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N550 Pharm > Endocrine 1, 2 > Flashcards

Endocrine 1, 2 Flashcards

1
Q

Insulin MOA

A

Insulin binds to plasma membrane receptors initiating an intracellular cascade of enzymatic events: Glucose diffusion into cells, glucose storage mode, uptake of AA/phos/K/mg, protein synthesis, inhibition of proteolysis, fatty acid/TG synthesis, dec lipolysis, regulate DNA/ gene expression (via insulin regulatory elements)

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2
Q

___ units of physiologic insulin is the average daily requirement

A

40 units

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3
Q

In what way does ANS control insulin release?

A

Alpha decreases insulin secretion

Beta and PSNS increases insulin secretion

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4
Q

Which insulins are mixed commonly?

A

R/NPH or rapid/NPH

Before breakfast, R covers breakfast, NPH covers lunch (or R dinner; NPH night)

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5
Q

Which types of insulin are ultra-rapid acting? Onset, peak, DOA?

A

Lispro (humalog)
Aspart (novolog)
Glulisine (apidra)
Onset 15-30 min, peak 30-60 min, DOA 3-5h

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6
Q

Which types of insulin are short acting? Onset? Peak? DOA?

A

Regular (humulin R, novolin R)
Onset 30 min (slight peak of glucose before insulin starts working)
Peak 1-5h, DOA 5-8h

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7
Q

Which types of insulin are intermediate acting? Onset? Peak? DOA?

A

NPH (humulin N, novolin N)
P=protamine (this is what we use to reverse heparin), they may develop protamine allergy over time
Onset 1-2h, peak 6-10h, DOA 16-20h

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8
Q

Which types of insulin are long-acting? Onset, peak, DOA?

A 
Glargine (lantus)- no peak, not mixed with other insulins
Detemir (levemir)
Ultralente
Stimulate basal release (no peak)
Onset 2-6h, DOA 24h
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9
Q

IV regular insulin pharmacokinetics? E1/2t, DOA, metabolism

A

E1/2t 5-10 min
DOA 30-60 min
Proteolytic enzyme metabolizes insulin in the liver and kidneys

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10
Q

Insulin adverse reactions?

A 
HYPOGLYCEMIA
Injection site reaction
Lipodystrophy at site
Protamine allergy (only NPH)
Weight gain
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11
Q

Hypoglycemia symptoms?

A

Diaphoresis, tachycardia, hypertension (epi response to raise BG), CNS agitation, seizures, coma

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12
Q

Drug interactions with insulin?

A

ACTH, glucagon, estrogens- oppose hypoglycemic effects
Epi decreases release of insulin (raises BG)
Tetracycline, chloramphenicol, salicylates- prolong DOA
MAOIs increase hypoglycemic effects

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13
Q

In type 1 DM, 1 unit insulin decreases BG by ____

In type 2 DM 1 unit insulin decreases BG by ____

A

Type 1: 40-50 mg/dL
Type 2: 30-40 mg/dL
Although it varies with individuals

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14
Q

Benefits of tight controlled BG vs. non-tight control?

A

Tight control: reduces risk of chronic complications in type 1 DM, also inc wound healing, dec infection, dec osmotic diuresis, dec DKA incidence
Non-tight control: when controlled to tightly, we risk hypotension, plus its annoying and more work

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15
Q

Hyperkalemia treatment

A

10u Reg insulin IV

25g glucose, 1 amp 50% dextrose in 5 min

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16
Q

Hypoglycemia treatment

A

OJ, soda, honey, sugar tablet/cube

25-50 mL 50% dextrose solution

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17
Q

Which of these oral antidiabetic medications cause hypoglycemia?
Sulfonylureas, biguanides, thiazolidinediones, alpha-glucosidase inhibitors, melitinides, GLP-1 mimetics/gliptons

A

Can cause hypoglycemia: Sulfonylureas, gliptons, and meglitinides all increase insulin secretion from B cells
Don’t cause hypoglycemia: biguanides and TZDs increase insulin sensitivity at target tissues, alpha-glucosidase inhibitors slow absorption from the gut

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18
Q

Sulfonylureas MOA?

A

Stimulate release of insulin from pancreatic beta cells
Binds to ATP sensitive K channes in the cell membrane resultinmg in depolarization, Ca influx, and insulin release (tricks the beta cell into thinking it is in a glucose-rich state)
Secondary MOA: enhance beta cell sensitivity to glucose, enhance tissue sensitivity to insulin, lower BG

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19
Q

Sulfonylureas effect on FBG and Hbg A1C?

A

Reduce FBG 60-70 mg/dL

Reduce Hgb A1C 2%

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20
Q

List 1st and 2nd generation sulfonylreas and their DOA

A

1st: Tolbutamine (orinase) DOA 6-12h; chlorpropamide (diabinese) DOA 36-72h
2nd: glipizide (glucotrol) DOA 12-24h; glymuride (micronase, diabeta) DOA 18-24h; glimepiride (amaryl)
1st gen has more drug interactions and SE than 2nd bc 2nd gen is 100x more potent

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21
Q

Sulfonylureas pharmacokinetics?

A

90-98% protein bound
Metabolized hepatically (avoid in liver dz), some active metabolizes
If renal impairment, use glipizide or tolbutamide

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22
Q

Sulfonylureas adverse effects?

A

HYPOGLYCEMIA (hold 1-2 days preop)
GI: N/V, fullness, heartburn, cholestasis, altered LFTs, appetite stimulant (exacerbate obesity)
GU: ADH effect- Na and H2O retention
Pruritis, rash

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23
Q

Biguanides: MOA

metformin

A

Dec hepatic and renal glucose production (decreased gluconeogenesis/glycogenolysis), inhibits aerobic metabolism

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24
Q

Biguanides benefits

A

No weight gain, possible weight loss
May increase HDL, decrease LDLs and TGs
Hypoglycemia rare when used alone

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25
Q

Biguanides adverse effects

A

GI distress (diarrhea, metallic taste, nausea)
Lactic Acidosis
Rash
Hold 1-2 days before surgery

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26
Q

Biguanides contraindications

A

Women with ESRD, creatinine over 1.4
Med with ESRD, creatinine over 1.5
Hepatic dysfunction
CHF, shock, hypoxic pulmonary disease

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27
Q

Thiazolidinediones (TZDs): MOA, and name a couple?

A

Improves insulin sensitivity/decreases insulin resistance peripherally
Pioglitazone (Actos)
Rosiglitazone (Avandia)

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28
Q

TZDs clinical effect and pharmacokinetics?

A

Effect: decreases FPG up to 50 mg/dL, decreases Hgb A1C 1-2%, resumes ovulation in premenopausal women who have insulin resistance
PO, hepatic metabolism

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29
Q

Alpha-gucosidase inhibitors MOA and name a couple of them

A

MOA: competitively and reversibly antagonizes enzymes in the intestinal brush border responsible for digesting complex carbohydrates (when in the GI tract, it doesn’t get reabsorbed to the blood) delays glucose absorption, lowers post-prandial hyperglycemia (after a meal)
Acarbose (precose)
Miglitol (glyset)

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30
Q

TZD side effects and black box warning?

A

SE: edema, weight gain, hepatotoxicity (monitor LFTs, look for jaundice)
Black ox warning: CHF (can cause or exacerbate), MI (from rosiglitazone)

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31
Q

Alpha-glucosidase inhibitors clinical effect and pharmacokinetics?

A

Decreases PPG 60-70
Decreases FBG 25-30 only
Decreases Hbg A1C 0.7-0.9%
Not absorbed after oral administration, excreted in stool

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32
Q

Alpha-glucosidase inhibitors adverse effects? Cautions?

A

Abdominal pain/distention, diarrhea, flatulence
Caution in patients with IBD, ulcers, intestinal obstruction
Tak with first bite of meal, if you skip a meal, skip the dose

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33
Q

Meglitinides MOA, how do they compare to sulfonylureas?

A

MOA: stimulates insulin secretion from pancreatic beta cells, quick onset and peak (1h), short DOA (4h), reduces PPH (postprandial hyperglycemia)
Compared to sulfonylureas, less hypoglycemia, shorter DOA, quicker onset

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34
Q

Name a couple meglitinides, what are adverse effects?

A

Repaglinide (prandin), nateglinide (starlix)
AE similar to sulfonylureas, hypoglycemia, n/v/c/d, heartburn, headache
Take it 15-30 min before meals, if a meal is skipped, skip the dose

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35
Q

GLP-1 Agonisits (gliptins) MOA

A

Inhibits DPP4 (an enzyme that inactivates uncertain hormones, GLP1), enhances glucose-dependent insulin secretion, reduces glucagon secretion, slows gastric emptying

36
Q

Sitagliptan (januvia)- what are the beneficial effects and adverse effects? E1/2t?

A

E1/2t 12h
Reduces postprandial and fasting BG
AE: rare fatal pancreatitis and anaphylaxis

37
Q

What is exenatide (byetta)?

A

Synthetic GLP1, mimics GLP1 (an incretin), similar to gliptin, used as an adjunct to metformin or sulfonylureas

38
Q

Exenatide (byetta) adverse effects?

A

N/V, delayed gastric emptying
Renal failure, pancreatitis
Antibodies developed against the drug
Hypersensitivity

39
Q

Pramlintide- what is it?

A

Amylin mimetics

Amylin is a pancreatic hormone released with insulin

40
Q

Pramlintide (amylin mimetic): effects? Uses?

A

Reduces postprandial blood glucose

Used in both DM 1 and 2 who fail to attain control with insulin

41
Q

Pramlintide pharmacokinetics? AE? Interactions?

A

Peaks in 20 min, E1/2t 50 min
Metabolized in the kidney (NOT liver)
AE: high risk for hypoglycemia, nausea, injection site reaction
Interactions: decreased absorption of ABX an oral contraceptives

42
Q

What does the thyroid do?

A

Responsible for growth and development of nervous system in infants
Regulates metabolism and body temp
Synthesizes and secretes thyroid hormones and calcitonin

43
Q

Thyroid hormones are made up of two tyrosine molecules that are ____ and linked by an _____

A

They are IODINATED. Iodine is an essential component of thyroid hormones.
Linked by an ether

44
Q

_____ releases thyrotropin-releasing hormone (TRH). THR causes release of TSH from the ____

A

Hypothalamus releases TRH

Anterior pituitary releases TSH

45
Q

Does the thyroid secrete more T3 or T4?

A

T4, which is then converted into T3 in the periphery

46
Q

What do anti-thyroid drugs do? Name a couple.

A

Tx hyperthyroidism/ Graves
Ex: propylthiouracil (PTU), methimazole
Blocks organification process by competing with thyroglobulin for oxidized iodide
Reduces synthesis of thyroid hormones

47
Q

Antithyroid drugs onset of action?

PTU, methimazole

A

1-2 weeks

48
Q

Is methimazole or PTU more potent, causing less side effects?

A

Methimazole is more potent, only requires daily dosing, less side effects

49
Q

Antithyroid drugs adverse effects?

A

Goiter formation (inhibition of thyroid hormone up regulates TSH, leading to thyroid gland hypertrophy)
PTU only- dec prothrombin, causes bleeding
Pruritic rash
Arthralgias
Rare: agranulocytosis, hepatotoxicity, vasculitis

50
Q

Other things that PTU does

A

Inhibits conversion of T4 to T3 in the periphery
Increased bleeding tendency
Preferred in pregnancy, doesn’t cross placenta
Preferred in thyroid storm (acute hyperthyroidism)

51
Q

What other meds treat hyperthyroid?

A

B-blocker: blocks hyperadrenergic effects (tachycardia, tremor, nervousness), use esmolol for thyroid storm
Corticosteroids: suppresses thyroid receptor Ab and inflammation
Iodide: blocks conversion of T4 to T3, decreases vascularity of thyroid gland, blocks thyroid hormone release (this is only temporary treatment)

52
Q

What other treatments besides meds for hyperthyroid?

A

Radioactive iodine, thyroid gland ablation
Surgical removal of thyroid gland
These options usually require thyroid replacement

53
Q

Levothyroxine (synthroid): what is it?

A

Tx hypothyroid

Chemically synthesized T4

54
Q

Levothyroxine half-life? What needs to be monitored?

A

LONG half-life of 7 days
Easy to titrate
Monitor TSH, T4, and s/s of hyperthyroid if dose is too high
Monitor for adverse reaction: rash

55
Q

When would you give T3 liothyronine (cytomel) instead of T4?

A

Life-threatening hypothyroidism, myxedema coma

Otherwise give T4- levothyroxine

56
Q

Levothyroxine drug interactions?

A

Inc levothyroxine metabolism- penobarbital, phenytoin, rifampin, carbamazepine
Dec T4-T3 conversion- PTU, b-blockers, amiodarone, glucocorticoids
Dec absorption from gut- cholestyramine, FeSO4, AlOH3, sucralfate, kayexelate
Inc thyroid binding- pregnancy, estrogen

57
Q

Name 3 drugs that alter thyroid status

A

Amiodarone: structure resembles thyroid hormone, can cause hyper/hypo-thyroid
Lithium: body thinks its iodine, leads to hypothyroidism
Metoclopramide: increases TSH

58
Q

Corticosteroids: what are mineralocorticoid effects vs. glucocorticoid effects?

A

Mineralocorticoid effects: reabsorption of Na and secretion of K in renal distal tubule (aldosterone effects)
Glucocorticoid: antiinflammatory, augmentation of SNS activity

59
Q

Corticosteroid MOA

A

Bind to steroid receptors in the cytoplasm
Note: Mineralocorticoid receptors are found in organs of excretion, glucocorticoids wide-spread
Steroid enters nucleus and influences DNA transcription (enhances/inhibits)

60
Q

Corticosteroid effects

A

Raises BG, amino acid, TGs

Inflammatory response inhibited (arachidonic acid pathway)

61
Q

Cortisol (solu-cortef) pharmacokinetics?

A

90% protein bound
Metabolized mostly in liver, the rest is eliminated unchanged in the urine
E1/2t 1.5-3h

62
Q

How much endogenous cortisol do we secrete per day?

A

10-20mg

50-150mg with extreme stress

63
Q

Which steroid, when given with zofran before surgery, has a synergist long term effect on reducing post-op nausea?

A

Dexamethasone (decadron)

DOA is very long, 36-54 hours

64
Q

Methylprednisolone, betamethasone, and prednisolone: do they have mineralocorticoid or glucocorticoid effects?

A

Methylprednisolone: glucocorticoid effects
Betamethasone: lacks mineralocorticoid effects
Prednisolone: both effects

65
Q

Corticosteroids big clinical uses?

A

Adrenal insufficiency: cortisol
Allergy/asthma: glucocorticoids, but takes 4-6h to see antiinflammatory effects
Antiemetic: Decadron

66
Q

If you swallow the inhaled glucocorticoid what are you risking?

A

Dysphonia- laryngeal muscle myopathy

67
Q

Corticosteroids 3 big clinical uses?

A

Adrenal insufficiency: cortisol
Allergy/asthma: glucocorticoids, but takes 4-6h to see antiinflammatory effects
Antiemetic: Decadron 8-10mg, inhibits COX resulting in post-op analgesic effect

68
Q

Other clinical uses for corticosteroids? (besides adrenal insufficiency, allergy, antiemetic)

A

Intracranial tumors
Aspiration pneumonitis
Immunosuppression (transplant)
Lumbar disc herniation (triamcinolone/methylprednisolone epidural injection)
RA, SLE, MG, sarcoidosis, ocular/cutanous inflammation
UC, RDS prevention, leukemia

69
Q

Corticosteroid side effects/interactions

A 
HPA suppression (CV collapse)
Fluid/electrolyte imbalance, CBC changes
Infection, ulcers
Osteoporosis, skeletal muscle weakness
Psych disorders, growth retardation, dec anticoagulant effectiveness
70
Q

Glucagon: what is it and what releases it?

A

Polypeptide hormone, produced by alpha cells in pancreas in response to hypoglycemia, an antagonist to insulin that raises BG

71
Q

Glucagon MOA

A 
Enhances cAMP (inc myocardial contractility, HR, gastric motility, renal flow, insulin secretion, gluconeogensis/glycogenolysis, relaxes smooth muscle, dec gastric motility)
Vasodilates
72
Q

Glucagon clinical uses

A 
Increased CO (helps with b-blocker OD, improves CHF)
Biliary dilation (helps with biliary stent placement)
Enhance AV node conduction, diagnose pheo
73
Q

Glucagon clinical uses? dose?

A

Increased CO (helps with b-blocker OD, improves CHF)
Biliary dilation (helps with biliary stent placement)
Enhance AV node conduction, diagnose pheo
1-5mg IV or 5 mcg/kg/min (20 mg/h)

74
Q

Glucagon side effects

A 
Hyperglycemia
Hypoglycemia
Hypokalemia
N/V
Inc HR (esp. with Afib pts)
75
Q

Somatostatin is a GI regulatory peptide secreted by _____

A

pancreatic delta cells

76
Q

Octreotide/ somatostatin

A

Octreotide is a SS analogue, both inhibit production and release of hormones from the GI tract and pancreas (inhibit growth hormone release, insulin secretion, and glucagon release)

77
Q

E1/2t differences between SS and octreotide?

A

SS E1/2t 3 min

Octreotide E1/2t 2.5h

78
Q

Octreotide uses?

A 
Carcinoid crisis (dec release of amines like serotonin, but watch out for HB/bradycardia)
Hepatorenal syndrome
Control of esophageal variceal bleeding
79
Q

Vasopressin/ADH: what happens at V1 and V2 receptors?

A

V1: arterial smooth muscle vasocontriction
V2: inc water permeability/reabsorption at the collecting ducts in nephron back into circulation (reabsorbs more water)

80
Q

Vasopressin uses? E1/2t?

A 
Diabetes insipidus
Esophageal varices r/t hemorrhage
Hemorrhagic/septic shock
Cardiac arrest resuscitation instead of epi
E1/2t 10-20 min
81
Q

Vasopressin side effects

A

Increased BP
Coronary artery vasoconstriction: MI, angina
GI hyperperistalsis: N/V, abd pain

82
Q

Vasopressin/ADH: what happens at V1 and V2 receptors?

A

V1: arterial smooth muscle vasocontriction
V2: inc water permeability/reabsorption at the collecting ducts in nephron back into circulation (antidiuretic!)

83
Q

How does dosmopressin (DDAVP) compare to vasopressin?

A

DDAVP has a longer E1/2 of 2.5-4.4 hours
More selective for V2 receptors (antidiuretic)
Better choice for DI
Stimulates secretion of vWF

84
Q

Oxytocin (ptosin): what is it used for and what does it do?

A

Causes uterus contraction: induces labor, inc uterine tone after C-section, dec postpartum hemorrhage
High doses dec BP

85
Q

Oral contraceptives are a combo of what drugs to inhibit ovulation?

A

Estrogen

Progesterone

86
Q

Estrogen prevents release of ____

Progesterone prevents release of ____

A

Estrogen prevents release of FSH

Progesterone prevents release of LH

87
Q

Oral contraceptive side effects?

A

Thromboembolism: DVT
MI/stroke
HTN

N550 Pharm (14 decks)

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