EXAM 1 Flashcards
(134 cards)
1
Q
Pathology
A
Study and diagnosis of disease through the examination of organs, tissues, cells, and bodily fluids
2
Q
Physiology
A
Study of the mechanical, physical and biochemical functions of living organisms
3
Q
Pathophysiology
A
Study of the abnormalities in physiologic functioning of living beings
4
Q
Etiology
A
Study of the causes or reasons for phenomena
5
Q
Idiopathic
A
Cause is unknown
6
Q
Iatrogenic
A
Cause is nosocomial (ex: ventilator associated pneumonia)
7
Q
Multifactorial
A
Multiple etiologic factors that contribute to its development
8
Q
Pathogenesis
A
Development or evolution of disease, from initial stimulus to ultimate expression of manifestations of disease
9
Q
Risk Factor
A
A factor that when present increases the likelihood of disease (MIGHT get disease)
-Modifiable vs non-modifiable
10
Q
Triggers
A
Promote the onset of clinical manifestations when someone already has the disease
11
Q
Symptoms
A
Subjective feeling of abnormality in the body
12
Q
Signs
A
Objective or observed manifestation of disease
13
Q
Syndrome
A
Set of signs and symptoms not yet determined to delineate a disease
14
Q
Incidence
A
New cases over a time period
15
Q
Prevalence
A
Existing cases over a time period
16
Q
Reliability
A
Same results when repeated
17
Q
Validity
A
Measuring what was intended
18
Q
Sensitivity
A
Correctly identifies a condition (true-pos)
-want tests to have high sensitivity
= # of true positive / # of total sick individuals in a population
19
Q
Specificity
A
Correctly excludes a condition (true-negs)
= # of true negs / # of total well individuals in a population
20
Q
Morbidity
A
Causes disease, illness, consequences or problems related to the disease
21
Q
Mortality
A
Causes death
22
Q
Point Prevalence
A
of cases in a defined population / # of persons in a defined population
23
Q
Incidence Risk
A
of new cases of disease / #of disease-free persons at the beginning of that time period
24
Q
Incidence Rate
A
of new cases of disease in a given time period / Total person-time at risk during the follow up period
25
Positive Predictive Value (PPV)
TP / (TP+FP)
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Negative Predictive Value (NPV)
TN / (TN + FN)
27
Syncope
Feeling of faint/dizziness
28
Autocrine cellular communication
Cell releases substance that in turn turns around and acts on itself
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Paracrine cellular communication
Substance released acts on a nearby cell (but does not enter the bloodstream)
30
Endocrine cellular communication
Distance signaling; hormones released into bloodstream and acts on a distant cell
31
Nervous cellular communication
Substances can be released in synapse causing following nerve to react
32
Reversible cell growth patterns
Atrophy, hypertrophy, metaplasia, hyperplasia, dysplasia
33
Irreversible cell growth patterns
Neoplasia
34
Atrophy
Decrease in cell size due to decrease in functional demand
| -can be caused by drugs/steroids
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Hypertrophy
Increase in cell size due to an increase in functional demand
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Hyperplasia
Increase in the # of cells due to an increase in functional demand/and or increased stress (ex: gingival hyperplasia, calluses)
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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
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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)
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Anaplasia
Undifferentiated cells with variable nuclear and cell structures
- Can imply a more advanced cancer
- NOT reversible
40
Neoplasm
"New growth" - commonly called tumor
| -NOT reversible
41
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)
42
Apoptosis
Cell suicide in response to injury that doesn't directly kill the cell but triggers intracellular cascades
-no inflammation
43
Ischemia
Lack of blood flow
| --> metabolic waste build up --> not enough O2/H2O/nutrients --> can't create ATP
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Hypoxic
Lack of O2
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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
46
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
47
Intracellular Accumulations
Accumulations of normal body substances (ex: lipids), substances from poor metabolism, exogenous products that are not processed by cells
48
Coagulative Necrosis
Begins with ischemia --> loss of energy --> inefficient Na/K pump --> swelling + acid build up --> rupture
Red = necrotic (pink = healthy)
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Liquefactive Necrosis
Once cell is damaged/spills --> dead cells are consumed by lysosomal enzymes --> the enzymes can damage surrounding healthy tissue --> cyst formation
50
Fat Necrosis
Death of adipose tissue (usually as a result of trauma)
51
Caseus Necrosis
Characteristic to lung damage + TB
| -clumpy cheese appearance
52
Gangrene
Cellular death in a large area of tissue as a result of interruption of blood supply to a particular part of the body
53
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)
54
Wet Gangrene
Large scale liquefactive necrosis
- found in internal organs but can be seen outwardly
- spread QUICKLY
55
Gas Gangrene
Result of infection of necrotic tissue by Clostridium (anaerobic bacteria)
- formation of gas bubbles
- can start as dry or wet gangrene
56
Pleomorphism
Undifferentiated cancer cells marked by a number of morphologic changes (size, shape, nucleus, DNA)
57
Stem Cells =
undifferentiated cells
| -can be triggered to enter cell cycle and produce large numbers of progenitor cells when needed
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Tumors =
mass of cells due to overgrowth = neoplasms
- malignant vs bening
suffix: -oma
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Adenoma
Benign tumor of glandular epithelial tissue
60
Adenocarcinoma
Malignant tumor of glandular epithelial tissue
61
Carcinoma
Malignant tumor of epithelial tissue
62
Obsteoma
Benign tumor of bone tissue
63
Sarcoma
Malignant tumor of connective tissue
64
Papillomas
Bening microscopic/macroscopic finger-like projections growing on a surface
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Metastasis
Development of secondary malignant growths at a distance from a primary site of cancer
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Angiogenesis
Development of new capillaries in the tumor (tumor's own blood and nutrient supply --> takes it away from tissue downstream)
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Superior Vena Cava Syndrome
Tumor impedes on vena cava, impeding on blood flow coming back to the heart (life threatening)
68
Cachexia
anorexia + fatigue + pain + stress
69
Effusions
(systematic effect of malignant tumor)
| -inflammation causes fluid buildup in body cavities
70
Infections
(systematic effect of malignant tumor)
- Occur frequently as resistance declines
- seen often in those anemic
71
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
72
TNM Classification system
```
T = primary tumor, graded on size
N = # of regional lymph nodes
M = metasasis
-0 = no
-1 = yes
```
73
Palliative Care
Pt is far along in prognosis (with no hope for cure/control) -- provide the best quality of life
74
Opsonization
(Complement Activation)
| -coding foreign cells to ease phagocytosis
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Chemotaxis
(Complement Activation)
| -involves release of chemical mediators like bradykinin and attracting leukocytes
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Complement Activation
opsonization, chemotaxis, anaphylatoxins, recruitment and activation of neutrophils, increased vascular permeability, cell lysis, mast cell degranulation
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Inflammation Exudate - Serous
Watery
- mostly fluid
- some proteins + WBC
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Inflammation Exudate - Sanguinous
Bloody
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Inflammation Exudate - Serosanguinous
Mostly serous with some RBC, maybe pinkish
80
Inflammation Exudate - Fibrinous
Sticky, thick, HIGH cell content
81
Inflammation Exudate - Purulent
Thick, yellow-green, microorganisms, leukocytes, cell debris
Ex: pus
82
C-Reactive protein
Inflammatory marker
| -a protein not normally in blood but appears with acute inflammation and necrosis within 24-48 hours
83
WBC normal range
4,500-11,000 cells/mL
Infection: > 11,000
84
Absolute Neutrophil count:
1000 - 1800 cells/mL
85
Bands (%)
3-6% (immature neutrophils)
86
Shift to the Left
increased WBC count (increase in immature neutrophils = bands)
87
Acetylsalicylic acids (ASA)
Ex - aspirin
- decreases prostaglandins synthesis at site, decreasing inflammatory response
- can increase bleeding
88
Acetaminophen
Ex - tylenol
| -decreases fever and pain, but DOES NOT decrease inflammatory response
89
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
90
Glucocorticoids
Ex - prednisone (steroids)
-decreased capillary permeability, decreased leukocytes and mast cells at site
(this decreases the release of histamines and prostaglandins)
91
Healing by primary intention
Approximated wound edges (paper cut, surgical incision, stitches)
-All areas heal simultaneously
92
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
93
Healing - Proliferative Phase
3-4 days after injury, lasts 2 weeks
| -foreign materials and cell debris removed by macrophages, monocytes, phagocytes
94
Healing - Remodeling Phase
Onset depends on wound size and whether it was initially open or closed
-scar tissue strengthens
95
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)
96
Hypovolemia
Decreased volume of circulating blood in the body
97
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
98
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
99
2 purposes of Immunity
(third line of defense)
- defend body against invasion or infection by antigens
- patrol for and destroy abnormal or damaged cells
100
Cytotoxic T Cell
Cell-Mediated immunity
CD8
Specific cellular antigen destruction
101
Helper T Cell
Cell-Mediated immunity
CD4
Activation of antigen-specific T cell
102
Plasma Cells
Humoral immunity
(B lymphocyte)
Secretion of antibody/immunoglobulins
103
Memory Cells
Humoral immunity
(B lymphocyte)
-Efficient, rapid antibody response to subsequent antigen recognition
104
HLA
Human Leukocyte Antigen (type of MHC protein)
| -HLA proteins label cells of the individual
105
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.
106
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
107
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
108
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
109
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
110
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
111
IgD - antibody
Found in tiny amounts in serum
- Located primarily on B cell membranes with IgM
- Co-expressed and facilitates IgM
112
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
113
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
114
Neutralization
Function of Antibodies
| -Functions as antitoxins that neutralize bacterial toxins
115
Opsonization
Function of Antibodies
| -Coat the foreign antigen so it can be recognized by phagocytic cells
116
Complement Activation
Function of Antibodies
| -Activates inflammatory response by triggering chemotaxis and other inflammatory mediators
117
Titer
Measures levels of serum immunoglobulins
-sees if the levels are high enough to respond/fight
118
Indirect Coombs test
Detects Rh blood incompatibility
-makes sure there are no issues in blood transfusions
119
Elisa
Looks for antibodies (which would show if we've been exposed to the disease)
Detects for HIV antibodies
120
MHC typing
Tissue matching before transplants
121
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
122
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
123
Graft versus host disease
Graft contains T cells that attack the host
124
Host versus graft disease
Host rejects graft
125
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
126
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)
127
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
128
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
129
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
130
Type IV Hypersensitivity
Delayed hypersensitivity - tissue damage resulting from a delayed cellular reaction (sensitized T lymphocytes) to an antigen
Cell-mediated
131
Type IV Hypersensitivity Ex - Cutaneous Basophil Hypersensitivity
Skin graft reactions and rejections
132
Type IV Hypersensitivity Ex - Contact Dermatitis
peaks in 48-72 hours; epidermal phenomenon to plant oils, chemicals, ointments, clothing, cosmetics, dyes, adhesives
-slow reaction
133
Type IV Hypersensitivity Ex - Turberculin-Type Hypersensitivity
Individual (who has been infected by tuberculosis) is exposed to tuberculin antigen in a PPD test
134
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
