Test 1 1/3 Flashcards
Etiology vs. pathogenesis
E: why a disease occurs
P: how a disease occurs
Three outcomes of cell injury
Reversible
Cell adaptation
Cell death
Causes of cell injury
No O2 Infectious agents Injury Chemicals Immune response Genetic abnormalities Nutritional imbalance
4 cell targets
Cell membrane
Mitochondria
Cell proteins
DNA
T/F clinical signs and symptoms appear at the same time as molecular/biochemical changes
FALSE - several steps removed
Mechanisms of cell injury (5)
ATP depletion ROS Ca2+/membrane permeability Mitochondrial damage DNA/protein damage
Hypoxia/ischemia increases what
Ca, Na, H20, K Lactic acid (anaerobic glycolysis)
ROSs cause damage in what 3 ways
Lipid peroxidation
Protein fragmentation
SS breaks in DNA
How does the body control ROS
Enzymes
Antioxidants
Serum proteins
After cell injury, 4 cell adaptations
Size
Number
Functional mods
Intracellular accumulations
4 types of necrosis and example of each
Coagulative (Aspirin burn, most common)
Liquefactive (abcess)
Caseous (tuberculosis)
Enzymatic (fat necrosis)
4 structures/processes that maintain cell viability
Plasma membrane
Mitochondria
Macromolecular synthesis
Nucleus
Apoptosis is involved in what 3 normal cell processes
Normal cell turnover
Embryogenesis
Immune function
Excessive apoptosis is involved in what diseases (5)
Aids Ischemia Neurogenerative diseases Myelodysplasia Toxin induced liver injury
What diseases can inhibit apoptosis
Cancer
Autoimmune diseases
Viral diseases
5 steps in apoptosis
Chromatin condensation Progressive cell shrinkage Plasma membrane blebbing Apoptotic bodies Phagocytosis
Differences b/t necrosis and apoptosis
Stimuli: N(pathologic), A(physiologic, pathologic)
N(multiple cells, swell, lysis)
A(single cell, shrinks, chromatin, apoptotic bodies)
Response: N(inflammation), A(no inflammation)
Chronic stress/injury cause cells to _
Undergo adaptive changes
T/F similar responses at the cell level can produce different morphological changes in different organs
TRUE
Metaplasia:
Alteration in cell differentiation with concurrent alteration of tissue/organ function
Increased cytoplasmic Ca causes what
Activate degradative enzymes
biochemical alterations occur _ to morphological changes
Before
Vasodilation is mediated by what 3 things
NO
PG’s
Histamine
Two types of fluid in inflammation and differences b/t them
Transudate: low protein, low specific gravity
Exudate: high protein, high spec. Gravity, can be fibrinous/purulent/sanguineous
Non-inflammatory transudate vs. inflammatory
NI - endothelium intact
I - early endothelial cell contraction
Endothelial cell contraction vs retraction
Con - forms intercellular gaps, mediated by histamine/bradykinin, occurs rapidly and lasts 30 min
Ret - restructuring of cytoskeletal proteins, 4 to 6 hours to develop and lasts 24 hours
What do activated endothelial cells do
Make PGI and NO (vasodilation)
Contract
Retract
Increased expression of cell adhesion molecules
Synthesis and release of inflammatory mediators
What are 5 things that leukocytes do
Margination Rolling (selectins) Adhesion (integrins) Emigration/transmigration Chemotaxis
4 steps in phagocytosis
Attachment
Engulfment
Degranulation
O2 burst
PMNs are also called
Neutrophils
_ cells are first responders
_ cells are second responders and more chronic
Neutrophils
Monocytes/macrophages
Monocytes/macrophages live for _ in tissues
Months
Difference b/t cellulitis/abscess/ulcer
C: warm swollen tissue, infiltration by PMN
A: collection of PMNs or pus
U: erosion of an epithelial surface exposing connective tissue
Acute vs chronic inflammation
Chronic has immune response, years, systemic, maybe not reversible, macrophages instead of neutrophils
Two types of chronic inflammation
Non-specific
Granulomatous
Inflammatory mediators (3)
Histamine
Prostaglandins/leukotrienes
Thromboxane
Labile vs. stable vs. permanent
L: continuously dividing
S: some replication
P: non-proliferative
First intention vs. second intention
First is a deep thin cut, little scarring if no infection
Second is wide and shallow, more scarring, less function
5 ways growth factors can affect wound healing
Epithelial proliferation Monocyte chemotaxis Fibroblast proliferation Angiogenesis Collagen synthesis
Besides growth factors, what else can affect wound healing
Infection Steroids Nutrition Mechanical factors Poor tissue perfusion
What is edema
Increased fluid in interstitial tissues
Hyperemia:
Congestion:
H: increased tissue blood volume due to increased flow (active)
C: increased blood volume due to impaired venous return (passive) blockage or backup
Internal bleeding from large to small
Hematoma
Ecchymosis
Purpura
Petechia
_ are like sandbags, the initial hemostatic plug
Platelets
3 parts to hemostasis
Endothelium
Platelets
Coagulation cascade
_ holds together platelets
Fibrinogen
Platelets do what 3 things, and what do they secrete to do them
Adhesion: vWf
Secretion: ADP, Ca2+
Aggregation: ADP, TXA, Thrombin
The extrinsic/intrinsic pathway are parts of the _. The extrinsic pathway deals with _ and the intrinsic pathway deals with _. The final products are _ and _
Coagulation cascade
Tissue factor
Factor XII
Thrombin and fibrin
_ and _ counter-regulate hemostasis
Fibrinolysis
Thrombomodulin
Virchow’s triad (pathogenicity of thrombosis)
Endothelial injury
Alterations in blood flow
Hypercoagulability
Hypercoagulability can be caused by either _ or _ such as:
Inherited conditions (factor V Leiden)
Acquired conditions (prolonged bed rest, extensive tissue injury)
T/F thrombosis looks the same in all locations
FALSE
arterial - white
Venous - red
DIC:
Caused by:
Disseminated intravascular coagulation - over activation of coagulation cascade
Caused by infection (G- bac) Pregnancy complications Neoplasm Shock Massive injury
Red vs. white infarction
Red- hemorrhagic, venous occlusion
White - pale, arterial occlusion in solid organ
4 things that influence infarct development
Nature of vascular supply
Rate of occlusion
Vulnerability to hypoxia
O2 Carrying capacity
Three types of shock
Cardiogenic - low blood pumping
Hypovolemic - have enough blood
Septic - bacteria
Septic shock mechanism
PAMPS bind to toll like receptors
3 stages of shock
Nonprogressive - compensatory mechanisms maintain perfusion
Progressive - inadequate perfusion, DIC, anaerobic metabolism, lactic acidosis
Irreversible - tissue injury unrecoverable, organ failure, death
Parenchyma vs. stroma
Parenchyma is functional tissue of organ
Stroma is supporting connective tissue and blood vessels
Adenoma vs papilloma
A: benign glandular epithelial tumor
P: benign surface epithelial tumor with finger like projections
Hamartoma
Choristoma
Teratoma
H: proliferation of tissue normally at that site
C: collection of tissue NOT normally at that site
T: derived from more than one germ layer