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Urinary > Lecture 6 - Control Of Body Fluid Volume And Osmolality > Flashcards

Lecture 6 - Control Of Body Fluid Volume And Osmolality Flashcards

1
Q

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

A

Macula densa cells

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2
Q

What cells doe the Macula densa cells send signals to?

A

Granular/juxtaglomerular cells

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3
Q

What substance do juxtaglomerular cells produce?

A

Renin

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4
Q

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

A

Prostaglandins

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5
Q

What system is stimulated when blood pressure is low?

A

RAAS (Renin-angiotensin-aldosterone system)

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6
Q

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

A

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

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7
Q

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

A

Angiotensin II

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8
Q

How does Angiotensin II increase BP?

A

Directly vasoconstriction efferent arterioles

Stimulates ADH production (aquaporin translocation in CD)

Stimulates thirst

Stimulates aldosterone production (zona Glomerulosa of adrenal gland)

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9
Q

How does aldosterone production increase blood pressure?

A

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

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10
Q

How does prostaglandins affect Na+ reabsorption?

A

Dilates afferent arteriole

Vasodilation
Leads to renin release (RAAS)

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11
Q

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

A

Cardiac atrial cells detect an increase in Extracellular fluid volume

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12
Q

How does ANP lead to decreased Na+ reabsorption?

A

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

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13
Q

How does ANP affect other factors regulating BP?

A

Vasodilates afferent arterioles increasing the GFR

Inhibits aldosterone secretion

Inhibits ADH release

Decrease renin release

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14
Q

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

A

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

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15
Q

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

A

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

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16
Q

What is pressure natriuresis?

What is pressure diuresis?

A

Increased sodium excretion in urine due to increased renal artery pressure

Increased water excretion in urine due to increased renal artery pressure

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17
Q

How does the kidney respond to increased BP summary?

A

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

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18
Q

How does the kidney respond to decreased BP summary?

A

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

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19
Q

What response does the kidneys have to Congestive Heart Failure?

A

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

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20
Q

Why is pulmonary oedema common with congestive heart failure?

A

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

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21
Q

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

A

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

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22
Q

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

A

Loop diuretics (furosemide)

ACE inhibitor (Enalapril)

Vasodilators

Nitrates

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23
Q

What is Hypervolemia?

A

Fluid overload

24
Q

What usually leads to Hypervolemia?

A

When theres high levels of sodium leading to water retention

25
Q

What often leads to Hypervolemia?

A

Kidney retention of Sodium and water

Excessive sodium or fluid intake
Cirrhosis
Hyperaldosteronism

26
Q

What are some symptoms of Hypervolemia?

A

Ascites
Pleural effusion
Pulmonary oedema

27
Q

What is Hypovolaemic shock?

A

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

28
Q

What are some symptoms of hypovolaemia?

A

Tiredness
Dizziness
Thirst

29
Q

What can lead to hypovolaemia?

A

Haemorrhage

Sepsis

30
Q

How can sepsis lead to hypovolaemia??

A

The widespread infection leads to widespread vasodilation

31
Q

Why does vasodilation occur in hypovolaemia?

How does this affect the kidneys?

A

Occur in vital organs like heart, lung and brain to maintain blood supply

Leads to acute tubular necrosis in kidney

32
Q

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

Why?

A

PCT

Very ATP sensitive since most reabsorption occurs here

33
Q

How does the body try to compensate for hypovolaemia?

A

Vasoconstriction

Increased strength of heart contraction (+ve inotropic response)

Increased heart rate (+ve chrontropic affect)

34
Q

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

A

Vulnerable organs undergo tissue hypoxia

Acute tubular necrosis

Acute kidney injury can develop to acute tubular necrosis

35
Q

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?

A

Prostaglandins

36
Q

How do you treat Hypovolaemic shock?

A

Give IV isotonic saline solution to restore extracellular volume

37
Q

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

A

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

38
Q

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

A

Arteriosclerosis of renal arteries

Hyaliniizzation of small vessels (looks glossy)

High BP can lead to Chronic Kidney Disease leading to reduced kidney size

39
Q

How can renal disease lead to hypertension?

A

Na+ and water excretion can be impaired

Renin may be stimulated to be

Renal artery stenosis

40
Q

How can renal artery stenosis lead to hypertension?

A

Reduced renal perfusion leads to excess RAAS activation

41
Q

What type of cells detect the plasma osmolarity?

Where these cells found?

A

Osmoreceptors in hypothalamus

42
Q

What pathways do the osmoreceptors stimulate?

A

ADH to reabsorb water

Thirst to take in more water

43
Q

What is the supraoptic nucleus?

A

Neurosecretory cells in the anterior pituitary that produce hormones like ADH

44
Q

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

A

Transported to posterior pituitary gland

45
Q

What type of hormone is ADH?

A

Peptide hormone

46
Q

What type of change in osmolality leads to ADH release?

A

Osmolality increase leads to ADH release

47
Q

How does ADH lead to decrease in Osmolality?

A

ADH binds to V2 receptor on the basal membrane of collecting duct cells

V2 = G coupled protein receptor (Gs)
Aquaporins fuse to luminal membrane

48
Q

How does an increase in osmolality affect ADH secretion??

How does a decrease in osmolality affect ADH secretion?

A

Increase = more ADH

Decrease = less ADH

49
Q

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

A

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

50
Q

When is thirst stimulated and then inhibited?

A

Stimulated when plasma Osmolality is increased (reduced ECF volume)

Stopped when the Osmolality returns back to its lower value

51
Q

When is thirst stimulated and then inhibited?

A

Stimulated when plasma Osmolality is increased (reduced ECF volume)

Stopped when the Osmolality returns back to its lower value

52
Q

How is ADH secretion affected in Diabetes Insipidus?

A

HYPOsecretion of ADH

53
Q

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

A

Polyuria
Thirst
Dehydration
Diluted urine
Dry mucuous membranes

54
Q

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

A

HYPERsecretion of ADH

55
Q

What are the effects of excess ADH from SIADH?

A

Fluid overload (oedema, ascites)

Weight gain (fluid mass)

Low urinary output

Conc urine

Hyponatremia

56
Q

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

A

Need to make Hypoosmotic urine (dilute urine)

Decrease ADH production

57
Q

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

A

Need to produce hyperosmotic urine (conc urine)

Produce ADH so water reabsorbed in CD

Urinary (24 decks)

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