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Pathophysiology > EXAM 1 > Flashcards

EXAM 1 Flashcards

1
Q

Pathology

A

Study and diagnosis of disease through the examination of organs, tissues, cells, and bodily fluids

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2
Q

Physiology

A

Study of the mechanical, physical and biochemical functions of living organisms

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3
Q

Pathophysiology

A

Study of the abnormalities in physiologic functioning of living beings

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4
Q

Etiology

A

Study of the causes or reasons for phenomena

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5
Q

Idiopathic

A

Cause is unknown

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6
Q

Iatrogenic

A

Cause is nosocomial (ex: ventilator associated pneumonia)

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7
Q

Multifactorial

A

Multiple etiologic factors that contribute to its development

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8
Q

Pathogenesis

A

Development or evolution of disease, from initial stimulus to ultimate expression of manifestations of disease

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9
Q

Risk Factor

A

A factor that when present increases the likelihood of disease (MIGHT get disease)
-Modifiable vs non-modifiable

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10
Q

Triggers

A

Promote the onset of clinical manifestations when someone already has the disease

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11
Q

Symptoms

A

Subjective feeling of abnormality in the body

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12
Q

Signs

A

Objective or observed manifestation of disease

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13
Q

Syndrome

A

Set of signs and symptoms not yet determined to delineate a disease

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14
Q

Incidence

A

New cases over a time period

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15
Q

Prevalence

A

Existing cases over a time period

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16
Q

Reliability

A

Same results when repeated

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17
Q

Validity

A

Measuring what was intended

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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

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19
Q

Specificity

A

Correctly excludes a condition (true-negs)

= # of true negs / # of total well individuals in a population

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20
Q

Morbidity

A

Causes disease, illness, consequences or problems related to the disease

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21
Q

Mortality

A

Causes death

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22
Q

Point Prevalence

A

of cases in a defined population / # of persons in a defined population

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23
Q

Incidence Risk

A

of new cases of disease / #of disease-free persons at the beginning of that time period

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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

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25
Q

Positive Predictive Value (PPV)

A

TP / (TP+FP)

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26
Q

Negative Predictive Value (NPV)

A

TN / (TN + FN)

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27
Q

Syncope

A

Feeling of faint/dizziness

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28
Q

Autocrine cellular communication

A

Cell releases substance that in turn turns around and acts on itself

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29
Q

Paracrine cellular communication

A

Substance released acts on a nearby cell (but does not enter the bloodstream)

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30
Q

Endocrine cellular communication

A

Distance signaling; hormones released into bloodstream and acts on a distant cell

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31
Q

Nervous cellular communication

A

Substances can be released in synapse causing following nerve to react

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32
Q

Reversible cell growth patterns

A

Atrophy, hypertrophy, metaplasia, hyperplasia, dysplasia

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33
Q

Irreversible cell growth patterns

A

Neoplasia

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34
Q

Atrophy

A

Decrease in cell size due to decrease in functional demand

-can be caused by drugs/steroids

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35
Q

Hypertrophy

A

Increase in cell size due to an increase in functional demand

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36
Q

Hyperplasia

A

Increase in the # of cells due to an increase in functional demand/and or increased stress (ex: gingival hyperplasia, calluses)

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37
Q

Metaplasia

A

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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38
Q

Dysplasia

A

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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39
Q

Anaplasia

A

Undifferentiated cells with variable nuclear and cell structures

  • Can imply a more advanced cancer
  • NOT reversible
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40
Q

Neoplasm

A

“New growth” - commonly called tumor

-NOT reversible

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41
Q

Necrosis

A

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)

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42
Q

Apoptosis

A

Cell suicide in response to injury that doesn’t directly kill the cell but triggers intracellular cascades
-no inflammation

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43
Q

Ischemia

A

Lack of blood flow

–> metabolic waste build up –> not enough O2/H2O/nutrients –> can’t create ATP

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44
Q

Hypoxic

A

Lack of O2

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45
Q

Free radical

A

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
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46
Q

Hydropic Swelling

A

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

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47
Q

Intracellular Accumulations

A

Accumulations of normal body substances (ex: lipids), substances from poor metabolism, exogenous products that are not processed by cells

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48
Q

Coagulative Necrosis

A

Begins with ischemia –> loss of energy –> inefficient Na/K pump –> swelling + acid build up –> rupture

Red = necrotic (pink = healthy)

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49
Q

Liquefactive Necrosis

A

Once cell is damaged/spills –> dead cells are consumed by lysosomal enzymes –> the enzymes can damage surrounding healthy tissue –> cyst formation

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50
Q

Fat Necrosis

A

Death of adipose tissue (usually as a result of trauma)

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51
Q

Caseus Necrosis

A

Characteristic to lung damage + TB

-clumpy cheese appearance

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52
Q

Gangrene

A

Cellular death in a large area of tissue as a result of interruption of blood supply to a particular part of the body

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53
Q

Dry Gangrene

A

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)
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54
Q

Wet Gangrene

A

Large scale liquefactive necrosis

  • found in internal organs but can be seen outwardly
  • spread QUICKLY
55
Q

Gas Gangrene

A

Result of infection of necrotic tissue by Clostridium (anaerobic bacteria)

  • formation of gas bubbles
  • can start as dry or wet gangrene
56
Q

Pleomorphism

A

Undifferentiated cancer cells marked by a number of morphologic changes (size, shape, nucleus, DNA)

57
Q

Stem Cells =

A

undifferentiated cells

-can be triggered to enter cell cycle and produce large numbers of progenitor cells when needed

58
Q

Tumors =

A

mass of cells due to overgrowth = neoplasms

  • malignant vs bening
    suffix: -oma
59
Q

Adenoma

A

Benign tumor of glandular epithelial tissue

60
Q

Adenocarcinoma

A

Malignant tumor of glandular epithelial tissue

61
Q

Carcinoma

A

Malignant tumor of epithelial tissue

62
Q

Obsteoma

A

Benign tumor of bone tissue

63
Q

Sarcoma

A

Malignant tumor of connective tissue

64
Q

Papillomas

A

Bening microscopic/macroscopic finger-like projections growing on a surface

65
Q

Metastasis

A

Development of secondary malignant growths at a distance from a primary site of cancer

66
Q

Angiogenesis

A

Development of new capillaries in the tumor (tumor’s own blood and nutrient supply –> takes it away from tissue downstream)

67
Q

Superior Vena Cava Syndrome

A

Tumor impedes on vena cava, impeding on blood flow coming back to the heart (life threatening)

68
Q

Cachexia

A

anorexia + fatigue + pain + stress

69
Q

Effusions

A

(systematic effect of malignant tumor)

-inflammation causes fluid buildup in body cavities

70
Q

Infections

A

(systematic effect of malignant tumor)

  • Occur frequently as resistance declines
  • seen often in those anemic
71
Q

Paraneoplastic Syndrome

A

(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
Q

TNM Classification system

A 
T = primary tumor, graded on size
N = # of regional lymph nodes 
M = metasasis 
-0 = no
-1 = yes
73
Q

Palliative Care

A

Pt is far along in prognosis (with no hope for cure/control) – provide the best quality of life

74
Q

Opsonization

A

(Complement Activation)

-coding foreign cells to ease phagocytosis

75
Q

Chemotaxis

A

(Complement Activation)

-involves release of chemical mediators like bradykinin and attracting leukocytes

76
Q

Complement Activation

A

opsonization, chemotaxis, anaphylatoxins, recruitment and activation of neutrophils, increased vascular permeability, cell lysis, mast cell degranulation

77
Q

Inflammation Exudate - Serous

A

Watery

  • mostly fluid
  • some proteins + WBC
78
Q

Inflammation Exudate - Sanguinous

A

Bloody

79
Q

Inflammation Exudate - Serosanguinous

A

Mostly serous with some RBC, maybe pinkish

80
Q

Inflammation Exudate - Fibrinous

A

Sticky, thick, HIGH cell content

81
Q

Inflammation Exudate - Purulent

A

Thick, yellow-green, microorganisms, leukocytes, cell debris
Ex: pus

82
Q

C-Reactive protein

A

Inflammatory marker

-a protein not normally in blood but appears with acute inflammation and necrosis within 24-48 hours

83
Q

WBC normal range

A

4,500-11,000 cells/mL

Infection: > 11,000

84
Q

Absolute Neutrophil count:

A

1000 - 1800 cells/mL

85
Q

Bands (%)

A

3-6% (immature neutrophils)

86
Q

Shift to the Left

A

increased WBC count (increase in immature neutrophils = bands)

87
Q

Acetylsalicylic acids (ASA)

A

Ex - aspirin

  • decreases prostaglandins synthesis at site, decreasing inflammatory response
  • can increase bleeding
88
Q

Acetaminophen

A

Ex - tylenol

-decreases fever and pain, but DOES NOT decrease inflammatory response

89
Q

Non-steroidal anti-inflammatory drugs (NSAIDS)

A

Ex - ibuprofen, naproxen sodium (aleve)

  • anti-inflammatory, anogesic, anti-pyrotic
  • acts by decreasing production of prostaglandins
  • can increase bleeding
90
Q

Glucocorticoids

A

Ex - prednisone (steroids)
-decreased capillary permeability, decreased leukocytes and mast cells at site
(this decreases the release of histamines and prostaglandins)

91
Q

Healing by primary intention

A

Approximated wound edges (paper cut, surgical incision, stitches)
-All areas heal simultaneously

92
Q

Healing by secondary intention

A

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
Q

Healing - Proliferative Phase

A

3-4 days after injury, lasts 2 weeks

-foreign materials and cell debris removed by macrophages, monocytes, phagocytes

94
Q

Healing - Remodeling Phase

A

Onset depends on wound size and whether it was initially open or closed
-scar tissue strengthens

95
Q

Chronic wound or pathological scarring

A

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
Q

Hypovolemia

A

Decreased volume of circulating blood in the body

97
Q

Hypertrophic scar tissue

A

fibrous tissue with excessive collagen deposits

  • leads to hard ridges of scar tissue or keloid formation
  • very disfiguring
  • can cause severe contractions
98
Q

Dehiscence

A

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
Q

2 purposes of Immunity

A

(third line of defense)

  • defend body against invasion or infection by antigens
  • patrol for and destroy abnormal or damaged cells
100
Q

Cytotoxic T Cell

A

Cell-Mediated immunity
CD8
Specific cellular antigen destruction

101
Q

Helper T Cell

A

Cell-Mediated immunity
CD4
Activation of antigen-specific T cell

102
Q

Plasma Cells

A

Humoral immunity
(B lymphocyte)
Secretion of antibody/immunoglobulins

103
Q

Memory Cells

A

Humoral immunity
(B lymphocyte)
-Efficient, rapid antibody response to subsequent antigen recognition

104
Q

HLA

A

Human Leukocyte Antigen (type of MHC protein)

-HLA proteins label cells of the individual

105
Q

MHC

A

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
Q

MHC Class I

A

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
Q

MHC Class II

A

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
Q

IgG - antibody

A

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
Q

IgM - antibody

A

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
Q

IgA - antibody

A

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
Q

IgD - antibody

A

Found in tiny amounts in serum

  • Located primarily on B cell membranes with IgM
  • Co-expressed and facilitates IgM
112
Q

IgE - antibody

A

Binds to receptors on basophils and mast cells

Degranulates mast cells –> releases histamine –> initiates inflammatory and allergic reactions

-Involved in immunity against parasites

113
Q

Precipitation and Agglutination

A

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
Q

Neutralization

A

Function of Antibodies

-Functions as antitoxins that neutralize bacterial toxins

115
Q

Opsonization

A

Function of Antibodies

-Coat the foreign antigen so it can be recognized by phagocytic cells

116
Q

Complement Activation

A

Function of Antibodies

-Activates inflammatory response by triggering chemotaxis and other inflammatory mediators

117
Q

Titer

A

Measures levels of serum immunoglobulins

-sees if the levels are high enough to respond/fight

118
Q

Indirect Coombs test

A

Detects Rh blood incompatibility

-makes sure there are no issues in blood transfusions

119
Q

Elisa

A

Looks for antibodies (which would show if we’ve been exposed to the disease)

Detects for HIV antibodies

120
Q

MHC typing

A

Tissue matching before transplants

121
Q

Autoimmunity

A

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
Q

Alloimmunity

A

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
Q

Graft versus host disease

A

Graft contains T cells that attack the host

124
Q

Host versus graft disease

A

Host rejects graft

125
Q

Hypersensitivity

A

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
Q

Type I Hypersensitivity

A

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
Q

Type I Hypersensitivity Management

A

Pharmacologic

  • antihistamines, corticosteroids, IgE Therapy
  • epinephrine = adrenergic agent given subQ or IV during acute allergic reactions

Pharmacotherapeutic prevention
-immunotherapy, pharmacologic densensitization

128
Q

Type II Hypersensitivity

A

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
Q

Type III Hypersensitivity

A

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
Q

Type IV Hypersensitivity

A

Delayed hypersensitivity - tissue damage resulting from a delayed cellular reaction (sensitized T lymphocytes) to an antigen

Cell-mediated

131
Q

Type IV Hypersensitivity Ex - Cutaneous Basophil Hypersensitivity

A

Skin graft reactions and rejections

132
Q

Type IV Hypersensitivity Ex - Contact Dermatitis

A

peaks in 48-72 hours; epidermal phenomenon to plant oils, chemicals, ointments, clothing, cosmetics, dyes, adhesives
-slow reaction

133
Q

Type IV Hypersensitivity Ex - Turberculin-Type Hypersensitivity

A

Individual (who has been infected by tuberculosis) is exposed to tuberculin antigen in a PPD test

134
Q

Host Defense Failure

A

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

Pathophysiology (8 decks)

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