Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
22 Cards in this Set
- Front
- Back
|
AFTER AN INJURY HAS OCCURED, WHAT ARE THE MAJOR PATHWAYS THE BODY CAN TAKE TO RETURN TO HOMEOSTASIS?
|
1. IN RENEWING TISSUES, SUCH AS TE EPIDERMIS, GI, HEMATOPOIETIC SYSTEM, CELL PROLIFERATION OCCURS TO REGENERATE THE DAMAGED TISSUE
2. IN STABLE TISSUES, SUCH AS THE LIVER AND KIDNEYS, COMPENSATORY GROWTH OCCURS TO REGENERATE THE DAMAGED TISSUE 3. IN NORMAL WOUND TISSUE, HEALING OCCURS ALONG WITH SCAR FORMATION 4. IN CHRONIC INFLAMMATION, FULL HEALING ISN'T POSSIBLE AND FIBROSIS OCCURS |
|
|
LYMPH SYSTEM
|
Wounds must be drained through the lymphatic system
Two circulatory systems: Blood and lymphatic Lymphatic removes liquid from the interstitial space move towards lymph nodes Liquid moves as the result of a pumping action when muscles move In healthy tissue: Liquid is clear with a few proteins In wound area: Liquid is cloudy with debris, bacteria, etc Lymphatic sys is a debris removal system |
|
|
GRANULATION TISSUE
|
WOUND REPAIR TISSUE
MACROPHAGES EMIGRATE INTO THE AREA OF DAMAGE WHICH BECOMES SEMI-LIQUID CAPILLARY BUDS GROW INTO THE DAMAGED AREA TO FOR A NETWORK BY WHICH NUTRIENTS AND WOUND REPAIR MATERIALS CAN BE TRANSPORTED TO THE SITE MACROPHAGES SECRETE FIBROGENIC AND ANGIOGENIC FACTORS FIBROBLASTS AND MYOFIBROBLASTS ENTER THE AREA FIBROBLASTS PROLIFERATE AND BEGIN TO DEPOSIT COLLAGEN COLLAGEN BECOMES DENSE FIBROBLASTS BECOME INACTIVE (FIBROCYTES) VASCULARITY IS REDUCED |
|
|
ANGIOGENESIS
|
Endothelial cells lose adhesiveness and
detach to move into the wound area. Endothelial cells proliferate and form tubes for flow EPC - Epithelial precursor cells New blood vessels can be made denovo via EPCs OR from pre-existing vessels Macrophages are coordinating everything In the wound area there are broken blood vessels -->Decreased O2 or hypoxia causes macrophages to secrete angiogenesis factors VEGF is the most important - Vascular endothelial growth factor Angiostatin or fragments of collegen - inhibit angiogenesis (Diabetic retinopathy can lead to blindness - uncontrolled angiogenesis) |
|
|
FIBROBLAST PROPERTIES
|
DIFFERENTIATE FROM MESENCHYMAL CELLS IN TISSUE
ACTIVELY PROLIFERATE IN CHRONIC INFLAMMATION SYNTHESIZE AND SECRETE COLLAGEN ACTIVATED BY MACROPHAGES - FIBROGENESIS |
|
|
COLLAGEN SYNTHESIS
|
PROCOLLAGEN IS THE BASIC NETWORK THEN CROSSLINKED PROCOLLAGEN BECOMES STRONGER COLLAGEN
Vitamin C is Necessary for Hydroxylation of proline and lycine in collagen Nutrition is part of the quality of repair Crosslinking provides the strength to collagen This process takes a long time |
|
|
COLLAGENASE
|
FACILITATES THE BREAKDOWN AND REMODELING OF COLLAGEN
|
|
|
FACTORS THAT EFFECT WOUND REPAIR
|
EXTENT AND LOCATION OF WOUND
EXTERNAL FACTORS SUCH A DIET INTERNAL FACTORS HEREDITY AGE BLOOD FLOW DISEASE |
|
|
HEALING BY FIRST INTENTION
|
AKA - Primary Union - a very localized minimal injury
can be easily repaired, favors regeneration in a tissue Which can divide. Little to no scar formation. No complications. Takes a few days to heal |
|
|
HEALING BY SECOND INTENTION
|
AKA - Secondary union - large gaping wound, granulation tissue involvement, scar tissue, more scar less functional tissue. Infected wound with pus. Complications.
Balance between regeneration and healing and scaring. Facial wounds - highly vascularized tissue will have a mainly healing result |
|
|
CLASSIFICATION OF INFLAMMATION
|
DURATION - ACUTE OR CHRONIC
ETIOLOGY INFECTIONS CHEMICAL CAUSES PHYSICAL CAUSES IMMUNE CAUSES LOCATION LOCALIZED VS. WIDESPREAD |
|
|
ACUTE INFLAMMATION
|
In acute inflammation there is a sequence of events that occurs linearly in time. There is a start and stop. At some point there is a complete/finish/done point.
|
|
|
CHRONIC INFLAMMATION
|
If the irritation or injury is persistent and the inflammation cannot be entirely removed. This is chronic inflammation and this is disease. Everything happens at the same time in a very disorganized. This is the most common cause of disease in developed countries.
|
|
|
EXAMPLES OF CHRONIC INFLAMMATION
|
GRANULOMAS
TB ULCER ABCESS BRONCHITIS ASTHMA |
|
|
TUBERCULOSIS
|
Caused by mycobacterium tuberculosis in the lungs
1 out of 3 people in the world have TB and some don't even know it This bacteria is very difficult to get rid of b/c: Due to bacterial coat difficult to digest - thick waxy cell wall Invasion gene - makes it difficult to impossible for the phagosome to fuse with the lysosome Most strains of TB are resistant to most antibacterial agents Forms a granuloma - area of necrosis surrounded by macrophages which are in turn surrounded by lymphocytes Part of a chronic inflammatory response Appearance of cheesiness - |
|
|
ULCER
|
CHRONIC INFLAMMATION CAUSED BY H. PILORI BACTERIAL INFECTION
|
|
|
FEVER
|
INTERNAL BODY TEMPERATURE 101 DEG OR HIGHER
Internal body temperature is a way to regulate the spped of leukocyte movement At higher temperatures WBCs move much quicker Regulated through the hypothalamus TNF and IL-1 cause the hypothalamus to make and secrete PGs to upregulate the thermostat causes high temp/fever TNF, LPS, IL-1, etc are pyrogens |
|
|
FIBROSIS
|
CAUSED BY CHRONIC INFLAMMATION AND THE ACTIVATION OF MACROPAHGES
The main cell typein chronic inflammation is again the macrophage (as with acute wound repair) Fibrosis results - excess scaring Fibrotic diseases - MI,Cirosis, abcess (on the skin = boil) |
|
|
ABCESS
|
Infection of the skin - Abcess = boil
Infection is not able to be able to be removed completely Bacteria, pus, WCBs, dead and live neutrophils are isolated in An abcess - pressure builds and can discharge |
|
|
LOW QUANTITIES OF LPS, TNF, IL-1, IL-6/IL-8, NO, PAF, AND OTHER MEDIATORS
|
MACROPHAGE ACTIVATION, ENDOTHELIAL ACTIVATION AND ACTIVE COMPLEMENT ACTIVATION
RESULT IN LOCAL INFLAMMATION |
|
|
MODERATE QUANTITES OF LPS, TNF, IL-1, IL-6/IL-8, NO, PAF, AND OTHER MEDIATORS
|
CNS ACTIVATION --> FEVER
LIVER ACTIVATION --> ACUTE-PHASE REACTANTS SYSTEMIC EFFECTS |
|
|
HIGH QUANTITIES OF LPS, TNF, IL-1, IL-6/IL-8, NO, PAF, AND OTHER MEDIATORS
|
LOW CARDIAC OUTPUT, LOW PERIFERAL RESISTANCE
BLOOD VESSEL INJURY, THROMBOSIS, DIC ARDS SEPTIC SHOCK |
