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Session 2 Flashcards

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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

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
A

Vasoconstriction if increased BP

Prevents transmission of high BP to glomerular capillary

Maintains normal glomerular capillary pressure

25
Myogenic mechanism at efferent arteriole
vasoconstriction if decreased BP Increased GFR
26
Tubuloglomerular feedback mechanism in high tubular flow
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
What happens when ATP is released in the Tubuloglomerular feedback mechanism in high bp
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
Tubuloglomerular feedback mechanisms in low bp
Release of prostaglandins- stop constriction of afferent arteriole renin released by juxtaglomerular cells
29
3 stimuli responsible for renin release by juxtaglomerular cells
Sympathetic nerve stimulation Decreased stretch of afferent arteriole Signals generated by macula densa cells in response to decreased NaCl delivery
30
What does systemic vasoconstriction do to renal blood flow
Reduces
31
What is the action of renin
Angiotensin 1 -> A2 -> Constriction of efferent arterioles -> Increased GFR
32
Renin key points
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
What do prostaglandins do
Acts on granular cells to release renin
34
things that cause release of renin
granular cells of JGA innervated by sympathetic system Wall tension in afferent arterioles falls Decreased Na+ to macula densa
35
What does Angiotensin 2 do
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
Other factors affecting Na+ resorption in low blood pressure
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
A significant reduction in BP may result in
Acute tubular necrosis
38
What adaptation do simple columnar cells have to help with resorption
Brush border- lots of villi
39
What adaptation do simple cuboidal epithelial cells have which helps to distinguish them from PCT cells
A wide lumen, no brush borders
40
What structure is formed from the merging of the collecting ducts and acts as the gateway to the cavity known as wider calyx
Papillary ducts of Bellini- open sieve like at area cribosa
41
Cavity of minor calyx is lined with
Transitional epithelium
42
Which region of the nephron is this from and what cells are these
Proximal convoluted tubule Brush border- simple cuboidal
43
Where is this and what are the cells
Descending limb of loop of henle Simple squamous epithelial
44
Where is this and what cells
Ascending limb of loop of Henle Simple cuboidal epithelial cells
45
Where is this and what Cells
Collecting duct Simple cuboidal epithelial cell
46
Clearance =
(Urine conc x urine flow rate) / Plasma conc
47
Secretion=
Excretion - filtration
48
Filtration rate =
Plasma conc x GFR
49
Excretion rate =
urine conc x urine flow
50
Excretion =
Filtration - (reabsorption + secretion)
51
What can be used as GFR
Clearance rate in something like inulin where it is not secreted or absorbed
52
What forces control capillary movement of plasma
Hydrostatic pressure in capillary Hydrostatic pressure in the Bowman’s capsule Oncotic pressure difference between capillary and tubular lumen Starlings forces
53
Hydrostatic pressure and colloid osmotic (oncotic) pressure due to
Water and then protein

Urinary (20 decks)

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