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Adrenal Flashcards

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1
Q

Structure of cholesterol

A

Multi aromatic ring with a long side chain of carbon units

27 amino acids

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2
Q

What is the rate limiting step in steroidogenesis

A

The transport of cholesterolfrom the outer to the inner mitochondrial membrane

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3
Q

Where is the first enzyme in steroidogenesis located

A

In the inner mitochondrial membrane (initial side chain cleavage of cholesterol)

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4
Q

What are the zone specific steroid hormone synthesis

A

Zona glomerulosa - mineralocorticoids

Zona fasiculata - glucocorticoids (mainly) and gonadocorticoids

Zona reticularis - glucocorticoids and gonadocorticoids (mainly)

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5
Q

What is zone specific steroidogenesis

A

Differential expression of biosynthetic enzymes in the different zones of the adrenal cortex

Each steroid is transferred between 2 sub cellular compartments as it progresses along its biosynthetic pathway

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6
Q

Action of aldosterone (main mineralocorticoid) made in the cortex

A

Principally act on DCT and collecting ducts of kidney to promote Na+ retention (-> H2O retention) and K+ elimination during formation of urine

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7
Q

Secretion of aldosterone

A

stimulated by increased plasma [K+] and renin- angiotensin system (largely independent of ACTH)

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8
Q

What is cortisol

A

The main mineralcorticoid and also a glucocorticoid

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9
Q

What is the pattern of levels of cortisol throughout the day

A

Peaks in the morning and falls during day but a small surge in late afternoon to help you get through evening

Associated with sleep wake cycle

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10
Q

What are the actions of cortisol

A

Metabolic effects

Anti inflammatory / immunosuppressive effects

Role in adaption to stress

Permissive role in action of other endocrine hormones

Actions on other tissues

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11
Q

Metabolic effects of cortisol

A

In muscle and adipose tissue - catabolic
In liver - stimulates gluconeogenesis and glycogen storage

Overall to elevate plasma glucose levels

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12
Q

Actions of cortisol

A

Anti inflammatory / immunosuppressive effects

  • stimulate production of lipocortin 1 (Annexin 1) which inhibits PLA 2, an enzyme that generates arachidonic acid the precursor for prostanoids and leukotrienes

Decrease number and activation of T lymphocytes
Decrease production of cytokines
Stabilises lysosomes
Decrease NO production

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13
Q

What is the integrated stress response

A

A state of threatened homeostasis or disharmony; the body responds by a complex repertoire of physiological and behavioural mechanisms to re establish homeostasis

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14
Q

What are stressors

A

Stimuli that induce state of stress

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15
Q

Stress response system

A

Sympathetic nervous system and adrenaline and CRH-ACTH - cortisol

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16
Q

What are the actions of SNS and adrenaline

A

Increased cardiac output and ventilation
Diversion of blood flow to muscles and heart
Mobilisation of glycogen and fat stores
‘Fight and flight’

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17
Q

What can prolonged elevated cortisol levels lead to

A

Muscle wasting
Hyperglycaemia
GI ulcers
Impaired immune response

(See Cushing’s syndrome)

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18
Q

Disorders of adrenal steroids

A

Glucocorticoid excess - Cushing’s syndrome

Mineralcorticoid excess- conns syndrome

Adrenal insufficiency - Addison’s disease

Congenital adrenal hyperplasia (cAH)

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19
Q

What is Cushing’s syndrome

A

Excessive glucocorticoid activity
Endogenous or exogenous (steroid medication) eg rheumatoid arthritis
Effects more women than men
Ages 20-60 mainly

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20
Q

What is cushings disease

A

Excessive production of ACTH
Main endogenous cause
Pituitary ACTH secreting tumour

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21
Q

What is the difference between Cushing’s syndrome and cushings disease

A

Cushings disease is a type of Cushing syndrome.
Disease occurs when a pituitary tumour causes the body to make too much cortisol
Makes up about 70% of Cushing syndrome cases

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22
Q

Signs and symptoms of Cushing’s syndrome

A 
Truncal obesity 
Buffalo hump 
Red round face 
Acne 
Female frontal balding 
Female hirsutism 
Menstrual irregularities 
Testicular atrophy 
Thin arms and legs 
Muscle weakness 
Thin skin 
Purple striae 
Poor wound healing 
Easy bruising 
Infections 
Cognitive difficulties 
Emotional instability 
Depression 
Sleep disturbances 
Osteoporosis 
Hypertension 
Diabetes
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23
Q

What is dexamethasone

A

A synthetic glucocorticoid
Low dose 0.5mg DEX every 6h for 48h, measure cortisol before and at 48h
Overnight 1mg DEX 11pm then cortisol measurement at 8am

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24
Q

What is the dexamethasone suppression test

A

Lack of suppression indicates hyper -/ autonomous secretion

- confirms Cushing’s syndrome

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25
What is the CRH stimulation test
Used to distinguish between pituitary dependent cushings and an ectopic source of ACTH Normally there is a rise in both ACTH and cortisol In pituitary dependent cushings patients, the response is exaggerated
26
Treatment of cushings disease
``` Localisation of the tumour Ant pituitary - MRI Adrenal - abdominal CT / MRI scan Bronchial tumour - chest x ray ACTH secreting tumour - octreoscan ``` Then surgery or radiation Medical, drugs to inhibit steroidogenesis eg metryapone, trilostane
27
What is conn’s syndrome (primary hyperaldosteronism)
Abnormally large amount of aldosterone produced - common cause = tumour Results in the initial retention of Na+, and Hanse increased water retention with increased K+ elimination Hypokalaemia -> weakness Chronic hypokalaemia -> renal dysfunction -> polyuria Main clinical finding in conn’s is hypertension Occurs in 1% of people diagnosed with hypertension If due to tumour surgery is the course of treatment
28
What is Addison’s disease
Adrenal insufficiency A rare chronic condition brought about by failure of adrenal glands Involved gradual destruction of adrenal tissue - often autoimmune or by TB or HIV Apparent when 90% of adrenal cortex has been destroyed Low aldosterone, low cortisol, low androgens but elevated ACTH
29
Symptoms of Addison’s disease
``` Postural hypotension Muscle weakness, fatigue, lethargy Hyponatraemia, hyperkalaemia Nausea, vomiting Weight loss, anorexia ```
30
Why do you get increased pigmentation in Addison’s disease
ACTH production increased as is MSH (melanocytes stimulating hormone) - increased melanin content in skin Often seen in skin creases, old scars, gums and inside of cheek
31
What is pro- opiomelanocortin
Undergoes extensive post translational processing | This processing is tissue specific
32
Diagnosis of Addison’s disease
Tests for adrenal failure - decreased cortisol and elevated ACTH levels ACTH stimulation test (stimulation test for adrenal function) - adrenal antibodies (if suspected autoimmune disease)
33
Treatment for Addison’s disease
Life long hormone replacement Glucocorticoid - hydrocortisone Mineralcorticoid - fludrocortisone Higher doses of glucocorticoids are given during times of illness or major stress eg surgery
34
What is secondary adrenal insuffiencey
Lack of ACTH production (tumour, damage to pituitary) Low cortisol with normal aldosterone levels (RAAs intact) May also be due to exogenous glucocorticoid use - secondary adrenal suppression often in patients with long term, high dose glucocorticoid use - suppression of ACTH levels leading to suppression and atrophy of adrenal cortex -> low endogenous cortisol
35
What can happen to patients with excess exogenous glucocorticoids
Can lead to cushingoid appearance (truncal obesity, round facies, dorsocervical fat pads, striae)
36
What happens with sudden withdrawal of exogenous steroids
- symptoms of acute adrenal insufficiency | Fatigue, N&V, anorexia, weight loss, hypotension, myalgia
37
What is an adrenal crisis
Medical emergency - acute adrenal insufficiency and expressed when patient is under stress eg infection - > hypotension, circulatory failure, potentially death ``` Urgent treatment (IV fluids, hydrocortisone, iv then oral) Oral once stabilised ```
38
What is congenital adrenal hyperplasia (CAH)
Inherited defect in an enzyme involved in the production of cortisol and aldosterone Several possible types >90% of CAH due to deficiency of 21B-hydroxylase
39
Difference between ACTH receptors and thyroxine receptors
ACTH receptors are found only on certain cells Thyroxine receptors are found on nearly all cells of the body
40
What does target cell activation depend on
Hormone amount Number of receptors on target cell Affinity of the receptors fro the hormone Following receptor activation there is termination of the signal (degradation of the hormone, inactivation of receptor or signalling)
41
What is receptor regulation
If increase in [hormone] -> down regulation of receptors Eg Inactivation of receptors Inactivation of signalling molecules Sequestration of recepotrs to inside of cell Degradation of internalised receptors Decreased production of receptors
42
What is upregulation of receptors
No reduced sensitivity Decreased inactivation of receptors and signalling proteins Decreased sequestration and degradation of internalised receptors Increased production of receptors
43
What are the 4 super families of receptors
Ligand fated ion channels (ionotropic receptors) G protein coupled receptors (metabotropic receptors) Catalytic receptors Nuclear (intracellular) receptors
44
Action of water soluble hormones
(amino acid based hormones except thyroid hormones) | - act on plasma membrane receptors (cannot enter cells)
45
Action of lipid soluble hormones
Steroid and thyroid hormones Act on intracellular receptors that directly activate genes (can enter cell)
46
What do Gq coupled receptors do
Phospholipase CB takes PIP2 and catalyses its breakdown into DAG and IP3 DAG activates PKC which phosphorylates many proteins such as ion channels and enzymes IP3 binds to IP3 receptors on endoplasmic reticulum which acts as a store for Ca2+ this causes a release which raises intracellular calcium levels
47
What are intracellular nuclear receptors
Mediate effects for steroid hormones, thyroid hormones and others such as bile acids, retinoic acid (derived from vit A), vit D and includes PPARs (peroxisome proliferator- activated receptors) Ligand regulated transcription factors Interact as homo- or heterodimers with DNA sequences in promoter region of target genes
48
What are type I nuclear receptors (steroid hormone receptors)
Glucocorticoid, mineralocorticoid, oestrogen, progesterone, androgen receptors Also plasma membrane receptors
49
What is primary adrenal insufficiency
Impairment of the adrenal glands (addisons disease)
50
What is secondary adrenal insuffiecey
Impairments of the pituitary gland (low ACTH)
51
What is tertiary adrenal insufficiency
Impairment of the hypothalamus (low CRH)
52
Symptoms of reduced glucocorticoid activity
Generally unwell (stress / immune regulation) Fatigue (hypoglycaemia Reduced appetite (metabolic effects) Confusion.
53
Reduced mineralocorticoid activity of glucocorticoids
Fatigue / weakness (electrolyte disturbances) Dizziness (hypovolaemia) Nausea (electrolyte disturbances)b
54
What should you do for symptomatic relief of Graves’ disease (primary hyperthyroidism)
Non selective beta blockers (needed for many months until reaching euthyroid state) Big build up of thyroid hormones
55
What happens to hormones in Graves’ disease (primary hyperthyroidism)
Rise in free T3 and T4 and decreased TSH
56
Why are cortisol levels measured at 24:00 and 08:00
These are the times when it is most extreme (high in the morning and low at night) If there’s a loss of this there’s a problems Loss of diurnal rhythm
57
Rate limiting step in steroidogenesis
Transport of cholesterol from outer to inner mitochondrial membrane
58
Where is the first enzyme of steriogenesis located
Inner mitochondrial membrane Initial side chain cleavage of cholesterol Cholesterol 20, 22 desmolase
59
Where are adrenal glands located
Superior to kidneys in renal fascia | Posterior to parts of diaphragm (retroperitoneal)
60
Blood supply of adrenal glands
Arterial: Superior suprarenal aa (from phrenic) Middle suprarenal aa (from abdoA) Inferior suprarenal aa (from renal aa) Venous: Right suprarenal vv (to IVC) Left suprarenal vv (to left renal vv)
61
What are the adrenal glands microscopically
Arterioles from capsular arteries Give rise to sinusoidal capillaries Drain into medullary vein
62
What is a sympathetic ganglion
Fight or flight - secretion controlled by preganglionic neurons -> secretory cell is functionally equivalent to postganglionic neurones of SNS so secretions are quickly released - act on adrenergic receptors (eg heart, blood vessels)
63
Ultrastructure of adrenal cortex
Smooth ER Lipid droplets Tubular Cristal in mitochondria
64
Ultrastructure of the adrenal medulla
Rough ER and golgi Granules Normal mitochondria
65
What is the commonest cause of addisons disease in the UK
Autoimmunity | As addisons disease is an autoimmune disease
66
Desribe the growth of the fetal adrenal gland
At 4 months gestation it is 4 times the size of the kidney but at birth it is a third of the size of the kidney This is due to the rapid regression of the fetal cortex at birth Disappears almost completely by age 1; by age 4-5 years, the permanent adult type adrenal cortex has fully developed
67
What electrolyte imbalance would be expected with addisons disease
Hyperkalaemia and hyponatraemia Aldosterone causes sodium reabsorption and potassium excretion. A lack of aldosterone would result in the following biochemical abnormality: hyperkalaemia and hyponatraemia
68
Primary causes of hypoadrenalism
``` Tuberculosis Metastases (eg bronchial carcinoma) Meningococcal septicaemia HIV Antiphospholipid syndrome ```
69
Differences between primary addisons and secondary adrenal insufficiency
Primary addisons is associated with hyperpigmentation whereas secondary adrenal insufficiency is not
70
Why do corticosteroids worsen diabetic control
Due to their anti insulin effects Glucocorticoids are the synthetic form of the natural hormone cortisol And cortisol raises blood glucose by acting on various organs to increase gluconeogenesis

Med 3 (10 decks)

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