Brainscape's Knowledge GenomeTM

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


See full index

Med 3 > Adrenal > Flashcards

Adrenal Flashcards

1
Q

Structure of cholesterol

A

Multi aromatic ring with a long side chain of carbon units

27 amino acids

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

What is the rate limiting step in steroidogenesis

A

The transport of cholesterolfrom the outer to the inner mitochondrial membrane

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

Where is the first enzyme in steroidogenesis located

A

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

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

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

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

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

Secretion of aldosterone

A

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

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

What is cortisol

A

The main mineralcorticoid and also a glucocorticoid

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

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

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

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

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

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

What are stressors

A

Stimuli that induce state of stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Stress response system

A

Sympathetic nervous system and adrenaline and CRH-ACTH - cortisol

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

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

What can prolonged elevated cortisol levels lead to

A

Muscle wasting
Hyperglycaemia
GI ulcers
Impaired immune response

(See Cushing’s syndrome)

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is cushings disease

A

Excessive production of ACTH
Main endogenous cause
Pituitary ACTH secreting tumour

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the dexamethasone suppression test

A

Lack of suppression indicates hyper -/ autonomous secretion

- confirms Cushing’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the CRH stimulation test

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Treatment of cushings disease

A 
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is conn’s syndrome (primary hyperaldosteronism)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is Addison’s disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Symptoms of Addison’s disease

A 
Postural hypotension 
Muscle weakness, fatigue, lethargy 
Hyponatraemia, hyperkalaemia 
Nausea, vomiting 
Weight loss, anorexia
30
Q

Why do you get increased pigmentation in Addison’s disease

A

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
Q

What is pro- opiomelanocortin

A

Undergoes extensive post translational processing

This processing is tissue specific

32
Q

Diagnosis of Addison’s disease

A

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
Q

Treatment for Addison’s disease

A

Life long hormone replacement

Glucocorticoid - hydrocortisone
Mineralcorticoid - fludrocortisone

Higher doses of glucocorticoids are given during times of illness or major stress eg surgery

34
Q

What is secondary adrenal insuffiencey

A

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
Q

What can happen to patients with excess exogenous glucocorticoids

A

Can lead to cushingoid appearance (truncal obesity, round facies, dorsocervical fat pads, striae)

36
Q

What happens with sudden withdrawal of exogenous steroids

A
  • symptoms of acute adrenal insufficiency

Fatigue, N&V, anorexia, weight loss, hypotension, myalgia

37
Q

What is an adrenal crisis

A

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
Q

What is congenital adrenal hyperplasia (CAH)

A

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
Q

Difference between ACTH receptors and thyroxine receptors

A

ACTH receptors are found only on certain cells

Thyroxine receptors are found on nearly all cells of the body

40
Q

What does target cell activation depend on

A

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
Q

What is receptor regulation

A

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
Q

What is upregulation of receptors

A

No reduced sensitivity

Decreased inactivation of receptors and signalling proteins
Decreased sequestration and degradation of internalised receptors
Increased production of receptors

43
Q

What are the 4 super families of receptors

A

Ligand fated ion channels (ionotropic receptors)

G protein coupled receptors (metabotropic receptors)

Catalytic receptors

Nuclear (intracellular) receptors

44
Q

Action of water soluble hormones

A

(amino acid based hormones except thyroid hormones)

- act on plasma membrane receptors (cannot enter cells)

45
Q

Action of lipid soluble hormones

A

Steroid and thyroid hormones

Act on intracellular receptors that directly activate genes (can enter cell)

46
Q

What do Gq coupled receptors do

A

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
Q

What are intracellular nuclear receptors

A

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
Q

What are type I nuclear receptors (steroid hormone receptors)

A

Glucocorticoid, mineralocorticoid, oestrogen, progesterone, androgen receptors
Also plasma membrane receptors

49
Q

What is primary adrenal insufficiency

A

Impairment of the adrenal glands (addisons disease)

50
Q

What is secondary adrenal insuffiecey

A

Impairments of the pituitary gland (low ACTH)

51
Q

What is tertiary adrenal insufficiency

A

Impairment of the hypothalamus (low CRH)

52
Q

Symptoms of reduced glucocorticoid activity

A

Generally unwell (stress / immune regulation)
Fatigue (hypoglycaemia
Reduced appetite (metabolic effects)
Confusion.

53
Q

Reduced mineralocorticoid activity of glucocorticoids

A

Fatigue / weakness (electrolyte disturbances)
Dizziness (hypovolaemia)
Nausea (electrolyte disturbances)b

54
Q

What should you do for symptomatic relief of Graves’ disease (primary hyperthyroidism)

A

Non selective beta blockers (needed for many months until reaching euthyroid state)
Big build up of thyroid hormones

55
Q

What happens to hormones in Graves’ disease (primary hyperthyroidism)

A

Rise in free T3 and T4 and decreased TSH

56
Q

Why are cortisol levels measured at 24:00 and 08:00

A

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
Q

Rate limiting step in steroidogenesis

A

Transport of cholesterol from outer to inner mitochondrial membrane

58
Q

Where is the first enzyme of steriogenesis located

A

Inner mitochondrial membrane
Initial side chain cleavage of cholesterol
Cholesterol 20, 22 desmolase

59
Q

Where are adrenal glands located

A

Superior to kidneys in renal fascia

Posterior to parts of diaphragm (retroperitoneal)

60
Q

Blood supply of adrenal glands

A

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
Q

What are the adrenal glands microscopically

A

Arterioles from capsular arteries
Give rise to sinusoidal capillaries
Drain into medullary vein

62
Q

What is a sympathetic ganglion

A

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
Q

Ultrastructure of adrenal cortex

A

Smooth ER
Lipid droplets
Tubular Cristal in mitochondria

64
Q

Ultrastructure of the adrenal medulla

A

Rough ER and golgi
Granules
Normal mitochondria

65
Q

What is the commonest cause of addisons disease in the UK

A

Autoimmunity

As addisons disease is an autoimmune disease

66
Q

Desribe the growth of the fetal adrenal gland

A

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
Q

What electrolyte imbalance would be expected with addisons disease

A

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
Q

Primary causes of hypoadrenalism

A 
Tuberculosis 
Metastases (eg bronchial carcinoma) 
Meningococcal septicaemia 
HIV 
Antiphospholipid syndrome
69
Q

Differences between primary addisons and secondary adrenal insufficiency

A

Primary addisons is associated with hyperpigmentation whereas secondary adrenal insufficiency is not

70
Q

Why do corticosteroids worsen diabetic control

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions