Practicals Flashcards
Fatty change
Accumulation of lipid droplets in cytoplasm
Karyolysis
Fading and loss of normal basophilic staining of DNA, nucleus disappears
Coagulative necrosis
Denaturing of proteins, making cytoplasm more eosinophilic
Key morphological features of apoptosis
Cell shrinkage Loss of surface contact with neighbours Chromatin condensation Fragmentation into apoptotic bodies Phagocytoais
Characteristic leukocytes of chronic inflammation
Lymphocytes and monocytes
Megakaryocytes produce
Platelets
Characteristic of neutrophil
Poly lobated nucleus
Fibrinogen:
Made in…
Converted to…
Liver
Fibrin
Collagen formed by…
Present in…
Fibroblasts
Chronic inflammation/healing
Trichromatic stain
Used to stain…
Fibrin scarlet
How does a viral infection become a bacterial infection?
Destruction of (bronchial mucosal) epithelium
Chronic inflammation
Prolonged inflammation
Tissue destruction, inflammation and healing simultaneously
Resolution
Inflammatory exudate cleared by macrophages
Organisation
Conversion of non-viable tissue to fibrous tissue
Regeneration
Replacement of damaged epithelium with new epithelium
Repair
Resolution and organisation
Healing
Regeneration and repair
Granulation tissue
Capillaries and fibroblasts forming fibrous tissue
Purulent exudate
Central pus
Neutrophils with few macrophages
Foreign body giant cells
Large multinucleated macrophages
Formed by the fusion of macrophages
Influences on gastric acid secretion
Stimulatory effect of histamine on H2 receptors on acid producing cells
Key initiating factor causing gastritis
Mucosal infection by Helicobacter
MALT
Mucosal associated lymphoid tissue
Birds : where do B lymphocytes mature?
Bursa of fabricius
How do lymphocytes enter lymph nodes?
Via high endothelial vessels
Sometimes by afferent lymph
High endothelial vessels
Lined by enlarged endothelial cells
Increased level of activation
Express cell adhesion molecules
Where are B lymphocytes in lymph nodes?
Aggregated around FDCs to form follicles in the cortex
If a B cell in follicle is activated …
With T help Enlarge and proliferate Somatic hypermutation Follicle is called germinal centre Considerable mitotic activity, and apoptosis of nonselected B cells
Mantle
Small B lymphocytes surround germinal centre as a dark rim
Resting
Become plasma cells during Humoral response
Where are T lymphocytes in the lymph node?
Some T helpers in follicles
Inter follicular areas/para cortex
Here APCs settle and become interdigitating cells
CD3 immunostaining
T lymphocyte marker
Brown
CD20 immunostaining
B cell marker
Brown
Cd68 immunostaining
Macrophage/dendritic cell marker
Brown
Red pulp of spleen
Sinusoids lined by macrophages
Reticulo endothelial system
Reticulo endothelial system
Phagocytosis of effete RBCs
Sessile macrophage
Attached to lining of sinuses
White pulp
Contains immune cells
- T and B lymphocytes
- Macrophages
Structure of thymus
Cortex and medulla
Rich vascular supply
What happens in the thymus?
Positive selection - on thymic epithelial/dendritic cells in cortex
Negative selection - on dendritic cells in medulla
Positive selection
Bind class 1 MHC retain CD8 expression Bind class 2 MHC retain CD4 expression
Negative selection
Dangerously high affinity for self peptides are deleted - signals from APC
Complete precipitation of antibody antigen occurs…
At an optimum ratio of antibody and antigen
Gel diffusion precipitation test
Agar
Line of precipitation where antigen and antibody meet in optimal proportions
Antigens common to both = lines which merge
Some common determinants = merge but show spurs
Different antigens = lines cross
What happens when complement is added to a solution containing antibody-antigen complexes?
Complement cascade will be activated and complement will be used up
Complement fixation test
Serum + antigen + complement
Add antibody coated RBCs as an indicator for residual conplement
Complement fixation test - positive
Complement consumed
RBCs remain unlysed
Complement fixation test - negative
Sufficient complement remains to lyse RBCs
What affect does the amount if complement have on the sensitivity of the test?
The more complement, the less sensitive the test will be
Anti-complementary activity
Complement is inactivated by substances other than antigen-antibody complexes
Anti-A and Anti-B are natural antibodies because..
Exposed to A and B antigens on microorganisms
Problem with rhesus antigens…
Non agglutinating
Coombs test
Test for rhesus antigen with antibody
Interaction detected using anti globulin to bring about agglutination
Immunodiffusion
Identical - smile
Non identical - X
Partially identical - Y shaped
Complement fixation test
Antibody present - Ag/Ig complex consume complement
Complement not available to lyse red blood cells
ABO blood group antigens -
Glycoproteins
Rhesus antigens -
Transmembrane proeins
Hypersensitivity type 1
- Type
- Mechanism
- Eg
Anaphylactic
IgE on mast cells
Asthma, hay fever
Hypersensitivity type 2
- Type
- Mechanism
- Eg
Cytotoxic
IgG or IgM binds antigen on cell
Acute rheumatic fever
Hypersensitivity type 3
- Type
- Mechanism
- Eg
Immune complex
IgG, IgM, IgA bind free antigen
SLE
Hypersensitivity type 4
- Type
- Mechanism
- Eg
Delayed type
APCs and T cells recruit macrophages, form granulomas or kill directly
Tb, transplant rejection
Polyp
Growth protruding from mucous lining of organ, often causing obstruction
Type 4 hypersensitivity - response at 2 separate sites:
Ghon focus - site of entry
Local lymph node
= primary complex
How do primary complexes heal? (type 4 hypersensitivity)
Fibrosis, often followed by calcification
Mycobacteria cell wall -
contains wax like mycolic acid
ZIEHL-NEELSEN STAIN
Granuloma
Collection of macrophages
What molecular mechanisms lead to fever?
Cytokines at site of inflammation (TNFa, IL1) at hypothalamus induce prostaglandin synthesis. Via neural mechanisms, vasoconstriction and shivering induced => heat
Physiological functions of CRP
Acute phase protein released by liver in response to IL1 IL6 TNFa
Opsonin
Activates complement cascade
What does cytokine production in chronic disease do?
Suppress bone marrow red blood cell production
Normal CD4:CD8
2:1
Th2 deficiency leads to…
Extracellular bacteria and parasites (helminths)
Th1 deficiency leads to…
Intracellular bacteria and parasites
Decrease in CD8 leads to…
Viral infections and intracellular parasite infections eg malaria
