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Pharmacology > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

thyroid and parathyroid glands

A

TH
thyroglobulin
PTH

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2
Q

Pancreas

A

exocrine: trypinogen, chymotrypsin, amylase, lipase
endocrine: insulin, glucagon

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3
Q

adrenal

A
  • cortisol
  • aldosterone
  • estrogens
  • androgens
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4
Q

bone formation

A

PTH: calcium, phosphorous

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5
Q

growth formation

A

estrogens, androgens: testosterone

-growth hormone releasing hormone-GH (somatropin)

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6
Q

metabolic rate control

A

TSH

TH

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7
Q

CHO metabolism

A

insulin

glucagon

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8
Q

blood pressure control

A

cortisol
aldosterone
ADH

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9
Q

bisphosphanates

A
  • used for osteoporosis and Paget’s disease
  • alendronate (fosomax), etidronate (Didronell), pamidronate (Aredia), risedronate (Actonel), tiludronate (Skelid)
  • alendronate, risedronate, ibendronate are used mostly for prevention
  • rational drug selection: high risk: white, Asian, hx of eating disorders
    • correct preexisting vit. D deficiency, hypocalcemia b/4 starting bisphonates
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10
Q

pharmacodynamics of bisphosphanates

A

-inhibits osteoclastic activity and bone resorption thus increases bone density
-bone density mass increases rapidly in first year and plateau’s after 2-3 yrs
ADRs: diarrhea, constipation, n/v, hypocalcemia, hypophosphatemia, dyspenia, esophageal ulcers, arthragia, myalgia, HA, rash, afib
-pathologic fx for tx >3 months
-osteonecrosis (jaw)
-muscular skeletal pain
-caution with patients with renal impairment, hrt failure, liver dz, active GI problems
-drug and food interactions: ranitidine doubles alendronate bioavailability, calcium supplements, antacids

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11
Q

pharmacokinetics of bisphonates

A
  • must be taken with 8 oz of water and fasting
  • pt. must remain upright for 30 minutes or one hour with ibandronate
  • onset 3-6 wks peak 3-6 months
  • half life ten years
  • metabolism-none
  • excretion: urine, feces (unabsorbed drug)
  • most pregnancy category C except pamidronate category D
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12
Q

Human growth hormone

A
  • stimulates growth and metabolism of every cell in body

- used for short stature men

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13
Q

pharmacodynamics of human growth horomone

A
  • initial insulin-like effect
  • simulates growth of linear bones, skeletal muscles and organs
  • simulates erythropoietin
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14
Q

pharmacokinetic human growth hormone

A 
IM and SQ well absorbed
-bioavailability 75% SQ
-metabolism: hepatic renal 90%
excretion: renal
ADRs: antibody development, hyperglycemia, edema, hypothyroidism, arthralgia, ha, dizziness, flu-like sx's
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15
Q

pancreatic enzymes

A

-used for cystic fibrosis and pancreatitis
-monitoring: CF-lifetime
pancreatitis-contraindicated during times of acute illness
hypersensitivity-may need products from vegetable sources
steatorrhea: needs monitoring

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16
Q

pharmacodynamics of pancreatic enzymes

A
  • inactivated by pH values
  • pancreatin (Ku-zyme) pancrealipase (Pancreas)
  • subsititute for pancreatic enzymes
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17
Q

pharmacokinetic of pancreatic enzymes

A

-taken immediately before of with meal
-absorption: none, because it acts locally in GI tract
-excretion: feces
-pancrelipase made from pork, pancreatin is made from pork, cow, or vegetable source-not good for people with gout or renal impairment
-antacids decrease effectiveness, decreases absorption of oral iron
ADRs: skin irritation, rashes, GI: n/v, stomatitis, hyperuicosuria, hyperuricemia

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18
Q

pharmacodynamics of inulin

A
  • total number of receptor sites can be decreased by obesity and long standing hyperglycemia
  • binds at insulin receptor sites on cell membrane allowing glucose to enter cells
  • acts on liver to increase storage of glucose as glycogen, decreases production of urea, catabolic activity and cAMP,
  • promotes protein synthesis on muscle cells
  • reduces circulation of free fatty acids and promotes storage of triglycerides in adipose tissue
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19
Q

types of inslin

A

rapid-acting: Lispro (Humalog), apart (Novolog), or glulisine (Apidra), onset about 5 minutes, peaks in one hour, duration 4-5 hours SQ
short-acting: humulin insulins, sometime used around mealtime; takes 30-45 minutes before eating, peaks in 3-4 hrs. duration 4-ten hours, can give IM off label use
intermediate-acting: NPH is mixed with protamine delaying absorption insulin looks cloudy and has to be mixed before its injected; onset half to hour peak 4 to ten duration twelve 24 hours
long-acting: glargine (Lantus), detemir (levemir) insulin onset 2-4 hours, duration 24 hours with little or no peak
ultra long lasting: Degludec, 42 hour duration

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20
Q

hypothalmic-pituitary system

A
  • thyrotropin-releasing hormone creates TSH
  • GnRh-leads to FSH, LH
  • prolactin releasing hormone-prolactin
  • oxytocin
  • antidiuretic hormone (ADH)
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21
Q

etidronate (Didronel)

A
  • bisphosphanate
  • reduces both bone resorption and formation (coupled together)
  • reduce vertebral fractures
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22
Q

pamidronate and risedronate (Aredia and Actonel)

A
  • bisphosphonate
  • inhibits resorption without inhibiting formation or mineralization
  • pamidronate only available in parenteral form
  • both reduce vertebral fractures
  • risedronate reduces non-vertebral fractures
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23
Q

alendronate (Fosamax)

A
  • bisphosphonate
  • 100-500x more potent then other drugs
  • highly selective inhibitor
  • inhibits osteoclastic activities without interfering with osteoclast recruitment or attachment
  • reduces both vertebral and nonvertebral fractures
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24
Q

tiludronate (Skelid)

A
  • bisphosphonate
  • inhibits osteclastic activity by interfering with osteoclasts attachment to bone surface and inhibiting osteclastic proton pump
  • decreases vertebral fractures
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25
Q

zoledronic acid (Zometa)

A
  • bisphosphonate
  • inhibits osteoclast activities and induces apoptosis
  • only IV
  • reduces vertbral fractures
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26
Q

ibandronate (Boniva)

A
  • bisphosphonate
  • inhibits osteoclastic activity and reduces bone resorption
  • reduces vertebral fractures
  • can be given IV every 3 months if po untolerated or unwilling
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27
Q

monitoring on bisphosponate

A
  • electrolytes-especially serum calcium

- alkaline phosphatase-increasing positive for paget’s dz

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28
Q

somatrem and somatropin

A

-for GH depression
-given to stimulate synthesis of somatomedins in growth plate cartilage resulting in increased linear, organ and skeletal growth and increased protein synthesis
-insulin-like effect
-contraindicated for patients with closed epiphyses, or active tumor growth
-close monitoring is needed for patient with thyroid disorders
-insulin resistance can occur–cautious with diabetic patients
ADRs: hyperglycemia, hypothyroidism, edema to secondary Na+ retention

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29
Q

pancreas

A
  • exocrine and endocrine glad
  • 2 major dz: CF and pancreatitis
  • both leads to obstruction of ducts resulting in activated digestive enzymes within pancreas and failure of releasing enzymes into duodenum to digest–malabsorption
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30
Q

diabetes

A

type one: destruction of beta cells to produce insulin
type 2: insulin resistant
-either one-disequilibrium between excess production of glucagon and lack of insulin

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31
Q

pharmacokinetics of insulin

A

-absorption dependent on type, injection site, and volume injected
-abdominal absorbs 50% more
-metabolism: induces CYP1A2
-excretion: urine
ADRs: hypoglycemia, diabetic ketoacidosis,
ETOH increases hypoglycemia
-drug interactions: beta blks increase insulin resistance and masks hypoglycemic symptoms

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32
Q

average dosing for insulin

A

0.6-0.8 U/kg

33
Q

monitoring for diabetes

A
  • routine glycohemoglobin, renal function and CBC
  • A1C test x2/yr when under control; once quarterly if tx goals not reached
  • goal usually is A1C
34
Q

type 2 diabetes

A
  • insulin resistance
  • 4 primary alterations: insufficient production of endogenous insulin by beta cells, tissue insensitivity to insulin, impaired response of beta cells to BG levels, excessive production of glucose secondary to increased glucagon levels
  • liver and incretin hormone system is the major organ
35
Q

sulfonyureas

A
  • helps with insufficient production of endogenous insulin by stimulating release from beta cells
    • improve insulin binding or increase # of receptors but does not improve insulin utilization
  • second line drug
  • not used as monotherapy
  • all potentiate effects of antidiuretic hormone
  • glipizide (Glucotrol), glyburide (Diabeta), glimeride (Amaryl)-
36
Q

pharmacokinetics of sulfonylureas

A
  • metabolism: liver CYP2C9
  • absorption: all with most
  • protein binding: >95%
  • excretion: urine and feces
37
Q

pharmacotherapeutics of sulfonylureas

A

-precautions/contraindications: cross sensitivity with sulfonamides and thiazide diuretics
-pregnancy C
-older adults more sensitive
-pediatric use for 10-18 yrs old but off label
ADRs: hypoglycemia, GI, derm rashes, SIDH, hemolytic anemia, leukopenia, thrombocytopenia, wt. gain

38
Q

clinical use/dosing for sulfonyureas

A
  • for type 2
  • use either first or second generation–first generation more hypoglycemia, wt. gain, and reduction of efficacy overtime
  • dose on individual response-titrate every 4-7 days
  • for neurogenic diabetes insipidus–chlorpropamide off label use
39
Q

rational drug selection/dosing for sulfonylureas

A
  • age: avoid using chlorpropamide and glyburide in older adults–use short acting glipizide
  • low cost-generic available
  • with comorbidities: renal impairment use glipizide/tolbutamide or glyburide
  • concurrent with insulin-only glimepiride by FDA, most 2nd generation
40
Q

monitoring of sulfonylureas

A

-HbA1C baseline every 6 months if meeting therapy goals or every 3 months if adjusting
CBC on onset and every8-ten months
-can be taken food except glipizide must be taken 30 minutes prior to meal

41
Q

biguanides

A
  • oral antihyperglycemic drug
  • first line drug for adults and children over age ten
  • metformin (glucophage)
  • monotherapy-lacks hypoglycemic effects, weight neutral, and decreased CVD events
42
Q

pharmacodynamics biguanides

A
  • decreases glucose in liver
  • decreases GI glucose absorption and improves insulin sensitivity by increasing peripheral glucose uptake and utilization
  • does not stimulate insulin from beta cells
  • inhibits platelet aggregation and reduces blood viscosity
43
Q

pharmacokinetics of biguanides

A
  • absorption: 50-60% after po dose; food decreases and delays absorption
  • no hepatic metabolism
  • excreted by kidneys
  • ETOH potentiates drug’s effect on lactate metabolism
44
Q

pharmacotherapies for biguanides-

A

precautions/contraindications

  • renal dz/dysfunction
  • metabolic acidosis
  • hepatic dz
  • withhold 48 hrs prior to test with iodine contrast
  • monitor pt. with b 12 deficiency
  • category B-not recommended
  • not for use of children
45
Q

rational drug selection/dosing of biguanides

A
  • IR v. ER-can safely switch btwn both.-just monitor glucose
  • start 500 mg BID with max of 2550 mg/day
    • if pts not responded after 4 weeks consider adding other oral agents like sulfonylurea
  • part of metabolic syndrome treatment protocol
  • monitoring: renal function, ketones, and HbA1C
46
Q

Alpha-glucosdiase inhibitors

A
  • acarbose (Precose)
  • migitrol (glyset)
  • NOT monotherapy *can be for pre-diabetes
47
Q

pharmacodynamics of alpha-glucosidase inhibitors

A
  • inhibits absorption of CHO from GI tract high lowers BG after meals
  • no hypoglycemia effect
48
Q

pharmacokinetics of alpha-glucosidase inhibitors

A

-

49
Q

Pharmacotherapies of alpha-glucosidase inhibitors

A

Precautions/contraindications
-not given to patients with IBS, possible bowel obstruction or renal impairment
-not for pregnant patients
ADRs: flatulance, diarrhea, abdominal pain
-drug interactions: acarbose and digoxin and miglitol and propanolol and ratadine

50
Q

Clinical use/dosing of alpha-glucosidase inhibitors

A
  • initial dose 25 mg TID titration 4-8 weeks

- take with first bite of meal

51
Q

pharmacodynamics of thiazolidinediones

A
  • pioglitazone (Actos), rosiglitazone (Avandia)
  • improves target cell response to insulin
  • increases utilization of insulin by liver and muscle cells
  • reduces liver glucose production
  • modest impact on lipids
  • no hypoglycemic effects
  • higher risk of bladder ca
  • increased risk of of HF
  • weight gain
52
Q

pharmacokinetics of thiazolidinediones

A
  • rapidly absorbed after po dose
  • metabolized by liver CYP2C8 and 3A4
  • 99% protein bound
  • excrete through urine and feces as metabolites
53
Q

pharmacotherapies of thiazolidinediones

A

precautions/contraindications
-chronic liver dz-increased concentrations of metabolites
-fluid retention-exacerbates HF
-restriction of use of rosiglitizone d/t increased risk of MI
ADRs: edema, URI, headache, fatigue
drug interactions: oral contraceptives need higher doses;
-any drug metabolized by CYP3A4-corticosteroids, ketoconazole

54
Q

meglitinides

A
  • short acting insulin secretagogues
  • add-on therapy
  • repalinide (Prandin), nateglinide (Starlix)
  • used in place of sulfonylurea
  • expensive
55
Q

pharmacodynamics of meglitinides

A
  • increases insulin release from beta cells by closing K+ channels leading to opening of Ca+ channels which then releases insulin
  • short time in plasm
56
Q

pharmacokinetics of meglitinides

A
  • absorbed rapidly and completely
  • metabolized in liver by CYP3A4 and CYP2C8
  • excreted within 96 hours; mostly in feces some in urine
57
Q

pharmacotherapies of meglitinides

A

precautions/contraindications
-liver impairment-higher concentrations of substrate
-pregnancy cat C
-not approved for pediatrics
ADRs: hypoglycemia
drug interactions: any drugs metabolized by CYP 3A4 or CYP 2C9
-antifungals and antimicrobials inhibit metabolism–increasing risk of hypoglycemia

58
Q

dosing for meglitinides

A
  • patient’s with HbAC 8 initial one mg before each meal

- titrate every 2 weeks for maximum of sixteen mg/24 hours

59
Q

dipeptidyl peptidase-4 inhibitors

A
  • “gliptins”
  • newest class of antidiabetic agents
  • sitagliptin (Januvia) and saxaglipin (Onglyza)
  • different mechanism of action: works on incretin hormone system
  • add-on therapy-*can be used as monotherapy but more effective in combination
  • once a day
60
Q

pharmacodynamics of dipeptidyl peptidase-4 inhibitors

A
  • inhibits DPP-4 which breaksdown GLP and GIP which are released in response to meals
  • increases secretion of insulin
  • suppresses release of glucagon from pancreas
  • promotes pre/post prandial glucose
  • slows gastric emptying
  • promotes weight loss
  • well tolerated
61
Q

pharmacotherapies for dipeptidyl peptidase-4 inhibitors

A

precautions/contraindications
-renal dysfunction-dependence on renal system for elimination
-pregnancy cat B
-not approved for pediatrics
ADRs: GI, headaches
drug interactions: ace inhibitors-increased risk for angioedema

62
Q

glucagon-like peptide 1 agonists

A
  • new drug of antidiabetic agents
  • exenatide (Byetta)
  • SQ injection twice daily; can be given weekly
  • given 60 minutes before meals
  • dose 6 hours apart
  • very expensive
  • add on therapy
63
Q

pharmacodynamics of glucagon-like peptide-1 agonists

A
  • promotes insulin release from beta cells when glucose level rises
  • decreases glucagon secretion
  • increases satiety
64
Q

pharmacotherapies of glucagon-like peptide agonists

A 
Precautions/contraindications
-severe GI dz-colitis, crohns
-pregnancy cat C
-renal dz
ADRs: n/v/d, pancreatitis
drug interactions: increased INR if given with warfarin, digoxin
65
Q

amylin agonists

A
  • pramlintide (Symlin)
  • adjunct therapy for type one and type 2
  • co-administered with insulin
  • lowers glucose by acting on glucagon secretion and slowing gastric emptying
  • via SQ injections
66
Q

pharmacodynamics of amylin

A
  • slows gastric emptying
  • suppresses glucagon secretion leading to decreased endogenous glucose
  • centrally mediated modulation of appetite–potential weight loss
67
Q

pharmacotherapies of amylin

A

precautions/contraindications
-high risk of hypoglycemia since administer with insulin
-pregnancy cat C
ADRs: GI
drug reactions: acetaminophen pharmacokinetics altered–must administer separately

68
Q

glucagon

A
  • considered antidote: used for diabetic patients who have hypoglycemia d/t insulin overdose
  • SQ, IM, IV
69
Q

pharmacodynamics of glucagon

A
  • stimulates hepatic gluconeogensis and glycogenolysis leading to increased BG
  • BG rises within ten minutes of injection with maximal effect after 30 minutes
  • hepatic stores necessary for glucagon to produce antihypoglycemic effect
70
Q

pharmacotherapies of glucagon

A

precautions/contraindications
-pregnancy cat B
-use caution with pt suspected having phenochromocytoma or insulinoma
ADRs: n/v
drug interactions: increased anticoagulant effects of po anticoagulants

71
Q

patient education on glucagon

A
  • educate family members/roommates on to administer IM
  • pt given supplemental CHO when awake and can swallow
  • lifestyle management
72
Q

thyroid hormones

A
  • levothyroin (T4), liothyronine (T3), liotrix (mixture of T3 and T4)
  • hypothalamus-pituitary-thyroid-hormone begins with secretion of TRH from hypotalamus in response to cold, stress, decreased levels of T4
  • TRH leads to secretion of TSH which: releases stored thyroid hormone, increases iodine uptake and utilization, increases synthesis of T3 and T4, increases synthesis of prostaglandins
  • create negative feedback loop to inhibit TRH and TSH
  • synthetic hormones produces feedback loop to stop secretion of TSH
  • levothyroxine drug of choice d/t longer half life
73
Q

pharmacokinetics of thyroid hormones

A
  • absorption is erratic with po and decreases with age, food, health of GI tract
  • majority is protein bound
  • excreted by bile/feces
74
Q

pharmacotherapies of thyroid hormones

A

precautions/contraindication
-contraindicated after acute MI or thyrotoxiocosis
-pregnancy cat A
-may need higher doses when pregnant
ADRs: symptoms of hyperthyroidism, long term use associated with decreased bone density in hips/spine
drug interactions: bile-acid sequestrants, iron salts, antacid decrease absorption; estrogen decrease response; warfarin, digoxin, and beta blockers may decrease action

75
Q

hypothyroidism

A
  • tx indicated with TSH>ten or btwn 5-ten if goiter or anit-thyroid peroxidase
  • thyroxin replacement is lifelong
  • levothyroxine drug of choice
76
Q

levothyroxine dosing

A

pts with CV: initial dose 50 mcg/day 2-4 wks may titrate
-average full replacement one hundred -one hundred twenty five mcg/day
pt>50 with CV or lifelong disease: initial dose twelve.5 to 25 mcg/day, titrate monthly

77
Q

antithyroid agents

A

-propylthiouracil (PTU), methimazole (Tapazole)
pharmacodynamics:
-blocks synthesis of thyroxine and trilodothyronine
-does not treat underlying pathology in hyperthyroidism

78
Q

pharmacokinetics of antithyroid agents

A

-rapidly absorbed after po dosing peaking within one hour
75-80% protein bound–except methimazole is NOT protein bound
-short half life
-excreted through urine

79
Q

pharmacotherapies of antithyroid agents

A 
precautions/contraindications
-pregnancy cat D
-high concentrations in breast milk
-PTU not recommended for children
ADRs: agranulocytosis, drowsiness, headache, alopecia, skin rashes, renal/hepatic failure
drug reaction: lithium, warfarin

Pharmacology (37 decks)

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