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V - KCU - RN (T2) - OMS1 > Immunological Aspects Of The Renal System > Flashcards

Immunological Aspects Of The Renal System Flashcards

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NCLEX-RN® flashcards
1
Q

Define AKI

A

No structural changes
Increase in SCr by 50%

Oliguria (decreased urine output)

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2
Q

Define CKD

A

FGR <60ml/min

Kidney damage

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3
Q

What does AKI lead to

A

Metabolic acidosis and ATP depletion which can lead to acute renal failure

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4
Q

Majority of causes in AKI cause what which then leads to AKI

A

Hypoxia

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5
Q

Sterile renal inflammation is induced by what

A

DAMPS

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6
Q

CRP is like what and can activate what

A

Is like IgM and can activate complement pathways via the classical pathway which leads to inflammation (C3a/C5a)

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7
Q

DAMPS and PAMPS activate what

A

TLR, NLR

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8
Q

Necrosis from AKI triggers what

A

DAMPS

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9
Q

Early stage AKI is mediated by what cells

What about late stage

A

Early - TH17

Late - Th1

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10
Q

What is the role of M1 and M2 in AKI

A

M1 - AKI mediation

M2 - tissue repair

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11
Q

What does DC cells lead to in AKI

A

TH1/TH17 differentiation

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12
Q

What does M1 lead to in AKI

What about M2

A

Increased TNF-a
Increased IL-6

Increased Arginase - 1
Increased IL - 10

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13
Q

What clears the early apoptotic cells

A

M2

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14
Q

What does the T-Cell lead to for AKI and tissue repair

A 
AKI:
Increased CD4, TH1 
Increased IFN - y
increased IL - 6 
Decreased IL - 4

Repair:
Ag-specific T-Cell expansion

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15
Q

M1 is activated by what

A

PAMPS/DAMPS through binding to TLR’s

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16
Q

M2 is activated by what

A

IL-4 and IL-13

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17
Q

Th - 17 is activated by what, produces what, and then causes what

A

activated by TGFb Produces IL - 17 and produces inflammation

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18
Q

M2 will do what, not what

A

Heal the tissue, not restore function

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19
Q

What causes M1 to become M2

A

CSF - 1, (M-CSF), IL - 10

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20
Q

What does CCL 20 do

A

Released from Th17 and used to recruit monocytes, Th1, and Th17

21
Q

Biopsies in any glomerulonephritis will have what

A

Compliment proteins

22
Q

C3b and C5b are important for what

A

Inflammation and forming MAC

23
Q

MAC leads to what

A

Apoptosis of cells

24
Q

In AKI, complement activation occurs downstream of what

A

Immune complex deposition (type III)

Or

Antibody mediated injury (type II)

25
Q

Type II and Type III hypersensitivites use what type of immune reactant

A

IgG or IgM

26
Q

In Type II, what does IgG and IgM do and where is this seen

A

Leads to cell lysis

Seen in patients with GBM mediated response

27
Q

In type III, what does IgG and IgM do and where is this seen

A

AG/Ab complexes are deposited in tissues

Compliment activation and inflammatory response which recruits neutrophils

Seen in RA, lupus, and post-strep glomerulonephritis

28
Q

Why do transplants not work

A

Ag’s on donor tissue is targeted for rejection

29
Q

Acute rejection occurs when and is caused by what

A

Occurs days to weeks after transplantation and is caused by T-cells

30
Q

Chronic rejection occurs when and is caused by what

A

Occurs months or years after transplantation and is caused by vascular trauma, inflammatory products of T-cells and abs

31
Q

Define autograft

A

Grafts exchanged from one part to another part of the same individual

32
Q

Define isograft

A

Grafts exchanged between different individuals of identical genetic constitutions (identical twins)

33
Q

Define allograft

A

Grafts exchanged between nonidentical members of the same species

34
Q

Define xenograft

A

Graft exchanged between members of different species

Very susceptible to rapid attack

35
Q

What does bradykinin cause

A

Vasodilation, SM contraction, increased vascular permeability

36
Q

What do fibrinopeptides cause

A

Increase local vascular permeability and attract neutrophils and macrophages

37
Q

Generally, an older person will fair how with a graft

A

Well, not able to mount an effective immune response

38
Q

Abs to A and B are on who

A

Individuals without these Ag on their RBCs

39
Q

ABO matching is not important for what

A

Non-vascular tissue

40
Q

Group A RBC has what Abs, Ags, and what donor allowed

A

Anti-B Abs
Ag A
Donor: A or O

41
Q

Group B RBC has what Abs, Ags, and what donor allowed

A

Anti-A Abs

Ag B

Donor: B or O

42
Q

Group AB RBC has what Abs, Ags, and what donor allowed

A

No Abs

A/B Ags

Universal recipient

43
Q

Group O RBC has what Abs, Ags, and what donor allowed

A

Anti A/B Abs

No Ags

Universal donor, only accepts O donations

44
Q

What will the Anti-whatever Abs do when come in contact with a recognized Ag

A

Activated the compliment pathway and cause apoptosis

45
Q

Least favorable donor is who

A

Mother

46
Q

If the dye is seen within the cells, then what has happened within anti-class I/II HLA abs

Explain this process

A

Patient has AgB and AbA

We need other donors to have AgB too

Put into tube, AbB to match with AgB on possible donor cells. This will allow the MAC to form, causing dye to be inside the cells, telling us that the specific donor cells have AgB and thus can be transplanted

47
Q

Successful transplantation is dependent on what

A

Successful matching f HLA Ags

48
Q

What are the HLA Ags encoded by

A

HLA Class I and Class II on the short arm of the chromosome

49
Q

Why is HLA matching required

A

Due to the extreme polymorphisim of HLA

V - KCU - RN (T2) - OMS1 (5 decks)

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