EXAM 1 Flashcards
Pathology
Study and diagnosis of disease through the examination of organs, tissues, cells, and bodily fluids
Physiology
Study of the mechanical, physical and biochemical functions of living organisms
Pathophysiology
Study of the abnormalities in physiologic functioning of living beings
Etiology
Study of the causes or reasons for phenomena
Idiopathic
Cause is unknown
Iatrogenic
Cause is nosocomial (ex: ventilator associated pneumonia)
Multifactorial
Multiple etiologic factors that contribute to its development
Pathogenesis
Development or evolution of disease, from initial stimulus to ultimate expression of manifestations of disease
Risk Factor
A factor that when present increases the likelihood of disease (MIGHT get disease)
-Modifiable vs non-modifiable
Triggers
Promote the onset of clinical manifestations when someone already has the disease
Symptoms
Subjective feeling of abnormality in the body
Signs
Objective or observed manifestation of disease
Syndrome
Set of signs and symptoms not yet determined to delineate a disease
Incidence
New cases over a time period
Prevalence
Existing cases over a time period
Reliability
Same results when repeated
Validity
Measuring what was intended
Sensitivity
Correctly identifies a condition (true-pos)
-want tests to have high sensitivity
= # of true positive / # of total sick individuals in a population
Specificity
Correctly excludes a condition (true-negs)
= # of true negs / # of total well individuals in a population
Morbidity
Causes disease, illness, consequences or problems related to the disease
Mortality
Causes death
Point Prevalence
of cases in a defined population / # of persons in a defined population
Incidence Risk
of new cases of disease / #of disease-free persons at the beginning of that time period
Incidence Rate
of new cases of disease in a given time period / Total person-time at risk during the follow up period
Positive Predictive Value (PPV)
TP / (TP+FP)
Negative Predictive Value (NPV)
TN / (TN + FN)
Syncope
Feeling of faint/dizziness
Autocrine cellular communication
Cell releases substance that in turn turns around and acts on itself
Paracrine cellular communication
Substance released acts on a nearby cell (but does not enter the bloodstream)
Endocrine cellular communication
Distance signaling; hormones released into bloodstream and acts on a distant cell
Nervous cellular communication
Substances can be released in synapse causing following nerve to react
Reversible cell growth patterns
Atrophy, hypertrophy, metaplasia, hyperplasia, dysplasia
Irreversible cell growth patterns
Neoplasia
Atrophy
Decrease in cell size due to decrease in functional demand
-can be caused by drugs/steroids
Hypertrophy
Increase in cell size due to an increase in functional demand
Hyperplasia
Increase in the # of cells due to an increase in functional demand/and or increased stress (ex: gingival hyperplasia, calluses)
Metaplasia
Mature cell type is replaced by a different mature cell type due to increased stress (ex: GERD) – cell is still a ‘normal’ cell just not in its normal location
Dysplasia
Cell has changed in size, shape, uniformity, arrangement, and or structure, typically due to increased stress (cell is not in normal structure)
- considered pre-cancerous
- cells become more immature
(ex: anemia)
Anaplasia
Undifferentiated cells with variable nuclear and cell structures
- Can imply a more advanced cancer
- NOT reversible
Neoplasm
“New growth” - commonly called tumor
-NOT reversible
Necrosis
Cell death/Tissue destruction
- characterized by cell rupture, spilling of contents into extracellular fluid, and inflammation
- caused by ischemia or toxic injury
Leads to loss of function, inflammation, fever, body aches, foci of infection, release of intracellular proteins (serum levels used as markers of cell death)
Apoptosis
Cell suicide in response to injury that doesn’t directly kill the cell but triggers intracellular cascades
-no inflammation
Ischemia
Lack of blood flow
–> metabolic waste build up –> not enough O2/H2O/nutrients –> can’t create ATP
Hypoxic
Lack of O2
Free radical
Electrically uncharged atom or group of atoms that contain an unpaired electron
- unstable
- produced by poor metabolism (oxidation/reduction)
- leads to lipid peroxidation (attack fat), attacks proteins disrupting transport channels, attacks membrane, attacks DNA
Hydropic Swelling
Cellular swelling due to the accumulation of water as a result of malfunctioning Na/K pump
-leads to increased size and weight of the organ
Intracellular Accumulations
Accumulations of normal body substances (ex: lipids), substances from poor metabolism, exogenous products that are not processed by cells
Coagulative Necrosis
Begins with ischemia –> loss of energy –> inefficient Na/K pump –> swelling + acid build up –> rupture
Red = necrotic (pink = healthy)
Liquefactive Necrosis
Once cell is damaged/spills –> dead cells are consumed by lysosomal enzymes –> the enzymes can damage surrounding healthy tissue –> cyst formation
Fat Necrosis
Death of adipose tissue (usually as a result of trauma)
Caseus Necrosis
Characteristic to lung damage + TB
-clumpy cheese appearance
Gangrene
Cellular death in a large area of tissue as a result of interruption of blood supply to a particular part of the body
Dry Gangrene
Large scale coagulative necrosis
- blackened, dry, wrinkled tissue
- separated by a line of demarcation from healthy tissue
- SLOW spreading
- seen in diabetic (poor blood flow to lower extremities)
Wet Gangrene
Large scale liquefactive necrosis
- found in internal organs but can be seen outwardly
- spread QUICKLY
Gas Gangrene
Result of infection of necrotic tissue by Clostridium (anaerobic bacteria)
- formation of gas bubbles
- can start as dry or wet gangrene
Pleomorphism
Undifferentiated cancer cells marked by a number of morphologic changes (size, shape, nucleus, DNA)
Stem Cells =
undifferentiated cells
-can be triggered to enter cell cycle and produce large numbers of progenitor cells when needed
Tumors =
mass of cells due to overgrowth = neoplasms
- malignant vs bening
suffix: -oma
Adenoma
Benign tumor of glandular epithelial tissue
Adenocarcinoma
Malignant tumor of glandular epithelial tissue
Carcinoma
Malignant tumor of epithelial tissue
Obsteoma
Benign tumor of bone tissue
Sarcoma
Malignant tumor of connective tissue
Papillomas
Bening microscopic/macroscopic finger-like projections growing on a surface
Metastasis
Development of secondary malignant growths at a distance from a primary site of cancer
Angiogenesis
Development of new capillaries in the tumor (tumor’s own blood and nutrient supply –> takes it away from tissue downstream)
Superior Vena Cava Syndrome
Tumor impedes on vena cava, impeding on blood flow coming back to the heart (life threatening)
Cachexia
anorexia + fatigue + pain + stress
Effusions
(systematic effect of malignant tumor)
-inflammation causes fluid buildup in body cavities
Infections
(systematic effect of malignant tumor)
- Occur frequently as resistance declines
- seen often in those anemic
Paraneoplastic Syndrome
(systemic effect of malignant tumor)
-tumor cells release substances that affect neurologic function and may have hormonal effects –> affects mineral/nutritional balance in the body and thus its metabolism
TNM Classification system
T = primary tumor, graded on size N = # of regional lymph nodes M = metasasis -0 = no -1 = yes
Palliative Care
Pt is far along in prognosis (with no hope for cure/control) – provide the best quality of life
Opsonization
(Complement Activation)
-coding foreign cells to ease phagocytosis
Chemotaxis
(Complement Activation)
-involves release of chemical mediators like bradykinin and attracting leukocytes
Complement Activation
opsonization, chemotaxis, anaphylatoxins, recruitment and activation of neutrophils, increased vascular permeability, cell lysis, mast cell degranulation
Inflammation Exudate - Serous
Watery
- mostly fluid
- some proteins + WBC
Inflammation Exudate - Sanguinous
Bloody
Inflammation Exudate - Serosanguinous
Mostly serous with some RBC, maybe pinkish
Inflammation Exudate - Fibrinous
Sticky, thick, HIGH cell content
Inflammation Exudate - Purulent
Thick, yellow-green, microorganisms, leukocytes, cell debris
Ex: pus
C-Reactive protein
Inflammatory marker
-a protein not normally in blood but appears with acute inflammation and necrosis within 24-48 hours
WBC normal range
4,500-11,000 cells/mL
Infection: > 11,000
Absolute Neutrophil count:
1000 - 1800 cells/mL
Bands (%)
3-6% (immature neutrophils)
Shift to the Left
increased WBC count (increase in immature neutrophils = bands)
Acetylsalicylic acids (ASA)
Ex - aspirin
- decreases prostaglandins synthesis at site, decreasing inflammatory response
- can increase bleeding
Acetaminophen
Ex - tylenol
-decreases fever and pain, but DOES NOT decrease inflammatory response
Non-steroidal anti-inflammatory drugs (NSAIDS)
Ex - ibuprofen, naproxen sodium (aleve)
- anti-inflammatory, anogesic, anti-pyrotic
- acts by decreasing production of prostaglandins
- can increase bleeding
Glucocorticoids
Ex - prednisone (steroids)
-decreased capillary permeability, decreased leukocytes and mast cells at site
(this decreases the release of histamines and prostaglandins)
Healing by primary intention
Approximated wound edges (paper cut, surgical incision, stitches)
-All areas heal simultaneously
Healing by secondary intention
Large breaks in tissue and inflammation
(pressure ulcer, compound fx)
Heals bottom up or inside out
- greater risk for infection and scarring (scar tissue buildup)
- takes longer to heal
Healing - Proliferative Phase
3-4 days after injury, lasts 2 weeks
-foreign materials and cell debris removed by macrophages, monocytes, phagocytes
Healing - Remodeling Phase
Onset depends on wound size and whether it was initially open or closed
-scar tissue strengthens
Chronic wound or pathological scarring
Phases of wound healing normally progress in a predictive, timely manner –> if not may progress to chronic wound (venus ulcer) or pathological scarring (keloid)
Hypovolemia
Decreased volume of circulating blood in the body
Hypertrophic scar tissue
fibrous tissue with excessive collagen deposits
- leads to hard ridges of scar tissue or keloid formation
- very disfiguring
- can cause severe contractions
Dehiscence
Surgical complication in which a wound ruptures around a surgical site (previously closed wound reopening)
- risk factors: age, diabetes, obesity, trauma, grabbing of sutures
symptoms: pain, bleeding, fever, inflammation
2 purposes of Immunity
(third line of defense)
- defend body against invasion or infection by antigens
- patrol for and destroy abnormal or damaged cells
Cytotoxic T Cell
Cell-Mediated immunity
CD8
Specific cellular antigen destruction
Helper T Cell
Cell-Mediated immunity
CD4
Activation of antigen-specific T cell
Plasma Cells
Humoral immunity
(B lymphocyte)
Secretion of antibody/immunoglobulins
Memory Cells
Humoral immunity
(B lymphocyte)
-Efficient, rapid antibody response to subsequent antigen recognition
HLA
Human Leukocyte Antigen (type of MHC protein)
-HLA proteins label cells of the individual
MHC
Major Histocompatability Complex (MHC) (includes HLA)
- molecules
- Each individual has a unique MHC profile
Protein fragments from inside the cell are displayed by the MHC complex on the cell surface, allowing the immune system to differentiate between the body’s own tissue and foreign substances.
MHC Class I
Located on self-cells and on virtually all nucleotide cells
-When a cell is damaged, whether by a virus or it becomes cancerous/non-functioning, the MHC class will trigger destruction by cytotoxic T cells by presenting degraded viral proteins from the infected cell
MHC Class II
Restricted to immune cells, antigen-presenting cells, B cells, and macrophages
-Engulfed antigen is degraded into free-peptide fragments within cytoplasmic vesicles –> then complexed with MHC - II molecules –> present on surface of those (above) cells –> T helper cells recognize them and become activated
IgG - antibody
Most common type (75-80% of circulating immunoglobulins)
- Smallest; allows them to enter interstitial space and cross the placenta
- Easily escapes bloodstream to enter interstitial fluid
- Antiviral, antitoxin, antibacterial
- Does most of the damage for subsequent exposures
IgM - antibody
Mostly found in intravascular pool
-cannot penetrate capillary wall
- First to be produced on exposure to antigens / initial responders to antigens and activates the compliment system
- the major antibody found on B-Cell surfaces
IgA - antibody
Produced by plasma cells located in tissue under skin/mucous membranes
- Helps prevent organisms from entering the body
- Found in saliva, tear,s tracheobronchial secretions, colostrum, breast milk, and GI/GU secretions
IgD - antibody
Found in tiny amounts in serum
- Located primarily on B cell membranes with IgM
- Co-expressed and facilitates IgM
IgE - antibody
Binds to receptors on basophils and mast cells
Degranulates mast cells –> releases histamine –> initiates inflammatory and allergic reactions
-Involved in immunity against parasites
Precipitation and Agglutination
Function of Antibodies
-Immunoglobin Y structure binds to an antigenic epitope –> becomes larger –> precipitates out of blood and is easier to find in tissue –> can be engulfed by macrophages
Neutralization
Function of Antibodies
-Functions as antitoxins that neutralize bacterial toxins
Opsonization
Function of Antibodies
-Coat the foreign antigen so it can be recognized by phagocytic cells
Complement Activation
Function of Antibodies
-Activates inflammatory response by triggering chemotaxis and other inflammatory mediators
Titer
Measures levels of serum immunoglobulins
-sees if the levels are high enough to respond/fight
Indirect Coombs test
Detects Rh blood incompatibility
-makes sure there are no issues in blood transfusions
Elisa
Looks for antibodies (which would show if we’ve been exposed to the disease)
Detects for HIV antibodies
MHC typing
Tissue matching before transplants
Autoimmunity
Individual’s immune system recognizes its own cells as foreign and mounts an immune response that injures self tissues
- Immune system can’t distinguish between healthy tissue and antigen
- Breakdown of self-tolerance
- Immune system forms antibody to self-antigens –> autoantibodies attack self antigens –> immune complexes deposit –> inflammation and tissue damage occur
Alloimmunity
Immune responds to cells from another individual of the same species by rejection
- often involves type IV hypersensitivity
- if the HLA match, it is more successful
- Examples: blood transfusion rejection
Graft versus host disease
Graft contains T cells that attack the host
Host versus graft disease
Host rejects graft
Hypersensitivity
Normal immune response that is inappropriately triggered, excessive, or produces undesirable effects on the body
-Type I, II, III are mediated by antibodies produced by B lymphocytes
Type I Hypersensitivity
Mediated by IgE activation of mast cells and basophils / classic allergic response
reaction occurs 15-30 minutes after exposure to the antigen
IgE attaches to mast cells –> sensitize mast cells –> on preexposure, allergen attaches to antibodies –> stimulates release of chemical mediators
- Mild manifestations: hives, seasonal allergic rhinitis, eczema
- or more problematic: throat constriction, localized edema, wheezing, tachycardia
- Anaphylaxis = most life threatening reaction (systemic reaction)
Type I Hypersensitivity Management
Pharmacologic
- antihistamines, corticosteroids, IgE Therapy
- epinephrine = adrenergic agent given subQ or IV during acute allergic reactions
Pharmacotherapeutic prevention
-immunotherapy, pharmacologic densensitization
Type II Hypersensitivity
IgG attacks antigens on surface of specific cells or tissues
aka cytolytic hypersensitivity
Examples:
- transfusion reaction
- hyperacute graft rejection (transplant donor tissue has an antigen to which recipient produces antibodies)
- hemolytic disease of the newborn
- Graves disease - overactivity of thyroid
- Myasthenia Gravis - autoimmune neuromuscular disorder
Type III Hypersensitivity
Caused by the formation of antigen–antibody immune complexes in the bloodstream, which are subsequently deposited in vascular epithelium or extravascular tissues and which activate the complement system and induce a massive inflammatory response
-IgM or IgG
Ex:
- Immune complex glomerulonephritis - inflammatory renal disorder (typically 10-14 days after Streptococcus infection)
- Rheumatoid arthritis
- Systemic lupus erythematosus
Type IV Hypersensitivity
Delayed hypersensitivity - tissue damage resulting from a delayed cellular reaction (sensitized T lymphocytes) to an antigen
Cell-mediated
Type IV Hypersensitivity Ex - Cutaneous Basophil Hypersensitivity
Skin graft reactions and rejections
Type IV Hypersensitivity Ex - Contact Dermatitis
peaks in 48-72 hours; epidermal phenomenon to plant oils, chemicals, ointments, clothing, cosmetics, dyes, adhesives
-slow reaction
Type IV Hypersensitivity Ex - Turberculin-Type Hypersensitivity
Individual (who has been infected by tuberculosis) is exposed to tuberculin antigen in a PPD test
Host Defense Failure
Results from functional decrease in one or more components of the immune system
- disease causing genotypes
- secondary/acquired dysfunction
- protein malnutrition, HIV/AIDS, genetics
Affects lymphocytes, antibodies, phagocytes, and or complement proteins
- suspected with severe recurrent, unusual, or unmanageable infections
- most cause moderate immune impairment that may not be diagnosed
