Week 11- regulation of fluid and electrolyte balance

Question 1

where is ADH synthesized?

Answer 1

cell bodies of paraventricular nucleus in hypothalamus and released in posterior pituitary

Question 2

delivery of ADH to general circulation?

Answer 2

stimulated by osmosensitive neurons, magnocellular neurons release the stored ADH into posterior pituitary and released into circulation

Question 3

regulation of ADH/ AVP?

Answer 3

plasma osmolality

Question 4

major actions of ADH?

Answer 4

reabsorbing water from renal tubules, binds to V2 receptors on the cells of DCT
induces production of water channels (aqua2) into luminal membrane
increases urine osmolality
control vasoconstriction of BV

Question 5

what are principle cells?

Answer 5

Na+ reabsorbing cells and site of action for aldosterone

located in DCT and CD

Question 6

mechanism of action for ADH?

Answer 6

protein hormone binds to ADH receptor and forms cAMP, this increases protein synthesis and makes water channels (A2) inserted into apical membrane
aquaporin 3 and 4 are in the basal membrane and V2 receptor. these are not dependant on ADH and help move water into the interstitial fluid

Question 7

what happens to the aquaporins if ADH is not there?

Answer 7

they’re taken back into the cell by endocytosis

Question 8

3 types of receptors for vasopressin:

Answer 8

V1a- vasoconstriction, present in blood vessels
V1b- present in anterior pituitary, corticotropes, increases ACTH secretion, increased cortisol, works during stress
V1a and V2a are by phospholipic C and increase Ca+
V2- present in nephron , increased water reabsorption by cAMP

Question 9

what stimulates ADH?

Answer 9

increased plasma osmolality:
- activates hypothalamic osmoreceptors, stimulation of neurons, stimulation of magnocellular neutrons to stimulate ADH release
decreased blood volume:
- decreased stretch of baroreceptors, sends signal to hypothalamus, goes to magnocellular neurons to increase ADH

Question 10

regulation of ADH?

Answer 10

hypervolemia (inhibits ADH)
decrease BP (stimulates ADH)
hypovolemia (increase renin-angiotensin system, increases brain angiotensin 2, increases ADH release)

Question 11

cause for diabetes insipidus?

Answer 11

vasopressin deficiency or kidneys fail to respond

Question 12

symptoms of DI?

Answer 12

dilute urine, tasteless
excessive urination
drinking large amounts of fluids
normal BG levels

Question 13

hypothalamic DI?

Answer 13

partial or complete lack of ADH, large volume of dilute urine is excreted
cause: head injury, hypothalamic tumours

Question 14

nephrogenic DI?

Answer 14

ADH is normal or increased, defect in the receptor or water channels (A2), no water reabsorption
Problem in kidneys (CD unresponsive)
defect in V2 receptor so prevent ADH from generating cAMP

Question 15

gestational DI?

Answer 15

deficiency of ADH only during pregnancy

Cause= increased synthesis of enzyme vasopressinase (breaks down ADH)

Question 16

dipsogenic DI?

Answer 16

increased thirst mechanism

Question 17

water deprivation test for nephrogenic DI?

Answer 17

synthetic AVP is used, urine still fails to concentrate

distal nephron unresponsive to DDAVP

Question 18

water deprivation test for cranial DI?

Answer 18

action of DDAVP on distal nephron, urine now becomes concentrated

Question 19

SIADH?

Answer 19

too much water retention, increased serum Na+

increased ADH secretion

Question 20

symptoms of SIADH?

Answer 20

concentrated urine, water retention, increased ECF, hypoosmolality, hyponatremia
causes head aches, nausea, confusion

Question 21

causes of SIADH?

Answer 21

ectopic production of carcinoma of lungs, pancreas
CNS trauma, infections, tumours
drug induced, nicotine, morphine

Question 22

factors regulating secretion of aldosterone?

Answer 22

serum Na+/K+, renin, angiotensin 2, ECF volume, renal blood supply, ACTH

Question 23

site of action for aldosterone?

Answer 23

DCT, CD

Question 24

mechanism of action for aldosterone?

Answer 24

acts on cytosolic receptors to alter the cell membrane Na+ transporters and NaK pump
to induce synthesis of proteins which are involved in Na+ transport

Question 25

circulatory effects of aldosterone?

Answer 25

increase BP and BV

Question 26

what is primary Conn's syndrome?

Answer 26

overproduction of aldosterone: primary- from adrenal hyperplasia and aldosterone producing adenomas ncreased aldosterone inhibiting angiotensin system low plasma renin

Question 27

what is secondary Conn's syndrome?

Answer 27

High angiotensin 2 stimulates adrenal cortex to release aldosterone high plasma renin

Question 28

clinical features of Conn's syndrome?

Answer 28

Na+ retention= water retention, increased ECF, increased BP, BV hypokalemia= muscle weakness, cardiac arrhythmias

Question 29

what is hypoaldosteronism?

Answer 29

deficiency of aldosterone but normal cortisol levels

Question 30

causes of hypoaldosteronism?

Answer 30

- reduced renin - deficiency of enzyme for renin synthesis - prolonged administration of heparin, reduced angiotensin 2 receptors in ZG and reduced aldosterone synthase - excision of aldosterone secreting tumour

Question 31

where is renin?

Answer 31

juxta glomerular cells of the kidney

Question 32

stimulus for renin angiotensin system?

Answer 32

renal ischemia, decreased BV/ BP, sympathetic nerve stimulation, Na+ depletion, diuretics

Question 33

major effets of renin angiotensin system?

Answer 33

increased angiotensin 2 increases aldosterone secretion increases sodium reabsorption increased BP

Question 34

inhibitors for renin angiotensin system?

Answer 34

increased Na/Cl reabsorption, angiotensin 2, vasopressin, increased BV

Question 35

what do the macula densa cells during regulation of renin angiotensin system do?

Answer 35

Stretch receptors present in arterial wall, increased stretch= increased BV and decreases renin secretion Increased angiotensin 2 formation, low BP baroreceptor reflex will be there, decreased blood flow to glomerulus decreased glomerulus filtration rate, so decreased Na+ in DT then macular densor cells are stimulated (paracrine action)

Question 36

what are the macula densa cells during regulation of renin angiotensin system?

Answer 36

a part of the distal convoluted tubule of the same nephron (juxta glomerular)

Question 37

what is the major action of renin?

Answer 37

split the decapeptide angiotensin 1 from the amino terminal end of angiotensinogen forms angiotensin 2

Question 38

what happens when angiotensin 2 is present?

Answer 38

increased aldosterone secretion increased sodium reabsorption increases BP restores renal perfusion pressure

Question 39

main points of renin angiotensin system?

Answer 39

Renin acts on angiotensin to convert it to angiotensin 1 (protein a2 globulin) so it is synthesized from liver and is in blood. Angiotensin 1 goes to capillaries in lungs and in endothelial cells capillaries of kidneys, then we have an enzyme called angiotensin converting enzyme (ACE) converts angiotensin 1 to angiotensin 2 (vasoconstrictor, increases Na+ abs)

Question 40

what else can ACE be used for?

Answer 40

Hypertensive patients receive ACE to reduce BP (decreases synthesis of angiotensin 2 so we decrease vasoconstriction= so we get vasodilation)

Question 41

where is angiotensin 2 formed?

Answer 41

in the blood

Question 42

what is the second messenger of angiotensin 2?

Answer 42

Ca2+

Question 43

what are the angiotensin 2 receptors?

Answer 43

AT1- blood vessels, heart, kidney, brain | AT2- fetus and neonates

Question 44

where is ANP released?

Answer 44

cardiac atrial muscles

Question 45

what stimulates ANP?

Answer 45

increased fluid volume/ BV, increased cardiac output, increased venous return stretch of atrial muscle

Question 46

ANP actions?

Answer 46

acts on kidney to increase Na+ excretion, inhibits reabsorption in renal tubules dilates afferent arterioles and relax mesangial cells in kidney increases capillary permeability decrease in BP