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Renal > 05.08 - Disorders of PCT, Water (Gosmanova) - PP, No reading > Flashcards

05.08 - Disorders of PCT, Water (Gosmanova) - PP, No reading Flashcards

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1
Q

Hormonal Function of PT

A

Final pathway in synthesis of active Vit D

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1
Q

Isolated PT dysfunctions are rare but typically result from

A

disorder of specific transport proteins

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2
Q

Mutation in AR Hypo-P Rickets

A

Several leading to increased FGF-23; or Na-Pi Iic transporter

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3
Q

What is Oncogenic Hypo-P Osteomalacia

A

Inc. production of FGF-23 by some tumors: fibromas, angiosarcomas, hemangiopericytomas

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3
Q

2 ways ADH regulates AQP-2

A

Short-term: reversibly shuttles channel to luminal membrane; Long-term: inc transcription of AQP-2 gene

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4
Q

Plasma Na ~

A

(Total Body exchangeable Na and K) / TBW

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5
Q

What causes Vit D-dependent Rickets Type 1

A

Mutation of 1alpha-Hydroxylase

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6
Q

Mutation in PHEX results in increased

A

levels of circulating factor FGF-23 (PHEX normally downregulates)

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6
Q

When is Normal Osmolarity Hyponatremia likely to occur

A

HyperTGemia, Paraproteinemia - when solid phase of plasma is greatly increased

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7
Q

To which is ADH release more senstive, Posm increase or decrease in BV

A

Posm increase: 1% increase in Posm triggers, but takes 7% decrease in BV to trigger

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8
Q

Hypernatremia usually develops if

A

Thirst is impaired or limitation in acess to free water

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9
Q

FGF-23 inhibits

A

Na-Pi cotransporter and alpha-1-hydroxylase

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9
Q

What causes Hartnup Disease

A

Defect in neutral AA transporter (SLC6A19)

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9
Q

Most important inherited cause of Fanconi Syndrome

A

Cystinosis - Cysteine not degraded normally

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9
Q

Main defence mechanism against hypernatremia

A

Thirst

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10
Q

Generalized PT dysfunctions are usually accompanied by

A

cause-specific extra-renal manifestations

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11
Q

Changes in Plasma Na are mainly determined by changes in

A

TBW

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12
Q

Normal Posm

A

285-290 mOsm/kg

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12
Q

When is Dilutional Hyponatremia likely to occur?

A

Glucose in absence of insulin, Mannitol, Glycine

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13
Q

Polyuria is defined as

A

Incr in urine volume > 3L/day

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14
Q

__ is always present in True Hyponatremia

A

Impaired urinary dilution mechanisms

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15
Q

How does increase in peritubular capillary hydrostatic pressure affect net reabsorption of Na and water

A

Reduces

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16
Q

Glomerulotubular Balance is the intrinsic ability of tubules to increase reabsorption in response to

A

Incr tubular load

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18
Q

Macro structure of PT epithelial cells

A

Microvili (brush border); Basolateral surface is thrown into folds - both extend surface area

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19
Inc production of FGF-23 by some tumors
Oncogenic Hypo-P Osteomalacia
19
Non-osmotic stimuli that stimulate ADH release
Dec ECV, Nausea, Pain, Drugs, Corticosteroid deficiency
19
In absence of ADH, urinary osmolarity can be lowered to
40-60 mOsm/kg
21
Ang 2 regulates ___ reabsorption and ___ secretion
NaCl and H20; H+ secretion
22
How is insulin taken up by PT cells
Pinocytosis
23
Water Excess =
0.6 x TBW x (1 - [Na]/140)
24
Most common inherited phosphate wasting disorder
X-Linked Hypophosphatemic Rickets
24
Osmotic threshold for thirst vs ADH
Slightly higher for thist: 290-295 vs 280-290
24
Hyponatremia with volume depletion is caused by
Renal, GI, or Skin losses; Third spacing
25
4 Acquired forms of Nephrogenic DI
(1) Defect in medullary interstitial tonicity; (2) Defect in cAMP generation; (3) AQP-2 downreg; (4) Pregancy
26
Cause of Cystinuria
Mutation of brush border transporter responsible for cysteine, and other AA's
27
Relationship of PHEX, FGF-23, and Na-Pi cotransporter
PHEX inhibits FGF-23, and FGF-23 inhibits Na-Pi cotransporter and Alpha1-Hydroxylase production
28
Proximal Straight Tubule is aka
Parse Recta
30
Reabsorption in PT is dependent on
Volume Status
31
Serum Glucose in Hereditary Renal Glucosuria
Normal
32
Mutation of brush border transporter responsible for cysteine, and other AA's
Cause of Cystinuria
32
2 most important acquired causes of Fanconi Syndrome
Tenofovir, Multiple Myeloma
33
How does X-Linked Hypophosphatemic Rickes present clinically
Rickets in children; Osteomalacia in adults
33
Hyperosmolar Hyponatremia is due to
Presence of other osmotically active substances that cause water movement out of cells = Dilutional Hyponatremia
34
True Hyponatremia occurs as a result of
Incr TBW, either absolute or relative
36
Mutation in X-linked Hypophosphatemia
PHEX
37
\_\_\_ is present in majority of cases of true hyponatremia
Appropriate or inappropriate increase in ADH
39
Phosphate vs Na: One can be reabsorbed transcellular and para, the other only trans
Phosphate is trancellularly reabsorbed, Na can be either.
40
3 functional segments of PT
S1-initial short segment; S2-remaining PCT and cortical parse recta; S3-medullary parse recta
42
Severity of Cystinuria
Relatively benign, rarely causes kidney failure
44
Hereditary Renal Glucosuria is caused by
mutation of SGLT2 Glucose transporter
44
FGF-23 normally inhibits
Na-Pi cotransporter
46
Classifications of PT dysfunction based on mechanism
Generalized vs Isolated Solute Transport Disorders
48
Inheritance of Hereditary Renal Glucosuria
Autosomal recessive
49
Water Deficit =
0.6 x TBW x ([Na]/140 - 1)
50
Hyponatremia with Volume Overload is caused by
Decreased ECV: CHF, Kidney failure, Cirrhosis, Nephrotic
51
Normal function of PHEX
Downregulate FGF23
53
Parathyroid hormone regulates what in PT
Pi excretion
54
Normal osmostic threshold for ADH release
280-290 mOsm/kg
56
Fanconi Syndrome can be \_\_, but is most commonly \_\_\_
Inherited, but most commonly acquired
58
Susceptibility of PT to ischemia
High
59
Osmotic threshold for thirst
290-295 mOsm/kg (slight higher than for ADH)
60
Patient with functional SGLT2 will have glucosuria if
[Glu] exceeds normal threshold
61
How does pregnancy cause Nephrogenic DI
Placental synthesis of Vasopresinase
62
Uosm in response to water deprivation in Primary Polydipsia
Increase
63
Congenital Nephrogenic DI results from mutations in
V2 or Aquaporin 2
64
Cwater =
V x (1 - Uosm/Posm) = V - Cosm
65
Normal Osmolarity Hyponatremia is due to
Limitation of some Na assays when Na is measure in the whole plasma while solid phase of plasma is greatly increased (eg. HyperTGemia, Paraproteinemia)
67
3 inherited causes of Isolated Phosphate Reabsorption defect
(1) X-linked hypophosphatemia; (2) AD Hypophosphatemic Rickets; (3) AR Hypophosphatemic Rickets
68
Acquired cause of Isolated Phosphate Reabsorption defect
Oncogenic Hypophosphatemic Osteomalacia
69
Cosm =
Uosm/Posm x V
70
Most common mutation related to phosphate reabsorption
X-Linked Hypo-P
71
Why is PT highly susceptible to ischemia
ATP dependence, Polarized structure of cells
72
K moving paracellularly is an example of
Simple diffusion requiring electrochemical gradient
73
Mutation in FGF-23
AD Hypo-P Rickets
74
In PT, 33% of Na is reabsorbed via \_\_\_, the rest by
33% via transporter proteins, the rest passively by solvent drug via paracellular route
76
Most common electrolyte disorder
Hyponatremia
77
Mitochondria in PT epithelial cells
Rich to provide sufficient energy for mass reabsorption
77
Where is 100% of glucose reabsorbed
PT
78
Mutation in AD Hypo-P Rickets
FGF-23
79
How quickly does ADH insert new AQP-2 channels
within minutes
81
Hyponatremia with normal volume status is caused by
Too much ADH (SIADH, Glucocorticoid def., Hypothyroidism)
82
Which are more severe: Generalized or Isolated PT Dysfunctions
Generalized
83
Hypoosmolar Hyponatremia is due to
Always due to impaired urinary dilution mechanisms
84
"Generalized" PT dysfunction is usually due to
Defect in energy generation (Na-K ATPase) or dysfunction of cellular organelles affecting transport recycling
85
25% of Na in PT is reabsorbed by what exchanger
Na-H
86
mutation of SGLT2 Glucose transporter
Hereditary Renal Glucosuria is caused by
87
What percent of Phosphorus is reabsorbed in PT
80%
88
FGF23 regulates what in PT
Pi excretion

Renal (31 decks)

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