Unit Test 1 Flashcards
Agranulocytes
Monocytes/Macrophages
Lymphocytes, T-cells, B-cells, NKC
Macrophages that live in connective tissue
Langerhan cells
Cells that secrete mucous in nose and upper respiratory tract
Goblet cells
Complement system
> 20 plasma proteins made by Liver (C1-C9)
Bind to microbial invaders
Form membrane attack complex
Attract phagocytosis cells (macrophages)
Neutrophils
1st responders
Most abundant
Fungal, bacterial infections
Eosinophils
Destroy parasitic worms
Elevated in allergic reactions(secrete histaminases)
Basophils
Secrete histamine
Similar to mast cells
Receptors for IgE antibodies
Monocytes/Macrophages
Phagocytosis
Act as antigen presenting cells (take to T helper cells)
Arrive after neutrophils
Natural Killer Cells
Part of innate
Recognize and kill tumor cells, cells infected with virus
As oppose to free floating pathogens
Lymphocytes
T and B cells (acquired immunity)
NKC (innate)
Most active in viral and chronic infections
CD4 T helper cells
Recognize pathogen, secretes cytokines
Activates B cell and macrophages
CD8 T killer
Cell mediated immunity
Similar to NKC but acquired
Eliminates intracellular pathogens such as virus by destroying cell
T-suppressor cells
Suppress immune response
Possibly not working in autoimmune
B Lymphocytes
Humoral (antibody-mediated) immunity
T helper cells instruct B cell to differentiate into plasma cell and produce antibodies
IgM
First responder
Acute problem, current infection
IgG
Produced after IgM, well designed for pathogen
Lifelong immunity
Cross placenta, don’t last but help for 6 mo
IgA
Mucosal secretions: saliva, breast milk
IgE
Mediates inflammatory, allergic, parasitic response
Binds to and activates MAST cells
IgD
Not in blood stream, membrane bound to B cells
Granulocytes
Neutrophils, Eosinophils, Basophils
5 signs of inflammation
Heat Swelling Redness Pain Loss of function
Causes of atrophy
Disuse, dennervation, inadequate nutrition, loss of endocrine stimulation, ischemia
Hyperplasia
Increase in number of cells Physiological -hormonal: increase in breast tissue -compensatory: wound healing Pathological -often hormonal, benign prostatic hyperplasia
Metaplasia
Change from one mature, well differentiated cell type into another
Often result of chronic inflammation
Dysplasia
Immature/undifferentiated cells replace mature cells
Result of chronic inflammation
Often precursor to cancer
Apoptosis
Programmed cell death
Does not activate immune response
No cell debris
Necrosis
Unregulated digestion of cell
Activates immune response
Products of cell death released into extra cellular space
Large area=gangrene
Dry gangrene
Interference with arterial blood supply to area
Line of demarcation
Area becomes dry, shrinks, and wrinkle
Slow progression
Wet gangrene
Interference with venous return Area becomes swollen Susceptible to bacteria infection Must amputate No line of demarcation
4 steps of acute inflammation
- damaged tissues secrete cytokines>cause cells to produce cell adhesion molecules>damaged mast cells secrete histamine
- histamine causes quick transit constriction>dilation>capillaries become more leaky
- immune cells enter tissue
- platelets seal wound
Hallmarks acute inflammation
rapid, transient response to injury
generally beneficial
predominance of neutrophils followed by macrophages
Hallmarks of chronic inflammation
self perpetuating(inflammation itself causes tissue damage) predominance of macrophages and lymphocytes proliferation of blood vessels damaging: tissue destruction, fibrosis (scar tissue), loss of organ function, calcification
Dystrophic Calcification
deposition of calcium salts in injured tissue
Ca comes from surrounding dead cells, blood, interstitial fluid
athlerosclerosis, hardening of arteries
Metastatic Calcification
deposits of Ca occur in normal tissue due to high serum Ca
kidney stones
Type I Hypersensitivity
Allergy
requires sensitization
involve IgE bond to mast cells and basophils
antigen binding triggers histamine release
Type II
antigen = fixed & intrinsic to tissue where reaction occurs
IgG and IgM
eg autoimmune, blood transfusion, tissue transplant
Type III
antibody, antigen complexes
free exogenous or endogenous antigen
IgG, IgM
eg strep complexes get stuck in KD
Type IV
Not antibody mediated
eg TB, CD8 try to kill infected macrophages, tissue in surrounding area ends up getting damaged
hypertrophy
increase in cellular size
from increased work load
physiological or pathological
skeletal and cardiac tissue(high BP)
Prion
protein without genome B sheath shape cellular proteins that we can't break down accumulate in the brain eg BSE-mad cow no treatment
virus
DNA or RNA, NOT BOTH surrounded by protein coat
eg polio
Bacteria
prokaryotic
both RNA and DNA
cell wall made of peptidoglycan (targeted by antibiotics)
Bacteria naming by growth pattern
Strepto- chains
Diplo- pairs
Staphylo- clusters
Bacteria by shape
- cocci: round
- bacilli: rod shaped
- vibrio: curved like boomerang
- spirilla: spiral
Diptheria
corynebacterium diphtheria spread by water droplet
binds to cells of respiratory tract and releases exotoxin that leads to cell death
layer of dead tissue develops in upper respiratory tract
Tetanus
Clostridium tetani (bacteria found in soil, dust, animal feces
exotoxin blocks inhibitory neurotransmitter release from spinal cord
spastic paralysis, “lock jaw”
Lyme Disease
Borrellia Burgdorferi (bacteria transmitted via tick bite) antigen/antibody complexes get lodged in vessels, nerves, joints classic lesion: bulls eye cardias, neuro, arthritic problems
Impetigo
caused by staph or strep infection
common in kids
red sores on face, honey crusted lesions, itchy
fungus
eukaryotic cell walls made of chitin cell membrane made of ergosterol (targeted by antifungals) yeasts=unicellular, ie Candida molds=multicellar
Tinea or ring worm
superficial fungal infection
Parasites
3 types
- Protozoa: eukaryotic, unicellular, human to human contact, i.e. malaria
- Helminths: wormlike, ie roundworms, tape worms
- Arthropods: ticks, mosquitos, lice, fleas, mites
Incubation Period
pathogen is replicating b4 sx appear
5 infectious disease stages
incubation
prodrome: vague sense of not feeling well
acute stage: max impact
convalescent stage: containment, repair
resolution stage: elimination of pathogen if possible,
HIV/AIDS
retrovirus(RNA)
bodily secretion
attacks anything with CD4 marker: T helper cells and macrophage/monocytes
HIV enzymes
Reverse transcriptase
Integrase
Protease
HIV proteins
p24: used for testing, our body makes antibodies to this
GP 120: attachment, binds to CD4 marker
GP41: helps fuse membranes
Seroconversion
enough antibodies to be detectable in HIV test, nothing to do with sx
window period
time btw infection and seroconversion
incubation period
time btw infection and sx
HIV progression
acute flu like infection 1-4wk after infection
latent period: 5-10yrs
overt AIDS: opportunistic infections, ie pnuemonia
Oral-Fecal Hepatitis
HAV, HEV
Blood Borne Hepatitis
B, C, D
HAV
abrupt onset, self-limiting, doesn’t become chronic
incubation: 15-50 days
vaccine available but not heavily pushed
HBV
blood born, very contagious
can become chronic and lead to cirrhosis
vaccine available
incubation: 45-160 days
HCV
blood to blood (IV)
chronic right off the bat, 85% develop cirrhosis
no vaccine
incubation: 14-180days
HDV
need HBV to develop
common in IV drug users
HEV
no chronic state
mostly in developing nation
mechanisms of tumor development
increase proto-oncogenes, decrease tumor suppressor genes
abnormality in apoptosis
dont respond to cell density limitations
telomerase re-elongates telomeres
benign neoplasia
well differentiated, slow dividing, non-invasive, enclosed in fibrous capsule
malignant cells
undifferentiated, rapidly dividing, no fibrous capsule, invade surrounding tissues, metastasis via blood and lymph
General sx, red flags of cancer
explained deep body pain, weightloss, fatigue, unexplained bleedin
naming benign tumors
-oma
ie osteoma, adenoma
naming cancerous tumors
ie adenocarcinoma, sarcoma
metastasis
spread via blood and lymph systems leading to secondary tumors
Paraneoplastic syndromes
disease or sx beyond actual tumor site due to: hormones secreted by tumor cytokines released in response to tumor production of clotting factors neurotransmitter interference
