Brainscape's Knowledge GenomeTM

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


See full index

Physiology and Pharmacology > The Kidney > Flashcards

The Kidney Flashcards

1
Q

What happens if there is a mutation in SGLT2?

A
  • Familial renal glycossuria
  • Increased urinary glucose
  • Autosomal recessive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When is aldosterone released?

A

1) Increase in plasma K by as little as 0.1mM
2) Decrease in plasma Na
3) Decrease in extracellular fluid volume

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

What does renin do?

A
  • Catalyses the conversion of angiotensin to angiotensis 1 (in the blood vessels)
  • AGT1 -> AGT2 by Angiotensin converting enzyme in the capillaries (the bulk of this happens in the lungs where the capillary density is larger)
  • Promotes the release of aldosterone from the zona glomerulosa
  • AGT2 also causes vasocontriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What channels are present in the proximal tubule and what do they allow?

A 
Apical:
SGLT1/ SGLT2 = Glucose and sodium cotransporter
Na/Amino acids = cotransporter
NApiII = Phosphate/Na cotransporter
NHE3 = Na/H symporter (H out Na in)

Basolateral
Na/KATpase = 3 NA out, 2 K in
K = K out
Na/HCO3 = 3 NA and 1 HCO3 out

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

What is uraemia?

A

A group of symptoms associated with chronic renal faliure

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

Symptoms of chronic renal faliure?

A

URAEMIA (a group of symptoms associated with chronic renal faliure)

  • Hypertension
  • Hyperkalemia
  • Mild acidosis
  • Nausea/ vomiting - due to increased cretanine and serum urea
  • Calcification
  • Amemia lethargy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the pelvis of the kidney?

A

1 per kidney, urine flows from the calyx into here and then into the ureter

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

What is different about the descending limb and the ascending limb of the loop of henle?

A

Decending- absorbs water but not ions

Acsending - absorbs ions but not water

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

What are the roles of the principle cells?

A

1) Concentrate urine
2) Secrete K and H
3) Reabsorb Na and H2O

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

What is the treatment for Liddle’s syndrome?

A

Amiloride, K sparing diuretic

- Blocks excess ENaC

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

What are the 3 regions of the adrenal cortex?

A
  • Zona reticularis
  • Zona fasciculate
  • Zona glomerulosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where are hypothalamic receptors present and what do they detect?

A
  • In the cell bodies of the neurosecretory cells in the supra-optic and and paraventricular nucleus in hypothalamus
  • They detect changes in osmolality +/- 3mOsm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Names of loop diuretics and what channel do they act on?

A

Bumetanide
Frusemide

Block the NKCC2 channel in the apical membrane of the TAL

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

What are the medullary rays?

A

Part of the medulla, show the orientation of the blood vessels

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

How does alcohol affect vasoreprssin release and what are the consequences?

A
  • Inhibit release when osmolality is normal
  • Less water reabsorbed
  • Increase urine flow rate
  • Dehydration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does aldosterone stimulate?

A

1) Resabsorption of Na
2) Secretion of K and H
3) Regulates the angiotensin system

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

What is the hilus of the kidney?

A

The point in the kidney where the ureter leaves

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

What is the progression of chronic renal faliure?

A
  • Thickening of the glomeruli membrane
  • Causes glomerulosclerosis (scarring)
  • Tubular atrophy (death of nephron and kidney)
  • Interstitial inflammation
  • Fibrosis (reduce in renal size)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the 3 types of diuretics and where do they act?

A

Loop diuretics - loop of henle
Thiazide diuretics - Early distil tubule
K sparing diuretics - Late distil tubule

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

How is Bartters symptoms different to Gittlemans syndrome?

A

Bartters involves hypercalciuria

Gittlemans involves hypocalciuria

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

What is the glomerulus?

A
  • A capillary bed embedded in the beginning of the nephron which filters the plasma
  • Has afferent and efferent arterioles
  • Liquid and ions are filtered though and proteins don’t
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the difference between superficial and juxtamedullary nephrons?

A

Superficial

  • Regulates urine
  • 85% of nephrons
  • Glomerulus and bowmans capsule is in the outer cortex

Juxtamedullary

  • Fine tunes urine
  • 15% of nephrons
  • Glomerulus and BC on the borderline between the cortex and the medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where does aldosterone act?

A

Late distil tubule and cortical collecting duct

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

What is the transport maximum for glucose?

A

375mg/min

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

What is the structure of the alpha intercalated cell?

A

Apical:
H ATPase - H out

Basolateral:
Cl channel - Cl out
AE1 - Cl in, HCO3 out

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

What does the release of renin cause?

A

1) Increase Na reabsorption
2) Increase in extracellular fluid
3) Blood pressure goes to normal

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

What do angiotensin converting enzyme cause?

A

Less constriction and less water retension

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

4 abnormalities of the kideny?

A

1) Horseshoe kidney, remain fused
2) Ectopic kidney, one or more kindeys form in the pelvis but they are normal
3) Polysystic kidney - kidneys are enlarged to 30cm
4) Renal agensis - kidney doesn’t develop. Incompatible with life

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

What is minimum flow rate?

A

300ml

30
Q

What does renin-angiotensin regulate?

A
  • Body fluid volume

- Plasma K and Na

31
Q

What percentage of fluid is extracellular?

A

38%

28% Intersitial, 7% plasma, 3% transcellular

32
Q

Causes of chronic and acute renal faliure?

A

Chronic:
Hypertension
Diabetes mellius
PKD

Acute:
Pre renal
Renal
Post renal

33
Q

What are diuretics?

A
  • Drugs which increase the flow rate of urine

- Treat hypertension and treat chronic renal faliure

34
Q

Example of a thiazide diuretic and what does it d?

A

Chlorothiazide

  • Targets NCC in the apical membrane of the early distil tubule
  • Side effects are Gittleman’s syndrome
35
Q

Treatment of chronic and acute renal faliure?

A

Chronic:
Dialysis
Dieuretics

Acute:
Dialysis

36
Q

How does ecstasy affect vasopressin release and what are the consequences?

A
  • Increase release
  • Retain water that would normally be secreted
  • If coupled with drinking lots -> odema and swelling of the brain
37
Q

What is the process of HCO3 reabsorption?

A
  • HCO3 + H -> H2CO3 (carbonic acid)
  • H2CO3 -.> H2O + CO2 (by carbonic anhydrase)
  • H2O + CO2 diffuse into the membrane
  • H2O + CO2 -> H2C03 (by carbonic anhydrase)
  • H2CO3 -> H + HCO3
    H out of apical membrane by NHE3
    HCO3 out of basolateral membrane by Na/HCO3 cotransporter
38
Q

What is an examples of a K sparing diuretic and where does it act?

A
  • Amiloride

- ENaC in the principle cells of the late distil tubule

39
Q

What are the channels in the early distil tubule?

A

Apical:
NCC - cotransporter (one Na and one Cl in)
Mg channel

Basolateral:
Na/KATPase
K channel 
Mg channel 
CLCK and Barttin
40
Q

Where is the site of action of vasopressin?

A

Collecting duct in the kidney

41
Q

What does too much angiotensin 2 cause?

A

Hypertension

42
Q

What percentage of fluid is intracellular?

A

62%

43
Q

What causes central diabetes insipidus and what is the treatment?

A

Problems which the CNS at the level of the hypothalamus or the posterior pituitary

Nasal spray (containing synthetic vasopressin)

44
Q

Principle cell model for vassopressin action?

A
  • Vasopressin activates V2 receptors on the basolateral membrane
  • Activation of protein kinase A (through G protein coupled pathway)
  • PKA attaches to the vesicles containing AQP2 channels
  • Channels fuse with the apical membrane
  • Increases the amount of water absorbed

When VP levels drop:
-Endocytosis of the channels

45
Q

What is Liddle’s syndrome?

A
  • Low aldosteone
  • BUT increase in NA absorption through ENaC
  • Increase in ENaC channels which can’t be removed from the membrane
  • Defect in endocytosis
  • Too much Na, too much water reabsorbed
46
Q

Intercellular composition of ions?

A 
[K] = 144mM
[Na] = 10mM 
[Other] = 40mM
[Cl] = 4mM
[Proteins] = 55mM
[Other] = 140mM
47
Q

What are the symptoms of ROMK knockouts in mice and humans?

A

Mice

  • Salt wasting
  • Polyuria
  • Acidosis

Humans
- Same symptoms but ALKALOSIS

48
Q

Function of the calyx?

A

Part of the medulla, urine drains through here into the pelvis

49
Q

What type of hormone is aldosterone?

A

A mineralcorticoid - regulates mineral content (especially Na and K)

50
Q

2 types of cell in the late distil tubule?

A

Principle cell

Intercalated cell - has alpha and beta configurations

51
Q

What is renal faliure?

A
  • When the glomerulus filtration rate falls below 125ml/min

- Accumulation of serum urea and creatine which are toxic

52
Q

Where is renin released from and how?

A
  • From the juxtaglomerular apparatus (glomerulus and early distil tubule) in the kidney

In early distil tubule:
- Macular densa cells release compounds which act on the afferent arteriole in response to urine flow rates

In glomerulus:
- Contains the afferent arterioles have granules containing renin, compounds cause renin release

53
Q

What is the structure of the beta intercalated cell?

A

Apical:
AE1 - Cl in, HCO3 out

Basolateral:
Cl channel - Cl out
H ATPase - H out

54
Q

What are the channels in the principle cell and what do they do?

A

Apical:
ENaC - 1 Na in
ROMK - 1 K out
AQP2 - H2O in

Basolateral:
Na/KATPase
Kir 2.3 - K out
AQP3 and AQP4 - water out

55
Q

What causes the release of vasopressin?

A
  • Increased plasma osmolality (how concentrated)
  • Stress
  • Dehydration
  • Injest solute
56
Q

When is renin released?

A
  • In response to a fall in extracellular fluid volume, which causes a fall in the glomerular filtration rate and a fall in urine flow rate
57
Q

Dimentions of the kideny?

A

150g
10cm x 5.5cm
Found between the 12th lumbar and the 3rd thoratic segment

58
Q

How is vasopressin released?

A
  • Activation of the hypothalamic receptors
  • Action potential generated down the axon into the posterior pituitary gland
  • Causes influx of Ca2+
  • Fusion of vesicles containing vasopressin with the presynaptic membrane
  • Vasopressin release into capillary bed
59
Q

What is the transport maximum and what is it limited by?

A
  • When the transport across the tubule has reached its maximum rate
  • Limited by the number of carrier channels
60
Q

What causes nephrogenic diabetes inspidus?

A
  • No activation of PKA due to V2 defect
  • AQP2 defect
  • No treatment
61
Q

What happens when injest salt?

A
  • Vasopressin release downregulated
  • If this didn’t happen there would be a opposing system as vasopressin aims to increase ECF volume and aldosterone aims to decrease it
62
Q

Where is aldosterone released from?

A

From the zona glomerulosa in the adrena cortex of the adrenal gland

63
Q

Onset for chronic and actute renal faliure differences?

A

Chronic:
Irreverisble
Progressive
Decreased Hb and renal size

Acute:
Reversible
Short

64
Q

What is albumin and why is it significant?

A

Small moleucular weight protein which is present in the ultrafiltrate but reabsorbed in the tubules
If still present in the turine - problem with the tubule

65
Q

What are the side effects of loop diuretics?

A 
Bartters-like symptoms:
Salt wasting 
Hypokalemia 
Hypotension
Alkalosis
Hypercalciuria
66
Q

Extracellular composition of ions?

A 
[K] = 5mM
[Na] = 140mM
[Other] = 8mM

[Cl] = 103mM
[Proteins] = 15mM
[Other] =36mM

67
Q

What is pseuodohypoaldosteronism?

A
  • High aldosterone
  • BUT high salt loss (Na)
  • Problem with the mineralcorticoid receptor
  • No production of protein channels
68
Q

Principle cell model of aldosterone?

A
  • Steroid hormone, enters through the cell membrane
  • Binds to intracellular mineralcorticoid receptor
  • Moves into nucleus and stimulates RNA transcription
- Increase in the proteins which synthesise:
ROMK
Na/H exchanger
ENaC
Na/KATPase
  • Increase capacity to reabsorb Na and secrete K and H
  • Same mechanism as in the alpha intercalated cells
69
Q

What are the channels present in the TAL and how does Mg and Ca move?

A

Apical:
NKCC2 - Na, K, 2 x Cl in
ROMK (kir 1.1) - K out

Basolateral:
Na/KATPase - 3 Na out, 2 K in
K channel
CLCK - Cl out, regulated by BARTTIN

Mg and Ca move by paracellular transport

70
Q

What is the function of the loop of henle?

A
  • To concentrate urine

- Removal of forgein compounds from the body (penicillin)

Physiology and Pharmacology (15 decks)

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