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Medicine block (Y3) > Week 5: Endocrine (2) > Flashcards

Week 5: Endocrine (2) Flashcards

1
Q

thyroid hormone investigation

A
  • HISTORY
  • Blood test e.g. TSH, TRH, T4
    • distinguish between hypo and hyper thyroidism
  • Thyroid ultrasound
    • Best way – structural isotope
  • Radioisotope scan
    • Give technetium- 99m via IV- a good uptake of iodine
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2
Q

Effect of T4 (thyroxin)

A
  • Controls your metabolism e.g. heart rate , body temp and the rate at which intestine digest food
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3
Q

Diagnosis of thyroid disorder

A
  • History
    • symptoms and signs
    • family history etc
  • Blood test e.g. TSH, TRH, T4
  • Imaging
    • Thyroid ultrasound- most useful at distinguishing bw cystic (fluid filled) and solid nodules.
      • Can guide biopsy of a thyroid lesion.
    • Radioisotope scan
      • Give technetium- 99m via IV- a good uptake of iodine
      • hyperthyroidsims and thyorid cancer
      • gamma camera used to detect gamma rays emitted from radioactive iodine
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4
Q

thryoid radioisotope scan findings

A
  • Diffuse high uptake is found in Grave’s Disease
  • Focal high uptake is found in toxic multinodular goitre and adenomas
  • “Cold” areas (i.e. abnormally low uptake) can indicate thyroid cancer
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5
Q

thyroid feedback system

A
  • The hypothalamus secretes thyroid releasing hormone
  • TRH stimulates the anterior pituitary to secrete thyroid stimulating hormone
  • TSH stimulates the thyroid to secrete T4
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6
Q

primary hypothryodisms

A

(underactive thyroid- usually autoimmune origin)

  • T4 low (2.4 pmol/L (8-25)
  • TSH high (150 miU/L (1-4.5)
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7
Q

primary hypothryodisms

A

(underactive thyroid- usually autoimmune origin)

  • T4 low (2.4 pmol/L (8-25)
  • TSH high (150 miU/L (1-4.5)
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8
Q

primary hypothryodisms

A

(underactive thyroid- usually autoimmune origin)

  • T4 low (2.4 pmol/L (8-25)
  • TSH high (150 miU/L (1-4.5)
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9
Q

primary hypothryodisms

A

(underactive thyroid- usually autoimmune origin)

  • T4 low (2.4 pmol/L (8-25)
  • TSH high (150 miU/L (1-4.5)
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10
Q

secondary hypothyroidism

A
  • Due to TSH deficiency and usually due to pituitary disease
  • Low T3 levels and non-elevated TSH
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11
Q

primary hyperthyroidism

A
  • T4 high (86 pmol/L (8-25)
  • TSH low (<0.05miU/L (1-4.5)
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12
Q

hypothyroidism presentation

A

Symptoms

  • Tiredness
  • Weight gain
  • Cold intolerance
  • Change in appearance
  • Depression
  • Psychosis
  • Joint/ muscle ache
  • Dry hair/ skin
  • Constipation
  • Puffy eyes

Signs

  • Peri-orbital oedema- swelling of the eyes
  • Loss of lateral eyebrows
  • Dry, thin hair
  • Bradycardia
  • Slow-relaxing reflexes
  • Carpal tunnel syndrome
  • Cold peripheries
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13
Q

causes of myxoedema (old fashioned descriptive word for hypothyroidism meaning swelling of eye and thickening of the skin

A
  • Autoimmune atrophic
  • Hashimotos’ thyroiditis
  • Post-partum thyroiditis
  • Dyshormonogenesis (babies born with under active thyroid)
  • Medication
  • Iodine deficiency
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14
Q

children who have hypothyroidism have

A

reduced I- cretinism

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15
Q

Special situations in hypothyroidism

A

Myxoedema coma

borderline or subclinical hypothyroidism

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16
Q

Myxoedema coma

A

Severe hypothyroidism usually in the elderly.

  • Hypothermia and fluid overload in heart
  • 50% mortality
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17
Q

Borderline or sub-clinical hypothyroidism

A
  • Low/normal T4 and high TSH
  • More common than severe hypothyroidism
  • Can be monitored until symptoms warrant treatment
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18
Q

Treatment of hypothyroidism

A

Thyroxine

replacement therapy

  • Levothyroxine (T4) for life
  • Starting dose depends on severity
  • 100ug for young and fit person
  • More caution in elderly and heart disease

Aims

  • Resolution of symptoms
  • Normalisation of blood tests (6-8 weeks)
  • High TSH suggests under replacement
  • Low TSH suggests over replacement
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19
Q

presentation of hyperthyroidism

A

Symptoms

  • Weight loss
  • Irritability
  • Restlessness
  • Insomnia
  • Malaise
  • Itching
  • Sweating
  • Palpitation
  • Tremor
  • Muscle ache
  • Diarrhoea

Signs

  • Tremor
  • Hyperkinesis
  • Tachycardia
  • Atrial fibrillation (irreg irreg)
  • Warm peripheries
  • Hypertension
  • Proximal myopathy
  • Lid lag
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20
Q

lid lag and hyperthyroidism

A
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21
Q

causes of hyperthyroidism

A

Causes

  • Graves disease
  • Nodular thyroid disease
  • Thyroiditis
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22
Q

graves disease

A
  • Most common cause of hyperthyroidism
  • Autoimmune mediated stimulation of TSH receptor on thyroid gland stimulates thyroid hormone synthesis

Effects

  • Graves ophthalmopathy
  • Pretibial myxoedema (Graves dermopathy)
  • Thyroid acropathy
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23
Q

thyroiditis

A
  • Inflammation of thyroid
  • Release of thyroxine into circulation
  • Viral infection- de quervains thyroiditis
  • After birth- post partum
  • Medication- amiodarone
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24
Q

nodular hyperthryodiisms

A
  • Single toxic nodule
  • Toxic multi-nodular goitre
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25
Q

treatment of hyperthyroidism

A

Medication

  • Carbimazole
  • Beware of agranulocytosis (reduces neutrophils)
  • Beta blocker for symptom control

Surgery

  • If side effects on medication or patient preference
  • Good cosmetic results
  • Small risk of laryngeal nerves palsy’s and hypocalcaemia

Radioactive iodine

  • Good definitive non-surgical option
  • Contra-indicated in pregnancy
  • Radiation restriction guidance after treatment
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26
Q

special situations in hyperthyroidism

A

thyroid crisis

hyperthyroidism and pregnancy

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27
Q

Thyroid crisis or thyroid storm

A
  • Rare condition with 10% mortality
  • Hyperpyrexia
  • Tachycardia
  • Cardiac failure
  • Liver dysfunction
  • Urgent treatment
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28
Q

Hyperthyroidism and pregnancy

A
  • In graves disease antibodies can cross placenta
  • Baby can be born with hyperthyroidism
  • Requires close monitoring in pregnancy
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29
Q

Types of goitre

A

Diffuse goitre

  • Simple goitre
  • Auto-immune
  • Thyroiditis

Nodular goitre

  • Multinodular goitre
  • solitary nodule (red flag )

Fibrotic goitre

  • Riedel’s thyroiditis – rare

Iodine deficiency

  • Common worldwide
  • Rare in UK
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30
Q

red flag symptoms of thyroid cancer : history

A
  • Very young or old patient
  • Rapid enlargement of lump in neck
  • Hoarse voice and dysphagia
  • Family history of thyroid cancer
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31
Q

red flag symptoms of thyroid cancer: examination

A
  • Hard irregular thyroid mass
  • Fixed to surrounding structures
  • Cervical lymph nodes
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32
Q

Investigation of suspected thyroid cancer

A
  • Thyroid ultra-sound
  • Fine need aspiration
  • CT scan thorax and mediastinum
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33
Q

if cytology suggest thyroid cancer

A

surgical removale

MUST BE DONE BY EXPERT TO PREVENT DAMAGE TO THE PARATHYROID GLANDS AND NOT DAMAGE TO THE RECURRENT LARYNGEAL NERVE -→ PALSY

34
Q

Anatomy of the adrenal gland

A
  • Pyramidal shape
  • Sits on top of the kidney
  • made up of cortex and medulla

SALT SUGAR SEX (DEEPER YOU GET THE SWEETER)

35
Q

layers of the cortex

A

GFR

zona glomerulosa

zona fasiculata

zona reticularis

36
Q

Zona glomerulosa- aldosterone

A
  • Salt and water
  • Mineralocorticoids e.g. aldosterone
  • Regulated by RAAS
  • RAAS: In response to low circulating blood volume, hyponatraemia or hyperkalaemia, renin is activated to catalyse the conversion of angiotensinogen to angiotensin I, which is converted by angiotensin-converting enzyme (ACE) to angiotensin II. Angiotensin II stimulates aldosterone release upon binding to the angiotensin receptor. Aldosterone acts mainly at the renal distal convoluted tubule on its receptor to cause sodium retention and potassium loss.
37
Q

Zona fasciculata- cortisol

A
  • Sugar
  • Glucocorticoids- cortisol
  • Cortisol synthesis is regulated by ACTH
    • Cortisol exerts a negative feedback on the hypothalamus top reduce CRH (and vasopressin) and on the anterior pituitary to reduce ACTH
    • Cortisol is highest at 0800 and lowest midnight
    • Investigation- cortisol immunoassays measure total (bound and free) cortisol, hence conditions which stimulate CBG (capillary blood glucose) e,g. oestrogen therapy, may increase measure cortisol levels without affecting biologically active free levels
38
Q

zona reticularis -testosterone

A
  • Sex
  • Androgens- Testosterone
  • Controlled by ACTH
  • More important role in women (in both sexes pre-pubertally), as adult men rely mainly on testicular production of androgens
  • DHEA and DHEA-S and androstenedione are converted to more potent testosterone and dihydrotestosterone in peripheral tissue
  • Androgens exert their effect on: sebaceous glands, hair follicles, the prostate gland and external genitalia
39
Q

adrenal medulla disease presentation

A

Presentation of adrenal medulla disease (noradrenaline/ adrenaline)

  • Excessive catecholamine secretion
  • Acute episodes
  • Sweating
  • Palpitations
  • High or low BP
  • Collapse
  • SUDDEN DEATH
40
Q

Biochemical assessment of adrenal medulla

A
  • 24 hour urine catecholamines
    • adrenaline (short half life)
    • noradrenaline (short half lif)
    • dopamine etc

Measuring 24 hour urine catecholamines gives an idea of how much adrenaline is being secreted by the tumour over the 24 hour period.

or

  • Plasma free metanephrines
    • metanephrines are breakdown products of catecholamine- longer half life- therefore more reliable diagnostic tool
  • Avoid certain foods: coffee, coke, bananas, chocolate, vanilla
41
Q

Adrenal hormone deficiency’s presentation

A
  • Cortisol (lack of glucocorticoid) deficiency (addisons disease) - weakness, tiredness, weight loss, hypoglycaemia
    • Cortisol does the opposite to insulin
  • Mineralocorticoid (aldosterone) deficiency– dizziness, hypotension, low Na, high K
  • Androgen deficiency– e.g. Addisons
    • In women- low libido and loss of body hair in women
      • Testosterone only produced in adrenal gland in women
    • In men- no symptoms because produced in testicals
42
Q

Adrenal hormone excess presentation

A
  • Cortisol excess- weight gain and cushingoid features (cushing’s syndrome)
    • Diabetes
    • Bone weakness
  • Mineralocorticoid excess (aldosterone)- high BP and low K
  • Androgen excess – increased male characteristics in women
43
Q

ACTH excess from pit

A
  • Skin pigmentation due to melanocyte stimulation
  • Pigmentation seen in Addisons and ACTH- driven cushings
44
Q

Diagnosis of suspected adrenocortical disease

A
  • Measurement of cortisol and ACTH
  • Measurement of 24hr urinary excretion of cortisol and its breakdown products
  • Dynamic function tests
    • Dexamethasone suppression test
      • Suppression of plasma cortisol by >50% is characteristic of Cushing’s disease, but suppression doesn’t normally occur in adrenal tumour or ectopic ACTH production
    • ACTH stimulation test
      • Admission of Synacthen would normally increase plasma cortisol, and a normal response to this usually excludes Addison’s disease
  • CT
  • MRI
  • Functional imaging: MIBG scan
  • PET scan
45
Q

Hyperaldosteronisms

A

A condition in which there is excessive production of aldosterone.

46
Q

Primary hyperaldosteronism

A

excess aldosterone production due to a defect in the adrenal cortex. Commonest form of endocrine hypertension.

  1. Bilateral idiopathic adrenal hyperplasia
  2. Or Aldosterone-secreting adenoma (Conns syndrome)
47
Q

primary hyperaldosteronism diagnosis

A
  • Hypertension and hypokalaemia
  • Elevated aldosterone independent of RAAS (suppressed renin)
  • Scan- shows adrenal adenoma or bilateral hyperplasia
48
Q

secondary hyperaldosteronism

A

excess aldosterone production due to overactivity of the RAAS

  • Renin- producing tumour or renal artery stenosis
49
Q

signs and symptoms fo hyperaldosteronism

A
  • High blood pressure
  • Left ventricular hypertrophy
  • Stroke
  • Hypernatremia
  • Hypokalaemia
50
Q

treatment of hyperaldosteronism

A
  • Dependent on cause
  • Surgical treatment for aldosterone-secreting adenomas or
  • Spironolactone (a mineralocorticoid receptor agonists) can be used for other causes
51
Q

cushings syndrome

A

A syndrome caused by excessive exposure to cortisol

→ different to disease

52
Q

causes of cushings syndrome can be

A

exogenous

endogenous

53
Q

ecogenous causes of cushings syndrome

A

main cause is being prescribed glucocorticoids e.g. being prescribed dexamethasone

54
Q

endogenous causes of cushings syndrome

A
  • Cushing’s disease: benign pituitary adenoma that secretes ACTH
  • Adrenal cushing’s: Adrenal tumour secreting glucocorticoids
  • Non- pituitary-adrenal tumours producing ACTH and/ or CRH (e.g. small cell lung cancer- very rare)
55
Q

cushings syndrome presentation

A
  • Moon shaped face
  • Buffalo hump
  • Abdominal obesity
  • Striae
  • Acute weight gain
  • Hyperglycaemia – increased gluconeogenesis
  • Hypertension- mineralocorticoid effects of excess cortisol
56
Q

steroid drug and cushings

A

(e.g. prednisolone and dexamethasone) are the same as the effects of higher levels of cortisol.

→ steroid dosage should always be decreased gradually and never stopped suddenly

57
Q

adrenal cushings syndrome

A

adrenal tumour

  • ACTH is suppressed- ACTH independent
  • Unlike pituitary and ectopic ACTH
    • Symptoms
      • Androgenic symptoms may be present
        • Hirsutism
        • Acne
        • Greasy skin
      • Virilising features in large tumours
        • Androgenic alopecia
        • Deep voice
        • Clitoromegaly
    • Treatment
      • Adrenalectomy- laparoscopic
      • Large tumours need open surgery
58
Q

androgens

A

Androgens are partially regulated by ACTH and CRH.

  • Promote axillary and pubic hair growth in both males and females
59
Q

androgens in males

A
  • In prepubescent males dehydroepiandrosterone (DHEA) released from the adrenal glands is converted to testosterone in the testes.
  • After puberty this production is insignificant as the testes themselves release testosterone
60
Q

androgens in females

A
  • Adrenal androgens promote libido and are converted to oestrogen in tissues
  • After menopause this is the only source of oestrogen in the body
61
Q

genital ambiguity in female infants

A

a rare condition in which an infant’s external genitals don’t appear to be clearly either male or female.

  • Genetic defect- deficiency of the 21-hydroxylase enzyme
    • Results in decreased glucocorticoid and mineralocorticoid production
    • Precursor of these hormones- 17a-hydroxypregnenolone is therefore diverted to more androgen synthesis (e.g. testosterone)-→ excessive testosterone
  • Can also cause salt wasting crises- high rate of sodium lost
62
Q

addisons disease

A

‘Primary adrenal insufficiency”

Hypocortisolism

63
Q

causes of addisons disease

A
  • Destructive atrophy of the adrenal glands by autoimmune response
  • Fungal infections
  • Adrenal cancer
  • Adrenal haemorrhage
  • TB (in old times- good time lol)
64
Q

presentation of addisons disease

A
  • Postural hypotension
  • Lethargy
  • Weight loss
  • Anorexia
  • Increased skin pigmentation hypoglycaemia
65
Q

addisons disease and increased skin pigmentation

A
  • Decrease in cortisol
  • Reduced negative feedback on the anterior pituitary
  • More POMC produced to synthesis ACTH
  • POMC also produces alpha-MSH
  • Increase in MSH= increase in melanin synthesis- hyperpigmentation
  • ACTH can also activate melanocortin receptors on melanocytes- hyperpigmentation
66
Q

maintence treatment of addisons

A
  • Lifelong replacement
    • Glucocorticoid: hydrocortisone, prednisolone
    • Mineralocorticoid: fludrocortisone
  • Education
    • Double dose of glucocorticoid at time of illness
    • Emergency HC injection if vomiting
    • Steroid card and bracelet
67
Q

Addisonian crisis

A

Life threatening emergency due to adrenal insufficiency

68
Q

causes of addisonian crisis

A
  • Abrupt steroid drug withdrawal
  • Severe stress
  • Salt depravation
  • Infection
  • Trauma
  • Cold exposure
  • Over exertion
69
Q

presentation of addisonian crisis

A

Signs and symptoms

  • Collapse
  • Nausea
  • Vomiting
  • Pyrexia
  • Hypotension
  • Vascular collapse
70
Q

treatment of addisonian crisis

A

fluid replacement and cortisol

71
Q

Congenital adrenal hyperplasia (CAH)

A

Congenital adrenal hyperplasia (CAH) is a group of rare inherited autosomal recessive disorders characterized by a deficiency of one of the enzymes needed to make specific hormones.

  • CAH effects the adrenal glands located at the top of each kidney.
  • Normally, the adrenal glands are responsible for producing three different hormones:
      1. corticosteroids, which gauge the body’s response to illness or injury;
      1. mineralocorticoids, which regulate salt and water levels; and
      1. androgens, which are male sex hormones.
  • An enzyme deficiency will make the body unable to produce one or more of these hormones, which in turn will result in the overproduction of another type of hormone precursor in order to compensate for the loss.
72
Q

most common cause of congenital adrenal hyperplasia

A

enzyme 21-hydroxylase

73
Q

CAH can cause

A

adrenal crisis and ambigious genitalia

74
Q

how can CAH cause ambigious genitalia and adrenal crisis

A
  • Block in adrenal cortex pathway
  • Presentation depends on enzyme defect
  • Lack of enzyme leads to:
    • Low cortisol and aldosterone
    • High male hormones (androgens)
75
Q

presentation of CAH

A

Presentation

  • Hypotension
  • Hyponatraemia
  • Hyperkalaemia
  • Hypoglycaemia
  • Virilisation – development of male body parts
76
Q

disorders of the adrenal meduall

A

Pheochromocytoma and paraganglioma

77
Q

Pheochromocytoma and paraganglioma presentation

A

a type of neuroendocrine tumor that grows from cells called chromaffin cells. These cells produce hormones needed for the body and are found in the adrenal glands. The adrenal glands are small organs located in the upper region of the abdomen on top of the kidneys.

  • Acute episodes
  • Sweating
  • Panic attacks
  • Palpitations
  • High or low BP
  • Collapse

Acute crisis

  • Hypertensive crisis
  • Encephalopathy
  • Hyperglycaemia
  • Cardiac arrhythmias
  • Sudden death
78
Q

investigations for Pheochromocytoma and paraganglioma

A
  • 24h urine metanephrines
    • 2-3 x collections needed
  • Plasma metanephrine
  • Neuro-endocrine marker: Chromogranin A
79
Q

Pheochromocytoma and paraganglioma managemetn

A
  • Alpha blockade- phenoxybenzamine
    • Always do alpha-block before b-block
  • B blockade- bisoprolol
  • Surgical excision
    • Perioperative management
      • Specialist anaesthetic team
      • Risk of crisis during operation
      • Maximal vasodilation and filling with IV fluids
80
Q

in an acute phaechromocytome crisis why always alpha block. before b-block

A

Unopposed alpha stimulation can cause hypertensive crisis

Medicine block (Y3) (38 decks)

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