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1 STEP Uworld immunology > Transplant > Flashcards

Transplant Flashcards

1
Q

Hyperacute. Onset time?

A

Minutes to hours

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2
Q

Hyperacute. Etiology

A

Preformed RECIPIENT antibodies against graft antigens

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3
Q

Hyperacute. Morphology

A

Gross mottling and cyanosis;

Arterial fibrinoid necrosis and capillary thrombotic occlusion

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4
Q

Acute. Onset time?

A

<6 monts

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5
Q

Acute. Etiology

A

Exposure to donor antigens induces activation of naive immune cells.
Predominantly CELL-MEDIATED

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6
Q

Acute. Morphology

A

CELLULAR (MAIN): lymphocytic interstitial infiltrate and endothelitis’
HUMORAL (not that dominant): C4d deposition, neutrophilic infiltrate, necrotizing vasculitis

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7
Q

Chronic. Onset time?

A

6 months to years

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8
Q

Chronic. Etiology

A

Chronic low-grade immune response refractory to immunosupression;
Mixed cell-mediated and humoral (aka antibody mediated)

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9
Q

Chronic. Morphology

A

Vascular wall thickening and luminal narrowing;

Interstitial fibrosis and parenchymal atrophy

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10
Q

Gross mottling and cyanosis;

Arterial fibrinoid necrosis and capillary thrombotic occlusion. What stage?

A

Hyperacute

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11
Q

CELLULAR: lymphocytic interstitial infiltrate and endothelitis’
HUMORAL: C4d deposition, neutrophilic infiltrate, necrotizing vasculitis

A

Acute

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12
Q

Vascular wall thickening and luminal narrowing;

Interstitial fibrosis and parenchymal atrophy

A

Chronic

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13
Q

KIDNEY from UW case.

Following transplant, T cells are activated and recipient antibodies are created against ……………

A

created against graft HLA and other antigens.

Donor graft MHC antigens (human leukocyte antigens).

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14
Q

KIDNEY from UW case.
The activated T cells can initially cause ……… acute rejection, which is generally reversible via an increase in immunosuppression (eg, high-dose glucocorticoids).

A

cell-mediated

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15
Q

KIDNEY from UW case.
The activated T cells can initially cause cell-mediated ACUTE rejection, which is generally reversible via ……………………

A

an increase in immunosuppression (eg, high-dose glucocorticoids)

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16
Q

KIDNEY from UW case.
Chronic rejection represents progression of cell-mediated and antibody-mediated inflammation (eg, via …………..) to the point that irreversible renal damage takes place;

A

activation of complement and recruitment of neutrophils

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17
Q

KIDNEY from UW case.
Chronic rejection represents progression of cell-mediated and antibody-mediated inflammation (eg, via activation of complement and recruitment of neutrophils) to the point that ………….. renal damage takes place.

A

irreversible

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18
Q

KIDNEY from UW case.

Chronic rejection. Kidney macro and micro?

A

The kidney grossly decreases in size;

histopathology shows obliterative vascular wall thickening with tubular atrophy and interstitial fibrosis.

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19
Q

KIDNEY from UW case.

Chronic. What metabolic changes are present?

A

Increased sodium retention, declining renal function in chronic rejection is also commonly accompanied by new or worsening hypertension.

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20
Q

KIDNEY from UW case.

Chronic. What is present due to metabolic changes?

A

declining renal function –> sodium retention –> HYPERTENSION

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21
Q

KIDNEY from UW case.

What is predominant glomerular injury in chronic?

A

Glomerular injury in chronic rejection is predominantly ischemic (no crescent formation nothing)

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22
Q

KIDNEY from UW case. What infiltration would be seen in acute phase?

A

A dense, interstitial, mononuclear (lymphocytic) infiltrate is characteristic of acute allograft rejection, which is most often a primarily T cell–mediated process.

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23
Q

KIDNEY from UW case.

Use of immunosupressants. Acute rejection often <6month. Why may occur acute but beyond 6 months?

A

Can occur later in a patient in whom posttransplant immunosuppression has been stopped.

24
Q

KIDNEY from UW case.

Vascular fibrinoid necrosis with capillary thrombotic occlusion occurs in …….

A

hyperacute

25
Q

KIDNEY from UW case.

Whats the course and scope of hyperacute?

A

A rapid and profound form of antibody-mediated rejection caused by preformed antibodies to graft antigen

26
Q

.

A

.

27
Q

KIDNEY from UW case.

Acute mechanism?

A

This process is mostly cell-mediated and results from sensitization of recipient T cells to donor graft MHC antigens (human leukocyte antigens).

28
Q

KIDNEY from UW case.

In acute what parameter starts to raise and is ,,asymptomatic’’?

A

asymptomatic rise in serum creatinine

29
Q

KIDNEY from UW case.

In acute what symptoms may have?

A

low-grade fever, malaise, joint pains, and graft tenderness

30
Q

KIDNEY from UW case.

What microscopic finding in acute?

A

dense lymphocytic infiltrate sometimes accompanied by vascular inflammation (endothelitis)

31
Q

KIDNEY from UW case. Acute reversible or not?

A

reversible with high-dose GK.

32
Q

KIDNEY from UW case. What combination helps to prevent acute rejection episodes?

A

Chronic immunosuppression with a calcineurin inhibitor–based regimen (eg, tacrolimus plus mycophenolate and low-dose prednisone) helps prevent acute rejection episodes.

33
Q

KIDNEY from UW case.

If in acute stage happens Host-B cells sensitization, what is seen in histopathology?

A

Histology is expected to show deposition of complement (eg, C4d), neutrophilic infiltrate, and necrotizing vasculitis; this patient’s mononuclear (lymphocytic) infiltrate is consistent with a cell-mediated T-cell response.

34
Q

KIDNEY from UW case. HUMORAL - more pronounced in acute or chronic?

A

In chronic. In acute more cell-mediated.

35
Q

LUNG UW table. Hyperacute etiology.

A

PREFORMED HOST antibodies to donor ABO or HLA

36
Q

LUNG UW table. Hyperacute patho?

A

Neutrophilic infiltration with fibrinoid necrosis and thrombosis

37
Q

LUNG UW table. Acute etiology?

A

Cell-mediated response to mismathched donor HLA.

38
Q

LUNG UW table. Acute patho?

A

Perivascular (small lung vessels) and submucosal (bronchiole) lymphocytic infiltrates

39
Q

LUNG UW table. Chronic etiology?

A

Chronic, low-grade, mixed cell-mediated and antibody response to HLA antigen

40
Q

LUNG UW table. Chronic patho?

A

Submucosal inflammation –> granulation, scarring and BRONCHIOLITIS OBLITERANS

41
Q

LUNG. The severity and timing of the rejection depends on ……?

A

degree of difference between the donor and recipient MHC antigens in addition to other variables.

42
Q

LUNG. Chronic lung transplant rejection is marked by submucosal …….. inflammation in the walls of the small airways

A

lymphocytic

43
Q

LUNG. Subsequent ingrowth of granulation tissue into the lumen leads to ……… and ………..

A

Airway obstruction and obliteration (bronchiolitis obliterans)

44
Q

LUNG. What symptoms is present in chronic?

A

Patients usually present with slowly worsening dyspnea and dry cough that begins months or years after transplantation.

45
Q

LUNG. Chronic. What lung examination findings?

A

Lung examination may reveal end-expiratory squeaks or pops, and spirometry typically demonstrates airflow limitation (obstructive pattern) with a drop in FEV1.

46
Q

LUNG. Hyperacute. Histo findings?

A

Histology generally shows fibrinoid necrosis with hemorrhage and ischemia (“white graft” reaction).

47
Q

LUNG. Acute. Histo findings?

A

Histology generally shows perivascular mononuclear infiltrates in the small blood vessels of the lung, which can expand to include the alveolar walls.

48
Q

LUNG. Restrictive allograph syndrome, what is it?

A

Restrictive allograft syndrome, a less common type of chronic lung transplant rejection, can result in fibrotic changes to the pleurae. However, pulmonary function tests would reveal a restrictive (reduced FVC), not obstructive, pattern.

49
Q

GVHD. Most commonly occurs after ……

A

Bone marrow transplantation

50
Q

GVHD. GVHD can also occur following transplantation of organs rich in …………. (eg, liver) or ……………….

A

GVHD can also occur following transplantation of organs rich in lymphocytes (eg, liver) or transfusion of non-irradiated blood.

51
Q

GVHD. Why it manifest in patients? What patients?

A

Patients affected by GVHD are generally severely immunodeficient due to the primary disease process or as a result of immunosuppressive medications.

52
Q

GVHD. Immunosupression/immunodef of the host allows …….

A

This allows immunocompetent donor T cells from the graft to survive and migrate into host tissues, where they recognize host MHC antigens as foreign and become sensitized. On activation, donor CD4+ and CD8+ T cells (not B cells) participate in host cell destruction.

53
Q

GVHD. What cells participate?

A

donor CD4+ and CD8+ T cells (not B cells) participate in host cell destruction.

54
Q

GVHD. What organs are most frequently affected?

A

Any organ may be a target of GVHD, but the skin, liver, and gastrointestinal (GI) tract are the most frequently affected.

55
Q

GVHD. Skin signs?

A

Early signs of GVHD include a diffuse maculopapular rash that has a predilection for the palms and soles and may desquamate in severe cases.

56
Q

GVHD. GI signs?

A

GI tract involvement causes diarrhea, intestinal bleeding, and abdominal pain.

57
Q

GVHD. Liver signs?

A

Liver damage will manifest as abnormal liver function tests.

1 STEP Uworld immunology (13 decks)

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