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From Flashcardlet > Pharm SS Exam 3 > Flashcards

Pharm SS Exam 3 Flashcards

1
Q

Type I Diabetes

A

Absolute deficiency in insulin - autoimmune destruction of beta cells.

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2
Q

Type II Diabetes

A

presence of insulin with inadequate compensatory increase in insulin secretion - insulin resistance and progressively lower insulin secretion.

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3
Q

Gestational Diabetes

A

diabetes developed due to the stress of pregnancy - glucose intolerance first recognized in pregnancy

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4
Q

Diagnosis of Diabetes

A

A1C >=6.5%, fasting glucose >= 126mg/dl, 2hr plasma glucose tolerance test >=200mg/dl or a patient with classic hyperglycemia sx and a random glucose test >=200mg/dl

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5
Q

Diagnosis of Prediabetes

A

A1C 5.7-6.4%, fasting glucose 100-125mg/dl, 2hr plasma glucose tolerance test 140-199mg/dl.

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6
Q

Diagnosis of Gestational Diabetes

A

all pregnant women should be screened at 24-28 wks. using 75g 2hr OGTT. Fasting >=92mg/dl, 1 hr >=180mg.dl, 2hr >=153mg/dl.
Screen post delivery for persistent diabetes 6-12 weeks postpartum. Continue to screen them for diabetes at least every 3 years and encourage lifestyle changes.

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7
Q

ADA A1C Recommendations

A

Perform A1C at least 2x per year in patients who are meeting tx goals and have stable glycemic control. Perform quarterly in patients whose therapy has changed or are not meeting glycemic goals.
Point of care testing allows for more timely treatment changes.

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8
Q

ADA Guideline: Diabetes care in the hospital for critically ill patients

A

insulin treatment for persistent hyperglycemia starting at the threshold of <=180mg/dl and a goal of 140-180mg/dl.

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9
Q

ADA Guildeline: Diabetes care in the hospital - dosing

A

Basal dose of long acting insulin (lasts 18-24 hours) and Bolus dose of short/rapid acting insulin for meal correction along with carb counting (Sliding Scale).

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10
Q

Insulin

A

contains protamine and zinc to help it maintain stability prior to use - delays the onset, peak and duration of effect. It is degraded in the liver, muscle and kidneys therefore insulin doses are lowered in those with end stage renal disease.

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11
Q

Patient is on insulin with normal K+ and hyperglycemia

A

Supplement insulin with K+.

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12
Q

Aspart (Novolog)

A

Rapid acting insulin - commonly used for sliding scale in the hospital.

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13
Q

Lispro (Humalog)

A

Rapid acting insulin

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14
Q

Glulisine (Apidra)

A

Rapid acting insulin

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15
Q

Regular (Humlin, Novolin)

A

Short acting insulin - Can be used as basal dose but still need a correction dose.

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16
Q

NPH (Humulin N, Novolin N)

A

Intermediate acting insulin - Can be used as basal dose but still need a correction dose.

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17
Q

Detemir (Levemir)

A

Long acting insulin - used as a basal dose. Duration of 14-24 hours. Give at night.

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18
Q

Glargine (Lantus)

A

Long acting insulin - used as a basal dose. Duration of 22-24 hours. Give at night.

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19
Q

Adverse reactions to insulin

A

Hypoglycemia (most common in patients on intensive regimens) and weight gain. Lipodystrophy can occur.

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20
Q

Type I insulin dose requirements

A

.5-.6units/kg per day with approx 50% as basal insulin and 50% as bolus meal coverage.

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21
Q

Homeymoon phase

A

particular periods when insulin increases, so their dose decreases to .1-.4units/kg.

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22
Q

Type II insulin dose requirements

A

PO preferred, but insulin eventually is started. Dosing varies by age, weight and stage of disease.

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23
Q

Exenatide (Byetta)

A

Inject-able GLP-1 Agonist - enhancing glucose dependent insulin secretion from pancreatic beta cells. Suppresses inappropriately elevated glucagon secretion and reduces both fasting and postprandial glucose. Reduce A1C by .9%
Side effects: weight loss and slow gastric emptying so that glucose entering the plasma better matches the glucose disposition. N/V/D are dose dependent.
DO NOT USE IN PATIENT WITH CRCL <30ML/MIN

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24
Q

Liraglutide (Victoza)

A

Inject-able GLP-1 Agonist - enhancing glucose dependent insulin secretion from pancreatic beta cells. Suppresses inappropriately elevated glucagon secretion and reduces both fasting and postprandial glucose. Reduce A1C by 1.1%
Side effects: can cause acute pancreatitis. May worsen gastroparesis (give erythromycin to increase motility).
Delays the absorption of other drugs like pain meds and abx.

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25
Q

Pramlintide (Symlin)

A

Inject-able Amylinomimetic - helps sensitize the tissues to insulin because it’s a hormone that is co-secreted with insulin. Decreases A1C bhy .6%
Side effects: Suppresses high post-prandial glucagon secretion, increases satiety resulting in weight loss and slowed gastric emptying. N/V and delay of absorption of other medications. Reduce prandial insulin by 30-50% when it is started to minimize severe hypoglycemic reactions.
Tmax is approx 20 minutes and the Cmax is dose dependent which appears linear. Bio availability after SQ injection is 30-40%.
Reduce A1C by .4-.5%

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26
Q

Glipizide

A

2nd generation Sulfonylurea, there are 3 types of this drug

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27
Q

Sulfonylureas

A

bind to specific sulfonylurea receptors on pancreatic cells enhancing the closing of K+ channels causing depolarization of the cell, Ca++ entry and subsequent secretion of insulin.
Can reduce the hepatic clearance of insulin.
Side effects: hypoglycemia and weight gain. Cross reactive with a sulfa allergy.
1st generation potency < 2nd generation potency.
Reduce A1C by 1-2%

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28
Q

Tolbutamide

A

1st generation Sulfonylurea that causes hyponatremia

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29
Q

Chlorpropamide

A

1st generation Sulfonylurea that causes hyponatremia

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30
Q

Tolazamide

A

1st generation Sulfonylurea

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31
Q

Glimepiride

A

2nd generation Sulfonylurea

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32
Q

Glyburide

A

2nd generation Sulfonylurea

33
Q

Short acting insulin secretagogues

A

stimulate insulin release by interacting with K+ channels on the beta cells. Absorbed in 30min-1hr with a very short half life of 1-1.5 hours.
Side effects: hypoglycemia and weight gain.
Interact with genfibrozil to double its half life and trimethoprim (bactrim) to increase repaglinide levels by 60%

34
Q

Repaglinide

A

Short acting insulin secretagogue that is hightly protein bound and metabolized by oxidative metabolism and glucuronidation. Can reduce A1C 1-2.4%.
Ok with renal insufficiency.
Moderate to severe hepatic impairment may prolong exposure.

35
Q

Nateglinide

A

Short acting insulin secretagogue that is highly protein bound and metabolized by CYP2C9 and CYP3A4 - conjugation allows for rapid renal elimination. Can reduce A1C by .8%

36
Q

Metformin

A

Biguanides - activate AMP dependent protein kinases to stimulate FFA oxidation and glucose uptake. Also reduces lipogenesis and gluconeogenesis. Increases insulin sensitivity in the liver and peripherally. Renal secreation with a half life of 6 hours. Lasts more than 24 hours. Reduce A1C by 1.5-2%.
reduces mortality and risk of stroke but contrainidcated if serum creat is >1.4 in females and >1.5 in males (renal insufficiency)
Side effects: abd discomfort, N/D, anorexia therefore weight loss,
Interactions: competes with Cimetidine so it increases serum metformin concentrations.

37
Q

Metformin dosing

A

Immediate release: 500mg BID with the largest meals. Can be increased by 500mg weekly up to 2,500 mg/day until glycemic goals are met.
Extended release: 750 mg tabs. Titrate weekly to the max dose of 2,250 mg/day.

38
Q

Thiazolidinediones

A

bind to the peroxisome proliferator activator receptor to enhance muscle, liver and fat sensitivity to insulin. Causes preadipocytes to differentiate into mature fat cells in subcutaneous fat stores.
Reduce A1C by 1.5%
Contraindicated in patients with heart failure!
Side Effects: fluid retention, increase risk of fracture, esp in women so supplement with Vit D and Calcium

39
Q

Pigolitazone (Actos)

A

Thiazolidinedione with a half life of 3-7 hours
Consistently decreases plasma triglycerides.
Max dose is 45 mg/day

40
Q

Rosiglitazone (Avandia)

A

Thiazolidinedione with a half life of 3-4 hours
Neutral triglyceride effect and increase LDL-C concentration
Max dose is 8mg/day - if given 4 mg BID it may reduce A1C by .2-.3% more

41
Q

Alpha-Glucosidase Inhibitors

A

competitively inhibit enzymes in the small intestines delaying the breakdown of sucrose and complex carbs. Reduces A1C by .3-1%.
Side effects: GI sx such as flatulance, bloating, abdominal discomfort, diarrhea.

42
Q

Alpha Acrabose (Precose)

A

Alpha-Glucosidase Inhibitor

43
Q

Miglitol (Glyset)

A

Alpha-Glucosidase Inhibitor

44
Q

Dipeptidyl Peptidase 4 Inhibitors (DDP-4 Inhibitors)

A

inactivate GIP glucose dependent insulinotropic polypeptide and GLP-1. Prolongs the half life of endogenous GLP-1 and GIP.
Reduces A1C .7-1%.
Drug interactions: Rifampin can decrease active levels by 50%
Side effects: hypoglycemia, utricaria and/or facial edema

45
Q

Sitagliptin (Januvia)

A

rapid absorption DDP-4 Inhibitor.

Drug Interactions: Neither an inducer or inhibitor of any CYP450 enzyme system

46
Q

Saxagliptin (Onglyza)

A

DDP-4 Inhibitor
Drug interactions: it is a p-glycoprotein substrate with neglible.
mod/strong CYP3A4/5 inhibitors or inducers (Diltiazem or Ketoconazole) can increase concentration 2-fold

47
Q

Bile Acid Sequesterants

A

acts in the intestinal to bind bile acid. Causes malabsorption of fat-soluble vitamins so may need to supplement.
Side effects: constipation, dyspepsia.
Contraindicated in patients with hx of triglyceridemia induced pancreatitis. Caution if patient has elevated triglycerides or hx of pancreatitis.
Drug interactions: cyclosporine A, warfarin and vitamin K

48
Q

Colesevelam

A

Bile acid sequesterant

49
Q

Bromocriptine

A

Dopamine Agonist that reduces A1C by .1-.4% from baseline, dosed in tablets 2 hours from waking from sleep and need a minimum of 1.6 mg/day

50
Q

ADA Guidelines: Pharm Therapy for T2 DM hyperglycemia

A

Metformin unless not tolerated or contraindicated.
Consider Insulin therapy with or without other agents at new onset if patient has markedly increased A1C or is symptomatic.
Add second oral agent, GLP-1 receptor agonist or insulin if noninsulin monotherapy at max dose does not achieve goal A1C

51
Q

ADA Guidelines: Glucose Monitoring

A

in patients >=25 with T1 DM along with intensive insulin it can be useful in lowering A1C. Success is related to the adherance.

52
Q

ADA Guidelines: BP Monitoring

A

Measure BP at all visits, goal =140/80 start ACEI or ARB, prior to that encourage lifestyle changes.
If pregnant female: 110-129/65-79 is target but an ACEI or ARB are contrainidcated.

53
Q

ADA Guidelines: Screening and Treating neuropathy

A

Screen for distal symmetric polyneuropathy and cardiovascular autonomic neuropathy at diagnosis for T2 and 5 yrs after diagnosis for T1.
Use meds to relieve sx.
Electrophysiological testing rarely needed.

54
Q

Tx of diabetic neuropathy

A

Low dose tricycyclic antidepressant, anticonvulsants (gabapentin, pregabalin, carbamazepine and maybe phenytoin), duloxetine, venlafazine, topical capsacin, and various pain meds including tramadol and NSAIDs.
Alpha lipoic acid 600mg/day

55
Q

what drug can cause hyperthyroidism?

A

amiodarone

56
Q

what is subclinical hyperthyroidism?

A

TSH is low but T3 and T4 are normal.

57
Q

propylthiouracil (PTU) and methimazole (MMI)

A

Thioureas - prevent the incorporation of iodine into iodotyrosines and ultimately iodothyronine (organification) and they inhibit the coupling of monoiodotyrosine and diiodotyrosine to form T3 and T4.

58
Q

Which is more potent - PTU or MMI?

A

MMI is about 10 times more potent because it is not protein bound like 60-80% of PTU is.

59
Q

Side effects to thioureas

A

puritic maculopapular rash, arthralgias and fevers. Benign transient leukopenia, agranulocytosis.
Hepatotoxicitiy - PTU not recommended in 1st tri of pregnancy, after that PTU is 1st line in pregnancy because of mmi teratogenic effects.

60
Q

radioactive iodine (RAI)

A

preferred drug therapy for Graves disease in US. Beta particle destroys the follicular cell causing a volume reduction and control of thyrotoxicosis.

61
Q

Indications/Contraindications for RAI

A

Indications - graves, toxic multinodular goiter, hyperfunctioning thyroid nodules, non-toxic multinodular goiter and thyroid cancer (surgery 1st then RAI for CA).
Contraindications - pregnancy, lactation, coexisting thyroid cancer or suspicion of CA, unable to comply with radiation safety guidelines and females planning pregnancy.

62
Q

RAI and antithyroid drugs

A

all antithyroid drugs must be d/c’d 2 days prior to administration.

63
Q

Iodide solution

A

acutely blocks thyroid hormone release, inhibits hormone synthesis by interfering with idodide utilization and decrease vascularity of the thyroid gland. Used as adjunctive tx to prepare graves pt. for therapy.
Side effects: hypersensitivity reactions, salivary gland swelling, gynecomastia.

64
Q

Lugol solution

A

iodide solution that is a “saturated solution of potassium iodide”
administer 7-14 days preop. As an adjunct to RAI give 3-7 days after RAI tratement so that the radioactive iodide can concentrate in the thyroid.

65
Q

Adrenergic blockers in Hyperthyroidism

A

Blocks T4 to T3 conversion at high doses, improves thyrotoxic sx such as palpitations, anxiety, tremor and heat intol. proranolol is preferred for nursing mothers, atenolol is shorter acting. there is no effect on urinary excretion of calcium, phosphorus, hydroxyproline, creatinine, or various amino acids.

66
Q

What drug can induce hypothyroidism?

A

Lithium

67
Q

Levothyroxine (Synthroid)

A

T4 DOC for thyroid replacement and suppressive therapy. Half life of 7 days but takes about 1 month to clear completely. Time to absorption is 2 hours, so avoid foods that decrease absorption in this period. Start patients with cardiac dz at a low dose and titrate slowly.

68
Q

Liothyronine

A

T3 chemically pure with a shorter half life than synthroid, but has a higher incidence of adverse cardiac events, is more expensive and is difficult to monitor.

69
Q

Liotrix

A

combination of synthetic T3 and T4 in a ratio that attempts to mimic natural hormone secretion. chemically stable and pure with predictable potency, but is expensive and has a lack of therapeutic rationale.

70
Q

Metyrapone, ketoconazole, etomidate and aminoglutethimide

A

Steroidogenesis inhibitors block the production of cortisol.

71
Q

Metyrapone

A

inhibits 11-hydroxylase resulting in a sudden decrease in cortisol levels within hours causing a compensatory rise in ACTH and eventually shifts to androgen production. Not readily available, but works immediately/rapid action. Side effects: androgenic side effects (hirsutism, increased acne), increased BP and electrolyte level variations.

72
Q

Ketoconazole

A

inhibits steroidogenesis via multiple mechanisms when used at lg. doses. Takes several weeks to be therapeutic. exhibits anti-androgenic activty. Side effects: gynecomastia and decreased libido in males. Can lower LDL cholesterol levels. **Monitor liver enzymes frequently even though severe hepatotoxicity is rare.

73
Q

Etomidate

A

imidazole derivative similar to Ketoconazole that inhibits 11-hydroxylase. Only available parenteral and is limited to emergency tx - works immediately/rapid acting.

74
Q

Aminoglutethimide

A

inhibits the conversion of cholesterol to pregnenolone and thereby inhibits cortisol, aldostrone and androgen production. Side effects: sedation, nausea, ataxia, and skin rashes. rarely used.

75
Q

Glucocorticoids

A

.75 Dexamethasone -> 5 prednisone

5 Prednisolone -> 5 prednisone

76
Q

Glucocorticoid side effects

A

infection, osteoperosis, Na+ retention, edema, hypokalemia, hypomagnesemia, cataracts, HPA axis suppression - require a taper if high dose short course or low dose for 21+ days. Don’t give with NSAIDs.

77
Q

mitotane

A

inhibits 11-deoxycortixol and 11-deoxycorticosterone in the cortex resulting in a net inhibition of cortisol and corticosterone synthesis. Takes weeks to become therapeutic. Will result in atrophy of the adrenal cortex.

78
Q

Ada guide for non critically ill pt

A

Premeal goal <180

79
Q

Glycemic recommendation for non pregnant adults with diabetes

A

A1C <180

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