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Endocrine > Adrenal > Flashcards

Adrenal Flashcards

1
Q

Does sodium follow water or water follow sodium

A

WATER ALWAYS FOLLOWS SODIUM

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2
Q

How does the ICF compartment compare to that of ECF?
What happens when water is gained or lost from the body?
What is it important to remember re this when thinking about clinical signs of water overload or deficit?

A

It is important to note that the ICF is double the size of the ECF. This is important, as when water is gained or lost from the body, it is distributed across all body compartments, since water is not confined to any one compartment.
This means that the clinical signs of water overload or deficit are correspondingly muted or ‘diluted’ if you like. So you can for example lose quite a lot of pure water without being obviously dehydrated clinically.

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3
Q

How do the concentrations of Na and K differ in the ICF compared to the ECF?
How is this maintained?
How does the body use this to maintain ECF fluid volume?

A

the normal concentration of sodium in the ICF is much smaller than that in the ECF. Potassium concentration is the opposite – it is much higher in the ICF than the ECF. The plasma membrane has a Na/K pump, which maintains these concentration gradients. The pump confines Na to the ECF compartment. The body uses the fact that Na is confined to the ECF to control the ECF volume.

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4
Q

What do your kidneys do if the ECF volume is too high or too low?

A

if your ECF volume is too high, the kidneys excrete more Na and thus you lose water with it. If the ECF volume is too low, the kidneys ‘hang on’ to Na in an attempt to retain water and restore volume to normal.

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5
Q

What are the clinical signs of reduced ECF volume?

Why are these specific?

A

Dry mucous membranes, postural decrease in blood pressure.

Because Na loss is confined to the ECF

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6
Q

If you lose control of Na excretion because of pathology, what happens to sodium?
What does this cause in the fluid compartments of the body?
How does this relate to the clinical signs?

A

Sodium loss
A reduction in the ECF volume. Because the volume loss is confined to the ECF (since the sodium is lost exclusively from the ECF), the clinical signs are obvious, and develop quickly.

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7
Q

What is sodium controlled by?
Which type of hormone regulates this and where are they produced?
What is the main mineralocorticoid hormone?
What does mineralocorticoid activity refer to?

A

SODIUM is controlled by mineralocorticoid activity.
Steroid hormones produced in the adrenal gland
Aldosterone (also cortisol)
Mineralocorticoid activity refers to sodium retention in exchange for potassium and/or hydrogen ions.

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8
Q

What two things does aldosterone cause in the kidney?

A

Aldosterone causes Na to be reabsorbed from that filtrate in exchange for K or H. You excrete positively charged ions – either K or H. You retain Na, so you retain H2O. You also lose more potassium and hydrogen.

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9
Q

What happens if you have too little mineralocorticoid activity?

A

If you have too little mineralocorticoid activity, you lose sodium, so lose water. Since this is from the ECF, the patient will be dry.

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10
Q

What does to much mineralocorticoid activity do to sodium?

A

Too much mineralocorticoid activity means sodium retention.

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11
Q

Where is ADH released from?
What type of stimuli cause this?
What does ADh do to the kidneys?

A

WATER is controlled by ADH (Anti-Diuretic Hormone).
ADH is released by the posterior pituitary in response to osmotic & non-osmotic stimuli.
The function of ADH on the kidneys is to cause water to be reabsorbed – pee out small amount of concentrated urine.

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12
Q

What is the term used when we assess urine concentration?

What does an increase or decrease of ADH to do urine concentration?

A

Urine osmolality
Increased ADH - concentrated urine - high urine osmolality
Decreased ADH - dilute urine - low urine osmolality

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13
Q

What does countercurrent multiplication refer to?

A

The concept of having a concentration gradient between what’s in the filtrate and whats surrounding the filtrate - you want a big concentration gradient between the two

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14
Q

What are the two possible causes of hyponutraemia?

Give two possible causes of each, with examples?

A

This can be caused by too much water, or too little sodium.
Too much water
- ↓excretion e.g. SIADH – syndrome of inappropriate ADH secretion
- increased intake e.g. compulsive water drinking – very unusual and very obvious
Too little sodium
- ↑ sodium loss - kidneys e.g. Addison’s, gut, skin
- increased sodium intake - rare cause

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15
Q

What are the two possible causes of hypernutraemia?

Give two possible causes of each, with examples?

A

This can be cause by too little water, or too much sodium.
Too little water
- ↑ water loss - diabetes insipidus (problem with ADH secretion or action)
- decreased water intake e.g. very young, elderly patients (insensible water loss continues)
Too much sodium - rare – may not be suspected
- Some IV medications are given as sodium salts
- Near-drowning in sea
- Infants given high-salt feeds

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16
Q

Is hyper or hyponutraemia more common?

A

Hyponutraemia

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17
Q

Is it more common to have problems with sodium balance or water balance?

A

In general it’s much more common to have problems with water balance rather than sodium.

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18
Q

A 24 year-old student presents with a six month history of malaise, tiredness, poor appetite and one stone weight loss. She has developed a craving for salty foods – crisps in particular. She has had a number of dizzy spells particularly while in warm places.
She is thin. She has low BP which falls further on standing. You have the impression that she is tanned, and you find increased pigmentation in her mouth and hand creases.
Her bloods show a low sodium [122] and a high potassium [5.8].
What is this a typical history of?

A

Addison’s disease

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19
Q

Addison’s disease

  • What is the basic problem?
  • What does this do to Na in the kidneys?
  • What does this do to the patient clinically?
  • What causes the excess pigmentation?
A

Basic problem is adrenal insufficiency – Addison means primary adrenal insufficiency
- So can’t make enough steroids
- So doesn’t have enough mineralocorticoid activity
- So can’t retain enough sodium in the kidneys – losing Na and water, and retaining K and H
So loses sodium (and water with it) from ECF
There is decreased ECF volume meaning patient is clinically dehydrated
Symptoms of dizziness etc reflect hypotension from decreased ECF
Excess pigmentation reflects excess ACTH from pituitary

20
Q
  • Patient often in hospital with other illness
  • Routine biochemistry shows decreased [Na]
  • On examination, volume status usually unremarkable
  • Patient usually has no symptoms specifically due to low sodium
  • Investigations for causes of sodium loss e.g. Addison’s negative
  • Patient presumed to have too much water
  • Most of these patients have ‘inappropriate’ ADH secretion
    What is this a classic history of?
A

SIAD: syndrome of inappropriate antidiuresis (inappropriate’ means inappropriate for the osmolal state).

21
Q

What are the two types of stimuli for ADH release?

Which occurs in health and which in disease?

A
  1. Osmotic (in health)

2. Non-osmotic (in disease) – very common, especially in hospital

22
Q

What are three examples of non-osmotic simuli for ADH release?

A
  1. Hypovolaemia/hypotension
  2. Pain
  3. Nausea/vomiting
23
Q

Syndrome of inappropriate antidiuresis

  • What is the basic problem?
  • What does this do to water?
  • Timeline of disease?
  • What does this do to the patients clinical volume status?
  • When does it usually come to your attention?
  • What is presumed to be the problem?
  • How is the diagnosis made?
A

Basic problem is ADH secreted in response to a non-osmotic stimulus
This causes water retention. This often occurs slowly and the retained water is distributed over all body compartments (ICF as well as ECF) – so patient’s volume status clinically may be unremarkable.
- It first comes to attention when U&E done and [Na] found to be low.
- Clinicians often aren’t sure why [Na] is low and investigate to exclude the other main mechanism of [Na] – i.e. too little sodium
- Diagnosis of water excess as the mechanism is often by exclusion – once adrenal insufficiency (and other sources of sodium loss) excluded, you start to think about water

24
Q

A 29 year-old man is admitted to ITU following a cycling accident in which he sustained a severe head injury. During his ITU stay his urine output is in excess of 12 litres daily; his IV fluid requirement is correspondingly large.
Serum sodium is 167 mmol/L on admission to ITU and slowly falls as fluid replacement ‘catches up’. He is in addition commenced on desmopressin (exogenous ADH) which produces a sharper fall in sodium.
What is this a typical presentation of?

A

Diabetes insipidus
He has transected his pituitary stalk – no longer secreting ADH from posterior pituitary. He is not reabsorbing water in the usual way, so he pees out lots of diluted urine.

25
Q

Diabetes insipudus

  • What is the basic problem?
  • What does this do to urine osmolality?
  • What does this do to [Na]?
  • How is it treated?
A

Basic problem is disruption of pituitary or pituitary stalk – so patient can’t secrete ADH from posterior pituitary
So there’s no ADH to act on kidneys to cause water to be reabsorbed
So LOTS of (pure) water is lost in urine
So patient’s [Na] is high, reflecting the water deficit
If the pituitary can’t make/release ADH, then we can give exogenous ADH (desmopressin) to replace it

26
Q

What is the most important clinical information in assessing Na and water balance?

A

Volume status

27
Q

If you get low water volume in a patient with low Na, then what is the problem?

A

Too little Na

28
Q

If the balance between capillary and ICF is altered so there is more water in the ICF then what happens to circulating volume?
What two things does the body do in response to this?
What does this do to the interstitial fluid?

A

Reduced circulating volume
1. Switches on aldosterone (secondary hyperaldosteronism), which causes Na to be reabsorbed in exchange for K and H, so you also reabsorb water
2. You also secrete ADH to try and restore blood volume back to normal
This goes some way to restoring the circulating volume, but some of the reabsorbed water goes back into the interstitial fluid.

29
Q

What does oedema tell you about water compartments?

A

Oedema tells you that the water is in the wrong place, not that there is too much of it. You are likely to have too much sodium, in the wrong place.
Basically, oedema signifies effective circulating volume depletion. Compensation for that (ADH & aldosterone to restore volume) produces a vicious circle.

30
Q

How can you tell if hypo or hypernutraemia is serious?
What symptoms might this cause?
What about if there has been a rapid change in [Na]?

A

[Na] itself is helpful. If very low (<120 mmol/L) or very high (>155 mmol/L), then YES it is serious
If [Na] is very low or high the patient may develop symptoms due to the abnormal [Na] e.g. altered consciousness, confusion, nausea. If the patient has these symptoms in context of very low or high [Na], then YES it is VERY serious.
If [Na] has fallen or risen rapidly to current level, that may be serious.

31
Q

A patient has low [Na]

  • What are the two possible causes?
  • what is the most helpful investigation?
  • What are the two possible causes of the Na problem?
  • What should you do if you suspect adrenal insufficiency?
  • What should you consider if the patient isn’t dry?
A

Has to be either too little sodium or too much water
Most helpful info is patient’s volume status
- If dry → too little sodium
- If not dry → too much water
If too little sodium then has to be either decreased intake or increased loss, either from gut, skin or kidney. Decreased intake uncommon. Gut/skin loss usually obvious
4If suspect adrenal insufficiency, then measure cortisol and ACTH, but if patient unwell DON’T wait – give patient sodium replacement.
If not dry, and adrenal insufficiency excluded, must be water excess.

32
Q

How should you treat a patient with the following problems?

  • Too little sodium
  • Too much water
  • Too little water
  • Too much sodium
A

Too little sodium → give sodium
Too much water → fluid restrict
Too little water → give water
Too much sodium → get rid of excess sodium e.g. diuretics to induce natriuresis, and then replace just the water

33
Q

Name the three zones that the adrenal cortex can be divided into and the hormones that each produces

A 
Zona Glomerulosa – 
- Mineralocorticoids
- Aldosterone
Zona Fasciculata – 
- Glucocorticoids
- Cortisol
Zona Reticularis – 
- Sex Steroids
- Glucocorticoids
34
Q

Adrenal Cortex Pathology

  • Give three causes of hyperfunction
  • Give two types of hypofunction and an example of each
A 
Hyperfunction
- Hyperplasia 
- Tumour 
- Carcinoma 
Hypofunction 
- Acute – Waterhouse-Friderichsen
- Chronic – Addison’s disease
35
Q

Congenital adrenocortical hyperplasia

  • What type of disorder?
  • What does this cause?
  • Symptoms?
  • Basic pathology?
A

Group of autosomal recessive disorders.
Deficiency / lack of enzyme required for steroid biosynthesis.
Altered biosynthesis leads to increased androgen production
- Masculinisation
- Precocious puberty
Reduced cortisol stimulates ACTH release and cortical hyperplasia (10-15x normal weight).

36
Q

Acquired adrenocortical hyperplasia

  • What hormone is produced and what does this cause?
  • What are the two types and what is the difference between them?
A 
Endogenous ACTH production
- Pituitary adenoma (Cushing’s disease)
- Ectopic ACTH - Paraneoplastic syndrome (small cell lung carcinoma)
Diffuse or Nodular
- Diffuse – ACTH driven
- Nodular usually ACTH independent
37
Q

Adrenocortical tumours

  • Who gets them?
  • M:F?
  • Presentation?
A

Mainly adults - can occur in younger patients (?Li-Fraumeni syndrome).
Males and females are equally affected.
Presentation
- Incidental finding (radiology, autopsy)
- Hormonal effects
- Mass lesion
- Carcinomas with necrosis can cause fever

38
Q

Adrenocortical adenoma

  • Describe the lesion itself
  • What does it resemble histologically?
  • Functional or not?
  • How are they usually found?
A

Well circumscribed, encapsulated lesions
Usually small – up to 2 to 3cm
Yellow / brown cut surface (lipid) – this is very characteristic of the adrenal cortex itself – because of the abundance of lipids present in the cells
Composed of cells resembling adrenocortical cells
Well differentiated, small nuclei, rare mitoses -> i.e. lack the usual histological features of malignancy
Can be functional, but more likely not
There are usually incidentally found.

39
Q

Adrenocortical carcinoma

  • Common or rare?
  • What do they resemble?
  • Where do they spread to?
  • Prognosis?
A

These are rare.
More likely to be functional - virilising tumours usually malignant
Can closely resemble adenoma - adenoma and carcinoma form a spectrum.
Spread of carcinoma
- Local invasion – retroperitoneum, kidney
- Metastasis – usually vascular (liver, lung and bone)
- Peritoneum and pleura
- Regional lymph nodes
5 year survival 20-35%, 50% dead in two years.

40
Q

Distinction between benign and malignant can be difficult.

Give five features suggesting adrenocortical carcinoma

A 
Large size (>50g, often >20cm)
Haemorrhage and necrosis
Frequent mitoses, atypical mitoses
Lack of clear cells
Capsular or vascular invasion
41
Q

Give three causes of Conn’s syndrome (primary hyperaldosteronism) in relation to adrenocortical tumours

A
  1. Usually (60%) associated with diffuse or nodular hyperplasia of both adrenal glands
  2. Adenoma (35%) – rarely carcinoma
    - Solitary, small, bright yellow and buried within the gland – do not cause a mass lesion
    - Spironolactone bodies
    - Do not suppress ACTH so adjacent & contralateral adrenal tissue is not atrophic
  3. Glucocorticoid remediable
    - Uncommon genetic disorder with production of hybrid steroids, cortisol and aldosterone
    - Under the influence of ACTH
42
Q

Which tumour produces spironolactone bodies?

A

Adrenocortial adenoma

43
Q

Give two causes of secondary hyperaldosteronism

A

Increased renin

Decreased renal perfusion, hypovolaemia, pregnancy

44
Q

What are the two tumours associated with the adrenal medulla?

A

Neuroblastoma

Phaeochromocytoma

45
Q

Neuroblastoma

  • When is it usually diagnosed?
  • Where does it arise from?
  • What is it composed of?
A

Usually diagnosed 18 months, 40% diagnosed in infancy.
40% arise in the adrenal medulla – the remainder mostly along the sympathetic chain.
Composed of primitive appearing cells but can show maturation and differentiation towards ganglion cells.

46
Q

Phaeochromocytoma

  • Derived from?
  • What might it cause?
  • What is laboratory diagnosis based on?
  • Describe the pathology
  • Where might it metastasize to?
A

This is a neoplasm derived from chromaffin cells of the adrenal medulla, which secretes catecholamines.
Rare cause of secondary hypertension.
Laboratory diagnosis - detection of urinary excretion of catecholamines and metabolites
Pathology
– Range from small to large necrotic tumour masses – 1g to >2kg described, average 100g
– May see adrenal remnants on the surface
– Yellow, red/brown to haemorrhagic and necrotic
Skeletal

47
Q

Phaeochromocytoma is a feature of which endocrine disease?
What are the two types?
Briefly describe each.

A

Multiple Endocrine Neoplasma (MEN)
1. MEN2A (sipple syndrome)
– Phaeochromocytoma (40-50%), Medullary thyroid carcinoma (100%), parathyroid hyperplasia (10-20%)
MEN2B
– Phaeochromocytoma, Medullary thyroid carcinoma, neuromas or ganglioneuromas, marfanoid habitus

Endocrine (9 decks)

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