Immunology Flashcards
All cells of immune system originally derived from
Multipotent haematopoetic stem cell
Multipotent haematopoetic stem cell splits into one of 2 cells depending on chemical signal involved
Myeloid stem cell
Lymphoid stem cell
Myeloid stem cell has potential to form 6 types of cell - PEMP (one P=3 Phils)
Erythrocyte
Platelet
Phils (Neutro, Baso, Eosino)
Macrophage
Lymphoid stem cell has potential to form 2 types of cell
Natural killer cell
Lymphocytes (T and B)
4 Lymphoid organs (STDL)
Lymph nodes
Spleen
Thymus
Diffuse lymphoid tissue (MALTs - Mucosa Associated Lymphoid Tissue) such as tonsils and peyer’s patches
Lymph nodes
Neck, armpit and groin
Contain T cells
Spleen has 2 pulps
Red pulp - Old RBCs destroyed
White pulp - Filters blood and antibody-coated bacteria
Thymus
Active in neonatal, then atrophies after puberty
Involved in development of T cells (Autoimmune T cells are destroyed here)
Innate immune response
Present at birth Non-specific No memory Phagocytes Complement proteins PAMPS Limited PR receptors
Adaptive immune response
Built over time Specific Memory Lymphocytes Antibodies Diverse PR receptors
4 components of innate immunity
PRR
Complement
Phagocytosis (Neutrophils and macrophages)
NK and mast cells, baso and eosinophils
2 Types of PRR
Secreted/circulating (Lectins and collectins)
Cell-associated (Toll-like R and nod-like R)
2 AMPS (Associated Molecular Patterns) which PRR recognise
PAMPS (Pathogen) - Lipopolysaccharides (LPS) endotoxins on gram negative bacteria
DAMPS (Damage)
5 step mechanism of PRR action
Trigger innate immune response and inflammatory response:
1) Opsonise pathogen
2) Activate complement
3) Activate inflammatory mediators
4) Secrete interferons and cytokines
5) Induce Apoptosis
3 Complement activation pathways - CAL
Classical pathway - AbAn complexes
Alternative pathway - Foreign An
Lectin pathway - Mannose-binding lectin (Mannose residues on pathogen surface)
3 Mechanisms of Complement action (LIP)
Lysis of microbe (MAC - Membrane attack complex)
Inflammation
Phagocytosis
Action of natural killer cells
Apoptosis of own cells that are infected/cancerous
Actions of mast cells, baso and eosinophils
Mast cells (Release histamine, heparin and cytokines) Baso and eosinophils (Release histamine in hypersensitivity reactions (raised in allergy))
6 components of adaptive immunity
Humoral (B cell) and cell-mediated (T cell) immune system: APC Major histocompatibility complex (MHC) T helper cell Cytotoxic T cell B cell Ab
What is major histocompatiblity complex (MHC)?`
Proteins that mark a cell as self
2 Classes of MHC
Class 1 - All cells
Class 2 - APCs
5 Immunoglobulin classes
IgG - Most common/Secondary response IgA - Mucus membranes IgM - Primary response IgE - Allergic reactions IgD - B cell activation
Allergy
Abnormal response to harmless foreign material
Atopy
Tendency to develop allergies
Anaphylaxis
Acute allergic reaction to Ag where body has become hypersensitive
Pathogenesis of allergy/hypersensitivity
IgE
MLS cells (Mast cell, Lymphocyte and Smooth muscle cell)
Mediators - Histamine, cytokines, prostaglandins
Genetic factors
Which of basophils and mast cells circulates and which is in tissues?
Basophils - Circulate
MasT cells - Tissues
5 Mast cell components in allergy/hypersensitivity
Histamine (Arteriolar dilation, bronchoconstriction)
Leukotrienes (LT) (Capillary contraction, increase vascular permeability)
Prostaglandin (Smooth muscle contraction)
Platelet aggregation factor (PAF) (Platelet aggregation increases vascular permeability)
Cytokines - IgE production
5 Allergic diseases - AARCI
Anaphylaxis Asthma Rhinitis (Hay fever) Contact dermatitis Insect venom
Anaphylaxis
Elevated histamine due to mast cell/basophil activation (serum) Lowered BP (Vasodilation) Bronchial contraction Rash and swelling (Skin) Pain and vomiting (GI)
Asthma
Eosinophil influx into lungs
Long term treatment - immune suppression
6 Treatment methods for allergy/hypersensitivity
1) Avoid allergens
2) Desensitisation to allergens (by increasing dose to Ag)
3) Lumiliximab (prevents IgE production)
4) Omalizumab (prevents IgE interaction with receptor - binds and inactivates)
5) Prednisolone - corticosteroid (prevents mast cell activation)
6) LT/PG antagonist (inhibit mast cell products)
What is systemic lupus erythematosus an example of?
Immunodeficiency
Systemic lupus erythematosus - Epidemiology 2 facts
More common in women>men
More common in african american
4 Hypersensitivity types
Type 1 - Allergy - IgE, mast cells and histamine (Asthma, Anaphylaxis)
Type 2 - Cytotoxic - IgM binds to Ag and kills cell via complement (Haemolytic anaemia)
Type 3 - Immune complex disease - IgG binds to Ag to form Ab-Ag complex which deposits in tissue and causes inflammation (Reactive arthritis)
Type 4 - Delayed type hypersensitivity - T helper cells and macrophages lead to inflammation
Systemic lupus erythematosus - Aetiology
Genetics - complement deficiencies
Hereditary - 1st degree affected relatives
Sex hormones - pre-menopause women
UV light
Systemic lupus erythematosus - Pathophysiology
1) Apoptosis leaves remnants of cells
2) Remnants not cleared, instead taken up by APC as Ag
3) B cells respond with Ab to form Ab-Ag complex
4) Ab-Ag complex deposited anywhere in body
5) Complement system activated (inflammation)
6) Ab binds to Ag on cell surface of RBC/WBCs which activates complement also
Systemic lupus erythematosus - Signs and symptoms (SOAP BRAIN MD)
Serositis
Oral ulcers
Arthritis
Photosensitivity - UV light causes rash
Blood disorder - Low RBC, WBC, platelets Renal disorder - Lupus nephritis Antinuclear Ab Immunological disorder Neurological disorder - Cerebral lupus
Malar rash - fixed erythema over malar (red cheeks due to increased blood flow)
Discoid rash - Erythematous raised patches with scarring
Systemic lupus erythematosus - 1 Complication
Lupus nephritis can lead to end stage renal failure if left untreated
Systemic lupus erythematosus - 3 Differential diagnoses (RAG)
Rheumatoid arthritis
Anti-phospholipid syndrome
Glomerulonephritis
Systemic lupus erythematosus - Diagnostic test
More than 3 signs from SOAP BRAIN MD = 95% specific
Systemic lupus erythematosus - Treatment
Lifestyle advice - UV protection
If no organ involvement - Hydrocortisone
If major organ involvement - Methyprednisolone
HIV - Epidemiology 3 facts
Male:Female = 3:1
UK prevalance = 100,000
Incidence falling due to antivirals
HIV - Medical science 3 steps
1) Protein on virus binds to Th cell
2) Viral Th cell proliferates in lymph nodes (Viral proliferation)
3) Reduced T cell function leads to infections
HIV - Aetiology 3 (SMC)
Sexual intercourse
Mother to child (Trans placental or breast feeding)
Contaminated needles/blood
HIV - Pathophysiology
1) Decline in T cells leads to dysregulation of B cells
2) Dysregulation of Ab production leads to dysregulation of Ag response
3) Unable to respond to infections
HIV - 4 Signs and symptoms
Fever Night sweats Diarrhoea Weight loss Opportunistic infections - Oral candida, oral hairy leucoplakia, recurrent herpes simplex
HIV - 4 Complications
Candidiasis
HSV
Kaposi sarcoma
Pneumocystis jiroveci pneumonia
Is there a differential diagnosis for HIV?
No
HIV - Diagnostic test
Adults - Serum HIV Ab levels
Babies - Ab levels test would be inaccurate because maternal Ab might be present, instead perform PCR or viral culture
HIV - Treatment (3 Lifestyle modifications and 1 medical therapy)
Sex education
Avoid sexual partners
Partner notification
HAART (Highly active anti-retroviral therapy)
HIV - Monitoring 3
CD4 T cell count
HIV RNA
Serum U&E and LFT
3 Physical/chemical barriers as part of innate immunity (SBG)
Skin
Bronchi - mucus and cilia
Gut - acid
What drug for peanut allergy?
Noradrenaline (Epipen)
What drug for anaphylaxis?
IV Hydrocortisone
