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BRS 2 - mine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Where does the posterior pituitary hypothalamic magnocellular neurons originate in

A

Supraoptic and paraventricular hypothalamic nuclei

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2
Q

What are the hormones of posterior pititary

A

AVP and oxytocin

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3
Q

What does diuresis mean

A

Production of urine

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4
Q

What is the action of AVP/ADH

A

Stimulation of water absorption in the RENAL COLLECTING DUCT, which concentrates the urine via V2 receptor in the kidney

Vasoconstriction via V1 receptor

Stimulates ACTH release rom anterior pituitary
CRH - corticotrophin releasing hormone stimulates ADH

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5
Q

How does vasopressin concentrate urine? -scientific pathway

A

??

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6
Q

How does posterior pituitary look on MRI

A

Bright spot

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7
Q

Is posterior pituitary bright spot absence on MRI an abnormal finding?

A

No it is not visualized in all healthy individuals

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8
Q

What stimulates vasopressin release

A

Osmotic:
Rise in plasma osmolality sensed by osmoreceptors in hypothalamus ( and also in carotid artery)

Non-osmotic:
Decrease in arterial pressure sensed by atrial stretch mechanoreceptors receptors / baroreceptors

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9
Q

What is the role of Organum vasculosum &
subfornical organ
??

A

The circumventricular organs (CVO) are structures that permit polypeptide hypothalamic hormones to leave the brain without disrupting the blood-brain barrier (BBB) and permit substances that do not cross the BBB to trigger changes in brain function.

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10
Q

Where does Organumvasculosum&

subfornical organ sit and what are they called and what is their featurical importance

A

Both nuclei sit around 3rd ventricle and are called circumventricular, they have no blood brain barrier so neurons can respond to changes in the systemic circulation
They are highly vascularised for this feature

Neurons project to supraoptic nucleus - site of vasopresinergic neurons

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11
Q

What are the 2 nuclei in posterior hyothalamus

A

Supraoptic and paraventricular

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12
Q

What change in osmoreceptor causes AVP release from hypothalamus

A

Increase in extracellular sodium causes the water in osmoreceptor cells to leave the cell and the cell shrinks

*this causes increased osmoreceptor firing and thus AVP release form hypothalamic neurons

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13
Q

What is the location of atrial stretch receptor pressure detection

A

Right atrium

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14
Q

What is the response of high pressure detection in stretch receptors

A

Inhibit vasopressin release via vagal affarent to hypothalamus

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15
Q

What is the response of reduction in circulating volume

A

Less strech of atrial receptors so less inhibition o vasopressin

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16
Q

Which receptors are responsible for vasopressin action on kidney for increased water reabsorption

A

V2

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17
Q

Which receptors are responsible for vasopressin action on vasoconstriction

A

V1

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18
Q

What happens to plasma osmolality during WATER DEPRIVATION and what is the cascade of events following this

A

Plasma osmolality increases
Osmoreceptor firing rate increases
This causes thirst and increased AVP release
Increased AVP release increases water absorption from renal collecting duct
Reduced urine volume
Increased urine osmolality
Reduction in plasma osmolality

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19
Q

What are other names for vasopressin

A

AVP
ADH
Arginine vasopressin
Antiduiretic hormone

20
Q

What are the symptoms associated with osmotic diuresis

A

Polyuria
Nocturia
Thirst - often extreme
Polydispia

21
Q

What are the symptoms of diabetes indispidus

A

Polyuria
Nocturia
Thirst
Polydipsia

22
Q

What is the most common cause of polyuria, nocturia, polydipsia

A

Diabetes mellitus

23
Q

What are two types of diabetes insipidus

A

Cranial (central) diabetes insipidus

Nephrogenic diabetes insipidus

24
Q

What is the problem in cranial (central) diabetes insipidus

A

Hypothalamus / posterior pituitary is unable to make arginine vasopressin
VASOPRESSIN INSUFFICIENCY

25
Q

What is the problem with nephrogenic diabetes insipidus

A

Kidney is unable to respond to vasopressin
But the vasopressin production is fine
VASOPRESSIN RESISTANCE

26
Q

What are the causes of cranial diabetes insipidus

A

Acquired:
Traumatic brain injury
Pituitary surgery
Pituitary tumors
Metastasis to the pituitary gland - eg. from the breast
Granulomatous infiltration of pituitary stalk - eg. TB, sarcoidosis ??
Autoimmune

27
Q

What is a congenital cause of nephrogenic diabetes insipidus

A

Mutation in the gene encoding V2 receptor, aquaporin 2 type water channel

28
Q

What is an acquired cause of nephrogenic diabetes insipidus

A

Drugs - lithium (used in bipolar disorder)

29
Q

What is a terminologic description of the state of urine and plasma in diabetes insipidus

A

Urine:
Hypo-osmolar (very dilute)
Large volume

Plasma:
Hyper-osmolar, hypotonic (increased concentration)
Hypernatraemia (increased sodium)
Glucose should be normal - check this in a patient with these symptoms

30
Q

How is the circulating volume maintained in a diabetes insipidus patient

A

Increased plasma osmolality
> stimulation of osmoreceptors
>thirst and polydipsia
> maintain the circulating volume AS LONG AS there is access to water

31
Q

What is psychognic polydipsia

A

Polydipsia, polyuria, nocturia
But no problem with arginine vasopressin

Patient drinks all the time so passes large volumes of dilute urine

32
Q

What is the cascade of events in polydipsia

A 
Polydipsia
> plasma osmolality falls
>less AVP by pp
> large volumes of hypotonic dilute urine
>plasma osmolality returns to normal
33
Q

How do you distinguish between diabetes insipidus and psychogenic polydipsia

A 
WATER DEPRIVATION TEST
Measure over time:
Urine volumes
Urine concentration - osmolality
Plasma concentration - osmolality
34
Q

What is the risk of water deprivation test and what should you do about it

A

Losing >3% body weight shows severe dehydration which can occur in diabetes insipidus so weight regularly

35
Q

What is the trend of urine osmolality in normal vs psychogenic polydipsia vs diabetes insipidus

A

Normal: goes up and levels off at about 6th hour

Psychogenic polydipsia: urine osmolality increases but at a slower rate than normal

Diabetes insipidus: stays the same > instead have progressive increase in plasma osmolality

36
Q

What is the name of replacement for vasopressin

A

Desmopressin - ddAVP

37
Q

How do you distinguish between cranial and nephrogenic diabetes insipidus

A

GIVE ddAVP
In cranial, there is a response to desmopressin, urine concentrates
In nephrogenic there is no response and urine osmolality stays the same

38
Q

What is the normal range for plasma osmolality for diabetes insipidus

A

275-285 mOsm/kg H2O

39
Q

What is the plasma osmolality ranges for diabetes insipidus and polygenic polydipsia

A

Diabetes insipidus >285

Psychogenic polydipsia<275

40
Q

How would you treat cranial diabetes insipidus

A

Desmopressin either tablet or intranasal, selective for V2 receptor (V1 receptor activation would be unhelpful)

41
Q

What is the problem with the nasal spray

A

Can be easily disregarded as not important and can lead to death if the person can not drink and do not have fluids

42
Q

What is the treatment of nephrogenic diabetes insipidus

A

Rare condition
Give thiazide diuretics eg. bendofluazide
Paradoxical unclear mechanism

43
Q

What is the name for the syndrome of too much arginine vasopressin

A

Syndrome of Inappropriate Anti-Diuretic Hormone SIADH

44
Q

What is the osmolality levels in SIADH

A

High urine osmolality
Low plasma osmolality - water retention
Dilutional hyponatraemia

45
Q

What can cause SIADH

A 
CNS
• Head injury, stroke, tumour, Pulmonary disease
• Pneumonia, bronchiectasis Malignancy
• Lung cancer (small cell) Drug-related
• Carbamazepine, Serotonin
Reuptake Inhibitors (SSSRIs)
Idiopathic
46
Q

What is the management of SIADH

A

Common cause of prolonged hospital stay

Restrict fluids
Can use vasopressin antagonist - vaptan, binds to V2 receptors in kidney but is very expensive

BRS 2 - mine (5 decks)

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