Unit 2 Flashcards

1
Q

-erol

A

-bronchodilation

Bronchodilators Adrenergic

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2
Q

Bronchodilators Xanthrine derivatives

A

-phylline
-bronchodilation

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3
Q

Cancer

A

large groups of diseases caused by uncontrolled cellular growth and spread of abnormal cells

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4
Q

What percentage of cancers are genetic?

A

5-10%

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5
Q

Differentiation

A

normal changes of cells with different physiologic functions

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6
Q

Malignant Cells

A

Become less recognizable from their parent cells

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7
Q

Anaplasic Cells

A

unrecognizable from parent cell, loss of differentiation, last level of metaplasia

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8
Q

Dysplasia

A

disorganization of cells that vary in size and shape

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9
Q

Metaplasia

A

1st level of dysplasia, reversible

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10
Q

Hyperplasia

A

increase in cell number

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11
Q

Neoplastic Hyperplasia

A

increase in abnormal cell mass

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12
Q

Tumor

A

Neoplasm, abnormal new tissue growth

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13
Q

Primary Tumor

A

tumor from local cells

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14
Q

Secondary Tumor

A

tumor from metastasized cells

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15
Q

Carcinoma in stitu

A

localized, pre-invasive, pre-malignant, epithelial tissue

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16
Q

-oma

A

benign

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17
Q

Epithelial tissue

A

carcinoma

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18
Q

Connective tissue

A

sarcoma, malignant

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19
Q

Hematopoietic tissue

A

leukemia, myeloma

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20
Q

Stage 0

A

carcinoma in stitu, pre-malignant

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21
Q

Stage I

A

Early, local

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22
Q

Stage II

A

increase risk of spread

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23
Q

Stage III

A

Spread but not to other regions

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24
Q

Stage IV

A

spread to other regions

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25
T
Primary Tumor
26
T(x)
cant be assessed
27
T(o)
no evidence
28
T(is)
in stitu
29
T(1-4)
progressive increase
30
N
Regional lymph nodes
31
Nx
cant be assessed
32
N(o)
no metastasis
33
N(1-3)
increased lymph node involvement
34
M
distant metastasis
35
Mx
can be assessed
36
M(o)
No distant metastasis
37
M(1)
distant
38
Most common cancers
Lung, breast, colorectal
39
Endogenous causes of cancers
genetics (prostate, breast, ovarian, colorectal)
40
Exogenous causes of cancers
environment (50%)
41
Carcinogens
agents capable of inacting malignant transformation
42
Carcinogenesis
carcinogens can cause cells to undergo malignant transformation, 7-8 steps
43
Hayflick Limit
cells can divide 50x before dying
44
Theory of Dysfunctional Senescence
Failure to die after increased mutations
45
Somatic mutation theory
neoplasia originates from a single cell through chromosomal changes
46
Oncogenesis
cancer causing genes, in all genes but can become malignant individually when activated by carcinogens
47
Tumor Suppressor Genes
anti oncogenes, chromosomal deletions (-p53, apoptosis of cells, activated by cellular stress
48
Stem Cell Hypothesis
abnormal stem cells feed cancer, chemo resistant, hard to kill
49
Tumor Specific Antigens
uniquely expressed on tumor cells, recognized by T Cells (fusion proteins and viral proteins)
50
Fusion proteins
translocations of genes that combine and create new genes
51
Viral proteins
aid in the replication of viruses
52
Tumor Associated Antigens
on tumorous and normal cells
53
Tumor Evasions
1. Loss of immunogenicity 2. antigenic modulation 3. induction of immune suppression (T Cells) 4. Prevention of NK and T Cell Activation
54
Cancer Immunotherapy
Anti-body based therapy, adoptive cell therapy, cancer vaccines
55
Most common metastase sites
lymph nodes, liver,lungs,bone, and brain
56
Seed vs. Soil
some cancers favor certain sites, target soil not seed
57
Percentage of cancers that metastasize
30%
58
Tumor Angiogenesis
new BV from existing to grow tumor
59
Most Common Nutrient Rich sites
Pulmonary (most common), Hepatic, Skeletal system, CNS
60
Osteolytic
decreased bone density, leads to hypercalcemia
61
Osteoblastic
increase bone density, dense scarring
62
CNS Sites
Brain: from lungs Spinal Cord: involves vertebrae
63
Opioids
pain management for cancer, (morphine, fentanyl, oxycodone)
64
Opioid Rotation
balance between analgesia and side effects
65
Paraneoplastic Syndrome
symptoms and signs at a distant site of a tumor
66
Anti-Neoplastic Treatment
management might be curative or palliative
67
Neoadjuvant Treatment
before surgical intervention, pair with chemo/radiation
68
Radiation Therapy
destroys h2 bonds in DNA strands, G2 most sensitive to radiation, done at different stages, G0 resistant
69
Cytotoxic Chemo Strategy
limit cell growth by killing
70
Growth Fraction
% of growing cells relative to neoplastic population, decrease as tumor grows
71
Cell Kill hypothesis
chemo kills 90%, never fully eliminate, 10% can be killed endogenously
72
Alkylating Agents Chemo
helix cant untwist for dna replication, initiates apoptosis
73
Features of Pancreas
sacroiliac joint and hip
74
Antimetabolites Chemo
endogenous metabolites, mimics other constituents that form nonfunctional genes or occupy enzymes, inhibit DNA synth.
75
Antibodies Chemo
antitumor antibiotics, cause DNA lysis or prevention of synthesis, form free radicals
76
Antimicrotubule Chemo
disrupt spindle formation
77
Topoisomerase Inhibitors Chemo
catalyzing cutting and re-ligating during unwinding/winding
78
Anticancer Hormones Chemo
mimic or block effects of sex hormones to treat hormone sensitive cancers, inhibit cancer cells
79
Platinum Coordination Complexes Chemo
heavy metal compounds, cross links between DNA strands to prevent replication
80
Target Cell Surface Glycoproteins Chemo
cell death, deliver chemicals and prevent cell growth
81
Cytokines Chemo
increase immune mechanisms
82
Adverse effects of Chemo
Alopecia, Gi toxicity, myelosuppression, fatigue, cardiotoxicity, pulmonary toxicity, renal toxicity, hepatic toxicity, neuropathies
83
-azole
azole antifungals
84
-avir
HIV protease inhibitors
85
-cillin
penicillin antibodies, bacterial infections
86
-cycline
tetracycline antibodies, bacterial infections
87
-micin and -mycin
various antibacterials, bacterial infections
88
Innate Immune System
1st response, limited specificity, internal and external defenses, inflammatory response (second)
89
Adaptive Immune System
specifc and memory driven, B cells and T cells, antigen and antibody driven, active vs passive
90
Neutrophils
1st response, short lived, polymorphonuclear cells, phagocyte and granulocyte, pus
91
Monocytes/Macrophages
longest lived, mono= blood, macro= tissues, phagocytes. MCH 2, Antigen presenting
92
Dendrites
main antigen presenting cell, MCH 2
93
Eosinophils
allergic responses and parasites, granulocytes release histamine, cytokines, and heparin
94
Basophils
granulocytes, allergic responses, increase blood volume
95
Mast Cells
granulocytes, allergic responses, anaphylaxis, increase blood volume
96
B Cells
produce antibodies, antigen presenting, mature in bone
97
T Cells
mature in thymus, have helpers and cytotoxic
98
Natural Killer Cells
kill cells with virus, don't express antigens, interact with ligands, initiate apoptosis
99
Major Histocompatibility Complex (MHC)
membrane proteins that present antigenic peptides for T cell recognition
100
MCH I
bind proteins that have been synthesized in cytoplasm, recognized by cytotoxic CD4+ cells
101
MCH II
bind fragments of previously phagocytized, pinocytosis, and endocised. Recognized by Helper CD+4 T cells
102
External Defenses of Innate Immune System
physical, chemical, and mechanical
103
Internal Defenses of Innate Immune System
soluble factors (complement system, cytokines, chemokines) Cellular Response (neutrophils, mono/macrophages)
104
Active Adaptive
usually permanent. Natural: contact with infection Artificial: inoculation of antigen, vaccine
105
Passive Adaptive
temporary. Natural: natural contact with antibody Artificial: inoculation of antibody Acquired: immune products between individual
106
Antigen
molecule on cells used for recognition by T cells or antibodies. Epitope: immunologically active site on antigen
107
Antibodies
produced by B Cells. Heavy Chains: determine type of antibody. Fab Fragment: portion that binds to antigen
108
Immunoglobulins
directly attack antigens, stimulate anaphylaxis and hypersensitivity. IgM, IgG, IgA, IgE, IgD
109
IgM
expressed on B cells, 1st secreted, predominant
110
IgG
antibacteral and antiviral, secondary, gestation
111
IgA
serum and secretory (breast milk, urine, saliva), defends external
112
IgE
low levels in blood, high affinitty receptors for basophils and mast cells (allergies and histamines), allergEEE
113
IgD
low levels in blood, antigen receptors on immature B cells
114
Immunologic Tolerance
Positive and Negative Selection. Positive: TCR gene rearrangement makes self identify. Negative: delete cells that recognize self peptides
115
Cytotoxic T Lymphocytes
CD8+, kills other cells, MCH I, kill virally affected cells and produce cytokines
116
Helper T Cells (CD4+)
1. Help B Cells make antibodies 2. Activate macrophages 3. Help CTLs 4. Help NK 5. Neutrophil Recruitment 6. Downregulation of Adaptive Immune Response
117
Regulatory T Cells (Tregs)
Prevent inappropriate responses against "self" antigen
118
Humoral Immunity
mediated by antibodies, body fluids (not urine), B Cell Development
119
Phases of Immune System
Recognition, Amplification, Effector, Termination, Memory
120
Recognition Phase
receptors bind to pathogens
121
Amplification Phase
complement cascades, cell recruitment, proliferation of B and T Cells
122
Effector Phase
removal of antigens
123
Termination Phase
decreased immune reactions after antigen clearance
124
Memory Phase
long lived B and T Cells
125
Neutrophil and macrophage clearance post-exercise
After 30min, 2-4 hours`
126
NK Cells post exercise
increase from epinephrine, then falls below pre-exercise level
127
Inaccurate Immune Responses
Immunodeficiency, hypersensitivity, transplantation, Autoimmunity
128
Immunodeficiency
immune response is lacking or absent. Primary: depletion due to genetics Secondary: pre-existing condititons
129
AIDS
destruction of immune system, caused by human immunodeficiency virus
130
HIV Virus
RNA retrovirus, reverse transcriptase from RNA to viral DNA. Affects CD4+ cells and macrophages
131
Acute HIV Infection
1-6 weeks, tests negative
132
Asymptomatic HIV
CD4+ 500+.1-20yrs, positive test. Seroconversion has occurred (emergence of HIV antibiotics)
133
Symptomatic HIV
200-500 CD4+.
134
Advanced HIV
CD4+ less 200. Kaposi Sarcoma
135
Type I Hypersensitivity
Immunoglobulin IgE. Seasonal allergies (histamines), anaphylaxis. CD4+ cells.
136
Antihistamines
competing with histamine receptors
137
Type II Hypersensitivity
Immunoglobulin IgG and IgM. Tissue specifc. Macrophages. Hashimoto’s.
138
Type III Hypersensitivity
Immunoglobulin IgG, IgM, and IgA. Immune complex mediated. Systemic. Neutrophils. Lupus
139
Type IV Hypersensitivity
T Cell mediated. No antibodies Delayed reaction. Graft rejection
140
Autoimmune Diseases
mechanisms directed against self-antigens. Localized tissue, lesions localized with distant antibodies, non-organ specifc
141
Central Tolerance
loss of self-reflective T and B Cells. Immature recognize self-antigens, leads to apoptosis
142
Peripheral Tolerance
mature lymphocytes that self-antigens become inactive or suppressed
143
Systemic Lupus Erythematosus (SLE)
chronic inflammation. Discoid: face. Systemic: everywhere.
144
Latent Lupus
symptoms without actually being lupus
145
Antiphospholipid Antibody Syndrome
immune, fetal loss, thrombosis
146
Late Stage Lupus
chronic 5+ years
147
Fibromyalgia (FMS)
chronic widespread pain of soft tissues, muscle/location specific
148
Leukocytosis
increased WBC
149
Leukopenia
Decreased WBC
150
Normal White blood cell count
5,000-10,000
151
Fever
96.8-98.6
152
Hypothalamus
temp-regulation center. pyrogens and cytokines
153
Intermittent Fever
temperature returns to normal in 24 hrs (sepsis)
154
Remittent Fever
temperature fluctuates but does not return (upper respiratory infection)
155
Sustained or Continuous Fever
temperature remains above normal with minimal variation
156
Recurring or Relapsing Fever
episodic fevers lasting 1-3 days with 1+ days of normal temperature
157
Signs and Symptoms of Infectious Diseases
Abscess, hypertension, rash, fever, red streaks, inflamed lymph nodes, joint effusion
158
Immunosenescence
thymus ages and becomes less active
159
Age related cell changes
Less naive T Cells, Increase memory T Cells, slower response to stimulus
160
Infection
organism has a parasitic relationship with its host
161
Infectious Disease
infection with 1+ clinical symptoms
162
Incubation Period
period b/wn pathogen entering and clinicial symptoms
163
Latent Infection
occurs after microorganism has replicated but remains dormant
164
Colonization of organisms
microorganisms present in tissues but dont cause symptoms
165
Period of Communicability
time when organism can be shed
166
Chain of Transmission
Pathogen, reservoir, portal of exit, mode of transmission, portal of entry, host susceptibility
167
Pathogen
organism with the ability to cause disease
168
Pathogenicity
ability of an organism to produce disease
169
Virulence
potency of pathogen in producing severe disease by fatality case rate
170
opportunistic pathogens
do not cause disease in healthy host but can be deadly for those compromised
171
Reservoir
an environment that an organism can live
172
Portal of Exit
place the pathogen leaves the reservoir
173
Mode of Transmission
Contact transmission (direct and indirect), airborne (small particles), droplet (large droplets), vehicle (food), vector-borne (animal)
174
Standard Precautions of CDC
assume anyone can be contagious
175
Healthcare-Associated Infections (HAI)
nonsocomial infections. develop from hostpitalizations. Pneumonia, GI, Surgical
176
Bacteria
single celled organisms with well defined cell walls. Cocci: sphere. Bacilli: rod. Spiral: spirochetes
177
Clostridiodies (c diff), clostridial myonecrosis (gangrene), pseudomonas
Bacteria
178
Bactericidal
kill bacteria
179
Bacteriostatic
limit growth and proliferation of bacteria
180
Antibacterial Inhibition of Bacterial Cell Wall
drugs can punch holes in cell walls or act as deterrents to break apart bilayer
181
Antibacterial Inhibition of Bacterial Protein Synthesis
bind to cell and bind to ribosomes, blocks protein synthesis
182
Antibacterial Inhibition of bacterial DNA/RNA synthesis
folic acid not nucleic synthesis, drug stops folic acid production
183
Viruses
subcellular organisms made up of RNA/DNA, smallest, dependent on host cells, lacks cellular components, only genetic material
184
Viral Replications
exocytose genetic material into cell and lysis causes new viruses to release
185
Herpesviruses
"to creep", 8 kinds. HSV-1: cold sores. HSV-2: sti. Treated with acyclovir
186
Varicella Zoster Virus
chickenpox or shingles
187
Infectious mononucleosis (Herpesvirus 4)
epstein-barr. mono.
188
Respiratory Syncytial virus
children, lung issues
189
Interferons
endogenous substances that exert nonspecific viral activity
190
Diaphragm Referral site
Shoulder, lumbar spine
191
Heart referral site
Shoulder, neck, upper back, TMJ
192
Urothelial tract referral site
Back, inguinal region, anterior thigh, genetalial
193
Pancreas, liver, spleen, galbladder referral site
Shoulder, midthoracic, or low back
194
Peritoneal or abdominal cavity referral site
Hip pain from abscess of psoas or obturator