week 7 Flashcards

and workshop 4

1
Q

Outcomes of the Immune Response:

A

Neutralization: Antibodies like IgM neutralize pathogens by binding to them, preventing them from infecting cells.
Opsonization: IgG antibodies tag pathogens for destruction by immune cells like phagocytes.
Killing of Target Cells: The immune system can directly kill foreign or altered cells, including those bearing tumor antigens.
Inflammation: The immune response can trigger inflammation, which is essential for fighting infections but can also cause tissue damage if unchecked

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2
Q

Types of Primary Immunodeficiency

A

People with primary immunodeficiency (PI) have an immune system that does not work correctly. This means that people with PI are more likely to get and become very sick from infections.

the types of primary immunodeficiency:

  1. Antibody Deficiencies:• Panhypogammaglobulinemia: Think of “pan” as all-encompassing (like a “panorama” view), meaning a decrease in all antibodies, leading to many infections.
    • Selective IgA Deficiency: “Selective” means only IgA is affected, and since it’s the most common, picture someone “selectively” choosing something common. Can be asymptomatic but may result in infections.
  2. Cell-Mediated Immunity Deficits:• SCID (Severe Combined Immunodeficiency): “Combined” = both T and B cells affected, so think of “severe” infections from both types being knocked out.
    • DiGeorge Syndrome: “Di” = two; focus on a dual issue, with T-cells affected due to thymus problems. Think “DiGeorge” for thymus and T-cells.
  3. Phagocyte Deficits:• Chronic Granulomatous Disease: “Granulomatous” = forming granulomas (due to ineffective phagocytosis), and think of phagocytes unable to “eat up” bacteria because they can’t produce bactericidal oxygen radicals.

All Sick Cats Despise Chronic Germs”

•	All – Antibody Deficiencies (Panhypogammaglobulinemia, Selective IgA Deficiency)
•	Sick – SCID (Severe Combined Immunodeficiency)
•	Cats – Cell-Mediated Immunity Deficits (DiGeorge Syndrome)
•	Despise – Deficits (Phagocyte Deficits)
•	Chronic Germs – Chronic Granulomatous Disease
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3
Q

Types of Secondary Immunodeficiency

A

immune system becomes weakened or compromised due to external factors such as infection or medications or medical conditons
Malnutrition: Reduced production of immune components due to poor nutrition.
Infections: Such as HIV, which leads to acquired immunodeficiency (AIDS).
Drugs: Immunosuppressive drugs, such as corticosteroids and cyclosporine, used in transplants or autoimmune diseases.
Burns/Nephrotic Syndrome/Protein-losing Enteropathy: Conditions that result in the loss of immune components or increased catabolism​

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4
Q

Three Types of Clinical Rejection

A

Hyperacute Rejection: Occurs within minutes to hours due to preformed antibodies attacking the donor tissue (Type II hypersensitivity reaction). It leads to endothelial damage, inflammation, and thrombosis.
Acute Rejection: Occurs within weeks or months, involving both antibody- and cell-mediated reactions (Type IV hypersensitivity). This results in graft vessel vasculitis and lymphocytic infiltrates.
Chronic Rejection: Takes months to years to develop and involves both antibody and cell-mediated reactions (Type II and IV hypersensitivity). It leads to fibrosis, thickening of the basement membrane, and progressive organ failur

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5
Q

Describe Graft verse Host disease

A

Graft-versus-Host Disease (GVHD) occurs when grafted immune cells recognize the host’s tissues as foreign and mount an immune attack. This is a major complication in bone marrow transplants and can occur 7 to 14 days after the transplant. rejection!

Symptoms: Skin rash, Fever, Hepatosplenomegaly (enlarged liver and spleen), Bloody diarrhea, Breathlessness

Progression:
GVHD can be fatal, with a mortality rate of 70% in severe cases and 30% in milder cases.

Difficult to Eradicate: Once GVHD begins, it is challenging to control or reverse, making it a serious complication​

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6
Q

whats this?

A

Primary Deficits in cell-mediated immunity
Absence of thymic shadow in adult ct

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7
Q

whats this?

A

Primary Deficits in cell-mediated immunity
Absence of thymic shadow. in infant ct

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8
Q

what disease is depicted here?

A

Name: Chronic Granulomatous Disease (CGD) - its Primary deficits in phagocyte function
Tissue:Granulomatous tissue: This tissue forms in response to chronic inflammation where the immune system attempts to wall off substances it cannot eliminate.
Organ:Can affect various organs, commonly the lungs, skin, liver, and gastrointestinal tract.
Key Features Seen in Histology: Presence of multiple abscesses.
Formation of non-caseating granulomas (granulomas without central necrosis).
Giant cells (multinucleated cells) within the granulomas.
cause:Failure to produce bactericidal oxygen radicals (NADPH oxidase deficiency).
Phagocytes are unable to kill certain bacteria and fungi because they can only use hydrogen peroxide from the pathogens themselves to generate reactive oxygen species.
This leads to the formation of granulomas as the body attempts to contain the infection.
symptoms: recurrent infection, pneumonia, chronic diarrhea, pulmonary and skin.al rate

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9
Q

what is Primary Complement Deficiency

A
  • Inherited
  • Varied manifestations
  • C1, C4 or C2 deficiency = red cheeks, chronic nephritis
  • C3 deficiency (usually secondary) = Life threatening;Pneumonia
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10
Q

Primary Complement Deficiency
Example

A

Hereditary angioedema
* Deficiency in C1 inhibitor
* Recurrent attacks of oedema = swelling (intestines and larynx, ariways)

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11
Q

tumour meaning

A

A tumor is an abnormal mass of tissue that may be benign, premalignant, or cancerous

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12
Q

Malignant

A

Abnormal cells divide without control and can invade nearby tissues

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13
Q

Benign

A

– Non-invasive, non-aggressive neoplasia.

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14
Q

Proto-oncogenes meaning

A

– Proto-oncogenes are a group of genes that cause normal cells to become cancerous when they are mutated.

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15
Q

The role of p53

A

supress uncontrolled cell growth. They are not specific to benign or malignant tumours and not all tumours of a certain type may express
the protein. Neoplastic cells commonly express normal proteins, that are commonly expressed under normal physiological conditions.

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16
Q

. In type I hypersensitivity reactions, __________ antibodies bind to mast cells and _________.

A

IgE, Basophils

17
Q

Type II hypersensitivity reactions ______

A

are mediated by IgG and IgM antibodies

18
Q

. In type III hypersensitivity reaction, antigens circulating within the bloodstream bind to antibodies, forming small____ that are deposited in tissues, creating localized inflammation.

A

complexes

19
Q

Contact dermatitis is a _________________, which is mediated by _______________, that are sensitised to
_________________.

A

type IV hypersensitivity reaction, T lymphocytes, antigens

20
Q

Order the types of hypersensitivity from fastest to slowest to manifest.

A

I > II > III > IV

21
Q

Grave’s Disease symptoms

A
22
Q

How could graves disease be treated?

A

Anti-thyroid medications (mathimazole), antihistamines, radioiodine ablation, surgical removal of thyroid.

23
Q

what organ is this, the cell features and the pathological process observed?

A

healthy kidney, has glomerolus and tubules. dense interstitial
inflammatory infiltrate is observed.

24
Q

what is this?

A

diseased kidney, as seen by the mononuclear inflammatory cells which are a type of infiltrate.

25
Q

What does the decrease and subsequent increase in creatine levels tell us?

A

Good kidney function was achieved, but after a week, rejection of the tissue resulted in loss of kidney function and
kidney damage.

26
Q

What is the differential diagnosis? e best test to confirm the diagnosis? patient can develop?

A

Acute rejection, Screening for donor-specific antibodies, Non-Hodgkin lymphoma (remember, cancer risk is increased in transplanted
kidneys)