Adrenal Flashcards
What are the different layers of the adrenal gland and what do they produce?
- Glomerulosa - mineralocorticoids
- Fasciculata - glucocorticoids
- Reticularis – sex steroids
Medulla: catecholamines (Adrenaline & Noradrenaline)
A 52-year-old man presents to the GP with an 8-year history of hypertension that has been difficult to control with antihypertensive medicines. His symptoms include frequent headaches, nocturia (3-4 times per night), and feeling tired. He has no other past medical history. On examination, his BP is 158/93mmHg, with no other remarkable findings.
What is the most likely diagnosis?
A – Chronic hypertension
B – Phaeochromocytoma
C – Primary hyperaldosteronism
D – Addison’s disease
E – Diabetes mellitus
C – Primary hyperaldosteronism
A 32-year-old woman presents to the GP complaining of weight gain and stretch marks on her stomach. She says she also feels weaker and finds that she bruises more easily than in the past. Her blood pressure today is 142/94 mmHg. On examination, you notice she has ankle oedema, as well as a large waist circumference and prominent purple striae on the abdomen.
What is the most likely diagnosis?
A – Metabolic syndrome
B – Primary hyperaldosteronism
C – Obesity
D – Cushing’s syndrome
E – Polycystic ovarian syndrome
D – Cushing’s syndrome
An anxious 27-year-old woman presents to the urgent care centre. She tells you she’s been having terrible headaches for several months which come and go at random intervals. During the episodes she also has palpitations and feels very sweaty. She has no past medical history, however her father had thyroid cancer a few years ago. On examination her BP is 215/117 mmHg and she is tachycardic.
What is the most likely diagnosis?
A – Phaeochromocytoma
B – Resistant hypertension
C – Addisonian crisis
D – Thyroid cancer
E – Pituitary tumour
A – Phaeochromocytoma
What is primary hyperaldosteronism?
What does hihg aldosterone do physiologically?
What are the different types ?
What are the treatment for them?
Excess secretion of aldosterone - with supression of plasma renin actiivty
- Excess aldosterone leads to increased Na+ and water retention
- This leads to hypertension
- It also causes increased renal K+ loss leading to hypokalaemia
- Renin is suppressed due to NaCl retention
- Conn’s (70%) - (adrenalectomy laparascopic) surgery
- Adrenal aldosteronoma (rare) - (adrenalectomy laparascopic) surgery
- Familial hyperaldosteronism
- Bilateral adrenal hyperplasia (30%) - spironolactone(aldosterone inhibitor) (potassium sparing diuretics)
What people are affected by conn’s syndrome?
What people are affected by bilateral adreanl cortex hyperplasia?
What people are affected by conn’s syndrome? young females
What people are affected by bilateral adreanl cortex hyperplasia? older males
What are symptoms and signs of hyperaldosteronism?
Symptoms
- Tend to be asymptomatic
- Often incidental findings on blood tests
- Symptoms of hypokalaemia
- Non-specific symptoms
Signs
- HYPERTENSION (HTN)
- Difficult to control with antihypertensive medications
- Complications of hypertension e.g retinopathy of hypertension, headaches
What are investigations for Hyperadrenalism?
SCREENING TEST
Bloods:
- Plasma K+ levels (low in 20%)
- Plasma aldosterone - high
- Plasma aldosterone:renin ratio – high
URINE:
- Urine K+ - high
Then more specialist:
- Salt loading
- Postural test
- Measure plasma aldosterone, renin activity and cortisol when the patient is lying down at 8 am
- Measure again after 4 hrs of the patient being upright
- Aldosterone-producing adenoma - aldosterone secretion decreases between 8 am and noon
- Bilateral adrenal hyperplasia - adrenals respond to standing posture and increase renin production leading to increased aldosterone secretion
- Fludrocortisone suppression test
- Aldosterone levels not suppressed, renin suppressed (BMJ best practice)
- CT/MRI
- Bilateral adrenal vein catheterisation
- -Elevated aldo in 1 vein indicates adrenal adenoma (lateralization)
What are complications of hyperadrenalosims?
What is the prognosis?
What are complications of hyperadrenalosims? complications of Hypertension
What is the prognosis? surgery may treat HTN or make it easier to be treated with medications
What are symptoms of cushings snd signs?
- Moon face
- Facial plethora
- Interscapular fat pad
- Proximal muscle weakness
- Central obesity
- Pink/purple striae on abdomen/breast/thighs
- Kyphosis (due to vertebral fracture)
- Hypertension
- Ankle oedema
- Pigmentation in ACTH dependent cases
- Fractures
What is the definition of cushings syndrome?
What is the aetiology?
What is the definition of cushings syndrome?
- Syndrome associated with chronic inappropriate elevation of free circulating cortisol
What is the aetiology?
- Exogenous steroid exposure is the MOST COMMON CAUSE
- Endogenous – 2 types
ACTH-dependent (80%)
- Excess ACTH from pituitary adenoma (Cushing’s disease)
- Ectopic ACTH e.g lung tumour, pulmonary carcinoid tumour
ACTH-independent (20%)
- Benign adrenal adenoma
- Bilateral adrenal hyperplasia
- Adrenal carcinoma (rare)
What are investigations needed for cushings syndrome?
- Serum glucose – high risk diabetes
- Pregnancy test
- 1st line high sensitivity tests - for patients with a high pre-test probability
- 24hr urinary free cortisol
- Late-night salivary cortisol
- Overnight dexamethasone suppression test
- Low-dose dexamethasone suppression test
A positive test is defined as morning cortisol >50 nanomol/L
FOR ACTH dependent:
- High plasma ACTH
- Pituitary MRI
- High dose dex suppression test
- Inferior petrosal sinus sampling
ACTH-independent
- Low plasma ACTH
- CT/MRI adrenals
What condition is this?
addison’s
What is the management in cushing’s?
What are teh comlipications of the different treatments?
MEDICAL
Metyrapone/ketoconazole – inhibit cortisol synthesis
Use pre-operatively or if unfit for surgery
SURGICAL – preferred treatment
Pituitary adenoma: trans-sphenoidal resection of adenoma
Adrenal adenoma/carcinoma: surgery to remove
Ectopic ACTH: treatment directed at tumour
COMPLICATION:
CSF leakage, Meningitis, Sphenoid sinusitis, Hypopituitarism
RADIOTHERAPY – if persistent post-operative high cortisol
complications: Hypopituitarism, Radionecrosis, Increased risk of second intracranial tumours and stroke
WHat are complications of cushings?
What is the prognosis?
- Diabetes
- Osteoporosis
- Hypertension
- Pre-disposition to infections
Prognosis:
- If untreated, 5yr survival rate is 50%.
- Depression often persists for years following successful treatment
What condition is this
PCOS
Phaechromocytoma
What is the definition?
What are common presentation?
What are risk factors
What are signs and symptoms?
What are investigations?
What is the definition?
= a tumour arising from catecholamine-producing chromaffin cells of the adrenal medulla
10% are bilateral
10% are malignant
10% are extra-adrenal: referred to as paragangliomas
What are common presentation?
REMEMBER PHEchromocytoma
- Palpitations
- Headaches
- Episodic sweating
- What are risk factors?
- Sporadic cases are of unknown aetiology
- Familial syndromes (up to 30% of cases)
- Multiple Endocrine Neoplasia 2a (MEN2a)
- Von Hippel Lindau syndrome (VHL)
- Neurofibromatosis type 1 (NF1)
What are signs and symptoms?
- Headaches
- Sweating
- Cardiorespiratory
- Palpitations
- Chest pain
- GI
- Epigastric pain
- Nausea
- Neuropsychiatric
- Tremor
- Anxiety
SIGNS:
- Hypertension
- Postural hypotension
- Pallor
- Tachycardia
- Fever
- Weight loss
What are investigations?
- 24 hr urine collection - check for catecholamines, metanephrines + normetanephrines
- Plasma free metanephrines/normetanephrines
- Genetic testing
Tumour localisation:
- CT > MRI
- I-123 MIBG scintigraphy
- Another way of visualizing the tumour
A 43-year-old man has a 3-month history of increasing fatigue and anorexia. He has lost 5.5 kg and noticed increased skin pigmentation, otherwise he has been healthy. Family history includes diabetes and thyroid problems. On examination his BP is 106/82 mmHg (supine) and 92/60 mmHg (sitting). There is diffuse pigmentation of his skin which is more pronounced in the mouth, palmar creases, and knuckles.
What is the most likely diagnosis?
A – Adrenal insufficiency
B – Haemochromatosis
C – Hyperthyroidism
D – Malignancy
E – Vitamin deficiency
A – Adrenal insufficiency
a) Which of the following is not a cause of hypokalaemia?
A – Vomiting
B – Anorexia Nervosa
C – Conn’s syndrome
D – Rhabdomyolysis
E – Salbutamol
b) Which of the following is the initial step in management of hyperkalaemia?
A – 10U actrapid
B – 10ml 10% calcium gluconate
C – 50ml 50% glucose
D – Nebulised salbutamol
E – 20ml SandoK
a) Which of the following is not a cause of hypokalaemia?
D – Rhabdomyolysis
b) Which of the following is the initial step in management of hyperkalaemia?
B – 10ml 10% calcium gluconate
chronic Adrenal insufficiency
Definition:
Types:
RF:
Epidemiology:
SIgns and symptoms:
Investigations:
Management:
Complications:
Prognosis:
Definition:
- deficiency of adrenal cortical hormones (mineralocorticoids; glucocorticoids and androgens)
- ~90% of the adrenal cortex needs to be destroyed to result in AI
Types:
- Primary AI
- Addison’s disease (usually autoimmune)
- May be either acute (adrenal crisis) or insidious
- Addison’s disease (usually autoimmune)
- Secondary AI
- Pituitary or hypothalamic disease
- Decreased adrenocorticotrophic hormone (ACTH) secretion: which ultimately results in adrenal failure
- Pituitary or hypothalamic disease
RF:
- TB
- Autoimmune
- sudden cessation of long term steroid therapy
Epidemiology: Most common causes are IATROGENIC – primary causes are rare
symptoms:
- Fatigue
- Weakness
- Myalgia
- Weight loss (+anorexia)
- Diarrhoea and Vomiting
- Abdominal pain
- Depression
Signs:
- Increased pigmentation
- Postural hypotension
- Loss of body hair in women (androgen deficiency)
- Associated autoimmune condition (e.g. vitiligo)
Investigations:
- 9am serum cortisol
- Short SynACTHen test
- Serum cortisol <550 nmol/L at 30 mins
- Long SynACTHen test
- Autoantibodies
- Abdo CT/MRI
Management:
Replace hormones hydrocortisone (time of acute illness/ stress increase dose) and fludrocortisone
Complications:
HYPERKALAEMIA
Death during Addisonian crisis
Prognosis:
Adrenal function rarely recovers
Normal life expectancy if treated
Auto-immune polyendocrine syndrome
What condition is this
cushing’s
What condition is this?
cushing
acute addisonian crisis
Signs:
symptoms:
Investigations:
Management:
Signs:
- Acute adrenal insufficiency à vomiting, diarrhoea, abdo pain
- Major haemodynamic collapse à shock
- Precipitated by stress (e.g. infection, surgery)
symptoms:
- Hypotensive shock
- Tachycardia
- Pale
- Cold
- Clammy
Investigations:
Bloods
->do NOT wait for blood results before starting treatment
- FBC
- U+Es
- High urea
- Low sodium
- High potassium
- CRP/ESR
- Low glucose
Blood cultures
Urinalysis: Culture + sensitivity
Management:
- Rapid IV fluid rehydration
- 50ml 50% dextrose
- IV 200mg hydrocortisone bolus
- 100mg 6hrly hydrocortisone till BP stable
- Treat precipitating cause e.g Abx for infection
- MONITOR
A 19-year-old female presents to the GP complaining of an excess of facial hair. She currently waxes her upper lip and chin twice a week and has also noticed hairs on her back and abdomen. Her periods have always been irregular (every 2-3 months) and the facial hair is affecting her social life, leaving her feeling very down.
What is the most likely diagnosis?
A – Hypothyroidism
B – Cushing’s disease
C – Gonadotrophin-secreting tumour
D – Polycystic ovary syndrome
E – Chromosomal abnormality
POLYCYSTIC OVARY SYNDROME
definition
association
aetiology
epidemiology
symptoms
signs
investigations
Definition: syndrome defined by 3 main features:
- Clinical features of hyperandrogenism
- Hirsutism
- Acne
- Oligo/amenorrhoea
- Polycystic ovaries on USS
Association:
- Obesity
- Insulin resistance
- Type 2 DM
- Infertility
aetiology:
- Genetic variants
- Environmental factors e.g poor diet à obesity
- Hyperinsulinaemia: increased ovarian androgen synthesis and reduced hepatic sex hormone binding globulin synthesis
- Leads to an increase in free androgens (which gives rise to the symptoms)
epidemiology: MOST COMMON cause of infertility in women
symptoms:
- Menstrual irregularities
- Acne
- Male-pattern hair loss
- Weight gain
- Infertility
signs:
- High BMI
- Hirsutism
- Acanthosis nigricans
investigations:
- bloods
- High LH
- High LH:FSH ratio
- High testosterone, androstenedione and DHEA-S
- Low sex hormone binding globulin
- Transvaginal USS:
- look for increased number of ovarian follicles and increase in ovarian volume
What is this graphic of
adissons
At the bottom left addisoniaan crisis
What does this graph show
hypokalaemia
what does this ECG show
hyperkalaemia
Hyperkalaemia
ECG changes
Symptoms:
Causes
Management
ECG changes:
- MILD: peaked t wave, ST depression, short QT
- SEVERE: prolongued PR interval, Absent P wave, Wide QRS
Symptoms:
- Emergency: can result in life-threatening arrhythmias (VF)
- 5.0-6.0: mainly asymptomatic
- >7.0: muscle weakness + ECG changes
Causes:
- Renal disease – HTN, DM
- Low RAAS activity – ACE-Is, ARBs, aldosterone antagonists, adrenal failure
- Systemic K+ release - rhabdomyolysis, metabolic acidosis (e.g DKA)
- Damage to the DCT - type 4 renal tubular acidosis, NSAID toxicity
- Spurious sample (recheck)
Management- 10 10 10 50 50
- 10ml 10% calcium gluconate
- 10U Actrapid
- 50ml 50% glucose
- Nebulised salbutamol
- 12-lead ECG (continuous)
->Aim to block cardiotoxic effects of K+ and increase K+ uptake into cells
Hypokaelaemia
- ECG changes
- Clinical features
- Causes
- Manangement
ECG changes: Prolongued QT and U wave + atrial and ventricular tachyarrhytmias
Clinical features: only seen if less than 3.0
- Muscle weakness & spasm
- Cardiac arrhythmia
- Polyuria and polydipsia (nephrogenic DI)
Causes:
- GI loss – vomiting, diarrhoea
- Redistribution of K+ into cells – insulin, B-agonists, metabolic alkalosis
- Renal loss – hyperaldosteronism, excess cortisol, natriuresis
- Decreased K+ intake – anorexia nervosa
Manangement: always correct magnesium
K+ 3.0-3.5 mmol/L
- Oral potassium chloride (SandoK)
- Recheck in 48 hours
K+ <3.0 mmol/L
- IV potassium chloride
- Max infusion rate 10 mmol/hr (peripheral irritant)
