Renal Anatomy Flashcards

1
Q

Of the total 42L of water in the body, which percentages of water are found where?

A

62% intracellular
28% extracellular interstitial (fluid surrounds cells)
7% plasma
3% transcellular (cerebrospinal)

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2
Q

The kidney sits between which sections of the spinal cord?

A

12th Thoracic to 3rd lumbar.

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3
Q

Complete failure to develop a kidney is called what?

A

Kidney agenosis

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4
Q

Horseshoe kidney is?

A

When two kidneys fused across the midline. Increased risk of kidney stones.

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5
Q

Label a kidney.

A

Capsule surrounds. Three main layers from outside in Cortex, Medulla, Pelvis. Papilla at the end of the medulla rays, which drain into the Calyx before into the ureter. Urethra, nerves and vessels pass through the hilum.

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6
Q

How many nephrons per kidney?

A

1-1.5million

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7
Q

Glomerular filtration rate?

A

all in both kidneys: 125ml/min

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8
Q

Percentage position of the nephrons?

A

85% superficial (cortex)

15% juxtamedullary (outermedulla)

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9
Q

Renal failure is defined as a fall in glomerular filtrate rate (GFR) leads to… This can be either ….. or ……

A

increase in urea and creatinine- toxic.
Acute-reversible
Chronic- irreversible

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10
Q

Acute vs chronic renal failure?

A

Acute- short term e.g. days, normal haemoglobin level, normal renal size no peripheral never damage.
Chronic- long term e.g. years, haemoglobin low, renal size decreased, peripheral neuropathy present.

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11
Q

Causes of renal failure? Leading to a reduction in renal size.

A

Thickening of glomerular membrane so harder to filter.
Leads to…damage to glomeruli, causing progressive scarring (glomerulosclerosis) and atrophy (dying off) fibrosis of tubules, leading to reduction in renal size.

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12
Q

Group of symptoms described by renal failure name?

A

Uraemia.

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13
Q

Uraemia symptoms? (4 main)

A

Failure to excrete water: hypertension > Hyperkalaemia
poor excretion: urea and creatine build up> neuropathy, pericardis (inflammation of the pericardium)
Failure to produce erythropoetin made in kidneys> low RBCs> anaemia> lethargy
Failure to excrete Phosphate, lowers serum calcium binds to> precipitates calcification> bone diseases

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14
Q

Causes of renal failure?

A

Glomerulonephritis- inflammation of glomerulus

Diabetes mellitus, hypertension, polycystic kidney disease.

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15
Q

Treatments for renal failure?

A

Chronic: dialysis, transplant
Acute: diet restrict salt, water, protein
Phosphate binders

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16
Q

In the proximal convoluted tubule …% of the filtrate is reabsorbed. …. H2O and Na, …% glucose and AA, ….%bicarbonate

A

70%
70%
100%
90%

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17
Q

In cell type 1 of the PCT what are the three pumps on the tubular fluid (apical side)?

A
  • Pumps into cell Na and Glucose= Sodium Glucose transporter protein e.g. SGLT1 and SGLT2.
  • Pumps into the cell Na and PO4 = NaPi II
  • Pumps in sodium and Amino acids.
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18
Q

In cell type 1 of the PCT what is actually getting reabsorbed?

A

Sodium, Glucose, Amino Acids, PO4 (phosphate)

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19
Q

In cell type 1 of the PCT what are the pumps on the basolateral side? (3)

A
  • Sodium potassium pump-ATPase pumping 3Na out into blood for every 2K back into the cells
  • Potassium channel- K out. (recycles K and sets negative pd so that the pumped out Na will go down the electrical potential gradient into the blood)
  • Facillitated diffusion through transport proteins of AA, Glucose and Phosphate.
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20
Q

What also follows in cell 1 of the PCT in being reabsorbed? why?

A

Water
ion levels such as sodium outside the basolateral side high so water follows by osmosis paracellularly. Wherever Na goes water follows.

21
Q

What happens in NaPi II knockout mice?

A

Lost ability to reabsorb phosphate. Leads to abnormal Bone development. But older mice can compensate for this.

22
Q

Amino acids number in the SGLT1 and SGLT2 channels?

A

SGLT1 664 amino acids

SGLT2 672 amino acids

23
Q

What’s renal Glycosuria? Familial?

A

Glucose found in the urine. Familial= inherited- results from mutations in the SGLT 2. Homozygous severe.

24
Q

Also in cell 1 of the PCT PH is controlled how? What are the pumps on the apical side? Basolateral?

A

Carbonic anhydrase in the filtrate dissociates into CO2 and H2O by carbonic anhydrase. These diffuse through the apical membrane and combine again to form Carbonic anhydrase. This dissociates again by carbonic anhydrase, releasing H+ ions and bicarbonate ions. The H+ is pumped back out the apical surface as a sodium ion comes in through the Sodium Hydrogen exchange protein 3 (NHE3).
The bicarbonate ions are then pumped out the basolateral surface along with 3Na+. (water follows).

25
Q

what happens in knockout NHE3 mice?

A

reduced ability to reabsorb bicarbonate, which is alkaline, therefore causes acidosis in the body. This also lowers blood pressure because less sodium is reabsorbed, therefore less water is reabsorbed so Extracellular fluid drops and so BP decreases.

26
Q

What is renal threshold?

A

the level of plasma glucose that’s higher than the rate of reabsorbtion so can be seen in the urine. >300mg/100, e.g. in case of diabetes mellitus.

27
Q

What are the two systems of secretion from peritubules to tubular fluid? positives and negatives?

A

Remove plasma protein bound substances.

Problem good at secreting drugs and lost in urine e.g. penicillin but good to get rid of chemotherapy drugs

28
Q

What happens in the loop of henle? Three parts?

A

More water is reabsorbed along with ions Na, Cl, Ca, Mg

29
Q

What is and happens in the first of 3 sections of the loop of henle?

A

Thin descending limb: impermeable to Na and Cl so maintains the high conc of ions in the medulla. H20 leaves via osmosis through the thin descending limb.

30
Q

What happens in the second and third of the 3 sections of the loop of henle? (brief)

A

Thin ascending limb and thick: both impermeable to water, sodium and chloride pumped out into the medulla.

31
Q

What are the channels on cell 2 in the thick ascending limb?

A

Apical: NKCC2 (sodium, potassium, 2 chloride cotransporter protein- transports Na, K and 2Cl into the cell.
Basolateral: The sodium is pumped out into the blood by the Sodium potassium ATPase on the basolateral side. The Potassium is also transported out.
Through CLCK the Cl- leaves when the Barttin accessory subunit is present.
The apical membrane is also partially leaky to K which leaks back through ROMK (kir1.1) ensuring the positive electrochemical gradient so Mg2+ and Ca+ moves paracellularly and is reabsorbed.
By the end of thick ascending limb there is not enough K to support the NkCC2

32
Q

What is Bartter’s syndrome?

A

Mutation in the genes encoding the NKCC2 channel. K not recycled so ROMK stops. Mg and Ca+ don’t follow paracellularly
Recessively inherited.

33
Q

Symptoms of Bartter’s syndrome?

A
  • Too much NaCl in urine-salt wasting.
  • As less ions absorbed less water follows so more excreted = Polyuria.
  • Water lost= Hypotension
  • Less K reabsorbed = hypokalaemia
  • Ca and mg not moved by diffusion paracellularly =Hypercalciuria- high Ca in urine.
  • High PH in body fluids= Metabolic alkalosis (due to less K reabsorbed affects H conc)
  • Kidney stones due to High Ca in urine= Nephrocalcinosis
34
Q

How do loop diuretics work?

A

They act upon the NKCC2 channel treat high blood pressure by reducing the water reabsorbed (by reducing Na), but can give barter like symptoms.
e.g.
Furosemide- blocks by binding.
Bumetanide.

35
Q

Function of the Early Distal tubule?

A

Reabsorbs Na, Cl, Mg, any left water. Sensitive to Thiazide diuretics.

36
Q

In cell 3 in the Early Distal Tubule what are the channels?

A

Apical: A cotransporter of sodium and chloride- NCC and a Mg channel in.
Basolateral: Mg efflux unknown, but a sodium potassium pump, K channel out and Barttin associated CLCK channel for Cl.

37
Q

What is Gitelman’s syndrome?

A

Recessive mutation in the genes coding for NCC channel in early distal tubule.Results in less Cl or Na being reabsorbed.

38
Q

What are the symptoms of Gitelmans?

A

Less Cl or Na reabsorbed= salt wasting and polyuria
Hypotension and hypokalaemia
Metabolic alkalosis
Only difference between Barrters is that patients have Hypocalciuria.

39
Q

What do Thiazide diuretics act upon?Uses?

A

The NCC transporter protein in call 3 on early distal tubule. Less Cl and Na reabsorbed less water follows.
Uses: High blood pressure and oedema.
Gittlemans like symptoms.

40
Q

Being a carrier for mutations in ….. ,…….. or ……. channels can confer an advantage in keeping blood pressure low. Where are these found?

A

NKCC2, NCC, and ROMK.
Thick ascending limb: ROMK and NKCC2
Early distal tubule: NCC

41
Q

Function of the Late distal tubules to collecting duct?

A

Reabsorb Na and H20 as well as secretion of K and H

42
Q

What are the two cell types found in the Late distal tubule?

A

Principal cells and Intercalated cells

43
Q

What are the functions of the Principal cells?

A

Na and H20 reabsorption

K and H secretion

44
Q

What are the functions of the Intercalated cells?

A

Switch between alpha or Beta IC depending on acid in the body.
H Secretion and absorption depedending on above.
HCO3 absorption or secretion.
Controls PH basically.

45
Q

What are the channels on the Principle cells?

A

Apical: Epithelial Na Channel (ENaC)- Na in
Aquaporin 2 to let H2O in. Regulated)
ROMK leaks K out back into nephron tubules.

Basolateral: Sodium potassium exchange protein
AQP3 and 4 to reabsorb H2O
Kir 2.3 recycles K.

46
Q

What is unique about Aquaporin 2?

A

On the apical surface of principal cell. Its regulated whether this is open or not whether water is present here or not.

47
Q

Examples of Principal cell diseases? (3)

A
  • Diabetes Insipidus- AQP2 problem, less water reabsorbed, BP down.
  • Liddle’s syndrome- mutation in ENaC.
  • Pseudohypoaldoateronism
48
Q

Diuretic that acts upon the …… in the late distal tubule?

A

Amiloride, blocks the ENaC channel. Potassium sparing.

49
Q

Up to alpha IC Cell.

A

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