Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Medicine Unit 8 > Renal physiology 2 > Flashcards

Renal physiology 2 Flashcards

1
Q

body composition female

A

45% solids
55% fluids

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

body composition male

A

40% solids
60% fluids

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

composition of total body fluid

A

2/3 intracellular fluid
1/3 extracellular fluid

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

composition of extracellular fluid

A

80% interstitial
20% plasma

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

why are there differences in body composition male and females

A

higher proportion of body fat in females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

water Balance

A

what goes in must come out
amounts will vary significantly
regulated intake and output from thirst and ADH

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

gaining water

A

from drinking
from food via oxidative metabolism

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

how is water lost

A

expired gas saturated with water vapour e.g. breathing

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

sweat

A

hypotonic
body fluid can become hypertonic if you sweat a lot

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

why osmoregulate

A

changes in volume of ECF will change the osmolality
can affect size of cells due to changes in tonicity

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

tonicity

A

solutes effect on cells volume

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

what happens if the body fluid becomes hypotonic

A

cells will swell
kidneys excrete filter urine to restore homeostasis

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

what happens if the body fluid becomes hypertonic

A

cells shrink
kidneys excrete concentrated urine to restore homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

osmolarity

A

number of particles in solution
usually referred to in comparison to another compartment
quantitive measure

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

central pontine myelinolysis

A

destruction of the myelin sheath in the pons
causes rapid osmotic changes

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

plasma osmolality

A

280-300 mOsm/kg-1 H2O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

urine volume

A

0.5 – 18L/day-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

urine osmolality

A

1200-50 mOsm/kg-1 H2O
(normally 300-500 mOsm/kg-1 H2O )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are plasma and urine osmolality and urine volume regulated by

A

ADH
from posterior pituitary

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

osmolality of ECF control

A

primarily controlled by regulating amount of water in the body
not NaCl

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

volume of ECf control

A

regulating NaCl in body
not water

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

osmoregulation dominates what

A

volume regulation

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

loop of henle

A

starts at the end of PCT and finishes at the macula densa
remaining 40-45% of filtrated isn’t handled by PCT
25-35% of Na+ and Cl-
salt and water reabsorption are separated
water passive in descending limb
salt is active in ascending limb

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

what is the main channel in the loop of henle used to absorb

A

Na+
K+
Cl-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
NKCC loop of henle
Na+, K+ and 2Cl- enter K+ removed paracellular transport
26
purpose of the loop of henle counter current
maximise reabsorption of water and sodium reabsorbed separately as the ascending loop is impermeable to water reabsorption in ascending loop affects the descending loop
27
counter current in LOH
1. ascending limb NKCC 2. interstitial osmolality increases 3. descending limb surrounded by the same interstitium 4. water moves out of the descending limb 5. urine moves down the limb and ascends counter current to teach other concentrated reaches thick ascending limb NKCC does job
28
urine osmolality entering and leaving the loop
the same
29
why is loop anatomy crucial
limbs tightly packed together change in interstitial osmolality in ascending limb directly affects the descending limb
30
urea reabsorption
in the collecting ducts contributes to interstitial osmolality
31
what does reabsorption of solutes in the ascending limb do
increase interstitial osmolality more water reabsorption in descending limb due to close proximity urine osmolality increases down the limb as more water is reabsorbed when urine travels up ascending limb there's a lot of salt to reabsorb via NKCC limbs/ urine move counter current
32
loop diuretics
furosemide bumetanide
33
action of loop directs
act on NKCC to inhibit reabsorption of Na+, K+ and Cl- increases osmolality in urine reduced concentration gradient less water reabsorbed by diffusion diuresis and natriuresis
34
production of concentrated urine in presence of max ADH
isosmotic fluid enters proximal tubule isosmotic reabsorption occurs descending limb is highly permeable to water so water leaves by osmosis until equilibrium of interstitial fluid ascending thin limb permeable to solute so solute passively diffuses out solute actively pumped out of thick ascending limb to maintain horizontal gradient as part of countercurrent mechanism maintains corticomedullary osmotic gradient early distal tubule impermeable to water so active dilution continues as NaCl is actively reabsorbed later distal tubule and CD are permeable in ADH presence water moves from tubule to intersittium by osmosis drive by the osmotic pressure difference of fluid in tubule and interstitium max ADH, small volume of high osmolarity urine is produced reabsorbed water enters capillaries returns to circulation decreases plasma osmolarity
35
urea trapping/recycling
tubule impermeable to urea except in medulla urea concentration increases as fluid flows along nephron and water reabsorbed medullary collecting duct urea concentration and permeability is high urea diffuses out of tubule down conc grad into the medullary intersittium increases osmolarity Medullary urea concentration increases (1) Some urea diffuses into loop of Henle in the medulla (2) Urea trapped in tubule as fluid leaves loop of Henle (3) and enters CD (4) Urea recycles from nephron to interstitium, back to nephron  Urea accumulates in medullary interstitium to help maintain cortico-medullary osmotic gradient (50% is excreted, 50% recycled) Urea excretion is minimal when water needs to be conserved
36
distal convoluted tubule
macula densa to connecting segment fine tuning of remaining Na+ and Cl- sodium chloride co transporter Na+/H+ and Cl-/HCO3- exchangers no water reabsorption
37
NCCT
Also powered by Na⁺K⁺ATPase Blocked by thiazide diuretics e.g. bendroflumethiazide, indapamide
38
Na+/H+ exchanger
Na+ in H+ out
39
Cl-/HCO3- exchanger
Cl- in HCO3- out
40
H+ and HCO3-
H⁺ + HCO₃⁻ = H₂CO₃ ⇌ H₂O + CO₂
41
calcium reabsorption in DCT
10-15% under influence of PTH and vitamin D
42
composition in DCT
low intracellular Na+ NCCT takes up the sodium impermeable to water filtrate leaving the DCT will become more dilute
43
main segments of the collecting duct
cortical medullary
44
main functions of the collecting ducts
Potassium excretion and sodium reabsorption (ENaC and Na,K,ATPase) – principle cells Acid-base handling – intercalated cells Hormonal influence – aldosterone and ADH Urea reabsorption via UT-A1 and UT-A3 (urea recycling)
45
intercalated and principle cells
potassium secretion
46
water reabsorption in the CD
Apical membrane (tubular side) is impermeable to water BUT Permeability can be increased Insertion of aquaporins (water channels) into apical membrane Under ADH influence Basolateral surface is permeable Water moves into the interstitium via osmosis This osmotic gradient has been set up by the LoH countercurrent multiplier
47
action of ADH over hydration
Little/no ADH released Few/no water channels inserted Water channels are internalised into vesicles, away from membrane Tubule impermeable to water Water is lost in high flow-rate, dilute urine 
48
action of ADH dehydration
ADH released from posterior pituitary Insertion of water channels on apical membrane Vesicles fuse with membrane Water is reabsorbed back into the bloodstream Small volume of concentrated urine lost 
49
what is ADH regulated by
hypothalamic osmoreceptors in response to changes in plasma osmolarity
50
ADH release
cells swell or shrink ADH synthesised and packaged into granules in neurons in hypothalamus transported down the axon and stored and released from nerve terminals into the posterior pituitary released into the blood stream
51
effect of plasma osmolality on ADH secretion
as plasma osmolality increases the ADH increases rapidly if <280 mOsm/kg (dilute) no ADH release
52
as plasma osmolarity increases
ADH secretion increases Water channels inserted into LDT & CD Water reabsorbed by osmosis  Urine flow rate decreases  Urine osmolarity increases (removed water from it)  Plasma osmolarity decreases back to normal limits  No change in total solute excretion
53
high osmolality, negative feedback
High plasma osmolality (eg dehydration) detected by hypothalamic osmoreceptors Secretion of ADH from posterior pituitary Increased aquaporins in LDT & CD Conservation of water by the kidney (concentrated urine) Water reabsorbed back into blood  Reduction in plasma osmolality
54
low plasma osmolality negative feedback
Low plasma osmolality (eg over-hydrated) Less/no ADH  Less/no aquaporins in LDT and CD Removal of water by the kidney (large volume, dilute urine) Increase in plasma (and hence ECF) osmolality
55
nephrogenic diabetes insipidus
Non-response of ADH to V2 receptors
56
cranial diabetes insipidus
Reduced production of ADH
57
drugs used to target collecting ducts
Mineralocorticoid antagonists (MRAs) e.g. spironolactone, stop salt and water retention in the distal nephron  drop in BP. MRAs cause hyperkalaemia
58
over expression of ENaC
Liddle’s syndrome (Autosomal dominant cause of hypertension associated with hypokalaemia)
59
diabetes insipidus, cranial and ADH
Diabetes insipidus Insufficient ADH secretion (cranial DI) Idiopathic (characterised by degeneration of hypothalamic ADH secreting cells) Caused by head trauma, infection or brain surgery  Familial (ADH gene mutation) tment with synthetic ADH (Desmopressin)
60
failing to respond to ADH in NDI
Failure to respond to ADH (nephrogenic DI) Kidney damage from certain drugs, or inherited Dietary management, diuretics (to reduce GFR) and NSAIDS Up to 18L/day urine output
61
alcohol and ADH
Inappropriately inhibits ADH Beating a hangover

Medicine Unit 8 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions