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151 Cards in this Set

  • Front
  • Back
Myeloid stem cells
in bone marrow- differentiate into red cells, neutrophils or megakaryoctyes.
Differentiation controlled by proteins
Erythropoietin
made in kidney, boosts red cell production
G-CSF
boosts granulocyte production
Hgb/Hct
Hgb- amount of oxygen carrying protein
Hct- fraction of blood volume occupied by RBCs
Leukocytes
WBCs
Neutrophils- phagocyte
lymphocytes- make antibodies
monocyte, eosinophil, basophil
T cells
regulate immune system
from bone marrow, thymus, lymph nodes
B cells
antibody production
from bone marrow, lymph nodes, spleen
NK cells
neither T nor B
kill infected cells
Monocyte/macrophage
phagocytose, produce cytokines
macrophage in tissue, monocyte in blood
lymph nodes
spleen=lymphoid organ
allow coordination of various immune cells
Anemia
reduction in total circulating red cells (low hgb and hct)
fatigue, dyspnea, chest pain, tachycardia, pallor
Aplastic anemia
decreased number stem cells, macrocytic or normocytic
cause- cytotoxins, radiation, infection, autoimmune
Anemia of inflammation
iron held in macrophages not released to red cells
Iron deficiency anemia
most common cause
microcytic, hypochromic
from blood loss, pregnancy, poor diet
Vitamin B-12 deficient anemia
Pernicious anemia
megalobastic
often due to stomach disorder
Thalassemia
inherited disorder of hemoglobin production
microcytic
major requires RBC transfusions
Hemolytic anemia
increased rate of RBC production, increased reticulocytes
high bilirubin- jaundice
Sickle cell anemia
recessive inherited structural abnormality of hemoglobin-- polymerization of hemoglobin
Autoimmune hemolytic anemia
production of antibodies against
detected by coombs test
treat w immunosupressants or splenectomy
Polycythemia
too many RBCs, blood is thick
vera/primary- myeloproliferative disorder- mutation in marrow
secondary- increased erythropoietin d/t low O2
Neutropenia
decreased neutrophils
decreased production- marrow failure or chemo
increased consumption- autoimmune, infection, enlarged spleen
Neutrophilia
increased production d/t infection
d/t demargination- unstick from vessel walls
Leukemia
cancerous proliferation of leukocyte production
acute- proliferation of immature cells (blasts)- rapid
chronic- proliferation of mature cells- slow
Manifestations of leukemia
marrow failure, accumulation in blood, accumulation in other tissues, release of toxins from leukemic cells
Acute lymphoblastic/lymphocytic leukemia
rapidly growing B or T cell blasts
most common cancer in children
often curable
Acute myelogenous leukemia
proliferation of immature granulocyte blasts
most common leukemia in adults
treatable, occasionally curable
Chronic myelogenous leukemia
proliferation of myeloid stem cells- overproduction of WBCs and platelets
treatable/curable
"philadelphia chromosome" mutation
Chronic lymphocytic leukemia
slow growing b-cell mature appearing cells
primarily in older adults
treatable but not curable
Lymphoma
proliferation of lymphocytes
behave as solid tumors
Non-Hodgkins lymphomas
low grade- slow growing but mature appearing cells, incurable but live long
high grade- faster growing less mature cells, potentially curable but aggressive
Hodgkins disease
Reed-sternberg cells (large, multinucleated)
One of the most common cancers in teens
predictable progression
most patients cured
Multiple myeloma
plasma (antibody producing) cell
secrete monoclonal immunoglobulin
causes bone destruction
not curable
Symbiosis
host and organism both benefit
Commensalism
organism doesn't really help or hurt the host
Saprophytic
organisms living off dead/decaying matter
Parasitism
organism inteferes with host function
pathogenic-- disease causing
virulent- poisonous
Barriers to infection
mechanical (skin)
secretions
epithelial (exfoliation)
chemical (pH)
microbial (normal flora compete with bad bugs)
Antibody mediated immunity
B cells
immunoglobulin binds to antigens
Cell mediated immunity
T cells
secrete substances to attract macrophages
Toxins
produced by organism or released when the organism is destroyed by the body
some organisms not toxic but damage is caused by body's effort to get rid of them
Candida albicans
fungal opportunistic pathogen
Spreading factors
produced by organisms and help breakdown tissues to allow organisms to spread
Transmission methods
fomites
food
fingers
flies
feces
Bacteria
prokaryotes
capsules can make them harder to kill
Anaerobic- no oxygen
Cross antigenicity
antibodies look like antigens normally in the body
Immune complex formation
causes inflammation
Bacteremia
viable bacteria in the blood
Septicemia
presence of pus forming organisms, pathogens and their toxins in the blood
Sepsis
systemic disease of organisms/toxins in blood
Gram + cocci
Staphylococcus
Streptococcus- beta is most dangerous
Streptococcus pyogenes
the only group A- causes strep, impetigo and endocarditis
Streptococcus pneumoniae
causes pneumonia and meningitis
capsule encased
Neisseria meningitidis
gram - cocci
causes fatal spinal meningitis
Gram - bacilli
E. coli
Shingella
Tuberculosis
acid fast bacteria
ingested by neutrophils but bacteria live and neutrophil dies
Superinfection
destroys the barrier, giving other parasites opportunity to cause infection
Rotavirus
most frequent cause of viral gastroenteritis
Viruses
obligate intracellular parasites
RNA or DNA
lyse of bud off of host cell
Yeasts
unicellular
reproduce via budding
Molds
long branching tubular cells
Cutaneous fungi
ringworm, athletes foot, jock itch
Candida albicans (monilia)
fungi
normal flora, can cause thrush and vaginitis
Aspergillosis
mold
common opportunistic pulmonary infections
Protozoa
unicellular eukaryotes
uncommon pathogenically in the US
Amebiasis
caused by entamoeba histolytica
usually in colon (diarrhea) but can spread
Malaria
replication in and rupture of RBCs
Worms (helminths)
roundworms, tape worms
infestation associated with high eosinophil count
Enterobiasis
pinworm
cause inflammation and itching on perianal skin
Neoplasias have relative autonomy
grow with little regard for host but still somewhat dependent
Benign neoplasms
slow growing, don't spread
can still cause morbidity by exerting local effects, producing hormones, causing pain or inducing bleeding
Malignant neoplasms
grow rapidly, spread beyond origin (invasion and metastasis)
carcinoma- in epithelium
sarcoma- from mesenchymal cells
Invasion
contiguous growth beyond their site of origin
requires malignant cells to be broken down by protolytic enzymes
Dysplasia
neoplastic cells that stay within tissue of origin but have features of malignancy
Metastasis
non-contiguous spread of neoplastic cells
invasion
intravasation
intravascular circulation
extravasation
grow in new location
angiogenesis
Differentiation
degree of resemblance of neoplasm tissue to tissue of origin
Anaplastic- no differentiation, high grade
Benign
non-invasive
encapsulated
no metastasis
normal N:C ratio
Malignant
invasive
metastatic
rapid growth
anaplastic
high N:C ratio
Stage determined by:
TNM
tumor (size, characteristics)
nodes (extension to)
metastases (presence of)
Cancer is a disease of genes
if germ cells are altered, affect all cells in body from birth
if altered during lifetime, affect subset of cells
Cancer is clonal
population of malignant cells is ultimately derived from a single mutated cell
Carcinogenesis is a multistep process
takes multiple mutations
8 basic functions in cells commonly disrupted by cancer
self sufficiency in growth signals
insensitivity to growth-inhibitory signals
evasion of apoptosis
defective DNA repair
limitless replicative potential
Self-sufficiency in growth signals
oncogene- mutated gene encoding growth factors-- activating mutation (only takes 1)
Insensitivity to growth-inhibitory stimuli
p53= most commonly mutated tumor suppressor gene (both alleles need to be mutated)
Evasion of apoptosis
BCL-2- anti apoptotic
4 causes of original mutation
familial
chemical
radiation
microbes
Chemical exposure
initiation- appearance of permanent damage
promoter stimulates proliferation
further accumulation (progression)
Cause of death
injury or disease producing physiological derangements in the body resulting in death
Mechanism of death
the actual physiological derangement that results in death
Manner of death
the circumstances surrounding the death (SHAUN)
suicide, homicide, accident, undetermined, natural
Cocaine death
benzoylecgonine indicates recent use
cocaethylene= cocaine+ethanol
Opioid death
pulmonary edema
foam cone
respiratory depression
Heroin death
monoacetylmorphine (6-MAM) indicates recent heroine use
Alcohol death
oxylate crystalizes in the kidneys
hepatic steatosis
cirrhosis
Vitreous humor
vitreous humor lags 2 hours behind blood, so can judge stage of alcohol intake
Carbon monoxide death
saturates hemoglobin so O2 cant bind- 50% sat is lethal
causes cherry red color (CO, cyanide, cold)
Judging time of death
algor mortis (cooling- within 12 hrs)
rigor mortis (12s- stiffens, fixed, relaxes)
livor mortis (blood settles and becomes fixed)
Osteoblasts
synthesize bone
Osteocytes
bone cells
Osteoclasts
reabsorb bone
multinucleated
Collagen
type 1 in bone and ligaments
type 2 in articular cartilage
Endochondral ossification
bone formation in long bones
cartilage mineralizes to become bone
Osteomalacia
defect in mineralization of bone d/t vitamin D deficiency
Osteoporosis
absolute decrease in bone mass
no serological changes
exercise for treatment
Process of fractures
Inflammatory phase
Reparative phase (callus)
Remodeling phase
Comminuted (high energy) fractures
multiple bone fragments
blood supply to bone disrupted
Osteomyelitis
infection of bone
hematogenous spread or direct inoculation
Osteosarcoma
neoplastic bone disease of children
highly malignant tumor that produces bone
Ewing sarcoma
malignant tumor of primitive mesenchymal cells in kids
systemic symptoms
Multiple myeloma
most common primary bone tumor in adults
disease of abnormal plasma cell production
Metastatic bone diseases
more common than primary bone tumors
stabilization to prevent pathologic fractures
Joint types
synoarthroses- no motion
amphiarthroses- little motion
diarthroses- most common, most mobile
Articular cartilage
made of type 2 collage
fibers parallel to axis of motion except deepest layer
Synovial tissue
lines diarthrodial joints
very vascular
Osteoarthritis
"wear and tear"
most common arthritis
normal ligaments- cartilage worn away
Rheumatoid arthritis
systemic autoimmune disease
primarily a disease of the synovium
Septic arthritis
more common in children
release inflammatory mediators which destroy cartilage
Gout
abnormal metabolism of uric acid
crystalizes in joints
Herniated disk
nucleus ruptures through annulus
Hyperventilation
low PaCO2
stimulate breathing
Hypoventilation
high PaCO2
Hypoxemia
caused by low inspired O2, impaired diffusion, hypoventilation, low V/Q (ventilation/perfusion ration- most common)
Hyperinflation
increased lung compliance
easy to inflate but bad recoil
Restriction
hard to inflate but recoil easily
Restrictive lung disease
decreased total lung capacity
secondary to parenchymal abnormality (decreased RV)
secondary to respiratory weakness (RV increased)
Airflow obstruction
best evaluated by FEV1/FVC
narrowing of airway lumen
dynamic airway narrowing
Pulmonary hypertension
acute in pulmonary embolism
chronic from lung disease or heart disease
Airway barriers
nose traps large
cillia traps medium
macrophages trap small
neutrophils against bacteria and fungi
anti-oxidants against gasses/pollutants
Bronchiolitis
infection of peripheral airway
viral
common in kids
Bronchitis
infection of central airway
viral or bacterial
common in adults
Bronchial obstruction
tumor, foreign body, secretions
Bronchiectasis
permanent dilation of airway secondary to destruction of elastin and muscle
Pneumonia
infection of lung tissue
inflammation
red hepatization
gray hepatization
resolution
Community acquired pneumonia
commonly bacterial
Nosocomial pneumonia
caused by gram - organisms or staph aureus
Opportunistic pneumonia
Pneumocystic carinni
Aspergillosis
Cytomegalovirus
Lung abscesses
local accumulation of pus
caused by aspiration
complicated by hemoptysis or empyema
Adult respiratory distress syndrome (ARDS)
rapid respiratory failure in in previously healthy patient
exudative phase, organizing phase, resolution
Diffuse alveolar damage (DAD)
non-specific pulmonary reaction to acute insults- counterpart of ARDS
COPD
non reversible decreased expiratory flows on PFTs
chronic bronchitis- chronic productive cough for 3 months
emphysema- enlarged airspaces w/o significant fibrosis (a1-anti-trypsin)
Asthma
reversible airway obstruction caused by increased airway responsiveness
Pneumothorax
accumulation of air in pleural space
Pleural effusion
accumulation of fluid in pleural space d/t increased pressure or inflammation
Idiopathic pulmonary fibrosis
fibrotic interstitial lung disease
Usual Interstitial Pneumonia- extensive fibrosis and abnormalities
Desquamative interstitial pneumonia- milder, minimal fibrosis, inflammation with macrophages
Sarcoidosis
chronic granulomatous interstitial lung disease
Hypersensitivity pneumonitis
pulmonary inflammation secondary to immune reaction to organic dusts
Pneumoconioses
disease caused by inhalation of inorganic dusts
Silicosis
silicone from sand blasting cause inflammation and fibrosis
increased risk for TB
Asbestosis
causes fibrosis that is apparently 20-30 years after exposure
can cause mesothelioma (lethal cancer) or bronchogenic carcinoma
Small cell carcinoma
highly malignant that is commonly metastatic
Non-small cell carcinoma
more localized and metastasize gradually usually surgically removed