Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

> 30 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What type of DM has a strong genetic link?

A

type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What type of DM is absolute deficiency of insulin production?

A

type 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

Type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

Type 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the goal of insulin therapy in T1DM Treatment?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is recombinant or the first “biologic” insulin?

A

human insulin, regular, short acting

100units/mL or 500units/mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the insulin analogs?

A

rapid “ultra short” acting

long-acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is NPH insulin?

A

intermediate acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the mixture insulins?

A

regular/intermediate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is insulin not given orally?

A

oral administration destroys protein

must be given parenterally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

may inject closer to mealtime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the advantage of long acting insulin analogs?

A

continuous coverage without injections

reduced solubility, slowing absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the long acting insulin analogs?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the duration of glargine?

A

22-36 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the duration of detemir?

A

12-20 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the duration of degludec?

A

greater than 42 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What long acting insulin causes less nocturnal hypoglycemia?

A

Toujeo and Degludec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

crystalline zinc insulin

positively charged polypeptide, protamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Who is Humulin manufactured by?

A

Eli Lilly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Who manufactures Novolin Novo Nordisk Human Insulin?

A

Novo Nordisk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is involved with intensive insulin therapy?

A

multiple self monitoring of blood glucose checks daily

greater than 3 insulin injections daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

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

A

4-6%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the AACE recommended guideline for HBA1C?

A

< 6.5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the ADA recommended guideline for HBA1C?

A

<7%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Type II DM is a disorder of: (4)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

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

A

individualize based on age and comorbidities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

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

A

therapeutic lifestyle changes AND mono therapy with metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

When should triple therapy be started?

A

if not at target A1C after 3 months of dual therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are highly effective hypoglycemic agents?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What long acting insulin is available OTC and cheaper?

A

NPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

When should rapid insulin analogs be given?

A

0-15 minutes before meals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

When should regular insulin be given?

A

30 minutes before meals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is considered first line for oral Type 2 treatment?

A

biguanides- metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

103
Q

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

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?

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?

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?

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions