11_01 Exam 6 - Adrenal

Follicles or follicular cells

Collect and transport iodine to the colloid

Regulate the release of thyroid hormones into the circulation.

Colloid

Synthesize thyroid hormones

Thyroglobulin

Glycoprotein (within colloid) containing tyrosine residues for thyroid hormone synthesis.

150mcg

iodide -> iodine (thyroid) - - -conv to iodide

iodine binds at 3 position = MIT
MIT iodized at 5 = DIT
2 DIT = 1 T4
MIT+DIT = T3

100%
20% 80%

protein bound

TSH, anterior pituitary

na

HT makes TRH
Ant Pit makes TSH

T4 -> T3 in the tissues NOT the glands

TRH from ht, triggers TSH which stims thyroid to make T3 and T4, high levels of both T3 and T4 then neg fb to TSH and TRH

Normal HypoT HyperT
TSH 0.5-5 high low
T4 0.8-2.7 low high
T3 60-181 low high
RAIU% 10-30 high


think! if hyperT - Thyroid will release less TSH b'c too much T3/4 around and vice versa for hypoT

Grave’s disease 3/1000
Activates receptor in the same way as TSH.

enlarged gland 2-3x normal size

Exophthalmos (bug eye), thyroid acropachy (club fingers), or pretibialmyxedemai (non pitting)


Increased T3 > T4

Increased free T4

TSH undetectable (< 0.1)

Negative feedback from high thyroid hormones

High RAIU

Thyroid gland overproducing

surgical - effective but invasive
radiactive - lifelong replacement
meds - low cure rate ~50%
pretreat for radioactive iodine

Propylthiouracil(PTU)Methimazole (MMI)

--Inhibit coupling of MIT and DIT to form T4to T3
--Inhibit peripheral conversion of T4to T3 (PTU only)

Cross the placenta and excrete in breast milk.

300-600 / 1200 mg/day
30-60 / 120 mg/day

Clinical effects seen with 4 to 8 weeks.

SERIOUS
AGRANULOCYTOSIS - <3mos thpy
HEPATOXICITY - < 3 mos thpy

MINOR
RASH= pruritic maculopapular (transient)
Artharalgia - >6mos thpy
fever
leukopenia

only if SEs were mild.

Acutelyblock thyroid release.

Inhibit thyroid hormone biosynthesis.

Decrease the size and vascularity of the thyroid gland.

SSKI, Lugols

used as adj thpy to surgery and RAI surgery

best candidates
-graves disease
-post RAI therapy
-thyrotoxic
-decompensated cardiac fx
sxs improve >7days

BBs W/CCB AS BACKUP

Beta-blockers: propranolol, nadolol

Adjunctive therapy to antithyroid drugs, RAI therapy, preparation for surgery, or in thyroid storm.

Effective for thyrotoxicsymptom relief such as palpitations, anxiety, tremor, and heat intolerance.

Partially block conversion of T4to T3

Little overall therapeutic effect.

Dosing:

Propranolol20 –40mg 4x/day

Nadolol40mg 2x/day

Titrate to response

Mechanism of action
131I incorporated into thyroid hormone and thyroglobulin
Follicular damage and necrosis
Small vessel destruction within the gland

Dosing
Colorless, tasteless liquid
Clinical impact seen in weeks
4000 to 8000 rads x 1 – may repeat in 6 months
80 – 120 mcCi / g of tissue

Best Candidates
Graves' Disease
Toxic autonomous nodules
Toxic multinodular goiter

Initial transient increase in TH due to release of stored hormone.
Patients with a cardiac history and elderly patients should receive a thionamide prior to (and occasionally after) RAI ablation
Usual practice is to discontinue thionamide 4 – 6 days prior to RAI and re-institute 4 days post RAI
Gland tenderness
Dysphagia

mos to yrs
prego
8 days
drink water

Common is Grave’s disease
Life-threatening: ~ 20% mortality with treatment
Fever (> 103F), tachycardia, tachypnea, dehydration, delirium, N/V, diarrhea, coma
Average duration 72 hours; can last up to 8 days.
Aggressive treatment can lower mortality rate by 20%.
Precipitants
Infection
Trauma
Surgery
RAI treatment
Withdrawal from antithyroid medications

mos to yrs
prego
8 days
drink water

Common is Grave’s disease
Life-threatening: ~ 20% mortality with treatment
Fever (> 103F), tachycardia, tachypnea, dehydration, delirium, N/V, diarrhea, coma
Average duration 72 hours; can last up to 8 days.
Aggressive treatment can lower mortality rate by 20%.
Precipitants
Infection
Trauma
Surgery
RAI treatment
Withdrawal from antithyroid medications