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Flashcards in Endocrinology Deck (84)
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1
Q

what is primary vs secondary hypothyroidism

A

primary hypothyroidism is an issue with the thyroid gland itself, most commonly autoimmune
secondary hypothyroidism is due to TSH insufficiency as a result of pituitary disease

2
Q

what is the difference between primary and secodnary hypothyroidism in terms of T3/T4 and TSH levels ?

A

in primary hypothyroidism T4 is low and TSH is high

in seocndary hypothyroidism T4 is low and TSH is also low

3
Q

what are the T3/T4 and TSH levels like in primary hyperthyroidism?

A

T3/T4 is elevated and TSH is supressed

4
Q

what drugs can affect thyroid results when testing?

A

lithium and amiodarone (also pregnancy)

5
Q

what are the causes of hyperthroidisim?

A
  • autoimmune (GRAVES - presence of TSH receptor stimulating antibodies)
  • nodular thyroid disease (older age)
  • thyroiditis (inflammation of thyroid gland causing release of thyroxine)
  • viral infection
  • medication
  • following childbirth
6
Q

what are the clinical features (signs and symptoms) of hyperthyroidism?

A

INCREASED SYMPATHETIC ACTION

symptoms:
- weight loss
- increased appetite
- insomnia
- irritability
- anxiety
- heat intoleranc e
- palpitiations
- tremor
- increased bowel frequency

signs:
- restign tachy
- warm peripheries
- resting tremor
- hypereflexia
- lid lag
- hypertension / flow murmur
- aggitated and hyperkinetic
- pretibial myxoedema
- nail changes

7
Q

what investigations are done in a patient suspected to have hyperthyroidism?

A

test T4/T3 levels and TSH
thyroid peroxidase antibodies (check for autoimmune cause)
thyroid US
nuclear imaging (iodine uptake isotope scan)

8
Q

what is teh treatment for hyperthyroidism?

A

medical - thionamides to reduce T3 and T4 synthesis
surgery - thyroidectomy
radioactive - radioactive iodine - single dose (can cause hypothyroidsim)

9
Q

what are the causes of primary hypothyroidism?

A
  • autoimmune (hashimotos thyroiditis)
  • pregnancy
  • iodine deficiency
  • genetic defect in thyroid hormone
  • drugs - amiodarone, lithium
  • iatrogenic (treatment of hyperthyroidism)
10
Q

what is the causes of secondary hypothyroidism?

A

TSH deficiency due to hypothalamic pituitary disease

11
Q

what are the clinical features fo hypothyroidism (hashimotos)?

A
  • weight gain
  • cold intolerance
  • fatigue
  • constipation
  • ## braydcardia

signs:
- thickened skin
- puffiness around eyes

12
Q

what are the investigations done to diagnose a patient with suspected hypothyroidism?

A
  • T4 and TSH levels
  • thyroid antiboides for autoimmue cuases
  • thyroid peroxidase antibodies are strongly positive in hashimotos thyroiditis
13
Q

what is the treatment of hypothyroidism?

A

thyroxine replacement

  • need to be careful as a suppressed TSH level means a n overeplacment which can lead to AFib, osteoporosis
  • patients who remain symptomatic should be investigated for non thyroid pathology
14
Q

what is the disease that results in primary adrenal insuffiency?

A

addisons disease

15
Q

what are teh clinical features of addisons disease?

A
  • fatigue
  • wekaness
  • anorexia
  • weight loss
  • nuasea
  • abdo pain
  • dizziness
  • postural hypotension
  • reduced libido
  • loss of axillary and pubic hair

signs:
- increased pigmentation (ACTH XS)

16
Q

what are teh investgiations done to diagnose addisons disease?

A
  • test for adrenal autoantibodies for autoimmune causes (MOST COMMON)
  • biochemically (hyponatremia, hyperkalaemia, raised urea, hypoglycaemia and mild aneamia)
  • low 9am cortisol and raised ACTH conc
  • synacthen test
17
Q

what is the managment of addisons disease?

A

lifelong glucocorticoid and mineralocorticoid replacemnt therapy - hydrocortisone first choice
minerlocorticoid given as fludrocortisone
(at times of illness thier doses need to be doubled)
+ need a steroid emergnecy card

18
Q

what is secondary adrenal insufficiency? what is it cuased by and how is it treated?

A

ACTH deficiency due to hypopituitarism
onyl need hydrocortisone (no fludrocortisone)

Patients taking long term steroids shoudl NOT STOP steroids ABRUPTLY = adrenal crisis

19
Q

name some disorders of the adrenal medulla

A

phaeochromocytoma and paraganglioma

20
Q

what is the difference between phaeochromocytoma and paraganglioma?

A

paraganglioma arises from the extra-adrenal chromaffin tissue (10% occurence)
phaeochromocytoma arise from the adrenal medulla (90%)

21
Q

what are the clinical features of the adrenal medulla tumours?

A
  • headahce
  • sweating
  • pallor
  • palpitation
  • anxiety /panic attacks
  • hypertension
    (can lead to hypertensive emergency)
22
Q

what investigations are done to diagnose phaeochromocytoma or paraganglioma?

A

biochemical confirmation of elevated catecholamines, followed by radiological localisation of the tumour
24 hr urine catecholamines and plasma metanephrines
CT or MRI abdo
genetic testing is present at a young age

23
Q

what is the management of phaeochromocytoma or paraganglioma?

A

surgical excision

+ alpha/beta blockade at diagnosis

24
Q

what are the 8 hormones released from the anterior and posterior pituitary gland?

A

PNUEMONIC: GOAT FLAP

Growth hormone 
Oxytocin (posterior) 
ACTH
TSH
FSH
LH 
ADH (posteior) 
Prolactin
25
Q

what is the role of ACTH? and what is it stimulated by?

A

ACTH has a circadian rhythm, with lowest activity at night. it stimulates cortisol release from the adrenal glands, and is under positive control by CRH
cortisol has a -ve feedback on ACTH

26
Q

what is the role of TSH? and what is it stimulated by?

A

TSH drives thyroxine release via stimualtion of TSH receptors in teh thyroid gland. TRH stimulates TSH secretion
thyroxine has a -ve feedback effect on TSH

27
Q

what are the common signs seen in a pituitary tumour?

A

can either present as a result of compression of surroundign structures e.g. optic chiasm (bitemporal hemianopia) or as the effects of hormone XS; acromeglay (GH), cushings (ACTH), prolactinoma (PRL), TSHoma (TSH)

28
Q

what are the two biochemical assessments for the pituitary gland ? explain each

A
  1. basal tests - assess TSH and fT4 (any time of day) and assess basal cortisol at 9am
  2. dynamic tests (syncathen test) - used to asses primary adrenal failure (after 2 weeks of ACTH deficiency, atrophy of the adrenal cortex = failure to respond to syncathen)
29
Q

what imaging can be done on the pituitary gland?

A

MRI - injection of ccontrast to highlight tumour

CT possible

30
Q

what are the causes of hyperprolactinaemia?

A
  • PCOS
  • profound hypothyroidism
  • pregnancy
  • antiemetics, anti-psychotics
  • non functioning adenoma of pituitary gland

(if prolactin is higher than 5000iU/L suggestive of a prolactinoma not a non functioning adenoma of pituitary gland)

31
Q

what are teh differences between a microprolactinoma and a macroprolactinoma?

A

microprolactinoma - <1cm and increased frequent in women, have menstrual disturbance, galactorrhea and infertility. (RULE OUT PCOS)

macroprolactinoma - >1cm and icnreased frequent in men

32
Q

what is the treatment for prolactinomas?

A

dopamine (D2) agonists

macroprolactinomas can lead CSF = meningitis due to rapid reduction in tumour size form treatment

33
Q

what causes acromegaly?

A

GH secreting pituitary tumour

34
Q

what are the clinical features of acromegaly

A
  • increased size of hands and feet
  • facial features becomes more coarse (frontal bossing of forehead, chin protrusion, spacing of teeth)
  • soft tissue swelling = tongue and soft palate enlargment = snorign and sleep apnoea + hands swell = carpal tunnel syndrome
  • hypertension
  • headaches
  • sweating
  • diabetes
35
Q

what are teh investigations done to diagnose acromegaly?

A
  1. oral glucose tolerance test (OGTT) - fialrue to suppress GH post OGTT
  2. IGF-1 - elevated
  3. Pituitary MRI shows a tumour (with contrast will show microadenomas)
36
Q

what is the managment of acromegaly?

A
  1. surgery (microadenomas have a high chance of surgical remission)
  2. medical - somatosatin analogues (monhtly injections)
  3. external beam or stereotactic radiotherapy - takes a while for tumour to reduce in size and not suitable for tumours near optic chiasm
37
Q

how are non functionign pituitary adenomas treated?

A

surgery by transsphenoial or trans cranial routes

38
Q

what are the most common causes of hypopituitarism

A
acquired - pituitary tumour - MOST COMMON 
inflammatory 
congenital 
infiltrative disorders 
radiotherapy 
traumatic brain injury
39
Q

what are the two mian signs of an acute hypo-adrenal crisis?

A

hyponatremia and hypotension

40
Q

what investigations are carried out when hypopituitarism is suspected?

A
  1. firstly exclude adrenal insufficiency
  2. can be confirmed by either:
    - low fT4 and non elevated TSH
    - low sex hormones with non elevated LH or FSH
    - GH deficiency suggested by low IGF-1
  3. MRI can show pituitary tumour or an empty fossa
41
Q

what is the treatment for hypopituitarism?

A

ACTH deficiency - hydrocortisone replacement
TSH deficiency - thyroxine replacement
Gonadotropin deficiency in men - testosterone
Gonadotropin deficiency in women - oestrogen and progesterone (COCP or HRT)
GH deficiency - GH injection

42
Q

what is cushings disease?

A

cushings disease is an increase in the cortisol released form the adrenal glands

43
Q

what are the signs of cushings disease

A

signs:
- central obesity
- dorso-cervical fat pad
- increased roundness of the face
- red face and thiin skin
- easy bruising
- proximal myopathy
- hypertension
- premature osteroporosis
- diabetes mellitus

44
Q

what are the investigations for cushings disease?

A

screening tests:

  • 24hr urine free cortisol (raised)
  • low dose dexamethasone suppression test and overnight dexamethasone suppression test (failure to suppress cortisol to <50nmol/L)
  • elevated late night cortisol salivary levels
  • BECAREFUL as alcoholism and severe depression can present as cushings
45
Q

what are the three potential cuases of cushings disease?

A

pituitary (e.g. tumour)
adrenal (e.g. tumour)
ectopic ACTH (e.g. lung cancer)

46
Q

what results/signs/symptoms would lead to a:
a - pituitary cause of cushings
b - adrenal cause of cushings
c - ectopic ACTH causing cushings

A

a - high ACTH due to high CRH, MRI shows pituitary tumour
b - significant and accelerated hirsutism, LOW ACTH due to negative feedback of high cortisol levels, also high dose DST can lead to some cortisol supression
c - hypokalaemia, Hx of smoking and weight loss as all point to lung cancer, normal/high ACTH, whole body CT or PET scan shows carcinoma

47
Q

what is the management of cushings disease?

A

if adrenal tumour found - laparoscope adrenalectomy
ectopic ACTH - treatment of underlying malignancy and medical control of cortisol levels
pituitary adenoma - transsphenoidal removal

MEDICAL -> metyrapone (inhibit cortisol release) and ketoconazole possible +/- radiotherapy

48
Q

what are the symptoms of hyponatreamia?

A
  • headache
  • nuasea
  • vomiting
  • general malaise
  • confusion
  • agitation
  • drowsiness
49
Q

what are the signs/symptoms of acute severe hyponatraemia?

A
  • seizures
  • resp depression
  • coma
  • death
50
Q

what are the investigations needed to be done if hyponatraemia is suspectded?

A
full history and examination 
drug history (thiazide duiretics cna be a cause) and hydration status 
biochemical investigations include serum osmolality, urine osmolality, urine sodium, thyroid function and an assessment of cortisol reserve (9am cortisol or syncathen test)
51
Q

what is teh immediate treatment for acute severe hyponatraemia?

A

hypertonic saline to prevent cerebral oedema

52
Q

what is the diagnostic algorithm to guide differential diagnosis when hyponatraemia has occured?

A
  1. confirm low serum osmolality (hypotonic hyponatraemia)
  2. check urine osmolality; if <100mosmol/Kg suggests primary polydipsia or inappropriate fluid administration, if >100mosmol/Kg then check urine sodium
  3. if urine sodium <30mmol/L then true dehydration or intravascualr depletion (GI salt loss, CCF, cirrhosis, nephrotic syndrome)
    if urine sodium >30mmol/L and patient euvolemic SIADH considered (ACTH deficiency must be excluded first), but if patients dehyrated then: addisons, renal and cerebral salt wasting, Hx of vomiting considered (and possible severe hypothyroidism)
53
Q

what are some causes of hyponatramia?

A
  • true dehydration
  • GI salt loss e.g. vomiting, diarrhoea
  • CCF
  • cirrhosis
  • nephrotic syndrome
  • SIADH
  • addisons
  • renal and cerebral salt wasting
  • severe hypothyroidism
54
Q

what is SIADH?

A

syndrome of inappropriate ADH - increased ADH release

55
Q

what is SIADH characterised by? what serum osmolality, urine osmolality and urine NA?

A

serum osmolality <275 momol/Kg
urine osmolality >100mosmol/Kg
urine Na >30mmol/L

56
Q

how can ACTH deficiency appear identical to SIADH?

A

as in ACTH deficiency = cortisol deficiency which leads to negative feedback causing increased release of ADH

57
Q

what are the main causes of increased ADH release that must be ruled out before diagnosing SIADH?

A
  • hypothyroidism
  • total salt depletion
  • ACTH deficiency
58
Q

what are the causes of SIADH?

A
  • underlying malignancy e.e.g lung cancer
  • lung disease
  • encephalitis
  • meningitis
  • brain tumour
  • brain injury
  • guillan barre syndrome
  • anticonvulsants
59
Q

what is the management for SIADH?

A

TREAT UNDERLYING CAUSE
specialist treatment and fluid restriction (1-1.5L per day)
medical - demeclocycline and ADH antagonists

60
Q

what is diabetes inspidus?

A

diabetes insipidus is cuased by decreased ADH or ADH resistance leading ot large volumes of urine being produced and profound unquenchable thirst

61
Q

what are teh biochemical hallmarks of diabetes inspipidus?

A

high serum osmolality, low urine osmolality and high urine volume

62
Q

what is teh difference between cranial ad nephrogenic DI?

A

cranial DI is usually seen in pituitary disease leading to ADH deficiency
nephrogenic DI is usually caused by metabolic and electrolyte disturbances (hypercalcaemia), renal disease and drugs affecting the kidney.

63
Q

what are the investgiation for suspected diabetes inspidus?

A

confirmed when urine volume >3L in 24 hours in presend of high serum osmolality and low urine osmolality
confirmed if serum osmolality >295 mosmol/Kg and urine osmolality <300mosmol/Kg

Water deprivation test !! - (dont do on patients with frank DI as significant weight loss could occur)
DI excluded if urine osmolality >600mosmol/Kg
in WDT, synthetic vasopressin given and in cranial DI, urine volume reduced and increaased urine osmolality occurs BUT no chnage in nephrogenic DI

64
Q

what is the managemnt for diabetes inspidus?

A

patients with cranial DI should be investigated for pituitary disease and managed appropriately e.g. DDAVP administration or desmopressin given (DDAVP overtreament = dilutional hyponatreamia, DDAVP undertreament = thirst and polyuria)

nephrogenic DI underlying cuase needed to be considered - pateitns need to drinka ccording to thirst and keep up with water loss
other than underlying cuases treatment should: low salt diet, low protein diet, diuretics, NSAIDS

65
Q

what is the serum calcium level of hypercalceamia?

A

> 2.6 mmol/L

66
Q

what are the two main causes of hypercalcaemia?

A

hyperparathyriodisism adn malignancy

67
Q

what is the main factor distinguishing hypercalcaemia of malignnayc with hypercalcaemia from hyperparathyroidism?

A

malignancy - low PTH levels due to negative feeedback

hyperparathyroidism - high or normal PTH levels

68
Q

what is the pathophysiology of malignancy cuasing hypercalceamia

A

with hypercalcameia nd supressed PTH = malignanyc must be ruled out !!
squamous cell epithelial tumours can secrete PTH-related peptide (PTHrP)
(mostly is larger/advanced tumours)

69
Q

what is another cuase bar malignancy for hypercalcaemia with supressed PTH levels?

A

benign granulomatous disease suhc as TB or sarcoidosis (secrete activated vit. D)

70
Q

what is pathophysiology behind hypercalcaemia with raised or normal PTH levels?

A

PRIMARY HYPERPARATHYROIDISM
due to parathyroid adenoma (most likely)
or parathyroid hyperplasia in more than one gland (genetic cuase)
or parathyroid cancer (very rare and serum calcium will be >3.5mmol/L)

71
Q

what are the clinical features of hypercalcaemia?

A

primary hyperparathyroidism usually asymptomatic and discovered by routine blood tests

  • tiredness
  • generalised aches and pains
  • polyuria (from nephrogenic diabetes insipidus)
  • polydipsia (from nephrogenic diabetes insipidus)
  • abdo pain
  • constipation
  • psychiatric symptoms
  • kidney stones (5%)
72
Q

what investigations are done when hypercalcaemia occurs in a patient?

A

test PTH levels for primary hyperparathyroidisim + check phosphate levels (low phosphate present usually as PTH causes excretion of phosphate)
High ALP = increased bone turnover and common in aptietns with existing vit D deficiency
renal US may show nephrocalcinosis

73
Q

what is the treatment of hyperparathyroidism?

A

surgery considered in serum calcium >2.85mmol/L or syptoms debilitating (parathyroidectomy)
medical - calcimimetic drugs (cinacalcet)

74
Q

what is familial hypocalciuric hypercalcaemia? hwo is it different to primary hyperparathyroidism?

A

genetic defect is calcium sensing receptor = increased calcium reabsorbed
difference to hyperparathyroidism as low urine calcium/creatinine ratio present

75
Q

how is a parathyroid adenoma localised?

A

SETAMIBI isotope scanning use alongside ultrasound

76
Q

what is the serum calcium level that = hypocalcaemia?

A

<1.9 mmol/L

77
Q

what is teh most common cuase of hypocalcaemia?

A

post surgical hypoparathyroidism post thyroidectomy

- may be permanent due to damage/removal of parathyroid glands

78
Q

name some other cuases of hypocalcemia bar post thyroidectomy?

A
  • pseudohypocalcemia
  • vit D deficiency (lack of sunlight, malabsorption, diet)
  • hypomagnesaemia (GI loss, alcohol, drugs, PPIs)
79
Q

how do phosphate levels distinguish a difference in hypocalcaemia cuased by hypoparathyroidism or vit D deficiency?

A

in vit D deficiency, phosphate levels are low, whereas they are high is hypoparathyroidism

80
Q

how does hypomagnesaemia cayse hypocalcaemia?

A

Hypomagnesemia causes hypocalcemia by interfering with the parathyroid cell release of PTH and by blunting PTH response

81
Q

what are the clinical features of hypocalcaemia?

A
  • muscle cramps
  • carpo-pedal spasm
  • peri-oral and peripheral parathesia
  • neuro-psychiatric symtoms
  • +ve Chvosteks signs
  • Trousseaus signs

acute severe hypocalcemia: cardiac dysrhythmias (prolonged QT intervals), seizures, laryngospasm)

82
Q

what is the treatment for hypocalcaemia?

A

calcium replacement + consider and reverse underlying cause
if vit d deficient - give cholecalciferol
hypoparathyroidism - alfacalcidol or calcitriol
oral calcium supplements
magnesium deficient - precipitating drugs stopped and iv magnesium given

KEEP calcium at LOW END of reference range to prevent NEPHROCALCINOSIS

83
Q

what is pseudo hypoparathyroidism?

How is it different to vit d deficiency and hypoparathyroidism in biochemical markers?

A

rare condition caused by mutation in a G protein coupled to the PTH receptor leading to PTH resistance
characterised by high phosphate and hypocalcaemia
AS high PTH and normal vit D suggest PTH resistance rather than deficiency
(apperance = short stare, round face and short 4th and 5th metacarpals)

84
Q

what is teh management on an addisonian crisis?

A
bloods: cortisol, ACTH, U+E, cultures 
Check CBG
IV crystalloids
hydrocortisone 600mg IV 6hrly
septic screen 
treat udnerlying cause