PATHO HEHEHEHA Flashcards
Atrophy
-Decrease in cell size
-Decreases organ sizes if enough cells shrink
-Physiologic (function) Normal in early development
-Pathologic (disease) Results from decreases in workload, pressure use, blood supply, nutrition, hormonal/neural stimulation
Hypertrophy
-Increase in cell size
-Increases organ size
-Physiologic (function) Results from increased demand, stimulation by hormones, growth factors
-Pathologic (disease) Results from chronic hemodynamic overload.
Hyperplasia
-Increase number of cells
-Increased rate of cellular division
-Physiologic (function)
Compensatory- enables organs to regenerate.
Hormonal-In organs that respond to endocrine hormonal control
Pathologic (disease)
Hormonal- abnormal proliferation of normal cells.
Dysplasia
-Abnormal changes in size, shape, and organization of mature cells.
-May be reversible if the triggering stimulus is removed.
-tissue appears disorderly, but it is not cancer.
(If changes penetrate the basement membrane: invasive neoplasm)
Metaplasia
-Reversible replacement of one mature cell type by another
-Associated with tissue damage, repair, and regeneration
-Reprogramming of stem cells or undifferentiated mesenchymal cells
Necrosis
- Rapid loss of plasma membrane structure, organelle swelling, mitochondrial dysfunction, lacks typical features of apoptosis
-May be regulated or programmed
-Autolysis (autodigestion)
Coagulative necrosis
-Protein denaturation
-Albumin is transformed from a gelatinous, transparent state to a firm opaque substance
-Infarct (small localized area without blood supply)
Liquefactive necrosis
-Neurons and glial cells of the brain
-Cells are digested by their own hydrolases (an enzyme that breaks down chemical bonds)
-Tissues become soft and liquefied
-Triggered by bacterial infection
ex: Staphylococci, Streptococci, and Escherichia coli
Caseous Necrosis
-Results from pulmonary tuberculosis infection (bacterial infection of the lungs)
-Combination of coagulative and liquefactive necrosis
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Fatty Necrosis
- Breast and other abdominal organs
-Action of lipases
-Fatty acids combine with elements to create soaps
-Tissue appears opaque and chalky white
Gangrenous Necrosis
-Death of tissue from severe hypoxic injury
-Dry (Skin becomes dry and shriveled, brown or black)
-Wet (Area becomes cold, swollen and black.) (Gas gangrene, caused by Clostridium)
Free Radicals
an electrically uncharged atom or
group of atoms with an unpaired electron that
damage:
* Lipid peroxidation
* Protein alteration
* DNA damage
* Mitochondrial effects
Ischemia
the decrease in blood supply to a tissue. It can be local, caused locally
by a thrombus or embolus, or global due to a low perfusion pressure.
Hypoxia (hypoxic injury)
The single most common cause of cellular injury
Results from:
* Ischemia—reduced supply of blood
* Reduced oxygen content in ambient air
* Loss of hemoglobin
* Decreased production of red blood cells
* Diseases of the respiratory and cardiovascular systems
* Poisoning of the oxidative enzymes (cytochromes) within
the cells
Anoxia—total lack of oxygen caused by
obstruction
Acute inflammation
Local manifestations
Result from cellular and vascular changes and
corresponding leakage of circulating components
into the tissue
Heat, swelling, redness, pain, loss of function
Exudative fluids
* Serous exudate (watery)
* Fibrinous exudate (thick and clotted)
* Purulent exudate (pus)
* Hemorrhagic exudate (erythrocytes)
4 phases of inflammation
- Vascular and Cellular
- VASODILATION (dilatation of blood vessels, which decreases blood pressure.)
- VASC PERMEABILITY: the blood vessels become more porous from
contraction of endothelial cells and leakage of fluid out of the vessel (exudate), causing swelling / edema at the site of injury, blood then starts to
move more slowly and collects at site of injury (ERYTHEMA) - WBC: sticks to inner walls of vessels and their migration through endothelial
cells
Thrombocytopenia
◦ Platelet count <150,000/mm3
◦ <50,000/mm3: hemorrhage from minor trauma
◦ <15,000/mm3: spontaneous bleeding
◦ <10,000/mm3: severe bleeding
*MAJOR causes = decreased platelet production, decreased platelet survival, splenic sequestration, and dilution
Hemophilia
Hemophilia A (classic hemophilia)
◦ Deficiency of factor VIII
◦ 80% of hemophiliacs
◦ 1:5000-10,000 live, white male
births
◦ Sex-linked recessive trait
Hemophilia B (Christmas disease)
◦ Deficiency of factor IX
◦ 15% of hemophiliacs
◦ Sex-linked recessive trait
Von Willebrand Disease
Most common hereditary bleeding disorder
Reduced platelet adhesion
Deficiency of von Willebrand factor
◦ Component of factor VIII
◦ Defective clot formation
Autosomal dominant trait
◦ Frequently a new mutation
◦ Males and females equally affected
-Easy bruising, epistaxis, gingival bleeding, increased
bleeding with laceration and with surgery, increased
menstrual bleeding19
Disseminated Intravascular Coagulation
Complex, acquired disorder in which clotting and hemorrhage simultaneously occur
Possible cause
◦ DIC is the result of increased protease activity in the blood caused by unregulated release of thrombin with subsequent fibrin formation and accelerated fibrinolysis
*both acute generalized, widespread activation of coagulation, which results in thrombotic complications due to the intravascular formation of fibrin, and diffuse hemorrhages, due to the consumption of platelets and coagulation factors.
Conjugated bilirubin
◦ Water soluble
◦ Excreted in bile
Unconjugated bilirubin
◦ If RBCs breakdown > bilirubin removal
◦ Causes what????
Sickle cell anemia
a severe, painful, acute exacerbation of RBC sickling causing vascular occlusion (blood no longer being able to go thru vessels.)
As blood flow is impaired, vasospasm occurs >hypoxia > further sickling
Sickled cells are broken down by the spleen > anemia
Tissue necrosis occurs from hypoxia > chronic leg ulcers.
Shock is possible caused by decreased cardiac output
Iron Deficiency Anemia
Blood loss or deficient diet
Low hemoglobin and hematocrit
Low serum iron and ferritin
Hypochromic and microcytic erythrocytes
Poikilocytosis (irregular shape)
Anisocytosis (irregular size)
Polycythemia
Increased RBC count and hematocrit greater than 50%
Relative polycythemia: loss of plasma volume
Absolute polycythemia: increased red cell mass
◦ Primary: neoplastic
◦ Secondary: increased erythropoietin
Benign
◦ Premalignant
◦ Originate from highly organized, differentiated cells
◦ Do not spread or invade surrounding tissues
malignant
◦ “Deadly”
◦ Clone of abnormal , proliferating cells, without function or differentiation
◦ Have the potential to metastasize or get bigger
◦ “Cancer”
Proto-oncogenes
Proto-oncogenes code for normal cell
division proteins.
◦ Growth factors, growth factor receptors,
transcription factors, cell cycle proteins,
apoptosis inhibitors
Proto-oncogenes mutate to oncogenes.
◦ Insertions, deletions, translocations
increased or activated
◦ Examples: ras, Philadelphia chromosome,
HER-2/neu
Neutrophil
Primary pathogen-fighting cells (Granulocyte)
Eosinophil
Help control allergic responses; fight
parasites (Granulocyte)
Basophil
Blood cells; release heparin, histamine, and
other inflammatory mediators (Granulocyte)
Mast cells
Tissue cells; release heparin, histamine, and
other inflammatory mediators; involved in allergic
reactions
Lymphocytes
◦B cells: Produce antibodies
◦T cells:
◦T-helper cells (CD4+): Activate immune response
◦Cytotoxic T cells (CD8+): Cell-mediated immunity
◦Natural killer cells: Kill antigenic cells
Monocytes > Macrophages
Antigen-presenting cells;
produce inflammatory mediators
Leukemia Acute
Acute: Site of origin - myeloid stem cell
* Sudden, stormy onset
* S/S related to (mature) WBC, RBC,
platelets
* ALL → 80% childhood acute leukemias
* AML → chiefly an adult disease
* Diagnosis based on:
* Blood/bone marrow tissue ↔
presence of immature WBC’s (blasts) –
may constitute 60-100% of cells
Hodgkin’s disease
- Characterized by PAINLESS,
progressive, rubbery enlargement
of a single node or group of nodes
– usually in neck area - Reed-Sternberg cell – distinctive tumor
cell found with lymph biopsy - GOOD PROGNOSIS
leukemia Chronic
Chronic: Site of origin - lymphoid stem cell
* More insidious onset
* May be discovered during a routine
medical exam by a blood count
* CLL → older adults
* Relatively mature lymphocytes that are
immunologically incompetent
* CML → adults & children
* Leukocytosis with immature cell types
Non-hodgkin’s disease
- Also neoplastic disorder of lymphoid
tissue - However, SPREADS EARLY → liver,
spleen & bone marrow - Also characterized by painless,
superficial lymphadenopathy; also
extranodal symptoms - POORER PROGNOSIS than Hodgkin’s
IgG
Most abundant class (80%-85%)
Accounts for most of the protective activity
against infections
Transported across the placenta to protect
newborn child
IgA
IgA molecules are found predominantly in the
blood
IgA-2 (secretory IgA) molecules are found
predominantly in bodily secretions (most
important) (breast milk)
Dimer anchored by a J chain and a “secretory”
piece
Secretory piece may function to protect IgAs
against enzyme degradation
IgM
Largest of the immunoglobulins
Pentamer stabilized by a J chain
First antibody produced during the primary
response to an antigen
Synthesized early in neonatal life
IgD
Low concentration in the blood
Function as one type of B cell antigen
receptor
IgE
Low concentration in the blood
Defense against parasitic infections
Initiates an inflammatory reaction to attract
eosinophils
When produced against innocuous
environmental antigens, they are a common
cause of allergies
Fc portions of IgEs are bound to mast cells
