Renal adaptation Flashcards

1
Q

Renal responses to various abnormalities

A

Deficient nephrons
Reduced renal mass
Reduced Nephron function

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

T or F

Deficient nephrons can be seen at birth

A

T

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

developmental abnormalities like hypoplastic kidney

A

CAKUT congenital abnormalities of the kidney and urinary tract

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

Low nephrons at birth

A

Autosomal recessive kidney disease
Urinary tract abnormalities with abnormal kidney
Dysplastic or Hypoplastic kidneys

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

kidney mass below two standard
deviations of age-matched normal or a
combined kidney mass of less than half
normal for the patient age

A

Dysplastic or hypoplastic kidneys

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

FACTORS CONTIRBUTING TO LOW NEPHRON

A

Decrease growth in utero
Low birth weight mothers= low birth weight babies
Calorie restrictions
Protein restrictions
Hi-fat intake prone to hypertension and renal fibrosis
Deficiency in Na, Zn, Fe, Vit A
Drugs taken during preg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

T or F
persistence of hyperglycemia can actually delay the kidney development and decrease in
the number of nephrons developed

A

T

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

calorie restriction of mothers may predispose their child to _____

A

albuminuria

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

Protein restriction decreases lifespan by

A

200mdays

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

Drugs that could contribute to deficient numbers of nephron

A

Dexamethasone
ACEI and ARBS
Gentamicin
Nsaids

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

This postulates what the kidney does when an
individual is born with deficient number [of
nephrons].

A

BENNER HYPERFILTRATION HYPOTHESIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

becomes maladaptive as it leads to progressive anatomical and functional deterioration of the kidney

A

BENNER HYPERFILTRATION HYPOTHESIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

adaptation in chronic kidney kidney injury

A
Counterbalance
Hypertrophy
systemic adap:
-potassium
-sodium
-Acid-base homeostasis
-mineral metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

an attempt on the part of the less injured or uninjured portion of the kidney to take over the work of the more injured portion

A

Counterbalance

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

growth or compensation due to overstimulation

A

acquired reserve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

related to increase in renal blood flow due to dilatation of the renal arterioles due to Nitric oxide production

increased size of the glomeruli and hyperfiltration

A

Hypertrophy

17
Q

factors implicated in compensated hypertrophy after nephron loss

A
inc renal blood flow
inc tubular absorption of Na with dec distal delivery and decreased afferent arterial resistance due to adaptive tubuloglomerular feedback
Hepatocyte growth factor
Gluc transporters
Inc renal nerve activity
Insulin like growth factor
Mammalian target of rapamycin signalling pathway activation
Transforming growth factor beta
18
Q

potassium is reabsorbed in the ______ and secretion determined by _____

A

proximal tubule; distal nephron

19
Q

hyperkalemia promotes potassium secretion by the principal cell of the _______

A

collecting duct

20
Q

Increases the density and activity of the
basolateral Na-K-ATPase and the
number of Na channels in the apical
membrane of the collecting duct

A

aldosterone

21
Q

In CKD: positive feedback=

A

increase distal delivery = increased filtration

22
Q

acid-base metabolism normal:

A

excrete 1 mEq/kg/day of dietary acid load

23
Q

adaptation to decreased mass (acid-base metab)

A

Increased H excretion
o Enhanced nephron ammoniagenesis
o Increased distal H ion secretion (RAS and endothelin-1)

24
Q

Mineral-metabolism response

A
•  Increased  secretion  of  PTH  and
FGF-23
•  Stimulate phosphaturia
•  Reduces  levels  of  Na-phosphate
cotransporter NaPi2a and NaPi2c
25
Q

mineral metabolism Maladaptive response:

A
•  Downregulation  of  Klotho-fibroblast
growth  factor  I  resulting  to  a
decrease in the ability of FGF-23 to
downregulate PTH production
•  Persistent  elevation  leads  to  soft
tissue  calcification,  left  ventricular
hypertrophy  and  subsequent
increased mortality in CKD.
26
Q

Activation of intrinsic defense mechanisms

to cope with pathologic conditions

A

PRECONDITIONING

27
Q

renders the organ resistant to subsequent ischemic injury

A

ISCHEMIC PRECONDITIONING

28
Q

Protection afforded in one vascular bed by
ischemia in another vascular bed in the
same organ or a different organ

A

remote ischemic preconditioning

29
Q

adenosine

A

akt (protein kinase b)

30
Q

antioxidants

A

autophagy

31
Q

bradykinin

A

dec in genes regulating inflammation

32
Q

extracellular single-related kinase

A

hypoxia induced factors

33
Q

heat shock proteins

A

protein kinase c

34
Q

JAK stat pathways

A

Jun N terminal kinase

35
Q

Mitochondrial connexin

A

Nitric oxide

36
Q

Opioids

A

Sirtuin activity

37
Q

Adaptive response to acute injury

A

Hypoxia
Acute renal success
Tubulogromerular feedback
Hypoxia-induced factor 1 alpha

38
Q

Induces upregulations of genes whose
protein products are involved in energy
metabolism, angiogenesis, and apoptosis

A

Hypoxia-induced factor 1 alpha

39
Q

ADAPTIVE RESPONSE TO TOXIC INJURY SPECIFIC TO THE PROXIMAL TUBULES

A

Response of the proximal tubule cells to direct

injury by Diphtheria toxin producing repair with minimal sequela.