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KG - Pharmacology 2 > KG - Pharm 2 Exam 3, Diabetes > Flashcards

KG - Pharm 2 Exam 3, Diabetes Flashcards

1
Q

rapid acting insulins?

A

insulin lispro
insulin aspart
insulin glulisine

*second part of name has something to do with an amino acid

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2
Q

short acting insulins?

A

regular insulin

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3
Q

intermediate insulins?

A

isophane insulin
NPH

*INtermediate (I = isophane, N = nph)

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4
Q

long acting insulins?

A

insulin glargine

insulin detemir

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5
Q

problem w/ Type 1 DM?

A
  • CIRCULATING INSULIN ABSENT

- pancreatic beta cells don’t respond to glucose

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6
Q

problem w/ type 2 DM?

A

insensitivity to circulating insulin

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7
Q

how do type 2 DM pts develop insensitivity to insulin?

A

chronic over feeding –>
sustained Beta cell stimulation –>
hyperinsulinism –>
receptor insensitivity

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8
Q

classical symptoms DM

A

3Ps

  • polydipsia
  • polyphagia
  • polyuria
  • weakness
  • fatigue
  • thirst
  • nocturnal enuresis
  • peripheral neuropathy
  • vulvo-vaginitis/pruritis in females
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9
Q

chronic diabetic syndrome - ocular signs

A
  • cataracts
  • lens changes
  • retinopathy
  • blindness
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10
Q

chronic diabetic syndrome - CV signs

A
  • gangrene
  • ATHEROSCLEROSIS
  • HTN
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11
Q

chronic diabetic syndrome - neurobiological signs

A
  • PERIPHERAL NEUROPATHY
  • postural hypotension
  • diarrhea/constipation
  • problems voiding
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12
Q

chronic diabetic syndrome - skin/mucous membrane signs

A
  • infection
  • xanthoma
  • shin spots
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13
Q

physiological changes in insulin deficiency?

A
  • hyperglycemia
  • hyperlipidemia
  • hyperketonemia
  • myoglobinuria
  • glucosuria
  • microangiopathy
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14
Q

diagnosis DM?

A
  • FASTING glucose > 126 on at least 2 separate occasions
  • following ingestion of 75 G GLUCOSE, plasma glucose > 200 at 2 hours and one other time during 2 hr test
  • HbA1c > 6%
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15
Q

HbA1c levels

A
  • NORMAL < 6%
  • POORLY CONTROLLED DM > 10%
  • DESIRABLE LEVEL FOR TIGHTLY CONTROLLED DM < 7%
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16
Q

insulin release activated by ____?

A
  • GLUCOSE
  • BETA 2 ADRENERGIC (epi/norepi) AGONISTS
  • other sugars
  • AAs
  • fatty acids
  • ketone bodies
  • vagal activation
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17
Q

insulin inhibited by ____?

A
  • ALPHA 2 AGONISTS

- conditions that activate SNS (hypoxia, hypothermia, surgery, burns)

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18
Q

insulin PROMOTES ___?

A

ENTRY GLUCOSE INTO:

  • SKELETAL MUSCLE
  • HEART MUSCLE
  • FAT
  • LEUKOCYTES
  • NOTE REQ FOR GLUCOSE TRANSFER INTO BRAIN, LIVER, RBCs
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19
Q

when insulin injected… what happens?

A
  • plasma glucose down
  • plasma pyruvate/lactate up
  • phosphate down
  • potassium down (bc potassium channels are closed)
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20
Q

Actions of insulin, general?

A

INHIBITS CATABOLIC PROCESSES (breakdown glycogen, fat, protein… promotes anabolic state)

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21
Q

actions of insulin - liver?

A
  • DECREASE GLUCONEOGENESIS

- INCREASE GLYCOGEN SYNTHESIS

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22
Q

actions of insulin - muscle?

A
  • STIMULATE GLUCOSE UPTAKE

- promote protein/glycogen synthesis

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23
Q

actions of insulin - adipose?

A
  • STIMULATES GLUCOSE UPTAKE

- increase lipogenesis

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24
Q

how to treat type 1 DM?

A

INSULIN!

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25
Q

how to treat type 2 DM?

A

ANTIDIABETIC AGENTS

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26
Q

toxicity/adverse rxn insulin?

A

HYPOGLYCEMIA

  • tachycardia
  • confusion
  • vertigo
  • sweating
allergy
lipodystrophy
lipohypertrophy
insulin resistance
drug interactions
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27
Q

tx for hypoglycemia

A
  • 50% glucose solution IV

- glucagon injection

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28
Q

insulin allergic rxns?

A
  • local allergic rxns 10x more common than systemic runs
  • inflammation can persist for several days
  • local inflammation/infection
  • -> unhygienic injection technique
  • -> impurities
  • systemic runs can manifest spectrum of responses
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29
Q

factors that increase insulin requirement

A
  • fever, thyrotoxicosis, pregnancy, stress, surgery, trauma, infection, increased metabolism
  • increased antibodies
  • excess GH (acromegaly)
  • excess adrenocortical hormone (Cushing’s)
  • altered sensitivity of muscle/fat to insulin
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30
Q

which insulins can be used IV?

A

rapid acting, short acting

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31
Q

method for insulin replacement?

A

INJECTION - create insulin profile & eat to fill it

PUMP - adjust boluses accd to what you eat

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32
Q

glucagon - MOA

A

increase blood glucose by mobilizing hepatic glycogen WHEN AVAILABLE
- regs glucose, AAs

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33
Q

glucagon - therapeutic effects

A
  • juveniles don’t respond as well
  • not as effective in pts w/ reduced glycogen stores
  • potent inotropic/chronotropic effects on heart (used in beta blocker overdose)
  • used in radiology to relax intestine
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34
Q

diazoxide - info

A
  • non-diuretic thiazide
  • vasodilator
  • hyperglycemic
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35
Q

diazoxide - MOA

A

hyperglycemia by:

  • directly inhibit insulin secretion
  • decrease peripheral glucose use
  • stimulate hepatic glucose production
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36
Q

diazoxide - therapeutic effects

A

pts w/ INSULINOMA

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37
Q

glucagon - pharmacokinetics

A
  • parenteral admin (SC, IM, IV)

- gradual onset of action

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38
Q

diazoxide - pharmacokinetics

A
  • oral admin

- fairly long duration action (half life = 24-36 hrs)

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39
Q

“other anti diabetic agents” - MOA

A
  • increase endogenous insulin release
  • decrease glucose levels
  • increase sensitivity to insulin
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40
Q

sulfonylureas - MOA

A
  • STIMULATE INSULIN RELEASE FROM PANCREATIC BETA CELLS
  • BLOCK K+ CHANNELS
  • INDIRECTLY potentiate action of insulin on target tissues
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41
Q

sulfonylureas - adverse effects

A
  • HYPOGLYCEMIA (more w/ long lasting ones, 2nd gen better)
  • GI side effects
  • WEIGHT GAIN
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42
Q

sulfonylureas - contraindications/precautions

A
  • renal dz/hepatic dysfunction

- SULFA ALLERGIES

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43
Q

first gen sulfonylureas?

A
  • Tolbutamide
  • Chlorpropamide
  • Tolazamide
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44
Q

Tolbutamide - distinguishing characteristics

A
  • infrequent hypoglycemia (least overall)
  • safest in elderly
  • rapid absorption
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45
Q

Chlorpropamide - distinguishing characteristics

A
  • worst hypoglycemia (first gen sulfonylureas)
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46
Q

second gen sulfonylureas?

A
  • Glyburide
  • Glipizide
  • Glimepiride
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47
Q

glyburide - distinguishing characteristics

A
  • 24 hour effect

- HYPOGLYCEMIA (worst of sec gen sulfonylureas)

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48
Q

glipizide - distinguishing characteristics

A
  • half life 2-4 hrs

- least hypoglycemia (of second gen sulfonylureas)

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49
Q

list meglitinides

A
  • repaglinide

- nateglinide

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50
Q

how are meglitinides different from sulfonylureas?

A

not sulfonamides so can be used w/ sulfa allergy

51
Q

meglitinides - therapeutic effects

A

EUGLYCEMIA

  • lower POSTPRANDIAL glucose
  • rapid, short action
  • LESS HYPOGLYCEMIA than sulfonylureas
  • lower HbA1c
  • little effect on weight
52
Q

meglitinides - MOA

A
  • receptors on K+ channels beta cells, increase insulin release
53
Q

meglitinides - pharmacokinetics

A
  • oral admin, PREPRANDIAL (1-10 min)
  • rapid action
  • liver metab - CYP3A4
54
Q

meglitinides - adverse effects

A

SLIGHT hypoglycemia

55
Q

meglitinides - contraindications/precautions

A
  • don’t use w/ sulfas
  • caution w/ liver probs
  • less hypoglycemia than 2nd gen sulfonylureas
56
Q

DOC newly diagnosed type 2 DM?

A

METFORMIN

57
Q

metformin - MOA

A

DOES NOT RELEAST INSULIN

  • increase glucose uptake (increase insulin action in muscle, fat)
  • decrease glucose absorption from GI
  • decrease glucagon
  • decrease gluconeogenesis
58
Q

metformin - therapeutic effects

A
  • decrease glucose - EUGLYCEMIA (NOT in normal pts)
  • decrease POSTPRANDIAL hyperglycemia
  • 15-20% decrease plasma triglycerides
  • DOES NOT INCREASE BODY WEIGHT
  • DECREASE MACROVASCULAR EVENTS
  • SAFE FOR KIDS > 10 y.o.
59
Q

Metformin + lifestyle changes = _____

A

NO INCREASE BODY WEIGHT

DECREASE MACROVASCULAR EVENTS

60
Q

Metformin - pharmacokinetics

A
  • oral admin

- can get once/day dose, extending release

61
Q

metformin - adverse effect

A
  • LACTIC ACIDOSIS (rare, but lethal)

- DIARRHEA, anorexia, n/v

62
Q

metformin - contraindications/precautions

A
  • LACTIC ACIDOSIS CONDITIONS
  • -> renal dz
  • -> hepatic dz
  • -> alcoholism
  • -> dz predisposing to tissue hypoxia (CHF, COPD)
63
Q

metformin - class?

A

biguanides

64
Q

list thiazolidinediones

(AKA - “TZDs” & “glitazones”

A
  • Pioglitazone

- Rosiglitazone

65
Q

thiazolidinediones - MOA

A

“INSULIN SENSITIZERS” - target insulin resistance

  • ligands of PPAR alpha receptor, can cause POST-RECEPTOR INSULIN-MIMETIC ACTION
  • -> increase glucose transporter synthesis in adipose
  • -> onset/offset action can take weeks-months
  • do not stimulate insulin secretion
66
Q

thiazolidinediones - therapeutic effects

A
  • LOWERS INSULIN RESISTANCE
  • decrease triglycerides in long term use
  • slight increase HDL
  • potential to REDUCE DEVELOPMENT OF TYPE 2 DM (PROPHYLACTIC USE)
  • improved glycemic control
67
Q

thiazolidinediones - pharmacokinetics

A
  • oral admin
  • long half life (103-158 hrs)
  • liver metab
68
Q

thiazolidinediones - adverse effects

A
  • WEIGHT GAIN
  • EDEMA (incr risk heart failure w/ CHF)
  • back pain, fatigue, HA
  • slight hypoglycemia
69
Q

Rosiglitazone - distinguishing characteristics

A
  • BLACK LABEL WARNING - often taken off market

- 2x increased incidence MI, angina

70
Q

thiazolidinediones - contraindications/precautions

A
  • HEPATIC DZ

- CHF

71
Q

list alpha-glucosidase inhibitors

A
  • Acarbose

- Miglitol

72
Q

alpha-glucosidase inhibitors - MOA

A

reduce glucose absorption

  • inhibit alpha-glucosidase in small intestine –> delayed carb digestion & absorption
73
Q

alpha-glucosidase inhibitors - these are used for which NON-FDA approved use?

A

Type 1 DM

74
Q

alpha-glucosidase inhibitors - therapeutic effects

A
  • decr postprandial glucose
  • min effects fasting glucose
  • modestly lower HbA1c levels
  • NO SIGNIFICANT EFFECTS ON WEIGHT
75
Q

alpha-glucosidase inhibitors - pharmacokinetics

A
  • oral admin
  • half life = 2 hrs
  • metab by intestinal digestive enzymes & microorganisms
76
Q

alpha-glucosidase inhibitors - adverse effects

A
  • GI EFFECTS - ab pain, diarrhea, GAS

- elevated hepatic enzymes, jaundice

77
Q

alpha-glucosidase inhibitors - contraindications/precautions

A
  • GI disease, obstruction, ileus, IBD, hiatal hernia
  • hepatic dz
  • renal impairment
78
Q

incretins - physiology?

A
  • GLP1 & GIP increase release insulin
  • GLP1 inhibits glucagon release
  • decreased hepatic gluconeogenesis

*incretins are released in response to glucose

79
Q

incretins - list

A
  • exanatide

- liraglutide

80
Q

incretins - info

A
  • synthetic version exendin 4

- RESISTANT TO ENZYMATIC DEGRADATION BY DPPV-IV

81
Q

incretins (Exenatide) - pharmacokinetics

A
  • morning and evening SC INJECTIONS - 60 MIN BEFORE TWO MAIN MEALS
  • -> half life 2 hrs
  • -> kidney elimination
  • -> new formula = ONCE/WK INJECTION
82
Q

incretins (Liraglutide) - pharmacokinetics

A
  • SINGLE DAILY SC INJECTION

- -> half life 12-13 hrs

83
Q

incretins - therapeutic effects

A
  • lowers postprandial AND fasting serum glucose
  • promotes better glycemic control
  • modestly lowers HbA1c
  • POTENTIAL INCREASED BETA CELL # and FUNCTION
  • WEIGHT LOSS
  • slows gastric emptying, pt eats less
84
Q

incretins - adverse effects

A
  • GI disturbance
  • hypoglycemia in combo therapy
  • hypersensitivity rxns
  • ACUTE PANCREATITIS POTENTIALLY
85
Q

incretins - contraindications/precautions

A
  • slow GI problems, GI disease
  • oral meds that cannot be exposed to stomach acid too long
  • renal impairment
86
Q

which incretin mimetic can cause thyroid cancer?

A
  • Liraglutide
87
Q

DPP-IV inhibitors - list

A
  • sitagliptin
  • saxagliptin
  • linagliptin
  • alogliptin
88
Q

DPP-IV inhibitors - MOA

A
  • DPP-IV inhibitors

- POTENTIATES EFFECTS ON INCRETIN HORMONES by inhibiting breakdown by DPP-IV

89
Q

DPP-IV inhibitors - therapeutic effects

A
  • lower postprandial and fasting serum glucose
  • cause modest decr HbA1c
  • NO EFFECT ON WEIGHT
90
Q

DPP-IV inhibitors - pharmacokinetics

A
  • ORAL ADMIN, once/day
  • eliminated by kidney
  • half life 12 hrs
91
Q

DPP-IV inhibitors - adverse effects

A
  • hypersensitivity rxns
92
Q

which DPP-IV inhibitor may be associated w/ ACUTE PANCREATITIS & PANCREATIC CANCER?

A

sitagliptin

93
Q

DPP-IV inhibitors - contraindications/precautions

A
  • slow GI probs

- renal impairment

94
Q

amylin-like peptide - list

A

pramlintide

95
Q

when to use pramlintide?

A
  • ONLY ADJUNCT TO INSULIN THERAPY

- TYPE 1 & TYPE 2

96
Q

pramlintide - MOA

A

SYNTHETIC ANALOG AMYLIN (hormone co-secreted w/ insulin)

  • works w/ insulin to REGULATE POSTPRANDIAL GLUCOSE BY
  • -> decr gastric emptying
  • -> suppress glucagon secretion
  • -> decr appetite/caloric intake
97
Q

pramlintide - therapeutic effects

A
  • modestly decr HbA1c

- WEIGHT LOSS

98
Q

pramlintide - pharmacokinetics

A
  • SC INJECTION, 3x daily (w/ meal bolus insulin)
  • elim by kidney
  • half life 48 min
99
Q

pramlintide - adverse effects

A
  • GI
  • hypoglycemia w/ insulin
  • injection site lipodystrophy
100
Q

pramlintide - contraindications/precautions

A

slow GI probs

101
Q

list dopamine agonist

A

bromocriptine

102
Q

bromocriptine - MOA

A
  • dopamine agonist
  • augments low hypothalamic dopamine levels –> inhibits excessive sympathetic tone w/in CNS –> decr postmeal plasma glucose levels due to ENHANCED SUPPRESSION of HEPATIC GLUCOSE PRODUCTION
103
Q

bromocriptine - indications/therapeutic effects

A
  • improves glycemic control
  • DECR FASTING & POSTPRANDIAL FFA & TRIGLYCERIDE LEVELS
  • modestly decr HbA1c
  • weight neutral
  • REDUCE CARDIOVASCULAR END POINT PROBLEMS (potentially)
104
Q

bromocriptine - pharmacokinetics

A
  • oral, w/in 2 hrs of awakening
  • quick release
  • eliminate by biliary system
105
Q

bromocriptine - adverse effects

A
  • mild/transient = nausea, weakness, constipation, dizziness

- non-cycloset = psychotic disorders, hallucinations, fibrotic complaints

106
Q

bromocriptine - contraindications/precautions

A
  • pregnant/nursing
107
Q

list bile acid binding resins

A

colesevelam

108
Q

colesevelam - MOA

A

unknown

109
Q

colesevelam - indications/therapeutic effects

A
  • DECREASE FASTING PLASMA GLUCOSE & HbA1c

- beneficial effects hyperlipidemia - HELPS CHOLESTEROL

110
Q

colesevelam - adverse effects

A
  • safe drug

- CONSTIPATION, BLOATING

111
Q

list SGLT2 inhibitors

A
  • canagliflozin
  • dapagliflozin
a = without
gli = glucose
flozin = flow
112
Q

SGLT2 inhibitors - MOA

A

inhibits sodium-glucose co-transporter 2 (SGLT2) in kidney

113
Q

SGLT2 inhibitors - indications/therapeutic effects

A
  • modest decrease HbA1c
114
Q

SGLT2 inhibitors - pharmacokinetics

A

oral

115
Q

SGLT2 inhibitors - adverse effects

A
  • common = female genital infections/UTIs
  • OSMOTIC DIURESIS – postural dizziness, orthostatic HTN, syncope, dehydration
  • renal probs = incr Cr, decr GFR
  • hyperkalemia
  • increased LDL-C
116
Q

SGLT2 inhibitors - contraindications

A
  • SEVERE RENAL IMPAIRMENT/DIALYSIS (can reduce GFR)

- prone to UTIs/GU infections

117
Q

which drug classes can cause bad hypoglycemia?

A
  • sulfonylureas

- meglitinides (not AS bad…)

118
Q

which antidiabetic drug classes can cause hyperinsulinemia?

A
  • sulfonylureas

- meglitinides

119
Q

which antidiabetic drug classes can cause lactic acidosis?

A

metformin (but rare)

120
Q

which antidiabetic drug classes must be injected?

A
  • incretin mimetics

- pramlintide

121
Q

which antidiabetic drug classes don’t have many GI side effects?

A
  • thiazolidinediones
  • gliptins
  • meglitinides (slight only)
122
Q

which is the newest class of anti diabetic drugs?

A

SGLT2 inhibitors

123
Q

w/ which drug were CVD deaths increased? (1970 study)

A

tolbutamide

124
Q

what should be done to maintain tight control of HbA1c in type 2 DM?

A
  • metformin
  • reduce macro vascular events in obese pts
  • BP control
  • tight control HbA1c reduces microvascular events

KG - Pharmacology 2 (10 decks)

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