Thyroid Deck 2 Flashcards

1
Q

Methimazole 10 to 50

A

10-50 times more active than propylthiouracil

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2
Q

Methimazole completely

A

Completely absorbed, but at variable rate

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3
Q

Methimazole slower

A

Slower excretion: 60-75% in urine in 48h

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4
Q

Methimazole half life

A

Half-life 6 hours

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5
Q

Methimazole onset of effects

A

Onset of effects in 1 week, peak 4-10 weeks

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6
Q

Methimazole crosses

A

Crosses placental barrier, caution in pregnancy

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7
Q

Methimazole is not

A

protein-bound

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8
Q

Propylthiouracil (PTU) rapidily

A

Rapidly absorbed, reaches peak after 1 hour

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9
Q

Propylthiouracil (PTU) incomplete

A

Incomplete absorption

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10
Q

Propylthiouracil (PTU) eliminated

A

Eliminated by kidney within 24 hours

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11
Q

Propylthiouracil (PTU) onset

A

Onset of effects in 10-21d, peak in 6-10 weeks

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12
Q

Propylthiouracil (PTU) crosses

A

Crosses placental barrier, but more highly protein-bound so crosses
less readily

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13
Q

Propylthiouracil (PTU) not secreted

A

Not secreted in breast milk in sufficient quantities to preclude breast
feeding

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14
Q

Adverse Effects of Thiourelynes or Thioamides

A
  • Maculopapular pruritic rash
  • Alopecia
  • Drowsiness, headaches
  • Fever, arthralgias
  • Nausea and vomiting
  • Nasal stuffiness
  • Transient leukopenia
  • Agranulocytosis (infrequent, but potentially fatal)
  • Renal/hepatic failure
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15
Q

Monitoring Thiourelynes or Thioamides

A

• Thyroid studies, complete blood count (CBC), liver/renal
panels before starting drug
• Recheck in 1 to 2 months after starting drug.

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16
Q

Interactions Thiourelynes or Thioamides

A

• Don’t use with decongestants; vasopressor action not
well tolerated
• Lithium
• Warfarin
• Antidiarrheals: Kaolin action interferes with absorption

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17
Q

Corticosteroids two types

A

Glucocorticoids and Mineralcorticoid

18
Q

Glucocorticoids role in

A

Adrenal cortex origin

19
Q

Glucocorticoids originate in

A

Adrenal cortex origin

20
Q

Glucocorticoids structure

A

Steroidal structure

21
Q

Glucocorticoids part of the body

A
Part of body’s FB loop to reduce
inflammation
• Anti-inflammatory
• Immunosuppressive
• Antiproliferative
22
Q

Glucocorticoids unique

A

receptors different from sex

steroids and mineralcorticoids

23
Q

Mineralcorticoid class of

A

Class of steroid hormones that cause

Na and H20 retention

24
Q

Mineralcorticoid primary example

A

Aldosterone comes from adrenal
cortex
• Essential to maintenance of
adequate fluid volume (CO/BP)

25
Q

Long acting glucocorticoid

A

Dexamethasone

26
Q

Glucocorticoid use in allergy and pulmonary

A

Asthma, allergic rhinitis, uricaria,anaphylaxis, food/drug

allergy

27
Q

Glucocorticoid use in skin

A

Acute severe dermatitis

28
Q

Glucocorticoid use in endocrinology

A

Adrenal disorders

29
Q

Glucocorticoid use in GI

A

IBD: Crohn’s Disease; ulcerative colitis

30
Q

Glucocorticoid use in hematology

A

Leukemia, lymphoma

31
Q

Glucocorticoid use in ophthalmology

A

Uveitis

32
Q

Glucocorticoid use in rheumatology

A

RA, SLE, vasculitis

33
Q

Glucocorticoid other use

A

MS, organ transplant, nephrotic syndrome, cerebral

edema

34
Q

crushing’s syndrome S/S

A
C – Cataracts
U – Ulcers
S – Striae, Skin thinning
H – Hypertension, Hirsutism
I – Immunosuppression, Infections
N – Necrosis of femoral heads
G – Glucose elevation
O – Osteoporosis, Obesity
I – Impaired wound healing
D – Depression/mood changes
35
Q

Addison’s disease is an

A

Impaired adrenocortical hormone synthesis
• Primary: adrenal steroidogenesis impairment
• Secondary: pituitary adrenocorticotropic hormone deficit
• Tertiary: hypothalamic corticotropin-releasing hormone deficit

36
Q

Symptoms of Addisons Disease

A

Low BP, HypoNa, HyperK+, Hypoglycemia, fatigue, anorexia, weight loss, hyperpigmentation

37
Q

Initial testing for adisons diseas

A

AM cortisol, Low DHEA-S for age and sex, ACTH test, BUN, CBC, Electrolytes plasma aldosterone
(renin)

38
Q

Treatment for Addisons disease

A

Treatment –Glucocorticoid replacement; Individualize!
• Challenges
• Inability to replicate circadian cortisol rhythm
• Uncertainties in dose adjustment and treatment monitoring
• Side effects of inadequate replacement; reduced QOL

39
Q

Tapering Corticosteroids there is no

A

standard taper

40
Q

Tapering Corticosteroids required if

A

Required if more than 2 weeks continuous

glucocorticosteroids

41
Q

Tapering Corticosteroids longer taper for

A

Longer taper for higher doses and longer-acting systemic
glucocorticoids
• Weeks to months to allow recovery of H-P-A axis