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Pharmacology > Week 12 > Flashcards

Week 12 Flashcards

1
Q

What are the characteristics of diabetes mellitus?

A

hyperglycemia
impaired metabolism of carbs, fats and protein
impaired insulin secretion, insulin resistance

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2
Q

What type of DM is 5-10% of cases?

A

Type I

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3
Q

What is the typical age of onset for type 2 DM?

A

> 30 years

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4
Q

What type of DM has a strong genetic link?

A

type 2

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5
Q

What type of DM is absolute deficiency of insulin production?

A

type 1

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6
Q

What type of DM is insulin resistance, defective insulin release?

A

Type 2

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7
Q

How is DM diagnosed by repeat?

A

HBA1C of 6.5% or more
FPG of 126 or more
symptoms + RPG >200
PG greater than 200 2 hour post GTT

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8
Q

What type of DM is typically an autoimmune medicated destruction of pancreatic beta cells?

A

Type 1

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9
Q

What are the 4 main features of type I DM?

A
  1. long pre-clinical period
  2. hyperglycemia when 80-90% of beta cells are destroyed
  3. transient remission (honeymoon period)
  4. established disease
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10
Q

What is the goal of insulin therapy in T1DM Treatment?

A

mimic normal physiologic levels
basal (long acting)
bolus (short acting)

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11
Q

What is recombinant or the first “biologic” insulin?

A

human insulin, regular, short acting

100units/mL or 500units/mL

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12
Q

What are the insulin analogs?

A

rapid “ultra short” acting

long-acting

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13
Q

What is NPH insulin?

A

intermediate acting

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14
Q

What are the mixture insulins?

A

regular/intermediate

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15
Q

What is insulin not given orally?

A

oral administration destroys protein

must be given parenterally

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16
Q

What is the advantage of rapid (ultra short) acting analogs?

A

may inject closer to mealtime

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17
Q

What is the advantage of long acting insulin analogs?

A

continuous coverage without injections

reduced solubility, slowing absorption

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18
Q

What are the long acting insulin analogs?

A

glargine (lantus and toujeo)
Detemir (levemir)
Degludec (tresiba)

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19
Q

What is the duration of glargine?

A

22-36 hours

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20
Q

What is the duration of detemir?

A

12-20 hours

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21
Q

What is the duration of degludec?

A

greater than 42 hours

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22
Q

What long acting insulin causes less nocturnal hypoglycemia?

A

Toujeo and Degludec

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23
Q

NPH insulin (Isophane) Intermediate- Acting Insulin is a suspension of what? (2)

A

crystalline zinc insulin

positively charged polypeptide, protamine

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24
Q

What is significant about NPH insulin (Isophane) Intermediate- Acting Insulin?

A

absorbed slower after subQ injection

duration of action is longer than regular (or analog) insulin
duration is shorter than glargine, detemir or degludec (long acting insulins)

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25
Q

Who is Humulin manufactured by?

A

Eli Lilly

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26
Q

Who manufactures Novolin Novo Nordisk Human Insulin?

A

Novo Nordisk

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27
Q

What is the total daily dose of insulin requires in T1DM?

A

0.4 to 1 units/kg/day of actual body weight

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28
Q

What is the total daily dose of insulin in T1DM of the honeymoon period?

A

0.2 to 0.5 units/kg/daily

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29
Q

What is the requirement for basal insulin in T1DM?

A

approximately half totally daily insulin dose
may use any intermediate or long acting inslin
NPH usually preferred as it can be mixed

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30
Q

What are the requirements for meal time insulin?

A

other 50% of the total daily dose
divided between meals based on type of meal, patient characteristics

*use rapid-acting or regular insulin

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31
Q

What is non-intensive insulin therapy- 2 injections?

A

“split mixed” dosing
2 daily injections (basal insulin if NPH)
2/3 TDD in morning
1/3 TDD in evening

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32
Q

What is non-intensive insulin therapy-3 injections?

A

same dosing as “split-mixed” but moves NPH to bedtime
decreases nocturnal hypoglycemia
increase effect at darn

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33
Q

What is involved with intensive insulin therapy?

A

multiple self monitoring of blood glucose checks daily

greater than 3 insulin injections daily

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34
Q

What is a glycosylated hemoglobin (HBA1C) in non diabetics?

A

4-6%

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35
Q

What is the AACE recommended guideline for HBA1C?

A

< 6.5%

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36
Q

What is the ADA recommended guideline for HBA1C?

A

<7%

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37
Q

How long does a HBA1C last?

A

process is irreversible and lasts the life of the RBC (120 days)
reflects average glucose over 3 months

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38
Q

Type II DM is a disorder of: (4)

A

insulin secretion
insulin resistance
excess glucose production
or all of the above

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39
Q

What is the glycemic goal and HBA1C based on for type 2 treatment?

A

individualize based on age and comorbidities

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40
Q

What is the recommended treatment for type 2 DM at diagnosis?

A

therapeutic lifestyle changes AND mono therapy with metformin

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41
Q

When should dual therapy be started in type 2?

A

if not at target A1C after 3 months of mono therapy OR is baseline A1C is greater than 9%

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42
Q

When should triple therapy be started?

A

if not at target A1C after 3 months of dual therapy

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43
Q

When should combo therapy be started?

A

if not at target after 3 months of triple therapy?

blood glucose is 300-350 and/or HBA1C is greater than 10-12%

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44
Q

What are highly effective hypoglycemic agents?

A

insulin
biguanides (metformin)
sulfonyureas (SUs)
rapid-acting secretagogues (Glinides)

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45
Q

Why is insulin now being used earlier in pharmacotherapy for type 2?

A

minimizes micro and microvascular complications

multiple drugs are being used earlier

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46
Q

When should insulin be started in Type 2?

A

not an HAB1C goal after 2 or more non-insulin hypoglycemics
those with FBG greater than 250
those with A1C levels greater than 10%
hyperglycemia symptoms
DO NOT use as a threat for reaching HBA1C goals

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47
Q

What insulin should you start with for Type 2 and why?

A

Basal (long acting)
causes less hypoglycemia
NPH & LA analogs are equally effective

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48
Q

What long acting insulin is available OTC and cheaper?

A

NPH

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49
Q

What are the steps when prescribing long acting insulin in type 2?

A
  1. 10 units or 0.1-0.2 units/kg/daily
  2. adjust once or twice weekly
  3. if not at goal or dose greater than 0.5 units/kg/d start prandial insulin
  4. if still not controlled, begin “basal-bolus” insulins
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50
Q

When should rapid insulin analogs be given?

A

0-15 minutes before meals

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51
Q

When should regular insulin be given?

A

30 minutes before meals

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52
Q

What is considered first line for oral Type 2 treatment?

A

biguanides- metformin

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53
Q

What is the mechanism of action for Biguanides-metformin (glucophage)?

A
  1. reduces hepatic glucose production
  2. reduces intestinal glucose absorption
  3. increase insulin sensitivity
  4. improves peripheral glucose uptake and utilization
54
Q

What are the benefits of metformin?

A 
promotes modest weight loss or weight neutral
lowers fasting BG 20% and A1C 1-2%
synergistic effect with SUs
minimal hypoglycemia
minimal side effect profile
55
Q

What are the adverse reactions of metformin?

A 
GI effects: N/V, diarrhea, flatulence
lactic acidosis (death)
56
Q

What are the contraindications of metformin?

A

males : SCr > 1.5

females: SCr >1.4

57
Q

What was the first biguanide that was recalled due to numerous fatalities and lactic acidosis?

A

phenformin

58
Q

When should metformin not be used?

A

when CrCl is less than 30mL/min (CKD stage 4 and 5)

59
Q

When should metformin be monitored closely?

A

when CrCl of 30-59 mL/min (CKD stage 3)

60
Q

What is important to monitor when taking metformin?

A

renal
dehydration
infection/sepsis
metformin overdose (lactic acidosis)

61
Q

What oral hypoglycemic agent is second line for oral therapy?

A

Sulfonylureas (SUs)

62
Q

Why is glimepiride (Amaryl) the most popular of the Sulfonylureas?

A

once a day dosing but has greater risk of hypoglycemia

63
Q

Why are sulfonylureas moderately effective as a class?

A

efficacy decreases over time (around 5 years, beta cell “burn out”)

64
Q

Why are first generation sulfonylureas rarely used?

A

due to potent second generation agents with fewer side effects

65
Q

What are the 3 main second generation sulfonylureas?

A

Glimepiride (amaryl)
Glipizide
Glyburide

66
Q

What sulfonylureas results in the most hypoglycemia?

A

glipizide (glucotrol) not preferred

67
Q

What is the MOA of sulfonylureas ?

A

stimulate the release of insulin
requires presence of insulin (functioning pancreas)
not effective in type 1

68
Q

What are the rapid secreting secretagogues?

A

“glinides”
nateglinide (starlix)
rapaglinide (prandin)

69
Q

What is the MOA of secretagogues?

A

stimulates insulin release from the pancreas
similar to SUs but shorter half life
faster onset than SUs, hence rapid acting

70
Q

Which secretagogues is slightly more effective at A1C reduction?

A

repaglinide (Prandin)

71
Q

What are the adverse side effects of secretagogues?

A

hypoglycemia (less than sulfonylureas)

weight gain

72
Q

What are the adrenergic manifestations of hypoglycemia?

A

shakiness, nervous, anxiety

palpitations, tachycardia, sweating (absent or diminished if on beta blockers)

73
Q

What are the glucagon manifestations of hypoglycemia?

A

hunger
nausea
vomiting
headache

74
Q

What are the neuroglycopenic manifestations of hypoglycemia?

A

impaired judgement, mentation
fatigue, lethargy, ataxia
stupor, coma, seizures

75
Q

What is the treatment for mild hypoglycemia (glucose less than 50)

A

3 glucose tablets
1/2 cup fruit juice
5-6 pieces of hard candy (no artificial sweeteners)
glucose gel

76
Q

What is the treatment for severe hypoglycemia? (glucose less than 40)

A

glucagon injection

50% dextrose IV push

77
Q

What are the moderately effective hypoglycemic agents?

A

TZDas
DPP4Is
SGLT2Is

78
Q

What are the thiazolidinediones (TZDs)?

A

Rosiglitazone (Amanda)

Pioglitazone (Actos)

79
Q

thiazolidinediones (TZDs) have a synergistic effect when combined with what?

A

sulfonylureas

metformin or insulin

80
Q

What is the MOA of thiazolidinediones (TZDs)?

A

increase insulin sensitivity in the liver fat and skeletal muscle by increasing glucose utilization and decreasing hepatic glucose production

81
Q

What mediation is an “insulin sensitizer” and requires its presence?

A

thiazolidinediones (TZDs)

82
Q

What are the adverse effects of thiazolidinediones (TZDs)?

A

weight gain (9 lbs)
increased total cholesterol, LDL, and HDL
edema
hepatic metabolism (avoid if LFTs greater than 2.5 ULN)

83
Q

What thiazolidinediones (TZDs) had an FDA warning in 2007 for increased risk of MI?

A

rosiglitazone (Avandia)

84
Q

What is the MOA of Dipeptidyl Peptidase-4 Inhibitors (DPP4Is)?

A

inhibits DPP-4, an enzyme that degrades intestinal incretin hormones (GLP-1, GIP)

85
Q

How do incretin hormones work?

A

increase insulin secretion in response to meals

86
Q

What is the effect of prolonging incretin levels by Dipeptidyl Peptidase-4 Inhibitors (DPP4Is?

A

stimulate insulin synthesis and release and decrease glucagon secretion from pancreatic alpha cells

87
Q

What medications are considered the “incretin enhancers”?

A

Dipeptidyl Peptidase-4 Inhibitors (DPP4Is

88
Q

What is the net result of Dipeptidyl Peptidase-4 Inhibitors (DPP4Is?

A

prolonged basal insulin secretion

89
Q

What Dipeptidyl Peptidase-4 Inhibitors (DPP4Is) does not have a renal adjustment?

A

Linagliptin (trajenta)

90
Q

What is a concern of Dipeptidyl Peptidase-4 Inhibitors (DPP4Is?

A

increased risk of heart failure

however in 2016, NEJM found no increased risk of hospitalization for HF

91
Q

What is the new, novel class of oral anti diabetics that are moderately effective?

A

Sodium-Glucose Cotransporter 2 Inhibitors (SGLT2Is)

92
Q

What is the MOA of Sodium-Glucose Cotransporter 2 Inhibitors (SGLT2Is)?

A

inhibition of Na-glucose co transporter 2
SGLT2 recovers filtered glucose from the urine
inhibition increases urinary glucose loss

93
Q

What medication increases urinary Na loss and therefore lowers BP and decreases weight?

A

Sodium-Glucose Cotransporter 2 Inhibitors (SGLT2Is)

94
Q

What are the adverse effects of Sodium-Glucose Cotransporter 2 Inhibitors (SGLT2Is)?

A

increases risk of genital fungal infections
dehydration
recent FDA safety communication (ketosis and UTIs and pyelonephritis)

95
Q

What are the minimally effective hypoglycemic agents?

A

alpha glucosidase inhibitors (AGIs)
Pramlintide
Glucagon- like peptide 1 receptor agonists (GLP-1-RAgs)

96
Q

What is the cost of alpha glucosidase inhibitors (AGIs)?

A

$30-60/30 days of treatment

97
Q

What is the MOA of alpha glucosidase inhibitors (AGIs)?

A

inhibits pancreatic alpha amylase and GI brush border alpha glucosides
delays hydrolysis of ingested carbohydrates
reduced postprandial insulin & glucose peaks

98
Q

What is alpha glucosidase inhibitors (AGIs) effective for both Type 1 and 2?

A

does not stimulate insulin secretion

DOES NOT cause hypoglycemia

99
Q

What are the adverse GI effects of alpha glucosidase inhibitors (AGIs)?

A

flatulence (73%)

diarrhea (31%)

100
Q

What medication is a synthetic analog of human amylin that decrease post-prandial glucose levels?

A

Pramlintide (Symlin)

101
Q

Why is Pramlintide (Symlin) effective for type 1 and 2?

A

it does not act on beta cells

102
Q

What is the effect of Pramlintide (Symlin) on weight?

A

LOSS

103
Q

What is the risk of hypoglycemia with Pramlintide (Symlin)?

A

neutral

104
Q

What medication is an additional SQ injection separate from insulin injection prior to each meal

A

Pramlintide (Symlin)

105
Q

What is the cost of Pramlintide (Symlin)?

A

$1,500 per month

106
Q

What are the side effects of Pramlintide (Symlin)?

A

nausea in 28-48%

107
Q

What is the MOA of Glucagon- like peptide 1 receptor agonists (GLP-1-RAgs)?

A

incretin mimetic
enhances glucose dependent insulin secretion of beta cells in pancreas
inhibits the release of glucagon after meals
slows the rate of gastric emptying
increase satiety (weight loss)

108
Q

Why were Glucagon- like peptide 1 receptor agonists (GLP-1-RAgs) recently discontinued?

A

increased risk of heart failure

109
Q

What other factors are important when starting pharmacotherapy in type 2?

A 
patient preference
route of administration
ability to lower A1C
risk of hypoglycemia (esp elderly)
cost
110
Q

What type is DKA most seen?

A

type 1

111
Q

What is DKA most often precipitated by?

A

omission of treatment (medication non adherence)
infection (if present usually hyperthermic)
alcohol abuse

112
Q

What is the presentation of DKA?

A

polyuria, polydipsia, polyphagia and weakness
“fruity odor” to breath
N&V
Dehydration (dry mucus membranes, tachycardia, hypotension)

113
Q

What is the treatment for DKA?

A 
fluids
insulin 
potassium
bicarbonate
sodium
114
Q

What are the two active thyroid hormones?

A

T4-thyroxine

T3- tri-iodothyronine

115
Q

What % of T3 is produced in the thyroid gland?

A

20%

116
Q

How is 80% of T3 produced?

A

produced peripherally by the breakdown of T4

117
Q

What is the steady state of thyroid hormone?

A

4-5 half lives

118
Q

What regulates the hormone production of the thyroid gland?

A

hypothalamic-pituitary-thyroid axis

119
Q

Where is TSH secreted?

A

by the anterior pituitary

120
Q

What is the most common type of primary hypothyroidism?

A

Hashimoto’s thyroiditis

121
Q

What is the cause of secondary hypothyroidism?

A

pituitary or hypothalamic disorder

122
Q

What is the clinical presentation of hypothyroidism

A

weight gain

depression

123
Q

When working up a patient for depression, what is essential?

A

thyroid function tests

124
Q

hypothyroid treatment that is desiccated beef or pro thyroid gland, measured in mg, potential for allergy and considered obsolete?

A

armor thyroid USP

125
Q

What medication is a T3 and T4 mixture that is expensive and lacks therapeutic rationale?

A

Liotrix

126
Q

What is the classic triad of symptoms of Grave’s disease?

A

hyperthyroidism
opthalmopathy
dermopathy

127
Q

What are the antithyroid medications for hyperthyroidism?

A

Propylthiouracil (PTU)

Methimazole (Tapazole)

128
Q

What medication inhibits peripheral conversion of T3 to T4?

A

Propylthiouracil (PTU)

129
Q

How often should patients on Propylthiouracil (PTU) be evaluated?

A

every 3 months for recurrence of hyperthyroidism

130
Q

What medication is 10x more potent than PTU

A

Methimazole (Tapazole)

131
Q

What mediation blocks oxidation of iodine in thyroid?

A

Methimazole (Tapazole)

No effect on circulating T3 or T4

132
Q

What are the major side effects of antithyroid medication?

A

agranulocytosis
aplastic anemia
thrombocytopenia

Pharmacology (17 decks)

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