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FLASHCARDS from MEDED lectures COPY > Adrenal > Flashcards

Adrenal Flashcards

1
Q

What are the different layers of the adrenal gland and what do they produce?

A
  • Glomerulosa - mineralocorticoids
  • Fasciculata - glucocorticoids
  • Reticularis – sex steroids

Medulla: catecholamines (Adrenaline & Noradrenaline)

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2
Q

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

A

C – Primary hyperaldosteronism

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3
Q

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

A

D – Cushing’s syndrome

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4
Q

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

A – Phaeochromocytoma

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5
Q

What is primary hyperaldosteronism?

What does hihg aldosterone do physiologically?

What are the different types ?

What are the treatment for them?

A

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
  1. Conn’s (70%) - (adrenalectomy laparascopic) surgery
  2. Adrenal aldosteronoma (rare) - (adrenalectomy laparascopic) surgery
  3. Familial hyperaldosteronism
  4. Bilateral adrenal hyperplasia (30%) - spironolactone(aldosterone inhibitor) (potassium sparing diuretics)
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6
Q

What people are affected by conn’s syndrome?

What people are affected by bilateral adreanl cortex hyperplasia?

A

What people are affected by conn’s syndrome? young females

What people are affected by bilateral adreanl cortex hyperplasia? older males

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7
Q

What are symptoms and signs of hyperaldosteronism?

A

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
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8
Q

What are investigations for Hyperadrenalism?

A

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)
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9
Q

What are complications of hyperadrenalosims?

What is the prognosis?

A

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

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10
Q

What are symptoms of cushings snd signs?

A
  • 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
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11
Q

What is the definition of cushings syndrome?

What is the aetiology?

A

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)
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12
Q

What are investigations needed for cushings syndrome?

A
  • 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
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13
Q

What condition is this?

A

addison’s

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14
Q

What is the management in cushing’s?

What are teh comlipications of the different treatments?

A

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

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15
Q

WHat are complications of cushings?

What is the prognosis?

A
  • Diabetes
  • Osteoporosis
  • Hypertension
  • Pre-disposition to infections

Prognosis:

  • If untreated, 5yr survival rate is 50%.
  • Depression often persists for years following successful treatment
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16
Q

What condition is this

A

PCOS

17
Q

Phaechromocytoma

What is the definition?

What are common presentation?

What are risk factors

What are signs and symptoms?

What are investigations?

A

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
18
Q

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

A – Adrenal insufficiency

19
Q

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

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

20
Q

chronic Adrenal insufficiency

Definition:

Types:

RF:

Epidemiology:

SIgns and symptoms:

Investigations:

Management:

Complications:

Prognosis:

A

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
  • Secondary AI
    • Pituitary or hypothalamic disease
      • Decreased adrenocorticotrophic hormone (ACTH) secretion: which ultimately results in adrenal failure

RF:

  1. ​TB
  2. Autoimmune
  3. 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

21
Q

What condition is this

A

cushing’s

22
Q

What condition is this?

A

cushing

23
Q

acute addisonian crisis

Signs:

symptoms:

Investigations:

Management:

A

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
24
Q

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

A
25
Q

POLYCYSTIC OVARY SYNDROME

definition

association

aetiology

epidemiology

symptoms

signs

investigations

A

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
26
Q

What is this graphic of

A

adissons

At the bottom left addisoniaan crisis

27
Q

What does this graph show

A

hypokalaemia

28
Q

what does this ECG show

A

hyperkalaemia

29
Q

Hyperkalaemia

ECG changes

Symptoms:

Causes

Management

A

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

30
Q

Hypokaelaemia

  • ECG changes
  • Clinical features
  • Causes
  • Manangement
A

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)

FLASHCARDS from MEDED lectures COPY (35 decks)

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