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Endocrinology Flashcards

1
Q

What is Cushing’s DISEASE?

A

Pituitary adenoma which secretes excess ACTH

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2
Q

What are the causes of Cushing’s syndrome?

A

Pituitary adenoma
Adrenal adenoma
Paraneoplastic ACTH secretion - in SCLC associated with very low K+
Exogenous steroid use: prescription or non-prescription

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3
Q

What are the features of Cushing’s syndrome?

A 
Central obesity with proximal muscle wasting
Round face / C-spine hump
Striae and skin thinning, easy bruising
Fatigue, depression, insomnia
Hypertension and hyperglycaemia
Osteoporosis

Hypokalaemic metabolic alkalosis

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4
Q

How do you diagnose Cushing’s syndrome?

A

Dexamethasone suppression test:

Low dose: if suppression of cortisol production, normal
1mg if no suppression of cortisol, Cushing’s syndrome present

High dose: if suppression of cortisol production, Cushing’s DISEASE (pituitary adenoma)
8mg if no suppression of cortisol, peripheral cause of disease
if ACTH suppressed = adrenal adenoma, if not = ectopic production

MRI brain can look for pituitary adenoma
CT TAP- look for SCLC, adrenal adenoma

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5
Q

How do you manage Cushing’s syndrome?

A

In pituitary adenoma: trans-sphenoidal surgery
In adrenal adenoma: surgical removal

Removal of adrenal glands and lifelong replacement
Medical management: metyrapone inhibits cortisol production, ketoconazole

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6
Q

What are the types of adrenal insufficiency?

A

Primary: Addison’s disease= autoimmune condition whereby there is reduced secretion of cortisol and aldosterone

Secondary: Inadequate ACTH production - Damage to pituitary gland / hypoperfusion e.g. Sheehan’s

Tertiary: inadequate hypothalamic production of CRH (usually after cessation of long-term steroids)

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7
Q

What are the symptoms/signs of adrenal insufficiency?

A

Fatigue
Reduced libido
Weight loss
Nausea, cramps, abdominal pain

Signs:
Bronze colouration of the skin- esp palmar creases
Vitiligo
Hypotension, hypoglycaemia

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8
Q

What U&Es would you expect in Addison’s disease?

A

Low sodium and High potassium

May also have low glucose and a metabolic acidosis

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9
Q

How is Addison’s disease diagnosed?

A

Short synacthen test: failure of cortisol to rise = primary insufficiency

ACTH stimulation testing can be used to diagnose secondary causes

Antibody testing: adrenal cortex ab, 21-hydroxylase ab

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10
Q

How can different types of adrenal insufficiency be differentiated?

A

ACTH level: high in primary failure, low in secondary and tertiary

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11
Q

How do you manage adrenal insufficiency?

A

Fludrocortisone to replace aldosterone
Hydrocortisone to replace cortisol

Steroid cards should be carried at all times
Double dose of hydrocortisone in illness, fludrocortisone should stay the same
Should be treated with IM hydrocortisone injections to treat adrenal crisis

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12
Q

What are the symptoms of Addisonian crisis?

A 
Reduced consciousness
Pyrexia
Hypotension
Hypoglycaemia
Hyponatraemia
HYPERKALAEMIA
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13
Q

How would you manage Addisonian crisis?

A

IV hydrocortisone 100mg STAT and 6 hourly
IV fluids
Correct hypoglycaemia
Manage hyperkalaemia

Close monitoring of fluid balance and electrolytes

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14
Q

What are the types of hyperaldosteronism?

A

Primary: Conn’s syndrome (adrenal adenoma, adrenal hyperplasia, adrenal carcinoma, familial hyperaldosteronism)

Secondary: renal artery stenosis, renal artery obstruction, heart failure causing INCREASED renin production which stimulates aldosterone production

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15
Q

What are the features of hyperaldosteronism?

A

Nocturia, polyuria, thirst
Fatigue
Mood changes, inability to concentrate

Hypertension
Hypokalaemia
Alkalosis on ABG

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16
Q

How would you investigate hyperaldosteronism?

A

Renin: Aldosterone ratio: low renin, high aldosterone = primary, both raised in secondary

CT/MRI adrenal glands

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17
Q

How is hyperaldosteronism managed?

A

Aldosterone antagonists: epleronone, spironolactone

Treat cause: surgical removal of adenoma, percutaneous renal artery angioplasty

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18
Q

What is the action of ADH?

A

Stimulates water reabsorption in the collecting ducts of the kidney.

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19
Q

What are the causes of SIADH?

A 
Post-operative
Atypical pneumonia / lung abscess
Head injury
Malignancy
Medication: Thiazides, NSAIDs, chemo, antipsychotics, SSRIs
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20
Q

What are the symptoms of SIADH?

A

Headache, fatigue, confusion
Muscle aches and cramps
May have nausea and vomiting but are generally EUVOLEMIC

Severe hyponatraemia can cause seizures and reduced consciousness

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21
Q

What would you find on investigation for SIADH?

A

Euvolemic on hydration status
U&E: hyponatraemia

Urinary sodium + osmolality raised
Serum sodium and osmolality low

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22
Q

How is SIADH managed?

A

Identify cause + treat e.g. stop causative medication
Slow sodium replacement with hypertonic saline (max 10mmol/L/24hr increase)
Fluid restriction to 500-1000ml per day

Tolvaptan can be used as a ADH receptor antagonist

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23
Q

What complication do you need to be careful of when replacing sodium in SIADH?

A

Central Pontine Myelinolysis

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24
Q

What is central pontine myelinolysis?

A

Osmotic demyelination syndrome
Water moves by osmosis across the BBB when there is low low sodium in the blood, the brain adapts to this and lowers solutes to prevent oedema. If hyponatraemia fixed too quickly, water will move back across too quickly and cause demyelination.

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25
Q

What are the symptoms of central pontine myelinolysis?

A
  1. Due to electrolyte imbalance:
    Encephalopathy, confusion, headache, nausea, vomiting
  2. Due to neurone demyelination
    Spastic quadraparesis, pseudobulbar palsy, cognitive and behavioural change, risk of death
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26
Q

What is diabetes insipidus?

A

Either reduced production or reduced sensitivity to ADH, preventing the kidneys from being able to concentrate urine

Two types: nephrogenic and cranial

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27
Q

What are the symptoms of diabetes insipidus?

A

Polydipsia and polyuria
Hypovolemia/dehydration
Postural hypotension

HYPERNATRAEMIA - may cause weakness, restlessness, lethargy, confusion, seizures

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28
Q

What are the symptoms of diabetes insipidus?

A

Polydipsia and polyuria
Hypovolemia/dehydration
Postural hypotension

HYPERNATRAEMIA - may cause weakness, restlessness, lethargy, confusion, seizures

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29
Q

What are the causes of diabetes insipidus?

A

Nephrogenic: Kidney does not respond to ADH
Medication especially LITHIUM, renal disease, hypercalcaemia/hypokalaemia, ADH receptor mutation

Cranial: Reduced ADH production
brain tumour, head injury, brain malformation/infection, surgery/radiotherapy

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30
Q

What are the investigations for diabetes insipidus?

A

Urine osmolality: low
Urine sodium: low
Serum osmolality: high
Serum sodium: high

Water deprivation test + desmopressin suppression test = gold standard
Water deprivation- no change in osmolality rules out psychogenic polydipsia
If desmopressin causes suppression: cranial DI, if no suppression: nephrogenic DI

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31
Q

What is the diagnostic test for DI?

A

Water deprivation + desmopressin suppression test

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32
Q

What is the management for diabetes insipidus?

A

Desmopressin - in nephrogenic, need much higher doses and close monitoring

Prevent dehydration + electrolyte imbalances

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33
Q

What is phaeochromocytoma?

A

Tumour of adrenal chromaffin cells -> catecholamine secretion
25% familial
Associated with MEN2

10% rules: 10% bilateral, 10% malignant, 10% located outside adrenal glands

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34
Q

What are symptoms of phaeochromocytoma ?

A

Often secrete in bursts, leading to periods of symptoms of worsening and settling

Anxiety, sweating, headache
Hypertension, tachycardia, palpitations
Paroxysmal AF

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35
Q

How is phaeochromocytoma diagnosed?

A

24 hourly urine catecholamines
Plasma free metanephrines
Genetic testing

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36
Q

How is phaeochromocytoma managed?

A

a-blockers: phenoxybenzamine
B-blockers once established on a-blockers
Adrenalectomy - symptoms should be medically managed before surgery

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37
Q

What is acromegaly?

A

Excessive growth hormone production.
Most commonly caused by pituitary adenoma (95%)
Can also be due to cancer secreting GHRH or GH, usually SCLC or pancreatic cancer.

38
Q

What symptoms are associated with acromegaly?

A

May have headache and bitemporal hemianopia associated with pituitary adenoma.

Tissue overgrowth: prominent forehead and brow, large nose, large tongue, large hands and feet, large protruding jaw, arthritis

Organ dysfunction: heart hypertrophy, HTN, T2DM, colorectal Ca

Raised GH: skin tags, profuse sweating and oily skin. 30% also present with ^ prolactin and galactorrhoea

39
Q

What complications are associated with acromegaly?

A

Hypertension
Diabetes
Cardiomyopathy
Colorectal cancer

40
Q

What investigations should be done in acromegaly?

A

IGF-1 = first line screening test
OGTT while measuring GH= usually high glucose and low GH, used to confirm
MRI brain
Visual field testing

41
Q

How is acromegaly managed?

A

Trans-sphenoidal surgery = 1st line

Management of ectopic hormone-producing cancers

Medical GH blockers: somatostatin analogues, dopamine agonists, GH receptor blockers

42
Q

What are causes of hypothyroidism?

A

Hashimoto’s thyroiditis : Anti-TPO antibodies
Iodine deficiency
Hyperthyroidism treatment
Medication: lithium, amiodarone
Central causes: hypopituitarism, tumours, infection, vascular, radiation

43
Q

What are symptoms of hypothyroidism?

A 
Fatigue, lethargy, weight gain
Intolerance of the cold
Dry skin, coarse hair, brittle nails
Hair loss
Menorrhagia
Constipation
44
Q

What are signs of hypothyroidism on examination?

A 
Weight gain
Fatigue
Cold
Bradicardia
Cerebellar ataxia
Ascites/oedema
Round face/obesity 
Ileus 
Goitre
Hyporeflexia
45
Q

What is the management of hypothyroidism?

A

Levothyroxine: review after 4 weeks and adjust 4-6weekly as needed
In pregnancy, dose needs to be increased 25-30% in T1

Caution should be taken in the elderly and those with ischaemic heart disease

46
Q

What are the causes of hyperthyroidism?

A

Grave’s disease: TSH receptor-stimulating antibodies
Solitary toxic nodule
Toxic multinodular goitre
Thyroiditis: drug-induced, post-partum, De Quervain’s

47
Q

What symptoms are specific to Grave’s disease?

A

Thyroid eye disease: exophthalmus, lid lag, ophthalmoplegia
Proximal myopathy
Pretibial myxoedema
Diffuse goitre

48
Q

What is De Quervain’s thyroiditis?

A

Hyperthyroidism triggered by infection
Fever + neck tenderness/pain + dysphagia + hyperthyroidism
Often followed by hypothyroid phase

Self limiting, supportive treatment with NSAIDs

49
Q

What are symptoms of thyroid eye disease?

A 
Grittiness, discomfort
Photophobia
Excessive lacrimation
Diplopia, reduced visual acuity
Pupil defects

Exophthalmus, proptosis, ophthalmoplegia, papilloedema

50
Q

How do you test for thyroid eye disease?

A

H-test
Lid lag
Fundoscopy

51
Q

What is the management for hyperthyroidism?

A

1st line = carbimazole, takes 4-8 weeks to work, often can stop after 18m
2nd line = PTU due to risk of severe hepatic reaction

B-blockers for symptomatic treatment

Radioactive iodine: can’t get pregnant for 6m, avoid contact with children and pregnant women for 3w

Surgical removal of thyroid + replacement

52
Q

What is the key side effect to look out for with carbimazole treatment?

A

Agranulocytosis

53
Q

Which drug is preferred in pregnancy for hyperthyroidism?

A

Propylthiouracil

54
Q

What are the symptoms of thyroid storm?

A 
Agitation, confusion
Tachycardia, hyperthermia
AF, palpitations, symptoms of heart failure
D&V
Thyroid bruit
Coma
55
Q

How do you manage somebody in thyroid storm?

A 
IV access + fluids
NG tube if vomiting
Cardiac and BP monitoring
Bloods: TFTs
Propranolol +/- digoxin
Antithyroid medication
Steroids to prevent peripheral conversion of T4 to T3
56
Q

What is the most common thyroid cancer?

A

Papillary (60%)

57
Q

What are the symptoms as hyperparathyroidism?

A

Renal stones
Painful bones
Abdominal groans : constipation, N&V
Psychiatric moans: fatigue, depression, psychosis

58
Q

What is the function of parathyroid hormone?

A

To increase calcium levels in the blood by:
Increasing osteoclast activity
Increasing intestinal absorption + renal reabsorption
Increasing vitamin D activity, which further increases calcium absorption

59
Q

What are the causes of different types of hyperparathyroidism?

A

Primary: parathyroid tumour

Secondary: renal disease/vitamin D deficiency, causes low calcium and PT glands compensate -> hyperplasia

Tertiary: Secondary HPT causes gland hyperplasia which causes higher baseline level of PTH

60
Q

What bloods would you expect in primary hyperparathyroidism?

A

Raised calcium, PTH and vitamin D, low phosphate

61
Q

What bloods would you expect in secondary hyperparathyroidism?

A

High PTH, high or normal calcium, low vitamin D

62
Q

What bloods would you expect in tertiary hyperparathyroidism?

A

High PTH, high calcium, high phosphate, low vitamin D

63
Q

How is primary hyperparathyroidism managed?

A

Surgical management of the tumour

64
Q

How is secondary hyperparathyroidism managed?

A

Calcium and vitamin D supplements

Renal transplant

65
Q

How is tertiary hyperparathyroidism managed?

A

Surgical removal of SOME of the parathyroid tissue

66
Q

What are the blood parameters for diagnosing diabetes?

A

Random/OGTT > 11 and fasting >7 mmol/L on 2 occasions

HbA1c over 48 mmol/mol

67
Q

What is the management for DKA?

A

FIGPICK

Fluids: 1L NaCl STAT, 4L + K+ over 12 hours
Insulin: actrapid 0.1unit/kg/hr
Glucose: add dextrose once gluc <14mmol/L
Potassium: monitor 4hrly and correct
Infection: treat underlying triggers
Chart fluid balance
Ketones- monitor

68
Q

What is the management of HHS?

A

Slow rehydration to prevent cerebral oedema
LMWH prophylaxis of VTE
Replace K+
Maintain blood glucose 10-15 for first 24 hours to prevent cerebral oedema

69
Q

What are the key side effects of metformin?

A

GI side effects

Lactic acidosis - not suitable in severe renal impairment

70
Q

In which populations are pioglitazone contraindicated?

A

Heart failure

Current or previous bladder cancer

71
Q

What are side effects of pioglitazone?

A

Weight gain, visual disturbance, bone fracture

72
Q

What are side effects of sulphonylureas e.g. gliclazide?

A

Weight gain
Hypoglycaemia
Nausea and diarrhoea
Increased risk CVD and MI

73
Q

Which diabetes medication increases risk of pancreatitis?

A

DPP4-inhibitors such as sitagliptin

74
Q

What are potential side effects of SGLT2 inhibitiors?

A 
Hypoglycaemia
Thrush, UTI
Genital necrotising fasciitis
Weight loss
DKA
75
Q

What is congenital adrenal hyperplasia?

A

Group of autosomal recessive disorders which affect steroid synthesis.

In response to loww steroid production, the anterior pituitary secretes a lot of ACTH which stimulates adrenal androgen production and causes hyperplasia

Can cause females to develop secondary male sexual characteristics

76
Q

What are features of congenital adrenal hyperplasia?

A

Virilisation of female genitalia
Precocious puberty in males
Hypertension
Salt losing crises

77
Q

What are the causes of pseudo-cushings?

A

Alcohol excess

Severe depression

78
Q

Which antibodies are associated with T1DM?

A

Antibodies to glutamic acid decarboxylase (anti-GAD)
Islet cell antibodies
Insulin autoantibodies (very common in young children with T1DM)

79
Q

What are examples of GLP-1 mimetics?

A

Liraglutide, Exenatide

Liraglutide often preferred as only needs to be administered once daily

80
Q

What are examples of DPP-4 inhibitors?

A

Sitagliptin, vildagliptin

81
Q

At what HBa1c should a second drug be added to metformin treatment?

A

58 mmol/mol

82
Q

Which diabetes medication is best for those taking part in ramadan?

A

Pioglitazone

83
Q

What is androgen insensitivity syndrome?

A

X-linked recessive condition.
Defect in androgen receptor results in resistance to testosterone & genotypically male children (46XY) to have a female phenotype.

Rudimentary vagina and testes present but no uterus.

Testosterone, oestrogen and LH levels are elevated

84
Q

What is 5-a reductase deficiency?

A

Autosomal recessive condition. 46 XY
Results in the inability of males to convert testosterone to dihydrotestosterone (DHT).

Individuals have ambiguous genitalia in the newborn period.
Hypospadias is common.
Virilization at puberty.

85
Q

What are the conditions for being able to drive with diabetes?

A

Awareness of hypos
No more than 1 hypo requiring help of another person within past 12 months
No visual impairment as a result
Neurological/physical ability to stop

86
Q

What is Kallmann’s Syndrome?

A

X-linked recessive condition which causes delayed puberty in men secondary to hypogonadotropic hypogonadism.

Typically: anosmia in a boy with delayed puberty.

Low levels of LH and FSH, usually normal or above average height

87
Q

What is Klinefelter’s syndrome?

A

47 XXY

Often taller than average with small, firm testes
Lack of secondary sexual characteristics
Infertile
Gynaecomastia
Elevated FSH/LH but low testosterone
88
Q

Which malignancies are associated with MEN 1?

A

3Ps:
Parathyroid
Pancreas
Pituitary

Most common presentation = hypercalcaemia

89
Q

Which malignancies are associated with MEN2?

A

Medullary thyroid cancer
Parathyroid
Phaeochromocytoma

Neuromas

90
Q

How does myxoedema coma usually present?

A

Hypothermia and confusion

91
Q

What is first line treatment for prolactinoma?

A

Bromocriptine

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