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Med Year 3 > Thyroid Disease > Flashcards

Thyroid Disease Flashcards

1
Q

anatomy of thyroid gland

A

anterior to trachea, below thyroid cartilage of larynx

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2
Q

what is the histology of the thyroid gland

A

colloid - resevoir hormone where thyroid hormones are made

columnair epithelium: thyroid follicular cells which make thyroglobulin

interspersed c-cells make: calcitonin

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3
Q

what is hypothyroidism

A

inadequate output of thyroid hormones by thyroid gland

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4
Q

what are the causes of hypothyroidism

A

hashimoto’s thyroiditis - auto immune inflammation of thyroid gland, associated with anti-thyroid peroxidase AB and anti-thyroglobulin AB

iodine deficiency

secondary to treatment of hyperthyroidism (carbimazole, PTU, thyroid surgery)

medications:
lithium inhibits production of thyroid hormones
amiodarone can cause thyrotoxicosis

pituitary - secondary hypothyroidism

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5
Q

what are the symptoms and signs of hypothyroidism

A 
weight gain
fatigue 
dry skin 
coarse hair and hair loss and nail changes 
cold intolerance 
fluid retention - oedema, ascites
heavy or irregular periods
constipation muscle cramps 
muscle weakness
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6
Q

what are the investigations for hypothyroidism

A

low free t3 and t4

TSH - high

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7
Q

management of hypothyroidism

A

oral levothyroxine (synthetic T4), 50-100mg

check T4 levels every 4 weeks and adjut in steps of 25ug

if pregnant; hypothyroid women need to have a higher dose

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8
Q

what are the side effects of levothyroxine

A

atrial fibrillation and osteoporosis

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9
Q

what is a myxoedema coma

A

severe hypothyroid state before death

what are the signs and symptoms often >65 years: hypothermia, hyporeflexia, decreased glucose, bradycardia, psychosis, coma, seizures

precipitants: thyroid surgery, radioidone, pituitary surgery.

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10
Q

what is the management of myxoedema coma

A

bloods for T4, T3, TSG, FBG, U&E, cultures, cortisol, glucose

ABG’s, for PaO2, high-flow o2 if cyanosed, may need ventilation

correct any hypoglycaemia
give liothyronine, 5-20 ug /12 h IV slowly, monitoring for precipitation of ischaemic heart disease

consider levothyroxine

give hydrocortisone 100mg/6h IV

treat suspected infection with co-amoxiclav 1.2g/8h IV

rehydrate with fluids, watching for cardiac dysfunction, inotropes may needed if BP does not respond

active warming if hypothermic

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11
Q

physiology of thyroid hormone synthesis?

A

HT releases TRH
APG release TSH
thyroig gland releases T4 and T4
iodide attaches to tyrosine (from thyroglobulin) to form MIT or DIT
hence forming either T3 or T4
transport in the blood bound to thyroid-binding globulin
more t4 is secreted but when they arrive at target cells t4 is converted to t3 because it is more active

-READ NOTES ON IPAD FOR MORE DETAIL

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12
Q

how does t3 act on target cells

A

binds to T3R, nuclear hormone receptor

binds to this, then binds to the DNA, causing gene transcription and producing mRNA

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13
Q

what effects do thyroid hormones produce

A

growth
increasing metabolic rate
CNS development
metabolism: increases o2 consumption, glc absorption and gluconeogenesis, lipolysis and protein synthesis,
CV: increases cardiac output and respiration

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14
Q

what is hyperthyroidism

A

overproduction of thyroid hormone by the thyroid gland

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15
Q

what is thyrotoxicosis and how is it different to hyperthyroidism

A

TTC is characterised by the clinical manifestations of high thyroid hormone ACTION in tissues

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16
Q

what is primary v secondary hyperthyroidism

A

primary: due to thyroid pathology
secondary: thyroid is producing excessive thyroid hormone as a result of overstimulation by TSH, so pathology is in HT or pituitary

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17
Q

what is grave’s disease

A

auto-immune condition where TSH receptor antibodies are abnormal, produced by the IS, that mimic TSH and stimulate TSH receptors on the gland causing hyperthyroidism

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18
Q

what are thyroid function tests

A

free T3, total T3, free T4, TSH
AB: TPO (antibodies against thyroid peroxidase: this is not normally present but if thyroid is destroyed then increased levels)

AB against TSH-R: AB may drive TSH for proliferation and indicates hyperactivity of follicular cells

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19
Q

what are the symptoms specific to grave’s disease

A

exophthalmos - bulging eyeball
pretibial myxoedema – mucin deposits under skin on front of leg as reaction to the TSH receptor AB
diffuse goitre
nail changes: thyroid acropachy

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20
Q

risk factors for graves disease

A

age: 40+

family history of any kind of immune disorder, eg coeliac or anything

21
Q

what is toxic multionodular goitre

A

cause of hyperthyroidism

nodules developing on the thyroid gland that act independently of the normal feedback system

continously produce excessive thyroid hormone

specific to:
goitre with firm nodules
most patients over 50

22
Q

what are the other causes of hyperthyroidism

A

solitary toxic thyroid nodule: single abnormal thyroid nodule acting alone to release thyroid hormone (benign adenomas usually)

thyroiditis: de quervains
viral infection with fever, neck pain, dysphagia
just need NSAID’s and beta blockers

thyroid storm

drugs: amiodarone and interferon

23
Q

what is a thyroid storm and what are the S&S

A

thyrotoxic crisis

symptoms: agitation and confusion, coma, tachycardia, diarrhoea and vomiting, goitre, thyroid bruit
causes: recent thyroid surgery, radioiodine, infection, MI, trauma

24
Q

how do you manage a thyroid storm

A

IV fluids
bloods for t3,t4, cultures
b blockers: propanolol, or diltiazem
antithyroid drugs: carbimazole, aqueous iodine
steroids: hydrocortisone or dexamethasone to prevent peripheral conversion of T4 to T3

25
Q

what are the signs and symptoms of hyperthyroidism

A 
anxiety and irritability
sweating and heat intolerance
tachycardia
weight loss despite good apetite 
fatigue
frequent loose stools
sexual dysfunction 
eyelid retraction
goitre
26
Q

risks and treatment of thyroid eye disease

A

intraocular pressure leading to optic nerve damage, corneal ulceration

treatments: steroids, immunosuppression, surgical decompression, radiotherapy

27
Q

CV effects of hyperthyroidism

A

higher pulse, BP

AF

28
Q

investigations of hyperthyroidism

A

free T4 and TT3 raised, suppressed TSH

29
Q

what is the first line management of graves; hyperthyroidism

A

CARBIMAZOLE:
treats patients with graves in 4-8 weeks

continue on maintenance carbimazole and either titration block or block and replace

complete remission usually within 18 months of treatment

side effects: neutropenia and agranulocytosis: see dr if sore throat

30
Q

what is the second line drug for hyperthyroidism

A

propylthiouracil
3x daily doses
remission less than carbimazole
side effects: rash, itching, nausea, agranuloyctosis, leukopenia

31
Q

what other treatments are there for hyperthyroidism

A

radioactive iodine:

beta and gamma emitter

drinking a single dose

taken up by thyroid gland and emitted radiation destroys proportion of thyroid cells

decrease of TH production

Remission can take 6 months = patients can be left hypothyroid and require levo
•Damages follicular cells
•As time increases, incidence of hypo after therapy increases to upto 80%

32
Q

how are beta blockers used in hyperthyroidism

A

blocks adrenalin related symptoms of hyper

propanolol: non-selectively blocks adrenergic activity as opposed to more selective ones that only work on the heart

33
Q

surgery for hyperthyroidism

A

remove whole thyroid or toxic nodules
effectively stops production of thyroid hormone, but will require levo

near-total thyroidectomy is standard
take T4 post op

34
Q

what is neonatal hyperthyroidism

A

thyroid stimulating antibodies in grave’s disease can cross the placenta and stimulate thyroid gland of fetus

35
Q

what is post-partum thyroiditis

A

inflamed thyroid within first year of child birth, can last weeks to months

1/3 of women develop permanent hypothyroidism

36
Q

what are the signs and symptoms of post partum thyroiditis

A

personal history of T1DM, tremor, tachycardia, warm moist skin, muscle weakness, lid retraction, lid lag

37
Q

what would you see on investigations for PPT

A

fT4 increased to a greater degree than fT3, and also will see TPO autoantibodies

reduced iodine uptake on radioactive scan

38
Q

what is a goitre

A

an enlarged thyroid

39
Q

how do you assess a goitre

A

toxic, hypo, euthyroid, is it multinodular, or diffuse, are there compression symptoms

40
Q

clinical signs to differentiate for thyroid cancer

A

age, duration, iodine status, radiation exposure
thyroid status, presence of solitary nodule v goitre,
multi-nodular disease
pressure symptoms, mobility, skin tethering, lymphadenopathy, RLN palsy

41
Q

what are the investigations for thyroid nodules

A

frequent benign disease but low risk of malignancy

USS
fine needle aspiration and cytology (before bloods is a lump is palpable and visible)

42
Q

what are the main kind of thyroid cancers

A

papillary carcinoma - 70% derived from follicular epithelium, good prognosis

follicular carcinoma -2 20%

anaplastic and medullary cell carcinoma - arising from c-cells

43
Q

how is thyroid cancer treated

A

surgery and post-op radioactive treatment or TSH suppression so tumour growth is not stimulated

44
Q

pregnancy and hyperthyroidism

A

grave’s: untreated can lead to difficulties conceiving

if conceiving: change from CMZ to PTU asap

do NOT use block and replace

45
Q

pregnancy and hypothyroidism

A

also more diff to concieve if untreated

higher doses of levo during pregnancy; increase by 25mcg so baby gets enough thyroid hormones

UK = babies have heel prick to test for hypo

46
Q

how else do you test pituitary gland function

A 
TFT's, free T4
LH, FSH, oestradiol, testosterone
prolactin
cortisol as a measure of ACTH 
IGF-1 as a measure of GH
47
Q

what is sheehan’s syndrome

A

condition that causes ischaemic necrosis to pituitary gland of woman, following hypovolemic shock or severe blood loss during or after childbirth

causes HYPOTHYROIDISM

48
Q

what are the symptoms of sheehan’s syndrome

A 
inability to breastfeed
infrequent menstruation
inability to regrow shaved pubic hair
hypothyroidism
low blood pressure and sugar
irregular heart beat

• May not have symptoms for many months or years, but trigger such as severe surgery, which triggers adrenal crisis and hence shows up because adrenal glands don’t produce enough cortisol

49
Q

what is the treatment for sheehans

A

HRT

Med Year 3 (25 decks)

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