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PT prep > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Hormones released from the anterior pituitary gland

A 
LH
FSH
TSH
Prolactin
ACTH
GH
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2
Q

Hormones released from the posterior pituitary gland

A

Vasopressin/ADH

Oxytocin

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3
Q

Pathophysiology of T1DM

A

Autoimmune destruction of pancreatic beta cells in the islets of Langerhans

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4
Q

Pathophysiology of T2DM

A

Decreased insulin secretion and increased insulin resistance peripherally

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5
Q

Maturity onset diabetes of the young is what kind of diabetes

A

Type 2

Rare autosomal dominant

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6
Q

What is an impaired glucose tolerance?

A

Fasting <7mmol/L (otherwise this is diabetes)

2 hour glucose >7.8mmol/L but <11.1mmol/L

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7
Q

What is impaired fasting glucose?

A

Fasting >6.1 but <7mmol/L

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8
Q

What is metabolic syndrome/ syndrome X?

A 
Central obesity (BMI>30)
BP 130/85
fasting glucose >5.6
T2DM
Various forms of hyperlipidaemia
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9
Q

Diagnosis of T2DM

A

Symptoms of hyperglycaemia and raised venous glucose detected once- fasting >7mmol/L or random >11.1
OR
Raised venous glucose on two separate occassions
HbA1c >48mmol/mol

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10
Q

Symptoms of hyperglycaemia

A

Polyuria, polydipsia, unexplained weight loss, visual blurring, genital thrush, lethargy

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11
Q

Clinical features of hypoglycaemia

A

Autonomic- sweating, anxiety, hunger, tremor, palpitations, dizziness
Neuroglycopenic- confusion, drowsiness, visual trouble, seizures, coma, rarely focal neurology, personality change, restlessness

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12
Q

Definition of hypoglycaemia

A

<4mmol/L plasma glucose

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13
Q

Fasting hypoglycaemia aetiology

A 
Insulin or sulphonylurea treatment in a diabetic is the top cause
Non-diabetics 
EXogenous drugs- insulin, oral hypoglycaemics
Pituitary insufficicency 
Liver failure
Addison's disease
Islet cell tumours- insulinoma
Neoplasms
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14
Q

Effect of active T3 and T4 in the body

A

Increase cell metabolism

Increase catecholamine effects

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15
Q

Why should TFTs be taken at the same time each day?

A

Trough at 2pm and higher in the night- variation throughout

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16
Q

Sick euthyroid tests

A

All low- should recover after illness, retest once recovered

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17
Q

What are anti-TPO antibodies and when are they raised?

A

Anti-thyroid peroxidase antibodies
Raised in autoimmune disease- Hashimoto’s or Graves’ disease
If positive in Graves then there is a chance of hypothyroidism following

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18
Q

TSH receptor antibody present in

A

Graves’ disease

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19
Q

Serum thyroglobulin useful as

A

A tumour marker to monitor the treatment of carcinoma

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20
Q

Clinical features of thyrotoxicosis

A

Symptoms- diarrhoea, weight loss, increased appetite, over-active, sweaty, heat intolerant, palpitations, tremor, irritability, labile emotions, oligomenorrhoea +/- infertility
Rarely psychosis, chorea, panic, itch, alopecia, urticaria

Signs- tachycardic, irregular pulse, warm moist skin, fine tremor, palmar erythema, thin hair, lid lag, lid retraction

Examination- goitre, thyroid nodules, bruit

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21
Q

Signs specific to Graves’ disease

A

Exophthalmos, ophthalmoplegia, proptosis
Pretibial myxoedema
Thyroid acropatchy

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22
Q

Tests in thyrotoxicosis

A 
May be mild normocytic anaemia
Mild neutropenia 
Raised T3 and T4
Low TSH
Raised ESR
Raised Ca
Raised LFTs
Thyroid autoantibodies- TPO and TSH receptor antibody
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23
Q

Treatment of thyrotoxicosis

A

Symptomatic control with beta blockers- propanolol
Anti-thyroid hormone- carbimazole ‘block’
Levothyroxine ‘replace’
Radioiodine if become hypothyroid post-treatment, though beware thyroid storm
Thyroidectomy

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24
Q

Causes of thyroid goitre

A

Physiological
Graves’ disease
Hashimoto’s thyroiditis
Subacute de Quervain’s thyroiditis (self-limiting post-illness)

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25
Q

Clinical features of hypothyroidism

A

Symptoms- tiredness, lethargic, decreased mood, cold intolerance, weight gain, constipation, menorrhagia, hoarse voice, decreased memory/ cognition, dementia, myalgia, cramps, weakness

Signs- bradycardic, reflexes relax slowly, ataxia, dry thin hair/ skin, yawning, drowsiness, coma, cold hands, ascites, round puffy face, defeated demeanour, immobile,

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26
Q

Aetiology of hypothyroidism

A

Primary atrophic hypothyroidism
Hashimoto’s thyroiditis-goitre
Drug induced- amiodarone, anti-thyroid, lithium, iodine
Secondary due to hypopituitarism

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27
Q

What is myxoedema coma?

A

The ultimate hypothyroid state before death

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28
Q

Risks from subclinical hyperthyroidism

A

AF and osteoporosis

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29
Q

Actions of parathyroid hormone

A

Increasing osteoclast activity releasing calcium and phosphate from the bones
Increases calcium reabsorption in the kidneys and acts as a phosphaturic agent
Increases hydroxylation of 1-hydroxycholecalciferol in the kidney to 1,25-dihydroxycholecalciferol which acts to increase calcium uptake from the intestines

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30
Q

Primary hyperparathyroidism clinical features

A

Symptoms- signs relating to hypercalcaemia
Bone pain, fractures and osteopenia/osteoporosis
HTN

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31
Q

Signs of hypercalcaemia

A 
Weak, tired, depressed, thirsty
Dehydrated but polyuric 
Renal stones
Abdominal pain
Pancreatitis 
Ulcers
Psychosis
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32
Q

Tests for primary hyperparathyroidism

A 
Calcium (increased)
PTH (increased)
Phosphate (decreased)
ALP (increased)
Pepper pot skull on XR
DEXA for osteoporosis
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33
Q

Secondary hyperparathyroidism

A

Low calcium

Appropriately raised PTH

34
Q

Aetiology of secondary hyperparathyroidism

A

Decreased vitamin D intake

Chronic renal failure

35
Q

Tertiary hyperparathyroidism

A

Increased calcium
Inappropriately increased PTH
Prolonged secondary hyperparathyroidism the glands act autonomously having undergone hyperplastic change

36
Q

Signs of hypocalcaemia

A 
Tetany- twitching, cramping, spasm 
Depression
Cataracts
QT prolongation
Trousseau's sign- BP cuff inflated
Chvostek's sign- tapping of parotid gland results in facial nerve twitching
Perioral paraesthesia
37
Q

Causes of hypocalcaemia

A 
Vit D deficiency
Renal disease
Hypomagnesaemia
Hypoparathyroidism 
End organ resistance to PTH or Vit D
38
Q

von-Hippel Lindau syndrome

A

Mutation of a tumour suppressor gene resulting in renal cysts and cancer, retinal and cerebellar haemangioblastoma and phaeochromocytoma

39
Q

Peutz-Jegher’s syndrome

A

Mutation of a tumour suppressor gene resulting in mucocutaneous dark freckles on lips, oral mucosa, palms and soles and multiple GI polyps- raising GI cancer risk by 15 fold

40
Q

Multiple Endocrine Neoplasm 1

A

Parathyroid hyperplasia
Pancreas endocrine tumours- gastrinoma or insulinoma
Pituitary prolactinoma or GH secreting tumour (acromegaly)

41
Q

MEN-2a

A

Thyroid medullary carcinoma- 100%
Phaeochromocytoma
Parathyroid hyperplasia

42
Q

MEN-2b

A

Similar to MEN-2a but with mucosal neuromas and marfanoid appearance without hyperparathyroidism

43
Q

Side effects of steroids

A

GI- peptic ulcer, acute pancreatitis
Endocrine- Cushing’s syndrome- intrascapular fat pad, moon-face, thin limbs, central obesity, impaired glucose tolerance leading to T2DM, increased appetite and weight gain
Immunosuppression
Growth suppression in children
Neutrophilia
MSK- proximal muscle myopathy, osteoporosis, avascular necrosis of the femoral head
Easy bruising, thinning of the skin
Ophthalmic- glaucoma, cataracts
Psychiatric- insomnia, psychosis, mania, depression
Fluid retention
Hypertension from the mineralocorticoid activity

44
Q

Adrenal cortex areas and steroids produced

A

Zona glomerulosa- mineralocorticoids
Zona fasciculata- glucocorticoids
Zona reticularis- androgens

45
Q

HPA axis

A

CRH (hypothalamus)–>ACTH (anterior pituitary)–> cortisol and androgens (cortex)

46
Q

ACTH dependent causes of Cushing’s syndrome

A

Cushing’s disease- bilateral adrenal hyperplasia from an ACTH secreting pituitary adenoma
Ectopic ACTH production- small cell lung carcinoma and carcinoid tumours

47
Q

ACTH independent causes of Cushing’s sydrome

A

Iatrogenic- steroids
Adrenal cancer
Adrenal nodular hyperplasia

48
Q

Investigating suspected Cushing’s syndrome

A

1st line tests
Overnight dexamethasone suppression test- 1mg at midnight, serum cortisol at 8am- normally should suppress but not in Cushing’s
24 hour free cortisol

2nd line tests
48 hour dexamethasone suppression test- give for 2 days and measure cortisol at 0 and 48hrs- failure to suppress cortisol in Cushing’s

Localising
Plasma ACTH- if undetectable then ACTH independent- adrenal tumour likely

49
Q

Treatment for Cushing’s syndrome

A

Depends on the cause
Stop medications
Removal of pituitary adenoma if Cushing’s disease
Adrenalectomy
If ectopic ACTH then locate and surgery if not spread

50
Q

What is Addison’s disease?

A

Primary adrenal insufficiency

51
Q

Aetiology of Addison’s disease

A 
Autoimmune
TB
Adrenal metastases 
Lymphoma
Opportunistic infections 
Adrenal haemorrhage
Secondary from long term steroid use
52
Q

Symptoms of Addison’s disease

A 
Lean, tanned, tearful and tired
Weakness
Anorexia
Faints
Myalgias and arthralgias 
Depression and psychosis
Nausea and vomiting, abdo pain, diarrhoea or constipation
53
Q

Investigations for Addison’s disease

A

Low mineralocorticoids leading to low sodium and raised potassium
Low glucose due to low glucocorticoid
Raised calcium

Short ACTH test- synacthen test- plasma cortisol before and after- expecting low cortisol (excluded above 550)
9AM ACTH inappropriately high
21 hydroxylase adrenal autoantibodies in 80%
Plasma renin and aldosterone to assess mineralocorticoid status

54
Q

Treatment for Addison’s disease

A

Replace steroids- hydrocortisone and mineralocorticoid- fludrocortisone

55
Q

Primary hyperaldosteronism

A

Excess production of aldosterone resulting in increased sodium and water retention and decreased renin release
Hypokalaemia and alkalosis

56
Q

Signs of hypokalaemia

A

Weakness, cramps, worsening DM control or polyuria
Palpitations
Psychological symptoms

57
Q

Aetiology of primary hyperaldosteronism

A

2/3 are Conn’s syndrome- aldosterone producing adenoma

1/3 due to bilateral adrenal hyperplasia

58
Q

Secondary hyperaldosteronism

A

Due to increased renin from decreased renal perfusion

Renal artery stenosis, HTN, CCF

59
Q

Tests for hyperaldosteronism

A

U&Es

Renin and aldosterone ratio

60
Q

Treatment for hyperaldosteronism

A

Conn’s- laparoscopic adrenalectomy

Adrenal hyperplasia- medical management with an MRA

61
Q

Classic symptoms of phaeochromocytoma

A

Sweating, episodic headache, tachycardia

Palpitations, anxiety, pallor

62
Q

Investigating phaeochromocytoma

A

24 urinary metanephrines

63
Q

Treatment of phaeochromocytoma

A 
Alpha blockade (phenoxybenzamine) then beta blockade (to avoid unopposed alpha adrenergic stimulation)
Surgery
64
Q

When to think of Conn’s with HTN

A

Hypokalaemia
Refractory (more than 3 drugs)
Early onset HTN <40, especially women

65
Q

What is virilism

A

The appearance of male secondary sexual characteristics in women

66
Q

Polycystic ovarian syndrome clinical features

A 
Bilateral polycystic ovaries (on ultrasound)
Oligo or amenorrhoea
Infertility
Hirsutism 
Obesity
Acne
67
Q

Management of PCOS

A

Healthy eating, optimize weight, shaving, laser photoepilation, wax, electrolysis
Oestrogens
Metformin and spironolactone
Clomifene for infertility

68
Q

The big three: organic causes of erectile dysfunction

A

Diabetes
Smoking
Alcohol

69
Q

Workup for erectile dysfunction

A

Full sexual and psychological history

U&Es, LFT, glucose, TFT, LH, FSH, lipids, testosterone, prolactin and Doppler- penile arterial inflow

70
Q

Side effects of sildenafil

A

Headache
Flushing
Dyspepsia
Transient blue-green tingeing of vision

71
Q

Features of local pressure from a pituitary adenoma

A

Headache
Visual field defects- bilateral temporal hemianopia- compression of the optic chiasm
palsy of cranial nerves III,IV,VI- pressure or invasion of the cavernous sinus
Diabetes insipidus
Disturbance of sleep and appetite

72
Q

What is pituitary apoplexy?

A

Rapid pituitary enlargement from bleeding into a tumour
Mass effects, cardiovascular collapse due to hypopituitarism
Sudden headache, meningism, decreasing GCS, visual defect

73
Q

Signs of acromegaly

A 
Increased growth of hands, jaw and feet
Coarsening facial features 
Macroglossia
Skin darkening
Acanthosis nigricans
Obstructive sleep apnoea
Goitre
Proximal weakness and arthropathy 
Carpal tunnel signs 
Signs from pituitary mass
74
Q

Complications of acromegaly

A

Impaired glucose tolerance
Vascular- cardiomyopathy, increased BP, LV hypertrophy,
Increased risk of colon cancer

75
Q

Why is random GH not an accurate test for acromegaly?

A

Secreted in a pulsatile fashion

Samples should be collected every 30 minutes

76
Q

What is diabetes insipidus?

A

Passage of large volumes of dilute urine due to impaired water resorption by the kidneys because of reduced ADH secretion from the posterior pituitary (cranial) or impaired response to ADH in the kidney (nephrogenic)

77
Q

Causes of cranial diabetes insipidus

A 
Tumour- craniopharyngioma, mets, pituitary 
Trauma
Infiltration- sarcoidosis
Vascular- haemorrhage
Infection- meningoencephalitis
78
Q

Causes of nephrogenic diabetes insipidus

A 
Inherited
Metabolic- low potassium, high calcium
Drugs- lithium
CKD
Post-obstructive uropathy
79
Q

How to calculate serum osmolality

A

(2xNa) + glucose + urea

80
Q

How to exclude DI with urine and serum osmolality

A

If the ratio of urine:serum osmolality is greater than 2:1

81
Q

Diagnosis of diabetes insipidus

A

Water deprivation test for 8 hours

Testing the kidneys ability to concentrate urine when dehydrated

82
Q

First line antihypertensive in a black T2DM of 59 years old

A

ARB- eg. losartan

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