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Renal ERIN > embryology and anatomy > Flashcards

embryology and anatomy Flashcards

1
Q

When does the pronephros form

A

week 4 then degenerates

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2
Q

How do the mesonephros and metanephros interact?

A

Ureteric bud from mesanephros interacts with metanephric mesenchyme to induce differentiation into the glomerulus to the DCt

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3
Q

what does the mesonephros give rise to?

A

ureter, pelvises, calyces, collecting ducts

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4
Q

what does the metanephros give rise to?

A

kidney and glomerulus to the DCT

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5
Q

what is the last part of the renal system to canalize?

A

ureteropelvic junction

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6
Q

What is potter sequence?

A

Oligohydramnios in utero -> compression of developing fetus -> limb deformities, facial abnormalities and pulmonary hypoplasia (from lack of fluid aspiration)

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7
Q

What complications may occur with potter sequence?

A

pulmonary hypoplasia
ARPKD
obstructive uropathy (posterior urethral valves)
bilateral renal agencies, chronic placental insufficiency

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8
Q

When is glucosuria normal?

A

pregnancy. increased GFR -> glucose in urine

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9
Q

are what concentration in the avg individual will there be glucose in the urine?

A

around 200 mg/dl

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10
Q

At what level of blood glucose will all the transporters in the PCT be saturated?

A

375 mg/dl

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11
Q

What is the splay phenomenon?

A

the fact that Tm (max reabsorption) for glucose is achieved gradually, not sharply, due to the heterogeneity of nephrons

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12
Q

If you see a child with a rash and amino acids in the urine what should you think of?

A

Hartnup disease

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13
Q

What is the pathophys of hartnup disease?

A

There is no trytophan transporter in PCT -> tryptophan deficiency -> pellagra and aa’s in the urine

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14
Q

what is fanconi syndrome?

A

Loss of all PCT functions - loss of bicarbs, glucose, amino acids, etc.

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15
Q

how does fanconi present?

A 
Patient urinates alot, polyuria, polydipsia, glocusira
BUT a normal serum glucose 
Non-anion gap metabolic acidosis
Hyopphosphatemias
Amino acids in the urine
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16
Q

Genetics of Fanconi syndrome

A

Inherited form - associated with cystinosis

Can be acquired

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17
Q

What is cystinosis?

A

A lysosomal storage disease that results in the build up of cysteine in cells, often the PCT is one of the first places

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18
Q

What is cystinuria?

A

A PCT defect that has impaired cystine reabsorption

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19
Q

What are aquired causes of fanconi syndrome?

A

Lead poisoning
Multiple myeloma
Cisplatin, valproate, etc.

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20
Q

What is the descending limb of the LOH permeable to?

A

Permeable to H2O, impermeable to NaCl

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21
Q

what is the ascending limb in the LOH permeable to?

A

Permeable to NaCl, impermeable to H2O

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22
Q

What is reabosbred in the distal tubule?

A

Na, Cl and Ca (via a Na/Ca exchanger)

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23
Q

What effect does PTH have on the DCT?

A

increases the Ca/Na exchanger leading to increased Ca reabsorption

24
Q

How is Ca reabsorbed int he thick ascending limb of the LOH?

A

some K leaks into the lumen causes an overall + charge which drives Ca and Mg to be reabsorbed paracellularly

25
What are the cell types in the collecting duct ?
principal cells and alpha-intercalated cells
26
Explain the fucntions of the principal cells
Primarily Na reabsorption and K secretion and water reabsorption Na/K ATPase is on the basal side and Enac channels are on the apical side
27
What are the effects on aldosterone on the CD?
increases Na/K ATPase activity and Enac upregulation ->increased Na reabsorption and K excretion in principle cells Also increases H secretion in intercalated cells
28
What stimulates aldosterone activity?
AT II | High K
29
What are the receptors for ADH and their functions?
V1 -> vasoconstriction | V2 -> H2O reabsorption
30
What are the stimuli for ADH release?
Hyperosmolarity | Volume loss
31
What effect does ADH have on urea reabsorption?
it increases it
32
Why is urea reabsoprtion importnat?
it concentrates the interstitium for H2O reabsorption in the LOH
33
Where in the nephron does AT II have effect?
the PCT where it increases Na reabsorption
34
What is the defect present in Fanconi syndrome?
Reabsorption defect in PCT that leads to excretion of amino acids, water, glucose, bicarb, phosphate, etc.
35
What are the effects of fanconi syndrome?
metabolic acidosis, hypophosphatemia, osteopenia
36
What causes fanconi syndrome?
``` hereditary defects (such as wilsons disease, tyrosinemia, cystinosis etc). Ischemia, multiple myeloma, drugs, lead poisoning ```
37
How does fanconi syndrome present?
Similarly to diabetes but wiht a normal blood glucose (maintained by insulin/glucagon)
38
What is the defect in bartter syndrome?
reabsorption defect in thick ascending loop of henle (the Na/K/Cl cotransporter)
39
which transport is defective in bartter syndrome?
Na/K/Cl
40
what are the effects of bartter syndrome?
metabolic alkalosis, hypokalemia, hypercalcuria
41
What is the cause of bartter syndrome?
Genetic (autosomal recessive)
42
what does bartter syndrome present very similarly to?
chronic use of loop diuretics?
43
What is the defect in Gitelman syndrome?
reabsorption defect of NaCl in DCT
44
Effects of Gitelman syndrome?
metabolic alkalosis, hypokalemia, hypomagnesemia, hypocalciuria
45
What is the cause of gitelman sydnrome?
Genetic (autosomal recessive)
46
What is the defect in liddl syndrome?
gain of function mutation -> Increased Na channel and increased Na reabsorption
47
What are the effects of liddle syndrome?
hypokalemia metabolic alkalosis hypertension and decreased aldosterone
48
what is the cause of liddl syndrome?
Genetic (autosomal dominant)
49
what does liddl syndrome present similarly to?
hyperalderonistm (but aldosterone is almost undetectable)
50
treatment of liddl syndrome/
amiloride
51
What is the pathophys of SAME syndrome?
Hereditary 11B-HSD deficiency | This usually converts cortisol to cortisone. Results in increased cortisol which can act on mineralcorticoid receptors
52
does cortisone act on mineralcorticoid receptors?
no
53
does cortisol act on mineralcorticoid receptors?
yes
54
What are the effects of SAME?
high BP hypokalemia metabolic alkalosis decreased serum aldosterone
55
what is the cuase of SAME?
genetic (autosomal recessive) | OR acquired via eating licorice
56
How to treat SAME?
K-sparing diurects (block mineralcorticoid effectS) | OR exogenous corticosteroids (decrease endogenous production)

Renal ERIN (5 decks)

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