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Pharmacology > Summer Exam 3 > Flashcards

Summer Exam 3 Flashcards

1
Q

Seven drug classes used for IBD?

A

Aminosalicylates (ASAa), corticosteroids, antimicrobials, immunosuppresives (azathioprine), Biologic TNF-a, anti-integrins, IgG monoclonal antibody

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2
Q

What is Ustekinumb and whats it used for?

A

IgG monoclonal antibody

Used in refractory crohns

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3
Q

First line med for low risk patient with mild crohns?

A

Bidesonide

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4
Q

Aminosalicylate MOA

A

azo structure reduces absorption in small intestine to reach terminal ileum and colon where bacteria cleave it into 5-ASA

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5
Q

Pharmacokinetics of 5ASA

A

not a lot of absorption- small amount undergoes acetylation in gut and liver to metabolite thats excreted by kidneys

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6
Q

5ASA MOA

A

interferes with production of inflammatory cytokines, may inhibit cellular function of natural killer cells, lymphocytes and macrophages
anti-inflammatory

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7
Q

5ASA uses

A

First line in mild-mod UC

can be used in crohns but not proven

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8
Q

How to treat IBD in proximal colon?

A

Azo compounds or mesalamine formulations

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9
Q

Treatment of crohns in small bowel (ileus)?

A

Mesalamine compounds (pentasa, asacol)

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10
Q

Mesalamine compounds

A

Pentasa-timed release in small intestine
Asacol-pH in distal ileum/proximal colon
Lialda-pH throughout colon
Rowasa/canasa suppositories-rectum and sigmoid colon

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11
Q

Olsalazine AEs

A

Secretory diarrhea

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12
Q

Mesalamine AEs

A

N/V, headache, interstitial nephritis in high doses

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13
Q

Sulfasalazine AEs/monitoring

A

N/V, headache, rash, anemia, hepatotoxicity, thrombocytopenia, orange skin

Folate replacement, CBC, LFTs

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14
Q

Glucocorticoids MOA

A

Inhibits production of inflammatory cytokines, reduces expression of inflammatory cell adhesion molecules, inhibits gene transcription

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15
Q

Glucocorticoid Use

A

IBD flare-up treatment; good anti-inflammatory but don’t cause remission

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16
Q

How do we reduce systemic absorption of steroids?

A

Rectal administration, only 15-30% absorbed and maxed tissue effects
*hydrocortisone! or budesonide (controlled release)

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17
Q

Budesonide PK

A

Controlled release in distal ileum/colon, rapid first pass hepatic metabolism resulting in low oral availability

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18
Q

Budesonide Uses

A

Mil-mod active UC or crohns in ileum or ascending colon

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19
Q

Which budesonide has delivery to ascending-descending colon?

A

Uceris (for UC only)

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20
Q

Treatment of mod-severe IBD

A

40-60mg pred (no higher!) initially, then taper after response

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21
Q

Budesonide vs prednisone pros/cons

A

Budesonide less AEs but less ability to achieve remission (but neither should be used for that, ASAs or immunosuppressives!)

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22
Q

Steroid AEs

A

Hyperglycemia, dyslipidemia, osteoporosis, hypertension, acne, edema, myopathy, psychosis

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23
Q

Purine analogs (immunosuppressants) options

A

Azathioprine (better option) and 6-mercaptopurine

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24
Q

Purine analog Pharmacokinetics

A

Azathioprine rapidly converted to 6MP which undergoes biotransformation via xanthine oxidase and thiopurine methyltransferase
Half life <2 hours and no onset for 17 weeks

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25
Q

Purine analog uses

A

Ulcerative colitis and Crohn’s initial and maintenance treatment, but takes 3-6 months to see results
Allows for steroid dose reduction

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26
Q

Purine analog AEs

A

Bone marrow depression, hepatic toxicity, risk of lymphoma, crosses placenta

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27
Q

Purine analog drug interactions

A

Allopurinol-reduces xanthine oxide catabolism of purine analogs>severe leukopenia

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28
Q

Antibiotic use in IBD

A

Used for septic complications like abscesses

Remission of active crohns

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29
Q

Methotrexate MOA

A

inhibits dihydrofolate reductase enzyme (need to prescribe with folate), interferes with interleukin actions, stimulate release of adenosine, apoptosis and death of t-lymphocytes

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30
Q

Methotrexate Uses

A

Induce and maintain remission in Crohn’s, weekly subQ injection

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31
Q

Methotrexate AEs

A

Bone marrow depression, alopecia, mucositis, peripheral neuropathy, liver damage

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32
Q

TNF MOA

A

release of proinflammatory cytokines, t-cell activation and proliferation

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33
Q

Anti-TNFs for Crohns

A

Infliximab, adalimumab, certolizumab, natalizumab, vedolizumab

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34
Q

Crohn’s treatment with Anti-TNFs

A

mod-severe disease

1/3 of patients lose response due to development of antibodies

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35
Q

Anti-TNF AEs

A

Infection due to suppression of T-helpers, development of antibodies (prescribe w/ methotrexate), increased risk of lymphoma, delayed serum-sickness

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36
Q

Anti-integrin MOA (natalizumab/vedolizumab)

A

Prevents binding to vascular adhesion molecules and migration into surrounding tissue

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37
Q

Anti-integrin uses

A

Refractory crohns

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38
Q

Anti-integrin AEs/monitoring

A

Risk of opportunistic infection

Monitor brain MRI, mental status, leukoencephalopathy

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39
Q

Vedolizumab vs Natalizumab

A

Vedolizumab doesn’t cause leukoencephalopathy (selectively blocks in gut not brain)
Used for crohns AND UC

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40
Q

Ustekinumab MOA

A

Blocks interleukin activity by inhibiting receptors on Tcells, NK cells and antigen presenting cells

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41
Q

Ustekinumab AEs

A

antibody development, infection, nasopharyngitis, malignancy (SCC), neurotoxicity

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42
Q

What medications cause hyperprolactinemia?

A

risperidone is MC
phenothiazines, metoclopramide, antihypertensives, SSRIs, cocaine, HIV drugs
(treated with dopamine agonists)

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43
Q

GH deficiency diagnosis

A

Peak GH serum concentration <10 in 2 hours after treatment with GH
Reduced IGF
No gold standard test
Treat those with short stature

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44
Q

Growth hormone treatments (drugs and MOA)

A

Somatropin (recombinant GH) and mecasermin (recombinant IGF)
Regulate lipid and carb metabolism and lean body mass, and production of IGF in peripheral tissues
Required for normal growth

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45
Q

Somatropin indications

A 
Short stature (turner, Noonan, prader-willi), failure to thrive, small for gestational age
Children and adults
Can also be used for short bowel syndrome
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46
Q

Somatropin AEs

A

Generally well tolerated in adults

Pseudotumor cerebri, slipped capital femoral epiphysis, scoliosis progression, hyperglycemia

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47
Q

Somatropin Interactions

A

Glucocorticoids may inhibit GH effect

other hormones may close epiphysis too soon compromising height

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48
Q

Mecasermin Indications

A

Children unresponsive to GH therapy who are deficient in IGF1

49
Q

Mecasermin AEs

A

Anaphylaxis, hypoglycemia (take with a snack/meal), tonsillar/lymphoid hypertrophy, coarse facial features

50
Q

Drugs used for GH excess

A

Dopamine agonists (bromocriptine and cabergoline), GH antagonists (pegvisomant), somatostatin analogs (creotides)

51
Q

Diagnosis of excess GH

A

oral glucose tolerance test-acromegaly will continue to secrete GH (will also have excess IGF)

52
Q

Pros and cons of dopamine agonists

A

Less effective, but reduced cost and available orally

FIRST LINE in acromegaly (cabergoline>bromocriptine)

53
Q

Somatostatin analogs in GH excess

A

More effective than dopamine agonist

Reduces GH and normalizes IGF

54
Q

GH antagonist (pegvisomant)

A

Highly effective in normalizing IGF (most effective option)

55
Q

Dopamine agonist AEs

A

headache, dizzy, nervous, fatigue, nausea, abd pain, diarrhea, nasal congestion/thickened bronchial secretions
Infertility with bromocriptine
Decreased BP in cabergoline

56
Q

Somatostatin analog MOA

A

Inhibits release of GH, glucagon, insulin and gastrin

57
Q

Somatostatin analog uses

A

acromegaly

neuroedndocrine tumors

58
Q

Somatostatin analog AEs

A

Gallstones, cardiac arrhythmia/conduction, hypertension, subclinical hypothyroidism, abnormal glucose metabolism

59
Q

Pegvisomant MOA and Use

A

Inhibits IGF productions and blocks GH effect on tissues

Refractory acromegaly

60
Q

Pegvisomant AEs

A

Increased LFTs, flu like syndrome, edema, nausea, diarrhea

61
Q

Persistent acromegaly treatment in men and postmenopausal women/ breast cancer pts

A

Selective estrogen receptor modulators (raloxifine and tamoxifen)- reduce IGF

62
Q

Hyperprolactinemia treatment

A

Dopamine agonists #1 (bromacriptine< cabergoline)
radiation +surgery
transphenoidal removal only if meds don’t work

63
Q

Panhypopituitarism Treatment

A

Lifelong replacement therapy of any hormones not secreted naturally, constant monitoring

64
Q

Drugs for hypothyroidism

A

Levothyroxine (synthetic T4)
Check TSH again in 4-5 weeks (7 day half life)
*T4 relationship with TSH is NOT linear!

65
Q

Drugs for hyperthyroidism

A

PTU (propothyrouracil) and MMI (methimazole)-thiourea drugs; PTU 1st line only in 1st trimester, otherwise MMI is 1st line
Used in kids and pregnancy (instead of surgery/radiation)
Iodide

66
Q

Thyroxine AEs

A

Heart failure, angina pectoris, MI remodeling of cortical and trabecular bone>reduced bone density
These are all with excessive doses*

67
Q

PTU/MMI AEs

A

Rash, benign transient leukopenia, agranulocytosis, arthralgia, lupus like syndrome, hepatotoxicity (more in PTU)
MMI teratogenic

68
Q

Dosing of hypothyroidism

A 
White always 50 mcg (least allergenic)
Average dose is ~125mcg/day (1.6 mcg/kg)
-young, healthy: start at 50, increase to 100 after 1 month
-elderly or CV risk: start at 25 mcg
Increase by 12.5-25 mcg each time
69
Q

dosing of hyperthyroidism

A

-PTU: 300-600 mg/day (in 3-4 doses); in pregnancy start at 300 and taper to 50-150/day to prevent fetal goiter
-MMI 30-60 mg/day in 2-3 doses (MMI is more potent)
Usually works in about 4-8 weeks, changes made on monthly basis

70
Q

Hyperthyroidism treatment in pregnant patient?

A

Average dose increases 25-50% (usually 2 extra tabs/week)
Monitor monthly during first trimester and 6 weeks postpartum
-1st tri: TSH 2-2.5
-2nd tri: TSH <3
-3rd tri: TSH <3.5

71
Q

levothyroxin as suppressive

A

Used in thyroid cancer: high risk we want TSH below 0.1, low risk we want it 0.1-0.5
To promote growth and function in abnormal thyroid tissue

72
Q

T3 vs T4

A

T4 is produced more in the body (thyroid gland only) but T3 is the active one, most of it comes from breakdown of T4

73
Q

Thyroid disorder labs

A
  • Hypo: high TSH, low T4
  • Secondary hypo: normal TSH with low T3/4
  • Hyper: low TSH with high T3/4
74
Q

What medications cause falsely high TSH?

A

Amiodorone* (blocks T4 to T3)
Estrogen/androgen excess
dopamine antagonists, salicylates, phenytoin

75
Q

Levothyroxine Interactions

A

Food impairs absorption- take on empty stomach and not with calcium, sulfate or other drugs (PPIs, H2 blockers, seizure meds)-4 hours!
Decreased sensitivity to warfarin

76
Q

Thiourea drugs MOA

A

Inhibit coupling of mono and diiodotyrosine to form T4/3 (preventing formation)
Diverts iodine from iodination sites

77
Q

Adjunctive therapy for hyperthyroidism

A

Propranolol (with PTU or MMI) for symptoms like palpitations, anxiety, tremor, heat intolerance (caution w/ asthmatics!)

78
Q

Iodide Uses/MOA

A

Graves’s disease
Blocks thyroid hormone release and inhibits thyroid hormone biosynthesis, decreasing size and vascularity of gland (symptoms improve within 2-7 days)

79
Q

Downside to iodide treatment

A

T3/4 still synthesized, just not released so gland has a lot of stored hormone

80
Q

Potassium iodide dosing

A

administered 7-14 days pre-op for graves after RAI/SSKI treatment

81
Q

Iodide AEs

A

Salivary gland swelling, Iodism (metallic taste, burning mouth/throat, sore teeth/gums, gynecomastia)

82
Q

Radioactive iodine

A

Cure of hyperthyroidism but causes permanent hypothyroidism

No pregnancy/breastfeeding for 6-12 months after

83
Q

What is the best treatment for toxic nodules and toxic mulitnodular goiter?

A

radioactive iodine

84
Q

Thyroid storm drug treatment

A

corticosteroids

85
Q

Treatment of hypoparathyroidism

A

Serum calcium/magnesium/ phosphate/creatine maintenance, calcitriol (vitamin D), phosphate binders PRN, thiazide diuretics

86
Q

Treatment of primary hyperparathyroidism

A

Operative management is curative

Otherwise bisphosphonates

87
Q

Treatment of secondary/tertiary hyperparathyroidism

A

secondary: calcium, vitD, phosphorous binding agents, calcimimetic
3: no treatment

88
Q

Cortisol pharmacokinetics

A

SHORT half-life-1.5 hours (hydrocortisone’s longer)

metabolized in liver, excreted in urine

89
Q

Adrenal crisis

A

Emergency state due to insufficient cortisol; low BP, dehydration, hyper pigmentation

90
Q

Treatment of adrenal crisis

A

Fluids and vasopressors first, if not responsive then IV hydrocortisone 100-300mg increasing Q6-8H, oral fludrocortisone added as hydrocortisone tapered off

91
Q

Fludrocortisone MOA/AEs

A

Agonist of mineralocorticoid receptors, activates glucocorticoid receptors
Causes edema, CHF, salt/fluid retention
Long duration of action!

92
Q

Addisons Disease

A

Dysfunction or absence of adrenal cortices

Hyperpigmentation, hypotension, small heart, low sodium, high potassium, calcium and BUN

93
Q

Treatment of addisons disease

A

Oral hydrocortisone 15-30mg 1st line (can use pred) +/- fludrocortisone (change dose of F but H stays the same)
-DHEA every morning

94
Q

Fludrocortisone dose changing in Addison’s treatment

A

Increased if: hypotension, hyponatremia, hyperkalemia, fatigue
Decreased if: edema, hypokalemia, hypertension

95
Q

DHEA

A

Improved sense of well being, increased muscle mass, reversal of bone loss at femoral neck
Monitor women for androgenic effects

96
Q

Treatment of Addison crisis

A

Aggressive IV saline, glucose, glucocorticoids

97
Q

Cushing’s syndrome vs disease

A

Syndrome is from exogenous steroid, disease is from over production of ACTH
Both have: hirsutism, purple striae, buffalo hump, hyperglycemia, hypokalemia

98
Q

Treatment of Cushing’s Syndrome

A

Surgery or meds-Metyrapone, ketoconazole, mitotane, mifepristone, cabergoline, pasireotide

99
Q

Hyperaldosteronism Treatment

A
  • Amiloride, eplerenone or spironolactone

- Watch for hyperkalemia and GI discomfort, monitor renal function

100
Q

Mechanism of teratogenesis

A

Caused by cytotoxicity

  • Some agents directly interact with DNA
  • some affect angiogenesis during development
  • some inhibit enzymes for organ development
  • nutrient and vitamin deficiencies can be teratogenic
101
Q

Which drug is the most famous teratogen?

A

Thalidomide

102
Q

Thalidomide Uses and Deformities caused

A 
Anti-emetic and sleep aid
Limb defects (phocomelia) when exposed in first trimester (inhibits angiogenesis during limb bud formation)
103
Q

FDA Pregnancy Categories

A

Pregnancy, lactation, females and males of reproductive potential (contraception, infertility, etc)

104
Q

Antiepileptic teratogenic drugs and effects/prevention

A

Carbamazepine, phenytoin, valproate

  • cause craniofacial and limb defects, fetal hydantoin syndrome (from phenytoin in any trimester)
  • use lowest dose and prescribe with folic acid
105
Q

Valproate neural tube defects

A

1st trimester exposure: small mouth, developmental delay, narrow forehead, flat philtrum

106
Q

Carbamazepine neural tube defects

A

about 1% risk; 10 times background rate

First trimester exposure!

107
Q

Isotretinoin teratogenic effects/prevention

A 
Cause miscarriage (40%), CNS, craniofacial (external ear defect/absence) and congenital heart defects, mental retardation, hydrocephalus, hypertelorism, clefts
Avoid pregnancy (bad through entire pregnancy)
108
Q

Anticoagulant teratogenic effects/prevention

A

Fetal warfarin syndrome

-switch anticoagulant before pregnancy (low molecular weight heparin is good)

109
Q

Fetal warfarin syndrome

A

From 1st trimester exposure

-nasal hypoplasia, calcific stippling of epiphysis, short stubby fingers

110
Q

Warfarin teratogenic effects after first trimester

A
  • 2nd semester causes: CNS defects from in utero hemorrhage w/ scarring; bone defects-dwarfism, scoliosis, skull defects
  • 3rd trimester: risk of bleeding, discontinue 1 month before delivery
111
Q

Lifestyle teratogens

A

Alcohol use
Obesity (can cause DM, HTN, VTE in baby)
Smoking

112
Q

Teratogenic effects of alcohol

A

IUGR and postnatal growth retardation, microcephaly, mental retardation, facial abnormalities (small eyes, smooth philtrum, thin upper lip, etc)

113
Q

ACE and ARBs teratogenic effects

A
  • Congenital renal failure reflecting fetal hemodynamic effect of ACE inhibition or angiotensin blockade
  • hypocalvaria
  • Entire pregnancy but esp 2nd and 3rd
114
Q

Methotrexate Teratogenic effects

A

Embryopathy (microcephaly, short limbs, IUGR, hypo plastic skull with wide fontanels and craniosynostosis)
Worst in first trimester

115
Q

Diethylstilbestrol (DES) teratogenic effects

A
  • Clear cell vaginal adenocarcinoma, premature labor in female offspring, hypospadias in male offspring
  • Bad in entire pregnancy
116
Q

Tetracycline teratogenic effects

A
  • Bad through entire pregnancy
  • Discolored teeth from deposition of antibiotic, altered bone growth
  • Doxy is the best option but can still produce staining
117
Q

Smoking teratogenic effects

A

Bad through whole pregnancy

IUGR, premature birth, SIDS, perinatal complications

118
Q

Somogyi Effect

A

rebound effect of high glucose from untreated nighttime hypoglycemia between 1-4AM; wake up and check BS at around 3 AM and eat snack if needed

Pharmacology (7 decks)

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