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Therapeutics 2 - Fall 2017 > Diabetes - Hockerman > Flashcards

Diabetes - Hockerman Flashcards

1
Q

Generic Name for Humalog

A

Insulin Lispro

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2
Q

Generic Name for Novolog

A

Insulin Aspart

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3
Q

Generic Name for Apidra

A

Insulin Glulisine

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4
Q

Generic Name for Lantus

A

Insulin Glargine

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5
Q

Generic Name for Levemir

A

Insulin Detemir

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6
Q

Generic Name for Tresiba

A

Insulin Degludec

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7
Q

List the VERY Rapid Onset/Short Action Insulins

A

Lispro, Aspart, Glulisine

humalog, novolog, apidra

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8
Q

List the rapid onset/short action insulins

A

Regular (R)

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9
Q

List the intermediate onset/action insulins

A

NPH (N)

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10
Q

List the slow onset/long action insulins

A

glargine, detemir, degludec

lantus, levemir, Tresiba

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11
Q

Describe “lente” insulins

A

insulin is complexed with Zinc to make an insoluble precipitate….

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12
Q

Explain NPH Insulin

A

Insulin is complexed with Protamine to delay absorption!

It is NOT genetically modified

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13
Q

Modification made to make Lispro Insulin?

A

lysine and proline switch positions on insulin B chain

P28 and K29

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14
Q

Modification made to make Aspart Insulin?

A

Proline 28 switched to aspartate

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15
Q

Modification made to make Glulisine Insulin?

A

Asn3 and Lys29 in B chain are switched to Lys and Glu

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16
Q

Modification made to make Glargine Insulin?

A
  • Asn 21 of alpha chain is changed to Gly

- 2 Arg Residues added to end of beta-chain

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17
Q

Modification made to make Detemir Insulin?

A

Thr 30 of b chain is deleted - Lys 29 is myristylated (aka fatty acid added so it can bind to serum albumin extensively)

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18
Q

Modification made to make Degludec Insulin?

A

Thr 30 of b chain is replaced by Glu and fatty acid added (so it can bind to serum albumin)

(what is added “gamma-Glu/C16 fatty acid)

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19
Q

Examples of Mixture Insulins

A

NPH and Regular (Humulin 70/30 and 50/50)

NPL and Lispro (Humalog 75/25 & 50/50)

Ryzodeg (70% degludec and 30% aspart)

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20
Q

what is Afrezza?

A

inhaled insulin

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21
Q

Qualities that allow Afrezza to be inhaled?

A

large surface area and it is a small particle

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22
Q

4 routes of administration for insulin

A

SQ, Infusion Pump, IV, Inhalation

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23
Q

Uses of Insulins in Diabetics:

1) ________ liver glucose output
2) _________ fat storage
3) _________ glucose uptake

A

decrease; increase; increase

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24
Q

List Adverse Reactions to Insulin

A
  • Hypoglycemia
  • Lipodystrophy
  • Lipoatrophy
  • Insulin Resistance
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25
Q

Signs/Sx of hypoglycemia

A

weakness, sweating, hunger, tachycardia, increased irritability, tremor, blurred vision, seizures, coma, increased sympathetic output

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26
Q

Hypoglycemia = blood glucose is < ______

A

60 mg/dL

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27
Q

what is lipodystrophy?

A

lump of fat at over used injection site of insulin

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28
Q

what is lipoatrophy?

A

concavities in SQ tissue

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29
Q

Agents that can interact with Insulin/ cause an INCREASE in blood glucose

A
  • catecholamines
  • glucocorticoids
  • Oral contraceptives
  • thyroid hormone
  • calcitonin
  • somatropin
  • isoniazid
  • Phenothiazines
  • morphine
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30
Q

Agents that increase the risk of insulin hypoglycemia

A 
ETHANOL
beta adrenergic receptors
ACE inhibitors
Fluoxetine
Somatostatin
Anabolic Steroids
MAO Inhibitors
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31
Q

What Antidiabetic drugs will decrease glucose production

A
  • Biguanides

- Insulin

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32
Q

What Antidiabetic drugs will decrease glucose absorption

A
  • alpha-glucosidase inhibitors

- amylin mimetics

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33
Q

What Antidiabetic drugs will increase glucose excretion

A

SGLT2 inhibitors

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34
Q

What Antidiabetic drugs will increase glucose utilization

A
  • thiazolidinediones

- insulin

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35
Q

What Antidiabetic drugs will increase insulin secretion

A
  • sulphonylureas
  • meglitinides
  • GLP-1 Activators
  • DPP-4 Inhibitors
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36
Q

type 1 or type 2 diabetes - which one uses antidiabetics

A

Type 2!

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37
Q 
ADA Diagnosis Criteria:
A1C 
Fasting Plasma Glucose
2-hours plasma glucose
Random Plasma Glucose
A

> 6.5%; > 126 mg/dL; > 200 mg/dL; > 200 mg/dL

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38
Q

Type 1 diabetes - when beta cell mass is decreasing - is there positive or negative results for ICA and IAA

A

positive! (antibodies against ICA and IAA can cause

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39
Q

Pathophysiology of Diabetes:
Hyperglycemia seen when…
- _______ glucose uptake in cells where glucose uptake is insulin dependent
- _________ glycogen synthesis
- ________ conversion of amino acids to glucose

A

decreased; decreased; increased

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40
Q

Will see Hyperlipidemia in Diabetes because……

increased _________ and increased ________

A

fatty acid mobilization from fat cells; fatty acid oxidation (ketoacidosis)

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41
Q

Complications of Diabetes - Neuropathy:

increased blood glucose levels lead to increased utilization of the __________ (_________)

A

polyol pathway; Aldose Reductase;

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42
Q

Complications of Diabetes - Neuropathy:

Increased _________ in neural cells

A

cystosolic

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43
Q

Complications of Diabetes - Nephropathy:

what issues are present?

A

renal vascular changes and changes in the glomerular basement membrane

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44
Q

Complications of Diabetes - Ocular:

what can happen?

A

cataracts, retinal microaneurysms, hemorrhage

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45
Q

Ideal Ranges for Blood Glucose:

Fasting

A

70 - 90 mg/dL

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46
Q

Ideal Ranges for Blood Glucose:

Pre-Parandial

A

70 - 105 mg/dL

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47
Q

Ideal Ranges for Blood Glucose:

Post-Prandial

A

< 120 - 160 mg/dL

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48
Q

Acceptable Ranges for Blood Glucose:

Fasting

A

70 - 110 mg/dL

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49
Q

Acceptable Ranges for Blood Glucose:

Pre-Parandial

A

70 - 130 mg/dL

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50
Q

Acceptable Ranges for Blood Glucose:

Post meal

A

< 180 mg/dL

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51
Q

Insulin’s Effect on the Liver

A

Inhibits: Gluconeogenesis; Ketogenesis; Glycogenolysis

Stimulates: Glycogen Synthesis; Triglyceride Synthesis

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52
Q

Insulin’s Effect on the Skeletal Muscle

A

stimulates: glucose transport and amino acid transport

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53
Q

Insulin’s Effect on the Adipose Tissue

A

stimulates triglyceride storage and glucose transport

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54
Q

Insulin Receptor has 2 subunits

A

alpha and beta

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55
Q

role of the alpha subunit in the insulin receptor

A

it is a regulatory unit of the receptor - will represses activity of beta subunit - repression gets relieved by insulin

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56
Q

Insulin _______ is a clear solution at a pH of 4.0 - but when administered it will precipitate

A

glargine

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57
Q

Hypoglycemia S/Sx:

_______ sympathetic output

A

increased

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58
Q

How to treat hypoglycemia

A

glucagon/glucose

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59
Q

For the use of sulfonylureas - what MUST be functioning

A

beta cells

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60
Q

Sulfonylureas will help diabetics how? (affect glucose or insulin more directly?)

A

will increase release of insulin

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61
Q

Effects of Sulfonylureas on Beta Cell Insulin Release:

1) binds to _________
2) _______ K+ channel
3) _________ cell polarization
4) Activates ________ channels
5) Increases ______ and activity of _____
6) Increased exocytosis of ______ containing granules

A

sulfonylurea receptor; inhibits; decreases; voltage sensitive Ca2+; Ca2+; microfilaments; insulin

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62
Q

Does the drug increases or decrease blood glucose?

Catecholamines

A

increase

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63
Q

Does the drug increases or decrease blood glucose?

Glucocorticoids

A

increase

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64
Q

Does the drug increases or decrease blood glucose?

Oral Contraceptives

A

increase

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65
Q

Does the drug increases or decrease blood glucose?

thyroid hormone

A

increase

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66
Q

Does the drug increases or decrease blood glucose?

Calcitonin

A

increase

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67
Q

Does the drug increases or decrease blood glucose?

Somatropin

A

increase

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68
Q

Does the drug increases or decrease blood glucose?

Isoniazid

A

increase

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69
Q

Does the drug increases or decrease blood glucose?

Phenothiazines

A

increase

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70
Q

Does the drug increases or decrease blood glucose?

Morphine

A

increase

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71
Q

Does the drug increases or decrease blood glucose?

Ethanol

A

decrease

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72
Q

Does the drug increases or decrease blood glucose?

Beta-adrenergic blockers

A

decrease

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73
Q

Does the drug increases or decrease blood glucose?

ACE Inhibitors

A

decrease

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74
Q

Does the drug increases or decrease blood glucose?

Fluoxetine

A

decrease

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75
Q

Does the drug increases or decrease blood glucose?

Somatostatin

A

decrease

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76
Q

Does the drug increases or decrease blood glucose?

Anabolic steroids

A

decrease

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77
Q

Does the drug increases or decrease blood glucose?

MAO Inhibitors

A

decrease

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78
Q

What Classes of Antidiabetic Drugs Increase Insulin Secretion

A
  • Sulphonylureas
  • Meglitinides
  • GLP-1 activators
  • DPP-4 Inhibitors
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79
Q

What Classes of Antidiabetic Drugs decrease glucose absorption

A
  • alpha-glucosidase inhibitors

- amylin mimetics

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80
Q

What Classes of Antidiabetic Drugs increase glucose excretion

A

SGLT2 inhibitors

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81
Q

What Classes of Antidiabetic Drugs decrease glucose production

A
  • biguanides

- insulin

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82
Q

What Classes of Antidiabetic Drugs will increase glucose utilization

A
  • thiazolidineodiones

- Insulin

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83
Q

Explain the Idea behind insulin being release from pancreatic beta cells

A

Glucose gets taken in by GLUT2;
Glucose encounters glucokinase –> G6P –> metabolism –> less ATP and more ADP
More ADP will close the K+ channel; causes depolarization; Ca2+ comes into cell; Ca2+ and microfilaments cause insulin granules to go to surface of cell and release insulin

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84
Q

which glucose transporter (GLUT#) has the HIGHEST Km

A

GLUT2

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85
Q

where is the highest Km GLUT# found?

A

beta cells (in pancreas)/liver

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86
Q

why does the pancreas and liver have a GLUT with such a high Km?

A
  • high Km = more glucose needed to stimulate response - don’t want beta cells to pump out insulin for just little amounts of glucose…
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87
Q

which glucose transporter (GLUT#) is insulin induced

A

GLUT4

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88
Q

where is GLUT4 found?

A

skeletal muscle/adipocytes (GLUT4- insulin induced)

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89
Q

which glucose transporter (GLUT#) has the lowest Km, where is it found, and why

A

GLUT3; its in neurons; very low because you wants neurons/brain to be able to take in glucose even at low levels because you constantly need glucose for functioning

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90
Q

What types of cells are found in islet of langerhans

A

alpha, beta, delta

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91
Q

what cell in the islet of langerhan releases glucagon

A

alpha

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92
Q

what cell in the islet of langerhan releases somatostatin

A

Delta

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93
Q

what cell in the islet of langerhan releases insulin

A

beta

94
Q

what cell in the islet of langerhan releases amylin

A

beta

95
Q

beta cells in the islet of langerhan release what?

A

insulin AND amylin

96
Q

alpha cells in the islet of langerhan release what?

A

glucagon

97
Q

delta cells in the islet of langerhan release what?

A

somatostatin

98
Q

what does Amylin do in the body?

A
  • slows gastric emptying
  • decreases food intake
  • inhibits glucagon secretion
99
Q

Insulin processing:

insulin is made in beta cells and is made as a ________ peptide that is deposited where?

A

single; secretory granules

100
Q

In the secretory granule, insulin is cleaved into what two things

A

1) alpha/beta chain

2) C connecting peptide (C peptide)

101
Q

List the sulfonylureas

A

1st gen (Tolbutamide, Chlorpropamide, Tolazamide)

2nd gen (glipizide, glimeperide, glyburide)

102
Q

Sulfonylureas work intermittently or constitutively?

A

constitutively (can wear out the cells!!)

103
Q

list the 2nd gen sulfonylureas

A

glipizide, glimeperide, glyburide

104
Q

Main difference between 1st and 2nd gen of sulfonylureas?

A

potency

105
Q

What drug class acts similarly to sulfonylureas but acts for a very short amount of time

A

Meglitinides (or the “glinides”)

106
Q

Describe the qualities of the “glinide” antidiabetic drug class (Metiglinides)

A
  • MOA: like sulfonylureas
  • V SHORT DURATION OF ACTION (1 hr = half life)
  • TAKE TABLET BEFORE EACH MEAL
107
Q

how should/how often should glinides be taken

A

before each meal (bc short acting)

108
Q

Examples of Glinides

A

Repaglinide, Nateglinide

109
Q

which glinide is selective for K(ATP) channels in the pancreas, and not the hear?

A

Nateglinide

110
Q

which glinide has a shorter half life?

A

Nateglinide (nate - works only at pancrease but v short half life)

111
Q

ADE’s for Sulfonylureas

A
  • lasting and prolonged hypoglycemia (b/c long af half life)
  • G.I. problems
  • Wt gain/
  • INCREASED # of SECONDARY FAILURES
112
Q

Drug Interactions for Sulfonylureas:
Which drugs may enhance the action of sulonylureas/increase risk of hypoglycemia due to the DISPLACEMENT of sulfonylureas from protein binding sites

A
  • salicylates
  • phenylbutazone
  • sulfonamides
  • clofibrate (Atromid S)
113
Q

“types” of drug interactions for sulfonylureas

A
  • may cause hypoglycemia (by displacing sulfonylureas from protein binding sites OR a drug has their own hypoglycemic effect and add as an additive)
  • drugs cause hyperglycemia
114
Q

what drugs can interact with sulfonylureas by having their own hypoglycemic effect

A

alcohol

high dose salicylates

115
Q

what are some drug interactions that can oppose the action of sulfonylureas

A
  • oral contraceptives
  • corticosteroids
  • epinephrine
  • thyroid
  • thiazide diuretics
116
Q

why does oral glucose give a higher insulin release than IV glucose?

A

incretin effect

117
Q

Idea behind “incretin effect”

A

peptide hormones (GIP and GLP-1) are released from the intestine after a meal - and go to islet of langerhans to stimulate beta cells

118
Q

what peptide hormones are released from the small intestine that will be used to stimulate beta cells

A

Pro-GIP and PRO-glucagon (will become GLP-1)

119
Q

Modes of Action for GLP-1:

_______ insulin secretion

A

stimulate

120
Q

Modes of Action for GLP-1:

_________ glucagon secretion

A

suppress

121
Q

Modes of Action for GLP-1:

________ gastric emptying

A

slows

122
Q

Modes of Action for GLP-1:

_________ food intake

A

reduces

123
Q

Modes of Action for GLP-1:

_________ beta cell mass and _______ beta cell function

A

increases; maintains

124
Q

Modes of Action for GLP-1:

________ insulin sensitivity

A

improves

125
Q

Modes of Action for GLP-1:

__________ glucose disposal

A

enhances

126
Q

GLP-1 Receptor Signaling:

GLP-1 is a small peptide ______ (agonist, partial, antagonist) for _______ (what kind of receptor)

A

agonist; GPCR

127
Q

GLP-1 Receptor Signaling:
Gs, Gq, and G(beta/gamma) pathways - will all (indirectly or directly) cause ________ (_____) which will cause increase in gene transcription and beta-cell proliferation

A

cause glucose-stimulated ERK1/2 phosphorylation (GSEP);

128
Q

GLP-1 Receptor Signaling:

what pathways lead to GSIS (Glucose stimulated insulin secretion)

A

Gs and Gq

129
Q

Recap on Signaling Pathways:

GPCR —> Gs —> ______ –> ______

A

AC; cAMP

130
Q

Recap on Signaling Pathways:

GPCR —> Gq —> ______ –> ______

A

PLC; Ca2+

131
Q

Recap on Signaling Pathways:

GPCR —> G(beta/gamma) —> ______ –> ______

A

PI3K; phosphorylation…

132
Q

GLP-1 is secreted from ______ cells in the ______

A

“L”; intestine

133
Q

GLP-1 levels may be ______ in T2DM

A

decreased!

134
Q

How to combat low levels of GLP-1 in T2DM

A
  • provide a long-lasting GLP-1 analog

- prevent degradation of endogenous GLP-1

135
Q

Benefits of GLP-1 treatment for T2DM:

  • _______ hyperglycemia with ____ risk of hypoglycemia
  • _____ loss
  • Increase _________
A

reduce; low; weight; beta cell mass

136
Q

List the GLP-1 Analogs

A
  • Exenatide (Exendin 4; Byetta)
  • Victoza (Liraglutide)
  • Tanzeum (Albiglutide)
  • Dulaglutide (Trulicity)
  • Lixisenatide (Adlyxin)

“tide-s”

137
Q

What drugs are are inhibitors of DPP-4

A

-Gliptins!
(januvia, tradjenta, onglyza, Nesina)
(sitagliptin, linagliptin, saxagliptin, alogliptin)

138
Q

DPP-4 inhibitors = GLP-1 _______

A

modulators

139
Q

which DPP-4 inhibitor(s) are NOT extensively metabolized

A

januvia, nesina, tradjenta

140
Q

which DPP-4 inhibitor(s) are extensively metabolized

A

onglyza (CYP3A4/5 substrate)

141
Q

which DPP-4 inhibitor(s) are excreted in the urine (kidney)

A

Januvia, Nesina, Onglyza

142
Q

which DPP-4 inhibitor(s) are excreted in the feces (liver)

A

Tradjenta

143
Q

ADE’s of GLP-1 Modulators

A

N/V; Constipation; HA; SEVERE SKIN REACTIONS

144
Q

DPP-4 is also present on _______ cells

A

immune

145
Q

DPP-4 is on present cells:
leads to reduced ________ –> _______
Potential increased risk of _______

A

WBCs; infections; cancers

146
Q

Amylin Analog name?

A

Symlin (Pramlintide)

147
Q

Amylin Analog - useful in type 1 or type 2 or both?

A

both!

148
Q

MOA of alpha-glucosidase inhibitors

A

decrease absorption of carbohydrates from the intestine by inhibiting gut alpha glucosidases

149
Q

what enzymes does alpha-glucosidase inhibitors inhibit?

A
  • sucrase
  • maltase
  • glucoamylase
150
Q

What are some examples of alpha-glucosidase inhibitors

A

Acarbose and Miglitol

151
Q

ADE’s for alpha-glucosidase inhibitors (and reasoning behind it)

A

diarrhea, nausea, flatulence (enzymes are not digesting it, so bacteria in gut DO digest it and leads to gas etc…)

152
Q

Acarbose has risk of _____ damage when doses exceed _______

A

liver; 100 mg TID

153
Q

what do SGLT2 inhibitor drug names end in…

A

-gliflozin

154
Q

what are the drugs that are SGLT2 inhibitors

A
  • jardiance
  • invokana
  • Farxiga
155
Q

how do SGLT2 inhibitors work?

A

they work in the kidney - they decrease the reabsorption threshold for glucose in the kidney —- leads to more glucose being excreted into the urine (will decrease blood glucose levels!!)

156
Q

are SGLT2 inhibitors for Type 1 , type 2 or both?

A

just type 2! should be used with diet/exercise

157
Q

ADE’s for SGLT2 inhibitors

A
  • increased risk of UTIs/genital infections (more sugar down there —- bacteria can grow better)
  • increased urine flow/volume
  • increased risk of hypoglycemia with sulphonylurea and insulin
158
Q

what is the contraindication for SGLT2 inhibitors

A

pts with renal impairment!

159
Q

which SGLT2 inhibitor should NOT be used in pts with BLADDER CANCER

A

Farxiga

160
Q

Possible causes of insulin resistance

A
  • polymorphisms in signaling pathways (rare)
  • Obesity (accum. of fat in abdominal cavity)
  • Inactivity
161
Q

Effect of Insulin Resistance in Skeletal Muscle

A
  • decreased glucose uptake
162
Q

Effect of Insulin Resistance in Adipose Tissue

A
  • impaired glucose uptake
  • impaired inhibition of lipolysis
  • mobilization of FAs to other tissues occurs
163
Q

Effect of Insulin Resistance in the liver

A

impaired inhibition of glucose output (via gluconeogenesis and glycogenolysis)

164
Q

Obese people - have ________ levels of free fatty acids

A

increased

165
Q

_______ FFAs lead to Insulin Resistance (IR)

A

acutely raising

166
Q

Insulin Resistance:

Polymorphism occurs how?

A

Ser gets phosphorylated (Tyr normally does!) this leads to inhibiting signaling

167
Q

what things lead to polymorphisms of Insulin resistance/pathway signaling

A

promoted FA uptake, lipid-by products, inflammatory mediators (cytokines)

aka

Excess nutrients(like FFA), adpionectin, cytokines

168
Q

Obesity Induced Inflammation and Insulin resistance:

_________ adipocytes are made by M1 infiltration

A

hypertrophied;

169
Q

Obesity Induced Inflammation and Insulin resistance:

Hypertrophied adipocytes release what factors that will cause insulin resistance

A
  • TNFa
  • IL-6
  • MCP-1
170
Q

Obesity Induced Inflammation and Insulin resistance:

_______ from the hypertrophied adipocyte will decrease adiponectin

A

MCP-1

171
Q

Obesity Induced Inflammation and Insulin resistance:

______ from hypertrophied adipocyte will go to monocyte

A

MCP-1

172
Q

Obesity Induced Inflammation and Insulin resistance:

M# —> M# due hyperphagia and due to lack of exercise

A

2 –> 1

M1 is the hypertrophied adipocyte

173
Q

Obesity Induced Inflammation and Insulin resistance:

what does MCP-1 stand for

A

monocyte chemoattractant protein - 1

174
Q

Advantages of biguanide over sulfonylureas

A
  • less chance of hypoglycemia

- rarely cause wt gain

175
Q

Metformin has a lower risk of _______ compared to older biguanides

A

lactic acidosis

176
Q

which drug is a part of the biguanide class?

A

metfomrin

177
Q

MOA of Metformin:

is an activator of ________

A

AMPK (AMP-activated kinase)

178
Q

MOA of Metformin:

increases efficiency/sensitivity of insulin where?

A

liver, fat, and muscle cells

179
Q

Metformin’s Action in the Liver:

Metformin binds to _______

A

OCT1

180
Q

Metformin’s Action in the Liver:

Metformin inhibits __________ at the mitochondria

A

oxidation at complex 1

181
Q

Metformin’s Action in the Liver:

Inhibited oxidation of mitochondria leads to ________ levels of AMP

A

increased (bc not making ATP = more AMP)

182
Q

Metformin’s Action in the Liver:

Inhibited oxidation of mitochondria leads to increased levels of ________

A

AMP

183
Q

Metformin’s Action in the Liver:

High AMP levels will inhibit what process _________

A

gluconeogenesis (bc it inhibits Fructose bisphosphase (FBP))

remember ATP is needed for gluconeogenesis

184
Q

Metformin’s Action in the Liver:

High AMP levels will increase/activate _______

A

AMPK

185
Q

Metformin’s Action in the Liver:

High AMP levels will increase/activate AMPK which leads to _________

A

DECREASED lipid and cholesterol synthesis

186
Q

where are the two main places that metformin affects

A

LIVER and SKELETAL MUSLCE

187
Q

what does OCT stand for? (OCT 1 is the metformin receptor)

A

oragnic cation transporter

188
Q

who is contraindicated for metformin

A

pts that have increased risk of lactic acidosis (ex: people w/ poor oxygenation - CHF pts…lung disease pts..)

189
Q

Which drug leads to decreased abosorption of Vit. B12

A

metformin

190
Q

Metformin leads to decreased absorption of _______

A

Vit. B12

191
Q

Can metformin and sulfonylureas be used together?

A

yes!

192
Q

Effect on lipid panel with metformin

A
  • decreased serum LDL

- decreased TGs

193
Q

How do thiazolidinediones decrease insulin resistance/improve target cell response

A

activates PPARy (PPAR gamma) aka a transcription factor

194
Q

what does PPARy stand for

A

peroxisome proliferator activated receptor GAMMA

195
Q

main target cells for thiazolidinediones

A

Adipocytes

196
Q

how do thiazolidinediones affect Adipocytes

A
  • enhance adipocyte differentiation
  • enhance FFA uptake into SQ Fat
  • reduce serum FFA
197
Q

_____ FFA = less insulin resistance

A

less

198
Q

Skeletal Muscles & Exercise:

______ accumulates during exercise and will activated ______

A

AMP; AMPK

more AMP b/c using ATP during exercise…duh

199
Q

Skeletal Muscles & Exercise:

_____ phosphorylates TBC1D(1/4) which will promote ______ activity of _______

A

AMP; GTPase; Rab

200
Q

Skeletal Muscles & Exercise:

Once Rab dissociates from ______ - it can translocate to the membrane

A

GLT4 (GLT4 will go to membrane)

201
Q

How will metformin work in the skeletal muscle to increase insulin sensitivity?

A

metformin will increase AMPK
AMPK will phosphorylate TBC1D(1/4) - which increases GTPase activity of Rab - Rab comes off of GLUT4 - which allows GLUT4 to go to the membrane and bring in glucose!

202
Q

what drugs are thiazolidinediones?

A

the “glitazone”s

  • Pioglitzaone
  • Rosiglitazone

(Remember pioglitzaone - looks like pig - pigs are fat - thiazolidinediones work on fat cells)

203
Q

which thiazolidinediones is assoc. w/ increased risk of bladder cancer

A

Pioglitazone

204
Q

Thiazolidinediones - can they cause hypoglycemia?

A

No!

205
Q

what is the contraindication for thiazolidinediones?

A

CHF (b/c of fluid retention)

206
Q

what are Adipokines

A

hormones that come adipose tissue

207
Q

what type of adipokine can cause insulin dependent glucose upake

A

adiponectin

208
Q

Structure and Function of PPAR-gamma:

PPAR has to bind to _____ - to make a _____ to regulate gene transcription

A

RXR; dimer

209
Q

Structure and Function of PPAR-gamma:

List components of the structure of PPAR-y

A

Ligand independent activation domain; Ligand- dependent activation domain;
DNA binding domain
Ligand binding/Dimerization domain

210
Q

List the factors that are regulated by activation of PPARy

A
  • resistin
  • adiponection
  • TNF-a
  • leptin
  • angiotensinogen (AGE)
  • plasminogen activator inhibitor (PAI-1)
211
Q

what does leptin do in the body?

A

suppresses appetite; tells brain that the body is “fed”

212
Q

PPARy is in control of releasing certain factors- all the factors are specifically released from

A

WAT - white adipose tissue

213
Q

Is it low or elevated in Obesity/T2DM?

Leptin

A

???

214
Q

Is it low or elevated in Obesity/T2DM?

Angiotensinogen

A

increased! — leads to HTN in obesity

215
Q

Is it low or elevated in Obesity/T2DM?

PAI-1 (plasminogen activator inhibitor)

A

increased! — leads to increased risk of clots in obesity

216
Q

Is it low or elevated in Obesity/T2DM?

Resistin

A

elevated

217
Q

what does resistin do?

A

stimulates glucose export by liver
&
stimulates insulin resistance

218
Q

what does adiponectin do?

A

decreases blood glucose and insulin resistance

219
Q

what does TNF-a do?

A

stimulates lipolysis in WAT (white adipose tissue)
&
stimulates insulin resistance in skeletal muscle

220
Q

when a TZD drug is given - what happens to levels of resistin

A

mRNA levels for resistin are DECREASED

221
Q

when a TZD drug is given - what happens to levels of adiponectin

A

mRNA levels for adiponectin are INCREASED

222
Q

when a TZD drug is given - what happens to levels of TNFa

A

mRNA levels for TNFa are DECREASED

223
Q

Metformin or TZD?

molecular target is AMPK

A

metformin

224
Q

Metformin or TZD?

molecular target is PPARy

A

TZD

225
Q

Metformin or TZD?

pharmacologic action is to suppress HGP (hepatic glucose production)

A

metformin

226
Q

Metformin or TZD?

pharmacologic action is enhanced insulin sensitivity

A

TZD

227
Q

Metformin or TZD?

which one decreases A1c quite significantly

A

metformin!

228
Q

Metformin or TZD?

which one reduces FFA quite significantly

A

TZD (bc they work on fat cells)

229
Q

Metformin or TZD?

which one stimulates adiponectin quite significantly?

A

TZD

230
Q

Metformin or TZD?

which on can cause wt gain

A

TZD

231
Q

Metformin or TZD?

which one can cause peripheral edema

A

TZD

232
Q

Metformin or TZD?

which one has increased risk of fracture and why/how

A

TZD; (TZD’s decrease differentiation of mesenchymal stem cells into osteoblasts!

Therapeutics 2 - Fall 2017 (22 decks)

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