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ENDOCRINOLOGY > 7. Adrenal Gland > Flashcards

7. Adrenal Gland Flashcards

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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
how is CHOLESTEROL CONVERTED TO ALDOSTERONE in MITOCHONDRIA of zona glomerulosa cells by conversion of
- 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
26
Diseases of the Adrenal Cortex: HORMONAL OVER-PRODUCTION examples:
Zona Glomerulosa: mineralocorticoid / Aldosterone excess - CONN'S SYNDROME Zone Fasciculate: glucocorticoid / Cortisol excess - CUSHING'S SYNDROME
27
Diseases of the Adrenal Cortex: HORMONAL UNDER-PRODUCTION examples:
primary: ADDISON'S DISEASE secondary: HYPOPITUITARISM (problem in pituitary)
28
other Diseases of the Adrenal Cortex:
* Incidentalomas * Adrenal carcinoma
29
Primary HYPERALDOSTERONISM is when there is...
EXCESS production of ALDOSTERONE
30
what can result from EXCESS ALDOSTERONE (hyperaldosteronism) (3)
- HYPERTENSION (increased Na+ retention and water retention contributes) - HYPOKALAEMIA (decreased K+) - METABOLIC ALKALOSIS
31
Conn’s syndrome: Diagnosis & Management
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
CORTISOL is produced in Zona Fasciculata by CONVERSION of...
CHOLESTEROL
33
COVERSION OF CHOLESTEROL TO CORTISOL
- cholesterol converted to PREGNENOLONE - pregnenolone converted to 17-HYDROXYPREGENOLONE - 17-hydroxypregnenolone converted to 11-DEOXYCORTISOL TO CORTISOL
34
ENZYMES used for CONVERSION of cholesterol to ALDOSTERONE / CORTISOL
3 BETA HSD 21-HYDROXYLASE 11 BETA-HYDROXYLASE 18-Oxidase for Aldosterone
35
Regulation of CORTISOL (negative feedback) starting from Hypothalamus..
HYPOTHALAMUS : CRH (Corticotrophin Releasing Hormone) ANTERIOR PITUITARY: ACTH (Adrenocorticotropic hormone) ADRENAL GLAND: CORTISOL
36
how is CHOLESTEROL produced in ZONA FASCICULATA CELLS for conversion into CORTISOL
cAMP to PROTEIN KINASE A converts CHOLESTEROL ESTER to CHOLESTEROL
37
when are CORTISOL levels highest
MORNING
38
CORTISOL released in response to...
STRESS and Stress Blood loss Severe infection Trauma Burns Illness Surgery
39
effects of CORTISOL on GLUCOSE levels
- INCREASED GLUCONEOGENESIS - INHIBITS peripheral glucose UPTAKE so INCREASED GLUCOSE LEVELS (Hyperglycaemia) - hepatic glycogen synthesis
40
effects of CORTISOL on FAT METABOLISM
LIPOLYSIS (breakdown of fats/triglycerides) INCREASED APPETITE FAT DEPOSITION (Central areas)
41
effects of CORTISOL on PROTEINS
PROTEIN CATABOLISM - breakdown of MUSCLE DECREASED PROTEIN SYNTHESIS
42
effects of CORTISOL on Na+, K+ (small effects)
Na+ RETENTION DECREASED K+ Anti-Inflammatory effect
43
what is CUSHING'S SYNDROME
CORTISOL OVER-PRODUCTION (hypersecretion)
44
why might you get EXCESSIVE CORTISOL (CUSHING'S SYNDROME)
- INCREASED ACTH (adrenocorticotropic hormone) from ANTERIOR PITUITARY (some LUNG CANCERS can stimulate excessive ACTH) - ADRENAL ADENOMA / CARCINOME producing excess cortisol
45
Cushing’s syndrome: clinical features
Diabetes Irritability Moon Face (fat and fluid retention in face) Muscle Wasting Bruising Hypertension Interscapular fat Striae (collagen destroyed) Osteoporosis
46
Diagnosis of Cushing’s syndrome
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
Treatment of Cushing’s syndrome
PITUITARY ADENOMAS: Transphenoidal hypophysectomy (surgery) ± radiotherapy Bilateral adrenalectomy ECTOPIC ACTH: Surgery, radiotherapy Chemotherapy ADRENAL TUMOURS Adrenalectomy Medical treatment – metyrapone, ketoconazole, mitotane
48
DEFICIENCY of CORTISOL : ADRENAL INSUFFICIENCY
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
ADRENAL INSUFFICIENCY (CORTISOL DEFICIENCY) Clinical Features
* 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
Diagnosis of ADRENAL INSUFFICIENCY
* 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
Management of Adrenal Insufficiency
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
what are the main adrenal ANDROGENS
Dehydroepiandrosterone (DHEA) Androstenedione
53
what stimulates production of ANDROGENS (Dehydroepiandrosterone (DHEA) & Androstenedione) from Adrenal Glands
ACTH (adrenocorticotropic hormone) from ANTERIOR PITUITARY
54
ANDROGENS (DHEA & Androstenedione) are formed from CONVERSION OF... (in Zona Reticularis)
CHOLESTEROL
55
CONVERSION OF CHOLESTEROL TO ANDROGENS (in Zona Reticularis)
- CHOLESTEROL converted to PREGNENOLONE - pregnenolone to 17-HYDROXYPREGNENOLONE - 17-hydroxypregnenolone to DHEA (Dehydroepiandrosterone) DHEA to ANDROSTENEDIONE (by 3 ALPHA HSD)
56
DHEA ANDROGEN peaks at what age
25
57
EXCESSIVE amounts of ADRENAL ANDROGENS can lead to...
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
Hormones of the Adrenal MEDULLA:
CATECHOLAMINES: EPINEPHRINE (dominant) aka adrenaline NOREPINEPHRINE aka noradrenaline
59
CATECHOLAMINES are released in response to...
STRESS (fight or flight response)
60
what happens in response to STRESS to release CATECHOLAMINES
SYMPATHETIC STIMULATION - ADRENAL MEDULLA CELLS STIMULATED - RELEASE OF EPINEPHRIN & NOREPINEPHRIN
61
what do CATECHOLAMINES act on
ADRENERGIC RECEPTORS on heart, blood vessels, bronchioles, muscle, Glycogenolysis
62
BIOSYNTHESIS OF CATECHOLEMINES, starts from...
TYROSINE
63
BIOSYNTHESIS OF CATECHOLEMINES TYROSINE CONVERSION TO NOREPINEPHRINE & EPINEPHRINE
-TYROSINE - converted to LEVO-DOPA (by Tyrosine hydroxylase) - converted to DOPAMINE (Dopa-decarboxylase) - converted to NOREPINEPHRINE (Beta-hydroxylase) - converted to EPINEPHRINE
64
CATECHOLAMINES are formed by .... of TYROSINE (2)
HYDROXYLATION & DECAROXYLATION
65
biosynthesis of catecholamines: TYROSINE is TRANSPORTED into...
CATECHOLAMINE-SECRETING NEURONS & ADRENAL MEDULLARY CELLS
66
biosynthesis of catecholamines: where is TYROSINE CONVERTED into DOPA & DOPAMINE
in the CYTOPLASM
67
CATECHOLEMINES are released from... (2) by...
AUTONOMIC NEURONS & ADRENAL MEDULLARY CELLS by EXOCYTOSIS
68
what are the Actions of CATECHOLAMINES to enables the body to deal with physical & physiological stress
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
what is Pheochromocytoma
Adrenal MEDULLARY hormone HYPERSECRETION - EXCESS CATECHOLAMINES
70
how can you get PHEOCHROMOCYTOMA (Adrenal medullary hormone hypersecretion)
Adrenal medullary catecholamine secreting TUMOUR Pheochromocytoma crisis: precipitated by straining, exercise, pressure on abdomen, surgery & drugs
71
PHEOCHROMOCYTOMA clinical presentations:
hypertension, palpitations, sweating, heat intolerance, pallor, flushing, pyrexia & headache
72
PHEOCHROMOCYTOMA Diagnosis
-INCREASED 24 hr urine cathecolamine excretion -INCREASED plasma meta & normetanephrines -MRI / CT scan -Meta-iodobenzylguanidine (MIBG) scan
73
PHEOCHROMOCYTOMA Treatment
Initial management: Alpha & Beta blockers Treatment: Surgery
74
RENIN is released by which cells in the KIDNEY
JUXTAGLOMERULAR CELLS

ENDOCRINOLOGY (11 decks)

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