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291 Cards in this Set

  • Front
  • Back
What do many diseases result from
an under-functioning immune system ( immunodeficiency ) or an immune system directed at the host (( auto immune disease)
Definition of Allergy
How our immune system responds to antigens
What is the medical terminology for allergy?
hypersensitivity
Immediate Type I hypersensitivity
- Develops within minutes of exposure to antigen
-Typically what we think of when we think of an allergic reaction
-range is from hives to anaphylactic shock
Mechanism of Type I (Immediate) Hypersensitivity
- IgE antibody production
-Mast cell degranulation
-release of mediators
Type II (Antibody Mediated) Hypersensitivity
immune reaction due to the binding of antibodies to cell surface antigens
autoimmune Hemolytic Anemia, Goodpasture Syndrome
Mechansim of Type II ( Antibody Mediated) Hypersensitivity
Production of IgM, IgG
-antibody binds to antigen
- phagocytosis or cell lysis
Type III ( Immune Complex Mediated) Hypersensitivty
-SLE
Serum Sickness
Arthus Reaction
Mechanism of Type III ( Immune Complex Mediated)
Vascular deposition of Ag-Ab complexes activates complement ---> recruits WBC
Type IV( Cell Mediated) Hypersensitivity
-initiated by T-cells
-function of T-cell response is to eliminate cells that are infected by intracellular pathogens
Contact Dermatitis, TB infection, Transplant Rejection
Mechanism of Type IV (Cell Mediated) Hypersensitivity
Activated T cells ---> Macrophage activation
What is a mast cell
a specialized type of white blood cell that are found in tissues near blood vessels
What do mast cells contain
many granules in their cytoplasm that are filled with potent biologically active mediators such as histamine
What is on the surface of the mast cell
binding sites for the Fc portion (non- antigen binding region) of IgE antibody. Circulating IgE is taken up by mast cells. When an antigen binds to the Fab portion of the IgE, the granules from the mast cells are released.
IgM
antibody that usually circulates as a large molecule comprised of 5 individual antibodies joined together as a pentamer

-seen early in the response to infection
IgG
primary antibody in the antibody response to infection and appears soon after IgM

-Unlike IgM, circulates as a monomer
IgA
found in secretions and on mucosal surfaces , in breast milk, and saliva
IgE
antibody associated with immediate hypersensitivity.

- can be found on the surface of most mast cells
IgD
found on the surface of developing B-cells as a receptor molecule
What happens when an antibody binds to the surface of a cell
the cell has been targeted for destruction
Immune complexes
Complexes comprised of antibody bound to circulating proteins that contain the target antigen

-helps immune system neutralize and eliminate foreign antigens
Anemia
a reduction in the tots circulating red cell mass(low hematocrit and hemoglobin )
Where do most blood cells come from?
bone marrow
Three Categories of Leukocytes(White blood cells)
-Neutrophils
-Monocytes
-Lymphocytes
Megakaryocytes
cells that fragment to form platelets
Stem Cell
precursor cell that all bone marrow derived cells (myeloid cells) descend from.

- Can differentiate into red cells, neutrophils, or megakaryocyte
Erythropoietin
hormone normally made by the kidney which boosts red blood cell production
hematologic malignancies
immature cells are unable to mature or reach full differentiation, so they keep dividing and accumulate in large numbers

Ex. Acute Leukemia
Plasma components
1. Fluid portion containing water, proteins, and nutrients
2. Serum= plasma- clotting proteins
Plasma Function
- maintain homeostasis (fight infection, prevent bleeding)
-Transport nutrients and electrolytes to cells
- transport waste products to kidneys, liver, lungs for excretion
Erythrocytes Function
-carry oxygen and CO2.
- occupy 40-45% blood volume
Hematocrit
fraction of blood volume occupied by red cells
* men usually have higher hematocrit level than women
hemoglobin
oxygen carrying protein responsible for red color of blood . Normal blood has about 15 g/ 100 ml
Leukocytes
1/1oooth as many as red cells
- fight infection
Neutrophil
phagocyte, eats bacteria
lymphocyte
(several subtypes) makes antibodies, recognizes and kills foreign cells (microbes, transplanted tissue, cells infected w/ viruses) regulate the immune system
Monocyte
phagocyte, works together w/ lymphocyte to control immune response
Eosinophil
involved in allergic reactions , kills certain parasites
Basophil
involved in allergic reactions
Platelets and function of platelets
-small cell fragments , about 1/10th as many red cells
-helps blood clot / prevents bleeding
Function of T lymphocyte (T Cell)
regulation of immune system; killing foreign or infected cells
Source of T cells
bone marrow, thymus, lymph nodes
Function of B lymphocyte (B cell)
antibody production
Source of B cell
bone marrow, lymph nodes, spleen, lymph, follicles in certain other tissue
Plasma cell
when stimulated to make antibodies the B cell differentiates into a plasma cell which is the cell type that makes most antibodies
Natural Killer Cell (NKC)
kills certain foreign or infected cells
Monocyte/ Macrophages
-phagocytosis(ingestion) of foreign cells, bacteria, etc
-digests foreign molecules and transfers pieces ("antigens") to T cells, which then tells Bcells what antibody to make
- produces hormones(cytokines) which mediate inflammation and regulate growth of other cells
source of Monocyte/ Macrophages
Bone marrow : first cousin of neutrophil
2 forms of Monocytes
a) circulating in blood= 3- 10% of blood leukocytes

b) In tissues= Macrophage
Lymph nodes
collections of lymphoid cells found scattered throughout the body
- connected by small vessels
lymph follicles
microscopic collections of lymph tissue contained in other organs
spleen
largest lymphoid organ in the body (fist sized)

-serves as a "filter" for blood and immune function
Lymph node
---->>>B cell location
in and around follicles
Lymph node
----->>>T Cell location
between follicles of node
Lymph node
----->>>Macrophage location
scattered throughout
What circulates through the nodes?
blood and lymph
What is anemia?
reduction in total circulating red cell masses.

- reflected by low hematocrit and/ or hemoglobin levels
Possible causes of decreased Red Cell Production- due to stem cells
1. Not enough stem cells due to generalized bone marrow failure or bone marrow replacement by non hematopoietic cells

2. Stem cells present but don not mature properly due to inherited or acquired mutation, or lack of iron or essential vitamin
Rapid Red cell Destruction (Hemolysis)
- due to inherited or acquired abnormality of the red cell that shortens it's lifespan

- due to abnormality of the blood or blood vessels that causes injury to or direct destruction of the red cell
macrocytic
larger than normal red cells
normocytic
normal sized cells
microcytic
smaller than normal cells
aplastic anemia
- Decreased #'s of stem cells; macrocytic or normocytic anemia
- caused by agents that can damage or destroy stem cells
ex> Cytoxic Chemicals, Ionizing radiation in Large doses
Anemia of inflammation
- Iron held in Macrophages and not released to red cell precursors
- normocytuc or microcytic
-physiological response to inflammation; when inflammation gets better, so does anemia
What is Iron used for in the body
Needed for hemoglobin synthesis
Pernicious Anemia
Caused by vitamin-B 12 deficiency
Purpose of Vitamin B-12
needed for DNA synthesis during Red Cell production
Megaloblastic
macrocytic w/ abnormal / delayed maturation
Folic Acid deficiency
needed for DNA synthesis by red cells
- macrocytic and megablastic
Lymphomas
cancerous proliferation of lymphocytes and their precursors
Low Grade non Hodgkin Lymphoma
-slow growing, mature appearing cells
-generally not curable
High Grade non Hodgkin Lymphoma
- Faster growing, less mature appearing cells
- potentially curable with chemotherapy
Hodgkin Disease (lymphoma)
-Large multi-nucleated Reed Sternberg cells
- common in adolescents and young adults
Stage 1 of disease
disease confined to single lymph node or group of nodes
Stage 2 of disease
disease in 2 or more lymph node groups on same side of diaphragm
stage 3 of disease
Disease in lymph nodes on both sides of diaphragm
stage 4 of disease
spread outside lymph nodes
ex....bone marrow, liver, bones, etc
multiple myleoma
-originates from plasma cell
- neoplastic cells often secrete antibody like protein
Acute leukemia
- caused by proliferation of immature leuocyte precursors(blasts) that have lost the ability to differentiate
Chronic Leukemia
- caused by proliferation of leukocyte precursors that have retained the ability to differentiate
- cells slow/ stop dividing when they differentiate
-progress slower
ALL
Acute Lymphoblastic leukemia
- B or T cells origin
- most common in children but also occurs in adults,
- often curable
Acute Myebgenous Leukemia
-malignant proliferation of immature granulocyte precursors leading to accumulation in blood, bone marrow and often other tissues
CML
chronic myelogenous Leukemia
- malignant proliferation of myeloid stem cell with over production of white cells and often platelets
What does CML cause?
enlarged spleen, fever, fatigue, weight loss
- can transform to fatal acute leukemia
CLL
Chronic lymphocytic leukemia
-originates in B cells and grows slowly
- primarily affects older people
Thrombocyopenia
low platelet count
qualitative platelet disorder
normal number of platelets bu abnormal function
neoplastic
cancerous
leukemia
cancerous cells replace normal bone marrow
-spread via blood and to other tissues
Causes of Leukemia
- Alterations in genes that regulate cell growth and division caused by exposure to radiation, mutagenic chemicals, or drugs , or other factors ( oncogenes)
- viral infections
- precursor to cancer must overcome cell signals and safe guards first
What test can detect antibody coated red cells
Coombs test
Treatment for autoimmune hemolytic anemia
corticosteroids( suppress immune system) or other immunosuppressive drugs
- spleenectomy( removes main site of red cell destruction)
Polycythemia
Too many red cells , blood is too thick
Disorder of Neutrophils:

Neutropenia
- decreased neutrophils production
- caused by aplastic anemia or other forms of marrow failure
- increased risk of bacterial or fungal infection
Diseases of Neutrophils:

Neutrophilia
increased neutrophils by marrow in response to physiological stimuli
ex. infection
Demargination
treatment of neutrophils with corticosteroids that make neutrophils less sticky so more show up in blood
Hypersplenism
Spleen soaks up leukocytes and platelets
asplenia
absence of spleen
Thalassemia
microcytic
- inherited disorder of hemoglobin production
Hemolytic anemia
anemia due to red cell destruction
Features of hemolytic Anemia
- increased rate of red cell production, red cell precursors in marrow, and increased numbers of newly made red cells ("reticulocytes") in blood
- high bilirubin in blood---->>>> indicates breakdown of hemoglobin
- Red cells may be taken up by macrophages in spleen and liver and then destroyed
Sickle Cell Anemia
- inherited structural abnormality ( single amino acid changes) of hemoglobin leading to polymerization of hemoglobin , damage to Red Cell membrane, premature destruction of red cells
How do sickle cells form
Repeated cycles of hemoglobin polymerization causes red cells to become rigid and clog small blood vessels causing tissue damage (infarction)
auto immune hemolytic anemia
production of antibodies against one's own red cells
- antibodies coat red cells , which are then eaten by macrophages in the spleen and destroyed.
symbiotic
when both the host and the parasite benefit from the relationship

Ex Bacteria in bowl that produce vit K
Commensalism
When an organism benefits from a host without causing the host any harm
ex. Bacteria in our mouth
Saprophytic
organisms live off dead and degenerate material material

ex. Vit K producing bacteria are both symbiotic and saprophytic because they help the host and live off degenerating material in the colon
What are the barriers to infection?
-Mechanical: skin and mucous membranes
- secretions
- epithelial by exfoliation
-Chemical( pH)
Parasitism
- interfere with the hosts integrity and function
- the more they interfere with host, the more pathogenic they are
virulence
quality of being poisonous
What determines how a host is affected by disease
virulence of a parasite and ability of host to deal with parasite
What are the 3 types of granular leukocytes
- neutrophils, Eosinophils, basophils
Tuberculosis Infection Process

Step 1
1. Usually enters via inhalation into lung
- 1st lesion called "Ghon" complex
- disease causing bacteria are ingested by neutrophils, but bacteria continue to multiply and neutrophils die
- Monocytes engulf bacteria, but cannot kill myobacteria
-monocytes w/ bacteria go to lymph nodes
Tuberculosis Infection Process

Step 2
- cell mediated immunity starts in 1-2 weeks
- organisms slowly destroyed
- granuloma forms
Tuberculosis infection process

Step 3
eventually most tuberculosis is walled off by a scar
Primary Tuberculosis
If cell mediated immunity doesn;t function properly, the bacteria may spread within 10-14 days
Re- infection of tuberculosis
- organism may remain dormant
-If CMI remains impaired, bacteria may break out
Spirochetes
long slender helically coiled organisms
Treponema Palladium
Spirochete that causes Syphilis
Borrelia Burgdorferi
spirochete that causes Lyme Disease
alpha hemolysis
incomplete green hemolysis
Beta hemolysis
complete clear hemolysis--->>> most dangerous
Gamma Hemolysis
no hemolysis
Group A B-hemolytic Streptoccus
has only one species : "streptococcus" pyogenes'
major cause of human infection
ex. strept throat, impetigo (skin infection)
Streptococcus Pneumoniae
grows in pairs and makes a capsule that protects it from being eaten
Gram (-) Cocci
- Gonococcus: gonorrhea
-Meningococcus: meningitis
-Nesseria Meningitidis: spinal meningitis
Gram (+) bacilli
-clostridium - botulism, tetanus, gas gangrene
-Coryne Bacterium - diptheria
Gram (-) bacilli
Enterobacteriacea: normal or disease causing inhabitants of the large bowel. Ex...E Coli

Shigella- non motile, cause dysentery
Acid Fast Bacilli
principally myobacteria
Tuberculosis
produced by myobacterium tuberculosis
- does not stain with ordinary gram stain, only acid fast and special media
What is the difference between prokaryotes and Eukaryotes
prokaryotes do not have a nucleus
Bacteriostatic action
process of regrowing a bacteria in culture with antibiotics to see if growth is suppressed.
Bactericidal
Process of regrowing a bacteria in culture of antibiotics to see if bacteria are killed
immunologically mediated disease
problems encountered by host are due to reaction host mounts against offending bacteria
Bacteremia
presence of viable bacteria within the blood
septicemia
presence of various pus forming organisms and other pathogens or their toxins in the blood or tissues
sepsis
systemic disease caused by the presence of microorganisms or their toxins in the circulating blood. may be associated with chills, fever, shock, death
Gram (+) cocci
Pyogenic or pus forming bacteria
- staphylococcus : grows in grape-like clusters Ex. boils, abscesses
- Streptococcus : grows in chains, classified by ability to lyse red blood cells in culture
non granular leukocytes
- lymphocytes
- monocytes
which leukocytes perform phagocytosis?
- neutrophils, eosinophils, monocytes
What are monocytes also referred to as?
- macrophages or histocytes
Humoral Immunity
- concerned with antibody production
Cell mediated immunity
directs specialized cells to recognize and destroy offensive agents.
- T cells mediate response
What are antibodies made in response to?
antigens
Opportunistic pathogens
cause disease only if they get into the wrong site or of host defenses are down. Have the ability to cause a disease when given the opportunity
carrier state
having a pathogenic organism, not showing clinical disease, but fully able to transmit the disease to others
Spreading factor
help break down tissue and allow organism to extend the region of infection
4 principle processes for the spread of infection
1. physical contact
- direct or indirect
2. airborne
3. food, H2O, or soil borne
4. insect borne
5 F's of infection spread
1. Food,
2. Fingers
3. Fomites,
4. flies,
5. feces
General Structure of Viruses
- submicroscopic, subcellular agents with a protective coat of protein wrapped around a central core of nucleic acid
- may be a surrounding lipoprotein envelope
What type of parasites are viruses
obligate intracellular
- cannot reproduce outside of host
- do not multiply by dividing
What kind of nucleic acid to viruses have?
DNA or RNA but never both
How are viruses classified
by type of nucleic acid they contain, size, type of tissues they infect
ways viruses may be spread
- lysing the host cell and releasing numerous progeny
-budding off from the host cell in a more controlled manner
-viral genomes becoming incorporated into the host genome and remain through mitotic cycles involving the hosts genome.
- Some may just enter the cytoplasm of a host cell and remain inactive and reactivate at a later time
superinfection
occurs when bacterial parasites have an opportunity to cause an additional infection to the one already occuring
Influenza structure
- 2 antigens: hemaglututinin & neuraminindase
- stimulate immune response
-lipid membrane beneath antigens
-protein layer surrounding the nucleocapsid
-RNA genome made up of 8 separate subunits that can exchange with other viruses-----allows viruses to continuously change
Virus attachment process
- attaches to host cell membrane by antigen spikes
-viral envelope fuses with host cell membrane
-virus loses its cover and nuclear material enters the cell and starts to take over the machinery of the host cell
Viral synthesis inside host cell
- synthesis of a new viral RNA
-new nucleocapsids migrate to cell surface where antigen spikes have been made on the surface of the hosts cells membrane by the action of the viral RNA on the host cell's synthetic machinery
-nucleocapsid buds from cell surface, taking the changed membrane with it
rota virus
most frequent cause of viral gastroenteritis in the young
Ways to diagnosis viral infections
-viral culture, measuring host antibody production, and or clinical picture
Characteristics of Fungi
- Do not perform Photosynthesis
-live off dying material or parasitize other organisms to survive
yeast
unicellular fungi that exist in a warm, moist environment.
- reproduce by budding
mold
-Fungi that exists in a colder dryer, climate
- reproduce by apical growth of hyphae
mycelium
mass of intertwining hyphae
mycoses or mycotic diseases
fungal infections
Amebiasis
- caused by Entamoeba histolytica (protozoan)
- comes from ingestion of contaminated water or food
- phagocytes RBC's or cyst
Malaria
caused by Plasmodium
- most widespread of infections
-spread by bite of female Anopheles mosquitoes
*reproduces sexually in mosquito and asexually in host
Worm infestations are often associated with a high count of?
Eosinophil
Enterbiasis
-pinworm, mainly infects children
- transmission by fecal-oral route
Bone consists of...
1. cells
2. Matrix components
3. blood vessels
Osteoblasts
synthesize bone, later become osteocytes
osteocytes
mature cells that occupy haversion systems
Osteoclasts
multinucleated cells that reabsorb and remodel bone
chondrocytes
cartilage cells
collagen
matrix component that is mostly Type I collagen in bone and ligaments and Type II collagen in articular cartilage
proteoglycans
form the matrix in cartilage
hydroxyapatite crystals
mineralized crystals that help to provide strength and structure to bone (matrix component)
Bone Marrow
contains fat cells and blood cell precursors ( matrix component)
Intramembranous ossification
mesenchymal cells directly become bone
Endochondral ossification
cartilage mineralizes to become bone, similar to how a fracture heals
Growth plate
where new bone is made for growing in a child
epiphysis
a portion of bone at the end of the growth plate next to a joint
metaphysis
bone adjacent to growth plate where new bone is mineralized
diaphysis
middle of tubular bone
periosteum
layer of tissue surrounding bone that provides nutrition and assists in circumferential growth
medullary cavity
contains trabecular bone and houses the bone marrow
cortical bone
thick, mature bone that gives bone its strength
woven bone
immature softer bone
Osteomalacia
defect in mineralization of bone due to a deficiency of vitamin D
Characteristics of Osteomalacia
- Rickets---> childhood form of disease
-alkaline phosphate activity is elevated in the serum
-often requires bone biopsy for diagnosis
-can be reversed with vitamin D supplementation
Osteoporosis
absolute decrease in bone mass
-no serological changes
- normal mineralization
Risk factors for Osteoporosis
-Post menapouse
-pregnancy
-immobilization
-steroids
-thyroid disease
-cigarettes
Treatment for Osteoporosis
Calcium, vitamin D, estrogen, fluorides, exercises
Fracture: inflammatory phase
mesenchymal cells turn into chondroblasts which make more cartilage that undergoes endochondral ossification
Fracture : Reparative Phase
A large callus is formed at the fracture site
Fracture: remodeling phase
mechanical forces on the bone cause it to slowly remodel into a more efficient and stronger structure
open fractures
skin over the fracture is torn= open or compound fracture
- often get infected due to contamination
Comminuted (high energy) fractures
-multiple fragments of bone
-blood supply to bone is disrupted so fracture heals slowly
Osteomyelitis
infection of bone
-can occur by hematogenous spread through the blood stream or direct inoculation into a wound
Osteosarcoma
-Children's Disease
- highly malignant tumor that produces bone
Ewing Sarcoma
-Children's Disease
- malignant tumor of primitive mesenchyma cells
- often present with systemic systems
Multiple Myeloma
-Adult disease
-most common bone tumor in adults
- abnormal plasma cell production in the bone marrow
Metastatic Disease in bone
- Adult Disease
-lesions destroy the bone and replace it with the same tumor cells as the primary lesion
- spine and proximal femur are areas most commonly involved
3 types of joints
1. Synarthroses
- suture lines in skull
2. Amphiarthroses
-little motion, pubic symphysis and disc space in spine
3. Fibrocartilaginous structure
Diarthroses
- most common, and mobile
contains synovial fluid membrane
ex. Hip, knew, ankle
Subtypes of diarthroses
-ball & socket in hip
-hinge in interphalangeal joints
Wolff's Law
In all types of joints, form follows function
Articular cartilage
made up of type II collagen
- fibers parallel to axis of motion
synovial tissue
lines all diarthrodial joints
- very vascular, produces variety of enzymes
Osteoarthritis
most common form of arthritis
- usually non inflammatory
-increased pain and loss of motion
Rheumatoid arthritis
- systemic autoimmune disease
-IgM directed against IgG
Septic Arthritis
-infected joints more common in children
-usually spread in blood
-staphyloccal in children
-Gonococcal in young adults
Gout
abnormality in metabolism of uric acid
- cause inflammatory response in joints
Intervetebral joints
amphiarthrodial joints
- no synovial fluid
- nucleus adjusts to different loads put on it (shock absorber)
-most common in lumbar spine
shooting pain --->> sciatica
Hyperventilation
reduced Co2
Hypoventilation
increased Co2
Hypoxemia
reduction of arterial PO2
ex...Hypoventilation : elevated alveolar PCO2 displaces alveolar O2 and hence, causes arterial hypoxemia
Most common mechanism causing hypoxemia
-low ventilation/ perfusion ratio
-venuous blood remains unoxygenated after contact with poorly ventilated alveoli
Right to left Shunt
venuous blood reaches the systemic circulation without contacting alveolar oxygen
How are the elastic properties of the lung usually described?
- plotting change in lung volume versus transpulmonary pressure
-slope= compliance of lung
Restrictive Lung disease
Total lung capacity is decreased ( restriction)
Restrictive Lung Disease:
Restriction secondary to parenchymal abnormal
ex fibrosis
TLC is reduced along with the rest of lung volumes including RV
Restrictive Lung Disease:

secondary to respiratory muscle weakness
TLC reduced with reduced inspiratory capacity, RV is increased because not inhaling or exhaling at a max
Key determinant of arterial PCO2
alveolar ventilation
Mucociliary blanket
lines airway epithelium
-composed of mucus type material that traps mid sized particles
*mucus moved outward by cilia
2-10 microns
alveolar macrophages
-non - specific/ immune defense mechanism
- most important phagocytic cell in the lung and serve to protect the lung from injuries by small particles(1-2 microns) and microorganisms
antioxidants
protect the lung against toxic injuries and pollutants and immunologlobins
Bronchiolitis
infections involving the peripheral airways
- mostly caused by viruses
- seen mostly in children
bronchitis
infection involving central airway
- mostly seen in adults
- caused by viruses and bacteria
Bronchial obstruction
pulmonary segment distal to the area of obstruction is susceptible to pneumonia, abscess formation and bronchic
otelectasis
completion of an obstruction that leads to a collapse of a lung tissue distal to the area of obstruction
- diagnosed by chest x ray
bronchiectasis
permanent irreversible dilation of the airway secondary to airway obstruction, infection, or cogenital abnormalities
pneumonia
an infection of the pulmonary parenchyma
- can be caused by bacteria , fungi, viruses, etc
community acquired pneumonia
occurs in persons outside the hospital
nosocomial pneumonia
occurs in patients who are already hospitalized and caused by organisms prevalent in hospital environments
opportunistic pneumonia
represents infections in patients with compromised immune status
What are most cases of community pneumonia caused by
streptococcus pneumoniae
Legionella Pneumonia
caused by legionella pneumophila
- can occur as a community or noscomial pneumonia
viral pneumonia
can be caused in immuno compromised hosts by varicella, measles, influenza
Fungal pneumonia
1. Infections acquired outside
2. Infections by ubiquitous organisms that afflict immune compromised hosts
Cause of nosocomial pneumonia
- gram negative organisms
- S. aureus, which is gram (+) organism
Opportunistic Pneumonia:
Pneumorystis Carinii Pneumonia
occurs in an immune compromised host ex...transplant chemotherapy, AIDS patients
Opportunistic Pneumonia:
Fungal Pneumonia
Invasive aspergillosis
occurs in patients with severe neutropenia and other immune compromised states
- invades pulmonary blood vessels
Cytomegalovirus
causes interstitial pneumonia in an immune compromised host
neoplasm/neoplasia
heritably altered, relatively autonomous growth of tissue
Implications of replicating fast
-genetic unstability
-not enough time to repair replicative errors
- could lead to more growth advantages of cell
Benign
slowly growing and do not spread to other tissues
- can still cause morbidity, and death
Malignant
- grow rapidly, have ability to spread beyond tissue of origin
Malignant tumor classification
- Carcinoma : cells arise from epithelium
-Sarcoma: cells arise from mesenchymal cells
Dyplastic
neoplastic cells stay within the tissues
-have features of malignancy and a high liklihood of behaving malignantly in the future
Invasion
requires that the malignant cells be able to degrade the surrounding tissue or stroma with proteolytic enzymes
Metalloproteinoses
attack the basement membrane to which epithelial cells are anchored
-------->>>epithelial layer is 1st layer that must be attacked in order to invade surrounding tissues
What proteinases attack extracellular matrix proteins in the tissues through which malignate cells migrate
Serine and Cysteine
Metastasis
non-continuous spread of malignant cells throughout the body
Ex------>>> colon cancer spreading to the brain
intravasation
growth of malignant cells through wall of blood vessel or lymphatic capillary
extravasation
tumor embolus adheres to vessel wall at distant site and migrate back out of it
angiogenesis
ability to establish own blood supply
somatic mutations
genes are altered during the lifetime of the individual and the mutations will affect only a subset of cells of the body
What leads to a malignant phenotype?
cummulative effect of genetic alterations
8 basic functions in cells corrupted in pathway to cancer:
1) Self -Sufficiency in growth cells
Proto-oncogene codes for growth factors, receptors
- oncogene- mutated and constitutively activated form of the proto-onco gene
-when the proteins involved in messaging are constantly in activating state, cells replicates more than normal
activating mutations
cause a proto oncogene to become an oncogene
- only takes mutation in 1 of 2 alleles
8 basic functions in cells corrupted in pathway to cancer:

2) Insensitivity to growth-inhibitory stimuli
tumor suppressor genes normally present in active state
- detect and repair DNA before cell can proliferate
-mutations can result in replication w/ altered DNA
- Becomes " fixed" in daughter cells
- both alleles have to be mutated for the regulatory function of tumor supressor genes to be lost
8 basic functions in cells corrupted in pathway to cancer:
3) Evasion of Apoptosis
prevent cell death
8 basic functions in cells corrupted in pathway to cancer:
4) defective DNA repair
-many DNA repair mechanisms in the nucleus that respond to and repair different kinds of damages
-when these cells do not function , the cell accumulates damage throughout the genome
8 basic functions in cells corrupted in pathway to cancer:
5) Limitless replicative potential
6) angiogenesis
7) invades and metastasis
8) evasion of immune system
5)cells / subclones can go through cell cycles indefinitely until host or organism dies
Iniation: time dependent
appearance of permanent DNA damage in a cell
------>>incurred by exposure to free radicals in the chemical.
------>>DNA damage done by a chemical carcinogen cannot be repaired
----->>must be induced to divide so damage becomes permanent/ fixed
promoters
agents that stimulate proliferation
- time dependent
progression
occurs when initiation and promoters stage happens in order and in a timely fashion
Tertiary prevention
treating diseases in its early stages
secondary prevention
management of risk factors
primary prevention
educating populations on risk factors
ARDS
Adult Respiratory Distress Syndrome
Clinical syndrome of rapidly progressive respiratory failure
- characterized by severe hypoxemia,
- usually requiring mechanical ventilation and featuring extensive radiologic treatments
DAD
Diffuse alveolardamage
non specific pattern of pulmonary parenchymal reaction to a variety of acute insults
--->>>ARDS counterpart
endothelial lung damage
results in a leakage of protein rich fluid from capillaries to alveolar space
epithelial lung damage
leads to a loss of epithelial basement membrane and of type I pneumocytes (flat epithelial cells that line the alveolar walls)
Alveolar Damage:
Exudative phase
develops over first week following an acute insult
-plasma protein exudation, accumulation of inflammatory cells and formation of hyoline membranes
- sloughing of Type I cells
Alveolar Damage: Organizing phase
Begin second week following the injury
-Marked by proliferation of Type II pneumocytes in the alveolar space and fibroblasts in the interstitium
Alveolar Damage: Resolution phase
Survival w resolution of diffuse alveolar damage or pulmonary fibrosis
COPD
-patients with a chronic bronchitis or emphysema
- decreased expiratory flows
Definition of chronic bronchitis
presence of chronic productive cough for greater than 3 months per year over a period of 2 years
pathology of Chronic Bronchitis
hyperplasia of mucus secreting cells
----thickening of bronchial wall by mucuous gland enlargement and edema
----increase in # of goblet cells
----increase in smooth muscle and excess mucus in airways
emphysema
enlargement of air spaces distal to termnal bronchioles with destruction of bronchial walls without significant fibrosis
pneumothorax
accumulations of air in pleural space
pleural effusion
accumulation of fluid in the pleural space
what are the key causes of ARDS
gastric aspiration, shock, trauma, sepsis
What is ARDS charcacterized by
respiratory failure, refractory hypoxemia, decreased pulmonary compliance, bilateral infiltrates on chest x rays
- increased mortality , so specific therapy
Causes of pleural effusion
high hydrostatic pressure ( congestive heart failure) or inflammation of the pleura
Sarcoidosis
chronic granulomatous interstitial lung disease of unknown etiology
-formation of non necrotic granulomas
Hypersensitiviy pneumonitis
pulmonary inflamation, secondary to immune reaction to inhaled organic dusts
pneumoconioses
group of interstitial pulmonary diseases causes by inhalation of organic dusts

ex. Silica asbestos, beryllium
-inhalation causes pulmonary inflamation which can be associated with granulomas and fibrosis
4 categories of carcinoma
-squamous cell
- Adenocarcinoma
- Large cell
- small cell