avp aldos DI

Question 2

Vasopression synthesis (1): Synthesised in _____neurones Packaged into neurosecretorygranules (w/ neurophysin) Transported along axons(supra-optic hypothalamic tract) Released from neuronal terminals in posterior pituitary via fenestrated ____–>inferior hypophyseal circulation

Answer 2

1. magnocellular (inhibited by alpha adrenoceptors)2. capillaries

Question 3

Vasopression synthesis (2):Some AVP in _______-neurones-Co-secreted with CRH-Potentiates CRH stimulation of _____- Some AVP secretion even ifsupraoptic- hypothalamic tract damaged

Answer 3

1. parvocellular 2. ACTH

Question 4

Other regulators of AVP1. ATII, adrenaline, cortisol, oestrogen, progesterone2. pain and trauma in __increase AVP3. increase ____stimulate AVP

Answer 4

surgery temperature

Question 5

Control of vasopressin secretion:1. increase plasma osmolality and AT II stimulates______ in hypothalamus2. via____Rs—> PVN—> AVP release3. baroreceptors tend to inhibit____ so less AVP released4. AT II also stimulates the _____organ

Answer 5

1. osmoreceptors2. nAChR3. PVN, (SON)4. sub-fornical

Question 6

Actions of AVP: via different GPCRs Pressor action - via ___receptors (will decrease GFR) Anti-diuretic action - via ___receptors t½ approx. 5 min so longer term regulationof salt and water balance also involves aldosterone, with a t½ approx. 20 min 3. ___stimulates insertion of aquaporin (AP2) channels in renal _____________

Answer 6

1. V1 2. V2 3. cAMP 4. collecting ducts longer term increased expression of AP2 (luminal membrane) and AP3 (apical membrane) i.e. prolonged dehydration

Question 7

aldosterone acts on MR which dimerises, and increases expression of ___ and ____ in luminal membraneSGK1 phosphorylates _________ converts cortisol—> cortisone, to confer aldosterone selectivity

Answer 7

1. ENaC and ROMK2. ROMK (+enac)3. 11betaHSD type 2

Question 8

Mineralocorticoid excess. Causes:Primary – low renin, high aldosterone1.Tumour of adrenal (rare) e.g. ____Primary – low renin, low aldosterone1.Deoxycorticosterone producing tumour 2.Cushing’s syndrome (but also diabetes mellitus)3. AMESecondary – high renin, high aldosterone1.Chronic _________/decrease in blood volume2.Heart failure –> decreased _____-

Answer 8

1. Conn’s syndrome2. haemorrhage3. GFR

Question 9

Mineralocorticoid deficiencyAddison’s disease,  CAH (P450C21 or P450C11B2 deficiencies Symptoms?___________

Answer 9

Hyponatremia / Hyperkalemia, fatigue, weakness, hypotension

Question 10

Aldosterone analogues: 1.________pure MR agonist2.________ MR antagonist

Answer 10

1. 9alpha-Fludrocortisone 2. Spironolactone

Question 11

DIABETES INSIPIDUSpolyuria (with decreased urine osmolality), polydipsia (check not psychogenic), increased plasma renin and aldosterone, hypovolemic hypotension. Cranial = Defect in ___________ Nephrogenic =______________

Answer 11

1. AVP synthesis and/orsecretion2. Defective V2 receptor protein /expression

Question 12

Head injury (damage to post.pit. / supra-optic hypothalamic tract) often results in cranial Diabetes Insipidus. Why isn’t plasma [ AVP ] decreased to zero?

Answer 12

1. AVP co-secreted with CRH fromsome parvocellular neurones

Question 13

What treatment option would be available for cranial DI but would not be applicable for nephrogenic DI?

Answer 13

Administration of AVP analoguese.g. Desmopressin (sometimes in combination with thiazide natriuretic diuretics)also for nephrogenic- low Na+ diet

Question 14

Vasopressin Hypersecretion or “Syndrome of inappropriate vasopressin ADH secretion” SIADHhypervolemia and pot. fatal hyponatremia low plasma osmolality–> v.concentrated urinetreat with fluid restriction and Na+ replacement

Answer 14

 Intra-cranial trauma / infection Pneumonia Malignancy esp small lung cell cancer,  narcotics / analgesics e.g nicotine, surgery Prolonged strenuous exercise

Question 15

What stimulates AVP secretion? (3)What inhibits AVP secretion?

Answer 15

 3 major stimuli- Increased plasma osmolality- Decreased plasma volume- Reduce O2 / Increased CO2 2 major inhibitors- Oropharyngeal reflex- Increased ANP (heart & CNS)

Question 16

AVP & Plasma Volume  Plasma volume must decrease >___%Exponential relationship:-  15% plasma volume -  2X [ AVP ]-  20% plasma volume -  4X [ AVP ]_____more effective than plasma volume

Answer 16

1. 82. Osmolality

Question 17

Vasopressin Analogues Lysine AVP (porcine) - low potency ____receptor agonist Arginine AVP Desmopressin :synthetic; highly selective ___receptor agonist O-ethyltyrosine substitutes (synthetic) - AVP receptor ___

Answer 17

1. V2 2. V23. antagonists

Question 18

Why might plasma aldosterone be elevated in the presence of normal systemic arterial BP and normal plasma [ K+ ]?(2)

Answer 18

Increased ACTH driveMay be suppressed by chronicglucocorticoid administration

Question 19

Conn’s SyndromePrimary hyperaldosteronism : rare due to over-expression of steroidogenic enzymes and/or expansion of Z.glomerulosa Kaliuresis / anti-natriuresis fluid resorption –>______  2ry decrease in [ AVP ] and plasma renin

Answer 19

hypervolemic hypertension

Question 20

Secondary Hyperaldosteronism ___renal perfusion (rel.common) ____secretion of renin Kaliuresis / anti-natriuresis fluid resorption –>______  2ry decrease in____

Answer 20

1. Decreased 2.Increased 3. hypervolemic hypertension4. AVP

Question 21

Pseudohypoaldosteronism ________Plasma renin activity ______ [ Aldosterone ] Symptoms = Hyponatremia / Hyperkalemiacaused by_________to actions of aldosterone

Answer 21

1. increased2. increased3.Resistance

Question 22

Why does increased production of DOC in salt-sparing / simple virilising CAH result in “malignant hypertension”?

Answer 22

DOC production insensitive tosuppression of renin-angiotensinsystem and increase in plasma [ K+ ]