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29 Cards in this Set

  • Front
  • Back
Hypothyroidism
deficient thyroid hormone production

results in slowing down of all body f(n)s

more common in women
Hypothyroidism

Types
primary-thyroid gland failure (common)
--Hashimoto's dz-90% of primary cases

secondary-pituitary failure

tertiary-hypothalamic failure

iatrogenic-follows exposure to radiation

other-thyroidectomy, iodine deficiency
Hypothyroidism

presentation
SX include
- cold intolerance
- fatigue, somnolence
- constipation, menorrhagia, myalgias
- hoarseness
SIGNS include:
- thyroid gland enlargement or atrophy
- bradycardia
- edema
-dry skin
- wt gain

Myxedema coma is end stage
Hypothyroidism

Pathophys
- T4 (thyroxine) secreted by thyroid
- T4 converted to more potent T3
(iodothyroxine) in tissue
- T4 secretion stimulated by TSH
- TSH secretion inhibited by T4
- negative feedback loop

- Hashimoto's dz is autoimmune
Hypothyroidism

Diagnosis
Plasma TSH levels are elevated in primary hypothyroidism

low plasma T4 confirms dx
Hypothyroidism

Treatment principles - doc
synthetic thyroxine (levothyroxine)
- 100 to 125 mcg PO QD
- 30 min before breakfast
- dec in elderly 50mcg qd
- goal is to maintain plasma TSH
in normal range
- change dose q6-8 weeks to optimize
- overtreatment = subnormal TSH
- leads to osteoporosis and a fib
Hypothyroidism

how long is one treated?
Lifetime
Levothyroxine drug interactions
antacids, BASs, sucralfate, Calcium, iron, decrease absorption of levothyroxine

separte by at least 4 hours
hypothyroidism

drugs
Levothyroxine (T4)
- Synthroid, Levothroid, Levoxyl, Unithroid
Thyro-Tabs

Desiccated thyroid USP
- Armour Thyroid
- Nature-Throid
- Westhroid

Liothyroine (T3)
- Cytomel
- Triostat

Liotrix (T4 and T3 4:1)
- Thyrolar
Hypothyroidism

monitoring
TSH q6-8weeks until normalized

S&Sx improve in a few weeks

TSH q 6 -12 months
desiccated thyroid USP
--use discouraged why

synthetic T3 (liothyronine)
--why not used often
b/c less predictable potency and stability


b/c T3 has shorter t1/2, higher incidence of cardiac s/e, and more difficult to monitor
Hyperthyroidism (thyrotoxicosis)

Types
Graves dz - most common cause

Toxic multinodular goiter (MNG)

amiodarone
idodine
Hyperthyroidism

Presentation
SX
-heat intolerance
-wt loss
-weakness
-palpitations
-anxiety

SIGNS
-tremor, tachycardia, weakness
-eyelid lag, warm, moist skin
-afib, CHF
Hyperthyroidism

Pathophys
Graves
-autoimmune dz that produces thyroid
stimulating antibodies that mimic TSH

MNGs
-masses of thyroid tissue that secrete
thyroid hormones independent of
pituitary control
Hyperthyroidism

Diagnosis
elevated t4 or t3 in presence of decreased TSH
Hyperthyroidism

treatment
3 methods:
1) surgery

2) radioactive iodide (RAI)
-treatment of choice in Graves and MNG

3) antithyroid (thionamide) drugs
-propylthiouracil (PTU) preferred in
pregnancy
-have no permanent effect on thyroid fn

adjunctive tx
BBs and CCBs to control tachycardia
Adrenals

Cushing's Syndrome
chronic glucocorticoid (GCC) excess

Types
- iatrogenic due to tx w/GCCs
- endogenous due to overproductoin of
adrenocorticotropic harmone (ACTH)
by pituitary gland adenomas
Adrenals

Cushing's presenation
*obesity - face, neck, trunk, abdomin
*HTN
*hirutism
*acne
*amenorrhea
*depression
*thin skin
*easy bruising, DM, osteopenia
Adrenals

Cushing's pathophys
hypothalamus produces corticotropin -
releasing hormone (CRH)

CRH stimulates anterior pituitary to release ACTH

ACTH stimulates adrenal cortex to produce cortisol
Adrenals

Cushing's treatment principles
iatrogenic
- minimization of corticsteroid exposure
is essential

Pharmacotherapy is aimed at dec ing
cortisol production or act'y w/drug, radiation, or surgery
Cushing's Drugs
ketoconazole (Nizoral)

aminoglutethimide (Cytadren)

mitotane (Lysodren)

metyraone (Metopirone)
Hyperthyroidism

thionamides a/e / monitoring
may cause agranulocytosis and cirrosis so pts must see physician if have fever, sore throat, abdominal pain, jaundice
Adrenals

adrenal insufficiency
Addison's disease
-autoimmune mediated destruction of the
adrenal cortex leads to glucocorticoid
and mineralocorticoid deficiency
Addison's dz

presentation
Glucocorticoid deficiency
-wt loss
-malaise
-abdominal pain
-depression

minearlocorticoud deficiency
-dehydration
hypotension
hyperkalemia
salt craving
Addison's

pathophys
- adrenal cortex synthesizes cortisol (requires ACTH)
- adrenal cortex secretes aldosterone, cortisol, and androgenic hormones
- mineralocorticoids (eg aldosterone) enhance reabsorption of na and water and increase urinary potassium excret

glucocorticoids
- affect glucose, CHO, and fat metab
- produce anti-inflammatory effects
- produce immunosuppresive effects

chronic admin of corticosteroids inhibits pituitary ACTH and therefore cortisol (ie Hypothalamic-pituitary-adrenocortical (HPA) axis suppresion)
Treatment of Addison's
lifelong glucocorticoid and mineralocorticoid replacement
Addisons

DOC for acute adrenal crisis
hydrocortisone 100mg IV q8h
Corticsteroids
cortisone (Cortone)
Hydrocortisone (Cortef, Hydrocortone)
prednisone (Deltasone)
prednisolone (Prelone, Delta-Cortef)
methylprednisolone (Medrol)
triamcinolone (Kenalog, Aristocort)
dexamethasone (Decadron, Dexone)
betamethasone (Celestone)
fludrocortisone (Florinef)
Miscellaneous Endocrine Drugs

What are the following used for:
1. cosyntropin (Cortrosyn) and
corticotropin (Acthar ie ACTH)


2. vasopressin (Pitressin)
desmopressin (Stimate ie DDAVP)
1. dx of adrenal indufficiency

2. Vasopressin:
- diabetes insipidus, v fib, shock,
variceal hemorrhage

Desmopressin:
- nocturnal enuresis, diabeter insipidus,
hemophilia A, von Willebrand's dz