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Year 3 Med 2 > Endocrine emergencies > Flashcards

Endocrine emergencies Flashcards

1
Q

Key roles of hypothalamus

A

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)

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2
Q

Pituitary gland

made of how many lobes?

which lobes secrete what?

A

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
    *
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3
Q

draw the general axis for a hypothlamic-effector-organ axis

A
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4
Q

what is hypopituitarism?

what is a primary pituitary disease?

secondary?

what is pituitary apoplexy? Sheehan’s syndrome?

A

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

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5
Q

causes of hypopituitarism

A
  • Tumours- pituitary, craniopharyngioma, gliomas, metastases
  • Trauma- including surgery
  • Infarction- pituitary apoplexy, Sheehan’s syndrome
  • Inflammation- sarcoidosis, haemochromatosis
  • Iatrogenic- radiotherapy
  • Drugs- opiates
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6
Q

Symptoms of hypopituitarism

A
  • 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

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7
Q

investigations

A
  • 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)
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8
Q

medications for hypopituitarism

A

Important to replace cortisol BEFORE giving thyroxine to avoid causing an Addisonian crisis in those with adrenal insufficiency.

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9
Q

why do you give cortisol before giving thyroxine?

A

thyroxine enhances cortisol clearance

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10
Q

draw the hypothalamic pituitary axis

A
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11
Q

What is adrenal insufficiency

primary

secondary

A

HYPOaldrenalism- therefore the opposite of Cushing’s

Primary- abnormality of the adrenal gland

Secondary- disorder of the HPA axis (ACTH secretion)

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12
Q

what is cortisol?

where is it produced?

functions?

A

what is cortisol?

glucocorticoid steroid

where is it produced?

zona fasciculata (gFr) of the adrenal cortex

functions?

metabolism and the immune response

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13
Q

causes of secondary adrenal insufficiency (7)

A

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
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14
Q

features of secondary adrenal insuffiency

A
  • lack of pigmentation (due to lack of melanocyte stimulating hormone which is also released from ant pit)
  • does not have a mineralocorticoid deficiency
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15
Q

Addison’s disease

A
  • 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

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16
Q

Causes of primary hypoadrenalism

A
  • *• 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*
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17
Q

Clinical features of primary hypoaldrenalism/ Addison’s disease

A
  • 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
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18
Q

Lab investigations for Addisons

A
  • decreased Na+/ increased potassium (due to loss of cortisol and aldosterone)
  • increased urea (due to hypovolaemia)
  • mild hypercalcaemia
  • anaemia (due to loss of EPO)
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19
Q

adrenal insufficiency diagnosis

A

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
20
Q

Adrenal insufficiency treatment

A
  • Glucocorticoid replacement therapy
    • Hydrocortisone 10mg on waking
      • 5mg midday
      • 5mg evening (alternatively can be given twice daily)
  • 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
21
Q

What is an addisonian crisis/ acute adrenal crisis?

clinical features

A

critically low cortisol medical emergency- urgent treatment is essential

clinical features:

  • Shock/ hypotension
  • Abdominal pain (think acute abdomen)
  • Fever
  • Hypoglycaemia
22
Q

management of an addisonian crisis

A
  • 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
23
Q

effects of long term steroid therapy

A
  • 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
24
Q

draw the hypothalamic pituitary thyroidal axis

A
25
Q

what is thyroid storm?

A
  • un/undertreated hyperthyroidism.
  • high mortality
26
Q

rfx for thyroid storm

A
  • Acute infection
  • Postpartum
  • Withdrawals of ATDs
  • Recent surgery
  • Radiographic contrast agents
27
Q

clinical features of thyroid storm

A
  • Altered mental state
  • Pyrexia
  • Tachycardia
  • Tachyarrhythmia
  • Vomiting
  • Diarrhoea
  • Jaundice
28
Q

which systems are affected in the multisystem decompensation?

A
  • Cardiac failure
  • Congestive hepatomegaly
  • Respiratory distress
  • Dehydration and pre-renal failure
29
Q

treatment for thyroid storm

A
  • beta blockers
  • steroids
  • ATDs
30
Q
  • What is myxoedema coma?
  • what are the clinical features?
A

Profound hypothyroidism

Clinical features:

  • Hypothermia
  • Hyporeflexia
  • Hypoglycaemia
  • Bradycardia
  • Seizures
  • Cerebellar ataxia
  • Cardiomegaly+ pericardial effusion
  • Psychiatric symptoms (depression/ psychosis)
31
Q

treatment for myxoedema coma

A

IV Liothyronine (T3)

32
Q

Causes of hyponatraemia

A

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

33
Q

clinical features of hyponatraemia

A

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
34
Q

investigations for hyponatraemia

treatment for hyponatraemia

A
  • 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)
35
Q

what is SIADH

A
  • 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
36
Q

causes of SIADH

A

• Tumours
- SCC Lung
- Thymoma
- Lymphoma
- Leukaemia
- Sarcoma
- Mesothelioma
• Chest Disease
- Infections (pneumonia, TB, empyema)
- Pneumothorax
- Asthma
- PPV
• Metabolic
- Hypothyroidism
- GC deficiency

and more

37
Q

SIADH diagnostic criteria

A
  • 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
38
Q

SIADH treatment

A
  • 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
39
Q

How do you know when you’re having an SIADH emergency

A
  • Vomiting
  • Seizures
  • Gcs<8
  • Cardiorespiratory distress
40
Q

Hyperkalaemia

ranges

A

5.5 – 6.0 mmol/L Mild
6.1 – 6.9 mmol/L Moderate
>7 mmol/L Severe

41
Q

causes of hyperkalaemia

A
  • ↓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)
42
Q

Clinical features of hyperkalaemia

hyperkalaemia ECG changes

A
  • 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
43
Q
A
44
Q

Hyperkalaemia management

A
  • 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
45
Q

causes of HYPOkalaemia

A

Relatively common

Causes:

  • Alcohol excess
  • CKD
  • Diuretics
  • DKA
  • Diarrhoea
  • Laxatives
  • Vomiting
  • Primary hyperaldosteronism
  • Curshings syndrome

Year 3 Med 2 (9 decks)

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