Immunology Flashcards

(43 cards)

1
Q

what are the 3/4 mechanisms of immunopathology

A

• Immunodeficiency = ineffective immune response
• Hypersensitivity reaction = overactive immune response
• Autoimmunity = inappropriate reaction to self

(also immune cell neoplasia)

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2
Q

what are the 3 general features of immunodeficiency diseases

A

o Increased susceptibility to infection
o Increased incidence of autoimmune disease
o Prone to virally induced cancers e.g. feline leukaemia virus

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3
Q

examples of innate immune system deficiencies

A

abnormal phagocyte function
complement deficiency

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4
Q

adaptive immune system deficiencies

A

B cell immunodeficiency (decreased immunoglobin production)
T cell immunodeficiency (decreased cell mediated immunity)
Combined – B and T cell (SCID)

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5
Q

primary vs secondary immunodeficiency diseases

A

primary are congenital, rare, and clinical signs develop after weaning

secondary are acquired, more common, and involve the animal initially having functional immunity, but subsequently the immunity becoming defective

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6
Q

causes of secondary immune deficiencies

A

o Failure of passive transfer
o Medical intervention e.g. chemotherapy, immunosuppressive drugs
o Infection of immune cells e.g. canine distemper virus, FIV, FeLV
o Hypercortisolaemia and stress
o Chronic disease = lymphoid depletion
o Environment e.g. starvation, malnutrition
o Old age (immunosenescence)

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7
Q

potential causes of failure of passive transfer

A

o Lack of colostrum ingestion – failure to suckle
o Lack of colostrum production – e.g. premature birth
o Absorption failure by newborn – something wrong with GIT

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8
Q

diagnostic approach to failure of passive transfer

A

• Index of suspicion based on history, signalment
• Measure IgG concentrations – stall-side testing kit
• Complete blood count
o Abnormal white blood cell count
o Toxic changes in white blood cells
• Serum biochemistry
o Low globulin concentrations

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9
Q

treatment of failure of passive transfer

A

IV administration of plasma containing immunoglobins (oral admin won’t work after 24 hours post-parturition as GIT is no longer able to absorb)

Antibiotics to treat infection

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10
Q

prevention of failure of passive transfer

A

• Prevention better than treatment
• Ensure the dam is healthy and vaccinated
• After birth, verify that the foal stands and nurses
• 12-18 hours after birth measure serum immunoglobins
o >8g/L = adequate
o <4g/L = failure
o 4-8g/L = partial failure

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11
Q

Iatrogenic immunosuppression

A

Acquired immunodeficiency due to administration of immune suppressant medication
Secondary opportunistic infections can occur - UTI, skin infections, blood stream infections

If an infection results, lower the dosage of the immune-suppressing meds and give antibiotics

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12
Q

hypersenstivity reactions

A

undesirable / harmful responses produced by normal immune system mechanisms.
Evolved to protect against infection – but overreact and react to harmless things, and react to self (autoimmunity) – can cause tissue injury and serious disease.

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13
Q

autoimmunity

A

an immune response directed against self-tissue, due to failure of self-tolerance.

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14
Q

Immune-mediated disease / autoimmune disease

A

the inflammation, tissue damage and resultant clinical signs that result from autoimmunity.

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15
Q

What’s the difference between autoimmunity and autoimmune disease?

A

Autoimmunity doesn’t always result in disease, but autoimmune disease is always due to autoimmunity.

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16
Q

What is the difference between autoimmunity and hypersensitivity?

A

Related abnormalities of the immune system
In autoimmunity, the immune system is reacting to self (no stimulus)
In hypersensitivity, the immune system is overreacting to a stimulus

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17
Q

why does autoimmunity occur?

A

genetic disposition
epigenetics - age, sex, lifestyle, diet
environmental triggers - infection, drugs, vaccines, cancer

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18
Q

primary vs secondary autoimmune disease

A

primary = no obvious triggers / idiopathic
secondary = suspected secondary to an obvious trigger

19
Q

types of immune system neoplasia

A

lymphocyte neoplasia - lymphoma, lymphosarcoma, lymphoid leukaemia

plasma cell neoplasia - multiple myeloma, extramedullary plasmacytoma

macrophage and dendritic cell neoplasia - histiocytoma, histiocytic sarcoma

20
Q

adverse effects of immune cell neoplasia

A

immunodeficiency (not very important)
local effects - disruption of physiologic function of affected tissues
paraneoplastic syndromes - hypercalcemia, hypoglycaemia, anaemia, thrombocytopenia, hyperglobulinaemia

21
Q

lymphoma

A

very common in small animal medicine
(the most common cancer in cats)

lymphoma = clonal proliferation of neoplastic lymphocytes

22
Q

WHO classification of lymphoma

A

stage 1 = single lymph node affected
stage 2 = regional lymphadenopathy
stage 3 = generalised lymphadenopathy
stage 4 = liver and/or spleen involvement
stage 5 = blood, bone marrow or other organ involvement

23
Q

substages of WHO classification

A

a = without systemic signs

b = with systemic signs

24
Q

Lymphadenomegaly

A

Submandibular, prescapular and popliteal lymph nodes are palpable in a normal dog

In a dog with lymphoma, the axillary and superficial inguinal lymph nodes may also be palpable

25
Pathophysiology of hypercalcaemia of malignancy
neoplastic cells produce parathyroid hormone-related peptide (PTH-rp) PTH-rp has the same effects in the body as PTH (increased calcium reabsorption in kidneys, increased calcium resorption from the bone) results in hypercalcaemia
26
why does hypercalcaemia of malignancy cause PU/PD
• Hypercalcaemia blocks ADH action on renal collecting ducts o Nephrogenic diabetes insipidus o Polyuria, with secondary polydipsia
27
Pathophysiology of paraneoplastic hypoglycaemia
neoplastic cells produce insulin-like peptides high insulin concentrations = glucose is moved intracellularly, glycogenolysis and hepatic glucose production is suppressed results in hypoglycaemia this can cause neurological signs - weakness, trembling, behaviour changes, seizures
28
Pathophysiology paraneoplastic anaemia
anaemia is common in lymphoma patients but is likely multifactorial - anaemia of inflammatory disease (iron deficiency, RBC lifespan shortened) - IMHA (autoimmunity triggered by lymphoid pathology) - microangiopathic haemolytic anaemia (more common with histiocytic sarcoma, RBC injured as they travel through capillary beds infiltrated by neoplastic cells)
29
diagnosis and staging of lymphoma
cytology first (start with least invasive) - usually with fine needle aspirate, differentiate neoplastic vs reactive lymph node histopathology from a biopsy sample PARR - PCR for clonal antigen receptor rearrangement, can be done if histopath or cytology inconclusive
30
Leukaemia
neoplastic leukocytes in the peripheral blood
31
2 main types of leukaemia
lymphoid leukaemia - acute and chronic lymphoblastic leukaemia myeloid leukaemia
32
Acute lymphoblastic leukaemia
Poorly differentiated lymphoblasts in circulation and bone marrow Concurrent cytopenias common (anaemia, thrombocytopenia, neutropenia) Treatment with multi-agent chemotherapy and supportive care Aggressive cancer with poor prognosis
33
Chronic lymphocytic leukaemia
Well-differentiated, small, mature lymphocytes in circulation and bone marrow Most T-cell (although B-cell origin reported) Treatment with less aggressive chemotherapy Long survival time expected
34
Multiple myeloma
systemic proliferation of malignant plasma cells within the bone marrow uncommon
35
Extramedullary plasmacytoma
plasma cell neoplasm outside the bone marrow
36
local and systemic pathophysiology of multiple myelomas
Local disease = osteopenia and cortical lysis = bone pain and fractures Systemic disease = paraneoplastic syndromes - Hypercalcaemia of malignancy - Monoclonal gammopathy -> hyperviscosity syndrome
37
Diagnosis of multiple myeloma
Clinical signs (non-specific): bone pain, lameness, PU/PD (if hypercalcaemic), behaviour / neurologic abnormalities (if hyperviscosity) Routine blood tests: hypercalcaemia (common but not always), high serum globulin concentration Serum protein electrophoresis – monoclonal gammopathy Radiographs or CT – lytic lesions in bone (usually multiple) Bone marrow cytology – identifies neoplastic plasma cells
38
Monoclonal gammopathy
(Serum protein electrophoresis) • Neoplastic plasma cells secrete large quantities of gamma globulins • Detected as a spike in serum electrophoresis
39
Histiocytic disease complex: 3 clinically recognised syndromes
1. Canine cutaneous histiocytoma complex (benign neoplasia) 2. Canine reactive histiocytosis (not neoplastic) 3. Histiocytic sarcoma complex (malignant neoplasia)
40
breeds predisposed to histiocytic sarcoma
bernese mountain dogs, rottweilers, golden retrievers
41
histiocytic sarcoma
Disseminated, neoplastic transformation of antigen-presenting cells (dendritic cell origin)
42
localised vs systemic histiocytic sarcoma
Localised histiocytic sarcoma: affects a single tissue or organ – with solitary or multiple foci Systemic histiocytic sarcoma: called “disseminated histiocytosis” - Previously called malignant histiocytosis - Considered disseminated once it has spread beyond the draining lymph node - Multi-system, rapidly progressive disease with simultaneous involvement of multiple organs - Discrete mass formation (sarcoma lesions) in spleen, LNs, lung, BM, periarticular tissue, brain
43
Haemophagocytic histiocytic sarcoma
Originates in the splenic red pulp and bone marrow macrophages - Diffuse splenomegaly - Neoplastic histiocytes phagocytose RBCs and platelets - Erythrophagocytosis results in severe cytopenias - Often suspected to have IMHA / ITP - Lack discrete masses in spleen and at metastatic sites e.g. liver, lung Worst prognosis of the two forms - Median survival time two weeks