• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/22

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

22 Cards in this Set

  • Front
  • Back
Describe basic renal processes (6)
1. Glom. filtration in Bowman's capsule
2. 70% filtrate reabsorbed in proximal tubule
3. High salt conc by active transport in Loop of Henlé
4. Secretion/reabsorption in distal tubule
5. control osmolarity of urine in collecting duct
6. Ureter
describe glomerular filtration (4)
1. each afferent arteriole divides to multiple capillary branches (tuft of vessels: large SA) forms 1 glomerulus

2. in Bowman's capsule (blind end/origin of nephron). Blood in glomerular capillaries and filtrate in Bowman's separated by 2 layers of epi cells, sharing a BM. BM thus is main barrier to filtration

3. Ultrafiltration: capillary pressure gradient to tubule forces water to filter from blood through membrane into lumen of Bowman's. Soluble substances also enter tubule depending on size and charge.

4. Glycoproteins on surface of glom. capillary cells negatively charged.
to what extent may substances enter tubule with the water in glomerular filtration? (2)
1. SIZE (ø)
< 4 nm (enter freely)
4-8 nm (partial entry)
> 8 nm (excluded)

2. CHARGE
~ -ve charged filter < half rate of neutral substances
~ +ve charged filter slightly > rate than neutral substances

∴ albumin (-ve, ø 7nm) doesn't filter through 8 nm pore
what is the net effect of glomerular filtration
1. water filtered, 125 mL/min or 180 L
2. cells completely retained
3. plasma proteins completely retained
4. small molecules and ions enter freely
~ Na+ radius 0.1 nm
~ Cl- radius 0.2 nm
~ glucose radius 0.3 nm

5. charge has no effect on very small ions
why may there be increased glomerular permeability? (2)
1. physical enlargement of pore

2. loss of -ve charged glycoprotein from surface of capillary cells e.g. nephritis [hence albuminuria]
how to control glomerular filtration? (3)
balance between
1. forces pushing fluid out of capillary
2. forces drawing fluid into capillary
3. filtration constant

too high: excessive loss of water and solute
too low: inadequate excretion of waste products
how to calculate filtration (hence GFR?)
Filtration = K [(Pgc - Pbc) - (πgc - πbc)]

1. K: filtration coefficient (permeability x SA)
2. Pgc: glomerular capillary blood pressure (constant along the whole capillary)
3. Pbc: Bowman's capsule fluid pressure
4. πgc: glomerular capillary oncotic pressure (rises along the capillary)
5. πbc: Bowman's capsule oncotic pressure

net filtration P = 15 mmHg at arterial end, may reach 0 mmHg at venous end
what forces favour filtration? (2)
1. Glomerular capillary blood pressure
2. Bowman's capsule Oncotic pressure
what forces oppose filtration?
1. glomerular oncotic pressure
2. Bowman's capsule fluid pressure
How to change GFR?
1. a, b, c
2. a, b
3. a, b
1. Change Pgc
a. constrict/dilate afferent or efferent arteriole
b. constrict afferent arteriole ↑Raff, ↓Pgc, ↓GFR
c. constrict efferent arteriole ↑Reff, ↑Pgc, ↑ GFR
[if both aff & eff arteriole constrict, capillary pressure remains unchanged but flow decreases

2. Change plasma oncotic pressure
a. dehydration leads to ↑πc and ↓GFR
b. starvation leads to ↓πc and ↓GFR

3. Change in filtration coefficient
a. change SA for filtration (no. of perfused capillaries)
b. contract mesangial cells (reduce perfusion of cap.)
How to regulate GFR?
(2 mechanisms)
1. (6)
2. (7)
tubuloglomerular feedback: change in GFR sensed and Pgc adjusted to return GFR to previous value.
If renal blood flow changes a lot, GFR can't be kept constant
2 mechanisms

1. ↓ NaCl delivered to macula densa (NaCl arrives at macula densa in DCT at proportional rate to GFR)
2. ↓ NaCl uptake and ATP breakdown
3. ↓ adenosine
4. ↓ afferent arteriole vasoconstriction
5. ↑ Pgc
6. ↑ GFR

a. ↓ Na+ & Cl- at macula densa cells
b. renin secreted from JG cells
c. angiotensinogen → angiotensin I
d. angiotensin I → angiotensin II (with ACE)
e. ↑ efferent arteriole vasoconstriction
f. ↑ glomerular capillary pressure
g. ↑ increase GFR
function of tubular cell (4)
They may
1. reabsorb some or all of substance back to blood
2. secrete more of substance to filtrate
3. do both: reabsorb in one part of tubule, secrete in a different part.
4. active transport of charged substances by epithelial cells creates potential difference between tubule lumen and ECF
what is reabsorbed in tubule?
~179/180 L of filtered water reabsorbed
~concentration of substances in filtrate ↑ as water removed (provides conc. gradient for passive reabsorption processes)
what are tubule walls made of?
single layer of tight epithelial cells,
~ providing minimal barrier to transport
~ controlling transport processes.
transport mechanisms of renal tubules
1. simple diffusion
~ driving force is concentration gradient
~ no carriers required

2. facilitated diffusion
~ driving force is concentration gradient
~ carriers required

3. primary active transport
~ uses ATP to transport substance
~ carrier pump required

4. secondary active transport
~ carrier transports a substance, plus another substance down conc. gradient
~ energy sets up conc. gradient for 1 substance
PCT transport mechanisms
iso-osmotic reabsorption of 70% (65-85%) filtered fluid
~70% filtered water
~70% Na+, Cl-, HCO3(-)
~all filtered K+, HPO4(2-)
for reabsorption processes, state how it is transported at the basolateral border and luminal border:
1. Na+ reabsorption
2. K+ reabsorption
3. Cl-, glucose, amino acid reabsorption
4. Water reabsorption
1. (B) active transport, Na+/K+ pump
(L) facilitated diffusion: subject to tubular maximum (transport maximum: if all available carriers saturated no further in ↑ in reabsorption occurs)
affects susbstances w. relatively few transporters: Na/glucose cotransporter

2. (B) passive diffusion through K+ channels
(L) active transport

3. (B) diffusion, Na+/K+ pump for Na
(L) co-transport with Na+ (sec. active transport)

4. (B) osmosis
(L) osmosis
what happens in the loop of henle (2)
1. salt transported out of loop to interstitial space

2. fluid leaving loop and entering DCT is hypotonic to plasma
what are the DCT transport mechanisms? (3)
1) 5% water reabsorbed
2) further Na+ reabsorption, K+ secretion
3) Aldosterone modifies extent of salt secretion/reabsorption
for reabsorption processes, state how it is transported at the basolateral border and luminal border:
1. Na+ reabsorption
2. K+ secretion
3. K+ reabsorption
4. Cl- reabsorption
1. (b) Na+/K+ pump if aldosterone present
(l) facilitated diffusion, pump pumps out Na+ which then enters at luminar border

2. (b) Na+/K+ pump if aldosterone present
(l) diffusion~passes through channels

3. (b) diffusion through basolateral channels to be reabsorbed.
(l) active transport if no aldosterone

4. (b) diffusion
(l) co-transport with Na+
what happens in the collecting duct (3)
1. little more Na reabsorption in uppermost part of collecting duct

2. Na crosses apical membrane using mainly epithelial Na channel (contrast to few of these channels in PCT/DCT: those were predominantly NaCl cotransporter)

3. water reabsoprtion under hormonal control
what is the distribution for Na reabsorption in the kidney?
1. 67% from proximal tubule
2. 25% from loop of Henle
3. 5% from distal tubule
4. 3% from cortical collecting duct

proportions depending on hormones present