Brainscape's Knowledge GenomeTM

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


See full index

Endocrinolgy > Adrenal > Flashcards

Adrenal Flashcards

1
Q

What is the average size and weight of an adrenal gland?

A

average size: 2-3cm wide, 4-6cm long and 1cm thick
mean weight: 4g irrespective of age, sex or weight
- At autopsy the adrenal gland may weigh up to 22g

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

What hormones are made in the adrenal gland in each region?

A

medulla: adrenaline and noradrenaline
cortex - steroid hormones:
● Zona glomerulosa - mineralocorticoid - aldosterone
● Zona fasciculata - glucocorticoid cortisol cortisol
● Zona reticularis - adrenal androgens - androstenedione dehydroepiandrosterone acetate (DHEA), (testosterone?)

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

What happens to the adrenal androgens?

A

Converted in to sex hormones in the periphery

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

How is cortisol synthesis regulated?

A
  • hypothalamus: CORTICOTROPIN RELEASING HORMONE (CRH) (41aa’s). CRH stimulates corticotrophs in anterior pituitary to produce to produce ADRENOCORTICOTROPIC HORMONE (ACTH) (39 amino acids).
  • ACTH stimulates the adrenal cortex to synthesize and release cortisol.
  • Cortisol feeds back on the corticotrophs of the anterior pituitary to decrease ACTH release and on the hypothalamus to inhibit release of CRH.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How are steroid hormones synthesised?

A

All steroid hormones - derived from cholesterol.
ACTH - G-protein coupled receptor - activates adenyl cyclase - - - increase in cAMP levels.
- activates protein kinase A
- activates cholesteryl ester hydrolase (CEH) which liberates cholesterol from lipid droplets.
- also stimulation of cholesterol 20,22-hydroxylase (desmolase) which is the first enzyme in the pathway and is the rate limiting step. This leads to increased synthesis of cortisol

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

Why can’t the zona glomerulosa synthesise cortisol?

A

Zona glomerulosa - lacks - 17-alpha-hydroxylase enzyme - Needed to make cortisol

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

Is the mitochondria involved in the synthesis of cortisol?

A

Yes

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

What percentages of cortisol in plasma are free, CBG bound, Albumin bound?

A

10%
75%
15%

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

What percentages of aldosterone in plasma are free, CBG bound, Albumin bound?

A

30-50%
5-10%
25 – 50%

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

What the mechanism of steroid receptor activation

A
  • Steroid hormones interact with nuclear receptors.
  • Steroid hormone enters cells by diffusion
    binds to cytoplasmic receptor.
  • This leads to dissociation of Heat Shock Protein (hsp90) from the receptor.
  • The hormone-receptor complex dimerises and is translocated to nucleus.
  • The complex binds to hormone responsive element (HRE) on DNA
  • increase in mRNA production and subsequently to increased protein synthesis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the metabolic effects of glucocorticoids

A
  • decrease glucose uptake
  • decrease glucose use
  • increase gluconeogenesis
  • hyperglycaemia
  • decrease protein synthesis
  • increase protein breakdown - muscle wasting
  • decrease Ca2+ absorption in gut
  • increase Ca2+ excretion in kidney
  • decrease activity of osteoblasts
  • increase activity of osteoclasts - osteoporosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What a the anti inflammatory effects of glucocorticoids?

A 
early phase: vs. redness, heat, pain, swelling late phase: vs. wound healing, repair, proliferation
- decreases:
expression of COX2 (cyclo-oxygenase 2)
cytokine production 
complement in plasma 
nitric oxide (NO) production 
histamine release 
IgG production 
increases: 
annexin-1 (lipocortin-1) which inhibits phospholipase A2 (PLA2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is the prevention of cortisol activation of mineralocorticoid receptors achieved?

A

cortisol and aldosterone have same affinity for mineralocorticoid receptor
11betaHSD converts cortisol to cortisone (inactive)
11betaHSD - 11-beta-hydroxysteroid dehydrogenase
11betaHSD2 isoform expressed in aldosterone sensitive tissues

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

What are the adverse affects of glucocorticoids?

A 
suppression of response to infection
suppression of endogenous glucocorticoid production
metabolic effects
osteoporosis
iatrogenic Cushing's syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What Is the difference between Cushing’s disease and Cushing’s syndrome?

A

Cushing’s disease - ectopic tumour - ACTH, cortisol

Cushing’s syndrome - more common - drug induced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the clinical manifestations of Cushing’s syndrome?

A 
easy bruising 
poor wound healing 
muscle wasting 
thinning of skin 
increased abdominal fat
buffalo hump 
moon face 
osteoporosis 
obesity 
increased appetite 
increased susceptibility to infection 
cataracts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q 
What are the percentage frequencies of the following clinical features of Cushing's disease or syndrome? Obesity
Hypertension
Hirsutism
Striae
Acne
Bruising
Neuropsychiatric effects
Menstrual disorders
Impotence
Glucose intolerance
Diabetes
A 
Obesity 90 
Hypertension 85 
Hirsutism 75 
Striae 50 
Acne 35 
Bruising 35 
Neuropsychiatric effects 85 
Menstrual disorders 70 
Impotence 85 
Glucose intolerance 75 
Diabetes 20
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the treatments for Cushing’s syndrome?

A
  • Metryrapone 11-beta-hydroxylase
  • Ketoclonazone inhibits steroid biosynthesis
  • Pasireotide (somatostatin analogue) SSTR5 agonist (Receptors highly expressed in tumours - shut down ACTH production) - Mifeprestone - glucocorticoid receptor antagonist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the clinical manifestations of Addison’s disease?

A 
muscular weakness 
low blood pressure 
depression
anorexia
loss of weight
Fatigue
Gastrointestinal disturbances
hypoglycaemia
Hyper pigmentation 
Salt cravings
Postural symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the percentage frequencies of these clinical manifestations of Addison’s disease?
Weakness, fatigue, anorexia, weight loss
Hyper-pigmentation
Hypotension
Gastrointestinal disturbances
Salt craving
Postural symptoms

A 
Weakness, fatigue, anorexia, weight loss 100
Hyperpigmentation 92
Hypotension 88
Gastrointestinal disturbances 56
Salt craving 19
Postural symptoms 12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In pre-menopausal women what percentage of androstenedione is derived from the adrenal and is converted in peripheral tissue to oestrogen and testosterone?
What effect can excess androgen secretion have in women?

A

In the pre-menopausal woman 50% of androstenedione is derived from the adrenal and is converted in peripheral tissue to oestrogen and testosterone. Excess secretion of these androgens in women can lead to hirsutism and virilisation.

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

What ‘advantage can obesity have in post-menopausal women?

A

In the post-menopausal woman, with the regression of the ovary, the main oestrogen in oestrone, peripheral conversion of androgen to oestrogen takes place in adipose tissue

  • the production of oestrone is higher in the obese postmenopausal woman than in the thin woman.
  • obese women suffer less from high testosterone in Cushing’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the effects of aldosterone and what is spironolactone?

A

Effects in kidney
Increased number of sodium channels in apical membrane
Increase in Na +/K +ATPase in basolateral membrane
Spironolactone: Aldosterone antagonist , Used as K+ sparing diuretic

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

See table on synthetic steroid in adrenal - basic notes

A

-

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

4 classifications of adrenal disorders

A

– Hypofunction
– Hyperfunction
– Cancer
– Genetic conditions

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

3 Types of hypofunction adrenal disease

A

– Hypothalamo-pituitary disease
– Primary adrenal failure
(Addison’s disease - destruction of cortex)
– Congenital adrenal hyperplasia

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

How does an adrenal gland appear on a CT scan?

A

Thin structure with lateral and medial limbs

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

From where do the cells of the adrenal medulla originate?

A

Migratory neural crest cells

29
Q

Aetiology of Adrenal Failure/ Primary adrenal insufficiency?

9 causes

A
  • Autoimmune (polyglandular failure)
  • Granulomatous infiltration (TB, sarcoid etc)
  • Haemorrhage
  • Fungal infection Fungal
  • AIDS
  • Congenital adrenal hyperplasia
  • Metastatic disease
  • Adrenalectomy
  • Toxic drugs
30
Q

Causes of secondary adrenal insufficiency?

A
  • Cessation of exogenous steroids

* Hypothalamo-pituitary hypofunction - Surgery - Radiotherapy - Tumours - Genetics

31
Q

What are the common features of Addison’s disease?

A 
Weakness - 100%
Weight loss - 100%
Pigmentation - 95%
Postural hypotension - 25%
Anorexia - 95%
Nausea - 95%
Abdominal pain - 30%
32
Q

What are the uncommon features of Addison’s disease?

A

Vitiligo - 20%
Salt craving - 15%
Hypoglycaemia - (in adults) - less than 1%
Aches and pain - 10%

33
Q

Treatment of adrenal failure?

A

• Emergency, life-threatening adrenal crisis:
– ICU care
– Fluids, sodium IV hydrocortisone @ high dose
– IV hydrocortisone @ high dose

• Maintenance treatment
– Glucocorticoid (hydrocortisone, prednisolone)
– Mineralcorticoid (fludrocortisone)
– ?DHEA

34
Q

What is Congenital adrenal hyperplasia CAH and what are its consequences?

A

• Recessive defect in cortisol biosynthesis leading to:
- elevated ACTH
- adrenomegaly
- excess androgens
Commonest defect = 21 OH enzyme – Commonest defect
Features:
– Salt-wasting crises
– Precocious puberty in boys
– Masculinisation of females leading to ambiguous genitalia at birth

35
Q

List the clinical manifestations of congenital adrenal hyperplasia CAH

A 
Classic CAH - presents in neonate
Non-classic CAH - presents in adolescence or adulthood
Urogenital sinus
Labial fusion
Scotilization of labia majora
Clitoromegaly
Penile enlargement
Precocious adrenarche
Bone age advancement
Rapid growth
Acne
Hirsutism
Menstrual abnormalities
Infertility
- this is the spectrum
36
Q

How is CAH treated?

A
  • In utero ideally
  • Use glucocorticoids to suppress ACTH
  • Antiandrogens
  • Mineralocorticoid
  • Genitoplasty – Controversial wrt age, degree of operation – Gender assignment
37
Q

What are the clinical manifestations of Addison’s disease (glucocorticoid deficiency)?

A 
Muscle fatique and chronic weakness 
Depression
psychosis 
Nausea
anorexia 
Hypoglycemia
38
Q

What are the clinical manifestations of Cushing’s disease (glucocorticoid excess)?

A 
Hyperglycemia 
Elevated blood pressure 
Obesity (thin limbs, fat trunk) 
Wasting of skeletal muscle 
Poor wound healing 
Mood swings (depression/euphoria)
hallucinations
39
Q

What is the aetiology of Cushing’s disease/syndrome?

A

ACTH - dependent 80%:
– Pituitary adenoma (Cushing’s disease)
– Ectopic (neuroendocrine tumour)

ACTH - independent 20%:
– Adrenal adenoma
– Adrenal carcinoma
– Carney’ syndrome (PPNAD)

40
Q

Diagnosis of adrenal Cushing’s syndrome?

A 
• Circadian serum cortisol (nmol/l)
– 0900 604 
– 1800 626 
– 2400 677 
• Plasma ACTH levels (ng/l) 
– 0900 s so ACTH stays high
41
Q

What is the treatment of Cushing’s?

A

Treatment

• Laparoscopic adrenalectomy
• Replacement GC – Hydrocortisone
– Periodic withdrawal
• Many of the features improve – BP, diabetes, psychological disturbance may continue

42
Q

What effect does noradrenaline have on force of myocardial contraction,Systolic blood pressure and Diastolic pressure?

A

Increases them all

43
Q

What effect does adrenaline have on force of myocardial contraction,Systolic blood pressure and Diastolic pressure?

A

Increases the first 2

Usually little effect on latter

44
Q

What affect do adrenaline and noradrenaline have on heart rate?

A

Adrenaline: increases
Noradrenaline: decreases because of reflexes

45
Q

What is the effect of adrenaline on the blood flow to skin, mucous membranes, gut, brain, skeletal muscle?

A 
skin - decreases
mucous membranes - decreases
gut - decreases
brain - increases
skeletal muscle - increases
46
Q

What is the effect of noradrenaline on the blood flow to skin, mucous membranes, gut, brain, skeletal muscle?

A 
skin - decreases
mucous membranes - decreases
gut - decreases
brain - may increase slightly 
skeletal muscle - little or no effect
47
Q

Does adrenaline affect anxiety?

A

Yes - increases the sensation of anxiety

48
Q

Does noradrenaline affect anxiety?

A

No

49
Q

What affect does adrenaline have on the blood levels of glucose, lactic acid, fatty acids?

A
  • Glucose: Raised
  • Lactic acid: Markedly increased
  • Fatty acids: Somewhat increased
50
Q

What affect does noradrenaline have on the blood levels of glucose, lactic acid, fatty acids?

A
  • Glucose: Little effect
  • Lactic acid: Slightly increased
  • Fatty acids: Increased
51
Q

STIMULI WHICH CAUSE EPI/NORAdrenaline RELEASE?

A
  • Stressful situations
  • Hypoglycemia (dietary or disease induced)
  • Postural hypotension
  • Exercise
52
Q

What is Phaeochromoctoma and what is its aetiology?

A 
• Tumour of the adrenal medulla(typically benign, typically cystic?)
– Secreting NA or A 
– 10 % bilateral 
- 10 % malignant  
– 10 % part of a genetic condition:
• MEN 2 
• Von Hippel Lindau 
• NF- 1
SDH
53
Q

How does Phaeochromoctoma present?

A
  • Headaches
  • Palpitations
  • Sense of Doom
  • Chest pain
  • Sweating
  • Weight loss
54
Q

How can you diagnose Phaechomoctoma?

A

• Plasma or urine assessment of levels of A, NA or their products – VMA / HMMA
– Metanephrins - almost exclusively used
– Imaging
• Nuclear medicine – MIBG
• Radiology – CT/ MRI

55
Q

Treatment of Phaechomoctoma?

A
  • Surgical removal after – Pretreatment with alpha and B blockade • Phenoxybenzamine
  • Doxazosin first then propranolol
56
Q

PHYSIOLOGICAL EFFECTS OF ALDOSTERONE?

A 
Regulation of water and electrolyte balance
- Decreases cellular K+
- increases cellular Na+ 
in kidney:
- Increases Na+ reabsorption 
- Decreases K+ reabsorption 
- Increases H+ secretion
57
Q

Volume-feedback loop between angiotensin 2 and aldosterone?

A 
• Action of angiotensin II on aldosterone results in negative feedback 
• 2 critical systems are regulated: 
– 1) sodium homeostasis ) 
– 2) regulation of arterial pressure: 
• Vasular smooth muscle 
• NA release 
• ADH 
• Volume expansion
58
Q

What is the action of aldosterone?

A

• Aldosterone binds to the type 1 mineralocorticoid receptor
– Increasing the number of “open” sodium channels channels
- Increased sodium resorption
• Negative gradient in the lumen – Consequent secretion of K and H

59
Q

What are the clinical features of Conn’s syndrome (primary hyperaldosteronism)?

A

– Hypertension, often difficult, younger people
– Spontaneous or diuretic associated hypokalaemia
– Oedema = rare
• Hypernatraemia, hypomagnesaemia, alkalosis, DI, neuromuscular symptoms

60
Q

What are the features of aldosteronism?

A
  • Often non-specific, hypertension
  • Hypokalaemia related to renal potassium wasting
  • Classical: hypertension, hypokalaemia & alkalosis
61
Q

What causes secondary aldosteronism?

A

–Renovasular

–Gitelmans, Barrters pseudo, nephrotic, cirrhotic, CCF

62
Q

What are the usual clinical manifestations do primary hyperaldosteronism?

A
  • Hypertension
  • Hypokalemia
  • Hypervolemia (without peripheral edema)
  • Metabolic alkalosis
63
Q

What are the ‘other’ clinical manifestations/effects do primary hyperaldosteronism?

A

-Due to hypertension:
•Headaches •Retinopathy (rare)
-Due to hypokalemia:
•Neuromuscular symptoms (cramps, paresthesias, weakness) •Nephrogenic diabetes insipidus
•Cardiac arrhythmia
•Glucose intolerance / impaired insulin secretion
-Due to direct actions of aldosterone on the cardiovascular system:
•Cardiac Hypertrophy/Fibrosis
•Vascular smooth muscle hypertrophy
•Due to a reset osmostat
•Mild hypernatremia

64
Q

What are the subtypes of Primary hyperaldosteronism?

A
  • Aldosterone producing adenoma (60%)
  • Bilateral adrenal hyperplasia (30-40%)
  • Glucocorticoid-remediable aldosteronism (1-3%)
  • Unilateral adrenal hyperplasia
  • Adrenal carcinoma
65
Q

What do you know about Aldosterone producing adenoma?

A
  • Small – 0.-2 cm
  • Women > men
  • Histology- difficult= benign cortical adenoma
  • CT appearance- low HU
66
Q

Diagnosis of primary aldosteronism?

A

• Biochemical screening – PRA, aldosterone= PA/ PRA

67
Q

Confirmation of primary hyperaldosteronism?

A
  • Measurement of PRA (suppressed) and aldosterone (high) in salt-replete individuals
  • Salt loading
  • Suppression with fludorocortisone
  • Catheter studies for selective venous sampling
68
Q

Treatment of Conn’s syndrome?

A 
• Remove the adenoma – Open or laparoscopic
• Drug treatment:
– Spironolactone 
– Eplerenone 
– Amiloride + others

Endocrinolgy (8 decks)

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