Lecture 6 - Control Of Body Fluid Volume And Osmolality

Question 1

What cells of the DCT detect levels of Na+ and Cl- in the filtrate?

Answer 1

Macula densa cells

Question 2

What cells doe the Macula densa cells send signals to?

Answer 2

Granular/juxtaglomerular cells

Question 3

What substance do juxtaglomerular cells produce?

Answer 3

Renin

Question 4

What hormone do macula densa cells produce to stimulate renin release from Granular cells?

Answer 4

Prostaglandins

Question 5

What system is stimulated when blood pressure is low?

Answer 5

RAAS (Renin-angiotensin-aldosterone system)

Question 6

What are the 3 mechanisms by which renin is stimulated to be produced by by the granular cells?

Answer 6

Granular cells innervated by sympathetic system

Decreased BP means less tension in afferent arteriole wall + granular cells so renin released

Less Na+ reaches Macula densa, stimulates them to make prostaglandins which makes granular cells to make renin

Question 7

What is the important substance produced in the RAAS system which helps increase BP?

Answer 7

Angiotensin II

Question 8

How does Angiotensin II increase BP?

Answer 8

Directly vasoconstriction efferent arterioles

Stimulates ADH production (aquaporin translocation in CD)

Stimulates thirst

Stimulates aldosterone production (zona Glomerulosa of adrenal gland)

Question 9

How does aldosterone production increase blood pressure?

Answer 9

More ENAC channels expressed in DCT so more Na+ reabsorbed so later down the line more water reabsorbed

Question 10

How does prostaglandins affect Na+ reabsorption?

Answer 10

Dilates afferent arteriole

Vasodilation
Leads to renin release (RAAS)

Question 11

What leads to the production of Atrial Natriuretic Peptide (ANP)?

Answer 11

Cardiac atrial cells detect an increase in Extracellular fluid volume

Question 12

How does ANP lead to decreased Na+ reabsorption?

Answer 12

Inhibits Na+/K+ ATPase and closes Na+ channels in collecting duct and DCT meaning less Na+ reabsorbed so more water excreted with the Na+

Question 13

How does ANP affect other factors regulating BP?

Answer 13

Vasodilates afferent arterioles increasing the GFR

Inhibits aldosterone secretion

Inhibits ADH release

Decrease renin release

Question 14

How does hydrostatic pressure affect reabsorption of Na+ and Cl- in the PCT?

Answer 14

Higher the blood pressure (extra cellular fluid volume), the lower the oncotic pressure meaning less NaCl and water reabsorbed by the PCT

Question 15

What happens in terms of Na+ and water reabsorption when renal artery blood pressure increases?

Answer 15

Less Na-H+ antiporter in PCT so less Na+ reabsorbed
Causes Pressure natriuersis and pressure diuresis

Question 16

What is pressure natriuresis?

What is pressure diuresis?

Answer 16

Increased sodium excretion in urine due to increased renal artery pressure

Increased water excretion in urine due to increased renal artery pressure

Question 17

How does the kidney respond to increased BP summary?

Answer 17

ANP made (cardiac atrial cells) inhibits Na/K+ ATPase reducing ENAC expression
So less Na+ reabsorbed

Inc pressure in peritubular capillaries so get pressure natriuresis and pressure diuresis

Question 18

How does the kidney respond to decreased BP summary?

Answer 18

Prostaglandins released
RAAS system gets activated
ANGII made:
-constricts efferent arteriole
-ADH made
-thirst
-Alodsterone release which increases expression of ENAC (more Na+ reabsorbed)

Question 19

What response does the kidneys have to Congestive Heart Failure?

Answer 19

Heart cant cope with its workload so CO falls and fails to peruse the organs like kidneys enough
Makes the kidneys think blood pressure is low leading to mechanisms which lead to increased Na+ and water reabsorption

Question 20

Why is pulmonary oedema common with congestive heart failure?

Answer 20

Blood backs up in the left side of the heart due to CO falling

Blood therefore backs up in the Pulmonary veins leading to increased pulmonary venous pressure

So increased hydrostatic pressure in the pulmonary veins > oncotic pressure

Question 21

What is the aim when treating pulmonary oedema with congestive heart failure?

Answer 21

Reducing the workload of the heart by reducing the fluid load of the body

Question 22

What are the 4 ways pulmonary oedema can be treated in congestive heart failure?

Answer 22

Loop diuretics (furosemide)

ACE inhibitor (Enalapril)

Vasodilators

Nitrates

Question 23

What is Hypervolemia?

Answer 23

Fluid overload

Question 24

What usually leads to Hypervolemia?

Answer 24

When theres high levels of sodium leading to water retention

Question 25

What often leads to Hypervolemia?

Answer 25

Kidney retention of Sodium and water Excessive sodium or fluid intake Cirrhosis Hyperaldosteronism

Question 26

What are some symptoms of Hypervolemia?

Answer 26

Ascites Pleural effusion Pulmonary oedema

Question 27

What is Hypovolaemic shock?

Answer 27

When theres a large loss of fluids leading to a very low circulating volume of blood meaning organs not perfused properly

Question 28

What are some symptoms of hypovolaemia?

Answer 28

Tiredness Dizziness Thirst

Question 29

What can lead to hypovolaemia?

Answer 29

Haemorrhage Sepsis

Question 30

How can sepsis lead to hypovolaemia??

Answer 30

The widespread infection leads to widespread vasodilation

Question 31

Why does vasodilation occur in hypovolaemia? How does this affect the kidneys?

Answer 31

Occur in vital organs like heart, lung and brain to maintain blood supply Leads to acute tubular necrosis in kidney

Question 32

What part of the kidney is especially vulnerable to acute tubular necrosis? Why?

Answer 32

PCT Very ATP sensitive since most reabsorption occurs here

Question 33

How does the body try to compensate for hypovolaemia?

Answer 33

Vasoconstriction Increased strength of heart contraction (+ve inotropic response) Increased heart rate (+ve chrontropic affect)

Question 34

What condition can happen if the bodies compensatory response to hypovolaemia isn’t enough?

Answer 34

Vulnerable organs undergo tissue hypoxia Acute tubular necrosis Acute kidney injury can develop to acute tubular necrosis

Question 35

What is produced when the body is trying to compensate for hypovolaemia to prevent excess vasoconstriction to ensure the blood flow through kidney is maintained to ensure suffient GFR?

Answer 35

Prostaglandins

Question 36

How do you treat Hypovolaemic shock?

Answer 36

Give IV isotonic saline solution to restore extracellular volume

Question 37

Why do we give isotonic saline IV in patients with hypovolaemia?

Answer 37

Most water stays in the Extracellular fluid compartment (interstitium and plasma) since the sodium in the saline can move very freely between the ECF compartment and Intracellular compartment Therefore water stays in blood helping with hypovolaemia

Question 38

What are some pathological changes that can be seen as a result of renal hypertension?

Answer 38

Arteriosclerosis of renal arteries Hyaliniizzation of small vessels (looks glossy) High BP can lead to Chronic Kidney Disease leading to reduced kidney size

Question 39

How can renal disease lead to hypertension?

Answer 39

Na+ and water excretion can be impaired Renin may be stimulated to be Renal artery stenosis

Question 40

How can renal artery stenosis lead to hypertension?

Answer 40

Reduced renal perfusion leads to excess RAAS activation

Question 41

What type of cells detect the plasma osmolarity? Where these cells found?

Answer 41

Osmoreceptors in hypothalamus

Question 42

What pathways do the osmoreceptors stimulate?

Answer 42

ADH to reabsorb water Thirst to take in more water

Question 43

What is the supraoptic nucleus?

Answer 43

Neurosecretory cells in the anterior pituitary that produce hormones like ADH

Question 44

What happens to ADH once its been made in the supraoptic nucelus in the anterior hypothalamus?

Answer 44

Transported to posterior pituitary gland

Question 45

What type of hormone is ADH?

Answer 45

Peptide hormone

Question 46

What type of change in osmolality leads to ADH release?

Answer 46

Osmolality increase leads to ADH release

Question 47

How does ADH lead to decrease in Osmolality?

Answer 47

ADH binds to V2 receptor on the basal membrane of collecting duct cells V2 = G coupled protein receptor (Gs) Aquaporins fuse to luminal membrane

Question 48

How does an increase in osmolality affect ADH secretion?? How does a decrease in osmolality affect ADH secretion?

Answer 48

Increase = more ADH Decrease = less ADH

Question 49

What is the relationship with BP, Osmolality values and ADH secretion?

Answer 49

Lower the BP the lower the Osmolality can be before ADH is released? Higher the Bp the higher the Osmolality must be before ADH is released

Question 50

When is thirst stimulated and then inhibited?

Answer 50

Stimulated when plasma Osmolality is increased (reduced ECF volume) Stopped when the Osmolality returns back to its lower value

Question 51

When is thirst stimulated and then inhibited?

Answer 51

Stimulated when plasma Osmolality is increased (reduced ECF volume) Stopped when the Osmolality returns back to its lower value

Question 52

How is ADH secretion affected in Diabetes Insipidus?

Answer 52

HYPOsecretion of ADH

Question 53

What is the affect of having low ADH secretion on the body?

Answer 53

Polyuria Thirst Dehydration Diluted urine Dry mucuous membranes

Question 54

How is secretion of ADH affected in SIADH (Syndrome of Inappropriate ADH secretion)?

Answer 54

HYPERsecretion of ADH

Question 55

What are the effects of excess ADH from SIADH?

Answer 55

Fluid overload (oedema, ascites) Weight gain (fluid mass) Low urinary output Conc urine Hyponatremia

Question 56

What is the bodies response if the plasma Osmolality is low?

Answer 56

Need to make Hypoosmotic urine (dilute urine) Decrease ADH production

Question 57

What is the bodies response if the plasma Osmolality is high?

Answer 57

Need to produce hyperosmotic urine (conc urine) Produce ADH so water reabsorbed in CD