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Year 5 Endocrine > Adrenals > Flashcards

Adrenals Flashcards

1
Q

What is adrenal insufficiency?

A

Destruction of adrenal cortex = ↓adrenal hormone output:

  • ↓Mineralocorticoids (Aldosterone) → Acidosis
  • ↓Glucocorticoids (Cortisol) → ↓blood glucose
  • ↓Androgens (Testosterone)
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2
Q

What is Addison’s disease?

A

Primary autoimmune destruction of adrenal cortex

Deficiency of glucocorticoid + mineralocorticoids

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3
Q

Who typically gets Addison’s?

A

30-50yo
Female
Metastatic Ca
Infection: TB - most common cause worldwide

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4
Q

What is Secondary Addison’s?

A

Inadequate pituitary/hypothalamic stimulation of adrenal glands

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5
Q

What causes secondary Addison’s?

A 
STEROIDS
Sepsis
Metastatic Ca, Lymphoma
SLE
Antiphospholipid syndrome
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6
Q

How does Addison’s present?

A 
Often diagnosed late
Lean: Anorexia, ↓weight
Tired
Postural hypoT → syncope
Tanned: Bronze skin, pigmented palmar creases + buccal mucosa
Tearful + weak: Depression
GI: N&V, abdo pain, D/C
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7
Q

What are the Sx of hypoaldosteronism?

A 
Hyperk
HypoNa 
Hypovolaemia 
Metabolic Acidosis (↓HCO3-) 
Muscle weakness
Palpitations & Arrhythmia
Cravings for salty food 
N&V Fatigue,Dizziness
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8
Q

What are the Sx of low cortisol levels?

A

Fatigue
Dizzy
Confused
Hyper-pigmented elbows, knees

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9
Q

What are the Sx of low androgen levels?

A

Low sex drive

Little pubic hair (women)

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10
Q

How is Addison’s investigated?

A 
SYNACTHEN TEST- DIAGNOSTIC
Bloods: U&E (↓Na + ↑K), ↓Glucose, FBC (↓Hb, ↓Eosin)
9am ↓Cortisol + ACTH levels
ABG: Met acidosis
Adrenal AutoAbx
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11
Q

What does a 9am cortisol level tell you?

A 
<100 = Addison's likely
100-500 = Synacthen test
>500 = Addison's unlikely
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12
Q

What does a 9am ACTH level tell you?

A 
↑= primary cause
↓/n = Secondary cause
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13
Q

How does a Synacthen test work?

A

Measure plasma cortisol
Give 250ug synacthen IM
Wait 30mins
Measure plasma cortisol

<500 = Addison's
>550 = NOT Addison's
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14
Q

How is Addison’s managed?

A

Hydrocortisone 15-30mg OD
DO NOT stop steroids abruptly + sick day rules apply (double dose)
Fludrocortisone 50-300ug
+/- Androgen replacement

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15
Q

What is an Addison’s crisis? What are the Sx?

A

Zona glomerulosa & fasiculata destroyed usually triggered by illness demand outweighs production)

  • Unresponsive hypotension
    • HyperK
  • Pain in back/abdo/legs
  • D&V = DEHYDRATION
  • HypoV = SHOCK
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16
Q

How is an Addison’s crisis managed?

A

Emergency admission
Tx underlying cause
IM/IV 100mg Hydrocortisone
IV 0.9% NaCl to correct ↓Na+

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17
Q

What is Conn’s Syndrome?

A

Primary hyper-aldosteronism

80% adrenal adenoma or bilateral adrenal hyperplasia

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18
Q

How does hyper-aldosteronism present?

A 
Asymptomatic
HypoK: Weakness, cramps, paraesthesia
HyperNa: Lethargy, irritable
Met alkalosis
HTN
Headache
19
Q

How is hyper-aldosteronism investigated?

A

Bloods: U&E (↓K+ ↑Na+ )
ABG: Met Alkalosis
Hormones: ↑Aldosterone ↓Renin - if ↑renin then NOT primary cause
HR-CT Abdo: Adenoma

20
Q

How is Conn’ syndrome managed?

A

Laparoscopic adrenalectomy

Spironolactone 4weeks post-op

21
Q

What are secondary causes of hyper-aldosteronism?

A 
Pathology outside of adrenals
↑renin from ↓renal perfusion 
RAS
Accelerated HTN
Diuretics
Hepatic failure
SIGNS: ↓K+ ↑Na+, ↑Aldosterone ↑Renin
22
Q

What is hyper-aldosteronism?

A

Excess levels of aldosterone
Produced in zone glomerulosa
Acts on DCT of nephron to stimulate ↑K+ excretion, ↑Na+ and ↑HCO3- retention

23
Q

What is Cushing’s syndrome?

A

Chronic excessive cortisol secretion
Decreased feedback to hypothalami-pituitary-axis
Loss of normal circadian rhythm of cortisol secretion

24
Q

What are the 2 types of Cushing’s?

A

-ACTH independent: Exogenous steroids!!, adrenal adenoma, adrenal nodular hyperplasia, albright syndrome
ACTH dependent: Cushing’s disease (B/L adrenal hyperplasia), ectopic ACTH producing tumours (SCLC), ectopic CRH production (thyroid & prostate Ca)

25
Q

What is Cushing’s disease?

A

Benign pituitary adenoma causes ↑ACTH

26
Q

What is the feedback loop of ACTH?

A

1) Hypothalamus secretes CRH
2) Stimulates ant pituitary to produce ACTH
3) Stimulates zona fasciculata in cortex to secrete cortisol
4) High cortisol negative feedback to pituitary to stop producing ACTH

27
Q

When is cortisol normally high?

A

Peak 8am

Trough 12am-midnight

28
Q

What are the Sx of Cushing’s?

A 
↑Weight → Central Obesity/ moon face
HyperG
HTN
Bruises + purple striae
Gonadal dysfunction: Erectile dysfunction + irregular periods
Muscle weakness + wasting= PROXIMAL MYOPATHY
Depression/lethargy/psychosis
Acne
Infection prone/poor healing
29
Q

How is Cushing’s syndrome investigated?

A 
OVERNIGHT DEXAMETHASONE SUPPRESSION TEST
24hr Urinary free Cortisol
Bloods: FBC, U&amp;E, plasma ACTH + Cortisol
ABG: Met Alkalosis
ECG: U waves (hypoK)
30
Q

How is an overnight Dexamethasone suppression test done?

A

1) 1mg Dex at midnight
2) Measure Cortisol at 8am

Cushing's= ↑Cortisol (No suppression)
Normal = Cortisol <50

If positive → High dose Dex test:

  • If Cushing’s disease then some sort of suppression
  • No suppression in ACTH dependent causes
31
Q

How is a 24hr Urinary free Cortisol carried out?

A

1) 3 separate urine collections
2) Measure creatinine excretion at same time
>280/24hours = Cushing’s

32
Q

How is Cushing’s syndrome managed?

A

Metyrapone

33
Q

How is Cushing’s disease managed?

A

Removal of pituitary adenoma

34
Q

What do the plasma ACTH + cortisol levels tell you?

A
  • Non-detectable ACTH, ↑Cortisol = INDEPENDENT- ACTH → CT Abdo to find cause
  • ↑ACTH ↑Cortisol = DEPENDENT ACTH → Dex suppression test/ CRH test to decide if pituitary or ectopic cause
35
Q

What is a Phaeochromocytoma?

A

RARE
Catecholamine producing tumour
Arising from chromatin cells of adrenal medulla
↑Adrenaline + ↑Dopamine

36
Q

How does a Phaeochromocytoma present?

A

Episodic headache
Sweating
Tachycardia & HTN
Often precipitated by stress/straining/exercise/beta-blockers/surgery

37
Q

How is Phaeochromocytoma investigated?

A

Bloods:
↑Glucose, ↑Ca2+, ↑Hb
24hr urinary collection of met-adrenaline= DIAGNOSTIC

38
Q

How is a Phaeochromocytoma managed?

A

1) A-blocker

2) Surgery- Definitive

39
Q

How can hypoaldosteronism be categorised?

A

1) Hyporeninemic: ↓ renin

2) Hyperreninemic: ↑ renin

40
Q

How is hypoaldosteronism investigated?

A

Plasma renin activity
Serum aldosterone
Serum cortisol

41
Q

How is hypoaldosteronism treated?

A

Low K+ diet
Fludrocortisone
AVOID: ACEi & K+ sparing diuretics
Hyporeninemic = Furosemide to correct K+

42
Q

What are the Sx of HPA suppression?

A 
Adrenal insufficiency
Flu-like Sx
Fever/chills
Headache
D&amp;V
Weakness
Fatigue
Vertigo
HypoT
Depression
Salt craving
Vitiligo (depigmentation)
43
Q

When is an Addison’s crisis most likely to occur?

A 
Infection
Surgery
Burns
Pregnancy 
MI

Year 5 Endocrine (6 decks)

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