Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

endocrinology > 9. Thyreotoxicosis - classification, clinical manifestation > Flashcards

9. Thyreotoxicosis - classification, clinical manifestation Flashcards

1
Q

describe the hypothalamus - pituitary - thyroid axis ?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

regulation of T3 and T4 occurs in what ways ?

A

hypothalamus pituory axis thyroid axis

and serum iodine
- high levels of iodine - decrease uptake of iodine - decrease t3/t4
vice vesa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how is T3 and T4 transported in the blood ?

A

TBG = thyroxine binding globulin
transthyretin (t4)
albumin

only free T3 and T4 can exert any function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how do we screen for thyroid dysfunction ?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

GOITER which is an enlargement of the thyroid gland can be divided into what ?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the cause of goiter ?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the signs and symptoms of euthyrodism of struma nodosa?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the treatment of iodine def ?

A

potassium iodine and levothyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is thyrotoxicosis ?

A

clinical syndrome when tissues are exposed to high levels of circulating thyroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the classification os thyrotoxicases by ETIOLOGY ?

A

HYPERTHYROIDISM (A)

EXOGENOUS HORMONES AND THYROID DESTRUCTION NO HYPERTYROIDISM (B)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the different causes which can cause hyperthyroidism thyrotoxicosis ?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does THYROID DESTRUCTION cause thyrotoxicosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the thyrotoxicosis caused by non hyperthyroidism and destruction or exogenous hormone consumption ?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the signs and symptoms of de quervian(Subacute granulomatous thyroiditis) ?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the difference between A and B thyrotoxicosis ?

A

A - high radioactive iodine uptake

B - low radioactive iodine uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the clinical manifestation of thrytoxicosis ?

A

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

17
Q

what is the diagnosis of thyrotoxicosis ?

A

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

18
Q

the severity of the thyrotoxicosis depends on and how do you classify it ?

A

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

19
Q

what are the complication os thyrotoxicosis ?

A

thyrotoxicosis cardiomyopathy = erm arrhythmia
heart failure

thyrotoxicosis cris 
above 39 degrees  
committing 
jaundice 
tachyarrythmia 
restlessness 
delirium
20
Q

what is the treatment for thyrotoxicosis ?

A

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

==============
THIONIMIDES NOT USED FOR SUBACUTE DE QUERVAN - BUT BETA BLOCKERS ARE
neither used for HASHIMOTO

21
Q

what are the side effects of thionamides ?

A

agranulocytosis ,aplastic anemia , fever , abnormal taste

serious - hepatitis , acute liver failure , lupus like syndrome , vasculitis

22
Q

The thyrostatics can only be taken for how many years ?

A

1- 1 1/2 years, because of the liver

toxicity and risk of agranulocytosis

23
Q

when is surgery indicated ?

A

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

24
Q

what is the complication of surgery ?

A

hypothyroidism
vocal cord paralysis - recurrent laryngeal nerve
hypoparathyroidism with hypocalcemia

25
Q

contra of radioactive iodine uptake ablation

A

Pregnant/breastfeeding women
Children < 5 years of age
Initial treatment for confirmed or suspected thyroid malignancy
Moderate to severe Graves ophthalmopath

endocrinology (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions