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Pathology (Healing and Repair (Factors that affects healing (Type, size…

- - - - Type III first then Type I
        
        Requires vitamin C
        
        Accumulation of collagen causes increase in tensile strength due to development of cross linkages
  - - - :tornado: Relevance to chemotherapy? :tornado:
        Able to predict the side effect of chemotherapy, most drugs target rapidly dividing cells etc hair, GIT epithelium, bone marrow
  - - - Complete wound healing and minimal scar
    - - Larger deforming scar (more wound contraction, more tissue fibrosis)
- - - - Vessels of microcirculation engorged with blood
        
        ACTIVE: Blood flow to organ is increased
        
        PASSIVE: Blood flow out of organ is decreased (congestion :red_flag:)
        
        Obstructed vein/Congestive heart failure
        
        Enlarged, Cyanotic, Firm and heavy
  - - - In Interstitial fluid
      - In cavity (peritoneum, pleural cavity)
      - Starling's law
        
        Primary cause:
        
        Increased hydrostatic pressure
        
        Reduced oncotic pressure
        
        Increased endothelial permeability
        
        Lymphatic obstruction
        
        Localised edema
        
        Impaired venous drainage
        
        Increased vascular permeability + hyperaemia (Inflammation)
        
        Obstruction destruction of lymphatics (filariasis :check:)
        
        Generalised edema
        
        Cardiac
        
        :tornado: What is the causes of cardiac edema :tornado:
        
        Decrease drainage, increases venous drainage
        
        RAAS system will increase aldosterone + ADH and lead to renal salt and water retention
        
        Renal
        
        Hypoproteinemia due to loss of albumin, drop in oncotic pressure
        
        RAAS aldosterone ADH
        
        Caused by liver disease cirrhosis protein malnutrition Filtration problem
        
        Hepatic
  - - - Anaphylactic :red_flag:
        
        IgE mediated hypersensitivity
        
        Vasodilation + capillary permeability due to histamine
      - Neurogenic :red_flag:
        
        Loss of vasomotor tone, dilation of both arteries and veins
      - Cardiogenic :red_flag:
        
        AMI, Cardiac failure, Cardiac tamponade :check:, pulmonary embolism
      - Septic :red_flag:
        
        DIC leading to inflammation and hyper coagulable state
      - Hypovolemic :red_flag:
        
        Due to inadequate blood volume
    - - Non-progressive stage --> Progressive --> Irreversible
  - - - Secondary Haemostasis
        
        Activation of coagulation factors
        
        Formation of fibrins
        
        Coagulation cascade
        
        Extrinsic by tissue factor from tissue injury [7,10]
        
        Common pathway [10+5, 2, fibrinogen, 13]
        
        Intrinsic by contact activation [12,11,9,10]
        8 + Ca involved
        
        :fire: Anticlotting regulators:
        
        Prostacyclin PGI2
        
        ADPase
        
        Thrombomodulin Activates Protein C (APC degrades 5 and 8)
        
        Antithrombin raised by heparin :fire:
        
        Tissue Plasminogen Activator forms D-dimer
        
        Estrogen, Serotonin
      - Primary Haemostasis
        
        Vasoconstriction
        
        Platelet Adhesion
        
        Platelet Aggregation
        
        Platelet plug
        
        Aggregation
        
        Platelet swell when exposed to damaged ECM, stick to vWF
        
        Stabilised by Gp1b
        
        Secrete plasminogen activator inhibitor to limit fibrolysis
        
        Thrombomodulin downregulated
        
        Adhesion
        
        Gp2b/3a increase integrin affinity to fibrinogen
        
        Fibrinogen induces adhesion
        
        Degranulation
        
        Releases of:
        
        ADP and TXA to recruit platelets
        
        Factor 13 to induce cross linking
        
        PDGF and VEGF induce healing by growth of vascular cells
      - Fibrinolysis
        
        Activation of fibrinolysis
        
        Lysis of plug
      - Lab Diagnosis
        
        Primary Hemostasis
        
        Platelet aggregation test (rarely used)
        
        Full blood count Look at the size and number of platelets
        
        Bleeding time to check for vWF
        
        Secondary haemostasis
        
        PT/INR
        
        aPTT
        
        mixing study
        
        Correctable: Just normal lack of factor
        
        Incorrectable: presence of inhibitor
        
        Firbinogen
        
        Most important to diagnose DIC :warning:
        
        D-dimer test
        
        Most important to diagnose DIC :warning:
        
        Thrombin time to assess ability to convert fibrinogen to fibrin
        
        Prophylaxis in thrombocytopenia
        
        Neurosurgery above 100
        
        Invasive surgery above 50
        
        Fever infection above 20
        
        Chemotherapy above 10
    - - Virchow's triad :red_flag:
        
        Injure to epithelial
        
        Exposure of sub endothelial collagen
        
        Depletion of PGI-2 and plasminogen activator
        
        Release of tissue factor (activate extrinsic)
        
        Alteration in blood flow
        
        Turbulent blood flow (eddy currents bring platelets together)
        
        Stasis
        
        Alteration in blood coagulability
        
        Predisposing factors:
        
        Atrial fibrillation :check:
        
        Prosthetic heart valves
        
        Post-operative, prolonged bed rest
        
        Disseminated cancer
        
        Oral contraceptive oestrogen :check:
    - - Resolution
        
        Propagation
        
        Organisation and recanalization (forming of blood vessels)
        
        Embolism
      - Embolus :red_flag:
        
        Solid
        
        Liquid
        
        Fat globules
        
        Gaseous
        
        Decompression sickness
  - - - In Lungs, Liver
    - - In Kidney, Spleen usually due to thromboembolism
- - - - Increased functional demand
        
        Hyperplasia :red_flag:
        
        Increased in cell number
        
        Hypertrophy :red_flag:
        
        Increased in cell size
      - Decreased functional demand:
        
        Lack of nutrients
        
        Denervation
        
        Poor blood supply
        
        Lack of endocrine stimulation
        
        Aging
        
        Atrophy :red_flag:
        
        Reduced cell size
        
        Involution :red_flag:
        
        Reduced number of cells
      - Metaplasia :red_flag:
    - - Chaperones to protect
        
        Aggregate to form inclusion bodies
      - Ubiquitin to remove damage proteins
        
        Aggregate to form inclusion bodies
        
        Mallory' bodies in Alcoholic liver damage
        
        Lewy bodies in Parkinsons
      - Autophagy
        
        Cells eat its own organelle, lead to atrophy of cell
        
        Formation of residual bodies accumulate to form lipofuscin
      - Hypertrophy of SER to remove toxins
  - - - Hepatitis
        
        HIV/AIDS
      - :tornado:Mechanism of apoptosis:tornado:
        Intrinsic pathway (Mitochondrial)
        Bax and Bak dimerase and insert to form MAC, leakage of SMAC, inactivates BCL and IAP, leakage of cytochrome c to activate capsase 3
        Extrinsic pathway (receptor mediated)
        Triggered by either TNF or Fas receptor, Fas and FasL forms DISC activate capsase 8 and 10 then activate 3 and 6
  - - - Hypoxia in all tissue except brain
    - - Cerebral infarct
    - - Cheese-like, granuloma TB
    - - Leakage of axctivated lipase, saponification due to calcification
    - - eosinophillic present injury to blood vessel
  - - - In germinal cell, telomerase present, normal cell no