Brainscape's Knowledge GenomeTM

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


See full index

5. Endocrinology > 12. Posterior Pituitary gland disorders > Flashcards

12. Posterior Pituitary gland disorders Flashcards

1
Q

Another name of ADH

A

Arginine Vasopressin = AVP = ADH

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

Define diabetes insipidus (DI).

A

Excretion of large volumes of dilute urine

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

Give 2 types of diabetes insipidus (DI).

A
  1. Cranial DI
  2. Nephrogenic DI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain the difference between cranial DI and nephrogenic DI.

A

Cranial DI = AVP deficiency = lack of vasopressin
* Uncommon but life threatening

Nephrogenic DI = AVP resistance = resistance to action of vasopressin
* Not common but life threatening

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

Give 5 symptoms of diabetes insipidus (DI).

A
  1. Polyuria (>3L/24h)
  2. Polydipsia
  3. Hypernatraemia
  4. Dehydration.
  5. Postural hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give 3 signs of diabetes insipidus (DI).

A
  1. Dry mucosa
  2. Sunken eyes
  3. Changes to skin turgidity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give 3 causes of cranial diabetes insipidus (DI).

A
  1. Tumours.
  2. Trauma.
  3. Infections (meningitis, encephalitis, TB)
  4. Idiopathic.
  5. Genetic - Autosomal dominant mutation
  6. Inflammation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give 3 causes of nephrogenic diabetes insipidus (DI).

A
  1. Osmotic diuresis - diabetes mellitus
  2. Drugs e.g. lithium toxicity
    - Decrease the production of aquaporin proteins in the collecting duct
  3. Chronic kidney disease (CKD)
  4. Metabolic e.g. hypercalcaemia and hypokalaemia
  5. Familial (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diagnosis / Investigations of diabetes insipidus (DI).

A
  1. Water deprivation test (ADH stimulation test)
    - Don’t drink any water (fluid deprivation) for 8 hrs
    - Hourly measurements of urine volume and osmolality are done
    - Give desmopressin drug
    - Measure osmolality 8 hrs after

1) Cranial DI -> Increase in urine osmolality
-ADH not made but kidneys still respond

2) Nephrogenic DI -> No effect on urine osmolality
- Desmopressin has no effect

Urine dip, glucose, U and E, fluid status

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

Management of cranial DI (AVP deficiency)

A
  1. Treat any underlying condition
  2. Desmopressin – high activity at V2 receptor
  • Tablets 100-600 micrograms/day
  • Nasal spray 10-20 micrograms/day
  • Injection 1-2 micrograms/day

Rare: If thirst disrupted may require twice daily body weight
and fluid ‘prescription’ and fixed dose of desmopressin

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

Management of nephrogenic DI (AVP resistance)

A
  1. Try and avoid precipitating drugs
  2. Mild cases managed by low sodium diet
  3. Treat underlying cause
  4. Desmopressin - very HIGH dose
  5. Thiazaide diuretic
    - Benzoflumethiazide
    - Produce mild hypovolaemia which encourages kidney to take up for Na+ and water in proximal tubule and offseting water losses
  6. NSAIDs
    - Inhibit prostaglandin synthase (prostaglandins locally inhibit ADH action) – NSAIDs thus lower urine volume and plasma Na+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give 2 complications of diabetes insipidus (DI).

A
  1. Dehydration
  2. Electrolyte imbalance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the normal serum sodium range?

A

Normal serum sodium = 135-144 mmol/l

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

Define hyponatraemia.

A

A condition where sodium levels in your blood are lower than normal I.E. serum sodium < 135 mmol/l.

Biochemical Severe = serum sodium < 125 mmol/l

Normal serum sodium = 135-144 mmol/l

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

What are the 4 different types of classification of hyponatraemia?

A
  1. Biochemical
  2. Symptoms-based
  3. Aetiology
  4. Acuity of onset
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Biochemical classifications of hyponatraemia

A

Mild 130-135mmol/l

Moderate 125-129mmol/l

Severe <125mmol/l

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

Symptoms-based classifications of hyponatraemia

A

Mild

Moderate

Severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Aetiology classifications of hyponatraemia

A

Hypovolaemic

Euvolaemic

Hypervolaemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Acuity of onset classifications of hyponatraemia

A

Acute < 48 hours

Chronic > 48 hours

20
Q

Give 5 signs + symptoms of acute hyponatraemia

A
  1. Headache
  2. Irritability
  3. Nausea / vomiting
  4. Mental slowing
  5. Unstable gait / falls
  6. Confusion / delirium
  7. Disorientation
21
Q

Give 3 symptoms of chronic hyponatraemia

A
  1. Stupor / coma
  2. Convulsions
  3. Respiratory arrest
22
Q

Treatment of hyponatraemia.

A
  1. IV 150 ml of 3% Saline (or equivalent)
    over 20 mins
  2. Check serum Na+
  3. Repeat twice until 5 mmol/L
    Increase Na+
  4. After 5 mmol/L increase
    - Stop hypertonic saline
    - Establish diagnosis
    - Na+ 6 hourly for 1st 24 hours
    - Limit increase to 10 mmol/l first 24 hour
23
Q

Management of hyponatraemia.

A

General
* Stop hypotonic fluids
* Review drug card – long list - PPI etc.

Specific
* Plasma and Urine Osmolality
* Urinary Na+
* glucose
* TFT’s
* +/- Assessment of Cortisol
* Assessment of underlying causes e.g. chest imaging

24
Q

Management + assessment of chronic hyponatraemia diagnoses

A
25
Q

Define SIADH / SIAD

A

SIADH = Syndrome of inappropriate ADH secretion

SIAD = Syndrome of inappropriate antidiuresis

Too much ADH = very concentrated urine and hyponatraemia

26
Q

Explain the pathophysiology of SIADH.

A
  1. Increased ADH release from posterior pituitary OR ectopic source (lung)
  2. ADH acts on collecting duct (AQP2) - water but not solute reabsorption
  3. Increases blood vol and decreases serum osmolality (decreased solute concentration)
  4. Increased vol → ANP/BNP release, which inhibits renin release and RAAS → promotes sodium and water excretion, which further increased ADH
  5. Kidneys adapt by reducing number of aquaporins available → leads to diuresis and natiuresis
  • Overall state is EUVOLAEMIA with HYPONATRAEMIA
27
Q

Give 3 causes of SIADH.

A
  1. Malignancy
    - e.g. small cell lung cancer, pancreas, prostate, thymus, lymphoma
  2. CNS disorders
    - e.g. meningitis, brain tumour, cerebral haemorrhage, encephalitis, Guillain-Barre syndrome
  3. Respiratory
    - e.g. TB, pneumonia, abscess
    (Due to renal vasoconstriction and antidiuresis in response to hypercapnia. The renal response eventually leads to hyponatremia due to water retention.)
  4. Endocrine
    - e.g. hypothyroidism
  5. Drugs (CARDISH)
    - Chemo, Antidepressants, Recreational, Diuretics, Inhibitors (SSRi, ACEi), Sulphonylureas, Desmopressin
28
Q

What types of malignancy can cause SIADH?

A

Small cell lung cancer, pancreas, prostate, thymus, lymphoma

29
Q

Name 3 diseases that you must exclude in someone who you suspect could have SIADH.

A
  1. Renal disease
  2. Hypothyroidism
  3. Hypocortism
  4. Recent diuretic use
30
Q

Describe 5 features of the essential criteria for SIADH.

A
  1. Hyponatreamia (<135mmol/L).
  2. Plasma hypo-osmolality (<275 mOsm/Kg).
  3. High urine osmolality.
  4. Clinical euvolaemia - NO Oedema!
  5. Increased urinary sodium excretion with normal salt and water intake.
31
Q

Despite water retention, what is NOT a feature of SIADH?

A

Oedema

32
Q

What is the main metabolic abnormality in SIADH?

A

Hyponatraemia

33
Q

Describe the urine of a patient with SIADH.

A

Concentrated urine with hyponatraemia and a low plasma osmolality

34
Q

Give 3 signs of SIADH.

A
  1. Raised JVP
  2. Oedema
  3. Ascites
35
Q

Give 3 symptoms of SIADH.

A
  1. Anorexia
  2. Nausea / Vomitting (N/V)
  3. Malaise
  4. Headache
  5. Confusion
36
Q

Investigations for SIADH.

A

ADH levels
U and Es (low sodium normal potassium)
Fluid status

37
Q

Treatment for SIADH.

A
  1. Restrict fluid < 1L/24 hr
  2. Treat underlying cause
  3. Give salt
    - If Na+ <115 mmol/l AND fitting hypertonic N/Saline on ITU
  4. Hypertonc saline loop diuretics e.g. furosemide
    - Urgent due to risk of cerebral oedema
  5. ADH-R antagonists
    - Selective V2 receptor -> competitive antagonist to AVP
    - e.g. demeclocycline / vaptans e.g. tolvaptan - can be used when people find fluid restriction challenging
  • In acute setting - daily U+E - hospital
  • In chronic setting - weekly to monthly U+E - hospital/GP
38
Q

Would you expect a patient with SIADH to be hypovolaemic, euvolaemic or hypervolaemic?

A

Euvolaemic.

39
Q

Would you associate SIADH with hyponatraemia or hypernatraemia?

A

Hyponatraemia <135mmol/L.

40
Q

Would you associate SIADH with plasma hypo-osmolality or hyper-osmolality?

A

Plasma hypo-osmolality <275mOsm/Kg.

41
Q

Would you associate SIADH with a high or low urine osmolality?

A

High urine osmolality.

42
Q

Complications of SIADH

A

Cerebral oedema
Seizure and coma
Death- a medical emergency!

43
Q

Give 2 clinical signs of hypervolaemia.

A
  1. Ascites.
  2. Oedema.
44
Q

Give 3 clinical signs of hypovolaemia.

A
  1. Hypotension.
  2. Tachycardia.
  3. Decreased skin turgor.
  4. Dry mucus membranes.
45
Q

Give 4 causes of polyuria.

A
  1. Hypokalaemia.
  2. Hypercalcaemia.
  3. Hyperglycaemia.
  4. Diabetes insipidus.

5. Endocrinology (20 decks)

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