Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CPR1 Exam 2 > 14- Immunological Aspects of Renal System > Flashcards

14- Immunological Aspects of Renal System Flashcards

1
Q

This means the kidney has no structural damage, and the functional criteria includes GFR ≥ 60 mL/min per 1.73 m2. Serum Creatinine is stable.

A

No Kidney Disease (NKD)

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

This disease has no structural criteria. The functional criteria includes an increase in SCr by 50% within 7 days, OR an increase in SCr by 0.3 mg/dL within 2 days, OR Oliguria.

A

Acute Kidney Injury (AKI)

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

This disease has structural criteria of kidney damage for >3 months. The functional criteria includes GFR <60 mL/min per 1.73 m2 for >3 months.

A

Chronic Kidney Disease (CKD)

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

The kidneys are the major filtering organ. They represent only 0.5% of the human body mass, and receive ______ of the total cardiac output (about 1 L/min).

A

20%

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

An ischemic acute kidney injury (AKI) leading to metabolic acidosis and ATP depletion is one of the major causes of…

A

Acute Renal Failure (ARF)

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

This is classically defined as an abrupt decrease in kidney function.

A

ARF

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

In most cases the cause of AKI is not an infection but rather a…

A

Sterile Inflammation

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

What do the following lead to?

    • Intravascular volume depletion and hypotension
    • Hepatorenal syndrome
    • Decreased effective intravascular volume
    • Medications
    • Sepsis
    • Renal Vascular Disease
A

Hypoxia

***Hypoxia then leads to AKI

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

Sterile renal inflammation is induced by ________, which are released from dying parenchymal kidney cells and generated during ECM degradation and remodeling.

A

DAMPs

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

Native ________ has five subunits like IgM. It can bind DAMPs and activate complement via the classical pathway.

A

CRP (C-reactive protein)

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

Immune cells can recognize DAMPs via ______ ______, become activated, and induce innate immune responses and renal inflammation.

A

Toll-like receptors

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

This type of DAMP is a protein passively released during necrosis and recognized by RAGE.

A

HMGB1

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

This type of DAMP is another diffusible danger signal recognized by NLRP3.

A

Uric Acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

This type of DAMP is another danger signal recognized by scavenger receptor class A.

A

HSPs

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

All DAMPs activate _________ pathway and release of inflammatory cytokines.

A

NF-kB

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

In the early stages of AKI, immune responses are mediated by pro-inflammatory _______ cells. These dominate in tissue injury.

A

Th17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

_______ macrophages play a key role in AKI (pro-inflammatory), while _______ macrophages play a key role in tissue repair (anti-inflammatory).

A

M1

M2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In the late stage of AKI, the pro-inflammatory _______ cells prevail.

A

Th1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Classically activated _______ _______ are induced by PAMPs and DAMPs through binding to TLRs and other PRRs.

A

M1 Macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

_______ are pro-inflammatory cytokines that promote differentiation of M1 Macrophages.

A

IFN-y

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Alternatively activated ________ ________ are induced by IL-4 and IL-13 produced by certain subsets of T cells.

A

M2 Macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

M2 Macrophages are important in tissue repair and renal fibrosis which both are controlled by ______ and ______.

A

IL-10

TGF-B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Accumulated Th17 cells secrete _______ that stimulates resident renal cells to produce inflammatory mediators, aka cytokines, chemokines, and other mediators.

A

IL-17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

IL-17 induces expression of chemokine _______ that primarily leads to the recruitment of neutrophils.

A

CCL20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Th17 cells facilitate infiltration of monocytes, Th1 cells, and Th17 cells directly by secretion of the CCL20. This is also called _________. Recruitment of other pro-inflammatory leukocyte subsets ultimately leads to the progression of immune-mediated kidney damage.

A

MIP-3 (Macrophage Inflammatory Protein-3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Complement proteins are seen in biopsies from patients with virtually all forms of __________, and each of the three activation pathways have been linked with various kidney diseases.

A

Glomerulonephritis

27
Q

The reason for the kidney’s unique susceptibility to complement-induced damage is that _________ favors tissue deposition of immune complexes.

A

Filtration

28
Q

AKI and tissue damage leads to excessive generation of DAMPs which activate resident immune cells via PRRs. Activation of the complement cascade leads to C3b and C5b deposition in the tissue and production of C3a and C5a. The engagement of C3aR and C5aR receptors for C3a and C5a leads to further activation of tissue resident cells. Deposition of _______ leads to massive cell death.

A

MAC (Membrane Attack Complex)

29
Q

Tissue damage and inflammation induces accumulation of…

A

Neutrophils

Monocytes – differentiate into inflammatory Macrophages

30
Q

C5a and C3a stimulate pro-inflammatory responses in neutrophils and Macrophages. Inflammation causes ________ of kidney cells. At the resolution stage, Macrophages acquire _______ phenotype and control tissue repair and _________.

A

Necrosis
M2
Fibrosis

31
Q

T/F. In kidney injury, complement activation may occur downstream of immune complex deposition (type III) or antibody-mediated injury (type II).

A

True

32
Q

Kidney _________ is used in the end-stage renal disease.

A

Transplantation

33
Q

The barrier to transplantation is the genetic incompatibility of donor and recipient. Today, successful organ transplantation depends on the use of…

A

Immunosuppressive drugs

34
Q

_______ matching is one of the methods (immunosuppression is another) for preventing graft rejection. Histocompatibility Ags are the targets for rejection.

A

HLA

35
Q

Host versus graft disease causes transplant rejection via mechanisms of what?

A

Hyperacute Rejection
Acute Rejection
Choric Rejection

36
Q

This type of rejection is immediate and caused by antibody.

A

Hyperacute Rejection

37
Q

This type of rejection occurs days to weeks after transplantation and is caused by T cells (Abs?).

A

Acute Rejection

38
Q

This type of rejection is seen months or years after transplantation and caused by vascular trauma, inflammatory products of T cells, Abs.

A

Chronic Rejection

39
Q

Graft versus host disease (GVHD) is caused by a reaction of donor immune cells against host tissues. The mechanism of GVHD can be ________ or ________.

A

Acute

Chronic

40
Q

This type of graft is exchanged from one part to another part of the same individual.

A

Autografts

41
Q

This type of graft is exchanged between different individuals of identical genetic constitutions (i.e., identical twins).

A

Isografts

42
Q

This type of graft is exchanged between nonidentical members of the same species.

A

Allografts (Allogeneic)

43
Q

This type of graft is exchanged between members of different species.

A

Xenografts (Xenogeneic)

44
Q

Xenografts are very susceptible to rapid attack by naturally occurring Abs that cause activation of complement. The insertion of human ________ into the genomes of the donor animals increases the chances of successful transplantation.

A

Genes

45
Q

______ incompatible kidney transplantation was previously considered to be an absolute contraindication for patients with end-stage kidney disease due to hyperacute rejection related to blood type barrier.

A

ABO

***Called ABOi-KT

46
Q

ABO matching is not important for what type of transplants because they’re non-vascularized?

A
    • Corneal transplantation
    • Heart valve transplantation
    • Bone and tendon grafts
47
Q

What Ags are present in all the blood types?

A

Blood Type A = A Ags
Blood Type B = B Ags
Blood Type AB = A and B Ags
Blood Type O = No Ags

48
Q

What Abs are present in all the blood types?

A

Blood Type A = Anti-B
Blood Type B = Anti-A
Blood Type AB = No Abs
Blood Type O = Anti-A and Anti-B

49
Q

What blood types can type A receive?

A

A or O

50
Q

What blood types can type B receive?

A

B or O

51
Q

What blood types can type AB receive?

A

A, B, AB, or O

52
Q

What blood types can type O receive?

A

O

53
Q

Who are the universal donor and universal recipient?

A 
Donor = O
Recipient = AB
54
Q

How do we test for pre-existing non-ABO Abs?

A

Test is called Microcytotoxicity Test for Preformed Abs

Step 1 = Recipient serum with Abs is added to donor cells

Step 2 = Complement is added

Step 3 = Dye is added

Step 4 = Preformed Abs are present

55
Q

The success of transplantation is dependent on matching of the _______ Ags. These Ags are encoded by the major histocompatibility complex, _________ and _________.

A

HLA
HLA Class-I
HLA Class-II

56
Q

Maternal and paternal HLA Ags are co-dominantly expressed. Each person has six HLA class I alleles (3 maternal and 3 paternal) and six HLA class II alleles (3 maternal and 3 paternal). The _________ Ags are the strongest barriers to transplantation because all nucleated cells express them. The _________ Ags are expressed by professional APCs only.

A

HLA Class-I

HLA Class-II

57
Q

How do we test for Class I HLA compatibility in donor and recipients?

A

Step 1 = Abs are added

Step 2 = Complement is added

Step 3 = Dye is added

Step 4 = If dye accumulates in both donor and recipient cells, then the HLA are identical. If dye only accumulates in donor cell, then HLA are nonidentical.

58
Q

How do we test for Class II HLA compatibility?

A

Donor cells are introduced to radioactivity and mixed with recipient cells. +3H-thymidine is added, and if proliferation of recipient cells occurs then radioactivity is incorporated in the DNA. If no proliferation, then there is radioactivity in DNA.

***Called Mixed Lymphocyte Response (MLR)

59
Q

What are the immune events in allograft rejection?

A

1) APCs trigger CD4+ and CD8+ T cells
2) Both a local and systemic immune response develop
3) Cytokines recruit and activate immune cells
4) Development of specific T cells, NK cells, or Macrophage-mediated cytotoxicity
5) Allograft rejection

60
Q

What are the 2 types of immune responses in transplantation?

A

Host vs. Graft Disease = When a kidney is transplanted and the recipient’s T cells attack the transplant

Graft vs. Host Disease = When bone marrow is transplanted the T cells in the transplant attack the recipient’s tissues

61
Q

For Host vs. Graft responses, the immune memory of previous encounters with donor Ags is important. From animal experiments, if a second graft is performed from the same donor, then it is rejected more (RAPIDLY/SLOWLY).

A

Rapidly

62
Q

During (DIRECT/INDIRECT) allorecognition, T cells recognize intact allogeneic MHC molecules on the surface of donor APCs in the graft.

A

Direct

63
Q

During (DIRECT/INDIRECT) allorecognition, alloantigens are recognized in the context of recipient’s MHC class II molecules after they have been processed and presented by recipient APCs.

A

Indirect

64
Q

Effector mechanisms of graft rejection are…

A

Humoral rejection Th2 (IL-4, IL-5, and IL-10)

Cellular rejection Th1 (IL-2, IFN-y)

CPR1 Exam 2 (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions