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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
Q

What are the cell types in the collecting duct ?

A

principal cells and alpha-intercalated cells

26
Q

Explain the fucntions of the principal cells

A

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
Q

What are the effects on aldosterone on the CD?

A

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
Q

What stimulates aldosterone activity?

A

AT II

High K

29
Q

What are the receptors for ADH and their functions?

A

V1 -> vasoconstriction

V2 -> H2O reabsorption

30
Q

What are the stimuli for ADH release?

A

Hyperosmolarity

Volume loss

31
Q

What effect does ADH have on urea reabsorption?

A

it increases it

32
Q

Why is urea reabsoprtion importnat?

A

it concentrates the interstitium for H2O reabsorption in the LOH

33
Q

Where in the nephron does AT II have effect?

A

the PCT where it increases Na reabsorption

34
Q

What is the defect present in Fanconi syndrome?

A

Reabsorption defect in PCT that leads to excretion of amino acids, water, glucose, bicarb, phosphate, etc.

35
Q

What are the effects of fanconi syndrome?

A

metabolic acidosis, hypophosphatemia, osteopenia

36
Q

What causes fanconi syndrome?

A 
hereditary defects (such as wilsons disease, tyrosinemia, cystinosis etc). 
Ischemia, multiple myeloma, drugs, lead poisoning
37
Q

How does fanconi syndrome present?

A

Similarly to diabetes but wiht a normal blood glucose (maintained by insulin/glucagon)

38
Q

What is the defect in bartter syndrome?

A

reabsorption defect in thick ascending loop of henle (the Na/K/Cl cotransporter)

39
Q

which transport is defective in bartter syndrome?

A

Na/K/Cl

40
Q

what are the effects of bartter syndrome?

A

metabolic alkalosis, hypokalemia, hypercalcuria

41
Q

What is the cause of bartter syndrome?

A

Genetic (autosomal recessive)

42
Q

what does bartter syndrome present very similarly to?

A

chronic use of loop diuretics?

43
Q

What is the defect in Gitelman syndrome?

A

reabsorption defect of NaCl in DCT

44
Q

Effects of Gitelman syndrome?

A

metabolic alkalosis, hypokalemia, hypomagnesemia, hypocalciuria

45
Q

What is the cause of gitelman sydnrome?

A

Genetic (autosomal recessive)

46
Q

What is the defect in liddl syndrome?

A

gain of function mutation -> Increased Na channel and increased Na reabsorption

47
Q

What are the effects of liddle syndrome?

A

hypokalemia
metabolic alkalosis
hypertension and decreased aldosterone

48
Q

what is the cause of liddl syndrome?

A

Genetic (autosomal dominant)

49
Q

what does liddl syndrome present similarly to?

A

hyperalderonistm (but aldosterone is almost undetectable)

50
Q

treatment of liddl syndrome/

A

amiloride

51
Q

What is the pathophys of SAME syndrome?

A

Hereditary 11B-HSD deficiency

This usually converts cortisol to cortisone. Results in increased cortisol which can act on mineralcorticoid receptors

52
Q

does cortisone act on mineralcorticoid receptors?

A

no

53
Q

does cortisol act on mineralcorticoid receptors?

A

yes

54
Q

What are the effects of SAME?

A

high BP
hypokalemia
metabolic alkalosis
decreased serum aldosterone

55
Q

what is the cuase of SAME?

A

genetic (autosomal recessive)

OR acquired via eating licorice

56
Q

How to treat SAME?

A

K-sparing diurects (block mineralcorticoid effectS)

OR exogenous corticosteroids (decrease endogenous production)

Renal ERIN (5 decks)

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