Cell and tissue Flashcards
Causes hyperplasia
BPH, HPV, breast puberty, wound healing
Causes hypertrophy
Uterus pregnancy, breast pregnancy, cardiac muscle in chronic hypertension
Cardiac hypertrophy
mechanical sensors
growth factors
vasoactive agent ( alpha ag, AT II, endothilin 1)
Cause signal to transcription factors GATA4, MFAT, MEF2
Columnar to squamous metaplasia
resp tract due to smoking / vit A deficiency
salivary, pancreatic, biliary duct
Squamous to columnar metaplasia
Barretts osophagus
Karyolysis
Pyknosis
Karyorhexis
fading of nucleus
Shrinking
fragmentation
Necrotic cell microscopy
eosinophilia, loss glycogen, myelin figures, nuclear degradation, lysosomal swelling
Coagulative necrosis
tissue architecture preserved - happens in gangrenous, solid organ ischaemia (brain liquefactive)
Fibrinoid necrosis
antibody/antigen complexes in vessel walls, bright pink area, seen in immunological disease e.g. lupus
caseous
friable and white, damages/ dead cells surrounded by inflam border
Cytochrome C
caspase released from mitochondria -.> apopoptosis
Antioxidants
Vits ACE, glutathione
enzymes - catalases, superoxide dismutase, glutathione peroxidase
Action on ROS
lipid peroxidation
oxidative modification proteins
lesions in DNA
Ischaemic reperfusion injury
free radicals from damaged mitochondria
ROS promote MPT pores inhibiting mitochondrial recovery
Inflamation + PMNs cause inc cytokines and adesion molecules
IgM deposition in tissue activating complement
C3b
opsonisation + phagocytosis
C3a and 5a
anaphylatoxins
histamine release
vasc permeability and vasodilation
C5a
chemotaxis - neutrophils, eosinophils, basophils
activates lipoxygenase arachidonic acid pathway
Complement outcome
inflamation (c3a and 5a)
Opsonisation and phagoytosis (C3b)
Cell lysis via MAC (C789)
Complement pathways
Classical - C1 antibody IgG/M
Alternative - C3 via surface molecules
Lectin - C1 mannose binding lectin binds to carb on microbe
Apoptosis
cell gets smaller, contents not leaked, no inflammatory reaction
morpphology - everything tightly packed, chromatin condensation, ytoplasmic blebs and apoptotic bodies
Apoptosis initiation pathways
extrinsic - death receptor TNFalpha binds cytokines
Intrinsic - mitochondrial, inc perm, regulated by BCL2 (antiapoptotic)
Apoptosis execution pathway
mediated caspases
8,9 initiate
3,6 execute
p53
tumour suppressor - cell cycle arrest at G1 / G2 checkpoint regulator
Common locations steatosis
liver, kidney, muscle
foamy appearance with macophages
Appearance protein acumulation
rounded eosinophilic droplets or russell bodies in ER
Glycogen appearance in cells
clear vacuoles in cytoplasm, renal tubular cells in DM
Dystrophic vs metastatic calcification
dystrophic normal Ca level on damaged tissue
Metastatic high Ca, on alkaline tissue kidney, resp gastric
telomere
repetitive nucleotide sequence at end of chromosome preventing degredation
TLRs
in vasc wall and inflam cells
Innate immunity
Recognise microbes
Step of leukocytes in inflamation
margination
rolling
firm adhesions with integrins
diapedesis
stimulated by IL 8
Cell response time
first 24 neutrophils
then moocytes/ macrophages
lymphocytes for viral
eosinophils for hypersensitivity
Professional phagocytes
monocytes, macrophages, neutrophils, eosinophils, dendritic cells, mast cells
Opsonins
Fc fragment IgG, C3b
Termination acute inflamation
arachidonic acidd metabplites - lipoxin A4 and B4
anti inflam cytokines TGFb and IL10
Anti inflam cytokines
4,10,11,13
TGFb
Actions serotonin and histamine
smooth muscle contraction GIT and bronchi
vasodilation locally
Nerve ending activation with itch
Arachidonic acid stimulators
mechanical
chemical
phospholipase A2
C5a
Platelet activating factor
from phospholipids via phospholipase A2
stimulate plt to form TXA2 -> aggregation
broncho and vasoconstriction
Leukocyte activation
Bradykinin
from kininogen (plasma protein) via kallikrein enzyme
inc vasc perm, vasodilation, contraction smooth muscle, pain
TXA2
from cox pathway
Vasoconstriction and plt aggregation
5 lipoxygenase pathway
from arachidonic acid
HETE + leukotriene B4 - chemotaxis and leukocyte adhesion
leukotriene C4 D4 E4 vasoconstriction and inc vasc perm
lipoxin A4 + B4 - supress inflamation
TNF, IL1
cytokines from macrophages, acute phase reaction
+IL6 -> fever
dec insulin sense
TNF cachexia + NO production
stimulate leukocyte production, adhesion to and migration through vessels
Serous inflammation
minimal cells, effusion
inc vasc perm or local irritation
e.g. burns or blister
fibrinous inflammation
fibrin passes out of blood to extracelular space
mainly pleura, pericardium, meninges
eosinophilic meshwork/ amorphous coagulation
broken down by fibrinolysis/ becomes scar
e.g. big injury or local to cancer
purulent inflammation
neutrophils, necrotic cells, oedema
bacteria cause liquefactive necrosis
central necrotic leukocytes, surrounded by preserved neutrophils and vascular dilation
Cells in chronic inflammation
macrophages, lymphocytes, plasma cells, eosipnophils
Macrophage activation
classical - M1 - activated by IFNy, TLR activation, acute defence + inflam reactions
alternative - M2 - IL4+13, tissue repair
Granulomatous inflamation
chronic inflammation with collections activated macropages
macrophage with abundant cytoplasm - epithelioid cell
2 fused - giant cell
FB type - non T cells
Immune - t cell mediated
Causes granulomas
TB - caseating (amorphous, eosinopilic debris in centre)
Cat scratch disease
Sarcoid
Syphilis
Schistosomiasis
Leprosy
Crohns
FB
Silicosis
Blastomycosis
Temporal arteritis
Labile tisue
constantly dividing + replaced by stem cells
haematopoetic cells
Epithelial cells:
stratified squamous - skin, oral, vagina, cervix
cuboidal - ducts
columnar - GI, uterus, fallopian tubes
transitional - bladder
Stable tissue
in G0 of cell cycle, can divide (limited except liver) in response to injury
solid organs
endothelial cells
Smooth muscle
Fibroblasts, lymphocytes
Permanent tissue
non dividing
neurons and cardiac tissue
TGF B
in plt, endothelium and lymphocytes and macrophages
fibroblast chemotaxis
collagen production
Associated with fibrosis
TIV collagen
Basement membrane, goodpastures
TI collagen
bone and skin, osteogenesis imperfecta
TII collagen
cartilage, IV discs
TIII collagen
hollow organs
TV collagen
blood vessels EDS
Elastin
elastin core surrounded by fibrillin
defects fibrillin in marfans
Hepatic regeneration
post partial heatectomy - 90% reenerated with proliferation hepatocytes
priming phase - IL6 from kuppfer
growth factor phase - HGF / TGFa restart cell cycle
termination phase
if damage to all liver cells some regen from oval stem cells
Cutaneous wound healing
D1 - VEGF, neutrophils
D1-2 - epithelial cells migrate meet in midline
D3 - macrophages replace neutrophils, granulation tissue with collagen
D5 - peak angiogenesis, fibriblasts
Week2 - decreased leukocytes, on going collagen and fibroblasts, blanching
1m - scar no inflam cells
Sutured wound strength
with sutures - 70%
1 week at suture removal - 10%
2-3m - 70-80%
Factors affecting wound healing
vit C deficiency, zinc deficiency, protein deficiency
Uraemia, DM
cytotoxics
Marfans, EDS, osteogenesis
rER
has ribosomes
protein synthesis (in ribosomes)
post translational sorting/ polypeptide folding
sER
lipis synthesis
steroid synthesis
carb and drug metabolism
gluconeogenesis
calcium regulation
Nucleus contents
nucleosomes -DNA wrapped around protein, for packaging, gene regulation and epigenetics (histone modification)
nucleolus - RNA for ribosomal synth
double layered membrane
Centriole
no membrane
organelle that organises microtubules
T1 hypersensitivity
IL4–> IgE, mast cells, histamine
anaphylaxis, asthma
T2 hypersensitivity
antibody mediated, IgG + M against self antigens, leukocytes
graves, goodpastures, autimmune haemolytic anaemia
T3 hypersensitivity
Antigen antibody complex, leukocytes + complement causing inflammation and necrotising vasculitis
SLE, serum sickness, Arthur’s reaction
T4 hypersensitivity
T-cell activation against self-antigens and T-cell–mediated cytotoxicity
MS, type 1 diabetes, TB, IBD, and rheumatoid arthritis
PGD2 and E2
vasodilation and increased vascular permeability
wear and tear pigment
lipofuscin
antigen presenting cells
dendritic cells, macrophages, Langerhans cells, and B cells
Post splenectomy bloods
Thrombocytosis
Heinz bodies in rbc
Howell jolly bodies
Nuceoli
Most numerous in growing cells
Site of ribosome synthesis
rER
Protein synthesis, folding etc
Ribosome
2 subuniys
RNA 65%
Translate mRNA into protein
In rER
Main site increased vascular permeability
Post capillary venules
Prussian blue staining
Detects iron in tissue
Day collagen deposition in wound healing
D3
Initially TIII then TI
