Unit 2 Flashcards
-erol
-bronchodilation
Bronchodilators Adrenergic
Bronchodilators Xanthrine derivatives
-phylline
-bronchodilation
Cancer
large groups of diseases caused by uncontrolled cellular growth and spread of abnormal cells
What percentage of cancers are genetic?
5-10%
Differentiation
normal changes of cells with different physiologic functions
Malignant Cells
Become less recognizable from their parent cells
Anaplasic Cells
unrecognizable from parent cell, loss of differentiation, last level of metaplasia
Dysplasia
disorganization of cells that vary in size and shape
Metaplasia
1st level of dysplasia, reversible
Hyperplasia
increase in cell number
Neoplastic Hyperplasia
increase in abnormal cell mass
Tumor
Neoplasm, abnormal new tissue growth
Primary Tumor
tumor from local cells
Secondary Tumor
tumor from metastasized cells
Carcinoma in stitu
localized, pre-invasive, pre-malignant, epithelial tissue
-oma
benign
Epithelial tissue
carcinoma
Connective tissue
sarcoma, malignant
Hematopoietic tissue
leukemia, myeloma
Stage 0
carcinoma in stitu, pre-malignant
Stage I
Early, local
Stage II
increase risk of spread
Stage III
Spread but not to other regions
Stage IV
spread to other regions
T
Primary Tumor
T(x)
cant be assessed
T(o)
no evidence
T(is)
in stitu
T(1-4)
progressive increase
N
Regional lymph nodes
Nx
cant be assessed
N(o)
no metastasis
N(1-3)
increased lymph node involvement
M
distant metastasis
Mx
can be assessed
M(o)
No distant metastasis
M(1)
distant
Most common cancers
Lung, breast, colorectal
Endogenous causes of cancers
genetics (prostate, breast, ovarian, colorectal)
Exogenous causes of cancers
environment (50%)
Carcinogens
agents capable of inacting malignant transformation
Carcinogenesis
carcinogens can cause cells to undergo malignant transformation, 7-8 steps
Hayflick Limit
cells can divide 50x before dying
Theory of Dysfunctional Senescence
Failure to die after increased mutations
Somatic mutation theory
neoplasia originates from a single cell through chromosomal changes
Oncogenesis
cancer causing genes, in all genes but can become malignant individually when activated by carcinogens
Tumor Suppressor Genes
anti oncogenes, chromosomal deletions (-p53, apoptosis of cells, activated by cellular stress
Stem Cell Hypothesis
abnormal stem cells feed cancer, chemo resistant, hard to kill
Tumor Specific Antigens
uniquely expressed on tumor cells, recognized by T Cells (fusion proteins and viral proteins)
Fusion proteins
translocations of genes that combine and create new genes
Viral proteins
aid in the replication of viruses
Tumor Associated Antigens
on tumorous and normal cells
Tumor Evasions
- Loss of immunogenicity
- antigenic modulation
- induction of immune suppression (T Cells)
- Prevention of NK and T Cell Activation
Cancer Immunotherapy
Anti-body based therapy, adoptive cell therapy, cancer vaccines
Most common metastase sites
lymph nodes, liver,lungs,bone, and brain
Seed vs. Soil
some cancers favor certain sites, target soil not seed
Percentage of cancers that metastasize
30%
Tumor Angiogenesis
new BV from existing to grow tumor
Most Common Nutrient Rich sites
Pulmonary (most common), Hepatic, Skeletal system, CNS
Osteolytic
decreased bone density, leads to hypercalcemia
Osteoblastic
increase bone density, dense scarring
CNS Sites
Brain: from lungs
Spinal Cord: involves vertebrae
Opioids
pain management for cancer, (morphine, fentanyl, oxycodone)
Opioid Rotation
balance between analgesia and side effects
Paraneoplastic Syndrome
symptoms and signs at a distant site of a tumor
Anti-Neoplastic Treatment
management might be curative or palliative
Neoadjuvant Treatment
before surgical intervention, pair with chemo/radiation
Radiation Therapy
destroys h2 bonds in DNA strands, G2 most sensitive to radiation, done at different stages, G0 resistant
Cytotoxic Chemo Strategy
limit cell growth by killing
Growth Fraction
% of growing cells relative to neoplastic population, decrease as tumor grows
Cell Kill hypothesis
chemo kills 90%, never fully eliminate, 10% can be killed endogenously
Alkylating Agents Chemo
helix cant untwist for dna replication, initiates apoptosis
Features of Pancreas
sacroiliac joint and hip
Antimetabolites Chemo
endogenous metabolites, mimics other constituents that form nonfunctional genes or occupy enzymes, inhibit DNA synth.
Antibodies Chemo
antitumor antibiotics, cause DNA lysis or prevention of synthesis, form free radicals
Antimicrotubule Chemo
disrupt spindle formation
Topoisomerase Inhibitors Chemo
catalyzing cutting and re-ligating during unwinding/winding
Anticancer Hormones Chemo
mimic or block effects of sex hormones to treat hormone sensitive cancers, inhibit cancer cells
Platinum Coordination Complexes Chemo
heavy metal compounds, cross links between DNA strands to prevent replication
Target Cell Surface Glycoproteins Chemo
cell death, deliver chemicals and prevent cell growth
Cytokines Chemo
increase immune mechanisms
Adverse effects of Chemo
Alopecia, Gi toxicity, myelosuppression, fatigue, cardiotoxicity, pulmonary toxicity, renal toxicity, hepatic toxicity, neuropathies
-azole
azole antifungals
-avir
HIV protease inhibitors
-cillin
penicillin antibodies, bacterial infections
-cycline
tetracycline antibodies, bacterial infections
-micin and -mycin
various antibacterials, bacterial infections
Innate Immune System
1st response, limited specificity, internal and external defenses, inflammatory response (second)
Adaptive Immune System
specifc and memory driven, B cells and T cells, antigen and antibody driven, active vs passive
Neutrophils
1st response, short lived, polymorphonuclear cells, phagocyte and granulocyte, pus
Monocytes/Macrophages
longest lived, mono= blood, macro= tissues, phagocytes. MCH 2, Antigen presenting
Dendrites
main antigen presenting cell, MCH 2
Eosinophils
allergic responses and parasites, granulocytes release histamine, cytokines, and heparin
Basophils
granulocytes, allergic responses, increase blood volume
Mast Cells
granulocytes, allergic responses, anaphylaxis, increase blood volume
B Cells
produce antibodies, antigen presenting, mature in bone
T Cells
mature in thymus, have helpers and cytotoxic
Natural Killer Cells
kill cells with virus, don’t express antigens, interact with ligands, initiate apoptosis
Major Histocompatibility Complex (MHC)
membrane proteins that present antigenic peptides for T cell recognition
MCH I
bind proteins that have been synthesized in cytoplasm, recognized by cytotoxic CD4+ cells
MCH II
bind fragments of previously phagocytized, pinocytosis, and endocised. Recognized by Helper CD+4 T cells
External Defenses of Innate Immune System
physical, chemical, and mechanical
Internal Defenses of Innate Immune System
soluble factors (complement system, cytokines, chemokines)
Cellular Response (neutrophils, mono/macrophages)
Active Adaptive
usually permanent. Natural: contact with infection
Artificial: inoculation of antigen, vaccine
Passive Adaptive
temporary. Natural: natural contact with antibody
Artificial: inoculation of antibody
Acquired: immune products between individual
Antigen
molecule on cells used for recognition by T cells or antibodies. Epitope: immunologically active site on antigen
Antibodies
produced by B Cells. Heavy Chains: determine type of antibody. Fab Fragment: portion that binds to antigen
Immunoglobulins
directly attack antigens, stimulate anaphylaxis and hypersensitivity. IgM, IgG, IgA, IgE, IgD
IgM
expressed on B cells, 1st secreted, predominant
IgG
antibacteral and antiviral, secondary, gestation
IgA
serum and secretory (breast milk, urine, saliva), defends external
IgE
low levels in blood, high affinitty receptors for basophils and mast cells (allergies and histamines), allergEEE
IgD
low levels in blood, antigen receptors on immature B cells
Immunologic Tolerance
Positive and Negative Selection. Positive: TCR gene rearrangement makes self identify. Negative: delete cells that recognize self peptides
Cytotoxic T Lymphocytes
CD8+, kills other cells, MCH I, kill virally affected cells and produce cytokines
Helper T Cells (CD4+)
- Help B Cells make antibodies
- Activate macrophages
- Help CTLs
- Help NK
- Neutrophil Recruitment
- Downregulation of Adaptive Immune Response
Regulatory T Cells (Tregs)
Prevent inappropriate responses against “self” antigen
Humoral Immunity
mediated by antibodies, body fluids (not urine), B Cell Development
Phases of Immune System
Recognition, Amplification, Effector, Termination, Memory
Recognition Phase
receptors bind to pathogens
Amplification Phase
complement cascades, cell recruitment, proliferation of B and T Cells
Effector Phase
removal of antigens
Termination Phase
decreased immune reactions after antigen clearance
Memory Phase
long lived B and T Cells
Neutrophil and macrophage clearance post-exercise
After 30min, 2-4 hours`
NK Cells post exercise
increase from epinephrine, then falls below pre-exercise level
Inaccurate Immune Responses
Immunodeficiency, hypersensitivity, transplantation, Autoimmunity
Immunodeficiency
immune response is lacking or absent. Primary: depletion due to genetics
Secondary: pre-existing condititons
AIDS
destruction of immune system, caused by human immunodeficiency virus
HIV Virus
RNA retrovirus, reverse transcriptase from RNA to viral DNA. Affects CD4+ cells and macrophages
Acute HIV Infection
1-6 weeks, tests negative
Asymptomatic HIV
CD4+ 500+.1-20yrs, positive test. Seroconversion has occurred (emergence of HIV antibiotics)
Symptomatic HIV
200-500 CD4+.
Advanced HIV
CD4+ less 200. Kaposi Sarcoma
Type I Hypersensitivity
Immunoglobulin IgE. Seasonal allergies (histamines), anaphylaxis. CD4+ cells.
Antihistamines
competing with histamine receptors
Type II Hypersensitivity
Immunoglobulin IgG and IgM. Tissue specifc. Macrophages. Hashimoto’s.
Type III Hypersensitivity
Immunoglobulin IgG, IgM, and IgA. Immune complex mediated. Systemic. Neutrophils. Lupus
Type IV Hypersensitivity
T Cell mediated. No antibodies Delayed reaction. Graft rejection
Autoimmune Diseases
mechanisms directed against self-antigens. Localized tissue, lesions localized with distant antibodies, non-organ specifc
Central Tolerance
loss of self-reflective T and B Cells. Immature recognize self-antigens, leads to apoptosis
Peripheral Tolerance
mature lymphocytes that self-antigens become inactive or suppressed
Systemic Lupus Erythematosus (SLE)
chronic inflammation. Discoid: face. Systemic: everywhere.
Latent Lupus
symptoms without actually being lupus
Antiphospholipid Antibody Syndrome
immune, fetal loss, thrombosis
Late Stage Lupus
chronic 5+ years
Fibromyalgia (FMS)
chronic widespread pain of soft tissues, muscle/location specific
Leukocytosis
increased WBC
Leukopenia
Decreased WBC
Normal White blood cell count
5,000-10,000
Fever
96.8-98.6
Hypothalamus
temp-regulation center. pyrogens and cytokines
Intermittent Fever
temperature returns to normal in 24 hrs (sepsis)
Remittent Fever
temperature fluctuates but does not return (upper respiratory infection)
Sustained or Continuous Fever
temperature remains above normal with minimal variation
Recurring or Relapsing Fever
episodic fevers lasting 1-3 days with 1+ days of normal temperature
Signs and Symptoms of Infectious Diseases
Abscess, hypertension, rash, fever, red streaks, inflamed lymph nodes, joint effusion
Immunosenescence
thymus ages and becomes less active
Age related cell changes
Less naive T Cells, Increase memory T Cells, slower response to stimulus
Infection
organism has a parasitic relationship with its host
Infectious Disease
infection with 1+ clinical symptoms
Incubation Period
period b/wn pathogen entering and clinicial symptoms
Latent Infection
occurs after microorganism has replicated but remains dormant
Colonization of organisms
microorganisms present in tissues but dont cause symptoms
Period of Communicability
time when organism can be shed
Chain of Transmission
Pathogen, reservoir, portal of exit, mode of transmission, portal of entry, host susceptibility
Pathogen
organism with the ability to cause disease
Pathogenicity
ability of an organism to produce disease
Virulence
potency of pathogen in producing severe disease by fatality case rate
opportunistic pathogens
do not cause disease in healthy host but can be deadly for those compromised
Reservoir
an environment that an organism can live
Portal of Exit
place the pathogen leaves the reservoir
Mode of Transmission
Contact transmission (direct and indirect), airborne (small particles), droplet (large droplets), vehicle (food), vector-borne (animal)
Standard Precautions of CDC
assume anyone can be contagious
Healthcare-Associated Infections (HAI)
nonsocomial infections. develop from hostpitalizations. Pneumonia, GI, Surgical
Bacteria
single celled organisms with well defined cell walls. Cocci: sphere. Bacilli: rod. Spiral: spirochetes
Clostridiodies (c diff), clostridial myonecrosis (gangrene), pseudomonas
Bacteria
Bactericidal
kill bacteria
Bacteriostatic
limit growth and proliferation of bacteria
Antibacterial Inhibition of Bacterial Cell Wall
drugs can punch holes in cell walls or act as deterrents to break apart bilayer
Antibacterial Inhibition of Bacterial Protein Synthesis
bind to cell and bind to ribosomes, blocks protein synthesis
Antibacterial Inhibition of bacterial DNA/RNA synthesis
folic acid not nucleic synthesis, drug stops folic acid production
Viruses
subcellular organisms made up of RNA/DNA, smallest, dependent on host cells, lacks cellular components, only genetic material
Viral Replications
exocytose genetic material into cell and lysis causes new viruses to release
Herpesviruses
“to creep”, 8 kinds. HSV-1: cold sores. HSV-2: sti. Treated with acyclovir
Varicella Zoster Virus
chickenpox or shingles
Infectious mononucleosis (Herpesvirus 4)
epstein-barr. mono.
Respiratory Syncytial virus
children, lung issues
Interferons
endogenous substances that exert nonspecific viral activity
Diaphragm Referral site
Shoulder, lumbar spine
Heart referral site
Shoulder, neck, upper back, TMJ
Urothelial tract referral site
Back, inguinal region, anterior thigh, genetalial
Pancreas, liver, spleen, galbladder referral site
Shoulder, midthoracic, or low back
Peritoneal or abdominal cavity referral site
Hip pain from abscess of psoas or obturator
