Endocrine 2 Flashcards

1
Q

definition of hypoparathyroidism

A

Relative or absolute deficiency of plasma parathyroid hormone (PTH) synthesis and secretion.

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2
Q

what are the biochemical changes in hypoparathyroidism?

A

low Ca2+

high phosphate

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3
Q

aetiology of hypoparathyroidism?

A

mainly due to surgical management of thyroid disease

thyroid surgery

parathyroidectomy

hypomagnesemia - severe low level leads to inhibition of PTH secretion

autosomal dominant conditions

autoimmune body resistance to PTH

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4
Q

clinical symptoms of hypoparathyroidism

A
asymptomatic 
chronic alcoholism 
malnutrition, malabsoption, diarrhoea 
muscle twitches, spasm, cramps - tetany 
paraesthesia, numbness, tingling 
poor memory slowed thinking 
anxiety 
dry hair, brittle nail 
cataracts 
•	Cheotveks sign- twitching of facial muscles on tapping facial nerve
•	Trousseau sign-carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure for 3 minutes
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5
Q

what is the acronym used for hypoparathyroidism

A

PTH

P - parathesis, positive Chetoveks & positive trousseau

T- tetany (muscle cramping and consultation)

H - hypocalcemia

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6
Q

differentials for hypoparathyroidism

A
low vit D 
hypomagnesaemia 
hypoalbuminemia 
pesudohypoparathyroidim 
renal failure, CKD
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7
Q

investigation and management of hypoparathyroidism

A
  • Refer to endocrinology
  • Bloods: serum calcium (low), serum albumin (normal, if low can give falsely low serum calcium level), PTH, magnesium (may be low), serum 25-hydroxyvitamin D ( low), serum phosphorus (elevated), UE.
  • ECG (prolonged QT)

• Oral calcium, Vitamin D, PTH injection

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8
Q

what are the different types of thyroid cancer

A
papillary 
follicular 
medullary
anaplastic 
- these 4 types of cancer make up 98% of thyroid cancer

other -
thyroid lymphoma
hurthe cell carcinoma

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9
Q

aetiology of thyroid cancer

A
ionising radiation
Hx of goitre
thyroid nodule
thyroiditis 
Fhx of thyroid disease 
female 
Asian
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10
Q

symptoms of thyroid cancer

A

thyroid nodule - hard and fixed, non-tender, rapid growth

hoarse voice - involvement of the recurrent laryngeal nerve

stridor - involvement of the airway

cervical lymphadenopathy

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11
Q

differentials for thyroid cancer

A

benign thyroid nodule

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12
Q

what are the investigations and management for thyroid cancer

A
  • Two-week referral pathway or same day referral if thyroid lump and stridor.
  • Bloods: TFT (normal), serum calcitonin (made by the thyroid and is a good tumour marker)
  • US, fine needle biopsy
  • I-123 thyroid scan and uptake – hot nodule = rule out
  • Rx: surgery, radioiodine ablation, RT.
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13
Q

definition of multi-nodular goitre

A

Multiple autonomously functioning nodules, resulting in hyperthyroidism. These nodules function independently of thyroid-stimulating hormone and are almost always benign

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14
Q

aetiology of mutli-nodular goitre

A

Most hyperfunctioning nodules have thyroid cell germline mutations that affect the thyroid-stimulating hormone (TSH) receptor.

RF - iodine deficiency, head and neck irradiation, > 40 years, female

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15
Q

clinical features of multi-nodular goitre

A

goitre - irrgular and rapidly growing

palpable multiple thyroid nodules

symptoms of hyperthyroidism

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16
Q

differential for multi-nodular goitre

A

-Grave’s Disease
-toxic adenoma
-thyrotoxic phase of painless/lymphocytic thyroiditis
-iodine-induced
hyperthyroidism

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17
Q

what are the investigation and management of multiple nodular goitre

A
  • Refer to endocrinology
  • Bloods: TSH, T3/T4, iodine thyroid scan and uptake, Tc-99 pertechnetate scan, thyroid ultrasound, TSH receptor antibodies, thyroid peroxidase antibodies.

• Rx: radioactive iodine therapy, antithyroid drugs, thyroid surgery, b-blockers

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18
Q

what are the causes of toxic nodules

A

thyroid adenoma (autonomously functioning thyroid nodule that causes hyperthyroidism)

cyst

cancerous tumour

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19
Q

aetiology of toxic goitre

A

arises after activating (gain of function) germline mutations in thyroid cells

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20
Q

RF for toxic goitre

A
iodine deficiency 
20-40 yrs 
female 
head and neck irradiation 
FHx
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21
Q

clinical symptoms of toxic goitre

A

palpable single thyroid nodule

symptoms of hyperthyroidism

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22
Q

investigation and management of toxic goitre

A

TSH, T3/T4, TSH receptor antibodies

thyroid peroxidase antibodies

thyroid US, thyroid scan and uptake

radioactive iodine therapy, antithyroid, thyroidectomy, beta-blocker

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23
Q

what is a simple goitre

A

enlarged thyroid gland

can lead to euthyroid, hyperthyroidism, hypothyroidism

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24
Q

aetiology for a simple goitre

A

Graves

Hashimoto’s thyroiditis

radiotherapy

iodine deficiency

drug (lithium and amiodarone)

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25
Q

clinical symptoms of a simple goitre

A

asymptomatic except swelling in neck

can be painless or painful (uncommon)

symptoms of either hyperthyroidism or hypothyroidism

difficulty breathing and swallowing as goire presses on the airway and the oesophagus

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26
Q

investigation and treatment for a simple goitre

A

refer to endocrinology

bloods - TSH, T3/T4, iodine thyroid scan, Tc-99 pertechnetate scan, thyroid USS

Tx - depends on cause, radioactive iodine (if hyperthyroidism), thyroidectomy (if cancer), iodine replacement (thyroxine if hypothyroidism)

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27
Q

definition of thyroiditis

A

swelling (inflammation) of the thyroid gland which can result in hyper or hypothyroidism

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28
Q

what are the different types of thyroiditis

A

Hashimoto - hypothyroidism

De Quervain’s (subacute thyroiditis. Painful swelling of the thyroid gland triggered by a viral infection)

post-partum thyroiditis - autoimmune hyperthyroidism 6 months after giving birth

silent thyroiditis

Drug-induced - amiodarone, and lithium

radiation-induced

acute or infectious thyroiditis - triggered by a bacterial infection and associated with a weakened immune system

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29
Q

what are the clinical symptoms of De Quervain’s thyroiditis

A

fever
pain in the neck, jaw, and ear
initially - hyperthyroidism (a few days)
followed by hypothyroidism (lasting weeks or months)
return to normal thyroid infection

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30
Q

what are the clinical symptoms of Post-partum thyroiditis?

A

6 months since delivery
initially - hyperthyroidism (a few days)
followed by hypothyroidism (lasting weeks or months)
return to normal thyroid function by 12-18 months

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31
Q

what are the clinical symptoms of silent thyroiditis?

A

painless
initially - hyperthyroidism (few days)
followed by hypothyroidism (lasting weeks or months)

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32
Q

what are the clinical symptoms of drug-induced thyroiditis?

A

symptoms short-lived and cease upon stopping medication

33
Q

what are the clinical symptoms of radiation-induced thyroiditis?

A

either symptom of over or underactive thyroid

34
Q

what are the clinical symptoms of acute or infectious thyroiditis?

A

pain in the throat, feeling generally unwell, swelling of the thyroid glands

symptoms of underactive/overactive thryoid glands

35
Q

investigations and treatment

A

• Refer to endocrinology or treat in PC if possible.
• blood - TSH, T3/T4, CRP
Tx: depends on cause

36
Q

definition of hypopituitarism

A

partial or complete deficiency of one or more pituitary hormones

37
Q

what are the hormones which are secreted in the anterior pituitary glands

A
growth hormone 
prolactin 
LH 
FSH 
ACTH 
TSH
38
Q

what are the hormones which are secreted in the posterior pituitary glands

A

vasopressin

oxytocin

39
Q

aetiology of hypopituitarism

A

Neoplastic - pituitary adenoma - most common cause of hypopituitarism

vascular - Sheehan’s, intrasellar aneurysm, pituitary apoplexy

inflammation and infiltrative lesion - lymphocytic hypophysis, hemochromatosis, sarcoidosis

infection - pituitary abscess, pituitary tuberculomas, fungal pituitary disease

congenital

RT

pituitary surgery

40
Q

what is the most common cause of hypopituitarism

A

pituitary adenoma

41
Q

clinical features of hypopituitarism

A
headaches 
FFT 
infertility 
hypoglycaemia 
amenorrhoea/oligomenorrhoea 
glatactorrhoea 
delayed puberty 
visual field defects/opthalmooplegia 
CVD
cold intolerance 
weight gain, N+V, constipation 
fatigue
42
Q

investigation for hypopituitarism

A
  • Refer to endocrinology
  • Bloods: all hormones secreted by the pituitary gland
  • Rx: depends on the cause.
43
Q

definition of pituitary tumors

A

tumor of the pituitary gland which is most commonly benign

44
Q

what is a RF associated with pituitary tumours

A

MEN 1

45
Q

what are the different types of pituitary tumours

A

non-functioning adenoma - reduced symptoms by pressure on surrounding structures

prolactinomas

growth hormone-secreting

adrenocorticotrophic hormone-secreting

Thyroid-stimulating hormone secreting

LH/FSH-secreting tumours

46
Q

clinical features of pituitary tumours

A

depends on the hormone secreted by the tumours as well as the pattern of growth of the tumour within the sell turcica

local effects resulting from a pituitary mass
- headache, neuro-ophthalmologic defect (bitemporal hemianopia), extensive extension into the hypothalamus

anterior pituitary deficiency

  • occurs in the following order, LH, GH, TSH, ACTH, FSH
  • infertility, oligo/amenorrhoea, dec libido, erectile dysfunction, dec muscle bulk, dec body hair, central obesity, small testes
  • in children - delayed or stunned growth
  • diabetes inspidius

hypersecretion
- acromegaly, hyperprolactinaemia, Cushing’s Disease, thyrotoxicosis

47
Q

investigation and treatment

A
  • Refer to endocrinology.
  • Pituitary function screen: GnRH, LHRH, TRH, ACTH, growth hormone, insulin tolerance test.
  • MRI.
  • Rx: depends on cause e.g. bromocriptine for prolactin-secreting tumors.
48
Q

which hormone proves to be a -ve feedback to HPA axis

A

cortisol

49
Q

what are the hormones released in the HPA axis

A

hypothalamus - corticotrophin-releasing hormone to stimulate anterior pituitary gland

anterior pituitary - releases adrenocorticotropic hormone to stimulate the adrenal cortex

adrenal cortex releases cortisol which act as -ve feedback for anterior pituitary gland and hypothalamus

50
Q

what is the main cause of HPA axis suppression?

A

excess glucocorticoids in the system, cortisol = glucocorticoids

51
Q

what is the overall consequence of HPA axis suppression?

A

dec production of both corticotropin-releasing hormone from the hypothalamus and adrenocorticotropic hormone from the pituitary glands –> dec in serum cortisol levels

52
Q

what are some of the causes of HPA axis suppression

A

exogenous glucocorticoids - most common cause

  • sudden cessation or rapid tapering of glucocorticoids
  • common in conditions like asthma and COPD
  • megestrol use
53
Q

clinical features of HPA suppression

A

Hx of weight gain and inc appetite
Hx depression, agitation or sleep disorders
Hx of easy bruising
fatigues, anorexia or weight loss
N+V
dizziness or orthostatic symptoms
mylagia or arthralgia
abdo pain
cushingoid features - moon faces, facial plethora, dorsocervical fat pad, bruising, violaceous abdo striae, thin skin, proximal muscle weakness and centripetal obesity
Hx of difficult to control diabetes or hypertension

54
Q

differentials for HPA suppression

A

primary adrenal insufficiency
pituitary compression, tumour, head trauma and surgery (non-Cushing)
corticosteroids withdrawal

55
Q

investigation and management of HPA suppression

A

refer to endocrinology
ix - serum cortisol (low), synathecen test (rise in cortisol > double, excludes adreneal insufficiency)
treatment - steriods

56
Q

what is pheochromcytoma

A

Benign or malignant tumour of adrenal gland which results in the release of too much epinephrine and norepinephrine.

57
Q

RF for pheochromocytoma

A
  • FHx
  • MEN type 2
  • Von Hippel-Lindau syndrome
  • neurofibromatosis type 1
  • germ-line mutations in succinate dehydrogenase (SDH) - B, -C or _D genes
58
Q

clinical features of pheochromocytoma

A

classic triad - palpitations, headache, diaphoresis

  • Episodic spells of symptoms which vary in duration and get worse as time goes on
  • Young age onset hypertension
  • Resistant intractable hypertension.
59
Q

differentials for pheochromocytoma

A

-anxiety and panic attacks
- essential or intractable hypertension
- illict drugs
- carcinodi syndrome
cardiac arrythemias
menopause
pre-eclampsia

60
Q

investigation for pheochromocytoma

A

Ix

  • 24 hours urine collection for catecholamine, metanephrines, normetanephrines - creatines
  • plasma catecholamines
  • genetics testing
61
Q

Treatment for pheochromocytoma

A

antihypertensives

alpha blockers

beta blockers

surgery

62
Q

definition of Cushing’s Syndrome

A

signs and symptoms that develop after prolonged abnormal elevation of cortisol

63
Q

definition of Cushing’s Disease

A

refer to specific condition where a pituitary adenoma secretes excessive ACTH

64
Q

aetiology of Cushing’s Syndrome

A
  • exogenous steroid
  • adrenal adenoma
  • paraneoplastic cushing’s - excess ACTH from cancer eg SCLC
65
Q

clinical features of Cushing’s Syndrome

A

round in the top and middle with thin limbs

  • moon face
  • central obesity
  • abdo striae
  • buffalo hump (fat pad)
  • proximal limb muscle wasting

high level of stress hormone

  • hypertension
  • cardiac hypertrophy
  • T2DM
  • depression
  • insomnia
  • oesteoporosis
  • easy bruising and poor skin healing
66
Q

investigation and treatment of Cushing’s syndrome

A

Dexamethasone suppression test - given at 10 pm at night and measure at 9am

if at low dose test - high/normal cortisol level –> then Cushing’s syndrome

MRI

treatment - surgery

67
Q

pathophysiology of adrenogenital syndrome

A

aka congenital adrenal hyperplasia

  • Deficiency of 21-hydroxylase = required for cortisol (stress response) and aldosterone (blood pressure and Na+ and K+) synthesis
  • Low cortisol increases ACTH = adrenal hyperplasia and increased synthesis of androgen

• Unable to produce aldosterone = salt loss.
- causing the development of male features in females and early puberty in both boys and girls

68
Q

what is the genetic patterns of adrenogenital syndrome?

A

autosomal recessive

69
Q

what are the clinical features of adrenogenital syndrome

A

female virilisation (inc muscle bulk etc), clitoral hypertrophy and fusion of labia (ambiguous genitalia)

male have enlarged penis and pigmented scrotum

salt losing adrenal crisis - vomiting, weight loss, hypotonia, circulatory collapse

non-salt losers - tall statures, muscle bulk, precocious pubarche, acne, pubic hair

70
Q

investigation for adrenogenital syndrome

A

RAISED 17 A hydroxy-progesterone
urine and blood steroids (low)
hyponatraemia, hyperkalaemia, hypoglycaemia

71
Q

treatment for adrenogenital syndrome

A

 Female- corrective and constructive surgery
 Salt losing crisis – sodium chloride, glucose and hydrocortisone IV.

1)Long-term
 Life long glucocorticoids (hydrocortisone)
 Mineral corticoids (for salt loss) (mineral cortisone)
 Monitor growth, skeletal maturity and plasma androgens and 17 a hydroxy progesterone
 Illness- IM cortisol

72
Q

what is the job of aldosterone?

A

regular blood pressure, blood volume, level of NA+, K+ and H+ through the RAA system

73
Q

what is Conn’s syndrome

A

primary hyperaldoseteronism

  • when adrenal glands are directly responsible for producing too much aldosterone
  • serum renin will be low as it is suppressed by the high BP
74
Q

aetiology of Conn’s syndrome

A
  • adrenal adenoma secreting aldosterone (most common)
  • bilateral adrenal hyperplasia
  • familial hyperaldosteronism type 1 and type 2 - rare
  • adrenal carcinoma (rare)
75
Q

what is secondary hyperaldosteronism

A

excessive renin stimulating the adrenal glands to produce more aldosterone

76
Q

aetiology of secondary hyperaldosteronism

A
  • serum renin will be high
  • renal artery stenosis
  • renal artery obstruction
  • heart failure
77
Q

clinical features of hyperaldosteronsims

A
high BP 
fatigue 
headache 
vision problems 
muscle weakness - caused by hypokalemia 
numbness 
temporary paralysis 
inc urination 
inc thrist
78
Q

investigation for hyperaldosteronism

A

investigation

  • renin/aldosterone ration (high aldoseterone + low renin = primary), (high aldosterone + high renin = secondary)
  • BP
  • U&E (hypokalaemia, hypernatreamia)
  • ABG (alkalosis) due to excretion of H+ ion

Treatment
- aldosteron antagonist –> eplerenone, spironolactone, surgery, percutaneous angioplasty for renal artery stenosis