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100 Cards in this Set
- Front
- Back
Pathogenesis
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Mechanism of Disease
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Cell injury leads to...
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Degeneration
Necrosis Apoptosis Neoplasia |
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Cell Adaptation leads to...
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Metaplasia
dysplasia |
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Cell injury- causes
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Hypoxia, Ischaemia
Disturbed Metabolism Genetic damage |
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Damage to cell membrane...
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Osmotic Disruption
Damage to ion pumps Loss of shape- cytoskeleton DNA damage Mitochondrial damage---> dec ox phosph, anaerobic glycolysis, ATP depletion ATP depletion---> Ion pump disruption---> osmotic swelling |
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Degeneration
eg |
Reversible, non lethal change
Cloudy swelling---> hydropic/ vacuolar degen---> eg fatty change |
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Fatty change
Normal during---> Pathological ---> |
Parturition and lactation in ruminants, neonates
Toxaemia, protein malnutrition, starvation (mobilisation)/ excess dietary fat, lipotrophic factor deficiency eg. Equine Hyperlipidaemia, feline hepatic lipidosis, preg toxaemia |
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Fat metabolism---> 3 stages
(Patho) |
Uptake- FFA---> goes to liver
(inc uptake- accumulation) Catabolism- FFA---> TG--->lipoproteins--->VLDL (dec utilisation/ oxidation (Damage)) Secretion- VLDL hydolysed in mm and adipose tissue (dec protein= dec lipoprotein creation and secretion) |
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Necrosis- 5 types
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Coagulative
Caseous Liquifactive Gangrenous Fat |
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Causes of Necrosis
Death occurs when... |
Toxins, free radicals, hypoxia, trauma
1) Mito irreversibly damaged. 2) Massive CA++ influx due to ATP deplet. 3) Enzymes activated (eg. phopholipases, ATPases, Proteases, Endonucleases) |
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Repurfusion injury
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Blood supply restored---> inc Ca++ brought to site of damage---> further activation of enzymes
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Cellular morphological changes in Necrosis
Nuclear changes |
Cytoplasm swollen, eosinophillic, detached
Pyknosis- basophillic, condensed nucleus Karyorrhexis- fragmentation Karyolysis- dissolution |
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Coagulative Necrosis
Cause- Gross- Micro- |
Due to ischaemia and toxins
Firm and pale Preservation of basic architecture- no proteolysis |
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Caseous
Cause- eg Gross- Micro- |
Bacterial dz- Tuberculosis and caseous lymphandenitis (C.pseudoTB)
Granular, friable, white/cream colour, chronic loss of architecture Cell coagulation, fragmentation, surrounded by granulomatous reaction Nuclear and cytoplasmic debris Mineralisation- calcification |
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Liquefactive
Causes- Gross- Micro- |
May follow coag. nec.
Due to bacterial infection + abscess formation in CNS (lipid content high- low CT) Cavity filled with pus Enzymatic digestion of cells PMN cells |
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Gangrenous- 2 types
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Dry- Mumified extremity after ischaemia and coag necrosis
Wet/Gas- Putrefied tissue (from bact. infect.)---> enzymatic liquefaction |
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Fat Necrosis
Cause- Gross- Micro- |
Due to- release of pancreatic enzymes
- trauma (eg parturition) White/cream colour and chalky (Fat+Ca2+---> soap) Outline of necrotic cells c blue mineral depos |
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Cholesterol Clefts
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Cholesterol xll from dead cells dissolve during fixing to leave clefts
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Results of Necrosis (x6)
(-ations) |
Inflammation
Disappearance of necrotic cells/debris- phagocytosis Encapsulation/ replacement/ regeneration Sequestration- seperation from healthy tissue Desquamation- sloughing Dystrophic calcification |
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Necrosis vs PM changes
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Autolysis without inflammation (still loss of structure)
Still have putrefaction- no inflam. |
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Apoptosis
Phases- Causes- Morphology- |
initiation-
inflam mediators ---> activation of caspases Execution- caspases cause cell death Causes- mito damage, DNA damage, T cells... Morphology- cell shrinkage + nuclear fragment./condensation Membrane retained until the end NO inflammation |
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Karyorrhexis
Karyolysis Pyknosis |
Fragmentation of nucleus
Dissolution of nucleus Condensation of nucleus |
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5 signs of inflammation
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Heat (calor)
Redness (rubor/tubor) Swelling (tumor) Pain (dolor) Loss of function |
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Inflammation leads to the activation of...
(x5) And accumulation of... (x3) |
WBCs (leukocytes)
Clotting factors + platelets Complement factors Mast cells fibroblasts fluids proteins Connective tissue inc elastin, collagen, proteoglycans |
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Chemical mediators of inflammation...
(x7) |
Histamines
PGE leukotrienes cytokines- (eg. IL-1, TNF IFN) NO Compliment WBCs |
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Definititions-
Exudation Exudate Pus Transudate Cytokines Chemokines Chemotaxis |
Escape of fluids, proteins and cells from BV to tissue
High protein extravascular fluid (SG> 1.020) Purulent exudate- contains WBC Low protein extra vascular fluid (SG<1.012) Soluble proteins which bind to cell and change funct. Attractant cytokines- induce cell movement Migration of WBC along chemoattractant gradient |
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5 stages of inflammation...
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Vascular changes
Cellular events Migration and activation of WBC Systemic reaction Repair/ regeneration |
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Acute inflammation
Causes- |
Rapid repsonse to trauma
Physical Chemical Infectious Hypersensitivity Tissue necrosis FB |
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Vascular changes in Acute inflam
(x4) |
(1) Coag cascade (intrinsic and extrinsic)
(2) Oedema- dilutes toxins and delivers Ab and enzymes (3) Activation of endothelium for WBC (4) Dec blood flow (loss of laminar flow)---> margination of WBC |
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Causes of oedema in Acute inflam
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Hyperaemia (may be a brief constriction then dilation)
---> due to insult or damage related mediators Inc permeability- endo contraction/ detatch/ damage --->damage from WBC release of FOS ---> Inc channels prod by VEGF inc hyrdostatic press. +dec osm. colloid press. ---> Net extravasation |
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Cellular events
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Influx of cells inc WBC and platelets
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Circulating cells...
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Neutrophils/Heterophils- Phagocytosis
- 6-12hrs Eosinophils- In parasitic infection +hypersens. - Release granules and cytokines Basophils- Similiar to Mast cells - IgE R present - Rare Lymphocytes- T and B Plasma Cells |
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Cells in tissue...
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Mast Cells
- Degranulate---> release histamine - Initiate vasc response - High IgE affinity Rs Macrophage- phag + APC - 12hrs+ |
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WBC activation- (Neut., mono., eos.,baso., lympho.)
Cause- Results- |
Complement/ microbes/ cytokine + WBC
--->---> Inc cytolsolic Ca++---> act of enzymes (Protein kinase C and PL a2 Result- expression of adhesion ("homing") molecules on WBC (L selectin and Integrin) and endothelium (P and E selectin) |
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Sequence of WBC activation/ extravasation...
(x5) |
1) Margination
2) Tethering/ rolling (tempory adhesion- req endothelial activation) 3) Adhesion ---> Pavementing -inc endothelial binding - Cytoskeletal reorg + GTPases (changes actin)---> inc motility---> allows amoeboid motion 4) Diapedesis/ emigration/ transmigration (along fibrin) 5) Chemotaxis -exogenous- bacterial products -endogenous- C5a, chemokines etc. |
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Phagocytosis
3 stages |
1) Recognition- Fc Rs on WBC/ opsonin eg IgG, C3
2) Engulfment - Actin psuedopods enclose particle - Phagosome and Lysosome---> Phagolysosome ---> dec pH +activates enzymes +ROS- oxidative burst (defect = Chediak-Higashi syndrome (persians)) 3) Killing and degredation - O2 dep.---> free radicals - O2 independ. ---> NO, BPI (increase perm.), MBP - Degredation via hydrolases |
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Byproducts of WBC activity
"collateral damage" |
Enzymes, ROS and eicosanoids released
---> cause tissue damage in surrounding cells --->amplify effects of injury (or create injury- RA) -Cytokines prod from activation---> MP chemotaxis -Prod of arachodonic acid metabolites (eicosanoids) PL---(PLa2)---> AracAcid---(LOX)---> Lipoxin+Leukotrienes ---(COX)---> PGE + thromboxane (PLa2 inhib by corticosteroids) |
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Plasma bourne chemical mediators...
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Complement
Coagulation cascade- thrombin activation end point ---> converts fibrinogen--->fibrin - intrinsic and extrinsic pathways Kinin (Hageman factor) Bradykinin---> BV dilation + inc perm., Inc AracAcid metabolite production., hyperalgesia Fibrinolytic system- (activated by hageman factor) ---> generates Plasmin---> cleaves C3 (activates Hageman factor (XII)) --->fibrin degredation products are chemotactic |
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Complement-
What- Cause- Pathways and stimuli- Important molecules- end point |
-20 plasma proteins secreted by liver as precursors
- Cause - Vascular change---> BV dil., Inc perm. - Opsonisation - Innate and adaptive immunity Classical/lectin- Ab and Lectin binding to bacterial proteins Alternative- Microbes Important- C3b---> opsonin C5a---> chemotactic and activates LOX pathway End point- MAC ---> lyse bacterial and fungal walls |
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Pain
Receptors- |
Mechanoreceptors- sense swelling
Thermoreceptors- detect Inc temp. Pain R- activated by PGE2, histamine and bradykinin |
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5 types of acute inflammation
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1) Serous
2) Catarrhal/ mucous 3) Fibrinous 4) Suppurative/ purulent 5) Haemorrhagic |
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Serous inflammation
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- Relatively mild
- Thin, clear/yellowy watery transudate/ fluid filled vesicles -eg. Early pneumonia/ blisters/ effusions/ oedema/ urticaria |
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Catarrhal/ mucous inflammation
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- Caused by low virulence microbes
- Yellow/green/grey mucoid discharge - +/- surface epithelia in exudate - +/- pus (mucopurulent) |
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Fibrinous inflammation
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- Inc vascular permeability---> loss of fibrin into ECS
---> fibrinous exudate -Gross - Yellow flecks/ strands in body cavity effusions - Yellow/red coating on peritoneal/visceral surfaces (mucous and serous membranes) -Fibrin may be voided as cast/ phagocytosed or fibrinolysed/ become organised eg. Traumatic pericarditis |
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Suppurative/ purulent
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-Usually of bacterial origin (esp Strep or Staph)
- Yellow/ green/ grey viscous liquid- high protein conc - +++ neutrophils, necrotic cells, bacteria, metabolites - Accomp. by immune resp. ---> Ab and fever - Retained pus ---> endotoxaemia/ septicaemia/ bacteraemia - May present as abscess- focal collection of pus - (Can also occur with chronic inflam) |
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Haemorrhagic inflammation
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-Haemorrhagic exudate due to v. virulent organisms/ toxins
-Tissues appear red/black, may have viscous (jam- like) exudate - e.g Anthrax |
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Ulceration
Definition- Causes- |
-Local defect/ excavation on surface of organ or tissue due to sloughing of necrotic inflam tissue which breaches muscularis mucosa or BM.
Diptheritic membrane formation - pseudomembrane of fibrin (prod by fibroblasts), inflammatory cells (MPs) and necrotic debris. |
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Erosion
Definition- Causes- |
- Loss of epi layers but muscularis mucosa and BM are intact
- Fibrinous exudate + inflam. |
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Termination of acute inflam
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-Expiry of short term mediators
- Apoptosis of neutrophils - Leukotrienes---> lipoxins (anti-inflam) -Anti-inflam mediators released by MPs eg TGFb |
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Outcomes of acute inflammation
(x5) |
1) Complete resolution- if minimal damage has ensued
2) Healing by fibrosis- can lead to loss of function 3) Abscess formation (which) 4) May become sterile- pus is resorbed and reorganised 5) Progression to Chronic inflam. |
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Abscess
Define- Morphology- |
- A focal collection of purulent inflammatory tissue
- Central necrotic area - Surrounded by neutrophils - outer layer of fibrosis/ fibroplasia |
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Response of acute inflammation...
(x5) |
Systemic inflam. resp. (SIRs)
- Pyrexia -Endog. (IL1) and exog. pyrogens (bact)---> Inc temp - PGE synth in hypothalamus - Plasma protein production and release moderated - eg C reactive Protein fibrinogen (rouleaux formation) serum amyloid A protein (2o amyloid. if prolonged) Other Acute phase proteins ---> Inc HR, BP, T etc - Leukocytosis (left shift due to Inc prod of precursors) or - Leukocytopaenia- If overwhelming infect. - Metal ions -Dec plasma Fe, Zn but Inc Cu Usually of benefit to host, otherwise---> Septic Shock occurs |
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Clinical signs of acute inflammation
(x5) |
Dec. sweating
Inc shivering Anorexia Somnolence Malaise |
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Chronic inflammation
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-Prolonged duration of active inflam., tissue destruction and repair occuring simult.
-Mononuclear cell infiltrate + accum. -MP, lympho, plasma cells -Tissue destruction -healing by fibrosis and angiogenesis -May follow acute or be chronic from the off. - Occurs when host cannot resolve/remove insult (Persistant (-eg. TB- delayed hypersensitivity) or autoimmune) |
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Chronic inflam. - Morphology
Gross- Micro- |
-Often grey/cream, frim, nodular or pitted surface
- Micro depends on cellular infiltrate- predom MP |
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Monocellular infiltration- 4 stages
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1) Recruitment- chemokines, GF, cellular debris
2) Activation 3) Division 4) Immobilisation- chemokines, oxidised lipids |
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Monocyte Activation
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- Activated by cytokines eg IFN/ endotoxins/ chemical mediators
-monocytes---> MP by fusion- become multinucleated - Inc size, may become epithelioid (adapted for inc protein secretion) |
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MP funct.
(x4) |
- Eliminate injurious agent
- Initiate repair - fibrosis +angiogenesis (stim by hypoxia, low pH, high lactate---> GF released) - Cause influx of other cells - Cause tissue injury in chronic inflam (enzymes, toxic o2 metab., chem fact., coag fact. etc) |
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Chronic inflam-
recruitment- |
-Recruited by cytokines and APCs presenting to CD4+ T cells.
- Bidirectional interaction of lympho + MPs - Act. T lymph---> IFNg---> Act. MP - Act MP---> IL12 or Ag ---> Act T lymph - Both prod TNF and IL |
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Chronic inflam-
Other cells and funct.- |
- Plasma cells- from B cells
- Eosinophils- med by IgE - Mast cells - prod cytokines ---> fibrosis + remod. - (acute inflam---> type 1 HS) - Platelets- trapped in thrombi - release GF---> stim gran. tiss - Fibroblasts- make collagen/ ECM ---> make fibrous tiss and scars - Myofibroblasts- contract wound during healing - Endo. cells- angiogen/ neovasc. - Neutrophils- med. by T cells/ MPs/persistent microbes |
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Granulomatous inflam.
Morphology- Seen in- |
- Presents as mass
- Can be solid or have purulent/necrotic center - Accum of activated, often epithelioid, MP around - Then layer of lymph., plasma Cs, MPs and fibrous tiss. - Diffuse or nodular (organised) - May be mineralised -May have fibrous capsule -Seen in -immune med. infects eg. TB - non immune med. eg FB -idiopathic |
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Granuloma Types
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- FB granuloma- Low turnover as little MP death, FB covered in MP- try to phag. (eg sutures)
- Microbe related granuloma - High turnover, MP present to T cells. (eg. type 4 HS) - Eosinophillic granuloma- nuclear material, lots of MP and eosinophils (eg bite reaction) |
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Regeneration
Define Requirements |
- Renewal or compensatory growth
- Req intact CT scaffold (ECM) - Occurs as nodules or as normal architecture - Capacity is tissue dep.- high= CT, BV, med= cart., tendons, low= nephrons, neurons |
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Cell Growth Cycle-
Cycle- Types- |
G1--CP--> S (synth) --->G2--CP--M (mitosis)---> G1--->...
G1---> G0 (resting phases) - Permenant cells- eg. neurons- no cycle - Quintescant/ stable- eg hepat.- in G0 but can progess - Labile- eg. epi -constant turnover |
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Healing-
Define- When- Fibrosis- |
- Combo of regen. and fibrosis---> scarring
- Occurs with damage to ECM- eg necrosis, or with abund. fibrinous exudate- organised - fibrosis occurs after 24hrs inflam - if no resolution then prolif of fibroblasts and endo cells --->organisation ---> Granulation tiss., Angio+neovasc. |
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Granulation tissue
Gross- Micro- Progression- |
Gross- roughen/ granular moist pink tissue above level of skin
- Capillary loops perp. to skin, fibroblasts parallel- "basketweave" - No nn---> bleeds lots -Initially very vasc. c MP, lympho and few fibroblasts - Later- less vasc. (capillaries atrophy), more fibroblasts, dec inflam cells - Finally GT replaced by fibrous tiss.- require degred. of ECM by MMP first |
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Angiogenesis requirements-
(x5) |
1) Mobilisation of endo precursor cells
2) Proteolysis of ECM 3) Migration and prolif. of cells 4) Lumen formation 5) Maturation and inhib of growth |
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Fibroplasia-
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- Plasma proteins- scaffold for ECM
-eg. fibrinogen -Collagen depo. -Fibroblast migration- stim by GF, IL1, TNF |
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First intention healing
Type of wound- Sequence of events- (x8) |
- Clean, uninfect. surgical incisions
1) Fibrin plug- scab 2) Clot removed by Neutro. 3) Epithelialisation- - Desmosomes dissolved, actin prod, - Prolif. and migr. of epi.---> BM deposited - Epi cells fuse midline (quicker if moist and well oxygenated) 4) Day 3- MP replace neutro. 5) Day 5- Granulation tissue and collagen 6) Week 2- Inflam gone, inc collagen, BV regress. 7) Tensile strength returns 8) Collagen scar Adnexae destroyed are permenantly lost |
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2nd Intention healing-
Type of wound- Sequence of events- (x6) |
- More extensive loss of cells and tissue ---> larger fibrin clot req. and inc inflam.
1) Fibrin clot 2) Granulation tiss. form. 3) Epi migration, fibro prolif., collagen prod. 4) Wound contraction- myofibroblasts (actin) 5) Fibrous scar and collagenous remodelling 6) Epi and keratin hyperplasia -(wound strength due to x-links and fibre size |
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Delays in wound healing
(x7) |
- Nutrition- protein/ vit C etc
- Mechanical- lack of immob. - Vasc inadequacies - Other dz - Glucocorticoids- inhibit MMP - Size of wound - Infection/ necrosis/ haem./ FB etc |
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Complications of wound healing
(x3) |
1) Inadequate granulation tiss./ scar form.
2) Contractures- excessive contr. 3) Excess fibrosis + angio from persist. stim.---> proud flesh |
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Bone # Healing
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1) # ---> Haemorrhage ---> Haematoma + inflam + bone necrosis (empty lacuna)
2) Organised haematoma= pro-callus (soft tiss.) 3) Cytokine release---> stim osteoprogenitor cells (eg osteo, chondro and fibroblasts) --->Remodelling of # ends 4) Deposit. of woven (immature) bone +/- cart. (inc cart with dec o2 tension)- Week 3- max callous girth 5) New cart. --(endochondrial ossif.)--> Trabecular bone (if gap <1mm---> trab. bone) (if gap >1mm---> woven bone) 6a) 1o callus- Trabec. join up (no woven bone) 6b) 2o callus- Mineralisation of woven bone---> replaced with lamellar trab. bone 7) Repair req direct osteonal bridging, no callus. Further remodelling due to stress. |
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Abnormal/ Delayed # repair
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-# is comminuted/ displaced
- # is inadequately immob. - Infect/ dz/ patho # - Dietary def. eg Ca++, P, Vitamins - Abnormal Callous (made of FT/ cart.) - Non-union - False joint formation |
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Vascular Changes and Circulatory Disturbances
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- Oedema
- Hyperaemia - Congestion |
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Oedema
Morph- Mech- |
- Controlled by starling's law- Filtration vs. Absorption
- Morph- excess clear fluid - Mech -Inc vasc. perm. - Inc hydrostatic fluid - Dec osmotic press. - Loss of protein - Lymphatic obstruct. eg. lymphadenitis - Na+ retention eg. renal failure. |
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Hyperaemia
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- Active inc. inflow of blood due to v.d.
- Phys.- assoc c inflam due to heat |
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Congestion
|
- Passive
- Stasis of blood---> low o2---> hypoxia---> cell damage - Hypostatic congestion- due to gravity eg recumbancy |
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Haemostasis
Components- |
- Vasc. wall- endothelium
- Anti-thrombotic- bloacks platelet adhesion, interfers c coag cascade - Pro-thrombotic- vasoconstrict., adhesion etc. - Platelets- Adhere to ECM via vWF bridge + become activated - secrete granules containing ADP and Ca++ - Expose PL complexes -Coag cascade - Prothrombin ---> Thrombin Fibrinogen ---> Fibrin |
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Normal Haemostasis
Sequence- |
1) Initial injury to vessel wall
2) Transient v.c (neuro reaction + local factors) 3) 1o Haem - Plug formation ( Platelet 1) adhesion, 2) shape change, 3) Granule release, 4) Recruitment, 5) Aggregation) 4) 2o haem- Coag cascade ( 1)Tissue factor, 2) PL complex expression, 3) Thrombin activation, 4) Fibrin polym.) 5) Regulated by tissue 1) plasminogen activator, 2) Thrombomodulin- blocks coag cascade |
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Haemorrhage
Forms- Causes- |
- Petechial- Pin point haem.
- Ecchymoses- foci <3cm - Haematoma- tumour like enlargement - Haemorrhagic disastheses- haem from insignif. insult Causes - Clotting fail. - Trauma - Destruct. of vessel - Toxins - Infectious agent - Defic.- eg. Vit C, K, E |
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Thrombosis
Define- Causes- Diff. from PM clot- |
- From dysregulation of haemostasis
- Predisp. by - Endo injury - Stasis/ turbulence - Hypercoag- genetic vs. acquired - All have a point of attachment unlike PM clot. - PM clot= gelatinous c dark red area + yellow supernatent where cells have dropped - May break off---> Embolus |
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Types of Thrombi-
|
-Arterial/ cardiac chamber thrombus
- Gross- friable, red/ grey, roughened surface - Micro- laminated- lines of Zahn- grey=platelets, red=RBCs + fibrin -Venous (often in areas of stasis) - Gross- Extend in direction of BF - Micro- Flocculent, amorphous eosinophillic mush- no lines - Heart valve clot- (esp LAV) occurs with valve damage |
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Thrombus sequalae-
Consequences- |
- Dissolution- removed by fibrinolysis
- Propogation- accum. fibrin and platelets - Embolism - Organisation and recanalisation - Obstruction - Embolism |
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Embolisms-
|
- Can be
- Solid- bone #, fat, thrombus - Liquid - Gas- Air - Bacteria Carried by blood |
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Infarction
Define- Gross- Consequences- |
- Area of ichaemic necrosis (coag (liquefactive in brain)) caused by occlusion of BV
- Gross- wedge shaped - Red- haemorrhagic- vessel damage - White- anaemic- from art. occlusion/ haemolysis/ Pressure - Consequences - Depends on - Nature of BS - Rate of occl. dev. - Vuln. of tiss. to hypox. - o2 conc in blood |
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Amyloid deposition morphology-
|
-Amyloid- (rare) insoluble proteinaceous fibrils folded abnormally into beta pleated sheets,
- Pink with Congo Red stain - May disrupt function/ compress surrounding tissues - Gross- firm, pale/white opaque, lard like - May appaear as black dots - Green under polarised light - Micro- Hyaline, glassy, eosin. c H&E |
|
Classification
|
- Classification-
-Generalised- kidneys, liver, spleen... -1o- B/plasma C dyscrasia (cancer)- Bence Jones test -2o- Assoc chronic inflam- serum amyloid A proteins - Senilei naturally occuring c age - Hereditary- eg abbessinians -Localised- Cardiac/ cerebral (Alzheimers)/ pancreas |
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Calcification
Types- |
- Dystrophic- in degen. + necro. tiss.- unrelated to blood
- Gross- white/grey honeycombed, gritty, hard to cut - Seen on degen invert. discs/ old TB lesions - Micro- Basophillic/ purple/ amorphous - Can be intra/extra cellular - Confirm with Alizarin red or Von Kossa tech. - Metastatic- persistently high blood conc---> ppt on organelles - Affects elastin in BV, trachea, heart valves, stomach and skin - Due to kidney failure/ excess Vit D/ hyperPT |
|
Calcinosis cutis
Define- Cause- Gross- |
- Ca++ depos. in dermis and sub cutis
- Cause - Dystrophic calcification- due to cushings - Metastatic - Iatrogenic - Idiopathic- generalised vs localised (Calcinosis circumscripta) -Gross - Firm plaques under/on surface of skin |
|
Calcinosis Circumscripta-
Location- Gross- Cause- |
- Uncommon lesion in dogs and Horses
- Affects skin, tongue, soft tissue on back. - Raised chalky/ putty-like/ gritty nodules seperated by CT - Hyperplastic epithelium -Caused by dystroph. Ca++ on damaged coll. at sites of trauma/ sutures |
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Uric acid/ urates
Define- Gross- Location- Pathology- |
- Xlls---> end point of purine metab. depos. in tiss. (Gout)
- Gross - Articular ---> White, chalky nodules - Serous ---> white/ grey layer - Visceral serous deposits most common- esp kidneys - FB reaction to xlls ---> acute and chronic inflam. |
|
Intracellular accum.
Define- |
-Normal cellular constituents in excess (glycogen/ TG/Chol/ PL etc.)
Or - Abnormal endog./ exog. substances -Range- Harmless---> Toxic// Temp.---> Permenant |
|
Haemosiderin
Define- Causes of haemosiderosis- Micro- Path- |
- Endogenous pigment derived from haemoglobin
- = Accum. of micelles (Fe+ apoferritin) -Part of Fe storage pool - Present normally in MP (haemosideroP) of spleen and bone marrow. - Excess present in haem./ bruising due to haemolysis -Haemosiderosis- - occurs due to systemic excess of Fe---> Haemo. depos. - Also H.A., chronic pass. congest.---> "heart failure cells" in lungs - Micro- Golden brown xlline or granular material - Use Perl's prussian blue Path- non harmful but indicator of haem. (haemoglobin toxin to renal tubules ---> black) |
|
Bile Pigments
Source- |
- Bilirubin prod. after seperation of haem+ Fe/Globin
- Excess= jaundice/icterus - Pre hepatic- haemolysis - Hepatic- hepatitis, liver degen. - Post hepatic- choleostasis |
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Other pigments
Lipofuscin- Ceroid- Melanin- |
Lipofuscin- "Aging pigment"- non harmful
- due to free radical damage (ROS) - Lipid + protein - Prominent in slowly dividing cells - Stained by Schmorl's technique - Ceroid- Pathological version of lipofuscin - From severe malnutrition/ Vit E def./ high unsat. fat/irradiation - Melanin- Brown/ black pigment - Melanosis- normal - Melanoma/cytoma- melanocyte/blast tumour - Path. depo in skin during chronic inflam./ cushings |
|
Carbon
Others |
- Common- from air pollution
- Anthracosis- collection in lungs/ LNs - Pseudomonas -Some fungi |
|
Lysosomal storage dz
|
- Lysosome= 1o disposal + recycling centre
- Catabolise cellular and EC macromolecules for use in cell -LSdz- rare- genetic basis- idiopathic/ acquired - Lack enzymes/ transport of enzymes---> accum. of catabolites |
|
Cellular aging
|
- Progressive decline in prolif. capacity
-Decline in functions- - Oxidative phosp. - Synth of NAs and protein - Repair - limited number of replications per cell - Telomere shortening - Genetics -Accum of metabolites |
|
Review- Acute vs Chronic inflam
Cause- Major Cell types- 1o mediators- Duration- Outcomes- |
-Acute- Pathogens or injury
-Chronic- Acute inflam, pathogens, FBs, auto-immune - Acute- Neutro., eosino., baso., monocytes and MP - Chronic- MN cells- MP, mono., lymph., plasma C, Fibro. - Acute- Vasoactive peptides + eicosanoids - Chronic- IFNg, cytokines, GF, ROS, enzymes - Acute- Few days - Chronic- Months, years - Acute- Resolution, abscess, chronic inflam - Chronic- Tiss. destruction, fibrosis, necrosis, resolution. |