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Urinary > Session 2 > Flashcards

Session 2 Flashcards

1
Q

Normal plasma glucose conc

A

2.5-5.5 mol/L

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2
Q

Virtually all filtered glucose is reabsorbed in the

A

Proximal convoluted tubule

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3
Q

Glucose Reabsorption by

A

Secondary active transport, driven by energy released from transport of sodium down its conc grad

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4
Q

What is Tm

A

Maximum tubular resorptive capacity for a solute

Limited number of Na+/glucose carriers

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5
Q

Why is glycosuria

A

When plasma glucose rises above 10mmol/L as in diabetes

Common in pregnancy as Tm for glucose falls and glucose is excreted in urine

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6
Q

Plasma conc of amino acids

A

2.5-2.5 mmol/L

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7
Q

Reabsorbtion and filtration of amino acids

A

Filter easily through glomerulus

Reabsorbed by proximal convoluted tubule by secondary active transport

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8
Q

Reabsorption by proximal convoluted tubule of amino acids

A

Symport with Na+, driven by Na+/K+ ATPase as with glucose

Tm limited process

5 different transport systems coupled with amino acid reabsorption

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9
Q

Sodium reabsorption in proximal convoluted tubule

A

Basolateral 3Na-2K-ATPase

Apical- Na H exchange, Co transport with glucose, AA, carboxyl is acids, phosphate

Aquaporin 1

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10
Q

Summary of proximal convoluted tubule

A

Reabsorption is isosmotic, responsible for bulk reabsorption of many solutes, very metabolically active, high conc of mitochondria, provide energy for Na/K ATPase

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11
Q

Beyond the loop of henle water permeability

A

Water permeability of early DCT is fairly low

Active Na+ reabsorption results in further tubular dilation- stimulated by aldosterone

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12
Q

Water permeability is variable depending on

A

ADH- low bp stimulated ADH increases water reuptake by aquaporin channels

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13
Q

Impaired ADH synthesis or secretion by hypothalamus can be due to

A

Brain injury, tumour, sarcoidosis or tuberculosis, aneurysm, encephalitis or meningitis

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14
Q

Not enough ADH can lead to

A

Not enough water reabsorbed from collecting ducts so a large quantity of urine is produced

Central diabetes insipidus - treat by ADH administration,

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15
Q

What is nephrogenic diabetes insipidus

A

Acquired insensitivity of the kidney to ADH

Water is inadequately reabsorbed from collecting ducts so a large quantity of urine is produced

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16
Q

Clinical management of nephrogenic diabetes insipidus

A

Low salt and protein diet reduces urine output

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17
Q

Causes of nephrogenic diabetes insipidus

A

Mutations in gene coding for V2 receptors, chronic pyelonephritis, Poly cystic kidneys, drugs such as lithium

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18
Q

What is too much ADH called

A

SIADH
Syndrome of inappropriate anti diuretic hormone secretion

Too much ADH released from PP gland or anther source

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19
Q

SIADH characterised by

A

Dilutional hyponatremia, plasma sodium conc lowered, total body fluid increased

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20
Q

2 mechanisms involved in auto regulation

A

Myogenic mechanism and tubuloglomerular feedback

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21
Q

Why is it important that the hydrostatic pressure within the glomerulus remains relatively constant

A

Doesn’t overload transporters

Maintains perfusion- stops kidney damage

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22
Q

Features of acute tubular necrosis

A

Reversible if quickly dealt with
Reduced oxygen and glucose getting to cells
Cells die, obstruction, back leak and tubular injury

23
Q

Explain myogenic mechanism

A

Arterial smooth muscle responds to increases and decreases in vascular wall tension

it is a property predominant of the preglomerular resistance vessels

24
Q

Myogenic mechanism at afferent arteriole

A

Vasoconstriction if increased BP

Prevents transmission of high BP to glomerular capillary

Maintains normal glomerular capillary pressure

25
Q

Myogenic mechanism at efferent arteriole

A

vasoconstriction if decreased BP
Increased GFR

26
Q

Tubuloglomerular feedback mechanism in high tubular flow

A

macula densa cells of DCT detect osmolality (rate of Na+ or Cl-)

higher flow of filtrate = higher Na+ conc in cells

Signal sent by Juxtaglomerular cells, due to increase in NaCl conc, ATP released

27
Q

What happens when ATP is released in the Tubuloglomerular feedback mechanism in high bp

A

ATP converted to adenosine, binds with A1 receptor on afferent arteriole

Further vasoconstriction of smooth muscle of adjacent afferent arterioles, Decreased renal perfusion pressure, decreased glomerular filtration rate

Renin synthesis inhibited

28
Q

Tubuloglomerular feedback mechanisms in low bp

A

Release of prostaglandins- stop constriction of afferent arteriole

renin released by juxtaglomerular cells

29
Q

3 stimuli responsible for renin release by juxtaglomerular cells

A

Sympathetic nerve stimulation
Decreased stretch of afferent arteriole
Signals generated by macula densa cells in response to decreased NaCl delivery

30
Q

What does systemic vasoconstriction do to renal blood flow

A

Reduces

31
Q

What is the action of renin

A

Angiotensin 1 -> A2 -> Constriction of efferent arterioles -> Increased GFR

32
Q

Renin key points

A

Enzyme that is synthesised and stored in JGA in kidneys. Fall in plasma Na+ leads to fall in ECF volume, causing release of renin

33
Q

What do prostaglandins do

A

Acts on granular cells to release renin

34
Q

things that cause release of renin

A

granular cells of JGA innervated by sympathetic system

Wall tension in afferent arterioles falls

Decreased Na+ to macula densa

35
Q

What does Angiotensin 2 do

A

Directly vasoconstricts efferent arterioles within glomerulus

Released ADH

Stimulate thirst

Stimulates zona glomerulosa of adrenal cortex to release aldosterone (directly increases Na+ reabsorption from DCT)

36
Q

Other factors affecting Na+ resorption in low blood pressure

A

Decrease in effective circulating volume= cortical prostaglandin synthesis. Occurs in kidney in cortex, medullary interstitial cells, collecting ducts epithelial cells

Results in vasodilators and renin release

37
Q

A significant reduction in BP may result in

A

Acute tubular necrosis

38
Q

What adaptation do simple columnar cells have to help with resorption

A

Brush border- lots of villi

39
Q

What adaptation do simple cuboidal epithelial cells have which helps to distinguish them from PCT cells

A

A wide lumen, no brush borders

40
Q

What structure is formed from the merging of the collecting ducts and acts as the gateway to the cavity known as wider calyx

A

Papillary ducts of Bellini- open sieve like at area cribosa

41
Q

Cavity of minor calyx is lined with

A

Transitional epithelium

42
Q

Which region of the nephron is this from and what cells are these

A

Proximal convoluted tubule
Brush border- simple cuboidal

43
Q

Where is this and what are the cells

A

Descending limb of loop of henle
Simple squamous epithelial

44
Q

Where is this and what cells

A

Ascending limb of loop of Henle
Simple cuboidal epithelial cells

45
Q

Where is this and what Cells

A

Collecting duct
Simple cuboidal epithelial cell

46
Q

Clearance =

A

(Urine conc x urine flow rate) / Plasma conc

47
Q

Secretion=

A

Excretion - filtration

48
Q

Filtration rate =

A

Plasma conc x GFR

49
Q

Excretion rate =

A

urine conc x urine flow

50
Q

Excretion =

A

Filtration - (reabsorption + secretion)

51
Q

What can be used as GFR

A

Clearance rate in something like inulin where it is not secreted or absorbed

52
Q

What forces control capillary movement of plasma

A

Hydrostatic pressure in capillary
Hydrostatic pressure in the Bowman’s capsule
Oncotic pressure difference between capillary and tubular lumen

Starlings forces

53
Q

Hydrostatic pressure and colloid osmotic (oncotic) pressure due to

A

Water and then protein

Urinary (20 decks)

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