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ENDOCRINOLOGY > 7. Adrenal Gland > Flashcards

7. Adrenal Gland Flashcards

1
Q

Where are ADRENAL GLANDS situated

A

above kidneys

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2
Q

why are adrenal glands yellow

A

due to LIPID content

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3
Q

very RICH ARTERIAL SUPPLY (very vascular organ)

main arterial supplies:

A
  • INFERIOR PHRENIC ARTERY
    • SUPERIOR SUPRARENAL ARTERIES
  • AORTA
    • MIDDLE SUPRA RENAL ARTERY
  • RENAL ARTERY
    - INFERIOR SUPRA RENAL ARTERY
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4
Q

because of the rich arterial supply, adrenal glands are PRONE TO…

A

HAEMORRHAGE
METASTATIC DEPOSITS

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5
Q

BLOOD supply of adrenal glands:
(seen in cross-section)

A

SUBCAPSULAR PLEXUS OF CAPILLARIES (below capsule)
CAPILLARIES
SINUSOIDS

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6
Q

VENOUS DRAINAGE - RIGHT

A

right suprarenal vein drains into INFERIOR VENA CAVA

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7
Q

VENOUS DRAINGAGE - LEFT

A

left suprarenal vein drains into LEFT RENAL VEIN

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8
Q

although rich arterial supply, how is VENOUS DRAINAGE of adrenal glands

A

only a SINGLE VENOUS DRAINAGE

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9
Q

SINGLE VENOUS DRAINAGE makes it prone to…

A

THROMBOSIS
(blood clots)

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10
Q

Adrenal Glands are made up of 2 parts

A

CORTEX (90%)
- derived from Mesoderm

MEDULLA
- derived from Neuroectodermal cells

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11
Q

3 PARTS OF CORTEX

A

ZONA GLOMERULOSA (15%)

ZONA FASCICULATA (80%)

ZONA RETICULARIS (5%)

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12
Q

what HORMONE is produced by ZONA GLOMERULOSA of adrenal CORTEX

A

ALDOSTERONE

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13
Q

which zone makes up MOST of the CORTEX

A

ZONA FASCICULATA (80%)

least - ZONA RETICULARIS (5%)

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14
Q

which HORMONE is produced by ZONA FASCICULATA of adrenal CORTEX

A

CORTISOL

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15
Q

which HORMONES are produced by ZONA RETICULARIS of adrenal CORTEX

A

ANDROGENS:
- ANDROSTENEDIONE
- DEHYDROEPIANDROSTERONE

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16
Q

which HORMONES are produced by the MEDULLA of adrenal glands

A

ADRENALINE
NOR-ADRENALINE

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17
Q

Adrenocortical Hormones (hormones produced by cortex) have what structure

A

Cyclopentanophenantharine structure

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18
Q

which hormone is the predominant Mineralocorticoid

A

ALDOSTERONE

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19
Q

what STIMULATES release of ALDOSTERONE

A

LOW BLOOD PRESSURE

LOW NA+ RETENTION

HIGH K+

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20
Q

renin-angiotensin-aldosterone system (RAAS) to stimulate ALDOSTERONE RELEASE from ADRENAL

A

LOW RENAL PERFUSION / BLOOD PRESSURE / RENAL BLOOD

  1. RENIN released from KIDNEY
  2. ANGIOTENSINOGEN from LIVER converted to ANGIOTENSIN 1
  3. ANGIOTENSIN 1 converted to ANGIOTENSIN 2 by ACE (angiotensin-converting enzyme) in LUNGS
  4. ANGIOTENSIN II stimulates release of ALDOSTERONE from ADNRENAL glands
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21
Q

results of ALDOSTERONE secretion from adrenal

A

INCREASED NA+ RETENTION

so INCREASED H20 ABSORPTION/RETENTION from kidney

DECREASE K+

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22
Q

to stimulate ALDOSTERONE release, ANGIOTENSIN II BINDS TO…

A

cell-surface RECEPTORS on ZONA GLOMERULOSA CELLS

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23
Q

ALDOSTERONE produced in MITOCHONDRIA of zona glomerulosa cells by conversion of

A

CHOLESTEROL

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24
Q

CONVERSION of CHOLESTEROL to PREGNENOLONE (…aldosterone) is promoted by… (2)

A

CALCIUM CA2+

PROTEIN KINASE C

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25
Q

how is CHOLESTEROL CONVERTED TO ALDOSTERONE in MITOCHONDRIA of zona glomerulosa cells by conversion of

A
  • enters mitochondria and by help of CA2+ and protein kinase C, converted into PREGENOLONE
  • pregnenolone to PROGESTERONE
  • progesterone to DEOXYCORTICOSTERONE
  • deoxycorticosterone to CORTICOSTERONE

TO ALDOSTERONE

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26
Q

Diseases of the Adrenal Cortex:
HORMONAL OVER-PRODUCTION examples:

A

Zona Glomerulosa: mineralocorticoid / Aldosterone excess
- CONN’S SYNDROME

Zone Fasciculate: glucocorticoid / Cortisol excess
- CUSHING’S SYNDROME

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27
Q

Diseases of the Adrenal Cortex:
HORMONAL UNDER-PRODUCTION examples:

A

primary: ADDISON’S DISEASE

secondary: HYPOPITUITARISM (problem in pituitary)

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28
Q

other Diseases of the Adrenal Cortex:

A
  • Incidentalomas
  • Adrenal carcinoma
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29
Q

Primary HYPERALDOSTERONISM is when there is…

A

EXCESS production of ALDOSTERONE

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30
Q

what can result from EXCESS ALDOSTERONE (hyperaldosteronism) (3)

A
  • HYPERTENSION (increased Na+ retention and water retention contributes)
  • HYPOKALAEMIA (decreased K+)
  • METABOLIC ALKALOSIS
31
Q

Conn’s syndrome: Diagnosis & Management

A

Diagnosis:
- HIGH Aldosterone / Renin ratio
- CT/MRI scan
- Adrenal vein sampling: allows differentiation between unilateral & bilateral aldosterone production

Treatment:
Surgical Rx: Adrenalectomy
Medical Rx (drugs) : Aldosterone antagonists (spironolactone, amiloride & triamterene)

32
Q

CORTISOL is produced in Zona Fasciculata by CONVERSION of…

A

CHOLESTEROL

33
Q

COVERSION OF CHOLESTEROL TO CORTISOL

A
  • cholesterol converted to PREGNENOLONE
  • pregnenolone converted to 17-HYDROXYPREGENOLONE
  • 17-hydroxypregnenolone converted to 11-DEOXYCORTISOL

TO CORTISOL

34
Q

ENZYMES used for CONVERSION of cholesterol to ALDOSTERONE / CORTISOL

A

3 BETA HSD

21-HYDROXYLASE

11 BETA-HYDROXYLASE

18-Oxidase for Aldosterone

35
Q

Regulation of CORTISOL (negative feedback) starting from Hypothalamus..

A

HYPOTHALAMUS : CRH (Corticotrophin Releasing Hormone)

ANTERIOR PITUITARY: ACTH (Adrenocorticotropic hormone)

ADRENAL GLAND: CORTISOL

36
Q

how is CHOLESTEROL produced in ZONA FASCICULATA CELLS for conversion into CORTISOL

A

cAMP to PROTEIN KINASE A

converts CHOLESTEROL ESTER to CHOLESTEROL

37
Q

when are CORTISOL levels highest

A

MORNING

38
Q

CORTISOL released in response to…

A

STRESS

and
Stress
Blood loss
Severe infection
Trauma
Burns
Illness
Surgery

39
Q

effects of CORTISOL on GLUCOSE levels

A
  • INCREASED GLUCONEOGENESIS
  • INHIBITS peripheral glucose UPTAKE

so INCREASED GLUCOSE LEVELS (Hyperglycaemia)

  • hepatic glycogen synthesis
40
Q

effects of CORTISOL on FAT METABOLISM

A

LIPOLYSIS (breakdown of fats/triglycerides)

INCREASED APPETITE

FAT DEPOSITION (Central areas)

41
Q

effects of CORTISOL on PROTEINS

A

PROTEIN CATABOLISM - breakdown of MUSCLE

DECREASED PROTEIN SYNTHESIS

42
Q

effects of CORTISOL on Na+, K+ (small effects)

A

Na+ RETENTION
DECREASED K+

Anti-Inflammatory effect

43
Q

what is CUSHING’S SYNDROME

A

CORTISOL OVER-PRODUCTION (hypersecretion)

44
Q

why might you get EXCESSIVE CORTISOL (CUSHING’S SYNDROME)

A
  • INCREASED ACTH (adrenocorticotropic hormone) from ANTERIOR PITUITARY

(some LUNG CANCERS can stimulate excessive ACTH)

  • ADRENAL ADENOMA / CARCINOME
    producing excess cortisol
45
Q

Cushing’s syndrome: clinical features

A

Diabetes
Irritability
Moon Face (fat and fluid retention in face)
Muscle Wasting
Bruising
Hypertension
Interscapular fat
Striae (collagen destroyed)
Osteoporosis

46
Q

Diagnosis of Cushing’s syndrome

A

confirm cortisol hypersecretion (Cushing’s syndrome) then determine the source of high cortisol

  • 24-hour urine free cortisol
  • Salivary cortisol
  • Midnight cortisol
  • Overnight dexamethasone suppression test
  • Serum ACTH
  • CRH / High dose dexamethasone suppression test
  • Pituitary MRI scan
  • Inferior petrosal sinus sampling
  • CT scan adrenals
47
Q

Treatment of Cushing’s syndrome

A

PITUITARY ADENOMAS:
Transphenoidal hypophysectomy (surgery) ± radiotherapy
Bilateral adrenalectomy

ECTOPIC ACTH:
Surgery, radiotherapy
Chemotherapy

ADRENAL TUMOURS
Adrenalectomy
Medical treatment – metyrapone, ketoconazole, mitotane

48
Q

DEFICIENCY of CORTISOL : ADRENAL INSUFFICIENCY

A

PRIMARY:
* Autoimmune adrenalitis
* Infections (TB, histoplasmosis, Candidiasis, CMV, HIV)
* Neoplastic infiltration & Metastasis
* Infiltration – hemochromatoisis, amyloid
* Thrombosis (antiphospholipid syndrome)
* Adrenal haemorrhage (anticoagulants)

SECONDARY:
* Pituitary diseases
* Drugs (long-term steroids)

49
Q

ADRENAL INSUFFICIENCY (CORTISOL DEFICIENCY) Clinical Features

A
  • Anorexia, weight loss & fatigue
  • Skin pigmentation (light-exposed & areas of pressure)
  • Dizziness & postural hypotension
  • loss of mineralocorticoid effect of aldosterone
  • loss of permissive effect of cortisol on vasopressor effects of catecholamines (low blood pressure)
  • Hypoglycaemia
  • Other endocrine conditions
50
Q

Diagnosis of ADRENAL INSUFFICIENCY

A
  • Hyponatraemia & hyperkalemia
  • Inappropriately low cortisol for the level of stress (<500 nmol/L)
  • Short synacthen test (30 minute cortisol <500 nmol/L)
  • Anti-adrenal antibodies - if autoimmune
  • Other endocrine tests (thyroid & pituitary hormones)
  • Imaging (CT abdomen & MRI pituitary)
51
Q

Management of Adrenal Insufficiency

A

Life-threatening condition
* Correct volume deficit (intravenous fluids)
* Initial treatment: IM/IV hydrocortisone
* Later oral hydrocortisone & fludrocortisone
* DHEA : may help vitality, fatigue & sexuality
* Double steroids in stressful situations / intercurrent illness
* Patients are encouraged to carry a medic-alert bracelet

52
Q

what are the main adrenal ANDROGENS

A

Dehydroepiandrosterone (DHEA)
Androstenedione

53
Q

what stimulates production of ANDROGENS (Dehydroepiandrosterone (DHEA) & Androstenedione) from Adrenal Glands

A

ACTH (adrenocorticotropic hormone) from ANTERIOR PITUITARY

54
Q

ANDROGENS (DHEA & Androstenedione) are formed from CONVERSION OF…
(in Zona Reticularis)

A

CHOLESTEROL

55
Q

CONVERSION OF CHOLESTEROL TO ANDROGENS (in Zona Reticularis)

A
  • CHOLESTEROL converted to PREGNENOLONE
  • pregnenolone to 17-HYDROXYPREGNENOLONE
  • 17-hydroxypregnenolone to DHEA (Dehydroepiandrosterone)

DHEA to ANDROSTENEDIONE (by 3 ALPHA HSD)

56
Q

DHEA ANDROGEN peaks at what age

A

25

57
Q

EXCESSIVE amounts of ADRENAL ANDROGENS can lead to…

A

MASCULINIZATION

In pre-pubertal boys excess adrenal androgens may lead to precocious (advanced) development of secondary sexual characteristics

In females foetus excessive adrenal androgens may lead to pseudohermaphroditism (external male genitalia)

58
Q

Hormones of the Adrenal MEDULLA:

A

CATECHOLAMINES:

EPINEPHRINE (dominant) aka adrenaline
NOREPINEPHRINE aka noradrenaline

59
Q

CATECHOLAMINES are released in response to…

A

STRESS
(fight or flight response)

60
Q

what happens in response to STRESS to release CATECHOLAMINES

A

SYMPATHETIC STIMULATION

  • ADRENAL MEDULLA CELLS STIMULATED
  • RELEASE OF EPINEPHRIN & NOREPINEPHRIN
61
Q

what do CATECHOLAMINES act on

A

ADRENERGIC RECEPTORS on
heart, blood vessels, bronchioles, muscle,
Glycogenolysis

62
Q

BIOSYNTHESIS OF CATECHOLEMINES,
starts from…

A

TYROSINE

63
Q

BIOSYNTHESIS OF CATECHOLEMINES
TYROSINE CONVERSION TO NOREPINEPHRINE & EPINEPHRINE

A

-TYROSINE
- converted to LEVO-DOPA (by Tyrosine hydroxylase)
- converted to DOPAMINE (Dopa-decarboxylase)
- converted to NOREPINEPHRINE (Beta-hydroxylase)
- converted to EPINEPHRINE

64
Q

CATECHOLAMINES are formed by …. of TYROSINE (2)

A

HYDROXYLATION & DECAROXYLATION

65
Q

biosynthesis of catecholamines:
TYROSINE is TRANSPORTED into…

A

CATECHOLAMINE-SECRETING NEURONS
& ADRENAL MEDULLARY CELLS

66
Q

biosynthesis of catecholamines:
where is TYROSINE CONVERTED into DOPA & DOPAMINE

A

in the CYTOPLASM

67
Q

CATECHOLEMINES are released from… (2)
by…

A

AUTONOMIC NEURONS
& ADRENAL MEDULLARY CELLS

by EXOCYTOSIS

68
Q

what are the Actions of CATECHOLAMINES
to enables the body to deal with physical & physiological stress

A

INCREASE GLUCOSE LEVELS:
- MOBILIZATION of GLYCOGEN RESERVES
- BREAKDOWN of GLYCOGEN to glucose

BREAKDOWN FATS TO FATTY ACIDS

INCREASE RATE & FORCE of CARDIAC MUSCLE CONTRACTIONS

69
Q

what is Pheochromocytoma

A

Adrenal MEDULLARY hormone HYPERSECRETION

  • EXCESS CATECHOLAMINES
70
Q

how can you get PHEOCHROMOCYTOMA (Adrenal medullary hormone hypersecretion)

A

Adrenal medullary catecholamine secreting TUMOUR

Pheochromocytoma crisis: precipitated by straining, exercise, pressure on abdomen, surgery & drugs

71
Q

PHEOCHROMOCYTOMA clinical presentations:

A

hypertension, palpitations, sweating, heat intolerance, pallor,
flushing, pyrexia & headache

72
Q

PHEOCHROMOCYTOMA Diagnosis

A

-INCREASED 24 hr urine cathecolamine excretion
-INCREASED plasma meta & normetanephrines
-MRI / CT scan
-Meta-iodobenzylguanidine (MIBG) scan

73
Q

PHEOCHROMOCYTOMA Treatment

A

Initial management: Alpha & Beta blockers

Treatment: Surgery

74
Q

RENIN is released by which cells in the KIDNEY

A

JUXTAGLOMERULAR CELLS

ENDOCRINOLOGY (11 decks)

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