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Year 3 OSCE > Case 16- Obesity > Flashcards

Case 16- Obesity Flashcards

1
Q

Cushings Syndrome Sx

A

Facial plethora, fat redistribution, skin bruising and thinning, violaceous abdominal striae, proximal myopathy, HTN, impaired glucose tolerance, hypokalaemia, osteoporosis, acne, hirsutism

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2
Q

Investigations for suspected cushings

A

BP, FBC (WCC), UE (hypernatraemia, hypokalaemia, metabolic acidosis)
Salivary night time cortisol- 2 samples taken or 24 hour urinary free cortisol
Overnight Dexamethasone suppression test- gold standard for outpatient (inpatient- 24 hour urinary cortisol). If abnormal do one of the following;

Venous sampling for ACTH
MRI brain
Chest CT- SCLC
Abdominal CT for adrenal tumours

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3
Q

Investigations for hyperaldosteronism

A

BP- HTN
FBC, UE, ABG- hypokalaemia and alkalosis
Aldosterone/ renin ratio- high aldosterone low renin for Conn’s. Should be first line
High resolution CT abdomen and adrenal vein sampling
Ct angiogram kidneys

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4
Q

Investigations for adrenal insufficiency

A

BP- hypotension
FBC, UE- hyponatraemia, hyperkalaemia, metabolic acidosis (normal anion gap)
Early morning cortisol (between 100-500, do short synacthen test)
Short synacthen test- gold standard
Serum ACTH (primary-high, secondary-low)
Adrenal antibodies
CT abdomen- if adrenal damage
MRI head- if suspect pituitary pathology

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5
Q

Nephrogenic causes of DI

A

Lithium
Intrinsic kidney disease

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6
Q

Cranial causes of DI

A

Cerebral tumours
Head injury
Brain surgery
CNS infection eg. Meningitis

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7
Q

Investigations for diabetes insipidus

A

FBC UE- hypernatraemia
Urine osmolarity- low
Serum osmolarity- high
Water deprivation test- gold standard
CT head- if water test positive, may want to exclude a brain tumour

NB- no glucosuria

NB- essential to exclude hypercalcaemia due to hyperparathyroidism before progressing
to a water deprivation test

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8
Q

Aetiology of Cushing’s syndrome

A

Exogenous steroids (most common cause)
Cushings disease- pituitary adenoma releasing ACTH (most common endogenous cause)
Adrenal cushings- adrenal adenoma realising cortisol
Paraneoplastic cushings- ectopic ACTH from SCLC

NB- adrenal adenoma is the only primary hypercortisol cause as the others all increase ACTH

NB- pseudo cushings- due to alcohol excess or severe depression (mimics symptoms and lab results, including dexamethasone suppression test)

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9
Q

Nelsons syndrome

A

Symptoms arising many years after a a bilateral adrenalectomy, where there is a rapidly enlarging pituitary adenoma (has been trying to increase ACTH levels for many years and this predisposes to tumour development)

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10
Q

Sx of conns syndrome (primary hyperaldosteronism)

A

Usually asymptomatic, HTN, hypokalaemia (fatigue, muscle wasting, cramps, headaches, polyuria, polydipsia, palpitations)

NB- classically a young pt with hypokalaemia and drug resistant hypertension

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11
Q

Adrenal insufficiency

A

Adrenal glands don’t produce enough steroid hormones, esp. cortisol and aldosterone

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12
Q

Addison’s disease

A

Where adrenal glands have been damaged (autoimmune) resulting in decreased cortisol and aldosterone (primary adrenal insufficiency)

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13
Q

Secondary adrenal insufficiency

A

Inadequate ACTH stimulating the adrenal glands, resulting in low cortisol release. Damage to the pituitary gland is most common cause (Sheehans syndrome)

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14
Q

Tertiary adrenal insufficiency

A

Inadequate CRH release by the hypothalamus. Usually when a patient is on steroids for numerous weeks then stops suddenly, the hypothalamus doesn’t reactivate quick enough and so endogenous steroids aren’t produced quickly enough

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15
Q

Sx Addison’s

A

Hypotension, weight loss, fatigue, myalgia, N & V, diarrhoea, salt cravings, loss of libido, loss of axillary and public hair, hyperpigmentation (increased ACTH), abdominal pain, hypoglycaemia, vitiligo

NB- hyponatraemia, hyperkalaemia

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16
Q

Sx of Diabetes Insipidus

A

Polyuria, polydipsia, nocturnal, signs of volume depletion eg. Hypotension, visual field defects (pituitary adenoma), hypernatraemia

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17
Q

Differentials for diabetes insipidus

A

Psychogenic polydipsia, diabetes mellitus, diuretic use

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18
Q

SIADH Sx

A

Hyponatraemia (anorexia, n and v, headache, cramps, lethargy), normotensive, euvolemic, absence of oedema

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19
Q

SIADH aetiology

A

Increased ADH secretion

Diseases of CNS- stroke, trauma, infection
Pulmonary disease- pneumonia, COPD
Drugs- SSRI
Endocrine disorders- glucocorticoid deficiency

Ectopic ADH- SCLC

Enhanced stimulation of ADH receptors in the kidney

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20
Q

SIADH Investigations

A

Fluid balance chart- check no excessive fluid intake
BP- normal (euvolemic)
Urinalysis- sodium and osmolarity increased
FBC UE- hyponatraemia
NB- if nothing found and someone has persistent hyponatraemia we do CT TAP- exclude malignancy

21
Q

Pituitary gland hormones

A

Anterior- TSH, GH, ACTH, FSH, LH, PRL, endorphins

Anterior- Oxytocin, ADH

22
Q

DM vs DI

A

Polyuria and polydipsia but no glucosuria in DI

23
Q

DI vs SIADH

A

High urinary output vs low urinary output
Low ADH (or can’t respond to it) vs high ADH
Hypernatraemia vs hyponatraemia
Dehydrated vs hydrated
Lose too much fluid vs retain too much fluid

NB- both present with excessive thirst

24
Q

Hypokalaemia and ADH

A

Hypokalaemia can cause a mild nephrotic diabetes insipidus

Kidneys don’t respond to ADH well in a hypokalaemia state

25
Q

How are steroids prescribed

A

High dose in morning

2 smaller doses in late afternoon/ early evening

(Naturally levels are lower overnight)

26
Q

Sx of Addisonian or adrenal crisis

A

Reduced consciousness
Hypotension
Hypoglycaemia hyponatraemia hyperkalaemia
Very unwell patients

27
Q

Triggers for an adrenal crisis

A

Infection
Trauma
Acute illness
Surgery
Steroid withdrawal
adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcaemia)

In patients with established Addisons or long-term steroid use

Treat before looking for cause eg. IV hydrocortisone

28
Q

Central pontine myelinolysis

A

When hyponatraemia is treated too quickly (or when too much insulin is given in HHS)

29
Q

Sheehan Syndrome

A

Women who lose a life-threatening amount of blood in childbirth or who have severe low blood pressure during or after childbirth can deprive the pituitary gland of oxygen and damage it

30
Q

Management of nephrogenic DI

A

Thiazides, low salt/protein diet

31
Q

Cranial DI Management

A

Desmopressin (vasopressin analogue)

32
Q

Causes of hypoadrenalism

A

Primary
Addisons disease (most common)
TB
Metastases (bronchogenic carcinoma)
Meningicoccal septicaemia (Waterhouse Friedrichsen syndrome)
HIV
Antiphospholipid syndrome

Secondary
Pituitary disorders eg. Tumour (non functioning), Sheehan’s syndrome, apoplexy
Exogenous glucocorticoid therapy

33
Q

Management of Addison’s disease

A

Give both mineralocorticoids and glucocorticoids

Hydrocortisone (majority in 1st half of the day)
Fludrocortisone

Don’t miss doses, steroid cards, medic alert bracelets, hydrocortisone for injection during adrenal crisis

34
Q

Management of inter current illness (not adrenal crisis) in Addison’s disease

A

Glucocorticoid dose doubled (hydrocortisone), fludrocortisone remains the same

35
Q

Management of an adrenal or addisonian crisis

A

Hydrocortisone 100 mg IM (patients should have this in the community)
1 litre saline over 30-60 minutes
Oral replacement after 24 hours

36
Q

Differentiate true cushings and pseudo cushings

A

Insulin stress test

37
Q

Features of a pituitary adenoma

A

Excess hormone in secretory adenomas- cushings (ACTH), acromegaly (GH), amenorrhea or galactorrhoea due to excess prolactin
Depletion of hormones due to compression of functioning gland- non secretory tumours therefore present with generalised hypopituitarism
Stretched dura- headaches
Compression of chiasm- bitemporal hemianopia

38
Q

Investigations for a pituitary incidentiloma

A

Pituitary blood profile- GH, prolactin, ACTH, FH, LSH, TFT
Formal visual field testing
MRI brain with contrast

39
Q

Treatment of pituitary adenomas

A

Hormonal therapy (bromocriptine for prolactinomas)
Surgery eg. If incidental adenoma is increasing in size or if it is a functioning/secretory adenoma

40
Q

Primary hyperaldosteronism

A

Bilateral idiopathic adrenal hyperplasia is most common cause
Unilateral adrenal adenoma- Conns syndrome (rarer)

41
Q

Investigations for primary hyperaldosteronism

A

Plasma aldosterone/renin ratio (should show high aldosterone with low renin)
CT abdomen
Adrenal venous sampling (AVS) fir source of aldosterone excess-unilateral or bilateral

42
Q

Management of primary hyperaldosteronism

A

Adenoma- surgery
Bilateral hyperplasia- spironolactone (aldosterone antagonist)

43
Q

Causes of Addison’s disease

A

UK- autoimmunity

Worldwide- infection (TB)

44
Q

Criteria for orlistat

A

Lipase inhibitor

BMI 30+ or BMI >28 with co morbidities

45
Q

Criteria for bariatric surgery

A

BMI 40+, or 35+ and significant co morbidities

46
Q

Secondary hyperaldosteronism

A

Renal artery stenosis or obstruction (renin and aldosterone raised)

47
Q

ABG cushings disease

A

Hypokalaemic metabolic alkalosis

48
Q

Corticosteroids

A

Fludrocortisone- min G, high M

Hydrocortisone- G, high M

Prednisolone- high G, low M

Dexamethasone, betmethasone- high G, no M

49
Q

Glucocorticoids and neutrphils

A

They are immunosuppressive, but they can cause neutrophilia

Year 3 OSCE (61 decks)

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