Brainscape's Knowledge GenomeTM

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


See full index

Finals Revision > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is primary adrenal insufficiency?

A

Adrenal glands are damaged
Reduction in secretion of cortisol and aldosterone
Commonest cause: autoimmune
Also called Addison’s

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

What is secondary adrenal insufficiency?

A

Inadequate ACTH
Low cortisol release
Loss or damage to pituitary
Fun fact: Sheehan’s syndrome is where massive blood loss during childbirth leads to pituitary gland necrosis

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

What is tertiary adrenal insufficiency?

A

Inadequate CRH release by the hypothalamus
Cause: long term oral steroids -> hypothalamus suppression. Long term steroids need to be tapered slowly for the adrenal axis to regain normal function

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

What are the symptoms of adrenal insufficiency?

A

Fatigue
Nausea
Cramps
Abdo pain
Reduced libido

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

What are the signs of adrenal insufficiency?

A

Bronze hyperpigmentation (ACTH stimulates melanocytes to produce melanin), particularly in skin creases
Hypotension (particularly postural hypotension)

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

What do investigations show in adrenal insufficiency?

A

Hyponatraemia
Hyperkalaemia
Early morning cortisol
Short synacthen test
ACTH
Adrenal cortex antibodies and 21-hydroxylase antibodies
Consider:
CT/MRI adrenals
MRI pituitary

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

What is the short synacthen test?

A

Give synacthen (synthetic ACTH)
Blood cortisol is measured at baseline, 30 and 60 minutes after administration. Cortisol should normally at least double - if not = primary adrenal insufficiency

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

What are the replacement steroids for adrenal insufficiency?

A

Hydrocortisone for cortisol
Fludocrotissone for aldosterone

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

What are the symptoms of an Addisonian crisis?

A

Reduced consciousness
Hypotension
Hypoglycaemia
Hyponatraemia
Hyperkalaemia

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

What is the management of an Addisonian Crisis?

A

IV hydrocortisone 100mg stat and then 100mg every 6 hrs.
IV fluid resus
Correct hypoglycaemia
Monitor electrolytes and fluid balance

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

Where in the adrenal cortex is aldosterone made?

A

Zona glomerulosa

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

What does aldosterone do?

A

Regulates BP
Regulates blood volume
Increases Na+ reabsorption by kidneys

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

What causes an increase in secretion of aldosterone?

A

Low BP
High levels of angiotensin II or K+ in the blood or ECF

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

What causes a decrease in the secretion of aldosterone?

A

High Na+ in blood or ECF

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

How does aldosterone work?

A

Increases no. of Na+/K+ pumps on the principle renal tubule cells and ENaC channels.
Increases the reabsorption of sodium and increases excretion of potassium
This increases the fluid volume and blood pressure in the capillaries.
Also increases H+ secretion

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

What are the symptoms of Conn’s syndrome (primary aldosteronism)

A

Benign tumour in the zona glomerulosa cells
Hypokalaemia
Mild metabolic alkalosis
Increase in blood volume -> increased BP
Decreased plasma renin levels
Muscle weakness due to low levels of ECF K+

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

What are the management options for hyperaldosteronism?

A

Tumour removal
Spironolactone: aldosterone antagonist

18
Q

What does ADH do?

A

Stimulates water reabsorption from eh collecting ducts in the kidneys

19
Q

What can cause SIADH?

A

Posterior pituitary secreting too much
Small cell lung cancer secreting ADH
Also:
Post-op
Infection such as atypical pneumonia and lung abscesses
Head injury
Medications: (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs)
Malignancy
Meningitis

20
Q

What does SIADH cause?

A

Dilution of sodium in the blood: euvoleumic hyponatraemia
More concentrated urine with him urine sodium

21
Q

What are the symptoms of SIADH?

A

Non-specific
Headache
Fatigue
Muscle aches and cramps
Confusion
Severe hyponatraemia: seizures and reduced consciousness

22
Q

How do you diagnose SIADH?

A

Exclusion of other causes of euvolaemic hyponatraemia (synacthen test, no diuretics, no D&V, no excessive water intake, no CKD or AKI)

23
Q

How do you manage SIADH?

A

Establish and treat the cause

24
Q

Why is important to correct sodium slowly?

A

To prevent central pontine myelinolysis (a change in sodium of less than 10 mmol/L per 24 hrs
You correct sodium by:
Fluid restriction
Tolvaptan (ADH receptor blockers) - but this can cause a rapid increase so only specialist use

25
Q

What happens in central pontine myelinolysis?

A

Water moves rapidly out of the brain cells and into the blood
The brain cells have become used to a low osmolality due to long term severe hyponatraemia
First phase: encephalopathic and confused +/- headache, nausea and vomiting
Second phase: demyelination: spastic quadriparxsis, psudobulbar palsy and cognitive and behavioural changes. Significant risk of death

26
Q

What can cause secondary acromegaly?

A

Ectopic GHRH or GH from lung or pancreatic cancer

27
Q

What types or organ dysfunction can GH cause?

A

Hypertrophic heart
Hypertension
T2DM
Colorectal cancer

28
Q

What are the investigations for acromegaly?

A

Insulin-like Growth Factor 1 (IGF-1) = raised
Oral glucose tolerance test whilst measuring GH = high glucose normally suppresses growth hormone but not in acromegaly
MRI brain
Formal visual field testing

29
Q

What medication can be used in the treatment of acromegaly?

A

Pegvisomant (GH antagonist given subcutaneously and daily)
Somastatin analogues to block GH release
Dopamine agonists to block GH release (e.g. bromocriptine)

30
Q

What do juxtaglomerular cells in the afferent arteriole of the kidney do?

A

Sense blood pressure and if low, they secrete renin.

31
Q

Where is angiotensinogen made?

A

Liver

32
Q

What does renin do?

A

Converts angiotensinogen to angiotensin I

33
Q

Where is angiotensin I converted to angiotensin II?

A

The lungs with the help of angiotensin converting enzyme (ACE).

34
Q

What does angiotensin II do?

A

Stimulates the release of aldosterone from the adrenal glands

35
Q

What is the most common cause of primary hyperaldosteronism?

A

Bilateral adrenal hyperplasia

36
Q

What causes secondary hyperaldosteronism?

A

Excessive renin stimulating the adrenal glands to produce more aldosterone.

37
Q

What can cause high renin levels?

A

Renal artery stenosis (often in patients who are atherosclerotic)
Renal artery obstruction
Heart failure

38
Q

What investigation for hyperaldosteronism?

A

Renin and aldosterone levels so that you can calculate a renin/aldosterone ratio

39
Q

What is the management for renal artery stenosis?

A

Percutaneous renal artery angioplasty

40
Q

A patient with high blood pressure that is not responding to treatment should be considered for investigation for what?

A

Hyperaldosteronism

Finals Revision (20 decks)

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