Endocrine emergencies Flashcards
Key roles of hypothalamus
homeostasis:
- HR+BP
- Body temperature
- Fluid and electrolyte balance- including thirst
- Appetite and body weight
- Sleep cycle
- GI secretions
Links the endocrine and nervous system
Regulates the anterior pituitary gland
Synthesizes hormones that are released by the posterior pituitary gland (e.g., oxytocin, ADH)
Pituitary gland
made of how many lobes?
which lobes secrete what?
Anterior lobe- synthesis and secretions of:
- Adrenal (ACTH)
- Gonads (LH/FSH)
- Thyroid (TSH)
- Growth (GH)
- Prolactin
- Melanocyte stimulating hormone
Posterior lobe- storage and release of:
- ADH
- Oxytocin
*
draw the general axis for a hypothlamic-effector-organ axis
what is hypopituitarism?
what is a primary pituitary disease?
secondary?
what is pituitary apoplexy? Sheehan’s syndrome?
Partial or complete deficiency of anterior/ posterior pituitary hormones
- 1ry pituitary disease- disease is within the organ itself
- 2ry disease- external pathology causes pathology in the pituitary
Pituitary apoplexy- pituitary infarction due to stalk compression
Sheehan’s syndrome- haemorrhage infarction of enlarged pituitary post partum
causes of hypopituitarism
- Tumours- pituitary, craniopharyngioma, gliomas, metastases
- Trauma- including surgery
- Infarction- pituitary apoplexy, Sheehan’s syndrome
- Inflammation- sarcoidosis, haemochromatosis
- Iatrogenic- radiotherapy
- Drugs- opiates
Symptoms of hypopituitarism
- GH–> fatigue, muscle weakness, increased body fat
- LH/ FSH--> females- fewer periods /less pubic hair
- male- ED /decreased facial + body hair/ mood changes
- TSH–> tiredness, increased weight/ dry skin/ cold intolerance/ constipation
- ACTH–> severe tiredness/ nausea/ vomiting
- Prolactin–> inability to produce breast milk (sheehans)
- ADH–> increased thirst / increased urine
generally patients may present with a combincation of mild aneamia and a lack of melatonin
investigations
- Baseline anterior pituitary hormones: prolactin, LH/FSH, testosterone/oestradiol, 9 am cortisol, Full TFTs, GH/ GF-1
- Serum and urine osmolarity
- Dynamic tests –> ITT/ SST/glucagon tests
- Pituitary MRI
- Visual fields assessment (presses on optic chiasm to cause bitemporal hemianopia)
medications for hypopituitarism
Important to replace cortisol BEFORE giving thyroxine to avoid causing an Addisonian crisis in those with adrenal insufficiency.
why do you give cortisol before giving thyroxine?
thyroxine enhances cortisol clearance
draw the hypothalamic pituitary axis
What is adrenal insufficiency
primary
secondary
HYPOaldrenalism- therefore the opposite of Cushing’s
Primary- abnormality of the adrenal gland
Secondary- disorder of the HPA axis (ACTH secretion)
what is cortisol?
where is it produced?
functions?
what is cortisol?
glucocorticoid steroid
where is it produced?
zona fasciculata (gFr) of the adrenal cortex
functions?
metabolism and the immune response
causes of secondary adrenal insufficiency (7)
Causes of secondary adrenal insufficiency
- Tumours – pituitary, craniopharyngioma, metastases
- Infarction – pituitary stalk compression, Sheehan’s syndrome
- Infections - TB
-
Inflammation – sarcoidosis, histocytosis X, haemochromatosis, lymphocytic
hypophysitis - Iatrogenic – surgery, radiotherapy
- Drugs – Opiates, Steroids*
- Other – trauma, isolated ACTH deficiency
features of secondary adrenal insuffiency
- lack of pigmentation (due to lack of melanocyte stimulating hormone which is also released from ant pit)
- does not have a mineralocorticoid deficiency
Addison’s disease
- Usually, an autoimmune disease that results in PRIMARY ADRENAL INSUFFICIENCY via destruction of the adrenal cortex.
- Can often be found amongst other autoimmune conditions –> e.g., vitiligo
- Affects adults 30-50 years
good differential for T1DM-as both have have weight loss but this is hypoglycaemia
good differential for hypothyroidism- lethargy but weight loss
Causes of primary hypoadrenalism
- *• Autoimmune** – 70%
- *• Infection** – TB, Fungal, Opportunistic
- *• Infarction** – Thrombosis in Anti-phospholipid syndrome
- *• Haemorrhage** – Waterhouse-Friedrichsen syndrome
- *• Infiltration** – Amyloidosis, Haemachromatosis
- *• Malignancy** – Lung/Breast/Kidney metastasis; Lymphoma
- *• Iatrogenic** - Adrenalectomy
- *- Drugs** - Ketoconazole / Fluconazole/Phenytoin / Rifampicin/ Steroids*
Clinical features of primary hypoaldrenalism/ Addison’s disease
- Lethargy
- Dizziness–> postural hypertension
- Anorexia or weight loss
- Hypoglycaemia
- Nausea, vomiting, abdominal pain, diarrhoea
- Hyperpigmentation
- Sun exposed areas, pressure areas
- Scars, palmar erythema, oral mucosa
- This is because ant pit works extra time to try and stimuate adrenal cortex more as it isnt responding, melanocyte relasing hormone also thrown out
Lab investigations for Addisons
- decreased Na+/ increased potassium (due to loss of cortisol and aldosterone)
- increased urea (due to hypovolaemia)
- mild hypercalcaemia
- anaemia (due to loss of EPO)
adrenal insufficiency diagnosis
9am serum cortisol
- > 425 nmol/L excludes insufficiency
- > 300 nmol/L makes it unlikely
ACTH levels
Short synacthen test
- Synthetic ACTH IM
- Sample cortisol at 0 30 60 mins
- Normal if after 60 mins cortisol > 425 nmol/L and there is a rise of 150 nmol/L
Long synacthen test
- 1mg depot synthetic ACTH
- Cortisol sampling as above + 2, 4, 8 and 24 hours
- Normal >170 and peak >900nmol
Adrenal insufficiency treatment
- Glucocorticoid replacement therapy
- Hydrocortisone 10mg on waking
- 5mg midday
- 5mg evening (alternatively can be given twice daily)
- Hydrocortisone 10mg on waking
- Aim for lowest dose that allows patient to feel well
- Doses should be doubled doubled during times of intercurrent illness
- Patients should carry steroid card and shock pack of IM hydrocortisone
- Mineralocorticoid therapy if primary insufficiency
What is an addisonian crisis/ acute adrenal crisis?
clinical features
critically low cortisol medical emergency- urgent treatment is essential
clinical features:
- Shock/ hypotension
- Abdominal pain (think acute abdomen)
- Fever
- Hypoglycaemia
management of an addisonian crisis
- IVT with 0.9% saline
- Give IV/ IM hydrocortisone 100mg bolus
- After that patient may need QDS IV hydrocortisone until they can switch to PO tablets
- Treat hypoglycaemia if present
effects of long term steroid therapy
- Negative feedback effect on HPA axis leads to
- Suppression of both CRH and ACTH secretion (2ry)
- Atrophy of adrenal cortex (1ry)
- If less than 3 weeks of use steroids can be stopped acutely
- Chronic users or supra users need to be tapered down
- Some patients HPA may never recover
draw the hypothalamic pituitary thyroidal axis
what is thyroid storm?
- un/undertreated hyperthyroidism.
- high mortality
rfx for thyroid storm
- Acute infection
- Postpartum
- Withdrawals of ATDs
- Recent surgery
- Radiographic contrast agents
clinical features of thyroid storm
- Altered mental state
- Pyrexia
- Tachycardia
- Tachyarrhythmia
- Vomiting
- Diarrhoea
- Jaundice
which systems are affected in the multisystem decompensation?
- Cardiac failure
- Congestive hepatomegaly
- Respiratory distress
- Dehydration and pre-renal failure
treatment for thyroid storm
- beta blockers
- steroids
- ATDs
- What is myxoedema coma?
- what are the clinical features?
Profound hypothyroidism
Clinical features:
- Hypothermia
- Hyporeflexia
- Hypoglycaemia
- Bradycardia
- Seizures
- Cerebellar ataxia
- Cardiomegaly+ pericardial effusion
- Psychiatric symptoms (depression/ psychosis)
treatment for myxoedema coma
IV Liothyronine (T3)
Causes of hyponatraemia
1) Excess water- dilutional hyponatraemia
- increase reabsorption- cirrhosis, CHF, nephrotic syndrome OR
- decreased renal excretion (SIADH. glucocorticoid dfeiciency)
2) Salt deficiency never due to low salt intake
- renal loss– PCKD, nalagesic nephropathy
- non-renal loss– skin, GI tract
3) Pseudohyponatraemia
- lipids
- proteins
4) glucose, mannitol, ethanol
osmotic effect due to shift of water from ICF to ECF
5) Sickle cell syndrome
clinical features of hyponatraemia
Depends on underlying cause and rate of development
<115 mol start to see symptoms –> <100 is life threatening
- Water excess ->brain injury -> confusion, headache, seizures, coma
- Hypervolaemia confined to ECF–> (CHF, cirrhosis, nephrotic syndrome) oedema and and fluid overload apparent
- SIADH–> no apparent fluid overload as fluid is evenly dispersed
- Salt deficiency–> hypovolaemia and tachycardia with postural hypotension
investigations for hyponatraemia
treatment for hyponatraemia
- Urine Na- most useful test in determining underlying cause
- TFT
- Glucose
- Cortisol
- Urine and serum osmolarity
- LFt
treatment
- Diuretics
- Drugs- carbamazepine, opiates, SSRI’s, ACE-I, PPIs, laxatives
- Glucocorticoid deficiency (e.g., Addison’s)
what is SIADH
- Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a condition in which the body makes too much antidiuretic hormone (ADH).
- This hormone helps the kidneys control the amount of water your body loses through the urine.
- SIADH causes the body to retain too much water
causes of SIADH
• Tumours
- SCC Lung
- Thymoma
- Lymphoma
- Leukaemia
- Sarcoma
- Mesothelioma
• Chest Disease
- Infections (pneumonia, TB, empyema)
- Pneumothorax
- Asthma
- PPV
• Metabolic
- Hypothyroidism
- GC deficiency
and more
SIADH diagnostic criteria
- Na and serum osmolarity <270mOsm/kg
- Inaproppriate urine osmolality
- Excess renal sodium loss
- Absence of clinical evidence of hypovolaemia or fluid overload
- Normal renal, adrenal and thyroid function
SIADH treatment
- Treat underlying cause
- Fluid restrict- 500-700mL/24Hr
- Drug treatment
- demeclocycline – induces partial nephrogenic DI
- (Tolvaptan) Vasopressin V2 receptor antagonist promotes aquapheresis -
- but expensive
- Saline infusion in emergency
How do you know when you’re having an SIADH emergency
- Vomiting
- Seizures
- Gcs<8
- Cardiorespiratory distress
Hyperkalaemia
ranges
5.5 – 6.0 mmol/L Mild
6.1 – 6.9 mmol/L Moderate
>7 mmol/L Severe
causes of hyperkalaemia
- ↓renal excretion:- AKI / CKD / K sparing diuretics (spironolactone)
- *- Cell injury**:- rhabdomyolysis / burns / blood transfusion / tumour cell necrosis
- *- K+ cellular shifts**:- acidosis / drugs (suxamethonium / B-blockers)
- *- Hyperaldosteronism** :- Addisons / Drug induced (NSAIDS / ACE-i)
- Spurious (fake)
Clinical features of hyperkalaemia
hyperkalaemia ECG changes
- Muscle weakness and cramps
- Paraesthesia
- Hypotonia
- Focal neurological deficits
- Often asymptomatic
Hyperkalaemia ECG changes
- High peaked T waves
- Small broad/ absent P waves
- Widening of QRS
- AV dissociation or VT/ VF
Hyperkalaemia management
- Urgent treatment if >6.5mmol/l
- Calcium chloride to stabilise cardiac membranes
- IV glucose/ insulin infusion
- Nebulised salbutamol
- Treat fluid deficiency/ acidosis
- Consider emergency dialysis
causes of HYPOkalaemia
Relatively common
Causes:
- Alcohol excess
- CKD
- Diuretics
- DKA
- Diarrhoea
- Laxatives
- Vomiting
- Primary hyperaldosteronism
- Curshings syndrome
