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Urinary > Session 4 > Flashcards

Session 4 Flashcards

1
Q

How does solute move across the PCT cells and enter interstitium

A

Solvent follows solute, solute transported primarily water follows passively

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2
Q

Driver for movement of solute across PCT cells into interstitium

A
  • Increased osmolarity of ICF as solute transported into PCT
  • Water from nephron lumen moves down gradient into PCT until equilibrated
  • Transient increase in ICF volume
  • 3Na-2K-ATPase moves Na+ into interstitium and water follows
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3
Q

What solute enters the cell across the luminal (apical) membrane

A

Sodium

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4
Q

What is the Net effect on the osmolarity of the PCT epithelial cells to the movement of sodium

A

No change as increased osmolarity of PCT cells means water follows

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5
Q

Which ions move in 3Na-2K-ATPase

A

3 Na+ out
2 K+ in

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6
Q

Primary driving force in interstitium for movement of solute and solvent from interstitium into peritubular capillaries

A

Hydrostatic pressure increased

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7
Q

Primary driving force in peritubular capillaries for movement of solute and solvent from interstitium into peritubular capillaries

A

Higher oncotic pressure (lower hydrostatic), left oncotic proteins behind

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8
Q

What is the function of the tight junctions between tubule cells

A

Barrier to prevent diffusion of transporter, channel and pump proteins between apical and basolateral membrane. Maintain polarity

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9
Q

Percentage and location of sodium iron reabsorption along nephron

A

PCT 67%
LOH asc 25%
LOH desc 0%
DCT 5%
CD 3%

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10
Q

Percentage and location of sodium ions and water reabsorption along the nephron

A

PCT 65%
LOH asc 0%
LOH desc 10%
DCT 0%
CD 5%

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11
Q

What causes release of renin

A

Fall in plasma sodium leads to fall in ECF volume

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12
Q

Renin is released by

A
  • increased sympathetic innervation (granular cells of JGA)
  • Wall tension in afferent arterioles fall, granular cells detect this which stimulates renin release
  • Decreased sodium to macula densa (if less NaCl reaches the macula densa, it i stimulated to secrete prostaglandins, acts on granular cells to simulate renin release)
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13
Q

Angiotensin II effects

A

Directly vasoconstricts efferent arterioles within the glomerulus

Stimulates zona glumerulosa of adrenal cortex to release aldosterone

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14
Q

What does aldosterone do

A

Directly increases Na+ reabsorption from DCT with ENAC channels

Releases ADH

Stimulate thirst

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15
Q

Prostaglandin synthesis

A

Decrease in effective circulating volume stimulates cortical prostaglandin synthesis

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16
Q

How does JGA respond if BP is high

A

ATP release

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17
Q

How does JGA respond if there is a drop in BP

A

Renin release, prostaglandin release

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18
Q

Prostaglandin synthesis occurs in

A

Cortex, medullary interstitial cells, collecting duct epithelial cells

Result in vasodilators and renin release

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19
Q

What is ANP (atrial natureric peptide)

A

Produced by cardiac atrial cells in response to an increase in ECF volume (high bp)

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20
Q

ANP acts to

A

-Inhibit Na+/K+/ATPase and close Na+ channels of CD and DCT, reducing Na+ reabsorption, water and Na+ excretion increased
- Vasodilate afferent arterioels increasing GFR
- Inhibit aldosterone secretion and ADH release
- Decrease renin release

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21
Q

What happens in high blood pressure to hydrostatic and oncotic pressure

A

NaCl intake increases so ECF increases

Hydrostatic pressure increases and oncotic pressure decreases, NaCl and water reabsorption by the PCT decreases

22
Q

Effectors of change in renal sodium excretion when renal artery BP increases

A

Reduced Na-H antiporter and reduced Na-K-ATPase activity in PT

Reduction in sodium resorption in proximal tubule (Glomerular tubular balance)

Reduction in water Resorption in PT

Pressure natriuresis and diuresis

23
Q

Summary of increased BP

A

Inhibits Na-K-ATPase and reduce ENAC expression
Decreased Na resorption DCT/CD
Increase in hydrostatic pressure of peritubular capillaries (pressure natriuresis and diuresis)

24
Q

Summary of decreased BP

A

Prostaglandin release
RAAS activated (ANG II causes constriction of efferent arteriole and release of aldosterone)
Aldosterone increases expression of ENAC, stimulates ADH and thirst

25
Q

Hypoperfusion due to congestive cardiac failure leads to

A

Na+ and water retention by the kidneys, leading to oedema, kidneys sense as hypovolemia, resulting in compensation by retaining NaCL and water to increase CFV

Stimulates low BP response

26
Q

Increased pulmonary venous pressure results in

A

Transudation from the capillaries in the lungs and in pulmonary oedema

Management involves reducing the fluid load e.g. diuretics, ACE inhibitors, nitrates, vasodilators

27
Q

First line diuretic

A

Furosemide

28
Q

What is hypervolaemia

A

Fluid overload, XS of total body sodium and water, leads to expansion of ECF compartment

29
Q

Hypervolaemia due to

A

Kidney retention of sodium and water
Reduced effective arterial volume e.g. CCF
XS sodium or fluid intake
Cirrhosis
Hyperaldosteronism

30
Q

Hypovolemia can lead to

A

Shock

31
Q

What is shock

A

A medical emergency in which the vital organs are not adequately perfused

Anaerobic metabolism and inefficient clearance of metabolites

Tiredness, dizziness, thirst

Vasodilation occurs in vital organs (heart lung brain) to maintain blood supply

Leads to acute tubular necrosis in kidney

32
Q

A severe decrease in circulating volume stimulates sympathetic activity to maintain BP by

A

Tachycardia
Peripheral vasoconstriction
Increase in myocardial contractility

33
Q

To counteract excessive vasoconstriction in Hypovolemic shock what happens in kidneys

A

Prostaglandins are secreted, maintains adequate blood flow through kidney and sufficient GFR

34
Q

2 major consequences of loss of large amounts of fluid

A

Volume depletion (decreases tissue perfusion), electrolyte and acid-base disturbances

35
Q

What is hypertensive renal disease

A

Renal autoregulation maintains Renal function despite variations in systolic BP

Arteriosclerosis of major renal arteries, hyalinization of small vessels with intimal thickening

Can lead to chronic renal damage (hypertensive nephrosclerosis) and a reduction in the size of the kidneys

36
Q

Renal causes of secondary hypertension

A

Impaired Na+ and water excretion increasing blood volume

Stimulation of renin release

Renal artery stenosis, reduces perfusion of kidney, XS RAAS

37
Q

Negative feedback loop for ADH

A

Increased ADH causes decreased renal water excretion

Decreased osmolarity inhibits ADH secretion

Negative feedback loops that begin with the anterior hypothalamus

38
Q

Changes in BP have an effect on the

A

Response to changes in osmolarity

(Volume is more important)

39
Q

Thirst is stimulated by

A

Increase in plasma osmolarity

40
Q

Symptoms of diabetes insipidus

A

Polyuria, polydipsia, low urine osmolality (dilute)

41
Q

Too little ADH in diabetes insipidus is

A

Inability to reabsorb water from the distal part of the nephron due to failure of secretion or action of ADH

42
Q

What is hypernatremia

A

Less prevalent clinically
More than 140mmol/L

43
Q

Causes of hypernatremia

A

Osmotic diuresis
Fluid loss without replacement
Diabetes insipidus
Incorrect intravenous fluid replacement
Primary aldosteronism

44
Q

Features of hyponatremia

A

Low sodium very common in hospital patients

Serum conc of Na lower than
130/135mmol/L

Symptoms: neurological, agitation, nausea, focal neurology, coma

45
Q

Causes of hyponatraemia

A

Diuretics
Water overload or retention
Increase in ADH secretion
Increased plasma osmolality
Increased plasma osmolality
Diuretics/renal failure
Peritonitis/Burns
D and V

46
Q

Hyponatraemia is generally caused by

A

Water loss than sodium directly

47
Q

Reference range of serum osmolality

A

275-295 mosm/kg

48
Q

How do you calculate osmolarity

A

2 Na + glucose + urea (all in mmol/L)

49
Q

What does hypovolemic hyponatremia tell us

A

Nonrenal loss e.g. GI, sweating, ascites, burns, cerebral salt-wasting syndrome

50
Q

People with inappropriate ADH secretion are generally

A

Uvoelemic

51
Q

Treatments for hyponatraemia

A

Fluid restriction

Pontine demyelination can occur with rapid correction

Infusion of hypertonic saline and furosemide

Urinary (20 decks)

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