Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Health.1 > Renal Physiology > Flashcards

Renal Physiology Flashcards

1
Q

3 Major functions of the kidney

A
  1. Filtration: removal
  2. Production
  3. Regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the 2 major waste products produced by body, cleared by kidneys

A

a. Ammonia NH3.

b. creatinine- made during muscle breakdown.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

whats creatinine used to indicate and what may create false positive/negative values?

A

muscle mass= relatively same day to day- indicates kidney func.
high= malfucntion

levels altered by: eating too much meat/excessive exercice/lean muscle mass in elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

why and how (outline) does kidney regulate body fluids?

A

volume (post.pituitary), conc, distribution of body fluid - homeostasis

Renal glands (aldosterone release) and brain (ADH release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

whats normal amount water in body and how do kidneys control conc + vol?

A
  • 40-45L water in body dont want to go above/below: de/overhydration
  • kidneys control urine vol thus conc
  • excess water- removed in dilute conc vice versa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

tonicity of solutions and effect on RBC

A

isotonic: normal in RBC cytoplasm
hypertonic: RBC shrivel as water leaves
hypotonic: RBC swell as water comes in

water travels by osmosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

location and compositions (%) of fluid compartments in average 70kg male?

A

total body water:45L 60% of body weight

extracellular fluid (ECF): 15L, 20%

  • plasma: 3L, 20% of ECF
  • Interstitial (IF): 12L, 80% of ECF

intracellular fluid (ICF):
-30L, 40% body weight
majority

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the functional barrier surrounding

a) plasma (also ECF)
b) ICF?

what do kidneys have access to?

A

a) capillary andothelium
b) cellular membrane

kidneys: control vol of all 3 compartments BUT only access to plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what pressures (+forces) regulate continuous exchange and mixing of body fluids?

A

hydrostatic and osmotic pressures

Starling’s forces: water and electrolytes freely cross, move by diffusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

process of fluid moving out of: plasma

A

starlings forces mmHg
drive DIFFUSION
changes in HP=fluid movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

effect of different amounts of ions in plasma, interstitium, intracellular on fluid osmolality

A

no effect.

although ions in different amounts, fluid osmolality still approx. 285mOsm/Kg/H2O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why are plasma and interstitial fluid compartments of ECF similar?

A

separated by only capillary endothelium- freely permeable to small ions.

but difference in ECF and ICF: plasma more protein, K+ = main cation of ICF
Na+K+ATPase=maintains distribution differences across plasma memb.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what 2 forced determine free and rapid movement of water between various fluid compartments?

A 
hydrostatic pressure (heart pumping)
osmotic pressure (exerted by plasma proteins - oncotic pressure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

effect of adding hypotonic NaCl IV infusion to ECF

A

osmolality of ECF decreases = water moves into ICF by osmosis: low to high solute conc.

after osmotic eqm,ICF and ECF osmolalities equal but volumes increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

effect of adding hypertonic NaCl IV infusion to ECF

A

osmolality of ECF increases = water moves out (low to high solute conc)- ICF –> ECF

after osmotic eqm,ICF and ECF osmolalities equal but ECF volume increased and ICF decreased

look at picture in lec notes last slide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

name 3 things that get filtered through kidney

A
  • metabolic waste: nitrogenous, excess ions. produced in body/excess from diet
  • drugs
  • toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

4 things produced in kidney and roles?

A
  • renin: BP
  • erythropoietin: RBC maturation. hormone made if anemic
  • prostaglandin: blood flow in the kidney. PGE2: vasodilation.
  • Vit D (Calcitriol-active form): made by cholesterol, activated in kidney
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what does the kidney regulate?

A
  • body fluids
  • Vol of extracellular fluid
  • Osmolal of bf
  • conc of electrolytes
  • blood pH- acid-base balance
  • BP
  • RBC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how is ammonia made and cleared from kidneys?

A

made from protein catabolism.
toxic, water soluble.

convert to urea (aa breakdown) -> uric acid (nucleotide breakdown)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what do high serum creatinine levels suggest?

A

serum levels= test of kidney function. high = impairment/disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why does kidney need to regulate body fluids: osmolality?

A
  • extreme variation=cells shrink/swell/burst

- damage cell struc and disrupt normal cell function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

normal kidney/ body osmolality?

A

285mOsm/Kg water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what do changes in HP =

A

continuous fluid movement between plasma and IF and IF and cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

process of fluid moving out of: ICF

A

osmotic pressure mosm/kgH2O
H2O free movement, not ions
OSMOSIS
changes in ionic content of IF =water movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what allows fluids in and out of cells?

A

no HP gradient across cell memb, only osmotic pressure diff between ICF and ECF = fluids in and out of cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what does plasma memb have that means fluids can easily cross?/permeate

A

plasma memb has h2o channels (aquaporins) = easily cross memb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Part 2: Glomerular filtration

basic kidney anatomy: what is the

a) inner layer called
b) outer layer called?

A

a) medulla

b) cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

the kidney is covered by what?

A

transparent fibrous renal capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

5 parts in the kidney

A
  • 5-8 renal pyramids
  • renal columns
  • renal papilla
  • renal pelvis: urine to ureter
  • ureter: urine to bladder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

where are the major blood vessels contained in the kidney?

A

renal columns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

where empties into renal papilla?

A

all urine filled collecting ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are nephrons?

A

functional units of kidneys-

hollow tubes. closed at proximal end and open at distal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

role and length of nephron?

A

a) each is its own unit, produces miniscule amounts of urine

b) 3-4mm long

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

3 main regions of nephron?

A
  • renal corpuscle
  • tubule
  • collecting tubule
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

a) what 2 structures are in the renal corpuscle?

A

bowmans capusles

glomerulus (capillaries)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

b) 3 structures in the tubule

A

PCT
loop of henle
DCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what regions of nephron found in the renal medulla?

A

LoH, collecting ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what enters the nephron and what leaves?

A

fluid (filtrate) in and urine out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what structure(s) modify the fluid passing through the nephron?

A

lining of nephron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what does the glomerulus provide?

A

capillaries that provide blood for filtration- enters in the coiled networks of capilalries with large pores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what leaves the nephron? specifically

A

urine: toxic urea, nitrogenous waste products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

name the first process of urine formation

A

glomerular filtration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what filters out of the capillaries into bowmans space?

A

plasma, low MW substances, electrolytes etc.

anything but blood cells and proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

where is glomerulus structure found?

A

sits inside bowmans capsule- filtrate collecting bag.

fist in a balloon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what arrives at glomerulus and what leaves?

A

arriving: afferent arteriole
exiting: efferent arteriole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

2 layers of BC and which one touches the glomerulus?

A

Parietal: outer wall
Visceral: inner wall, lines glom capillaries. !

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

where are podocytes found?

A

highly specialised epithelial cells of visceral layer of BC.

wrapped around glom capillaries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

role of podocytes?

A

along with the monolayers of fenestrated endothelium lining caps and glom basement in between,
form the filtration barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what 3 layers of filtration barrier does plasma pass through to get from glom to BC?

A

fenestrated Endothelial cells: line glom caps that have large pores.

basement membrane: v thick fibrillar layer

podocytes:epithelial cells of BC visceral layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what helps plasma getting forced through pores in the fenestrated endothelial cells of the filtration barrier?

A

high hydrostatic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

why does the basement memb of filtration barrier exclude proteins on size and negative charge?

A

the BM has negatively charged proteoglycans on it

  • stops - passing through
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what molecules can filter through the - charged basement memb into BC space?

A

+ charged molecules attracted to BM and uncharged mols.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

why is blood pressure crucial for renal function?

A

need high pressure in glomeruli for filtration.

wide afferent arteriole and narrower efferent generates a high hydrostatic pressure in caps = favour net filtration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what does high hydrostatic pressure in capillaries ensure?

A

glom filtration.

plasma forced into nephron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Starlings forces in capillaries- what causes outward filtration? (fluid leaves)

A

HP (of blood in caps) > OP (of BC = 0)
AA wider and longer than EA no proteins filtered

towards arteriole end (left)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Starlings forces in capillaries- what causes inward filtration? (fluid enters)

A

OP (of caps) > HP (of filtrate in BC)
proteins in blood drawn fluid back fluid entering nephron, getting fuller with filtrate, pushed back to caps

towards venule end (right)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

why is net fluid outward = net fluid in, not favoured for nephron?

A

= no fluid accumulation inside, eqm.

- wont make urine. makes cap OP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

where does the fluid filtered out of glomerulus go to?

A

high HP = fluid filtered out –> BC –> PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what would the starlings forces be for outward fluid movement?

A

glom HP: 50mmHg - out of glom
glom OP: 25mmHg - into
BC HP: 15mmHg - into
BC OP: 0mmHg -x

net filtration = 50-25-15-0 = 10mmHg
shoved out (HIGH HP) due to long efferent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

why is glomerulus capillary HP 50mmHg (greater than normal cap: 35mmHg)?

A

due to narrow and long efferent

afferent arteriole, which delivers blood to the glomerulus, has little vascular resistance because it is short and wide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

regarding water, elecs, glucose, waste products, how does glom filtrate composition compare to plasma?

A

identical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

why is albumin (69,000Da) not filtered and kept out of filtrate?

A

filtration barrier cut off = 70,000Da.

Albumin also - charged= repelled by BM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what is difference in appearance of plasma and glom filtrate?

A

the blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

3 main causes of proteinuria (protein in urine)

A
  • diabetes mellitus: high plasma gluc-damage filter
  • hypertension: high glom HP damage filter
  • glomerulonephritis: inflamm damage from immunological attack
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what is proteinuria and how detected?

A

proteinuria: protein in urine due to filtration barrier disrupted.

detected in urinalaysis- dipstick test.
green instead of yellow for proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

proteinuria: how do the proteins enter urine?

A

leak out form glomerulus into bowmans capsule due to disruption in filtration barrier for 3 reasons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what condition may cause decreased plasma protein levels on fluid movement across capillaries and affect?

A

increased BP/ diabetes.

loss from plasma > gain to plasma instead of =.
imterstitial fluid vol increases= oedema

decrease in plasma proteins lowers plasma OP.
HP > OP: fluid moves out normal

here, glom damaged, protein leaks out into urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

consquences of excessive proteinuria? (3)

A

low level protein in plasma = oedema
* swolled around eyes, hands, feet

frothy/bubbly urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

whats GFR and what does it tell us?

A

fluid volume filtered from renal glom caps into BC during certain period of time.

overall index of renal function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

normal GFR by both kidneys a min and a day?

A

125ml/min or 180L/day

must be maintained. will change if kidneys not working well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

how many times a day is the plasma in body filtered?

A

60 times a day

3L plasma but GFR is 180L/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what is urine and how much excreted a day?

A

non-reabsorbed filtrate that leaves kidneys/ minute

GFR x %(above) = 0.8%
0.8% x 125 = 1ml urine/ min or 1.5L urine/day

99% goes back into body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

why ECF composition precisely regulated?

A

plasma reg precisely and often = urine often v important for removing unwanted substances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

GFR depends on increased HP

consequence of:

a) GFR too high
b) GFR too low

A

a) needed substances not reabsorbed quickly, lostin urine. (goodies in urine)
b) everything reabsorbed inc waste (baddies in blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Part 3: tubular function - PCT

what are the 4 basic renal processes that occur for filtration in nephron?

A
  1. glom filtration
  2. tubular reabsorption
  3. tubular secretion
  4. excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

how is urine volume formed calculated?

approx how much is it a day?

A

Urine = Filtered - Reabsorbed + Secreted

1.5L urine a day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

why is all the plasma not filtered?

A

How much plasma is filtered by the kidneys?
About 20% of the plasma volume passing through the glomerulus at any given time is filtered

would lead to sludgy cells leaving EA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Filtration, Reabsorption, Secretion (Urine).

what is the filtrate?
whats ultrafiltrate?

A

the plasma filtered from glomerulus into BC.

ultrafiltrate: whats left after cells, proteins, large mols filtered out of glomerulus. similar to plasma but no proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what drives filtration?

filtration is non selective

A

Starlings forces

HP forces plasma to BC.
everything gets through

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Filtration, Reabsorption, Secretion (Urine).

what is reabsorption and whats reabsorbed?

A

selective process.

solutes and water needed by body brough back in from PCT filtrate, into peri-tubular caps.

  • organic nutrients (gluc, aas)
  • inorganic ion if not excess
  • water if not excess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what is reabsorption driven by?

A

active transport, diffusion, osmosis, starlings forces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Secretion is a 2nd chance to…?

A

actively eliminate unwanted substances from blood into urine.
only 19-20% filtered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is secreted from blood to urine?

A
  • nitrogenous waste( NH3, creatinine, urea, uric acid)
  • inroganic ions if excess
  • unwanted drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

where are secreted substances moved from and to?

and what is the process driven by?

A

from peritubular caps into PCT lumen.

active transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what is the busiest part of the renal nephron and why?

A

PCT as most (2/3) reabsorption happens- lots of substances too valuable to risk losing by waiting later on.

all filtrate passing through and A LOT is reabsorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

how is pct specialised for reabsorption?

A

PCT = approx 1/3 length of nephron and has increased SA due to brush border on tubular cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

PCT: whats reabsorbed?

A
  • ions: 65%
  • water: 65%
  • glucose: ALL
  • AAs: ALL
  • vitamins: ALL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what 2 types of reabsorption processes can take place in PCT and how do they differ?

A

active reabsorption: uses ATP energy

passive reabsorption: e.g. osmosis high–>low solute conc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

why is the same amount (65-67%) ions and water reabsorbed in the PCT?

A

same % as move together.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

difference between clearance and excretion of drug?

A

clearance: VOLUME OF BLOOD (vol) cleared of drug per unit of time.
excretion: AMOUNT OF DRUG (mg) excreted over period of time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what does the clearance of drug depedn on? 5

A
  • whether drug filtered/secreted/reabsorbed
  • GFR
  • structure of drug
  • age
  • disease
    …
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

whys it important to know clearance rates of drugs?

A

determines dosage- correct to maintain plasma conc and = therapeutic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

affect of renal function on clearance and plasma half life?

A

LOW renal func = LOW clearance and HIGH plasma half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

whats meant by

a) high clearance
b) low clearance

A

a) rapid elimination from blood by kidneys

b) inefficient excretion. only administer low levels tomaintain level in blood and prevent ADRs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

effect of low GFR from malfunctioning kidneys on clearance and dose of drug?

A

low GFR with age/disease etc = low clearance = may need to increase dose of drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what does PCT have a lot of for driving the reabsorption process?

A

mitochondia for energy

also brush border: increase absorptive capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

why do DCT cells look like they have alarger lumen than PCT cells?

A

absence of brush border (which increases surface area) on DCT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

2 methods of reabsorption transport through PCT to the peritubular capillary?

A

1: transcellular (straight through)
- across apical memb
- through tubular cell cytosol
- across basolateral memb
- through interstitium to blood vessels

2: paracellular (between)
- through leaky ‘tight’ junctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

with transcellular reabsorption, why does the substance move into blood vessel passively by diffusion once in the interstitium?

A

when in interstitium, conc is higher than in peri-tubular caps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

how are peritubular caps specialised for allowing reabsorption of substances back into them?

A

more porous than normal caps
have v low Blood pressure (as theyre second set of caps)

= good at allowing material to diffuse back into them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

role of Na+K+ATPase pump?

A

pumps approx 100 Na+ ions per second
establish ionic gradient across tubular cell membrane.

Na+ pumped out of cell = intracellular Na+ lowered
= driving force for reabsorption of Na+ from filtrate to tubular cells, then out into blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

what can the entry of Na+ through Na+K+ATPase also bring?

A

other solutes in too, which can be transported by ‘secondary active transport’ process with reabsorbed Na+ (symport).

grabs Na+ out of filtrate and likely to grab glucose too

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

why and how (literally) is Na+ reabsorbed?

A

non-selective

high Na+ conc = use ATP to move out, can take glucose with it :)
dont want to leave valuable nutrients till end to reabsorb.

movement of water by osmosis highest if NA+ absorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q
  1. using the Na+K+ATPase, what is energy invested in ?
A
  • to get Na+ out of filtrate and create Na+ electrochemical gradient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

where are the 3Na+ molecules pumped out of by Na+K+ATPase in exchange for 2K+?

A

from the basal and basolateral side of tubular cell.

the high [Na+] conc in interstitium diffuses into blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

process by which sodium enters into proximal tubule cell from lumen and how moved in interstitium?

A

through Na channels, moving down its electrochem gradient.
by diffusion,
pumped into interstitium by Na+K+ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

what else happens when Na moves down its EC gradient (from tubule lumen into proximal tubule cell)?

A

glucose pulled into cells too using SGLT1 and SGLT2 co-transporter channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

where from and how does glucose diffuse out of proximal tubule cells?

A

out of the basolateral side of the cells using GLUT2 channel

Na pumped out by Na+K+ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

what channel is used to exchange NA+ for H+ in PT cell?

A

Na+/H+ anti-porter- Na+ exchanged for H+.

Na+ pumped out by Na+K+ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

How is CO2 and H2O formed in the tubule lumen?

what does the process require?

A

secreted H+ combines with filtered HCO3-. = CO2 and H2O.

requires carbonic anhydrase located on apical brush border of PCT tubulae cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

what happens to the CO2 produces from H+ and HCO3- using carbonic anhydrase in the tubule lumen?
where will it exit from after this?

A

CO2 diffuses into tubular cell and recombines with H2O –> HCO3-: exits cell from basolateral side and diffuses into blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

what is reabsorbed into the peritubular capillary? (2) from diagrams

A

HCO3- and Na+.

recycled- (reabsorb bicarbonate H2CO3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

the equation for substances being filtered at PCT? (acid base transport)

A

CO2 + H2O ⇌ H2CO3 ⇌ HCO3− + H+

Slow Fast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

why are carbonic anhydrase enzymes critical for HCO3− reabsorption and the creation of new HCO3−?

A

The carbonic anhydrase enzymes effectively bypass the slow reaction in the sequence CO2 + H2O ⇌ H2CO3 ⇌ HCO3− + H+
(first bit)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

what process and route(s) does water reabsorption in the PCT occur by?

A

osmosis.

paracellular and transcellular (AQP1 aquaporin 1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

why is water obliged to follow sodium into peritubular capillary?

A
  • Na+ moves down EC grad due to ATPase
  • many substances co-transported
  • H2O reabsorbed by osmosis- many solutes (Na+) been reabsorbed and H2O obliged to follow as low Na+ conc inside.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

what happens to conc of solutes left in filtrate and what is now moved?

A

conc of solutes left increases in filtrate. now move down chem gradient by diffusion.

filtrate conc > blood = gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

how do the following travel from PCT tubule lumen into cell and peritubular capillary?

a) lipids
b) Cl-, K+, Ca2+….

A

a) transcellularly

b) paracellularly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

which 2 processes in ‘Na+ reabsorption aids reabsorption of water and many other solutes’ are active?

A

1: Na+ in and K+ out of peritubular cap into PCT via ATPase = PRIMARY ACTIVE
2. Na+ and something else cotransported into PCT= SECONDARY ACTIVE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

which 2 processes in ‘Na+ reabsorption aids reabsorption of water and many other solutes’ are diffusion?

A

lipids and ions, urea… via trans/paracellular pathway:

PASSIVE DIFFUSION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

what process in ‘Na+ reabsorption aids reabsorption of water and many other solutes’ is driven by passive osmosis?

A

water following Na+, into peritubular cap from PCT lumen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

what 2 molecules weakly/not absorbed in PCT?

A

urea and Cl-: conc higher at end of PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

what 6 molecules absorbed from PCT?

A
  • water
    -Na+
    -K+
    -H3O-
    same conc at end of PCT
strongly:
-glucose
-amino acids
           none at end of PCT
(done at start)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

how is there same osmolality at beginning and end of PCT if volume decreases?

A

35 things in 1L = approx same as 12 things in 350mL

change in volume AND concs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

how does filtrate remain isotonic with plasma by end of PCT despite going through glom filtration etc?

A

squash through sieve analogy:
filtrate not diluted or reabsorbed = same conc and osmolality.

non-selective filtration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

what is reabsorption of water by osmosis linked to? in context of PCT?

A

reabsorption of solutes.

obligatory H2O movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Part 4: tubular function - LoH

What is the role of the ‘straight nephron’ inland animals adapted from aquatic, and why is it needed?

A

glom: filters plasma
PCT: reabsorbs good things and water -65%

ensure max water absorption as water reabsorbed from plasma not sufficient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

what is the LoH (loop of henle) designed for?

A

looped region of nephron- has countercurrent flow inside it- going in opposite directions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

what does the filtrate going around the LoH and changing concentrations as it moves down descending and up ascending limb, contain?

A

water and solutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

role of LoH (regarding other structures of nephron too)?

A

creates a hyperosmotic medullary inetrstitium to ensure maximum water rebasorbed form LoH, but primarily from DCT and collecting ducts!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

the water absorbed in LoH is taken up by?

A

specialised blood vessels: vasa recta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

where is filtrate osmolality highest in the nephron? what does this mean?

A

at bottom of LoH 1200mOsm/kg/water. = means water mustve come out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

at which site of nephron is the filtrate:

a) hypotonic with plasma
b) hypertonic with plasma

A

a) top of and after LoH, just before DCT. 90mOsm

b) bottom of collecting tubule- urine. 400-1000mOsm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

what does the cortico-medullary hyperosmotic interstitial gradient allow?

A

concentrated urine formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

the cortico-medullary hyperosmotic interstitial gradient makes XXX have a very high solute osmolality

A

fluid of the medullary interstitium surrounding LoH AND also surrounding collecting ducts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

hat is the corticomedullary/ corticopapillary osmotic gradient?

A

outer renal cortex –> inner renal medulla:

interstitium of medulalry region becomes more concentrated (saltier)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

whats the role of the thick ascending limb of the LoH?

affect of this?

A

actively extrudes solutes into surrounding interstitium
- will increase interstitial osmolality but
- decrease that of filtrate
= hypo-osmotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

how is the tonicity of fluid entering and leaving LoH changed?

A

isotonic fluid from PCT enters
hypotonic fluid leaves to DCT

  • Na+ and Cl- leave at LoH ascending limb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

what does the removal of Na and Cl from filtrate in LoH require?

A

lots of energy so lots of Na+K+ATPase found on tubular cells here

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

why does water not follow the Na leaving in ascending limb/diluting segment of LoH?

A

as this part of LoH is impermeable to H2O and only permeable to solutes.
H2O stays in filtrate!
osmolality changes!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

what affect does the action of ascending limb of LoH have on the medullary interstitium surrounding it?

A

throws out solutes: Na and Cl = making it hyperosmotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

what drugs act on the thick ascending limb of LoH? how?

A

Loop diuretics: diuretics that act on the Na-K-Cl cotransporter along the thick ascending limb of LoH of the kidney.

  • block channel, diuretics increase urine as make kidneys pass out more fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

what does the Na-K-Cl cotransporter along the thick ascending limb of the loop of Henle do?

A
  • when all 3 are present, picks up Na, 2Cl and K follow, on apical side.
  • then Na+K+ATPase transports Na and 2Cl- out of LoH, in exchange for K+

water cannot enter at transporter OR actual LoH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

what do drugs acting on thick ascending limb of LoH treat? give an example drug.

A

loop diuretics e.g. Furosemide (suphonamide derivative)

Treat hypertension and edema often due to congestive heart failure/ CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

what is the role of the thin descending LoH (concentrating segment)?

A

extrudes water.

H2O passively reabsorbed by osmosis. enters medullary interstitium and picked up by vasa recta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

what is the filtrate in descending LoH surrounded by?

A

hyperosmotic medulla thanks to ascending LoH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

what happens to filtrate when is equilibriates with interstitium? (descending LoH)

A

becomes hyperosmotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

difference in water reabsorption from PCT, at descending LoH?

A

not obligatory H2O reabsorption.

not directly linked with Na+ reabsorption as with at PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

what is the concentrating segment/ descending LoH behaviour towards solutes and water and meaning?

A

impermeable to solute
permeable to water

solute stays in filtrate and water thrown out using aquaporins! = salty gradient and v conc filtrate at bottom of LoH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

what is the consequence of extrusion of Na+ / Cl- from ascending limb and H2O reabsorption from descending limb of Loh?

A

creates ! increasing vertical ! hyperosmotic gradient in medullary interstitium.
Thus, LoH, DCT, collecting ducts are bathed in very concentrated interstitium.

=water can be reabsorbed by osmosis from descending LoH BUT will have same effect on DCT and collecting ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

why is a vertical corticomedullary gradient creates in LoH i.e. what is the menaing?

A

outer cortex = less hyperosmotic (closer to plasma osmolality)
inner medulla = more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

what happens at LoH after Na and water pumped out?

A

equilibriate = reason for the gradient- differing concs down the LoH!
until 200mOsm difference because cells get tired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

why is the interstitial fluid made only 200mOsm/Kg H2O more concentrated than the fluid in the ascending LoH at each level?

A

energy needed to pump Na+ and Cl- out and uses Na+K+ATPases.

millions on each basolateral side BUT have their limits.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

what is the countercurrent multiplication mechanism? (reason for concentration values)

A

although ascending limb can generate gradient of only 200mOsm/L at each horizontal level, this effect is multiplied into a large vertical gradient because of the countercurrent flow within the loop.

hence LoH= countercurrent multiplier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

role of the LoH/ countercurrent multiplier?

A

establish an osmotic gradient (300-1200mOsm) from renal cortex through to medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

how can urine be made more concentrated from cortex to medulla?

A

because H2O can be removed from collecting ducts by osmosis

extruded Na+/Cl- accumulate in interstitium aroudnd LoH and collecting ducts = both can use gradient to reabsorb water and cocn urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

describe the postive feedback cycle that uses flow of fluid to multiply power of salt pumps

A
  • water leaves descending limb
  • filtrate conc here increases (as does osmolality)
  • more solute available for pumping out of ascending limb
  • increased interstitial fluid osmolality

salt pumped out, increase osm of IF, water leaves, increase osm of filtrate,..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

difference in filtrate osmolality between ascending and descending limbs of LoH/ countercurrent multiplier?

A

Descending:
INcreases to 1200mOsm/KgH2O at base of LoH: hypERosmotic

Ascending:
DEcreases to 90-100mOsm/KgH2O before start of DCT: hypOsmotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

difference in permeability to water/ Na and Cl

between ascending and descending limbs of LoH/ countercurrent multiplier?

A

Descending:
H2O: freely permeable
Na+ and Cl-: impermeable

Ascending:
H2O: impermeable
Na+ and Cl-: permeable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

what is the permeability in ascending LoH mediated by?

A

impermeable to water but Na+ and Cl-: permeable -

mediated by Na+/K+/2Cl- apical carrier - inhib by loop diuretics e.g. Furosemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

what do the specialised blood vessels: vasa recta do?

A

descending limb :
carry away the water passing out of filtrate from descending limb into hyperosmotic medullary interstitial fluid

ascending limb:
carry some of solute away that passes out of filtrate to make the hyperosmotic medullary interstitial fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Role of urea?

A

extrusion (very osmotically active) also increases the medullary osmotic gradient- makes it stronger/more hyperosmotic

contributes approx half the osmotic gradient and Na, Cl the rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

Where does the passively reabsorbed urea accumulate?

A

passively reabsorbed from the inner medullary region of collecting duct, accumulates in medullary interstitium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

affect of water reabsorption from collecting duct filtrate on urea conc?

A

urea conc increases, so can move out of these urea-permeable areas of nephron by diffusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

3 points of urea recycling

A
  • some reabsorbed from terminal CDs and accumulates in surrounding interstitium
  • most urea lost in urine
  • urea secreted into LoH and recycled - dont job, not needed. thrown out
    loop-can have gradient!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

what does the presence of ADH mean for water reabsorption?

specific region?

A

generation of vertical cortico-medullary gradient = more water reabsorbed by osmosis mainly from CDs when ADH present.
especially from inner medullary region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

normally late DCT and collecting ducts not permeable to water, but what may change this?

A

ADH presence: aquaporins are inserted and tubules become water permeable.
= allows for small vol conc urine to be produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

how do loop diuretics work?

A

increase urine frlow by acting on thick ascending LoH.

  • block Na K 2Cl ion channels in ascending LoH
  • no reabsorption/ Na/Cl extrusion into med interstitium
  • no corticomedullary gradient formed
  • no hypertonic interstitium around loh, dct, cds
  • more urine made, less in body = DIURETIC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

how do loop diuretics decrease blood pressure?

why used for hypertension treatment

A

decreased Na+ reabsorption at asc. LoH = more Na+ excreted
blood volume decrease
blood pressure decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

summary:

effect of increasing interstitial osmotic gradient with Na, Cl, urea from isotonic –> hypertonic parts of kidney?

A

= more and more water reabsorbed by osmosis as filtrate goes down LoH, CDs
= concentrate urine

conservation of water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

Part 5: Renal blood supply

renal autoregulation (mechanisms later)
myogenic control of GFR
vasa recta importance in maintaining corticom.....

whats the main thing kidneys need in order to regulate pH, fluid volume, BP, osmolal, electrolytes…..

A

need a rich blood supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

how much of the cardiac output is supplied to the kidneys and via what?

A

renal arteries supply approx 20% - 1.1L blood/ min

A LOT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

a) how does blood enter the kidney?

A

through renal artery - branches to smaller ones, some divide more into afferent arterioles, supply glomerullar capillaries. = where ultrafiltration happens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

b) what happens after ultrafiltration and blood coming to glomerular capillaries?

A

blood flows to efferent arterioles - supply second capillary network: peritubular capillaries and subset: vasa recta.
involved in reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

c) how does blood leave the kidney?

A

through the small venules and veins and finally: renal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

what are the two capillary networks in the kidney?

A

first capillary network: glomerular caps

second capillary network: peritubular caps (branch to vasa recta)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

levels of blood supply travel to kidney

A 
renal artery and arteries (interlobular artery)
afferent arteriole
glomerulus
efferent arteriole
(arcuate artery)

peritubular caps vasa recta (reabsorption)
venules
renal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

what artery branches to form the afferent artery of glomerulus?

A

interlobular artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

why is the efferent artery smaller in diamerter than afferent?

A

efferent leaving G: smaller than A arriving.

maintain hydrostatic pressure (HP) in glomerular caps = allows plasma to be filtered into bowmans space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

what is blood pressure in glomerulus controlled by?

A

different diameters of EA and AA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

from what are the peritubular capillaries formed and what do they surround?

A

EA gives rise to them and they surround the renal tubules.

towards medulla, they become vasa recta, then renal venous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

role of the peritubular capillaries? (2)

A

branch off efferent arterioles and give nutrients to epithelial and interstitial cells there

also supply blood for reabsorption and secretion in PCTs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

role of vasa recta?

A

long hairin shaped blood vessels, run alongside loh

provide nutrients and O2 to cells here

mainly: countercurrent exchangers!- contribute to urine conc by CDs.

184
Q

a) external mechanism of tight regulation of GFR?

A

sympathetic and hormonal mechanisms
(cardiac physiology lecs)

BP maintained in response to nerves and hormones

185
Q

b) intrinsic mechanism of tight regulation of GFR?

A

autoregulation- help itself by changing diameter of AA and EA = blood vessels consrict, pressure increases= alter GFR
MYOGENIC CONTROL

and
TUBULOGLOMERULAR FEEDBACK later lec

186
Q

3 major physiological body systems that activated and respond to drop in BP?

A

cardiovascular
renal
neuroendocrine: ADH released from pit. gland

187
Q

how does cardiovasc system respond to drop in BP?

A

aorta and carotid arteries. –> detected by baroceptors = activates sympathetic nervous system (ANS) constricts the blood vessels

188
Q

how does renal system respond to drop in BP?

A

renin released from JGA (juxtaglomerular apparatus)
and
aldosterone from adrenal cortex

189
Q

regardless of BP fluctuation, GFR and renal blood flow remain contant. at what values?

A

80-180mmHg

190
Q

myogenic mechanism:

what changes in EA and AA diameters are ideal when BP increased?

A

constrict afferent, dilate efferent: less blood enters glom caps
or
dilate both: blood leaves glom caps quicker

= net cap HP and glom filt DECREASED

191
Q

myogenic mechanism:

what changes in EA and AA diameters are ideal when BP decreased?

A

dilate afferent/ constrict efferent. or both:

more blood enters glom caps
or
blood stays in glom caps lonegr

= net cap HP and glom filt INCREASED

192
Q

when is constriction of efferent arteriole most useful?

A

when BP drops.

= getting more blood to glom caps.

193
Q

what is the role of prostaglandins produced by kidney?

A

released locally, counteract with Angiotensin II etc.
blood flow within kidney

modulate renal microvascular response to drop in BP.

194
Q

how do prostaglandins cause vasodilation?

A

PGs protect renal hemodynamics against excessive vasoconstrictors: Ang II.
essentially minimise/ offset any potent vasoconstriction.

dont want everything to construct: would decrease kidney function

195
Q

what drugs interfere with PG synthesis and what would this lead to?

A

NSAIDs.
= renal func deterioration and renal blood flow insufficiency in patients with vasoconstrictor stimuli to kidney.
e.g. those losing blood/ with low BP

196
Q

what occurs in volume depleted states? (NSAIDs and renal failure) (2)

A

Ang II released = renal efferent vasoconstriction to maintain GFR
or
PG release to offset potent vasconstriction- NSAIDs TARGET. detect hypoxic kidney
this one is cancelled by NSAIDs

197
Q

how do NSAIDs = renal failure?

A

target PGs- then not released to offset potent vasoconstriction in volume depleted states.

unopposed vascoconstriction –> poor renal perfusion –> acute renal failure

198
Q

how is perfusion of kidney different compared to perfusion of otehr organs?

A

done to retain filtration funcs instead of regulated to maintain organ nutrition

199
Q

paracrine factors: NO and PGs are released locally by kidneys. which is AA more sensitive to?
role of PGs?

A

vasodilator effects of NO.
PGs modulate effects of vasoconstrictors (AngII) and protect against potent vasoconstriction,

renal symp nerves also innervate AA and EA = vasconstriction

200
Q

what do vasa recta specifically allow- blood flow in what?

what are they permeable to?

A

coutercurrent loops. blood flows SLOWLY in opposite directions to filtrate in LoH.

freely permeable to water and solutes

201
Q

why are the vasa recta looped?

A

prevent high conc of solutes in medullary interstitium being washed away

202
Q

2 things vasa recta provide/allow?

A

provide oxygenated blood to renal medullary region, carry away metabolic toxins (same as normal cpas)

preserve corticomedull osmotic gradient - doesnt wash away, prevents rapid salt removal from medullary interst.

203
Q

what does vasa recta remove?

A

reabsorbed water.

water entering VR from descending VR/ reabsorbed from descending LoH and CD.

204
Q

3 causes of oedema in ankles

A

Diet: salty foods
LVF heart failure: can’t pump blood and remove fluid
Less plasma protein: reduced OP caused by kidney failure- glom filtration

205
Q

Effect of furosemide on kidney

A

Loop diuretics block NaClK transporter in asc LoH.
Na absorption and plasma volume reduced
Fluid put back into circulation to be excreted and BP decreased

206
Q

How does furosemide essentially lower BP and swelling?

A

Helps body get rid of excess salt and water by increasing urine amount

207
Q

How does furosemide reach its site of action?

A

Orally admin
Absorbed in GI tract
Binds to plasma proteins- albumin, made harder to get to site, limiting glom filt and enters LoH to exert effect

Actively secrete into PCT

208
Q

Why would furosemide be given IV sometimes instead of orally?

A

Faster onset of action

209
Q

What problems may furosemide cause?

A

Loop diuretic:

Electrolyte imbalance: metabolic alkalosis due to hypokalaemia loss of K, nausea

Dehydration: headaches, dizziness fatigue postural hypotension
Want to avoid risk of fall

210
Q

How to check and monitor decrease of oedema in ankles?

A

Weigh patient regularly

211
Q

Drug class of Spironolactone and effect on kidneys?

A

Aldosterone antagonist
Block aldosterone production, Na rea sorted by kidneys so more water excreted
Can lower BP and fluid around heart

212
Q

Affect of using aldosterone antagonist e.g. spironolactone with ACEi/ARB

A

When used with ACEi/ARB may cause high K in blood/ decline in kidney function

Sodium and water secreted
K sparing!!! K retained

213
Q

Drug class of bendroflumethiazide and affect on kidneys

A

Thiazide: DCR
reduce Na absorption, and plasma volume and BP.

Increase urine flow promote diuresis

Reduce hypertension 
K lost too through collecting duct

214
Q

Why must BP be controlled with using thiazide? I.e how are kidneys affected by BP?

A

=maybe damaged arteries and won’t filter blood well at nephrons

Hypertension is asymptomatic:

  • Damage filter and lumen: direct kidney damage
  • HF
  • damage to brain stroke
  • eyes
215
Q

What to monitor with diuretic and how often?

A

Blood:
-pressure
-K+ and Na+
Every 3 months then 6 months onwards etc

Impaired glucose tolerance- not suitable for diuretic and already have that

216
Q

Part 6: Urine conc and dilution

what is urine normally like compared with plasma?

A

urine normally HYPEROSMOTIC compared with plasma

400-1000mOsm/Kg H2O

217
Q

concentrated urine is produced by reabsorbing water from:? (4)

A

PCT: obligatory Na+ reabsorption
LoH (descending): needs medullary gradient
DCT: needs medullary gradient and ADH
CDs: needs medullary gradient and ADH

218
Q

where are decisions made to conc/dilute urine?

A

in last part of nephron- DCT and collecting ducts

219
Q

what does urine look like with:

a) high osmolality
b) low osmolality?

A

a) darker, more conc with toxins = hyperosmotic

b) paler, more dilute

220
Q

roughly what % of the 180L/day filtered water from glomerulus is reabsorbed in:

a) PCT
b) DCT
c) LoH
d) CD

A

a) 70%
b) 10%
c) 5%
d) 15% - 23L/day that VARIES!

221
Q

what would be the consequence if collecting duct failed?

A

would produce 23L urine a day as no decisions made to reabsorb any of it.
= 1L urine an hour! approx

222
Q

what does solute and water conc in man vary depending on?

A

diet
external factors
climate
…

223
Q

affect on urine of

  • low water intake
  • excess water intake
A
  • need to conserve water, product little, conc urine
    pungent smell as urea toxins etc removed with little water
  • need to excrete water, produce more, dilute urine
224
Q

what happens to body fluid osmolality when you drink too much? and therefore to urine?

A

increased water intake absorbed in blood
bf = hypo-osmolar:
<285mOsm/Kg H2O.

in healthy person: when BF become hypo-osmolar, so does urine.
= produce lots of dilute

225
Q

what happens to body fluid osmolality when you drink little? and therefore to urine?

A

bf = hyper-osmolar:
>285mOsm/Kg H2O.

insufficient water= kidneys pass out less water.

in healthy person: when BF become hypo-osmolar, so does urine.
= produce lots of dilute

226
Q

what does ADH do?

A

regulated water reabsorption from the collecting ducts (the fine tuners)
therefore segment can fine tune electrolyte and water concs in urine thus plasma

227
Q

whats the major factor that = conc/dilute urine?

A

ADH- tells CD when to draw water out

228
Q

what does the LoH create to then help with fine tuning of urine?

A

corticomedull. hyperosmotic interstitial gradient.
very salty cortex –> medulla.

water moves out CD to blood vessel as result of salty grad outside.
ONLY if ADH tells it to draw water out

229
Q

how does water move out of CD? (gradient)

A

from LOW to HIGH solute conc

230
Q

where does the water reabsorbed from CD go to?

A

nearby peritubular capillary/ vasa recta etc.

231
Q

affect of drinking lots of water on ADH production?

A

little ADH produced as dont reabsorb a lot

232
Q

what does ADH precisely control?

A

plasma OSMOLALITY not volume

233
Q

steps to dilute urine production from over hydration? (3)

A
  • low osmolality of ECF in plasma
  • less ADH release- no water reabs from DCT and CD
  • lots of dilute urine made. low as 100mOsm/Kg water
234
Q

steps to conc urine production from dehydration? (4)

A
  • high osmolality of ECF
  • more ADH release- aquaporin insertion to facilitate water reabs from DCT and CD
  • less, conc urine made. high as 1200mOsm/Kg water
235
Q

whats the real problem as a results of decreased ECF osmolality from overhydration?

A

hyponatremia! low Na
- affect heart AP, nerve stimulation

normally: plasma has higher Na than in blood

236
Q

affect of drinking TOO MUCH water?

A

water intoxication
affects electrolyte balance in blood.
Na+ dilution/hyponatraemia occurs in ECF. = water enters cells by osmosis (low -> high solute conc) ECF->ICF

237
Q

who is particularly at risk of water intoxication (too much water)?

A

athletes- sweat a lot and when dehydrated person drinks lot of water without accompanying electrolytes (energy drinks).

238
Q

adverse effects of water intoxication?

how is it fixed?

A

irregular heart beat
brain and nerve damage

need saline drip= solution to replenish salts and electrolytes in body

239
Q

where and when is ADH secreted?

A

secreted into blood from pituitary gland in response to hypovalaemia and plasma hyperosmolality

240
Q

what does amount of water absorbed in presence of ADH depend on?

A

interstitial hyperosmolality gradient made by LoH

thus urine becomes conc in medullary CD as it equilibriates with surrounding interstitium

241
Q

what 2 factors work together to allow CD to reabsorb water?

A

interstitial hyperosmolality: nice and salty (estab by LoH)
&&
ADH

= help CD pull out water from lumen by osmosis

242
Q

how are CDs acting in absence of ADH?

A

CDs not permeable to water even with the gradient, if no ADH

243
Q

what type of urine produced in presence of ADH?

A

released when dehydrated.

small volume of conc urine as maximum watre reabsorbed

244
Q

what does production of ADH depend on?

A

how hydrated.
very = little ADH
dehydrated = some ADH

245
Q

when dehydrated, urine gets v concentrated and interstitium osmolality can go up to?

A

up to 1200mOsm/kg water. max due to LoH

-> pull out lot of water! = conc urine

246
Q

ADH makes the CD permeable to water and what else?

A

urea.

- helps salt pull out more water

247
Q

to produce dilute urine, at the end of these regions filtrate is…

a) PCT
b) desc LoH
c) asc LoH
d) DCT and CD

A

FIXED:

a) isotonic
b) hypertonic
c) hypotonic

varied
d) hypotonic- 65-70mOsm

248
Q

to produce conc urine, at the end of these regions filtrate is…

a) PCT
b) desc LoH
c) asc LoH
d) DCT and CD

A

FIXED:

a) isotonic
b) hypertonic
c) hypotonic

varied
d) hypertonic- up to 1200mOsm

249
Q

why is filtrate always ISOTONIC at end of PCT?

A

285mOsm.

similar water and solute reabs. into peritubular caps

250
Q

why is filtrate always HYPERTONIC at end of desc LoH?

A

up to 1200mOsm
lots of water reabs into vasa recta.
no solute reabs

251
Q

why is filtrate always HYPOTONIC at end of asc LoH?

A

90mOsm
lots of solute into interstitium and some into vasa recta
no water reabs

252
Q

what disease state is caused by no ADH production?
whats a consequence/symptom?
nothing reabsorbed

A

Central diapetes insipidus.

v HIGH urine vol = 25L a day. = frequent urination as bladder capacity only 400mls.

253
Q

affect of extreme ADH: maximal on urine osmolality (and whats this same as) and urine volume?

A

urine osm: 1200mOsm
same as interstitial osm of deepest part of medulla/close to papilla

urine vol: 300-400ml/day
v little

254
Q

2 possible causes of central diabetes insipidus?

A

No ADH:

  • not produced by pit gland
  • OR kidneys dont respond to it
255
Q

what drug is a synthetic version of ADH and why is it prescribed?

A

Descmopressin
when simply drinking water not enough for pateints with central diabetes insipidus.
also used in nocturnal enuresis and bed wetting in kids

256
Q

how does desmopressin compare to ADH and work?

A

more powerful than endogenous ADH.

stops kidneys producing urine

257
Q

affect of too much desmopressin OR drinking too much fluid with it and symptoms of this?

A

= water retention.

headaches
dizzy
bloated
HYPONATRAEMIA- seizures
      too much water in body
258
Q

what 5 factors work together hand in hand to control urine conc?

A 
LoH: creates hyperosm... grad
urea recycling
vasa recta
CDs
ADH
259
Q

what 3 structures/ factors involved in the two counter currents created and maintained for increasing urine conc?

A

LoH (CC multipliers)
Urea recycling = makes gradient stronger
maintained by vasa recta (CC exchangers)

260
Q

Part 7: Osmoregulation

what 3 things does kidney control regarding body fluids?

A
  1. correct osm (285mOsm)
  2. vol of fluid in body
    too much = increase plasma = increase BP :(

linked.

  1. correct pH
261
Q

A variation of how many mOsm/KgH2O triggers sensors in the body to return osmolality back to normal?

A

± 3mOsm/KgH2O

262
Q

How do changes in plasma/ECF osmolality affect cell volume?

A

can increase or decrease it, due to movement of water created between compartments

263
Q

Which organ’s interstitial fluid compartment has varying osmolality?

A

kidney, due to LoH ascending limb throwing out salt into interstitium

264
Q

The 4 stages of body fluid osmolality regulation?

A

1) stimulus
2) receptor (sensor)
3) control centre
4) effector

265
Q

What is the stimulus that triggers ADH release?

A

a change in osmolality e.g. eating salty meal or sweating

266
Q

What receptors detect a change in osmolality?

A

osmoreceptors in the hypothalamus, communicate with control centre (pituitary gland)

267
Q

What is the control centre’s action in response to osmoreceptors’ signal?

A

ADH is triggered to be released from the posterior pituitary gland

268
Q

What is the effector response to ADH?

A

Change in the H2O permeability of Renal DCT and COLLECTING DUCTS:
- ADH -> insertion of aquaporins into CD wall

269
Q

Where is the pituitary gland located?

A

by the eye socket

270
Q

Where is ADH made?

A

in the hypothalamus

271
Q

ADH regulates which of the following?
A) H2O retention or loss
B) solute amount

A

A) H2O retention or loss

it only affects the reabsorption of water at the CD, but doesn’t directly change the salt content

272
Q

role of hypothalmic osmoreceptors and how sensitive are they?

A

detect small changes is plasma osmolal. and regulate release of ADH (vasopressin) - modulates water retention/loss.
NO effect on solutes

273
Q

affect of the following on urine production:

a) diuretic (drugs)
b) ADH hormone

A

a) increase urine production

b) decrease

274
Q

affect of eating salt on urine volume?

A

-> salty conc blood -> ADH makes you urinate less. reabsorb fluids etc
also stimulate thirst-> dilute body fluid

275
Q

What other receptors are located close to the osmoreceptors?

A

thirst receptors (lateral pre-optic area)

276
Q

Where is ADH stored?

A

posterior pituitary

277
Q

Why is ADH said to be unstable in circulation?

A

it has a half-life of 10 minutes

278
Q

ADH is released into the blood when plasma osmolality increases or decreases?

A

ADH is released when plasma osmolality increases

279
Q

ADH release is inhibited when plasma osmolality increases or decreases?

A

ADH release is inhibited when plasma osmolality decreases

280
Q

What is the main effect of ADH?

A

Causes kidneys to conserve H2O by stimulating passive H2O reabsorption from CDs
- normally these areas are not H2O permeable

281
Q

ADH leads to the insertion of what in collecting ducts? What is the effect on the collecting ducts’ permeability to H2O?

A

ADH =insertion of aquaporins in CDs = increases their permeability to H2O thus = H2O reabsorption

282
Q

How does ADH release affect urine concentration?

A

increases it, increasing its osmolality

283
Q

Apart from a rise in plasma osmolality, what else triggers ADH release?

A
  • change in plasma volume
  • E.g. if you cut arm, lose blood and volume is decreasing
  • Fluid and salt are being lost at the same time - osmolality isn’t changing but fluid volume change is massive
284
Q

affect of too little solute in plasma (low plasma osmol) on water and ADH?

A

too little solute in plasma
plasma too dilute
low plasma osmolal.

need to lose water to concentrate it
LESS ADH
dilute urine

285
Q

affect of too much solute in plasma (high plasma osmol) on water and ADH?

A

too much solute in plasma
plasma too conc
increased plasma osmolal

need water to dilute it (conserve water)
MORE ADH
conc urine

286
Q

ADH release can be completely suppressed with only a XXmOsm/Kg water drop?

A

5mOsm/Kg water

287
Q

for every 1mOsm/Kg increase in plasma osmolarity, hm will [ADH] increase?

A

by 0.38pg/ml

288
Q

How does the osmolality of urine change as you continue to insert aquaporins?

A
  • At top - assume 300mOSm interstitium, water leaves, aquaporins inserted until urine reaches 300 too-If dehydrated, more aquaporins inserted further down duct
  • As outside is 400, water leaves until it’s 400
  • going down, osmolality will increase so more aquaporins will be required to be inserted
  • Urine will match interstitium’s osmolality up to which aquaporins were inserted
289
Q

Why does ADH also make the collecting ducts permeable to urea?

A

increases osmotic gradient of the already salty medullary interstitium, so more water can be pulled out by osmosis

290
Q

summary of effect of increased plasma osmolality. (6)

A

Plasma osmolality increased….

  • osmoreceptors in hypothalamus detect
  • more ADH released from pituitary gland
  • CDs become more permeable to H2O
  • increased water reabsorption by osmosis into blood
  • decreased volume of conc urine produced
  • H2O in blood reduces plasma osmolality
291
Q

summary of effect of decreased plasma osmolality. (6)

A

osmoreceptors in hypothalamus detect

  • less ADH released from pituitary gland
  • less ADH travels in blood to kidneys
  • CDs less/ not permeable to H2O now
  • decreased water reabsorption by osmosis into blood
  • increased volume of dilute urine produced
  • H2O in blood increases plasma osmolality
292
Q

following release from pituitary, how does ADH travel? and where to?

A

in bloodstream to the V2 receptors on basolateral memb of cells lining the CDs.

293
Q

Describe the steps that lead to the insertion of aquaporins in collecting ducts (4)

A

1) ADH release from pituitary
2) ADH binds to V2 receptors on basolateral membrane of the cells lining CD
3) raises cAMP levels -> intracellular vesicles containing AQP2 (aquaporins) fuse with apical membrane
4) H2O reabsorbed from CDs by osmosis, gradient bought about by high solute conc in he surrounding medulla, into the vasa recta

294
Q

result of ADH binding to V2 receptors on basolat memb of cells lining CD?

A

cAMP levels raised = intracellular vesicles containing AQP” fuse with apical memb

295
Q

What is the maximum concentration of urine that can be reached and why?

A

1400 mOsm/kg H2O - highest osmolality of interstitium at base of collecting duct

296
Q

What is the shape of the cells lining the collecting ducts that aquaporins are inserted into, and on what 2 sides?

A
  • columnar

- luminal / apical surface

297
Q

What is necessary on the collecting ducts in order for water to be reabsorbed under the effect of ADH?

A

V2 (vasopressin) receptors

298
Q

why is no water reabsorbed from regions when no ADH released?

A

no ADH = no aquaporins in luminal/apical surface of columnar cells lining CDs = no water reabsorbed here.

299
Q

where are aquaporins always present?

A

on basolateral surface to allow water into these cells for survival

300
Q

Why is drinking sea water bad?

A
  • Sea water osmolality 2000mOsm/KgH2O
  • Urine osmolal can reach 1400mOsm/Kg H2O
  • To clear 1Kg (1L) of sea water will require : 2000mosm/1400mOsm= 1.4L of water to clear
  • therefore result in dehydration - more body water removed than amount drank
301
Q

What is diabetes insipidus caused by?

A

hyposecretion of/ insensitivity to the effects of, antidiuretic hormone (ADH), also known as arginine vasopressin (AVP)s

302
Q

What are the 2 types of diabetes insipidus?

A
  • Cranial DI: less ADH;cant concentrate urine- polyuria and polydipsia
  • Nephrogenic DI: cant concentrate urine. resistance to ADH in the kidney.

both= produce lot of dilute urine

303
Q

What are the symptoms of diabetes insipidus?

A
  • polyuria
  • polydipsia (excessive thirst)
  • nocturia
  • urinary incontinence may occur
304
Q

What will the plasma and urine osmolality be in patients with diabetes insipidus?

A

raised: >295 mOsmol/kg, despite having dilute urine <700 mOsmol/kg

305
Q

what does osmoregulation actually do (and not do)?

A

controls plasma Na+ conc by changing water volume

NOT controlling actual bodys water content.

306
Q

Part 8: regulation of body fluid volume

After ingesting NaCl, what happens to the: a) osmolality,

b) thirst,
c) ADH concentration,
d) collecting duct permeability to H2O and e) H2O retention?

A

all increase:
osmolality- salt only goes in ECF compartment but this draws H2O out of ICF and increases osmolality in ICF compartments
thirst and ADH increase, collecting duct permeability to H2O increase
=H2O retention

all restore the osmolality to 285mOsm /KgH2O

307
Q

How do osmoregulation and volume link?

A

osmoregulation disturbs volume, so you need a volume regulator

308
Q

affect of adding salt to fluid volume?

A

does not change water volume but changes osmolality = increased fluid volume

309
Q

How are [Na+] and H2O volume in body connected?

and what does this therefore mean for volume regulation?

A

water follows Na due to the gradient Na generates
therefore ECF volume can be regulated by body Na+ content

↑ Na+ = osmolal = ADH = water ↑
↑ ECF Na+ = ↑ ECF vol

↓ Na+ = osmolal = ADH = water ↓
↓ ECF Na+ = ↓ ECF vol

310
Q

Renal handling of Na+ sets plasma volume or plasma osmolality?

A

Plasma volume is set by renal handling of Na+

linked with ADH

311
Q

ADH action on H2O reabsorption sets plasma volume or plasma osmolality?

A

ADH action on H2O reabsorption sets plasma osmolality

linked with Na+

312
Q

What is effective circulating volume (ECV)?

and normal value?

A

part of ECF that is in the arterial system (normally about 700 mL in a 70 kg man) and is effectively perfusing tissues.

(blood volume to kidneys)

313
Q

What does the body directly control the volume of? (terms of effective circ volume)

A

the intravascular fluid -> influences vol of the other compartments

314
Q

body cant measure total body water volume in all cmptms easily , but can monitor what instead?

A

blood perfusing tissues/ ECV effective circ volume

315
Q

Why is ‘effective circulating volume’ used rather than ‘total blood volume’ in physiology?

A

‘effective’ vol of blood perfusing organs/tissues can change even w no changes in blood vol

  • kidney ‘sees’ the ECV + decides if low/ high
  • e.g. in heart failure, lot of blood may remain in ventricles instead of perfusing organs but total blood volume > that perfusing organs = dec ECV
316
Q

how does ECV affect organs/ systems in

a) heart failure
b) liver cirrhosis

A

a) ↓ cardiac output
b) ↑ splanchnic vasodilatation- less diffusing, blood vessels smaller in liver- harder to push out. liver dilates- more blood held there

317
Q

What detects the changes in pressure of the effective circulating volume?

A 
baroreceptors
detect pressure (stretch) perfusing through them rather than volume

overstretch (overhydrated)
not enough stretch (dehydrated)

318
Q

What are the 2 types of baroreceptors? (that detect changes in ECV)

A
  • Systemic arterial baroreceptors
    in aortic arch and carotid sinus - cardiovascular physiology
  • Renal glomerular afferent arterioles: hence can detect changes in body H2O volume by getting kidneys to scrutinise blood volume going through
319
Q

What are the baroreceptors within the afferent arterioles called? (they are modified from the smooth muscle)

A

juxtaglomerular cells (or granular cells)

320
Q

juxtaglomerular cells (or granular cells) act as baroreceptors but also the same cells do what?

A

release renin enzyme when blood volume/ pressure drops

321
Q

4 things that may induce renin secretion?

A

through BP/ blood volume drop
haemorrhage
sweating
diarrhoea

322
Q

What other receptors are found in the nephron that help regulate blood volume?

A

chemoreceptors (osmoreceptors)in the DCT

323
Q

What are chemoreceptors called in the DCT? (they are modified from the tubular cells as it reaches the glomerulus)

A

macula densa cells - modified tubular cells (can also cause renin release from juxtaglomerular cells when Na+ is low)

324
Q

In actuality, how far are the DCT and the glomerulus?

A

very close, hence the name of the juxtaglomerular cells

325
Q

What is the juxtaglomerular apparatus made of?

A

chemoreceptor macula densa cells of the DCT and
the baroreceptor and renin releasing juxtaglomerular cells of the afferent arteriole just before it enters the glomerulus

326
Q

what does the JGA do?

A

maintain BP and act as a quality control mechanism to ensure proper GFR + efficient Na+ reabsorption

detects vol change and pressure (baroreceptors) in blood vessels

327
Q

How is renin release triggered by low fluid volume/BP (juxtaglomerular cell version)?

A
  • AA have less blood volume to them
  • JGA cells detect lack of stretch in arteriole

release renin into bloodstream

328
Q

How is renin release triggered by low fluid volume/BP (macula densa version)?

A
  • Filtrate flows slowly through PCT =more time to reabsorb lots of Na+
  • By the time filtrate hits macula densa in DCT, not enough fluid in filtrate due to more Na absorbed (macula densa detect low Na content)

More renin released by JGA cells

329
Q

what is the RAAS system? role

A

hormone based system.

increase effective circulating volume.

330
Q

what 2 things does RAAS system regulate?

A

BP:
-cardiovasc and symp. NS regulate BP. renal system can also help

fluid volume:
- Na+ content through renal reabs and excretion can change fluid volume

both work together :)

331
Q

how does renin production change if BP too high?

A

decreased renin produced

332
Q

how does renin production change if BP too low?

A

BP/ vol decreased.
filtrate through PCT flows slower = more time to reabsorb lots of Na+.
= less Na+ appears in DCT, sensed by macula densa cells.
paracrine signals sent by these to nearby JG cells = MORE renin released.

baroreceptors detect as not stretched out as much with low BP

333
Q

pressure receptors on PCT release renin when..?

A

blood volume decreased. as baro. not stretched out as much.

334
Q

What is necessary for renin to have a physiologic function?

A

angiotensinogen, produced by the liver

= a globulin released in bloostream and acted upon by renin.

335
Q

What does renin need to do to have an action?

A

cleave angiotensinogen –> angiotensin I

336
Q

What is angiotensin I further cleaved into and what by?

A

angiotensin II by ACE (angiotensin-converting enzyme)

337
Q

Where is angiotensin I converted to angiotensin II?

A

Pulmonary and renal endothelial cells

338
Q

Summarise how renin results in production of angiotensin II

A
  • renin cleaves angiotensinogen into ang I

- ang I cleaved by ACE in renal/pulmonary endothelial cells into ang II

339
Q

role of angiotensin II (Ang II), the final product formed in process of angiotensinogen->angI->angII. ?

what 5 things does it affect?

A

exerts affects to bring blood volume back up!.

affects:
- vasoconstriction
- EA constriction
- ADH
- Aldosterone
- Thirst

340
Q

What is the aldosterone action of angiotensin II?

A

Aldosterone secretion stimulated from adrenal cortex = increases Na+ absorption from DCT/CD’s

341
Q

how does AngII stimulate aldosterone to stimulate Na+ reabsorption?

A

Na+/Cl- reabsorption enhanced in DCT and CDs (principle cells) and hence obligatory H2O reabsorption from the PCT (increases Na+/H+ exchange).

342
Q

What is the ADH action of angiotensin II?

A

ADH release stimulated from posterior pituitary – aquaporin insertion in CDs = H2O reabsorption

343
Q

What is the vasoconstriction action of angiotensin II?

A
  • Vasoconstriction of arterioles/venules in the body = raise BP and
  • renal efferent arteriole to increase GFR through inc glom HP = ensures kidneys still filter depsite drop in BP.
344
Q

What is the thirst action of angiotensin II?

A

thirst centres in hypothal stimulated

encourage increased fluid volume as drop in water volume (from dry mouth too) will increase fluid osmolality

345
Q

RAAS system: myogenic control affect on GFR?

what is this an indicator of?

A

myogenic control on EA contriction… narrower. = inc pressure = inc GFR.

check kidney still working through GFR

346
Q

RAAS system: effect of vasoconstriction on arterioles?

A

inc TPR = inc BP as:

BP = CO x TPR

347
Q

RAAS system: effect of vasoconstriction on venules?

A

increased:

  • venous return (blood back to heart)
  • EDV
  • stroke volume
  • BP as:

CO = SV x HR
and BP = CO x TPR

348
Q

What is the action of aldosterone? from stim by RAAS system

A

reduces NaCl excretion by stimulating = Na+ reabsorption/uptake by thick ascending LoH, CD, DCT (apical cell membrane)

349
Q

ACE enzyme reaction happens where?

A

pulmonary blood- lungs!

350
Q

what is renin released from JGS in response to ? (2)

A
  • afferent baroreceptors detecting low fluid volume/BP and

- paracrine signals from macula densa cells detecting low Na+

351
Q

how does ADH inc water reabs?

A

it causes aquaporins to move to CD plasma membrane = increases water reabsorption

352
Q

physiological response of renin?

A

does not have direct response.

its substrate = circulating protein: angiotensinogen = produced by liver

353
Q

2 important sites for conversion of AngI and AngII?

A

pulmonary and renal endothelial cells

354
Q

summary of the 5 key actions of AngII to increase ECV?

A

aldosterone secretion stim from adrenal cortex = inc Na+ abs from DCT/CDs

Na+/Cl- reabs enhanced so oblig water reabs from PCT (inc Na+/H+ exchange)

ADH release stim from post pit.- aquaporin insertion in CDs = inc water reabs

Vasoconstriction of arterioles/venules in body = raise BP and renal efferent arteriole to increase GFR.

thirst stimulated

355
Q

What is inhibiting RAAS useful in treating?

A 
hypertension,
congestive HF,
LV dysfunction,
pulmonary and systemic oedema,
diabetic nephropathy,
liver cirrhosis,
migraines

as this system works to increase fluid volume (and hence, BP)

356
Q

4 drug classes that inhibit RAAS system? Clinically inhibit

A

Renin inhibitors: Aliskiren
ACEi: ramipril
AngII rec antagonists/blockers (ARB): Candesartan
Aldosterone rec antagonists: Spironolactone

357
Q

how may Aliskiren be prescribed?

A

a renin inhibitor.

used alone/ combine with other anti-hypertensives

358
Q

What are ACE inhibitors used to treat?

A

used alone or combination with other anti-hypertensives to treat
hypertension, congestive heart failure, acute MI, cardiac failure, diabetic nephropathy

359
Q

When are Ang II receptor blockers (ARBs) used?

A

to treat hypertension and heart failure when ACE inhibitors are not tolerated

360
Q

How do aldosterone antagonists work?

A

by blocking aldosterone receptor sites and promoting renal excretion of Na and H2O.
= prevents Na+ absorb.
diuretic.

361
Q

What are aldosterone antagonists used to treat?

A

hypertension as well as oedema associated with cirrhosis, congestive heart failure etc.

362
Q

What is the role of atrial natriuretic peptide (ANP)?

what happens when blood volume increases?

A

atrial = heart, Na = sodium, riuretic = urine

  • acts to put Na in urine
  • when blood volume increases, the atria of the heart are stretched - they release ANP
363
Q

What stores and secretes atrial natriuretic peptide? ANP

A

cardiac myocytes

364
Q

ANP. 2 ways the renal system excretes Na+ in urine and thus restores volume?

A

switch off RAAS system

heart releasing ANP. when blood vol inc, heart atria stretched - ANP released.

365
Q

ANP and lack of renin = ?

A

removes excess Na+ from body

all work to dec blood volume

366
Q

how are the following interlinked and maintained?

a) osmolality
b) volume

A

a) maint. at expense of volume changes -> ADH
b) main. by altering Na+ content -> RAAS system (mulitple pathways).

both communicate and linked
changes affect both

367
Q

what 2 things regulate

a) Na+?
b) water?

A

a) volume changes & RAAS and ANP

b) osmolality changes & ADH

368
Q

summary of factors that maintain water balance

A

green table in lc 8 revisit

369
Q

Part 9: Regulation of body fluid pH

What is the normal body pH?
and what is this dictated by?

A

7.35-7.45

The concentration of H+ ion dictates body pH

370
Q

role of buffer

A

too few H+: could go into alkalosis and death
release H+ into fluid/blood

too many H+: could go into acidosis and death
need to mop up H+

restore pH to 7.34

371
Q

What happens if the body pH goes outside the range of 7.35-7.45?

A 
proteins denatured, 
enzyme function lost, 
nerves hypersensitive, 
muscle spasms, 
heart rate changes etc.
372
Q

What type of processes cause pH changes?

A

daily metabolic - produce and consume substantial volumes of free H+ ions/acids that are efficiently removed from body

373
Q

What 6 examples of H+ ion sources?

A
  • Ingested protein metabolism
  • Cell metabolism - produce CO2, can disturb acid-base balance if not breathed out !
  • Food: processed, sodas, sweetened drinks, meats, citrus fruits, yoghurt, sauerkraut…
  • Meds - aspirin, warfarin, indomethacin
  • Metabolic intermediate by-products e.g. exercise produces lactic acid
  • Disease processes - e.g. diabetes may cause improper breakdown of fats and generation of keto-acids
374
Q

why must ingested protein metabolism be kept in check?

A

source of H+ ions and produces amino acids

375
Q

What buffer systems exist in the intracellular fluid compartments?

A
  • phosphates (HPO42-)
  • amino acids
  • both accept H+ relatively quickly
376
Q

What buffer system exists in the interstitial fluid compartments? ICF

hint: very powerful buffer!

A

the carbonic acid/bicarbonate buffer system

H2CO3/HCO3-

377
Q

What buffer systems exist in the blood? (3)

A
  • haemoglobin
  • plasma proteins
  • carbonic acid/bicarbonate buffer system

Hb also accepts H+ relativey quickly

378
Q

What 2 organs use the carbonic acid/bicarbonate buffer system to restore pH?

A

the kidneys and the lungs

great ECF buffer

379
Q

Carbonic acid/bicarbonate buffer system equation

A

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3–

380
Q

What end of the carbonic acid/bicarbonate buffer system equation can be altered by the lungs?

A

left - it alters depth and rate of ventilation to alter arterial PCO2

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3–

381
Q

What end of the carbonic acid/bicarbonate buffer system equation can be altered by the kidneys?

A

right - it causes either tubular excretion or reabsorption of H+ and HCO3-

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3–

382
Q

What are the 3 defence mechanisms in the body buffering against pH changes in decreasing speed?

A
  • 1st defence: Chemical buffering – seconds (< 1sec)
  • 2nd defence: Respiratory – minutes
  • 3rd defence: Renal – days (5-7)
383
Q

why are multiple organs involved in regulating body fluid pH?

A

if one organ unable to do job e.g. kidney damage/ lungs etc, others can compensate

384
Q

How do we check if the pH, PCO2 and HCO3- levels in a patient are normal?

A

using arterial blood gas samples obtained from radial artery

385
Q

What is the normal values from an arterial blood gas sample for:

a) pH
b) PCO2
c) HCO3-

A

a) 7.4
b) 40mmHg (35-45)
c) 24mmol/L (22-26)

386
Q

what 2 things must be kept constant for pH to remain unaltered

A

CO2 and HCO3- levels

387
Q

What do the kidneys do to HCO₃⁻ and H⁺ when the pH is too low?

A
  • reabsorb HCO₃⁻
  • excrete H⁺
  • generate HCO₃⁻

acidic want kidneys to excrete it into urine

all HCO₃⁻ reabsorbed abck into blood stream

388
Q

What do the kidneys do to HCO₃⁻ and H⁺ when the pH is too high?

A
  • excrete HCO₃⁻

alkaline: bic. into urine

389
Q

Why is there a limit to how much free H⁺ can be excreted in the urine? (hint: what does H⁺ do to the urine?)

A

H⁺ increases the acidity (decreases the pH) of urine; if it becomes too acidic it will become painful to excrete and damage the bladder and urethra

390
Q

How else can H⁺ be excreted in the urine to prevent it from changing the pH of the urine?

A
  • buffered with phosphate (HPO₄²⁻) to form H₂PO₄⁻ (titratable acid)
  • buffered with ammonia (NH₃ - produced by PCT cells) to form NH₄⁺ released into urine

(but wont change urine pH)
acidic urine will hurt urethra etc.

391
Q

Why is there a limit how much H⁺ that can be excreted as H₂PO₄⁻?

A

75% of HPO₄⁻ is reabsorbed as our body needs it to mineralise bones and teeth and act as a buffer within cells

392
Q

reminder from lec 3:

How is HCO₃⁻ reabsorbed by the kidneys?

A

in tubule lumen
secreted H+ combines w filtered HCO₃⁻ = h2o and co2.
requires carbonic anhydrase on apical brush border of PCT tubular cells.

back into proximal tubule cell
co2 difffuses into cell, recombines w h20 = hco3- = exits cell from basolateral side and diffuses back into blood.

393
Q

Until what pH can H⁺ be excreted in the urine freely and unbound?

A

until the urine pH reaches 4.4

after this, acidosis dealt with by kidneys in 2 ways…

394
Q

….acidosis dealt with by kidneys in 2 ways which are?

A

removes some excess H+ via:
H2PO4- or NH4+

bind to remove acidity.
generate extra bicarbonate

395
Q

renal phosphate buffer system

What is generated by the renal tubules when HPO₄⁻/ NH₃ buffers H⁺ before being excreted in the urine?

A

new HCO₃⁻

the system can be used as an intracellular buffer

396
Q

renal ammonia buffer system

How is ammonia produced in the PCT cells of the kidney?

A

glutamine (added/ alr in) into the PCT cells is converted to ammonia which accepts a base H+ to become ammonium

again new HCO3- gen by renal tubules

397
Q

Why is 99% of HCO₃⁻ reabsorbed back into the body?

A

if lost, it would result in acidosis as nothing could buffer H⁺ from metabolic processes

398
Q

ammonia buffers and excretes how much of excess H+ in urine and contributes to how much of new HCO3-?

A

50/50

399
Q

Under what circumstance is HCO₃⁻ excreted in the urine?

A

when the plasma is too basic, to allow H⁺ to build up and decrease the pH

400
Q

what can acid base imbalances arise due to?

A

respiratory dysfunction: change in PCO2
or
metabolic dysfunction: change in [HCO3-]

therefore change in [H+]/pH are reflected by changes in [HCO3-]:[co2]

pH = [HCO3-]/PCO2

401
Q

definition of repiratory acidosis

A

Low pH < 7.35

High pCO2 >45mmHg

402
Q

causes of respiratory acidosis

A

hypoventilation (CO2 retained. not ventiliating alveoli)
holding CO2 in body- most common AB disorder
lung problems: emphysema/obstruction/oedema
trauma to resp centre
dysfunction of resp muscles

403
Q

how does repiratory acidosis affect carbonic acid equation?

A

more to RIGHT as (MORE CO2) and MORE HCO3- and H+

CO2 accumulation in blood stream increases H+/HCO3-

404
Q

renal compensatory mechanisms of repiratory acidosis

A

peripheral chemoreceptors sense pH change, try to change ventilation rate. BUT lungs unresponsibe as this is where problem is

therefore kidneys try and remove excess H+ in acidic urine and conserve HCO3-

INCREASED:

  • renal secretion and excretion of H+
  • renal reabs of HCO3-
  • renal generation of HCO3-
405
Q

whats a davenport diagram? (resp acidosis)

A

representation (simple) of pH/ HCO3- and PCO2 (isobars)

shows the 4 types off AB disturbances and renal/resp compensations that happen to restore pH.

406
Q

renal compensatory mechanisms of repiratory acidosis 3 steps to increase blood pH?

A

excrete H+ into urine
retain HCO3-
generate HCO3-

blood pH increased

(think of pH = [HCO3-]/pCO2 )

407
Q

renal compensatory mechanisms of respiratory ALKALosis 2 steps to increase blood pH?

A

retain H+
excrete HCO3- into urine
blood pH decreased

(think of pH = [HCO3-]/pCO2 )

408
Q

definition of respiratory alkalosis

A

high pH > 7.45

low pCO2 <35mmHg

409
Q

causes of respiratory alkalosis

A

hyperventilation
removing co2 from body too quickly
anxiety, fear, pain- hysterical overbreathing not just panting
lungs: pneumonia
aspirin OD/toxicity; too much caffeine
over ventilation on mechanical respirator

410
Q

how does repiratory alkalosis affect carbonic acid equation?

A

more to LEFT as LESS CO2 and (LESS HCO3- and H+)

CO2 loss from blood stream decreases H+/HCO3-

411
Q

renal compensatory mechanisms of repiratory alkalosis

A

peripheral chemoreceptors sense pH change, try to change ventilation rate. BUT lungs unresponsibe as this is where problem is

therefore kidneys RETAIN H+ and EXCRETE HCO3-

INCREASED:

  • renal excretion of HCO3- (dont reabsorb/ generate)
  • renal reabs of H+ (dont excrete)
412
Q

whats metabolic alkalosis

A

high pH > 7.45

high HCO3- > 24mEq/L

413
Q

5 things that may lead to metabolic alkalosis?

A
  • severe vomiting= acid loss (common)
  • gastric suction
  • diuretics -> renal dysfunction
  • excesisve intake of alkaline drugs - antacids
  • excessive intake of fruits (fad-diets ricch in fruits)
414
Q

what drug class (excessive use of) may lead to metabolic alkalosis?

A

alkaline drugs- antacids

415
Q

what direction would the carbonic eqn shift in metabolic alkalosis?

A

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3–
RIGHT

loss of H+ (or gain of HCO3-) = increased HCO3-
hold onto CO2

416
Q

compensatory mechanisms in metabolic alkalosis?

i.e. which system has major role?

A

peripheral chemoreceptors sense change in pH
lungs hypOventilate to retain CO2 (and thus H+)
- pulmonary compensation for metabolic alkalosis
= will raise HCO3- even more!

kidneys remove excess HCO3- in urine, conserve H+

417
Q

compensatory mechanisms FOR change in HCO3- and H+ in metabolic alkalosis?

A

INCREASED:
renal excretion of HCO3- (dont reabsorb/generate it)
renal reabsorption of H+ (dont excrete it)

418
Q

Metabolic alkalosis increases blood pH. how does pulmonary and renal system respond/compensate for this change?

A

renal:

  • retain H+
  • excrete HCO3- in urine
  • blood pH decreased

pulmonary

  • hypoventilate
  • blood pH decreased
419
Q

Summary:
How is Acidosis responded/compensated for by: pulmonary and renal systems

i.e. what happens to the H+? (3)
H2CO3 -> H+ + HCO3-

A

Problem = Addition of H+/loss of HCO3-

H+:
- more turned into H2CO3 –> goes to lungs and leaves as CO2 (inc resp rate to remove and lower PCO2

  • more absorbed by other buffers in body
  • more excreted in acidic urine –> HCO3- reabsorbed and generated
420
Q

Summary:
How is Alkalosis responded/compensated for by: pulmonary and renal systems

i.e. what happens to the H+? (3)
H2CO3 -> H+ + HCO3-

A

Problem = Addition of HCO3-/loss of H+

H+:
- Resp rate decreased to retain thus increase PCO2 = inc H2CO3
(lungs hold onto CO2)

  • more donated by other buffers in body
  • more reabsorbed from kidneys–> HCO3- secreted in alkaline urine
421
Q

Part 10: Revision session

Why is the glomerular filtration barrier effective? (4)

A
  • tiny pores in endothelial layer only let plasma through (no big MW mols)
  • BM thicker than normal
  • BM = negative so large proteins repelled
  • podocytes = 3rd barrier to plasma components
422
Q

what are the 3 layer sof the glomerular filtration barrier?

A

endothelial cells- fenestrates lining of glomerulii
basement membrane
podocytes- cover whole glomeruli

423
Q

which force favours filtration:

a) glom cap HP
b) capsular HP
c) glom cap osmotic P
d) capsular osmotic P

A

= a) glom cap HP
reason= Bowmans Capsule not interstitium surrounds glomerulus = should not be any proteins in filtrate (oncotic pressure)

424
Q

net filtration pressure favours XXX fluid movement?

reason and what is the net filtratiion pressure?

A

net filtration pressure favours OUTWARD fluid movement

Starlings forces:
OUT
glom HP: 50mmHg

IN
glom OncoticP: 25mmHg
BC’s HP: 15mmHg

BC’s OncoticP: 0mmHg

net = 50-25-15-0=10mmHg

425
Q

Meant arterial pressure (MABP) increases from 90mmHg to 110mmHg.

what could happen to prevent an increase in pressure in glom caps?

A

constriction of AA.

= less blood into glom caps. could occur when BP increased to decrease it

426
Q

which out of the following hormones does NOT influence kidney function?

ADH
erythropoeitin
ANP (atrial natriuretic peptide)
aldosterone

A

erythropoetin

  • produced and secreted by kidney when hypoxic to increase RBC production - hence acts on RBC progenitors and precursors in bone marrow!
427
Q

plasma levels of erythropoetin usually low but when may it increase?

A

in hypoxic stress/ anaemia

up to 1000 fold inc!

428
Q

how does ANP (atrial natriuretic peptide) act on kidney?

and when is it released

A

produced by heart myocytes
released in response to atrial stretch due to high blood volume
acts on kidney to decrease Na+ reabsorption

429
Q

where does most of the 99% of glom filtrate produced each day, get reabsorbed and what ion reabsorption is it linked to?

A

PCT… linked ot reabsorption of Na+

430
Q

what do Na+K+ pumps in basal membrane do to Na+? i.e. whats their effect

A

move Na+ out of tubule cell, keeping intracellular Na+ conc low.
Na+ is filtered so filtrate conc is high

431
Q

how does Na+ get through apical membrane of tubule cell?

then what happens regarding organic nutrients?

A

diffuses through co-transporters in apical membrane of tubule cell

then organic nutrients reabsorbed across apical surface by secondary active transport with Na+.

432
Q

what does reabsorption of Na+ create? what does this lead to?
(4)

A

osmotic gradient => h2o reabsorption
conc of solutes left behind in tubule lumen increases
lipid soluble subs diffuse through apical and basal mem bilayers
remaining solutes (K+,Ca2+…) diffuse betweent ubule cells

433
Q

which is not included in the system for formulation of conc/dilute urine?

CDs
Medullary interstitium
LoH
PCT
Vasa Recta
A

PCT.

434
Q

what parts of nephron are:

a) concentrating
b) diluting
c) least permeable to water

A

a) desc LoH
b) ascending LoH
c) ascending LoH- throwing out Na+. now ater

435
Q

which solutes = main contributors to high osmolality of interstitial fluid in renal medulla?

A

Na+
Cl-
Urea

salts and urea help strengthen cortico-medullary interstitium. urea secreted back into desc LoH

436
Q

what are the 3 major solutes contributing to plasma osmolality of 285mOsm/Kg

A

Na+ 140mOsm/Kg
Cl- 115mOsm/Kg
HCO3- 25mOsm/Kg

= 280mOsm/Kg

437
Q

5 steps in the journey of Na+/Cl- through the counter-current exchanger

A

Na+/Cl-…

  1. leaves thin and thick asc Loh
  2. accumulates in medullary interstitium
  3. absorbed by desc vasa recta
  4. flows into asc vasa recta
  5. returned to medullary interstitium
438
Q

in renal tubule, what hormone regulates:

a) water volume
b) sodium reabsorption

A

a) ADH

b) aldosterone

439
Q

whats the principal regulator of plasma osmolality?

Plasma [Na+]
ADH
aldosterone
AngII
volume of water
A

ADH

440
Q

in sosmeone with excess water consumed, you would expect to see:
X ADH, Y dilute urine, Z urea permeability

A

less ADH, more dilute urine, less urea permeability

441
Q

4 factors to tell if patient had diabetes indipidus?

A

extreme thirst
decrease in ADH
large volume urine
urine with very low osmolality

442
Q

which RENAL substance works with CVS to raise BP:

ADH
aldosterone
renin
ANP
ACE 
?
A

renin.

ACE can be found in renal endothelial cells and pulmonary endothelium but renin is purely form kidney

443
Q

whats the function of macula densa cells?

A

monitor NaCl conc in filtrate

444
Q

what happens to blood osmolality and volume when severly dehysrated?

A

blood osmolal: increase = stim osmorec in hypothal

blood volume: decrease = decrease BP= more renin released and Ang II made

= thirst

445
Q

where is thr key hormone in reg water reabs secreted from?

A

post pit gland

446
Q

there are osmoreceptors in hypothalamus

T/F?

A

true

447
Q

how is body volume regulated?

A

changing body sodium content and maintaining normal osmolality

448
Q

what provides info about body volume?

A

stretch receptors

449
Q

what provides info about osmolality?

A

rec in hypothalamus (osmoreceptors)

450
Q

whats the main influence of body volume?

A

renal sodium exretion

451
Q

normally in urine what is most of H+ tied up wiht?

A

ammonia

452
Q

how to decide if metabolic/resp alka/acidoss is COMPENSATED?

A

pH is normal

regardless of low/high Co2/HCO3-

453
Q

what does the vasa recta preserve?

A

Countercurrent Exchange in the Vasa Recta Preserves Hyperosmolarity (Salty gradient) in renal medullary interstitium

454
Q

Why is there lots of bicarbonate in blood? What’s it’s role

Na, Cl, Bicarbonate

A

Acts as buffer

455
Q

What’s acidosis?

A

H+ sitting in blood, not being breathed out

Hyperventilate to help
Breathe out acid
Inc resp rate

456
Q

What ion is most abundant inside cell and outside cell?

A

Na extracellular
K intracellular

Salty banana

Health.1 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions