Endocrinology Flashcards

1
Q

what is Cushing’s syndrome

A

a syndrome caused by prolonged exposure to an excess of glucocorticoids

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2
Q

what is cushing’s disease

A

Cushing’s disease refers to cases caused by a pituitary adenoma. These are responsible for the majority of endogenous cases

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3
Q

what is cortisol secretion controlled by

A

Cortisol secretion is controlled by the hypothalamus-pituitary-adrenal axis

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4
Q

where is cortisol released from

A

adrenal cortez

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5
Q

what is the pattern of its concentration

A

diurnal variation

It reaches a zenith (highest point) at around 8 am and a nadir (lowest point) at around midnight to 1 am.

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6
Q

List 4 causes of Cushing’s syndrome

A

ACTH dependent:
- Cushing’s disease: pituitary adenoma releasing excess ACTH

ectopic ACTH producing tumour

ACTH independent

  • therapeutic corticosteroid medication
  • adrenal tumour
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7
Q

What hormones are inivolved in cortisol homeostasis

A

Corticotroponin-releasing hormone (CRH)

adrenocortocotropic hormone (ACTH)

cortisol

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8
Q

symptoms of cushing’s syndrome

A
Tiredness
Depression
Weight gain
Easy bruising
Amenorrhoea
Reduced libido
Striae
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9
Q

signs of cushing’s disease

A
Acne
Moon facies
Plethora
Buffalo hump
Hypertension
Proximal muscle weakness
Hyperpigmentation (in ACTH dependent causes)
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10
Q

investigations in Cushing’s Syndrome

A

24 hour urinary cortisol (multiple collections; 3-4x normal = highly suggestive of Cushing’s syndrome

midnight (salivary) cortisol: demonstrate loss of normal circadian pattern

1mg overnight dexamethasone suppression test: demonstrates loss of normal negative feedback on pituitary gland and hypothalamus

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11
Q

what are risks of untreated Cushing’s syndrome

A

Untreated Cushing’s syndrome can be lethal with death from cardiac, thromboembolic or infective complications.

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12
Q

management of Cushing’s syndrome

A

definitive treatment: surgical resection

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13
Q

what is SIADH

A

The syndrome of inappropriate anti-diuretic hormone (SIADH) results from excess ADH secretion.

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14
Q

what is the relationship between osmolality and ADH

A

ADH release is governed by the plasma osmolality

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15
Q

What does SIADH result in

A

This results in a low plasma osmolality and a euvolaemic hyponatraemia.

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16
Q

What part of the kidney does ADH act on

A

ADH acts on the distal convoluted tubule and collecting duct to increase water reabsorption independent of sodium. ADH stimulates the insertion of aquaporin-2 channels onto the luminal membrane, allowing the free entry of water. ADH also causes vasoconstriction of arterioles.

17
Q

CNS causes of SIADH

A

Stroke
Subarachnoid haemorrhage
Trauma
Psychosis

18
Q

neoplastic causes of SIADH

A

Small cell lung cancer (paraneoplastic syndrome)
Other lung cancers (less commonly)
Neuroblastoma

19
Q

infective causes of SIADH

A

pneumonia

HIV

20
Q

drugs that cause SIADH

A

Carbamazepine
Cyclophosphamide
Selective serotonin reuptake inhibitors (SSRIs)
MDMA (Ecstasy)

21
Q

hormonal causes of SIADH

A

Hypothyroidism

Hypopituitarism

22
Q

iatrogenic causes of SIADH

A

Common following many procedures

Particular risk in transsphenoidal pituitary surgery

23
Q

clinical features of SIADH

A
  • similar to hyponatraemia
    symptoms: headache, confusion, lethargy, anorexia
    signs: seizuresm reduced GCS, coma, myoclonus, ataxia, hyporeflexia, asterixis
24
Q

what is the risk of rapid correction of hyponatraemia

A

osmotic demyelination syndrome

aka cerebral pontine myelinolysis

25
Q

management of SIADH

A
  • fluid restriction
  • vaptans
    severe: ICU, hypertonic saline, furosemide
26
Q

what is the typical starting dose for metformin

what is the maximum dose of metformin

A

500mg daily

2g daily

27
Q

side effects of metformin

A

commonest: GI upset (nausea, abdominal pain, diarrhoea)
rare: lactic acidosis

28
Q

what is the mechanism of metformin

A

Metformin reduces hepatic glucose production and acts systemically to increase glucose uptake.

29
Q

what are contraindications of metformin

A

acute metabolic acidosis e.g. DKA: stop treatment

eGFR<30

30
Q

criteria for HHS

A

hypovolaemia
severe hyperglycaemia >30
mild or absent ketones
high osmolality > 320

31
Q

complications of HHS

A
AKI 
electrolyte disturbance 
hypotension 
coma 
VTE
32
Q

precipitants of HHS

A
Infection
High-dose steroids
Myocardial infarction
Vomiting
Stroke
Poor treatment concordance
33
Q

signs of HHS

A
Dehydration (dry mucous membranes, sunken eyes, reduced capillary refill, decreased skin turgor)
Hypotension
Decreased urine output
Decreased conscious level
Coma
Focal neurology signs
Features of the precipitating cause
34
Q

symptoms of HHS

A
Polydipsia
Polyuria
Nausea
Vomiting
Muscle cramps
Weakness
Altered mental status
Seizures
Coma
35
Q

HHS investigations

A

The key investigations for management of HHS include a laboratory glucose, urea & electrolytes blood test, a blood gas (venous/arterial) and a blood or urinary ketone level.

additional tests looking for potential causes/ complications e.g. ecg

36
Q

management principles of HHS

A

Aggressive fluid resuscitation: controlled to prevent cerebral oedema 0.9% saline

normalise glucose:consider insulin therapy if ketonaemia or slow drop in BM

Electrolytes including sodium, potassium, phosphate and magnesium should be monitored regularly (4 hourly minimum) and replaced as necessary.

cardiac monitoring
LMWH prophylaxis