MCBoM- Definitions Flashcards
Solenoid
Collection of nucleosomes
= chromatin filament
Then wound into chromosome
Azidodeoxythymidine
AZT
Inhibits reverse transcriptase of HIV
Good as doesn’t effect human cells
Retrovirus
Vector to deliver gene in gene therapy
Infects replicating cells only
Integrates to RNA genome
Lentivirus
Vector to deliver gene in gene therapy
Infects non-dividing as well as dividing cells
Integrates to RNA genome
Adenovirus
Vector to deliver gene in gene therapy
Double stranded DNA
Doesn’t integrate to RNA, in episome
Adeno-associated virus
Vector to deliver gene in gene therapy
Single stranded DNA
Doesn’t integrate to RNA, in episome
Coagulation necrosis
Denaturation of all cytoplasmic proteins including proteolytic enzymes
Necrotic cells become tomb cells, swollen, no nuclei or any cytoplasmic detail, are just gel like structures holding tissue in place
Liquefaction necrosis
Results from actin of proteolytic enzymes which convert necrotic tissue to fluid consistency
Brain tissue
Caseous necrosis
Results in tissue being converted to a firm dry friable material
In tuberculosis, what happens inside granulomas
(dying cells burst in inflammation, immune response walls off diseased cells by granulomas, stops spread of bacteria so useful, but also stops O2, nutrients etc so cells die
Gangrenous necrosis
Necrotic tissue secondarily affected by saprophytic organisms
Dead tissue invaded by saprophytic bacteria-> gangrene, invading healthy tissue alongside
Dry (slow moving), wet or gaseous (fast)
Serous inflammation
Collection of thin exudate serous fluid below epithelium in vacule (blister)
Autoimmune- antibodies are injurious agent
Fibrinous inflammation
Rich in fibrin
Eg fibrinous pericarditis so heart can’t contract properly
Supperative inflammation
Rich in dead/dying neutrophils (pus)
Ulcer
Abscess containing pus, surface epithelium replaced by granulation tissue (fibroblasts and newly formed blood vessels)
Type I Hypersensitivity
Allergic (Immediate), eg asthma
Soluble antigens (not on surface of infected cells)
Quick onset and recovery
TH2 cytokines IL4 and IL13 switch to make IgE (TH1 cytokine IFNy suppresses)
IgE and mast cells critical
Dendritic cell picks up allergen, presents to CD4 lymphocyte, B cells make IgE, activates mast cells causing…
-increased fluid in tissues, increased blood flow and permeability
-diarrhoea and vomiting
-congestion and airway blockage, swelling and mucus secretion
Type II Hypersensitivity
Cytotoxic, eg Mum/baby placenta
TH2 mediated
Mediated by antibodies and complement system to react with cell surface antigen leading to cell death
IgG or IgM expressed, binds to surface of host cells and opsonises
PHAGOCYTIC LYSIS
Target cell expresses antigens, antibodies bind, expose Fc portion, phagocytes bind, release cytotoxic material and kill target
CLASSICAL COMPLEMENT PATHWAY
Antigens on target cell bind to IgG/IgM antibodies, recognise and activate MAC (membrane attack complex) to punch hole in target cell surface leading to the lysis of the cell
ANTIBODY DEPENDENT CELLULAR CYTOTOXICITY
NK cells attach to Fc portion of antibodies, release perforins and granzymes, apoptosis
Type III Hypersensitivity
Immune complex mediated, eg Lupus (butterfly rash)
Soluble antibody (IgG/M) complexes form in large amounts, overwhelm the body, become insoluble as oversaturated
Lodge in capillaries and become trapped
Activates classical complement pathway
Destroys capillary by inflammation and tissue death
Type IV Hypersensitivity
Delayed, eg transplant rejection
Cell mediated, not antibody mediated
TH1 CD4 lymphocytes sensitised to antigen, produce cytokines eg IFNy to interfere with viral replication
CTL CD8 lymphocytes produced
CTLs, cytokines and macrophages cause tissue damage
