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Immune mediated disease Flashcards

1
Q

What are the two main types of immune responses?

A

Innate immunity: Immediate, non-specific (e.g. macrophages, NK cells)

Adaptive immunity: Slower but specific (e.g, T-cells, B-cells, antibodies)

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2
Q

What is the key failure in immune-mediated diseases?

A

Failure of self-tolerance (usually peripheral) leading to immune system attacking body’s own healthy cells

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3
Q

What are the two types of immune tolerance?

A

Central tolerance: Deletion of self-reactive T-cells in thymus

Peripheral tolerance: Regulation of T-cell response in body (e.g. Tregs, anergy, apoptosis)

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4
Q

How does the immune system prevent attacking its own cells?

A

Through immune tolerance, which prevents self-reactive immune responses

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5
Q

What are the key mechanisms of peripheral tolerance?

A

Anergy – T-cells recognise self-antigens but fail to activate due to lack of secondary signals (CD80/CD28)

Activation-induced cell death – Auto-reactive T-cells are destroyed (FAS-ligand mediated)

Regulatory T-cells – Suppress immune responses to prevent self-damage

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6
Q

What are cryptic antigens, and how can they cause immune-mediated disease?

A

Cryptic antigens aren’t expressed in thymus during development

If tissue damage exposes these antigens, immune system may mistakenly attack them

E.g.: Post-traumatic uveitis (immune response triggered by eye trauma)

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7
Q

What are common cytotoxic immune-mediated diseases in dogs?

A

IMHA (Immune-Mediated Hemolytic Anemia) – destruction of red blood cells

IMT (Immune-Mediated Thrombocytopenia) – destruction of platelets

IMPA (Immune-Mediated Polyarthritis) – inflammation of joint capsule

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8
Q

What are common immune-mediated endocrine diseases in dogs?

A

Addison’s Disease (Hypoadrenocorticism) – destruction of adrenal glands, leading to no production of mineralocorticoids or glucocorticoids

Type 1 Diabetes – destruction of pancreatic islet cells, causing no insulin production

Hypothyroidism – destruction of thyroid follicular epithelium, leading to no thyroid hormone production

Exocrine Pancreatic Insufficiency (EPI) – destruction of pancreatic exocrine glands, resulting in no pancreatic digestive enzymes

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9
Q

What are the two broad categories of immune-mediated disease (IMD) management?

A

Reversible IMD – Use drugs to control immune response (e.g. IMHA)

Irreversible IMD – Replace missing hormone or function (e.g. Type 1 Diabetes)

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10
Q

What is Type II hypersensitivity, and how does it cause immune-mediated disease?

A

Antibody-mediated cytotoxicity (IgG or IgM bind to cell surface antigens)

Can lead to complement activation or macrophage destruction of targeted cells

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11
Q

How does Type II hypersensitivity cause IMHA (Immune-Mediated Haemolytic Anaemia)?

A

Autoantibodies (IgG or IgM) bind to red blood cell antigens

Cells are then:
- Opsonised for removal by macrophages in liver/spleen
- Destroyed by complement lysis

(More common in dogs than cats)

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12
Q

How does Type II hypersensitivity cause Myasthenia Gravis?

A

Autoantibodies target acetylcholine receptors at neuromuscular junction

This blocks or destroys receptors, preventing nerve signal transmission

Leads to muscle weakness & fatigue

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13
Q

What are two possible outcomes of autoantibody binding in Type II hypersensitivity?

A

Destruction of target cells (IMHA – red blood cells destroyed)

Blocking of receptor function (Myasthenia Gravis – acetylcholine receptor blocked)

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14
Q

What is Type III hypersensitivity, and how does it cause immune-mediated disease?

A

Immune complex hypersensitivity – circulating antigen-antibody complexes deposit in small capillaries

Activates complement –> inflammation & tissue damage

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15
Q

What are common sites where immune complexes deposit, and what diseases do they cause? (Type III hypersensitivity)

A

Renal glomerulus → Glomerulonephritis

Synovium (joints) → Polyarthritis (IMPA)

Uveal tract (eye) → Uveitis

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16
Q

How does immune complex deposition cause tissue damage? (Type III hypersensitivity)

A

Triggers inflammatory response –> tissue destruction

Can cause local ischaemia due to vessel inflammation

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17
Q

What is Type IV hypersensitivity, and how does it cause immune-mediated disease?

A

Cell-mediated hypersensitivity – CD8+ cytotoxic T cells attack cells displaying self-antigens

Leads to direct tissue destruction without antibody involvement

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18
Q

How does Type IV hypersensitivity cause hypothyroidism?

A

Cytotoxic T-cells destroy thyroid follicular cells

Results in thyroid hormone deficiency

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19
Q

How do Th2 lymphocytes contribute to immune-mediated disease?

A

IL-4 & IL-5 drive B-cell activation, leading to autoantibody production

Autoantibodies cause Type II (cytotoxic) & Type III (immune complex) hypersensitivity

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20
Q

How do Th1 lymphocytes contribute to immune-mediated disease?

A

IL-12 & IFN-γ drive cytotoxic T-cell activation

Causes Type IV hypersensitivity (T-cell-mediated destruction of self-tissues)

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21
Q

What is a multisystemic immune-mediated disease (IMD)?

A

Most IMDs target specific organ or cell type due to single autoantigen

Multisystemic IMD occurs when immune system attacks multiple organs

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22
Q

What are the two mechanisms leading to multisystemic IMD?

A

Common Target – Autoantibodies target widely distributed antigens (e.g. SLE-like syndrome in dogs, where nucleic acids are attacked in multiple tissues)

Different Targets – Concurrent unrelated autoimmune diseases due to genetic predisposition

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23
Q

How do genetics influence immune-mediated diseases (IMD)?

A

Certain breeds (e.g. Cocker Spaniel) have genetic predisposition to IMD

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24
Q

What immune-mediated diseases are Cocker Spaniels at increased risk for?

A

Immune-Mediated Hemolytic Anemia (IMHA)

Immune-Mediated Thrombocytopenia (IMT)

Hypothyroidism

Keratoconjunctivitis Sicca (Dry Eye Syndrome)

Immune-Mediated Pancreatitis

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25
Why are mid-to-older age dogs more likely to develop immune-mediated diseases (IMD)?
Age-related immune changes reduce immune regulation Immunosenescence leads to reduced T-cell mediated immunity Increased CD8+ cells & reduced CD4+ cells
26
How does aging affect different parts of the immune system?
Cell-mediated immunity is most affected Humoral immunity (antibody response) is less affected Innate immunity remains largely preserved with minor defects
27
What is primary (idiopathic) immune-mediated disease?
Occurs in genetically susceptible individuals without identifiable trigger Likely involves multiple unknown factors E.g. Immune-mediated haemolytic anaemia with no known cause
28
What is secondary immune-mediated disease?
Triggered by distinct factor E.g. drugs, infections, topical flea treatments causing hypersensitivity
29
Why is identifying a trigger important in immune-mediated disease?
Primary IMD often requires long-term immune suppression Secondary IMD (ie identifying trigger) may be treatable by removing trigger (e.g. stopping drug, treating infection)
30
How can drugs trigger secondary immune-mediated disease (IMD)?
Some drugs act as haptens, bind to cells (RBC, platelets, WBC) & trigger immune response Examples: - Trimethoprim-sulphonamides (antibiotics) → Can cause IMHA or IMT - Carbimazole & Methimazole (for hyperthyroid cats) → Can induce IMHA or IMT
31
How can neoplastic diseases trigger secondary immune-mediated disease?
Tumours may express cryptic antigens or expose new antigens, triggering immune attack Key associations: Lymphoma & Splenic Hemangiosarcoma → Known triggers for IMHA & IMT If IMHA or IMT is diagnosed, consider screening for underlying neoplasia
32
How can inflammation contribute to secondary immune-mediated disease (IMD)?
Chronic pancreatitis/enteropathy is associated with immune-mediated cytopenias Acute enteritis is linked to Type III immune-mediated polyarthritis (IMPA)
33
Why is it difficult to link infections to secondary immune-mediated disease (IMD)?
Infectious agents are hard to identify & difficult to culture Some pathogens (e.g. Babesia, Leishmania, Ehrlichia) are sequestered in tissues Triggering infection may have occurred weeks before IMD symptoms appear - Time lag makes it harder to establish cause-&-effect relationship
34
Why is identifying an infection (if possible) in IMD cases important?
Prevents misdiagnosis (e.g. distinguishing haemolytic parasites from IMHA) Allows targeted treatment of infection, rather than just suppressing immunity
35
What are the key clinical signs of immune-mediated polyarthritis (IMPA)?
Pyrexia Palpable joint effusions Pain on joint manipulation
36
What laboratory and radiographic findings are associated with immune-mediated polyarthritis (IMPA)?
C-reactive protein (CRP) elevated Joint effusion analysis: Neutrophilic inflammation, but no infectious agents detected Radiography: Joint effusions present, but no erosive changes
37
What is the pathophysiology of immune-mediated polyarthritis (IMPA)?
Type III hypersensitivity reaction - Immune complex deposition in synovial basement membrane - Complement cascade activation - Recruitment of inflammatory cells (neutrophils & macrophages) → Release of nitric oxide, free radicals & proteases → tissue damage Prompt treatment is crucial to prevent further damage If trigger antigen is found, treating underlying cause may avoid need for immunosuppressive drugs
38
How is immune-mediated polyarthritis (IMPA) categorized based on trigger factors?
Classified based on trigger factor: - Type I (Idiopathic IMPA) – Most common, no trigger identified - Type II – Associated with infection remote from joints (e.g. Lyme disease, Leishmaniasis, focal infections) - Type III – Associated with inflammatory GI disease - Type IV – Associated with neoplastic disease
39
What clinical findings may indicate IMPA as part of a broader immune-mediated disease?
Joint disease along with: - Glomerular disease - Skin lesions (mucocutaneous junction erosions & ulcers) - IMHA +/- thrombocytopenia (Evan’s Syndrome)
40
Why is it necessary to reduce/stop overactive immune response?
To prevent further damage & manage symptoms
41
How does the severity of immune-mediated disease influence treatment goals?
Some diseases allow for partial control, while others require complete suppression to prevent life-threatening complications (e.g. Immune-mediated thrombocytopenia (risk of fatal bleeding))
42
What is a major challenge when using immunosuppressive drugs?
Balancing disease control with significant adverse effects of drugs
43
What are the main functions of immunomodulatory drugs?
Stimulate, suppress, or modify immune system
44
What drug is commonly used for immune stimulation?
Achieving immune stimulation is challenging with limited options Interferon omega is commercially available & used in severe viral infections (e.g. poxvirus & parvovirus)
45
How does immune modification work in allergy (and cancer therapy)?
Allergy immunotherapy increases T-regulatory cells, reducing IgE & T-helper cells Some cancer treatments enhance immune responses to tumours
46
Why is immune suppression the most common immunomodulatory strategy?
Many immune-mediated diseases require suppression to prevent severe damage
47
What is an example of a broad vs. targeted immunosuppressive drug?
Broad drugs like steroids affect many immune pathways, while targeted drugs like Lokivetmab specifically block IL-31, reducing side effects
48
What are the challenges of using broad immunosuppressive drugs?
They can cause systemic immunosuppression, leading to adverse effects beyond intended target, increasing infection risk & other complications
49
Why are steroids widely used as immunosuppressive agents? How well tolerated are they in cats, dogs and horses?
They have broad immunosuppressive effects & can be used alone or in combination with other drugs They are well-tolerated in cats, less so in dogs & can be problematic in horses
50
How do steroids work at the cellular level?
1. They bind to glucocorticoid receptors in cytoplasm of most nucleated cells 2. Steroid-receptor complex translocates to nucleus, altering gene transcription in cell-specific manner (activate or inhibit genes --> varied effects)
51
What additional effects do steroids have beyond gene transcription?
They exert non-genomic effects by stabilising immune cell membranes, reducing release of granules from mast cells, eosinophils & neutrophils, thereby limiting inflammation
52
How do steroids reduce immune and inflammatory responses?
They reduce protein synthesis, leading to lower antibody production & inhibition of immune cell function
53
What are the key effects of steroids on the immune system?
Suppress Immune Cells: ↓ granulocyte, mast cell & macrophage activity by stabilizing membranes, ↓ mediator release & phagocytosis ↓ Cytokines: Downregulate IL-1, IL-6, TNF-α → ↓ immune activation ↓ T-cell Activity: Inhibit function & induce apoptosis (useful in cancer therapy) ↓ Antibodies: Gradual B-cell suppression → ↓ antibody levels ↓ Fc Receptors: Less antibody binding → dampened immune response
54
Why do steroids cause widespread metabolic effects?
They are hormonal drugs that act systemically, leading to inevitable side effects
55
What are the key metabolic effects of steroids?
Increased gluconeogenesis → Higher blood glucose & insulin resistance Protein catabolism → Muscle wasting & increased blood proteins Lipolysis & fat redistribution → Altered body fat distribution
56
How do steroids affect the skin and connective tissue?
Cause cutaneous atrophy --> thin, fragile skin & hair loss
57
What is the effect of steroids on calcium metabolism?
Mobilise calcium --> calcinosis cutis (calcium deposition in skin)
58
How do steroids impact the gastrointestinal system?
They increase gastric acid secretion, raising risk of ulcers
59
What additional effects do some steroids have due to mineralocorticoid activity?
Can cause salt & water retention, affecting blood pressure, heart & kidney function
60
Why can high-dose steroid use lead to euthanasia in some cases?
Severe side effects (esp. metabolic & tissue damage) can outweigh benefits of treatment
61
How does Azathioprine cause immunosuppression, and why does it mainly affect immune cells?
Azathioprine is metabolised in liver to 6-mercaptopurine, which incorporates into DNA, disrupting rapidly dividing cells like bone marrow & immune cells Since these cells undergo frequent mitosis, they are more affected, while slower-dividing cells (e.g. hepatocytes) experience less impact
62
How is Azathioprine metabolised, and why do some individuals experience severe side effects?
Azathioprine is broken down by xanthine oxidase & thiopurine methyltransferase (TPMT) into inactive metabolites for excretion Some dogs lack TPMT enzyme, leading to toxic accumulation of active metabolites & increased side effects
63
What are the major risks associated with Azathioprine?
Pancreatitis → Often linked to concurrent steroid use; usually resolves when steroids are withdrawn Hepatotoxicity → Can be severe & may not resolve with drug withdrawal
64
Why should Azathioprine never be used in cats?
Can't tolerate drug well due to severe toxicity risks & difficulty in dosing
65
Why does Azathioprine require haematology and biochemistry monitoring, and what are the expected haematologic side effects?
Mild anaemia & lymphopenia are common & can indicate appropriate therapeutic dose However, drug’s effects are variable, so monitoring every 2-4 weeks is essential to ensure safe dosing & detect severe side effects early
66
What is Chlorambucil, and why is it commonly used in cats?
Alkylating agent derived from nitrogen mustard with cytotoxic effects on DNA. Commonly used in cats as alternative to Azathioprine
67
How does Chlorambucil work, and how does its action compare to Azathioprine?
It cross-links DNA, causing cytotoxic effects Has slower onset (6 weeks) than Azathioprine (2-3 weeks) Haematology & biochemistry monitoring every 2 weeks initially, then extending to every 4 weeks once stable
68
What are the common side effects of Chlorambucil, and how can they be managed?
Myelosuppression (less common than Azathioprine) → requires monitoring GI signs (more with daily dosing): anorexia, vomiting, diarrhea Reducing dose frequency (e.g. every other day or extended intervals in small cats) can help minimise GI side effects
69
How does Mycophenolate Mofetil work?
Inhibits de novo purine synthesis, disrupting DNA synthesis & suppressing both T & B cells more than other immune cells Faster acting than drugs like azathioprine or chlorambucil, taking only a few days to take effect instead of weeks
70
In which conditions is Mycophenolate Mofetil particularly useful?
Often used as adjuvant drug, esp. in canine pemphigus foliaceus (pF) & sporadically in other immune-mediated diseases
71
What are the most significant side effects of Mycophenolate Mofetil?
Acute severe GI toxicity—some dogs develop vomiting, diarrhea, or become systemically unwell, making drug unsuitable for them Hepatitis may develop (less common)
72
How does Ciclosporin work as an immunosuppressant?
1. It binds to cytoplasmic cyclophilin 2. Forms complex that inhibits calcineurin (preventing dephosphorylation of NF-AT) 3. Leads to reduced IL-2 & cytokine activation 4. Results in suppressed T-cell function Unlike steroids, Ciclosporin doesn't cause significant metabolic effects, making it a more targeted immunosuppressant
73
In which conditions is Ciclosporin licensed for use?
Licensed for atopic dermatitis in dogs & non-flea hypersensitivity disease in cats
74
How is Ciclosporin dosed in immune-mediated diseases?
Used at higher doses for immune suppression & at lower doses for immunomodulation in conditions like allergic skin disease
75
Why is Ciclosporin a poor choice for rapidly progressive immune-mediated diseases?
Has very slow onset of action, making it unsuitable for life-threatening diseases like IMHA or immune-mediated thrombocytopenia that require immediate control
76
When is Ciclosporin most useful?
Best suited for T-cell mediated diseases or as secondary drug in antibody-mediated diseases Effective in chronic conditions like pemphigus foliaceus, cutaneous lupus & severe symmetric lupoid onychodystrophy (SLO)
77
What are the common side effects of Ciclosporin?
Gastrointestinal issues: Vomiting and diarrhea Metabolic effects: Hirsutism (abnormal hair growth), gum hyperplasia Immunosuppression: Increased risk of infections
78
Why should Ciclosporin use be monitored with other medications?
Its metabolised by cytochrome P450 enzyme system, which interacts with other drugs
79
How does Leflunomide work as an immunosuppressant?
Inhibits mitochondrial enzyme dihydroorotate dehydrogenase (DHODH), preventing expansion of activated & autoimmune lymphocytes, effectively slowing down immune response
80
In which immune-mediated diseases is Leflunomide used?
Immune-mediated polyarthritis (IMPA) Immune-mediated hemolytic anemia (IMHA) Immune-mediated thrombocytopenia (IMT)
81
What are the potential side effects of Leflunomide?
Diarrhoea Lethargy Unexplained haemorrhage Thrombocytopenia Increased liver enzymes
82
How does Oclacitinib work as an immunosuppressant?
It inhibits JAK-1, blocking cytokine receptor signaling for cytokines in IL-2 & IL-6 family, which includes IL-2, IL-10, IL-4, IL-13, and IL-31
83
What is Oclacitinib licensed for, and how is it being used beyond that?
Licensed for canine atopic dermatitis & allergic skin disease Higher doses used for immune-mediated diseases, particularly as steroid-sparing agent
84
Why is Oclacitinib not preferred for critical immune-mediated diseases?
Not as potent as other immunosuppressants & may be less effective for severe conditions like IMHA or IMT Better suited for maintenance therapy or non-critical diseases
85
What are the main side effects of Oclacitinib?
Neutropenia Haematological abnormalities Diarrhoea (uncommon)
86
How do Omega-3 fatty acids help in inflammatory and immune-mediated diseases?
They reduce production of inflammatory mediators by interfering with arachidonic acid pathway & promoting synthesis of anti-inflammatory factors, helping to modulate both innate & adaptive immune responses
87
What is Vitamin E used for in immune-mediated diseases?
Acts as adjunct antioxidative treatment, particularly in sterile pyogranulomatous panniculitis
88
How does Vitamin D influence the immune system?
Enhances innate immunity by boosting immune response against pathogens & modulates adaptive immunity by influencing T-cell activation & antigen-presenting cells
89
What is main risk of excessive Vitamin D supplementation?
Hypercalcemia, which can lead to renal failure if prolonged
90
How does glutamine support the immune system and gut health?
Normally non-essential amino acid, but in diseased states, it becomes essential Preferred energy source for enterocytes, supporting gut barrier integrity Plays role in nitrogen metabolism, immune modulation & antioxidant function
91
What is potential role of arginine in immune-mediated disease?
May have immune-enhancing properties, esp. in critical illness
92
What is the typical strategy for using immunosuppressive drugs in immune-mediated diseases (IMD)?
Most cases start with high-dose steroids, & additional drugs are added later to reduce steroid side effects or enhance immunosuppression
93
Which drugs are commonly added to reduce steroid adverse effects?
1. Azathioprine or Chlorambucil – used early as second-line agents 2. Ciclosporin – slower-acting but more targeted, esp. in T-cell mediated diseases like erythema multiforme or discoid lupus erythematosus 3. Mycophenolate, Oclacitinib, Leflunomide – typically used when other options have failed, with variable success
94
What is the main risk of using multiple immunosuppressive drugs together?
Increased risk of profound immunosuppression, leading to higher susceptibility to infections While none of these drugs have strong contraindications when combined, unexpected adverse effects can still occur
95
What factors should be considered when choosing immunosuppressive therapy?
Phase of treatment: Induction vs. Maintenance Severity: Is disease life-threatening? Mechanism of immunological damage: - Humoral (antibody-mediated) → often requires steroids - Cellular (T-cell/NK cell damage) → may respond better to calcineurin inhibitors (e.g. Ciclosporin)
96
How do direct vs. indirect immunosuppressive drugs differ in their use?
Direct-acting drugs work immediately on immune cells & are often used for acute, severe cases Indirect-acting drugs have more delayed onset but are better for maintenance therapy
97
What are the key stages in managing immunosuppressive therapy?
98
What is the underlying cause of IMHA?
IMHA occurs when immune system mistakenly targets & destroys red blood cells
99
What are the two main types of IMHA?
Primary (idiopathic - likely genetic or environmental predisposition) & Secondary (caused by underlying disease, infection, neoplasia, or drugs)
100
How does IMHA lead to pyrexia?
Pro-inflammatory cytokines act on hypothalamus, altering body’s temperature regulation Pyrexia could also indicate underlying infectious disease as trigger factor for IMHA
101
Why does IMHA cause jaundice?
Haemolysis releases bilirubin, which accumulates when liver can't process it fast enough
102
What causes splenomegaly in IMHA?
Spleen is site of phagocytosis of opsonised RBCs (RBCs bound to circulating antibody &/or complement) by macrophages Could also occur because spleen is site of secondary haematopoiesis activated in response to anaemia
103
What are common clinical signs of IMHA?
Lethargy, pale/jaundiced mucous membranes, tachycardia, tachypnea, pyrexia, lymphadenopathy, splenomegaly
104
Why does IMHA lead to tachycardia and tachypnea?
Decreased oxygen-carrying capacity triggers compensatory increases in heart & resp rates
105
What are common quick tests to assess anaemia severity in suspected IMHA?
Packed Cell Volume (PCV) & Total Solids (TS)
106
Why is normal total solids (TS) important in IMHA?
It helps differentiate IMHA from blood loss anaemia, where both PCV & TS would decrease
107
How can you tell if anaemia is regenerative on blood smear and haematology?
Blood smear - look for markers of regeneration: - Polychromasia – immature RBC - Anisocytosis – variable RBC sizes (immature tend to be larger than mature) - Increased nucleated RBC Haematology: - High MCV - High reticulocyte count - Low MCHC
108
Label S, P & NE
P= large polychromatic RBCs likely reticulocytes (immature RBC) ME= nucleated RBC (erythrocyte) S= spherocytes
109
Why might anaemia appear non-regenerative early in IMHA?
Bone marrow takes 3-5 days to mount a regenerative response
110
What additional tests help diagnose IMHA?
Blood smear - Look for spherocytes & neutrophilia Look for evidence of extreme type II hypersensitivity response: - Evidence of autoagglutination (speckles on surface of blood tube (EDTA best anticoagulant) seen when tipped gently) - Saline agglutination test - Coombs test (if saline agglutination test is negative) PCR for infectious causes Radiographs & ultrasound for underlying disease
111
What are spherocytes?
Smaller & rounder/denser than normal RBCs (no central pallor seen) They are fragments of RBCs that result from damage by partial phagocytosis by macrophages in spleen &/or liver
112
What is autoagglutination?
IgM/IgG auto antibodies attach to antigens on surface of RBCs & draw together RBC --> clumping: autoagglutination
113
How is the saline agglutination test done?
Mix 1 drop of EDTA blood with 4 drops of saline on slide Examine under microscope to assess for autoagglutination Helps differentiate true agglutination (grape-like clusters due to antibody binding) from rouleaux formation (stacks of coins due to increased plasma proteins) True agglutination supports diagnosis of immune-mediated hemolytic anemia (IMHA)
114
What is the purpose of the Coombs test in diagnosing IMHA?
Direct antiglobulin test used if saline agglutination test is -ve Detects immunoglobulins (auto antibody) &/or complement bound to RBCs in dogs with IMHA
115
Why is it important to rule out secondary causes before treating IMHA?
Treating underlying cause (e.g. infection, neoplasia) may resolve IMHA without need for strong immunosuppressants
116
What are the possible mechanisms causing red blood cell (RBC) damage in IMHA?
Primary IMHA (1ry IMHA) - Idiopathic: No underlying cause identified - Autoantibody to RBC membrane antigen: Immune system attacks its own RBCs Secondary IMHA (2ry IMHA) - Cross-reacting antibodies against infectious agents - Antibody against drug-adherent RBCs - Drug, infection, or neoplasia modifies RBC antigen or exposes hidden antigens Alloantibody-Mediated IMHA - Blood transfusion reaction (incompatible donor-recipient) - Neonatal isoerythrolysis (maternal antibodies attack neonatal RBCs)
117
What are the main treatment goals for IMHA?
Suppress abnormal immune response Provide supportive care Manage complications (e.g. thrombosis & transfusion reactions)
118
How do you monitor response to IMHA treatment?
PCV trends, reticulocyte count, resolution of autoagglutination, improved clinical signs
119
What are the first-line immunosuppressive drugs for IMHA?
Prednisolone or dexamethasone
120
When is a blood transfusion indicated in IMHA, and why is packed RBC preferred?
Indicated when PCV is critically low & patient is unstable Packed RBCs preferred over whole blood as they provide oxygen-carrying capacity without volume overload

LEAH FCP (151 decks)

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