Brainscape's Knowledge GenomeTM

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


See full index

Physiology 1 > Disorders of Adrenocortical Dysfunction > Flashcards

Disorders of Adrenocortical Dysfunction Flashcards

1
Q

What are the actions of cortisol?

A
  1. Glucose sparing effects
  2. Lipolysis
  3. Glyconeogenesis
  4. Glycogenesis
  5. Na and water mention
  6. Anti-inflammatory
  7. Increased gastric production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is cushing syndrome?

A

Excess cortisol

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

What is Cushings disease?

A

Excess cortisol in the blood due to an ACTH secreting pituitary tumour

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

What are the clinical features of Cushing’s disease?

A

High blood pressure
Fluid retention

Due to salt and water retention

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

What are the 3 stages of investigating cushings disease?

A
  1. Screening
  2. Confirmation of the diagnosis
  3. Differentiation of the cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe what happens in the Screening and Confirmation of the diagnosis

A

Urinary free cortisol
Diurnal Rhythm
Over night dexamethasone suppression testing

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

What happens in the Overnight Low Dose Dexamethasone Suppression Test?

A

Cortisol is measured at 8am

Dexamethasone 1mg is given at 11pm

Cortisol is measured at 8am the next morning

Cortisol suppression to <50nmol/l is normal

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

What happens in the differential diagnosis?

A

True Cushing’s Syndrome

Pseudocushing’s Syndrome:
Depression
Alcoholism
Anorexia Nervosa
Obesity
Exogenous steroids:
Inhalers
Eyedrops
Nasal Drops
Skin Creams
Health Food Shops
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the dosage and results of a Dexamethasone Suppression Test?

A

LOW DOSE
0.5 mg Dexamethasone six-hourly, 48 hrs

Result
complete suppression in normal subject

If cortisol detectable then patient has CUSHING’S SYNDROME

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

What does the differential diagnosis determine?

A

Cushing’s Disease
Pituitary Adenoma

Adrenal Tumour
Benign
Malignant

Ectopic ACTH production
Benign
Malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do we differentiate between the cause?

A

High dose Dexamethasone Suppression testing

ACTH

Imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens at a high dose of Dexamethasone Suppression Test

A

HIGH DOSE
2 mg Dexamethasone six-hourly for 48 hrs

If cortisol suppresses to < 50% of baseline then the patient has Pituitary dependent Cushing’s Disease

If the Cortisol does not suppress then the patient has ectopic ACTH production or an adrenal tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the lab features of it?

A

Hypokalaemia

Metabolic Alkalosis

Hyperglycaemia

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

What happens in a CRH test?

A

0.1 µg/kg of human CRH is given

Blood is assayed for ACTH and cortisol at time -15, 0, 15, 30, 60, 90, 120.

An exaggerated response indicates pituitary dependant Cushing’s Disease

A flat response indicates ectopic ACTH production

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

What methods can be used to locate or see the problem?

A

Pituitary
MRI
IPSS

Adrenal
CT or MRI

Ectopic
Octreotide Scan
ACTH Sampling

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

What treatment is available for Cushing’s?

A

Cortisol Production Blockers

  • Metyrapone
  • Ketoconazole

DXT three field or gamma knife

Following treatment patients may require replacement of other pituitary hormones too

Adrenal source
Removal of adrenal tumour

Patients need to have steroid replacement tablets at the time of and following surgery

The adrenal tumour suppresses the function of the normal gland

Many will not need the steroid tablets long term

17
Q

Give some clinical features of additions disease

A 
Tiredness
Weakness
Anorexia
Weight loss
Postural hypotension
Myalgia
Salt Craving
Nausea Vomiting
Hyperpigmentation
Vitiligo
Hyponatraemia 
Hyperkalaemia
Acidosis
Hypercalcaemia
Hypoglycaemia
Increased urea and creatinine
Eosinophilia
18
Q

What is the cause of Addison’s disease?

A 
Autoimmune
TB
Steroid Withdrawal
Metastases
Infiltration
 - Amyloid
 - Haemochromatosis 
Waterhouse- Freidrichson
Apoplexy 
Infection
 - Fungal
 - Viral 
Enzyme defect
Congenital Adrenal hyperplasia
 - Adrenolucodystrophy
 - Adrenomyolneuropathy
Drugs
19
Q

What treatment is available for additions disease?

A 
Hydrocortisone
 - 10mg 5mg 5mg
 - Mimicks the diurnal rhythm
 - Last dose before 6pm
Fludrocortisone
 - 50-200mcg o.d.
20
Q

What is 21-hydroxylase Deficiency (Classical)?

A

Excess sex steroids cause
virilisation, hirsutism, premature adrenarche, infertility.

No aldosterone, hence salt-losing crisis
hyperkalaemia, hypotension.

21
Q

What is 11b-hydroxylase Deficiency (Non-Classical) caused by?

A

Excess sex steroids
virilisation, hirsutism, premature adrenarche, infertility

No aldosterone but high DOC, which is an agonist at MC receptors
hypertension and hypokalaemia

22
Q

How can we investigate 11b-hydroxylase Deficiency (Non-Classical)?

A

Synacthen
No cortisol rise
Increased 17OH Progesterone levels

Prednisolone suppression
Androgens should fall into normal range

23
Q

What is the treatment for 21-hydroxylase Deficiency (Classical) and 1b-hydroxylase Deficiency (Non-Classical)

A

Both entities comprise a spectrum of disease – partial deficiencies complicate matters.

Rx of 11b- and 21- hydroxylase deficiency lies mainly in the use of glucocorticoid therapy

Surgery to virilised female genitalia.

Treatment of Mother to prevent foetal Virilisation

Fludrocortisone is used only in 21-hydroxylase deficiency to replace absent mineralocorticoid activity

24
Q

Describe aldosterone syndromes

A 
Primary Excess
Conn’s Syndrome
Bilateral Adrenal Hyperplasia
Steroid Treatable hypertension
Aldosterone producing adrenal carcinoma
Secondary Excess
With HT
Renal artery stenosis
Renin Secreting Tumour
Malignant nephrosclerosis
Normal BP
CCF
Cirrhosis
Nephrotic syndrome
Dehydration
25
Q

What drugs treat conns syndrome?

A

Spironolactone
Amiloride / Triampterine
Potassium Supplementation
Treatment of the Primary Tumour

26
Q

What is Phaeochromocytoma?

A 
Tumour of the enterochromaffin cells of the adrenal medullar
Produce Adrenaline ( nor adrenaline, dopamine)
27
Q

What are the symptoms of Phaeochromocytoma?

A 
Sweating
Anxiety
Fever
Paroxysmal hypertension
Palpitation
(Hypotension)
Angor aminii
Constipation
Abdominal Pain
Headache
Fits
Visual disturbance
Pallor or Flushing
Eosinophilia
Hyperglycaemia
Hypercalcaemia
Raised urinary 
Metanephrines
catecholamines
28
Q

How can we manage Phaeochromocytoma?

A 
Emergency
Alpha blockade
Non competitive alpha antagonist
Phenoxybenzamine phentolamine
Beta blockade
Nonselective beta blocker
Propranolol
Fluid Resuscitation
Surgery

Physiology 1 (72 decks)

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