Q

symptoms of hypog

A

anxiety, blurred vision, palpitations, shakiness, slurred speech, sweating

63
Q

is pig and human insulin similar?

A

yes

64
Q

where did early on insulin come from?

A

porcine pancreas

65
Q

treatment for hypoglycemia?

A

glucose/ simple sugars, soda, candy

66
Q

further treatment of hypoglycemia

A

glucagon injection

67
Q

glucagon uses GLUT __ to get into pancrease

A

2

68
Q

is glut 2 low affinity?

A

yes

69
Q

does glut 2 use concentration gradient?

A

yes

70
Q

is atp going to close or open the inward rectifiying potassium channel

A

close

71
Q

how insulin is released via GLUT 2 in beta cell

A

high glucose->metabolized to ATP-> shuts K channel ->opens Ca channel -> vesicle fuses to membrane ->releases insulin

72
Q

oral antidiabetics

A

biguanides, insulin secretagogues, thiazolidinediones, a-glucosidase inhibitors, bile acid sequestrant, amylin analogs, incretin-based therapies, SGLT-2

73
Q

are the tyrosine kinase receptors dimerized?

A

yes

74
Q

IRS means

A

insulin response substrates

75
Q

what does IRS affect?

A

IP3 and MAP Kinase pathways

76
Q

high Km means

A

low affinity

77
Q

low affinity means what?

A

low glucose levels->doesn’t work well
works better w higher levels

78
Q

what is the first line therapy?

A

biguanides

79
Q

what is metformin drug class

A

biguanide

80
Q

what organ toxicities with biguanides?

A

GI toxicities

81
Q

MOA of biguanides

A

reduction of hepatic glucose production

82
Q

MOA of insulin secretagogues

A

bind to K channel, rectifier current, causes depolarization of cell

83
Q

classes of insulin secretagogues

A

sulfonylureas, meglitinde, phenylalanine derivatives

84
Q

leptin produced by what cells?

A

adipose cells

85
Q

Orinase is given in __ doses

A

divided

86
Q

sulfonylureas drugs

A

orinase, tolinase, diabinese, diabeta, glucotrol, amaryl

87
Q

Risk of __ with Tzds

A

MI

88
Q

insulin secreted in how many min?

A

6 min

89
Q

MOA of thiazolidinediones

A

decrease insulin resistance, PPAR mediated, increase insulin signal transduction

90
Q

how is MI risk increased with Tzds

A

increased with insulin, nitrates, avandia access program

91
Q

70/30 is not ___ control

A

tight

92
Q

MOA of alpha glucosidase inhibitors?

A

block digestion of complex carbs

93
Q

alpha-glucosidase inhibitors are beneficial in what pts

A

pre-diabetics

94
Q

what GI effects with alpha-glucosidase?

A

farting, diarrhea, abd pain

95
Q

Acarbose is an example of a ___

A

alpha-glucosidase

96
Q

MOA of bile acid binding resin

A

large cation exchange resins - not absorbed
bind bile acids - prevent reabsorption

97
Q

what organ is affected by bile acid binding resins

A

GI upset

98
Q

what cells also release amylin

A

beta cells

99
Q

what does amylin suppress

A

glucagon release

100
Q

amylin analog is ____ with insulin

A

concomitant (accompanies, given together)

101
Q

incretin works on ___ hormones

A

GI

102
Q

incretin based therapy agonist

A

GLP-1 agonists

103
Q

antagonists of incretin based

A

dipeptidyl peptidase-4 antagonists

104
Q

what cancer risk with incretin

A

pancreatic cancer

105
Q

Semaglutide is a ___ drug

A

GLP-1 agonist

106
Q

Sitagliptin is a __ drug

A

DPP-4 inhibitor and decreases glucose

107
Q

MOA of gliflozins

A

SGLT2 inhibitors and prevents glucose reabsorption in PCT

108
Q

drugs for SGLT2 inhibitors

A

“gliflozin”s

109
Q

when decreasing glucose reabsorption in PCT we see what in the urine

A

glycosuria

110
Q

what else do we see with glycosuria?

A

BP reduction, weight loss, dehydration

111
Q

typical combination therapy in NIDDM

A

biguanide, biguanide with insulin or biguanide and secretagogues, biguanide with 2-3 other classes, intensive insulin therapy

112
Q

adjunctive therapy

A

diet, stress, exercsies

113
Q

what type of diet

A

low carb, low diet, calorie-restricted diet

114
Q

gluconeogenesis is what

A

makes glucose out of other things

115
Q

ideal glucose

A

90mg/dL

116
Q

sys BP goal with therapy

A

<130 mmHG

117
Q

how to treat the HTN, CV disease first line treatment

A

ACE inhibitor, ARB

118
Q

what is the LDL goal of type 2 diabetics

A

<100 mg/dL

119
Q

first line therapy for dyslipidemia

A

statins

120
Q

antiplt agents such as ___ can be used to prevent ischemic attacks

A

aspirin

121
Q

order of insulin treatment for type 2

A

metformin, sulfonylurea, basal insulin, basal and meal time insulin

122
Q

when do we release insulin?

A

when BG too high

123
Q

75% of pancreatic islet is what

A

beta cells

124
Q

insulin from beta cells binds to what kind of insulin receptor

A

tyrosine kinases

125
Q

glucose transporters transport glucose from ___ to ____

A

bloodstream to the inside of the cell

126
Q

by bringing the glucose into the cell, what happens to the level in the blood

A

lowers

127
Q

if we eat a meal high in carbs, what gets stimulated and what gets released

A

beta cells release insulin

128
Q

what does the liver do with the glucose?

A

stores it for long term storage in the form of glycogen

129
Q

when blood level sugar decreases below 90 and closer to 70 or even 60

A

alpha cells of pancrease release glucagon and liver breaks down glycogen to be released into the blood

130
Q

glucagon receptors are what kind of receptor

A

GPCR

131
Q

glycogenolysis is what

A

break down of glucose

132
Q

insulin secretagogue means what

A

causes secretion of insulin

133
Q

what subunits in the tyrosine kinase receptor become activated when insulin binds?

A

beta units

134
Q

primary effect when insulin receptor activates IRS in the cell

A

movement of glucose transporter from inside the cell to the outside

135
Q

GLUT2 found where

A

pancreatic beta cells, liver, kidney, gut

136
Q

if allergic to sulfa, can take ___

A

meglitinide

137
Q

are meglitinides safer

A

yes

138
Q

how do bile acid binding resins work in the intestines

A

blocks the reabsorption

139
Q

GLP-1 works by inhibiting ___ release and stimulates ___ release

A

glucagon
insulin

140
Q

DDP4 antagonists do what to GLP1

A

block DDP4 and increase GLP1

Pharm (22 decks)

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