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93 Cards in this Set
- Front
- Back
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what dose hydropic change cuase?
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rupture of the cell
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how can hydropic change occur?
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increasing cell membrane perm
direct damage to the pump interfering with ATP production |
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where is iron stored
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liver and bone marrow
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what are two examples of pigments
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endogenous
exogenous |
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what examples of endogenous pigments
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melanin found in skin and eye
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what is a non specific indicator of cell injury that is pink staining glasslike
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hyaline change
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what is a type of residual body?
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lipofuscin granule which is found in myocardibum neurons and liver as a wear and tear pigment
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what insoluble protein due ot mutation accumulates in hepatocytes leading to cirrhosis
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alpha antitrypsin deficiency
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what does the liver oxidize fa's into? what accumulates?
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oxidized into TG and TG accumulates
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what is an exmaple of dysplasia?
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acid reflux in the esophagus
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what is an example of metaplasia?
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respiratory airways lined with stratifiedd squamous instead of pseudostratified in smokers
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what are the examples of hyperplasia
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endometrial cells in mentrual cycle
RBC's at high altitude smokers airways or skin calluses |
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how does hyperplasia occur?
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new cells formed by mitosis
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what are the main causes of hypertrophy
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physiologic
abnormal hormonal hypertrophy increased functional demand |
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what are the five major adaptive responses
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intracullular retention of materials
atrophy hypertrophy hyperplasia meta and dysplasia |
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____ inferefere with cell eprmeability, osmotic homeostasis and enzyme or cofactor
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toxins
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what six things cause trauma?
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temrperature extremes
radiation chagnes in pressue mechanical retained foreign materials microbial agents |
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thickening of the arteriolar wall is a _____ of hypertension
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sequel
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what are three types of pathogensis
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acute
crhonic insidious |
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what are the four causes of disease?
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genetic
congenital acquired idiopathic |
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what are examples of pathology at each level
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protein changes in DNA
unusual cells mitosis funcitonal alveoli crowded out by dense tissue hard mass in lung weight loss and fatigue |
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what happens in transytosis?
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emgrating cells icnrease permeability
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what happens in leukocyte induced cell injury?
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oxygen radicals and proteolytic enzymes injury endothelium
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what cytokines disrupt the endothelial cell junctions?
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tumor necrosis factor TNF and IL1
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describe acute inflammation immediate transient response.
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endothelial cells contract and increase the intercellular gaps. this is elicited by histamine bradkinin and luekotriens. occurs due to flood.
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what are the benefits of exudation
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dilutes toxin
increases pain limits use releases circulating antibodies phagocytosis of microorgs. |
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what is margination and emigration
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neutrophiles line up by endothelial lining. they leukocytes squeeze between the endothelial cells into the interstitialo space
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why is the loss of plasma beneficial?
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RBCs concentrate
slows circulation (stasis) slows blood loss allows clotting time limits fluid loss into tissue |
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what is the main cause of swelling
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exudates
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what can initiate acute inflammation?
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substances released from injured cells is K+
direct stimulus to mast cells ie trauma cold microbial products basement membrane complement activation deposition of antigen/antibody disruption of vascular integrity |
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cholelithiasis =
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gall stones
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what are the major vitamin deficiences
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A lungs and cuts
Thiamine B encephalopathy B12 pernicous anemia impaired RBC synth C scurvy D rickets and osteomalacia |
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what is deposited during necrosis?
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calcium leading to dystrophic clacification
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what are the four types of necrosis and examples?
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coagulation MI
liquefaciton gangrene caeous TB fat pancreatic injury |
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what are three good examples of apop?
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embryonic devlepment
liver cells damaged damaged cyto T |
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what three things happen to the nuclear envelope
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karyloysis fade away
karryohexis break up pyknosis shrink or condense |
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what are the structural changes that occur with cell death
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distorted plasma membrane
mitochondria and ER distort change in nuclear envelope |
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what causes necrosis
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strong inflammatory response. necrosis is exogenous stresss.
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what are the structural cell changes that may occur in cell death?
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plasma membrane distorted
mitochondria and ER changes changes in nuclear envelope karr and pyk |
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what are examples of good apoptosis
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embryologic development (between toes)
damaged liver cells cytotoxic T cells |
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what are the four types of necrosis
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coagulation
liquefaction caseous fat |
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what can be seen in any type of necrosis
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calcification
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what are examples of the four types of necrosis
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MI
gangrene TB pancreatic injury |
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what are the six leukocytic envets
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SPACEM
systemic activation of inflammatory response results in leukocytes phagocytosis adhesion chemotaxis emigration margination |
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what are the types of chemotactic agents
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soluble bacgterial products
complement components C5a cytokines leukotrines B4 |
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binding of igG antibody triggers a _____ ______
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complement cascade
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when the complement cascade is triggered ___ coats the targeted particle
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C3b
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____ ____ can also activate the complement system or altnerative pathway
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microbial surfaces
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describe what happens in the fusion of the phagocytic vacuole with a leukocyte
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NADPH oxidase superoxide radical
with 2H+ to form H2O2 in Cl- myeloperoxidase converts to HOCL. |
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hageman factor =
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clotting factor XII
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what are the four enzyme cascades of hageman factor
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coagulation
fibrinolytic complement kinin |
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what does the kinin system do
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increases vascular permeability, contraction of bronchial smooth muslce, inflammatory cella ctivation, plasma extravesion
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what does kiallikrein do
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activated Hageman factor helps it convert kinningoen and plasminogen
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describe the complement system
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C5-C9 membrane attack complex holes in bacterial cell walls
C3a and C5a anaphylaxins C5a lipoxygenase pathways C3b opsonin |
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what are four cellular mediator sources of inflammation
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platelets
tissue cells endothelial cells WBCs |
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what are cellular mediators derived from
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metabolism of phospholipids and arachidonic acid
prostaglandins trhomboxanes leukotriens lipoxins platelet activating factor |
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what are the two vasoactive amines?
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histamine and serotonin
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what are leukotrienes important for
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chemotaxis
aggregation of neutrophils increased vascular permeability |
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arachidonic derivatives stimulate what five things
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platelets
neurtophils moncytes/macrophages endothelial cells SM cells |
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what is the major effect of arachidonic acid derivatives
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potent vasodilator
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what are the five types of cytokines
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interleukins
TNF a inferferons growth factors chemokines |
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what does tnf alpha do
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fever
sleep decreased appetite secretion of ACTH which stimulates cortisol and release of neutrophiles formt he bone marrow into cifculation |
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what do interferons do
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activated macrophages and neutrophils
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what are the four bacterial defenses
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produce endotoxins that resist lymphocytes
produce slimy coat to resist phagocytosis produce cells walls with glycolipids that resist free radicals produce substances that bind to opsonins |
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name examples of bacteria of each
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yersinia perstis streptococcus pyogenes
streptococcus pneumonia mycobacerium leprae mycobacterium tuberculosis |
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what are four cellular mediator sources of inflammation
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platelets
tissue cells endothelial cells WBCs |
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where are cellular mediators derived from
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metabolism of phospholipids and arachidonic acids
prostaglandins thromoxanes leukotrienes lipoxins platelet activating factor |
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what are the two pathways of arachidonic acid derivatovies
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lipoxygenase and cyclooxygenase
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arachidonic derivatives stimulate what five things
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platelets
neutrophils monocytes/macrophages endothelial cells SM cells |
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what are three types of GF
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epidermal GF
platelet derived GF vascular endothelial GF |
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describe day 1 on of primary intention
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Day 1 scab
day 2/3 granulation day 6 collagen fibers two weeks inflammatory cells and edema reduce 2 months scar 1/3 3 months scar 70-80% |
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define chronic
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a standoff between the inciting agent and the inflammatory cells
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what is fibrosis
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deposition of collagen as scar tissue
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what causes crhonic inflammation
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persistant infections like syphyllis
chronic exposure to toxic agents asbestos autoimmune RA and SLE |
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what six things do macrophages produce?
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protesases
complement coagulation factors reactive oxygen specides includign NO eiocsanoids cytokines including IL1 and TNF |
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what is granulomatous inflammation
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giant cells and macrophages like TB and sarcoidosis
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what are two main types of immunity
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innate and specific
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what are the six innate response
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physical barriers
antibacterial agents commensal organisms ongoing phagocytosis inflammatory response fever |
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what is responsible for the promotion of phagocytosis
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CRP
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what are the four main traits of specific immunity
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recognition
learning memory self discrimination |
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what are the two types of specific immunity
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humoral and cellular
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where are T cells found?
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lymph nodes and spleen
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what are the three major types of T cells
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cytotoxic
helper suppressor |
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where are b lymphocytes found
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marrow
peripheral lymhoid |
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what are five types of antibodies
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AMGDE
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what do macrophages do
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process and present antigens to helper T APC
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what are the types of class I MHC
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HLA A B C
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class II MHC have tendency to bind ____ from _____
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peptides from bacteria
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what lymphocytes recognize the calss I MHC
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cytotoxic via killer inhibitor receptor
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what recognizes calss II MHC
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helper T
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B27
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chronic uveitis
akylosing spondylytis inflammatory bowel disease |
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DQ
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diabetes
RA |
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DR
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chronic hepatits
psoriaosis DM 1 graves p vulgaris termporal arteritis |
