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BRS YEAR 2 > Endo - Disorders of Vasopressin > Flashcards

Endo - Disorders of Vasopressin Flashcards

1
Q

What type of neurones are found in the PPG?

A

Mangocellular neurones

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2
Q

Why is the PPG neural in origin?

A

it develops continuously with the hypothalamus

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3
Q

Where do magnocellular neurones originate from?

A

Supraoptic and paraventricular nucleus

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4
Q

What are the PPG hormones?

A

AVP

Oxytocin

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5
Q

What is the physiological action of AVP?

A

Concentrations urine in the collecting duct

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6
Q

What does AVP bind to?

A

V2 receptors

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7
Q

What type of receptor is V2?

A

G protein coupled

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8
Q

What does V2 binding stimulate?

A

Adenylate cyclase leads to cAMp and protein kinase A activity which leads to aquaporin 2 channels to move to the apical membrane of tubular cells

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9
Q

What does the PPG normally show in an MRI?

A

Bright spot

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10
Q

Is the PPG always seen in health?

A

No

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11
Q

What are the 2 ways vasopressin release is stimulated?

A

Osmotic and non osmotic

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12
Q

What is the osmotic route of AVP stimulation?

A

Increase in plasma osmolarity is sensed by hypothalamic osmoreceptors

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13
Q

What is the non osmotic route of AVP stimulation?

A

Decreased blood volume leads to less atrial stretch detected by stretch receptors

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14
Q

Where are osmoreceptors found mainly?

A

In the hypothalamus in the subfornical organ and the organum vasculosum

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15
Q

What is an advantage of the osmoreceptors?

A

They lack a blood brain barrier therefore respond directly to the systemic circulation

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16
Q

Where do osmoreceptor neurones project?

A

Into the supraoptic nucleus which is a site of vasopressinergic neurones

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17
Q

Outline how water deprivation increases AVP secretion

A

Increase in plasma Na means that water leaves the osmorecpetors due to osmotic balance, osmoreceptor shrinking leads to increased firing and thus increased AVP release

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18
Q

Where are atrial stretch receptors found?

A

Right atrium

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19
Q

How do atrial stretch receptors work?

A

They are usually inhibitory on AVP secretion via the vagus nerve

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20
Q

Outline how water deprivation causes AVP release non osmotically?

A 
Decrease in water
Decrease in blood volume
Less stretch detected
Disinhibition by less firing 
AVP release
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21
Q

Why is AVP released following a haemorrhage?

A

Following a haemorrhage there us a lower circulating volume, this allows for us to try and increase our blood pressure

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22
Q

Alongside AVP release, what else happens during a haemorrhage?

A

We get vasoconstriction by AVP acting on V1 receptors

Junta glomerular apparatus stimulates aldosterone release to increase blood volume

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23
Q

Alongside AVP release, how else do we correct plasma osmolarity?

A

Stimulation of osmoreceptors increases thirst therefore plasma osmolarity is reduced when drinking

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24
Q

What is diabetes insipidus?

A

When there is a problem with insufficient AVP effect

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25
Q

What are the symptoms for diabetes insipidus?

A

Polyuria
Polydipsia/extreme thirst
Nocturia

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26
Q

What is the more common form of diabetes?

A

Mellitus

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27
Q

Why does diabetes mellitus cause osmotic symptoms?

A

Increase in blood glucose
Water enters blood due to osmotic effect
Increased water loss in urine

28
Q

Describe urine production in diabetes insipidus

A

Large volume, hypo-osmoloar urine

29
Q

Describe the plasma in diabetes insipidus

A

Hyper-osmolar with increasing thirst
Hypernatremia
Normal glucose

30
Q

What are the 2 types of diabetes insipidus

A

Cranial

Nephrogenic

31
Q

What is the more common form of diabetes insipidus

A

Cranial

32
Q

What happens in cranial diabetes insipidus

A

Problem with hypothalamus or pituitary whereby we don’t make sufficient AVP

33
Q

What happens in nephrogenic diabetes insipidus

A

AVP production is normal but collecting duct doesn’t respond - vasopressin resistance

34
Q

What are the causes of congenital cranial diabetes insipidus

A

Very rare

35
Q

What are the causes for acquired cranial diabetes insipidus

A 
Traumatic brain injury
Pituitary surgery
Pituitary tumours
Metastasis (breast to pituitary)
Granulomatous infiltration of pituitary stalk e.g. TB, sarcoidosis.
Autoimmune
36
Q

How does granuloma cause cranial diabetes insipidus?

A

Stalk inflammation causes thickening thus preventing passage of AVP

37
Q

What are the causes of congenital nephrogenic diabetes insipidus

A

Rare e.g. V2 receptor or aquaporin 2 gene mutation

38
Q

What are the causes of acquired nephrogenic diabetes insipidus

A

Drugs e.g. lithium

39
Q

What is the treatment for cranial diabetes insipidus

A

Desmopressin - oral or intranasal

40
Q

What does desmopressin act on?

A

V2 receptors - not V1 receptors

41
Q

What is the treatment for nephrogenic diabetes insipidus?

A

Thiazide diuretics e.g. bendrofluazide

42
Q

How can diabetes insipidus cause death?

A

We constantly lose water through lack of AVP mechanism therefore if we don’t drink water and the DI is not managed correctly, we die

43
Q

qWhat is psychogenic polydipsia?

A

Mental health disorder in which the patient drinks too much water - seen in the context of other mental health disorders

44
Q

What are the symptoms of psychogenic polydipsia?

A

Polyuria
Nocturia
Polydipsia

45
Q

How do we distinguish DI from PD?

A

Water deprivation test

46
Q

What happens in a water deprivation test?

A

We give the patient nothing to drink over the course of a few hours

47
Q

What do we measure in water deprivation test?

A

Urine volume
Urine osmolarity
Plasma concentration
Body weight

48
Q

When do we stop a water deprivation test?

A

If patient loses more than 3% of their body weight indicating significant dehydration

49
Q

What do we see in a water deprivation test for normal patient

A

As we have less water, AVP increases therefore urine osmolarity increases

50
Q

What do we see in a water deprivation test for PD

A

Water deprivation means AVP still works, but it is generally lower osmolarity than normal person due to large amounts of dilute urine

51
Q

What do we see in a water deprivation test for DI

A

AVP problem therefore urine is never concentrated, osmolarity stays low

52
Q

How do we distinguish between CDI and NDI?

A

We give desmopressin

53
Q

What do we see in CDI deprivation test?

A

CDI responds, urine osmolarity rises

54
Q

What do we see in NDI deprivation test?

A

NDI is resistant to ddAVP therefore osmolarity of urine is unaffected

55
Q

What is a normal plasma osmolality

A

280 mOsm/kg H20

56
Q

What is the plasma osmolarity for DI?

A

290

57
Q

What is the plasma osmolarity for PD?

A

270

58
Q

What is Syndrome of Inappropriate ADH?

A

Too much AVP

59
Q

What are the effects of SIADH?

A 
Water retention 
Low urine output
High urine osmolarity
Low plasma osmolarity
Dilution hyponatremia
60
Q

What are the 5 main causes of SIADH?

A 
Drugs
Idiopathic 
Pulmonary disease
Malignancy
CNS causes
61
Q

What malignancies cause SIADH

A

Small cell lung cancer

62
Q

What drugs cause SIADH

A

SSRIs

Carbamazepine

63
Q

What pulmonary diseases cause SIADH

A

Bronchiectasis

Pneumonia

64
Q

What CNS problems cause SIADH

A

Head injury
Stroke
Tumour

65
Q

How do we manage SIADH

A

Vaptan - V2 receptor antagonist (very expensive)

BRS YEAR 2 (37 decks)

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