endocrine (pharm) Flashcards

1
Q

glycemic goals of tx in dM hgbA1c and preprandrial and postprandial plasma glucose

A

hgbA1c

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

why is correlation between patient report of SBG and hgb A1c important?

A

it pts feels like blood sugars good but A1c comes back high, think about glucose monitor needing recalibrating, strips, etc

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

dm patient ed

A

Describing the diabetes disease process and treatment options
• Incorporating nutritional management and physical activity into lifestyle
• Using medication(s) safely and for maximum therapeutic effectiveness
• Monitoring blood glucose and other parameters and interpreting and using the results for selfmanagement
decision making
• Preventing, detecting, and treating acute and chronic complications
• Developing personal strategies to address psychosocial issues and concerns, and promote
health and behavior change

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

lifestyle change for dM

A
Nutrition
 Self-monitoring
 Physical activity
o Improves insulin sensitivity
o May improve glucose tolerance
 Adherence to medication regimen (if meds necessary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

4 main pathogenetic features DM meds target

A

decreased insulin secretion, increased glucose made by liver, sugar absorption in gut, decreased glucose use by tissues

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

effect on A1C with physical activity (decreasing weight) and nutriton

A

decrease in 1-2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
metformin
trade name
mechanism of action
advantages
disadvantages
cost
A1C effect
A
metformin
trade name glucophage
mechanism of action ↓ Hepatic glucose
production
advantages• Extensive experience
• No hypoglycemia
• ↓ CVD events (UKPDS)
disadvantages
• Gastrointestinal side effects (diarrhea,
abdominal cramping)
• Lactic acidosis risk (rare)
• Vitamin B12 deficiency
• Multiple contraindications: CKD#,
acidosis, hypoxia, dehydration, etc.
cost: low
A1c 1-1.5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
sulfonylureas: glipizide
trade name
mechanism of action
advantages
disadvantages
cost
A1C effect
A
glipizide
trade name glucotrol
mechanism of action • Closes KATP channels
on -cell plasma
membrane
• ↑ Insulin secretion
advantages• Extensive experience
• ↓ Microvascular risk (UKPDS)
disadvantages • Hypoglycemia
• ↑ Weight
• ? Blunts myocardial ischemic
preconditioning*
• Low durability
cost low 
A1C effect 1-1.5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
thizolidinediones: pioglitazone
trade name
mechanism of action
advantages
disadvantages
cost
A1C effect
A
thizolidinediones: pioglitazone
trade name acts
mechanism of action ↑ Insulin sensitivity
advantages• No hypoglycemia
• Durability
• ↑ HDL-C
• ↓ Triglycerides (P)
• ? ↓ CVD events (ProACTIVE, P)
disadvantages • ↑ Weight
• Edema/heart failure
• Bone fractures
• ↑ LDL-C (R)
• ? ↑ MI (meta-analyses, R)
cost low
A1C effect 1-1.5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
alpha glucosidase inhibitors
trade name
mechanism of action
advantages
disadvantages
cost
A1C effect
A
alpha glucosidase inhibitors
trade name acarbose=precose
mechanism of action Inhibits intestinal
a-glucosidase
• Slows intestinal
CHO digestion/
absorption
advantages • No hypoglycemia
• ↓ Postprandial glucose
excursions
• ? ↓ CVD events (STOP-NIDDM)
• Nonsystemic
disadvantages • Generally modest A1C efficacy
• GI side effects (flatulence, diarrhea)
• Frequent dosing schedule
cost moderate
A1C effect 0.5-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
DPP-4 inhibitors
trade name
mechanism of action
advantages
disadvantages
cost
A1C effect
A
DPP-4 inhibitors
trade name sitagliptin=januvia
mechanism of action • Inhibits DPP-4
• ↑ Postprandial active
incretin (GLP-1, GIP)
• ↑ Insulin secretion†
• ↓ Glucagon†
advantages • No hypoglycemia
• Well tolerated
disadvantages• Angioedema/urticarial, other immunemediated
derm effects
• ? Acute pancreatitis
• ? ↑ HF hospitalizations
• ? Severe joint pain (rare)
cost high 
A1C effect not great
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
GLP-1 receptor agonists
trade name
mechanism of action
advantages
disadvantages
cost
A1C effect
A
exenatide: byetta
trade name
mechanism of action • Activates GLP-1
receptors
• ↑ Insulin secretion†
• ↓ Glucagon secretion†
• Slows gastric emptying
• ↑ Satiety
advantages • No hypoglycemia
• ↓ Weight
• ↓ Postprandial glucose
excursions
• ↓ Some CV risk factors
disadvantages • GI side effects (N, V, D)
• ↑ Heart rate
• ? Acute pancreatitis
• C-cell hyperplasia/medullary thyroid
tumors in animals
• Injectable
• Training requirements
cost high 
A1C effect 1-1.5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

drug that is often used with insulin in type II DM

A

amylin mimetics (pramlintide)

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

drug for DMII that is also used for HLD

A

bile acid sequestrants: colesevelam

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

drug for DMII that inhibits reabsorption of glucose in proximal tubule and has added benefits of decreased wt and bp

A
Sodium-glucose cotransporter
2 (SGLT2)
inhibitor
• Canagliflozin
• Dapagliflozin‡
• Empagliflozin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T or F: if A1c is >9, consider starting at dual therapy

A

T

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

where should you consider starting if BG >300-350

A

combo injectable therapy

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

what is 1st line DM tx? where to go from there?

A

metformin, check A1c in 3 months, if not at goal and fully titrated and adherent, move on to dual therapy

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

initial immediate release dosing of metformin

A

500 mg bid or 850 mg daily

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

universal dose of regular insulin100 units/ml OTC

A

100 units/ml OTC

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

indication for rapid acting insulin

A

covers for meals

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

examples of long acting insulin

A

glargine, detemrir

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

name of ultra long acting insulin

A

degludec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

best place to keep insulin

A

 Best place is the refrigerator
 Can be kept at room temperature if used within 30 days
 Do not expose to extreme temperatures or sunlight; no not allow to freeze
f:

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

don’t use insulin if

A

Insulin is discolored
Particles have clumped together or are sticking to side of bottle
Past expiration date on bottle or has been unrefrigerated for > 1 month

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

insulin starting dose for DM1 AND 2

A

DM1: 0.5-0.6 units/kg/day
DM2: 0.1-0.2 units/kg/day
Usual DMI1 dose: 0.5-1 unit/kg/day in divided doses
50% Basal insulin (long acting)
50% Prandial insulin (prebreakfast, prelunch, predinner)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

treatments of hypoglycemia

A

Conscious patient
 Oral glucose tablets 15-20 gm (chew), MR in 15 min if SMBG shows continued
hypoglycemia
 Food (orange juice)
 Meal or snack once BG normalizes to prevent hypoglycemia recurrence
 Unconscious patient
 Glucagon: 1 mg SQ, IM or IV produces a response in 5-20 min, MR x 1 or 2 prn
 IV dextrose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what do all diabetic patients on insulin and PO agents with r/o of hypoglycemia need to know?

A

signs and sx of hypoglycemia and how to tx with oral tablets, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

is acute illness a problem for T2DM patients?

A

usually not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how to manage BG in T1DM patients with an acute illness?

A

Patients need to monitor BG frequently,
check urine ketones, use short-acting
insulin as needed
continue usual insulin regimen
and use supplemental rapid-acting insulin basedon BG results
 Give additional insulin if ketonuria develops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how do you manage BG in hospital setting?

A

Scheduled insulin with additional short-acting insulin as needed is recommended, esp b/c you need to hold metformin b/c of risk of renal failure in hospital and possible need for CT with contrast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

BP goal for diabetes according to ADA? pregnancy?

A

Blood Pressure Goal*

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

what type of management (lifestyle vs. drugs) is appropriate for BP in DM? for which BP ranges? which drug should be used?

A

Lifestyle therapy** alone (max 3 months) > 120 > 80
Lifestyle therapy** + pharmacologic therapy > 140 > 90
drug: ACEI 1st line, ARB 2nd line

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

monitoring of BP drugs (ACE/ARB) in diabetcis

A

BP, serum creatinine, GFR, serum K

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

what statin intensity should be taken by those 40-75 with no known ASCVD RFs?

A

moderate, b/c DM is a CVD risk equivalent

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

what kind of statin tx by ACS and LDL >50 in patients who can’t tolerate high dose statins?

A

Moderate statins + ezetimibe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

anyone with ASCVD should receive what kind of statin therapy?

A

high dose statins

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

who with DM should get aspirin?

A

YES if >50 and RFs and 10 years risk >10 %, NO if

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

T or F: everyone with DM should be on aspirin therapy

A

F: If

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

how do you decide who should be on aspirin therapy?

A

need to look at 10 year CV risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

increased urine albumin to creatinine ratio (30-299) is an early indicator of what?

A

diabetic kidney disease

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

what’s the best way to prevent diabetic kidney disease?

A

optimize BG & BP and screen for urinary albumin and GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how often should someone on insulin therapy check BG?

A

1-6 x/day

44
Q

preprandial BG goal

A

80-130

45
Q

post prandial BG goal

A
46
Q

hgb A1c goal, how often to check?

A
47
Q

how to manage pre diabetes ?

A

Refer to an intensive behavioral counseling program targeting:
• Weight loss of 7% of body weight
• Regular physical activity (≥ 150 min/week of moderate activity, e.g. walking)
• Follow-up counseling appears to be important for success

48
Q

in those without DM, who should be considered for metformin?

A
  • BMI > 35

* Age

49
Q

when should patients monitor their BG?

A

SMBG prior to meals and snacks, occasionally postprandially, at hs, prior to exercise, when
they suspect low BG, after treating low BG until normoglycemic, and prior to critical tasks, e.g. driving.
 For patients using less frequent insulin injections or non-insulin therapies, SMBG may be useful as aguide to management

50
Q

factors that affect blood glucose patterns

A

meals, exercise, illness, stressful events

51
Q

T or F: to change BG patterns, Adjust the insulin dose taken after the time of the pattern

A

F: adjust the one before hand

52
Q

what is typical number of carbs 1 unit of insulin covers?

A

12-15

53
Q

Total daily insulin dose

A

weight (Kg) x 0.55 units/Kg

54
Q

carbohydrate coverage equation

A

500 ÷ TDI (for rapid acting insulin; 450 for regular insulin) then divide carbs in meal by coverage ratio to cover carbs

55
Q

gold std for pharm tx of hypothryoidism

A

levothyroxine

56
Q

AE of thyroid replacement therapy

A

HTN, tachycardia, insomnia, diarrhea
 Excessive doses may lead to heart failure, angina pectoris, MI (rarely caused by coronary
artery spasm) Reduced bone density with excessive doses

57
Q

T or F: levothyroxine dose is in mcg

A

T!

58
Q

indications for an increased thyroid hormone dose

A

decreased absorption, certain drugs/diets, pregnancy, increased TBG, incresed clearance, impaired deiodination, other: streamline, lovastatin

59
Q

decreased dose requirements of thyroid hormone

A

aging, delivery, withdrawal of interacting substance

60
Q

what needs to happen with warfarin dose when hypothyroid? euthyroid?

A

increase warfarin dose when hypothyroid, decrease when euthyroid

61
Q

dosing of levothyroxine

A

Average dose: ~1.7 mcg/kg/day (typically 100-125 mcg/day); > 75 yo, 1 mcg/kg/day
 Take first thing in the morning on an empty stomach (absorption can be  by calcium, iron,
fiber); wait ≥ 30 minutes before eating and 4 hours to take calcium iron, magnesium or
aluminum, sucralfate, cholestyramine, and orlistat

62
Q

who should be started on decreased doses of levothyroxine?

A

those >50 and those with cardiac disease (don’t want to tax heart with too much hormone)

63
Q

tx of myxedema coma

A

300-500 mcg levothryoxine IV + 50-100 mg hydrocortisone q 6h (in case of simultaneous adrenal insufficiency)

64
Q

what’s best lab to check after levothryoxine therapy and wheN?

A

TSH q6-8 weeks until euthyroid and then q 6-12 months forever

65
Q

antithyriod agents: methimzaole and propylthiouracil
MOA
AE

A

MOA inhibit the synthesis by blocking the oxidation of iodine, do not inactivate circulating T3 and T4; PTU
inhibits peripheral conversion of T4 to T3
AE: maculpapular rash, arthralgias, fevers, agranulocytosis, GI intolerance, hepatoxicity

66
Q

1st line drug for hyperhtyroidism

A

methimazole (mmi)

67
Q

indications for propylthiouracil (PTU)

A

patients who can’t tolerate other tx; ♀ trying to conceive or
during 1st trimester, tx of thyroid storm

68
Q

other drugs that can be used to tx hyperthyroidism

A

beta blocker (“bridging” just controls sx) and iodides (blocks conversion and release)

69
Q

CI of radioactive iodine

A

pregnancy (don’t want to expose fetus to radioactive iodine)

70
Q

1st line tx of hyperthyroid in graves is what for who?

A

antithyroid drugs for children, adolescents, and in pregnancy or pre-op

71
Q

best tx for toxic nodules and toxic multi nodular goiter in hyperthyroidism by graves

A

radioactive iodine

72
Q

what needs to happen to patients before they can get thytroid surgery?

A

need to be euthryoid

73
Q

tx of thyroid storm

A

Short acting beta blocker, e.g. IV esmolol
IV or oral iodide
Large doses of PTU (900-1200 mg/day in 3 to 4 divided doses)
Supportive care: APAP for fever, fluid and electrolyte management, antiarrhythmic agents
IV hydrocortisone 100 mg q8h due to the potential presence of adrenal insufficiency

74
Q

Modest weight reductions of ____ have been shown to improve obesity-related health risks

A

5-10%

75
Q

drug that began as “when-fen” (fen had valve problems, which works by increasings NE and DA; mild CNS stimulant, helps people lose about 8 pounds, OLD–developed in 1960s, only approved for ST use causes AE of hyperactivity (palpitations, increased BP, HR), and class 4 controlled substance. what do you need to monitor?

A

phentermine; monitor BP, HR

76
Q

drug similar to phentermine

A

diethylpropion

77
Q
orlistat 
indication
MOA
Short or long term?
AE
CI
A
orlistat
indication obesity
MOA: decreases absorption of fat
Short or long term? long term
AE GI/malabsorption stuff (steatorhrea..)
CI: pregnancy, certain drugs (warfarin)
78
Q

trade names of orlistat

A

xenical (rx) and alli (OTC)

79
Q

drug that targets satiety center in brain. what are a few big adverse effects?

A

lorcaserin (belviq). CNS stuff (serotonin) and serotonin syndrome, euphoria, priapism, valvular heart disease

80
Q

weight loss drug that combines phentermine with an AED at low doses to lose weight

A

phentermine/topiramate

81
Q

drug that is also used to tx alcohol dependence that can be used in obesity. CI?

A

naltrexone/bupropion, contraindications of higher risks of seizures (anorexia nervosa, alcohol withdrawal, seizure disorder)

82
Q

drug for weight loss originally made by DM

A

liraglutide

83
Q

tx of any cholinergic overdose symptoms (wet, SLUDGE)

A

atropine

84
Q

tx of suspected organophosphate (commercial) pesticides to regenerate acetyl-cholinesterase enzyme and saves it from permanent covalent bond

A

Pralidoxime (2-PAM)

85
Q

tx of anti-cholinergic toxidrome (bloated as a boat, mad as a hatter)

A

benzodiapezines to prevent seizures and agitation

86
Q

tx of opiates

A

naloxone (be careful not to fully reverse if going to hate you b/c they’ll be OK with some o2 unless heart is failing) and flumezenil

87
Q

tx of sympathomimetic agents

A

diazepam, cooling

88
Q

tx of serotonin syndrome

A

diazepam, cooling, antipyetics

89
Q

GI decontamination that absorbs toxins within 1 hour of ingestion

A

activated charcoal

90
Q

whole bowel irrigation when charcoal won’t bind to drug

A

polyethylene glycol osmotically balance solution

91
Q

approach to patient with overdose

A

ABCs, when did it occur? (charcoal?), any other toxins?, acetaminophen level? LFTs? bill? BUN/SCR? coags? CBC?

92
Q

tx of TCA overdose

A

bicarb

93
Q

injury from a medicine or lack of an intended medicine

A

adverse drug event

94
Q

stop the medication and look for an improvement

A

dechallenge

95
Q

if possible, give again and look for similar reaction

A

rechallenge

96
Q

FDA program launched in June of 1993 that reports adverse drug evetns

A

medwatch

97
Q

who should reports ADEs?

A

ALL health care practitioners who suspect an ADE

 Manufacturers are required to report ADEs discovered to FDA

98
Q

what ADEs should be reported?

A

SERIOUS ADEs defined by the FDA as type A or B reactions where the outcome is:
Death
Life-threatening event
Hospitalization (initial or prolonged)
Disability
Congenital anomaly
Medical or surgical intervention was required to prevent permanent damage
ADEs related to newly released agents are particularly important

99
Q

prescriber problems related to medication errors

A
Illegible handwriting
 Incomplete medication orders
 Use of improper abbreviations
 Use of apothecary system (gr = grains, grams)
 Use of improper drug names (5-FU, 6-MP)
 Ambiguous drug orders
 Improper expression of drug strengths
 Unnecessary verbal orders
100
Q

high hazard meds

A
Benzodiazepines
 Calcium
 Chemotherapeutics
 Heparin
 Insulin
 Lidocaine
 Magnesium Sulfate IV
 Opiate Narcotics
 Potassium Chloride IV
101
Q

tips to prevent med errors

A

stay up to date, use current references, double check calculations, always use a leading zero but never a trailing one, avoid verbal orders, include reason for use, avoid dangerous abbreviations, educate patient and caregiver

102
Q

places to report medication errors to

A

individual hospital, USP , FDA, ISMP ((institute for safe medical practice)

103
Q

components of a fiduciary relationship

A

expertise, holds trust of others, held to high standards, avoid conflicts of interest, is accountable legally

104
Q

good questions to ask yourself when considering gifts

A

What is the purpose of the gift and does it truly benefit your patients in some manner?
• What would my patients and colleagues think about this arrangement?

105
Q

markers of an “appropriate gift”

A

primarily benefits patients; not of substantive value; if an educational activity,
unbiased and legitimate, no “strings” or conditions