Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

Name the three layers of the adrenal cortex, how they are regulated and what they secrete

A

Zona glomerulosa
Regulated by angiotensin II & (plasma) K+
Secrete mineralocorticoids (aldosterone)
————————————————————————————
Zona fasciculata
Regulated by ACTH
Secrete glucocorticoids (cortisol)
————————————————————————————
Zona reticularis
Regulated by ACTH
Secrete adrenal androgens (DHEA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name the cells of the adrenal medulla and what they produce

A

Chromaffin cells
Catecholamines (epinephrine & norepinephrine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What substance are all corticosteroids (aldosterone, cortisol, DHEA, testosterone…) derived from?

A

Cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the HPA axis (cortisol & androgen production regulation)

A

Hypothalamus secretes corticotrophin releasing hormone (CRH)
Anterior pituitary secretes adrenocorticotropic hormone (ACTH)
Adrenal cortex secretes cortisol (& small amounts of DHEA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the regulation of the HPA axis

A

Negative feedback control of CRH & ACTH
Variation of CRH secretion with illness, stress and time of day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Briefly describe the RAAS system

A

Drop in blood pressure →
Kidneys release renin →
Angiotensinogen converted to angiotensin I →
Angiotensin I converted to angiotensin II by ACE →
Aldosterone secreted by adrenal cortex →
Salt retention & Increase in BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Aldosterone is secreted in response to what level of plasma K+

A

High K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the main actions of cortisol
(Cardiac, renal, CNS, bone, connective tissue, metabolic, immunological)

A

CARDIAC - Increased CO & BP
RENAL - Increased renal blood flow & GFR
CNS - Decreased libido, mood lability
BONE - Accelerated osteoporosis
CONNECTIVE TISSUE - decreased wound healing
METABOLIC - Increased blood glucose, lipolysis & proteolysis
IMMUNOLOGICAL - Decreased inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name some conditions that are treated with glucocorticoids

A

Asthma, RA, UC, Crohn’s, sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where are mineralocorticoid receptors located (4)

A

Kidneys
Gut
Salivary glands
Sweat glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the main actions of aldosterone

A

Na/K balance (K/H excretion, Na reabsorption)
Extracellular volume & blood pressure regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Adrenal insufficiency aetiology

A

Primary insufficiency
- Addison’s disease
- Congenital adrenal hyperplasia
- Adrenal infection e.g. TB
- Adrenal malignancy
- Bilateral adrenal haemorrhage (sepsis, anti-coagulants)
- Bilateral adrenalectomy
- Bilateral adrenal infiltration e.g. haemochromatosis

Secondary/ tertiary insufficiency
- Excess exogenous steroids
- Pituitary/ hypothalamic disorders causing lack of ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define primary adrenal insufficiency

A

Destruction of the entire (>90%) adrenal cortex causing decreased production of adrenocortical hormones (glucocorticoids, mineralocorticoids, and adrenal androgens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Primary adrenal insufficiency/ Addison’s disease clinical presentation

A
  • Anorexia, fatigue, lethargy
  • Loss of appetite, salty food cravings
  • Dizziness & low bp
  • Abdominal pain, vomiting, diarrhoea
  • Skin & oral mucosa pigmentation (excess ACTH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What clinical sign differentiates primary from secondary adrenal insufficiency and what does it indicate

A
  • Skin & oral mucosa pigmentation
  • Caused by excess ACTH from the pituitary gland
    • ACTH molecule contains sequence for MSH within it
    • ACTH is degraded by proteases eventually exposing MSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the most common cause of adrenal insufficiency in infants (< 6 months)

A

Congenital adrenal hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Primary adrenal insufficiency/ Addison’s disease bloods findings

A
  • Adrenal autoantibodies positive in 70%
    • Biochemistry - ↓ Na+, ↑ K+, may be hypoglycaemic
      (especially in paediatrics)
    • ACTH levels very high (results in skin pigmentation)
    • Renin/aldosterone levels - ↑↑ renin, ↓ decreased
      aldosterone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Primary adrenal insufficiency/ Addison’s disease ‘stimulation’ test

A

Short synacthen test
- Measure plasma cortisol before IV/IM ACTH injection
- Measure plasma 30 mins after IV/IM ACTH injection
- Normal baseline cortisol >250 nmol/L,
- Normal post ACTH cortisol >550 nmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Investigations to determines the aetiology for primary adrenal insufficiency

A
  • 17-OH-Progesterone blood levels (High in CAH)
  • 21-OH antibody (Addison’s, anti-phospholipid syndrome)
  • CT adrenals (infection/ infiltration/ haemorrhage/
    malignancy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Primary adrenal insufficiency/ Addison’s treatment

A
  • Hydrocortisone as cortisol replacement
    • If unwell IV first
    • Usually 15-30mg PO daily in divided doses
    • Try and mimic diurnal rhythm (higher dose in morning)
  • Fludrocortisone as aldosterone replacement
    • Careful monitoring of BP and K+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Primary adrenal insufficiency/ Addison’s disease ‘sick day rules’

A

Increase steroid replacement when unwell or undergoing other stress e.g. preoperative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Adrenal crisis treatment

A
  • 0.9% IV NaCl (normal saline)
  • 100mg IV hydrocortisone
  • Cardiac monitoring
  • ?underlying cause/precipitant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Adrenal crisis definition/ aetiology

A

Acute, severe glucocorticoid deficiency caused by either

  • stress in a patient with underlying adrenal insufficiency or
  • sudden discontinuation of glucocorticoids after prolonged glucocorticoid therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Congenital adrenal hyperplasia definition/ aetiology

A
  • Inherited group of disorders characterised by a deficiency in one of the enzymes necessary for cortisol synthesis
  • 90% due to an autosomal recessive 21⍺-hydroxylase deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Congenital adrenal hyperplasia pathophysiology
- 21⍺-hydroxylase deficiency prevents the production of aldosterone and cortisol - Increased volume of precursors will be diverted into the androgen pathway → increased testosterone and dihydrotesterone - Reduced cortisol stimulates ACTH release and cortical hyperplasia
26
Classic vs non-classic CAH clinical presentation
Classic CAH - Presents at birth or shortly after - Genital ambiguity (virilisation) in females - Adrenal failure - collapse, hypotension, hypoglycaemia, poor weight gain - Biochemical patten of Addison's disease Non-classic CAH - Partial 21⍺-hydroxylase deficiency - Presents later (adolescence/adulthood) (hyperandrogenaemia) - Precocious puberty - Hirsutism - Acne - Oligomenorrhoea, infertility or sub-fertility
27
Congenital adrenal hyperplasia investigations
- Basal (or stimulated) 17-OH progesterone - would be high as it is converted by 21⍺-hydroxylase (which is deficient) - Genetic analysis
28
Congenital adrenal hyperplasia management
Paediatrics - Glucocorticoid replacement - Mineralocorticoid replacement in some - Surgical correction - Achieve maximal growth Adults - Glucocorticoid replacement, avoiding steroid over-replacement - Control androgen excess - Restore fertility
29
Secondary/ tertiary adrenal insufficiency is different from primary adrenal insufficiency in two ways. Name these.
No excess ACTH => no skin pigmentation Intact aldosterone production => less hypotension
30
Secondary vs tertiary adrenal insufficiency
Secondary: lack of production of ACTH by the pituitary gland Tertiary: lack of CRH secretion by the hypothalamus
31
Secondary/tertiary adrenal insufficiency investigations
Insulin tolerance test CRH stimulation test (secondary vs tertiary) MRI of hypothalamus & pituitary gland
32
Secondary/tertiary adrenal insufficiency treatment
Hydrocortisone replacement alone (Fludrocortisone unnecessary)
33
Cushing’s syndrome vs disease
Cushing’s syndrome - increased cortisol Cushing’s disease - increased cortisol (cushing’s syndrome) due to functioning pituitary adenoma
34
Cushing’s syndrome aetiology
ACTH dependant - Cushing’s disease (pituitary adenoma) - Ectopic ACTH secretion (e.g. SCLC) - Ectopic CRH secretion (e.g. medullary thyroid carcinoma) ACTH independent - Exogenous steroids (most common) - Adrenal adenoma or carcinoma - Adrenal corticol nodular hyperplasia - Mccune-Albright syndrome - Pseudo-Cushing’s (severe depression/ alcoholism)
35
Differences in adrenal enlargement in ACTH dependent vs independent Cushing’s syndrome
ACTH dependent - (usually) diffuse enlargement ACTH independent - (usually) nodular enlargement
36
Cushing’s syndrome clinical presentation - excess cortisol effects (ACTH independent & dependant)
Inflammation & (central) fat deposition - Facial plethora & swelling (‘moon face’) - Central obesity - Dorsocervical fat pad - Conjunctival oedema (chemosis) ———————————————————————————— Increased blood sugars, lipolysis & proteolysis - Proximal myopathy - Glycosuria/ diabetes mellitus ———————————————————————————— Decreased collagen formation & wound healing - Thin skin - Easy bruising - Striae ———————————————————————————— Increased bone resorption & decreased bone formation - Osteoporosis ———————————————————————————— Cortisol effects on CNS - Depression/psychosis ———————————————————————————— Cortisol effects on cardio & renal (increased CO & BP) - Hypertension
37
Cushing’s syndrome clinical presentation - excess ACTH & androgen effects (ACTH dependant)
Increased ACTH - Skin pigmentation Increased adrenal androgens - Acne - Virilization/ hirsutism - Oilgo/ammenorhea - Frontal balding
38
Cushing’s syndrome first line screening test & 3 other screening tests available (to establish excess cortisol)
First line - Overnight dexamethasone suppression test - Normal: cortisol <50 nmol/l next morning - Abnormal: cortisol >130 nmol/l Other screening tests - 24hr urine free cortisol, diurnal cortisol variation, late night salivary cortisol test
39
Cushing’s syndrome diagnostic test
Low dose dexamethasone suppression test - 2 day 2mg/day dexamethasone - Normal: cortisol <50 nmol/l 6 hours after last dose - Cushing's: cortisol >130 nmol/l + Repeat to confirm
40
Cushing’s syndrome aetiology focused investigations
1) Serum ACTH (ACTH dependent vs independent) 2a) If serum ACTH high => pituitary MRI (pituitary adenoma) => biochemical tests e.g. CRT +/- HDDST (ectopic ACTH/ CRH) 2b) If serum ACTH low => exogenous steroids?? => Adrenal glands CT
41
Cushing’s syndrome management
Aetiology based - Pituitary adenoma => hypophysectomy +/- radiotherapy - Adrenal adenoma => adrenalectomy - Ectopic => remove source +/- radiotherapy OR bilateral adrenalectomy - If all other treatments fail => metyrapone (/Ketoconazole/Pasireotide)
42
Explain the effect of prolonged high dose steroid therapy on the pituitary gland & adrenal gland.
Initially there is an excess of cortisol (iatrogenic Cushing’s) This causes chronic suppression of pituitary ACTH secretion This then leads to adrenal atrophy & suppression If they then suddenly stop taking the steroids it could lead to an adrenal crisis
43
Define primary hyperaldosteronism
Autonomous production of aldosterone independent of its regulators (angiotensin II/ plasma K+), causing elevated aldosterone & hypertension
44
Describe the (cardiac) effects of excess aldosterone
Sodium retention in the kidneys Excessive cardiac collagen formation, inflammation & fibrosis Abnormal endothelial function & increased oxidative stress Baroreceptors dysfunction & increased sympathetic outflow => Increased BP, LVH & atheroma formation (^ CV risk)
45
Primary hyperaldosteronism aetiology
- Adrenal adenoma (conn’s syndrome) - Bilateral adrenal hyperplasia (most common) - Genetic mutation (rare)
46
Primary hyperaldosteronism clinical presentation
Significant hypertension Hypokalaemia (~30% cases) Alkalosis
47
Primary hyperaldosteronism investigations
1) Plasma aldosterone: renin ratio 2) If ratio raised => saline suppression test 3) If limited suppression => Primary aldosteronism 4) Adrenal CT to demonstrate adenoma 5) If present => adrenal vein sampling (to confirm adenoma is source of aldosterone excess)
48
Primary hyperaldosteronism management
Adrenal adenoma - Unilateral laparoscopic adrenalectomy (Cures hypokalaemia & may cure hypertension) Bilateral adrenal hyperplasia - mineralocorticoid receptor antagonists (e.g. spironolactone)
49
Adrenal adenomas can be benign (functioning/ non functioning) or malignant. If you identified an adrenal adenoma on CT, what would make you likely to surgically remove it?
- If functional lesion ie. Produces cortisol (Cushing’s) or aldosterone (conn’s) OR - If large adenoma (thought to be at risk of malignancy)
50
When giving fludrocortisone to a patient. What would you consider giving first?
IV fluids e.g. saline (to prevent sudden fluid overload)
51
What happens to aldosterone, cortisol & dihydrotestosterone production in 21α hydroxylase deficiency (CAH)
Mineralocorticoid/ Aldosterone - none/low Glucocorticoid/ cortisol - none/low Adrenal androgens/ dihydrotestosterone - normal/high
52
Secondary hyperaldosteronism definition
Increased adrenal production of aldosterone in response to nonpituitary, extra-adrenal stimuli such as renal hypo perfusion
53
Secondary hyperaldosteronism aetiology & pathophysiology
Reduced blood flow due to: - Obstructive renal artery disease (eg, atheroma, stenosis) - Renal vasoconstriction (in accelerated hypertension) - Oedematous disorders (e.g. HF, cirrhosis with ascites) Leads to excess renin & hence angiotensin II
54
Secondary hyperaldosteronism clinical presentation
Hypertension
55
Secondary hyperaldosteronism investigations
- Renin/aldosterone ratio: high aldosterone AND high renin - Imaging: doppler US or CT angiogram to look for for renal artery stenosis/ obstruction
56
Secondary hyperaldosteronism management
Treat cause! Mineralocorticoid receptor antagonists (Spironolactone)
57
Adrenal cortex tumours are likely benign adenomas. What would make you suspect adrenocortical carcinoma (a very rare malignancy)
- Medical history of Li-fraumeni syndrome - Functional, virilising tumour - Haemorrhage, necrosis, atypical mitoses & invasion
58
A patient presents with an adrenal cortex tumour and fever, what is a differential diagnosis
Adrenocortical carcinoma with necrosis (necrosis causes fever)
59
What is a phaeochromocytoma
Catecholamine-secreting tumour Typically derived from chromaffin cells of adrenal medulla
60
Phaeochromocytoma vs paraganglioma
Phaeochromocytoma - adrenal medulla Paraganglioma - extra-adrenal, sympathetic chain
61
What would make you suspect a familial condition associated with a phaeochromocytoma/paraganglioma
- Younger patient - Paraganglioma or BILATERAL phaeochromocytoma
62
Phaeochromocytoma/paraganglioma clinical presentation
- Insidious onset - Classical triad -hypertension, headache, hyperhidrosis (3H’s) - Other symptoms - postural hypotension, tachycardia, pyrexia, SOB, palpitations, anxiety, weight loss, constipation (excess catecholamines effect)
63
Why is phaeochromocytoma known as the ‘10% tumour’?
10% extra-adrenal (more commonly familial) 10% bilateral (more commonly familial) 10% malignant 10% not classic triad (hypertension, headache, sweating) >10% familial
64
Complications of a phaeochromocytoma/paraganglioma
LV heart failure (due to overstimulation of cardiac muscle) Myocardial necrosis (due to cardiac muscle injury) Stroke (due to hypertension & arrhythmias) Shock (due to cardiomyopathy => Cardiogenic shock) Paralytic ileus of bowel (due to sympathetic overstimulation)
65
What biochemical changes can be expected in phaeochromocytoma/paraganglioma
Hyperglycaemia (sympathetic overstimulation) Hypokalaemia (due to K cell influx, more likely with vomiting), Hypercalcaemia High Hb concentration (erythrocytosis) Lactic acidosis - in absence of shock
66
What would make you suspect and investigate for a phaeochromocytoma/paraganglioma
Resistant hypertension Young person with hypertension Classic triad of symptoms (3H’s) Family history Adrenal incidentalomas
67
Phaeochromocytoma/paraganglioma investigations
CONFIRM CATECHOLAMINE EXCESS - 2 x 24 hr urinary metanephrines (sensitive) - Plasma metanephrites, ideally at time of symptoms (specific) CONFIRM TUMOUR - MRI abdomen or whole body (neck for paraganglioma) - MIBG scan - PET scan
68
Phaeochromocytoma/paraganglioma treatment
PRE-OP (a before b) - Full ⍺-blockade (phenoxybenzamine/ doxazosin) - Then once stable, full β-blockade (propranolol/atenolol etc) - Fluid &/ blood replacement - High salt diet DEFINITIVE - laparoscopic excision (or de-bulking if not possible) - chemo/ radio-labelled MIBG if malignant POST-OP - Genetic testing & long-term follow up/monitoring
69
Genetic conditions associated with phaeochromocytoma/paraganglioma
•Multiple Endocrine Neoplasia 2 (MEN2A/MEN2B) •Von-Hippel-Lindau syndrome •Succinate dehydrogenase mutations •Neurofibromatosis •Tuberose sclerosis

Endocrine (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions