9. Thyreotoxicosis - classification, clinical manifestation Flashcards
describe the hypothalamus - pituitary - thyroid axis ?
1) hypothalamus release - TRH (thyrotropin releasing hormone ) - which goes to the pitutory gland
2) to stimulate - TSH (thyroid stimulating hormone)
3) TSH = goes to the thyroid gland =
and also stimulates the uptake of iodine
follicular lumen of the thyroid gland called the colloid
colloid contain thyroglobulin
thyroglobulin is attached to either there (T3) or four (T4) iod atoms
by the enzyme thyroid peroxidase (TPO)
TPO also converts the iodine absorbed from the gastrointestinal tract to iod
t3 nd t4 released
4) T4 in the blood is converted to T3 by
TETRA IDO THYRONINE 5 DEIODINASE
5) the T3 has target tissues such as the heart , the liver , the bones and CNS
= increase hr
increase catabolism of carb and protein
sympathetic effect of nervous system by catecholamines
increase bp
increase ventilation
large number aof T4 converted to reverse T3 = INACTIVE
high T3 and T4 acts as a negative effect on thyroid gland and pituitary gland
regulation of T3 and T4 occurs in what ways ?
hypothalamus pituory axis thyroid axis
and serum iodine
- high levels of iodine - decrease uptake of iodine - decrease t3/t4
vice vesa
how is T3 and T4 transported in the blood ?
TBG = thyroxine binding globulin
transthyretin (t4)
albumin
only free T3 and T4 can exert any function
how do we screen for thyroid dysfunction ?
hypo and hyperthyroidism is done by screening TSH levels
overt hyperthyroidism
increase FT4 AND FT3 and very low TSH
subclinical hyperthyroidism
normal FT4 FT3
and low TSH
normal TSH
0.4 - 2.5 mIu/L
subclinical hypothyroidism
normal FT4 AND ft3
increased TSH
overt hypothyroidism
decrease FT4 AND FT3
really increased TSH
GOITER which is an enlargement of the thyroid gland can be divided into what ?
diffusely enlarged thyroid gland
more than 18ml women
more than 25ml men
struma diffusa
struma nodosa
thyroid gland with nodules but the size might be normal
Euthyroid struma nodosa (euthyroid nodular goiter) can be shown with normal thyroid function = most common
hypothyroidism
hyperparathyroid
what is the cause of goiter ?
most cases iodine deficiency = compensatory goiter = help produce normal t3 and t4 levels , despite iodine def
= resulting in normal function of thyroid even with goiter = most cases
compensatory goiter can even lead to hyperthyroidism even in the midst of iodine def ?!
in continuous iodine def = autonomic nodules = produce t3 and t4 without stimulated by TSH
TSH receptor stay activated all the time
= autonomic nodule develop
hashimoto
graves
adenoma
carcinoma
what are the signs and symptoms of euthyrodism of struma nodosa?
enlarged thyroid gland palpated = pressure in neck disturbs swallowing and breathing
hoarseness - compression of n recurrent - if malignant growth
no other symptoms because T3 AND T4 normal
what is the treatment of iodine def ?
potassium iodine and levothyroxine
what is thyrotoxicosis ?
clinical syndrome when tissues are exposed to high levels of circulating thyroid hormones
what is the classification os thyrotoxicases by ETIOLOGY ?
HYPERTHYROIDISM (A)
EXOGENOUS HORMONES AND THYROID DESTRUCTION NO HYPERTYROIDISM (B)
what are the different causes which can cause hyperthyroidism thyrotoxicosis ?
1) diffusely toxic goiter = only in graves disease / basedow disease
(can be nodules)
2) autonomous toxic goiter
a) multi nodular struma goiter = PLUMMER DISEASE
due to iodine deficiency
single hyper functionng = toxic adenoma
3)Iodine-induced thyrotoxicosis A condition of thyrotoxicosis that develops in iodine-deficient individuals with thyroid abnormalities after administration of iodine
how does THYROID DESTRUCTION cause thyrotoxicosis?
inflammation destroys the follicular cells and all the
stored T3 and T4 is released from them
this will lead to a transient (tempoäre)
thyrotoxicosis
here the production is normal and thus we do not call it hyperthyroidism
what are the thyrotoxicosis caused by non hyperthyroidism and destruction or exogenous hormone consumption ?
exogenous thyrotoxicosis
levothyroxine(iodine intake) in patients with hypothyroidism
or t3 and t4
subacute de quervian thyroiditis = or subacute granulomatous thyrodidtis
(giant cells histologically)
transient thyrotoxcosis by hashimoto thyroiditis
what are the signs and symptoms of de quervian(Subacute granulomatous thyroiditis) ?
subacute onset within couple of days
slightly enlarged thyroid - which is DIFFUSE AND FIRM
severe pain in throat , ear and jaw
difficulty swallowing
its a cycle of hyperthyroidism to euthryosisim and hypothyroidism
what is the difference between A and B thyrotoxicosis ?
A - high radioactive iodine uptake
B - low radioactive iodine uptake
what are the clinical manifestation of thrytoxicosis ?
increased basal metabolic rate - heat and sweating intolerance
weight loss
accelerated insulin and insulin resistance
CV - supraventricular tachycardia = atrial arrhythmia
high systolic and low diastolic pressure = high myocardial contractilitya nd decreased peripheral resistance = widening of pulse pressure
nervous system = activation of sympathetic nervous system = tremor , nervous , anxiety , hunger , hyper reflexibility
SLEEP DISTURNANCE
gastrointestinal = weight reduction despite increased appetite , diarrhea
eyes :
NOT GRAVES DISEASE=
lid lag
lid retraction
GRAVES :
- exophthalmus = ssh receptor antibodies stimulates the muscles of the eyelid to contract
- erythema and edema of the eyelids and conjuctiva
- double vision = extra ocular muscles inflammation and fibrosis
decrease eye motility
increased pressure around optic nerve and corneal ulcerations
thyrotoxic myopathy =proximal muscles of the limbs atrophic and weak due to protein catabolism
periodic paralysis
osteoporosis due to the direct effect of T3 on osteoclastic bone resorption , fractures (in the elderly) = hypercalcemia and hypercalciurea
skin and hair hair loss thinning of skin cutaneous vasodilation and excessive sweating = warm and moist skin soft nails
reproductive
oligomeorrhea , reduced fertility
men = gynecomastisa and impotent
what is the diagnosis of thyrotoxicosis ?
iodine induced = different
palpations
graves disease - diffuse and soft goiter
toxic multi nodular goiter /plummer disease
multi nodular
de quervian thyroiditis/ subacute granulomatous thyroiditis
= diffuse and firm
in all reduced TSH = suppressed due to negative feedback
de quervian - in thyrotoxic phase increase in TSH (opposite in hypothyroidism phase)
in all suppressed TRH
FREE!! T4 AND T3 = increased
plummer disease = MAINLY T3 ELEVATED
scintigraphy
radioactive iodine uptake scintigraphy =
graves - high diffuse uptake
plummer - Hot areas’ or ‘areas of uptake’ describe areas that are using the most iodine and show up black on imaging. ‘Cold areas’ or ‘inactive areas’ describes areas that are not using iodine as much, and show up white on imaging. The scintigraphy report shows some ill-defined hot areas and an overall irregular dispersal of hot and cold areas. This describes a ‘patchy uptake’ picture
thyroid destruction = reduced
iodine induced - reduced
Hot nodules indicate autonomously functioning nodules, warm nodules suggest normal thyroid function, and cold nodules indicate hypofunctional
autoimmune
TSH receptor antibodies = TRab = only in graves disease
TSI - thyroid stimulating gig antibodies = in graves = causing the diffuse enlargement
TPO antibodies = in graves but higher in hashmito thyroiditis
thyroglobulin antibody - graves disease
slightly MORE hashimoto slightly
sodium iodine symporter antibodies = graves disease
ultrasound
nodules or enlargement
graves : Thyroid gland is often enlarged and can be hyperechoic
Results depend on the form of Hashimoto thyroiditis.
Atrophic phenotype: reduction in thyroid size (mainly observed)
Goitrous phenotype: heterogeneous enlargement
Increased perfusion: either diffuse (Graves disease, toxic adenoma) or nodular (toxic MNG)
Decreased perfusion:
——–
thyroid fine needle aspiration
hashimoto : Diffuse lymphocytic infiltration (cytotoxic T lymphocytes) with germinal center, oncocytic-metaplastic cells (Hurthle cells) and fibrotic tissue
autoimmune :lymphocytic infiltration of gland
the severity of the thyrotoxicosis depends on and how do you classify it ?
heart rate , weight loss , fatigue and neurological symptoms
mild
HR below 100
10 percent weight reduction
fatigue in afternoon
moderate
100-120
10-20 percent
heavy fatigue
severe ( PRECRISIS)
above 120
20-50 percent
somnolence
what are the complication os thyrotoxicosis ?
thyrotoxicosis cardiomyopathy = erm arrhythmia
heart failure
thyrotoxicosis cris above 39 degrees committing jaundice tachyarrythmia restlessness delirium
what is the treatment for thyrotoxicosis ?
thionamides
= propylthiouracil (PTU) , methimazole , carbimazole
- inhibit TPO function
propylthiouracil inhibit deionisation of T4 and T3
betal blockers = propranolol / metoprolol
decrease sympathetic activity
block T4 to T3 conversion in periphery
radioactive iodine therapy - graves
radioactive iodine ablation= plummer wilson and toxic adenoma
and thyroid surgery for large goiters plummer and if there is graves disease orbitopathy
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THIONIMIDES NOT USED FOR SUBACUTE DE QUERVAN - BUT BETA BLOCKERS ARE
neither used for HASHIMOTO
what are the side effects of thionamides ?
agranulocytosis ,aplastic anemia , fever , abnormal taste
serious - hepatitis , acute liver failure , lupus like syndrome , vasculitis
The thyrostatics can only be taken for how many years ?
1- 1 1/2 years, because of the liver
toxicity and risk of agranulocytosis
when is surgery indicated ?
failure of drug treatment with recurrence of the disease
serious side effects of thionamide treatment
very enlarged and nodulated goiter
toxic adenoma !!!
suspicion of malignant thyroid tumour
moderate to severe Graves’ ophthalmology
what is the complication of surgery ?
hypothyroidism
vocal cord paralysis - recurrent laryngeal nerve
hypoparathyroidism with hypocalcemia
contra of radioactive iodine uptake ablation
Pregnant/breastfeeding women
Children < 5 years of age
Initial treatment for confirmed or suspected thyroid malignancy
Moderate to severe Graves ophthalmopath
