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HSC 411 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Parenchyma

A

Normal functioning tissue
“Resident cells” - cells that are supposed to be in that area

EX) hepatic cells in liver

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2
Q

Stroma

A

Structural framework within tissue
“Stromal”
-structure/framework of cells “scaffolding”

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3
Q

Fibroblasts

A

CT cells that form collagenous matrix

  • secrete collagen
  • -white fiber (protein)
  • -very strong
  • -supports tissue
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4
Q

Cell Classification (based on regenerative ability)

A

Labile cells
Stable cells
Permanent (fixed) cells

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5
Q

Labile Cells

A

Regenerate throughout our lifetime
EX) epithelial cells

  • highly mitotic
  • continuous replicators

only thing that will stop it is overcrowding
-called contact inhibition

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6
Q

Stable Cells

A

Stop dividing when growth ceases, but are capable of regeneration if properly stimulated. For these cells to regenerate properly, the underlying structural framework must be intact.
EX) liver cells

  • conditional replicators
  • will under mitosis ONLY if everything is intact
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7
Q

Permanent (fixed) Cells

A

Cells that are unable to divide
EX) muscle cells (heart after MI) and neurons

  • NO ABILITY to undergo mitosis
  • cannot replenish them
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8
Q

Two ways to heal injured tissue

A

Regeneration

  • when tissue is replaced from parenchyma cells
  • “best case scenario”

Repair

  • when fibrous scar tissue fills in gap left by damaged tissue
  • “next best thing”
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9
Q

Regeneration

A

Process in which damaged cells are replaced with parenchymal and normal structure, and normal function is restored.

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10
Q

2 Requirements for Regeneration

A
  1. The injury must not be too severe
  2. The tissue must be mitotic (labile or stable)

MUST HAVE BOTH!

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11
Q

Repair

A

When the injury is too severe OR the tissue is not mitotic, the parenchymal tissue will be replaced with fibrous connective tissue replacing structure, but sacrificing function

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12
Q

Revascularization

A

Whether healing occurs through regeneration or repair, the blood vessels in the area need to be restored. (replace blood vessels when they are lost during injury)

Angiogenesis

New capillaries formed from vessels adjacent to wound.

Dividing endothelia cells form buds or cords that extend into damaged area that eventually meet forming anastomoses

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13
Q

Angiogenesis

A

Growing new blood vessels

  • normal process, happens every day
  • important to growth of tumors
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14
Q

Healing Within the Skin

A
  • Reepithelialization - replacement of epithelium
  • New epithelial cells divide near damage
  • New cells move to denuded area
  • Cells secrete a new basement membrane as they migrate
  • Cells then get anchored to membrane
  • Dividing cells now move up towards surface of tissue
  • contact inhibition tells them to stay
  • overgrowth of epithliod causes large, uprised scar
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15
Q

Nervous Tissue Repair

A

Cannot Replace Neurons!

  1. CNS (Brain and Spinal Cord)
  2. PNS
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16
Q

CNS (nervous tissue repair)

A

If soma intact, some axonal regeneration may begin to occur. However, after 14 days, glial cells form scar tissue that blocks further regeneration.
No function is restored.

  • neuroglial cells prevent regeneration
  • could cause “rewiring” of brain
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17
Q

PNS (nervous tissue repair)

A

If soma and schwann cells are intact, axonal regeneration may occur

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18
Q

Factors Affecting Wound Healing

A 
Age 
Nutrition
Presence of infection 
Hormones
Blood Supply 
Size of wound 
Presence of foreign bodies
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19
Q

Age (factors affecting wound healing)

A

YOUNG: increase capacity for repair, but lack reserves for repair combined with an ignorant immune system

OLD: decreased cell replacement potential, decreased immune system

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20
Q

Nutrition (factors affecting wound healing)

A

Decreased proteins and fibroblasts prolong the inflammatory phase

Fats: needed for new cell membranes

Carbohydrates: provide energy to leukocytes

Vitamins: C for collagen synthesis

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21
Q

Presence of Infection (factors affecting wound healing)

A

Impairs the healing process

  • wound contamination
  • impaired leukocyte function function (diabetes, certain medications)
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22
Q

Hormones (factors affecting wound healing)

A

Corticosteroids decrease capillary permeability, impair phagocytosis, and inhibit fibroblast function, all of which impairs inflammation and healing

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23
Q

Blood Supply (factors affecting wound healing)

A

Poor blood supply may result from swelling, cardiovascular disease, etc.

Oxygen necessary for collagen synthesis

Necessary to remove debris and waste

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24
Q

Size of Wound (factors affecting wound healing)

A

Suturing greatly enhances healing process

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25
Q

Presence of foreign bodies (factors affecting wound healing)

A

Wood, metal, glass, sutures

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26
Q

Acquired Immunity

A

adaptive/specific immunity

  • adapts to pathogen every time it encounters one
  • developed over lifetime
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27
Q

Specificity

A

Reacts to specific substances

-Antigen, Pathogen

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28
Q

Antigen

A

Molecule that elicits an IR (immune response)

ex) allergies

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29
Q

Epitope

A

Binding site on antigen

-spot on antigen that immune system can react with

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30
Q

Pathogen

A

disease causing agent

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31
Q

Memory

A

Long-term retention

encounter again = rapid response

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32
Q

Tolerance

A

Ability to distinguish between self and foreign antigens. (Self recognition)

  • will attack anything that is foreign, but leave own cells alone
  • very important part of immunity

Tolerance depends largely on a group of cell surface proteins known as MHC

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33
Q

Major Histocompatibility Complex (MHC)

A

Protein on surface of cell “ID tag”

*Code for making MHC is on chromosome 6

MHC is also called Human Leukocyte Antigen (HLA)

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34
Q

MHC Class I

A

Molecules found on the surface of all cells
Offer evidence of intracellular abnormalities
-acts as a billboard and gives an idea of what is going on in that cell

-important for transplants

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35
Q

MHC Class II

A

Molecules made by antigen presenting cells (APC)
Offer evidence of extracellular activities

-Macrophages - eat something and display as a trophy

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36
Q

Phagocytes

A

neutrophils and macrophages

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37
Q

Lymphocytes

A

B cells and T cells

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38
Q

B lymphocytes

A

Responsible for Humoral Immunity (Antibody Molecules)

Plasma cells: antibody synthesis
-“antibody factory” - kicks out a lot of antibodies (2000/second/cell)

Memory B: long lived immunity
-hang out and if encounter pathogen again - IR is quick

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39
Q

T lymphocytes

A

Responsible for cell mediated immunity

Produced in bone marrow and thymus: maturation occurs in thymus

-T cells learn hat they should attack and what they should leave alone

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40
Q

T Lymphocyte Subgroups

A

Helper T/CD4
Memory T
Cytotoxic

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41
Q

Helper T

A

(also called CD4)

Recognizes MHC II from APC’s
Direct the immune response via cytokine release

-“commander in chief”, “conductor”, “quarterback”

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42
Q

Memory T

A

Long term retention

-strike pathogen faster if it returns

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43
Q

Cytotoxic

A

(also called T/CD8/Killer T)

Recognizes MHC I
Destroy via perforin

  • checks out cells to see if they are doing what they are supposed to
  • drills holes in cell membrane
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44
Q

B lymphocytes (more details)

A

Antibody-mediated immunity (Humoral Immunity)
Create antigen specific antibodies
Maturation occurs in red bone marrow

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45
Q

Antibodies

A

Y-shaped protein molecules that provide a means for linking defenses to pathogen
-do not do destruction themselves, but plant a “kiss of death”

Have fragment of antigen binding (FAB) (variable region) that attaches to foreign epitopes.
-changes all of the time - lots of shapes

Have FC region (constant region) for single, simple binding site 
-doesn't attach - determines class of antibody
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46
Q

The antibody response to an antigen

A

Production of masses of antigen-specific antibodies that bind to that specific antigen

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47
Q

Antibodies: How they Destroy

A
  1. Attracting IS cells
  2. Agglutination
  3. Activate Complement
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48
Q

Attracting IS cells (antibodies)

A

Opsonization

  • “to prepare to eat”
  • hook onto anything where shapes match
  • makes it easier for phagocytes to get ahold of it
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49
Q

Agglutination (antibodies)

A

Clumping

  • “bigger bite” for macrophages - easier to eat
  • makes it harder for pathogen to get into cells
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50
Q

Activate Complement (antibodies)

A

To form Membrane Attack Complex (MAC)

  • activated in a cascade
  • -end product is called MAC
  • -involves 30 different proteins
  • DESTROYS the cell!
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51
Q

Five main types/CLASSES of antibodies

A 
IgG - immunoglobin G
IgA - immunoglobin A
IgM - immunoglobin M
IgD - immunoglobin D
IgE - immunoglobin E
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52
Q

IgG - immunoglobin G

A

Principle circulating antibody
Only one to cross placenta
Binds to macrophages

(secondary response antibody)

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53
Q

IgA - immunoglobin A

A

Secreted in saliva, breast milk, respiratory, and urogenital tract
Protects mucous membranes (from invasion)

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54
Q

IgM - immunoglobin M

A 
In plasma
Star Shaped (very big!)

(Primary/First antibody produced)

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55
Q

IgD - immunoglobin D

A

Found on B lymphocyte
Needed for B cell activation
(Dumb!)

(Function unknown)

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56
Q

IgE - immunoglobin E

A

Found on mast cells in allergic response

important for allergies

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57
Q

Long Term Immunity

A

First antibody response to antigen takes about a week. It peaks at about 12 days and then tapers off.

Second and subsequent challenges produce faster rise in antibody production, which is retained at higher levels for a longer time. (increases antibodies immediately)

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58
Q

Immune System Diseases (types)

A

Autoimmunities - loss of tolerance
Hypersensitivity - overreaction
Immunodeficiencies - insufficient response

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59
Q

Autoimmune Diseases

A
  • Result from breakdown in the integrity of immune tolerance such that a humoral (B cell) or cellular (T cell) immune response is mounted against host cells antigens
  • Etiology = idopathic
  • Ability of immune system to distinguish foreign from native antigens is responsibility of MHC complexes
  • Current Theories: Genetic (chromosome 6), hormonal (more women affected), environmental
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60
Q

Molecular Mimicry

A

When similarities exist between foreign and self antigens sufficient enough to trigger IR

(“mistaken identity” - antibodies attack similar shapes of own cells)

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61
Q

Select Autoimmune Disorders (listed)

A 
Graves' Disease
Insulin-Dependent Diabetes Mellitus 
Myasthenia Gravis 
Rheumatoid Arthritis 
Systematic Lupus Erythematosus (SLE)
Multiple Sclerosis (MS)
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62
Q

Graves’ Disease

A

Autoantibodies bind to TSH receptors = hyperthyroidism

eyes bulge, weight loss, anxiety

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63
Q

Insulin-Dependent Diabetes Mellitus

A

Beta cell destruction

Type 1 - immune system attacks Beta cells of Pancreas - need insulin injections

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64
Q

Myastenia Gravis

A

Autoantibodies block/destroy ACh receptors

antibody hooks onto ACh receptors at neuromuscular junction; progressive muscle weakness and then paralysis

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65
Q

Rheumatoid Arthritis

A

Immune response targeting synovial membranes

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66
Q

Systematic Lupis Erythematosus (SLE) is also called ___ ?

nickname

A

“Great Imitator”

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67
Q

Etiology of SLE

A

Idiopathic

  • Genetic (chromosome 6, African Americans more often)
  • Environmental (UV light, sunlight, stress = increased flare ups)
  • Hormonal (estrogen - more in women)
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68
Q

Statistics of SLE

A

1 in 2,500 general population
1 in 700 females
1 in 250 black females

*understand trends, not numbers

Age - women 20-40 are most affected (peak instance)

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69
Q

Pathogenesis of SLE

A

Autoantibodies produced against a variety of targets

Multisystem disease characterized by remission and exacerbation. (exacerbations triggered by sunlight and stress)

Ag/Ab complexes deposit in basement membrane of tissues triggering inflammation and clogging organs

70
Q

Signs and Symptoms of SLE

A

Depend on target and vary widely

Common Sites:
90% SKIN involvement
90% JOINT involvement
50% KIDNEY involvement

Sometimes causes pericarditis, endocarditis, and other HEART problems (~25%)

71
Q

Diagnosis of SLE

A

ANA and S&S

ANA=anti-nuclear antibodies which are the antibodies against DNA/RNA

72
Q

Treatment of SLE

A

Control symptoms and reduce the immune response.

Corticosteroids and NSAIDS

Immunosuppressants in SEVERE cases

73
Q

Multiple Sclerosis (MS)

A

Demylenation of axons in the CNS and optic nerve

74
Q

Etiology of MS

A

Idiopathic

  • Genetics/ancestry
  • Hormones (2x more common in women)
  • Viral
  • Environmental (more vitamin D decreases risk for MS - it interacts with chromosome 6)

Age - 20-40 is peak incidence

75
Q

Pathogenesis of MS

A

Autoimmune destruction of the myelin sheath = CNS lesions - infilm and scarring (gliosis) depending on area of demylination

76
Q

Common S&S of MS

A

Has many different symptoms

  • Visual impairment
  • Muscle weakness
  • Ataxia (loss of coordination)
  • Speech
  • Mental impairment

Characterized by remission and exacerbation (usually caused by stress but really unknown)

77
Q

Diagnosis of MS

A

(hard to diagnose because of many symptoms)

Evoked potentials (EEG and flashed lights should evoke certain action potentials at certain speeds - if slower than normal, MS likely)

MRI

S&S

78
Q

Treatment/Prognosis

A

Palliative
Corticosteroids (reduce inflammation)
Interferon
Immunosuppressants (dangerous)

Vitamin D (low levels in etiology of MS; increase in dose to go into remission faster)

Prognosis varies widely

(treat as early as possible!)

79
Q

Hypersensitivity Reaction

A

Abnormal immune response to a relatively harmless environmental agent, an allergen (exogenous antigen)

80
Q

Hypersensitivity Reaction - Type 1

A

Anaphylactic-type reaction (immediate hypersensitivity reactions)

  • Mediated by IgE and mast cells
  • Clinical examples: hay fever, bronchial asthma, anaphylactic shock, food allergies, and latex glove allergies.
81
Q

Hygiene hypothesis (hypersensitivity)

A

Lack of exposure to antigens increase susceptibility

82
Q

Etiology of hypersensitivity

A

Idiopathic

  • Genetics (runs in families)
  • Environment
83
Q

Pathogenesis of hypersensitivity

A

Reactions require presentation, meaning they must have been exposed to antigen previously to show symptoms

84
Q

Hypersensitivity - FIRST exposure

A

Allergen is processed by the immune system
Plasma cells produce antibodies (IgE) against the allergen.
IgE becomes fixed on mast cells. They are now termed “sensitized mast cells”.

85
Q

Hypersensitivity - SECOND exposure

A

Allergen binds with IgE causing degranulation of mast cell and release of histamine.
Histamine causes vasodilation and increased capillary permeability resulting in the signs and symptoms of the allergic response.

86
Q

Herminthic Therapy

A

Involves the use of hook worms

87
Q

Anaphylaxis

A

(Anaphylactic Shock)
Severe life threatening systematic hypersensitivity

Examples: penicillin, bee stings, food (nuts, shellfish)

88
Q

(anaphylaxis) SECOND exposure results in:

A

Systemic vasodilation (decreases BP)

Bronchospasm (smooth muscle contracts and blocks airflow - minutes count!)

Increases capillary permeability

89
Q

Treatment of anaphylaxis

A

EPI pen

  • epinephrine
  • vasoconstricts
  • bronchodilator
90
Q

S&S of anaphylaxis

A 
Skin - urticaria (hives)
Eyes - conjunctivitis (red/runny)
GI Tract - nausea (vomiting, diarrhea)
Nose - runny, sneezy
Bronchopulmonary - coughing/wheezing (edema)
91
Q

AIDS is a disease cause by:

A

infection with human immunodeficiency virus (HIV)

92
Q

AIDS is characterized by:

A

Profound destruction of Helper T cell directed immune response with resultant opportunistic infections, causing death

(The primary disease lowers the victims immunity, and a secondary, unrelated disease produces the symptoms that cause death)

93
Q

Opportunistic Infection

A

An infection caused by pathogens that do not usually cause disease in a healthy immune system

94
Q

AIDS was first recognized in:

A

June 1981 in the LA area

95
Q

HIV was first isolated in

A

1983

96
Q

HIV/AIDS Statistics - US

A

Number of new HIV infections in 2009 = 0.5 million
Number of people living with HIV/AIDS = 1 million, (including more than 0.5 million with AIDS)
Number of AIDS deaths since the beginning of the epidemic = 0.5 million

70% of these new infections occur in men and 30% occur in women

In 2010, the age group 20-24 accounted for
the highest rate of new HIV diagnosis

By race, 45 percent of the new infections in the US occur among African Americans

21% of people are infected with HIV and do not know (about 1 in 5)

97
Q

Racial and ethnic minorities are disproportionally affected

A

Although black people represent only about 1 in 8 Americans, 1 in every 2 living with HIV in the US, is black

98
Q

HIV/AIDS Statistics - worldwide

A

In 2010, there were 34 million people infected (living with HIV/AIDS) worldwide, and 1.8 million deaths
Globally, women account for 50% of infections
Since inception, >30 million have died
90% of HIV infections are in poor countries
2/3 are in Africa
-Hardest hit region is sub-saharan Africa - accounts for 68% of all infections worldwide

In 2005, 1 person died every 13 seconds. That is 23 people every 5 minutes.

99
Q

AIDS: Life Expectancy

A

Sub-Saharan Africa sees reduction in life expectancy

US:

  • In 2003 - a 20 year old diagnosed had a life expectancy of 49 years old
  • In 2008 - a 30 year old diagnosed had a life expectancy of 69 years old
100
Q

HIV: virus structure

A
  1. Core of 2 strands of RNA with 3 transcription enzymes
  2. These are surrounded by core proteins/capsid (p24)
  3. Glycoprotein/Capsid - outer protein coat (gp120). This binds to CD4 and CCR5 on helper T cells
  4. At least 2 different types of the virus
    - HIV-1: around the world, most concerning, transmitted easier, progresses quicker
    - HIV-2: not as easy to transmit, mostly in Africa (west), slower progressed
101
Q

More on the HIV virus

A
  1. It is a retrovirus, its genetic material is carried on RNA, and it changes the coding to DNA by reverse transcriptase
    (it is also a lentivirus - attacks immune system)
  2. Once it produces DNA from RNA, its DNA is integrated into the host cell’s DNA
  3. There, it can take over the cell’s protein machinery and start making copies of itself
  4. Replication of HIV
102
Q

8 Steps of Replication (HIV virus)

A
  1. HIV binds to CD4 and CCR5
  2. Uncoating of virus
  3. Reverse transcriptase makes viral DNA
  4. Integration into cell’s DNA (via integrase)
  5. Transcription of viral DNA to make messenger RNA
  6. Translation of mRNA to produce HIV polyprotein
  7. Cleavage into individual proteins (protease)
  8. Assembly and release of new HIV virus from host cell
103
Q

Why is HIV so devastating?

Host Cell Functions and HIV Properties

A

Host Cell Functions

  • recognize foreign antigens
  • stimulate B cell response (antibody mediated)
  • stimulate CTL (“killer T”)
  • stimulate macrophages

HIV Properties

  • host choice
  • replication rate
  • mutation rate
  • escapes detection (NEF)
104
Q

Primary HIV Infection

A
  1. Some develop mono-like symptoms early - fatigue, fever, swollen glands, headache, night sweats, myalgia (muscle pain), sore throat, nausea, vomiting
  2. Lasts 2-4 weeks
  3. During this stage there is a large amount of HIV in the blood and the immune system begins to respond to the virus by producing HIV antibodies. This process is known as SEROCONVERSION. If an HIV antibody test is done before seroconversion is complete, then it may not be positive.

(takes 1-3 months for antibodies to show up in the blood)

105
Q

Clinically Asymptomatic Stage

A
  1. Lasts for an average of 10 years, and is free from major symptoms, although there may be lymphadenopathy. The level of HIV in the blood is low, but people remain infections and HIV antibodies are present.
  2. Research has shown that HIV is not dormant during this stage, but is very active in the lymph nodes. A test is available to measure the small amount of HIV that escapes the lymph nodes. This test which measures HIV RNA (HIV genetic material) is referred to as the VIRAL TEST LOAD.
106
Q

Symptomatic HIV/Progression to AIDS

A
  1. As the immune system fails, symptoms develop. Initially many of the symptoms are mild, but as the immune system deteriorates the symptoms worsen.
  2. Symptomatic HIV infection is mainly caused by the emergence of opportunistic infections that the immune system would normally prevent.
107
Q

Classification of HIV Infection

A

Based on the CD4 (TH cells) count per microliter of blood.

  • Category 1: more than 500
  • Category 2: 200 to 499
  • Category 3: less than 200
108
Q

AIDS defining illnesses/Identifier Diseases/Opportunistic Infections

A

As CD4 count decreases, susceptibbility to opportunistic infections increases. These are some examples:

  1. Kaposi’s sarcoma
  2. Pneumocytis pneumonia (PCP)
  3. Tuberculosis
  4. Candidiasis
  5. Cryptosporidium
  6. Wasting Syndrome
109
Q

Kaposi’s Sarcoma

A

Cancer of the endothelial cells that line small lymph vessels (KSHV = Karposi’s Sarcoma Herpe’s Virus - causes transformation of epithelial cells)

  • used to be rare
  • lymph vessels fill with blood and lesions appear on the surface of skin, and also internally
110
Q

Pneumocytis Pnemonia (PCP)

A

Caused by a fungas

111
Q

Tuberculosis (TB)

A

MDR strains from lack of compliance

  • # 1 cause of death in persons with AIDS (1/2 of people with AIDS has TB)
  • In people with AIDS, TB moves outside of the lungs to other parts of the body
112
Q

Candidiasis

A

Thrush.
Fungal

Is present in body, but with AIDS can get “out of check”

113
Q

Cryptosporidium

A

Protozoa that causes severe diarrhea

-Happens in healthy or poor immune system, but people with AIDS will not recover from it

114
Q

Wasting Syndrome

A

Loss of lean body mass

-with AIDS, the metabolic rate is faster than normal

115
Q

AIDS Transmission

A

HIV is found in blood, semen, vaginal fluid, CSF, tears, and saliva, but it seems that sufficient virus for transmission is limited to the blood, semen, vaginal secretions, and breast milk

Best suited sites for establishment of infection after exposure appear to be the cardiovascular system, open wounds of the skin, the penis, the vagina, and rectum.

(Tissue injury/STDs pose greater risk)

116
Q

Transmission Routes (HIV/AIDS)

A
  1. Blood to blood
    - 10-15% IV drug use
    - transfusions, needle sticks <1% since 1985
  2. Sexual
    -75-85% (all types)
    –M to M - 77% of HIV+ men
    –M to F - 86% of HIV+ women
    –F to M - 12% of HIV+ men
    (it is much easier for a male to give to a female than the opposite)
  3. Perinatally (mom to baby - crosses the placenta and found in breast milk)
    - WITHOUT treatment - 20-30% during delivery and 5-20% during breastfeeding
    - WITH treatment - 1-3%
117
Q

Prevention of Transmission (HIV/AIDS)

A
  1. If infected, do not have vaginal, oral, or anal intercourse (positive prevention strategy)
    - If not infected, use ABCs
  2. If have intercourse, effective whether HIV+ or HIV-, use effective barrier, latex condoms. (NO N-9 - can increase transmission)
  3. Blood and Blood products - must be tested for HIV
  4. Care in the handling of needles/use universal precautions/needle exchange
  5. If infected, females who are pregnant, need treatment
  6. Circumcision - New 2007 Guideline - WHO AIDS Cheif, Kevin deCock, Strongly advises circumcision (can decrease transmission by 51-60% (heterosexually))
118
Q

Treatment (HIV/AIDS)

A

HAART - Highly Active Anti-viral Therapy/ Antiretroviral Therapy (ART)
-attempts to keep virus low

  1. Reverse transcriptase inhibitors - AZT
  2. Protease inhibitors bind to active sites of HIV-1 protease
  3. Fusion inhibitors - inhibit HIV from binding to Helper T’s
  4. Integrase inhibitors - inhibit insertion into DNA
  5. CCR5 antagonists - fusion inhibitor
119
Q

When to start treatment for HIV/AIDS

A

Offer to all regardless of CD4

-500 microliters or below - strongly recommend!

120
Q

When to switch treatment for HIV/AIDS

A
  • ART - “3 drug cocktail”

- toxicity or tolerance (viral load test)

121
Q

Compliance is Critical (HIV/AIDS)

A

or resistance will develop

64% are non-compliant
14% say side effects are too awful

122
Q

Vaccine for HIV/AIDS

A

HIV vaccine 2009 - only 31% effective (reduces transmission by 31%)

Difficulties

  • HIV mutates
  • Vaccines trigger Ab formation
123
Q

Neoplasm

A

(New growth) - Abnormal mass growing by uncontrolled proliferation that serves no useful purpose or function
-may be malignant (cancer) or benign

124
Q

Oncology

A

The study of tumors

125
Q

Benign

A

“kind” - growth is slow, orderly, and localized

126
Q

Malignant

A

“with malace or intent to cause harm” - characterized by rapid, disordered, uncontrolled growth by aggressive invasion into adjacent normal tissues and ability to metastasize.

127
Q

Metastasis

A

Spread of cancer to locations distant from the origin

Only occurs in malignant tumors, not benign

128
Q

Primary Site (tumor)

A

Origin (original location of cancer cells_

1 CELL loses control and forms a tumor

129
Q

Secondary Site (tumor)

A

Site of metastasis

Does not have to change tissue type
-Example: breast cancer tissue found in bone will look like breast tissue

130
Q

Cancer Statistics

A
  1. Second ranking cause of death in North America
  2. 25% of population has some form
    - 15% of those die as a result
  3. Most common = skin cancer
  4. Cancer Incidence/Deaths (US) - Estimated 2011
    - Males
    - -1. prostate/lung
    - -2. lung/prostate
    - -3. colon/colon
    - Females
    - -1. breast/lung
    - -2. lung/breast
    - -3. colon/colon
131
Q

Naming of Tumors

A

“-oma” = tumor (used for benign tumors)

carcinoma = glands and epithelial
sarcoma = muscle and (CT) bone, adipose, cartilage
-(used for malignant tumors)

Some Prefixes:

  • “adeno-“ = gland
  • “chondr-“ = cartilage
  • “lipo-“ = fast
  • “sarco-“ = muscle
  • “osteo-“ = bone
132
Q

Modes of Metastasis

A

Blood
Lymph
Seeding (movement of cancer in body cavities because of gravity)

SITES: bone, brain, liver, lungs (areas of high blood flow)

133
Q

Carcinogenesis/Oncogenesis

A

Cell growth control system failure

All cancers are thought to be due to genetic mutation

134
Q

Cancer-Associated Genes (listed)

A

Proto-oncogenes
Oncogenes
Tumor Suppressant Genes (TSGs)

135
Q

Proto-oncogenes

A

Genes that control responsible cell proliferation (“go button”)

Tells cells when to begin growth

136
Q

Oncogenes

A

Mutated proto-oncogenes = unlimited mitosis

137
Q

Tumor Suppressant Genes (TSGs)

A

Safeguard against irresponsible growth (“stop button”)

Produce a protein that tell the cell to exit cycle

EX) p53

138
Q

What do TSGs do?

A
  1. DNA repair

2. Trigger apoptosis

139
Q

Neoplasia, or uncontrolled cellular proliferation, can result either from:

A
  1. mutations that “turn on/amplify” that stimulate growth

2. Mutations that result in loss of tumor suppressor genes and their products that inhibit cellular growth

140
Q

Multi-hit model of Carcinogenesis:

A

More than one mutational event is required in the development of cancer

141
Q

3 Steps Involved in Carcinogenesis/Tumor Cell Transformation

A
  1. INITIATION - mutations the result of exposure of a cell or cells to a carcinogen, which permanently alters its genetic material
    - virus, radiation, and some chemicals
  2. PROMOTION - mitagens. A substance that involves induction of unregulated growth in initiated cells.
    - hormones, alcohol, most chemical exposure
  3. PROGRESSION - Tumor cells acquire malignant characteristics via accumulated genetic mutations ac
142
Q

Complete carcinogen

A

Substance that is both initiator and promoter, such as “tobacco smoke”

Has both MUTAGENS and MITAGENS

143
Q

Etiological Factors in Carcinogenesis (listed)

A

Radiation
Chemical Exposure
Genetics
Viral

144
Q

Radiation (Etiological Factors in Carcinogenesis)

A

2 Sources:

  • Ionizing Radiation
  • UV Radiation
145
Q

Chemical Exposure (Etiological Factors in Carcinogenesis)

A

Alcohol, coal tar, cigarette smoke, radon, asbestos, etc.

146
Q

Genetics (Etiological Factors in Carcinogenesis)

A

Currently >50 cancers are considered inherited (parents give you the mutations)

BRCA1 and BRCA2 mutations - early onset breast and ovarian cancers

147
Q

Viral (Etiological Factors in Carcinogenesis)

A

Oncogenic viruses - HPV, KSHV, HBV, EBV

148
Q

Adaptive Cell Responses

A

HYPERPLASIA - increased mitosis in response to specific growth stimulus
HYPERTROPHY - increase in cell size due to an increased demand
METAPLASIA - conversion of one cell type to another
ANAPLASIA - undifferentiated; cells lose specialization
DYSPLASIA - Disordered cell growth. Cells are variable in size, shape, and structure. Usually a precursor to tumor, precancerous lesion/carcinoma in situ

149
Q

Pleomorphism

A

The condition of dysplasia

150
Q

Benign Tumor Characteristics

A

CELL STRUCTURE: normal; well differentiated; nuclear cytoplasm ratio (n/c) = 4:1
TISSUE STRUCTURE: organized, resembles tissue in which it grows
GROWTH RATE: above normal. Growth fraction = ~3%
INVASION: local by expansion
METASTASIS: never
CAPSULE: often = well circumscribed/demarcated (makes for easier removal)
PROGNOSIS: depends on: site, size, and products

151
Q

Malignant Tumor Characteristics

A

CELL STRUCTURE: bizarre and anaplastic; pleomophic (many shapes); nuclear to cytoplasm ration 1:1; mitotic figures are present; hyperchromatic (stain darker)
TISSUE STRUCTURE: unorganized
GROWTH RATE: measured by growth fraction = % of cells that are dividing. Slow growers = 10% GF (aggressive)
ANGIOGENSIS: Vascular Endothelial Growth Factor (VEGF)
INVASION: collagenase - enzyme to dissolve surrounding tissue; underexpression - of E. cadheren = loss of cohesion; loss of contact inhibition - overgrow and form mounds
CAPSULE: rare or incomplete
METASTASIS: 3 Routes - blood, lymph, seeding. Common sites: areas of high blood flow (bone, brain, liver, lungs)
PROGNOSIS: depends on site, stage, and response to treatment

152
Q

Liver Metastasis

A

Common due to hepatic portal system, which drains GI Tract

Parentineal cells likely to set up second site in liver b/c of this pathway

153
Q

Cancer kills by:

A

Spreading to vital tissue, replacing parenchymal tissue, compressing, obstructing, and destroying normal tissue

154
Q

Lung Metastasis

A

Common via lymph or venous

155
Q

Bone and Brain Metastasis

A

Via systemic circuit

156
Q

Tumor Effects

A
  1. Tissue destruction
  2. Obstruction/Compression
  3. Infection
  4. Anemia
  5. Pain
  6. Cachexia (“wasting” syndrome involving general weakness, fever, weight loss, can pallor)
157
Q

Cancer Diagnosis

A

An attempt to accurately identify the site of origin and the type of cells involved.

158
Q

Steps to Cancer Diagnosis

A
  1. Diagnostic Tests/S&S - imaging studies, scans
  2. Biopsy - removal of tissue for microscopic evaluation (cannot diagnose cancer until biopsy is done)
  3. Tumor Markers - substances that can be found in abnormal amounts in the blood, urine, or tissues of some patients with cancer. Limited Use. Different markers in different cancers. Used for screening, monitoring, diagnosis, and prognosis
159
Q

A cancer is typically undetectable until…

A

it contains more than 1 billion cells!

160
Q

Different Tumor Markers

A

CA 125: ovarian cancer
-present in high numbers when cancer is advanced. Not useful as a screener because it is found too late. Used to monitor treatment.

PSA: elevated with prostate CA > 10 ng/mL = abnormal

  • currently the only screening marker (detects early)
  • problem: too many false positives

p53 mutations: colon CA cells shed in stool
-new area - high cost limits use

HER-2/neu: an oncogene in breast CA indicates aggressive growth likely
-codes for protein that becomes receptor on breast cancer cells

Estrogen receptors/progesterone receptors: Determines treatment in breast cancer

  • intracellular receptors
  • have drugs that block receptors and can cause some breast cancers to shrink
161
Q

Strain

A

Stretching injury to a muscle or musculotendinous unit cause by mechanical overloading.

  • usually the result of excessive stretch or unusual contraction
  • pain, stiffness, and swelling are present

common sites of injury: lower back, cervical spine, elbow, and shoulder

treatment: application of heat and massage. if serious, traction and bed rest

162
Q

Sprain

A

Involves the ligaments surrounding a joint. Pain and swelling subside more slowly.
Caused by abnormal or excessive movement of the joint.

Symptoms: pain, rapid swelling, heat, disability, discoloration, and limitation of function

Ankle joint is most common site of sprains (foot turns inwards). Also common in knees and elbows.

May see a chip on an x-ray

Four grades, 1-4

163
Q

RICE

A

Rest
Ice
Compression
Elevation

164
Q

Classification of Fractures: Open/compound

A

When bone fragments have broken through the skin

165
Q

Classification of Fractures: closed

A

When bone fragments have not broken through the skin

166
Q

Classification of Fractures: greenstick

A

Only one side of the bone broken; bent. Seen in children because bones are more resilient

167
Q

Classification of Fractures: comminuted

A

Has more than two pieces (shatter)

168
Q

Classification of Fractures: compression

A

Two bones squeezed or crushed together. Vertebrae are common site

169
Q

Classification of Fractures: impacted

A

Fracture pieces wedged together

170
Q

Five Stages of Healing (fracture)

A
  1. Hematoma formation
  2. Cellular Proliferation
  3. Callus Formation
  4. Ossification
  5. Remodeling
171
Q

Fat Emboli

A

When the fat in the medullary cavity is released into venous blood = pulmonary embolism

172
Q

Osteosarcoma

A

Seen in long bone metaphysis, typically by knee or elbow

Peak incidence is in adolescence

HSC 411 (4 decks)

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