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182 Cards in this Set

  • Front
  • Back
infection
invade and cause damage to the host; disrupts normal body function
which disease inhibits dna, rna, or protein synthesis
poliovirus
which diseases insert into the hosts cell membrane and damage its integrity or promote cell fusion
HIV, measles, herpes
which diseases replicate efficiently and lyse host cells
rhinovirus, influenzavirus, yellow fever, polio, rabies
which diseases have viral proteins on the host cell's surface that may be recognized by the immune syst.
HBV, respiratory syncitial virus
which diseases can cause cell proliferation and transformation leading to cancer
EBV, HPV, HBV, HTLV-1
what structures bind bacteria to host cells
adhesins
which bacteria bind to CR3
legionella, m.tuberculosis, leishmania
mechanism- shigella and e.coli
inhibit host cell protein synth., replicate and lyse host cell
mechanism- salmonella and yersinia
replicate within phagolysosomes
mechanism- mycobacterium and legionella
inhibit the acidification that occurs after endosome fusion w/ lysosome
microorganisms escape the immune syst. by:
1)remaining inaccessible 2)cleaving Ab, resisting comp. mediated lysis 3) varying or shedding Ag 4) causing immunosuppresion
directly spread
neisseria gonorrheae
spread by droplets
influenza virus
spread by water
cryptosporidium parvum
spread by food
listeria monocytogenes
spread by soil
blastomyces dermatitidis
spread by fomites
HBV
spread transplacentally
cytomegalovirus
spread perinatally
HSV
spread by animal reservoir
rabies
spread by insect vector
plasmodium vivax
suppurative pmn inflammation
due to acute tissue damage; inc. vascular permeability and pmns(bc of chemoattractants and endotoxin); pus formation
spread by water
cryptosporidium parvum
spread by food
listeria monocytogenes
spread by soil
blastomyces dermatitidis
spread by fomites
HBV
spread transplacentally
cytomegalovirus
spread perinatally
HSV
spread by animal reservoir
rabies
spread by insect vector
plasmodium vivax
suppurative pmn inflammation
due to acute tissue damage; inc. vascular permeability and pmns(bc of chemoattractants and endotoxin); pus formation
adenoma
benign epithelial neoplasm producing gland patterns or a neoplasm derived from glands
chondroma
benign cartilaginous tumor
papilloma
benign, epithelial neoplasm that produces finger like fronds
fibroma
a benign tumor arising in fibrous tissue
sarcoma
malignant neoplasm derived from mesenchymal tissue
carcinoma
malignant neoplasm derived from epithelial tissue
adenocarcinoma
carcinoma in which the lesion begins to grow in gland patterns
teratoma
consists of more than one germ layer; well differentiated=benign, not well differentiated=malignant
mesothelioma
rare; mesothelial cells; usually in parietal or visceral pleura; related to asbestos in air
leiomyoma
benign; found in smooth muscle; often in uterine wall
rhabdomyosarcoma
malignant mesenchymal neoplasm that exhibits skeletal muscle differentiation; most common soft tissue sarcoma in child.
osteosarcoma
neoplastic cells produce osteoid; primary form: arise de novo, secondary form: arise as a complication of a known underlying process
seminoma
malignant testicular tumor arising from germ cell lines
hamartoma
an excessive but focal overgrowth of cells native to the organ in which it occurs
lymphoma
malignant lymphocytic neoplasm
choristoma
a heterotropic rest of cells left behind as embryonic structures form
dysplasia
disorderly but non-neoplastic proliferation
oncogenes
mutated forms of DNA, which no longer effectively regulate cell replication
proto-oncogenes
genes which encode products that regulate cell replication
oncoproteins
products of oncogenes which resemble normal products except they do not have important regulatory elements
promoters
non-carcinogenic chemicals that augment the actions of chemical carcinogens
classes of carcinogens
chemicals, radiant energy, and oncogenic viruses
Philadelphia chromosome
translocation that causes genetic damage, characteristic of chronic myeloid leukemia; chromosomes 9 and 22; the hybrid has potent tyrosine kinase activity
suppressor genes
aka antioncogenes; encode proteins that inhibit cell proliferation; related to knudson's 2 hit hypoth.
paraneoplastic syndrome
a symptom complex other than cachexia that appears in cancer patients and cannot readily be explained
benign neoplasms
well differentiated; usually progressive and slow growth; mitotic figures are rare and normal; do not invade surrounding tissue; no metastases
malignant neoplasms
some lack of differentiation w/ anaplasia; pleomorphic; erratic growth; mitotic figures numerous and abnormal; locally invasive; metastatic
3 pathways for metastasis
1) seeding-neoplasms invade a natural body cavity 2) lymphatic spread- usually carcinomas; lymph nodes and then blood 3)hematogenous- usually sarcomas; worst case; veins first; liver and and lungs most likely sites
renal cell carcinoma often invades
renal vein to inf. vena cava to right side of heart
prostatic carcinoma often invades
bones
bronchogenic carcinomas often invade
adrenals and brain
neuroblastomas often invade
liver and bones
top 3 cancers for men
prostate(31%), lung(14%), colon(11%)
top 3 cancers for women
breast(31%), lung and colon(12% each)
top cancer deaths for men
lung, prostate, colon
top cancer deaths for women
lung, breast, colon
3 classes of hereditary forms of cancer
1)inherited cancer syndromes(autosomal dominant) 2)familial cancers 3) syndromes of defective dna repair(autosomal recessive
preneoplastic disorders
1)persistent regenerative cell replication 2)hyperplastic and dysplastic proliferations 3)chronic atrophic gastritis 4) chronic ulcerative gastritis 5) leukoplakia of the the oral cavity, vulva, or penis 6) villous adenomas of the colon
cancers associated w/ smoking
lung, renal cell carcinoma, bladder tumors, oral, laryngeal, esophageal, pancreatic, and vulvular
3 classes of normal regulatory genes that are the target of genetic damage
1)growth promoting proto-oncogenes 2) growth inhibiting cancer suppressor genes 3) genes that regulate apoptosis
chemical carcinogens
can be direct acting(weak) or procarcinogens that are activated by promoters which turn them into ultimate carcinogens
radiation carcinogens
can cause chromosome breakage, translocations, and point mutations; latent period is very long
5 types of cancer that have been related to infections
HTLV-1, HPV, EBZ, HBV, HHV8
human t cell leukemia virus type 1
RNA retrovirus; targets CD4 t cells; stim. production of t cells by the TAX gene that encodes IL2; there is also inc. prod. of GM-CSF
human papilloma virus
causes benign squamous papillomas and may cause sq.cell carcinomas of the cervix(also anal, perianal, vulvar and penile cancers); related to products of viral genes E6 and E7
Epstein-Barr virus
can cause Burkitts lymphoma, lymphomas in AIDS patients, a subset of Hodgkins lymphoma, and nasopharyngeal carcinoma(only non Bcell tumor); EBV encoded gene LMP-1 sends signals that mimic CD40
hepatitis b virus
linked to liver cancer, mech. unknown
human herpes virus 8
assoc.w/ rare group of tumors present as malignant effusions; usually immunosuppressed
anti-tumor effects within our immune system
1)CD8-specific sensitivity 2) NK cells-possible 1st line of defense 3) macrophages-TNF 4)humoral mechanisms
4 ways cancers evade the immune syst.
1) selective outgrowth of Ag variants 2)loss of histocompatibility Ags 3)lack of co-stimulation 4)immunosuppression
tumor grade
based on level of differentiation and the # of mitoses
tumor stage
more important for prognosis; based on size of lesion and extent of spread
frozen section diagnosis
allows evaluation w/in minutes; examine margins of excised tumor
flow cytometry
leukemias and lymphomas; fluorescent ab against cell surface molec. are used to obtain the phenotype of malignant cells
immunohistochemistry
detects cytokeratin to diagnose an undiff. carcinoma rather than a large cell lymphoma
colonization
bacterial population that doesnt elicit an immune response or harm the host
papanicolaou smear
neoplastic cells shed into fluids and secretions; fluids are smeared and evaluated
molecular profiling
two tissue samples of mRNA are extractedand cDNA copies are synthesized in vitro w/ fluorescently labeled nucleotides and they are analyzed
mononuclear inflammation
acute response to intracellular parasites(bacteria,viruses,spirochetes,helminthes); predominant cell type depends on host response
cytopathic-cytoproliferative inflammation
little inflamm.response; usually caused by viruses and have inclusion bodies and giant cells
necrotizing inflamm.
rapid and severe inflamm. results in cell death; usually b/c of bacterial toxins
chronic inflamm. and scarring
ex. cirrhosis, gummas
carbuncle
localized bacterial infect. of skin and subcutan. tissue; several openings discharging pus
furuncle
circumscribed pus-filled inflamm. of skin and subcutan. tissue often b/c of staph. infec.
abscess
focal collections of pus caused by deep seeding of pyogenic organisms or by 2ndary infect of necrotic foci; have central necrotic region surrounded by PMNs surrounded by an area of early repair
empyema
pus in a body cavity
cellulitis
spreading inflamm. of subcut. or CT
exotoxins
protein produced by gram + and -; secreted by living organisms; located in cytoplasm; ex. cholera , diphtheria,tetanus
endotoxins
LPS produced by gram -; released through autolysis of dead organisms; located on outer membrane of cell envelope;ex.septic shock,meningococcus
endotoxic shock
lps binds to lps binding protein and the complex binds to WBCs which activates the cytokine cascade in high doses causes liver,kidney,and CNS failure
inhbit host cell dna, rna, or protein synth.
poliovirus
insert into host's plasma membrane
hiv, measles, herpes
replicate efficiently and lyse host cells
rhinovirus, influenza
lymphocytes attack the virus infected cells
HBV, resp. syncytial virus
viruses that can lead to cancer
ebv,hpv,hbv,human t cell lymphotropic virus
pmn inflammation
bacterial infections- chemoattractants and endotoxins released; pus formation
mononuclear inflammation
bacterial-indicates intracellular invasion(ex.plasma cells in syphilis& granulomas); viral-lymphocytes
cytopathic-cytoproliferative inflammation
viral-little inflamm.response; inclusion bodies, polykaryons, can cause cell proliferation
necrotizing inflamm.
bacterial-strong toxins; viral-ex. HBV and liver destruction
chronic inflamm.
bacterial-ex. chronic gonnococcsl salpingitis; viral-ex. HBV-cirrhosis
virus
obligate intracellular;contains DNA or RNA w/in capsid
prions
composed of a modified host protein(PrPSc);lack RNA and DNA
prion diseases
known as transmissible spongiform encephalopathies; can be infectious or inherited; ex bovine spong. enceph., creutzfeld jakob dz
interferons
produced naturally; part of innate immunity; destroy viruses by 1)inhibiting viral translation 2)prevent viral replication 3) enhance T and NK cells
4 methods by which fungal infections are spread
1.resp.inhalation 2.cutaneous inoculation 3.systemic invasion by opportunists 4.contact w/ infected host
yeast
larger than bacteria, budding organisms, stain gram +, carb rich cell wall
mold
look like common bread mold, produce spores
thermally dimorphic species
blastomyces and histoplasma
4 mech. by which aspergillus cause dz
1. allergic to spores 2.colonization(fungus ball) 3. invasive systemic infec. in debilitated hosts 4. aflatoxin
histopathological response to candida
acute pyogenic abscess
h.p. response to histoplasma
chronic granuloma
...dermatophytes
chronic,localized dermal infiltration
...blastomyces
mixed pyogenic and granuloma rxn
...mucor
blood vessel invasion w/ thrombosis and infarction
...aspergillus
hypersensitivity w/out tissue rxn
4 ways parasites produce dz
1.kill hosts by multiplying in them(taxoplasma gondii) 2.eat host cells(ancylostoma duodenale) 3.take up space in host(taenia solium) 4.induce destructive immune response(schistosoma mansoni)
opportunistic fungi
histoplasma, candida, aspergillus, cryptococcus
role of smooth muscle cells in atherosclerosis
phagocytize the excess lipids; produce fibrous CT to form a fibrous cap over lesion
role of platelets
release paracrine type growth factors which stim inflamm cells; release ADP which stim. clotting cascade
major clinical consequences of atherosclerosis
MI, cerebral infarct, aortic aneurysms, periph. vascular dz, chronic ischemic heart dz
unchangeable risk factors for heart dz
inc age, male, family history,genetics
changeable risk factors
hyperlipidemia, hypertension, smoking, diabetes
hepatitis A virus
icosahedral capsid,ssRNA, picornavirus,fecal oral trans., 2-6wks incub.,rarely fulminant
hepatitis B
enveloped dsDNA,hepadnavirus serum hep.,4-26 wks incub., <1% fulminant, <1% carriers, 90-95% chronic, can cause cancer
hep.C
enveloped ssRNA, flavivirus, parenteral trans., 2-26 wks incub.,rare fulminant, <1%carriers, >70%chronic, can cause cancer
hep D
enveloped ssRNA, parenteral trans., 4-7wks incub., fulminant-3-4% in co and 7-10% in super, chronic- <5% in co 80% with super
hep E
unenveloped ssRNA, caliciviridae, waterborne or fecal oral trans., 40%seroprevelence in india, 2-8 wks incub., 20% fulminant in preg. women
hepatitis carrier state
no apparent dz or subclinical chronic hepatitis
asymptomatic infection
serological evidence only
acute hepatitis
preicteric-nonspecific symptoms; icteric- cholestasis, jaundice
fulminant hep.
massive hepatic necrosis
chronic hepatitis
continuing or relapsing for more than six months; w/ or w/out progression to necrosis; common in HCV
jaundice
caused by hepatocyte damage; occurs during symptomatic icteric phase; due to conjugated hyperbilirubinemia
4 phases of acute viral hepatitis
incubation, symptomatic preicteric, symptomatic icteric, convalescence
diagnosis of HAV
cant be cultured in vitro; presence of HAV-specific IgM in blood
diagnosis of HBV by viral Ag
HBsAg(means virus is replicating in liver), HBeAg (high levels of rep. occurring), HBcAg(not found in blood)
diagnosis of HBV by Ab response
antiHBs(detectable late in convalesc.,indicates immunity), antiHBe(detectable as replication falls, indicates low infectivity), core IgM(rises early in infection, indicates recent infect.), core IgG(rises soon after IgM, present for life
diagnosis of HCV
HCV specific IgGindicates exposure not infectivity; PCR detects viral genome in serum
HBsAg
present before onset of symptoms; peaks during onset overt dz; envelope glycoprotein; immunogenic
HBeAg
present before onset of symptoms; peaks during onset overt dz; nucleocapsid core protein; immunogenic; indicates active replication,infectivity, and probable progression to chronic hep
HBcAg
present before onset of symptoms; peaks during onset overt dz; Hep B core Ag; retained in infected hepatocyte
anti-HBc IgM
present before onset of symp.; slowly replaced w/ anti-HBc IgG prioir to convalescence
anti-HB IgG
present once acute dz is over; peaks during recovery phase and may persist through life; basis for vacc.
anti-HBc IgG
present once acute dz is over; peaks during recovery phase; replaces anti-HBc IgM
likelihood of the potential clinical outcomes of HBV
65% subclinical, 25% acute(1% fulminant),10% healthy carrier, 4% persistent(10-30% chronic)
morph. acute hepatitis
diffuse swelling, cholestasis, ground glass hepatocytes,inflamm. present
morph. chronic hepatitis
also has hepatocyte injury, necrosis, and regeneration;smoldering hepatocyte necrosis, liver arch. well preserved,scar tissue(cirrhosis)
rocky mountain spotted fever
rickettsia rickettsii; rash over entire body,petechia, acute necrosis,dec fibrin, and thrombosis, vasculitis; tick trans
infections that can be observed using H&E stain
CMV and herpes(inclusion bodies), bacterial clumps, candida and mucor, most protozoans, all helminthes
...gram stain
most bacteria
...acid fast stain
mycobacterium, nocardia
...silver stain
fungi, legionella, pneumocystis
...periodic acid-schiff
fungi, amoeba
...mucicarmine
cryptococci
...giemsa stain
campylobacter, leishmania, malaria plasmodium
...Ab probes
viruses and rickettsia
...PCR
slow growing in culture(CMV or mycobacterium) or cant be cultured(HBV and HCV)
...DNA sequence analysis
bacteria that have never been cultured (tropheryma whippelii, hepatic peliosis, and bacillary angiomatosis
bacterial diagnosis methods
gram stain,KOH,stool exam, darkfield, PAS stain, GMS stain, silver stain,culture, serology, PCR, Ag detection, skin testing
viral diagnosis methods
PCR, viral load, tissue culture, serology
albumin
most abundant plasma protein (3-5%), made in liver, 1/2 life 15-19 days, maintains colloid osmotic press. and acts as a buffer
which conditions would have a low total protein on SPE
burns, malnutrition, malabsorption, hemmhorrage
SPE for MI
dec albumin; inc alpha globulins(AAT and Hp)
albumin
most abundant plasma protein (3-5%), made in liver, 1/2 life 15-19 days, maintains colloid osmotic press. and acts as a buffer
3 main components of acute inflammation
1.inc. vascular permeability 2.vasodilation 3.PMN emigration
3 main components of chronic inflammation
1.infiltration of mononuclear cells 2.tissue destruction 3.attempted repair
albumin
most abundant plasma protein (3-5%), made in liver, 1/2 life 15-19 days, maintains colloid osmotic press. and acts as a buffer
which conditions would have a low total protein on SPE
burns, malnutrition, malabsorption, hemmhorrage
Wilson's disease
1:30,000; appears after age 8; if untreted fatal before 30;caused by accumulation of copper in liver; diagnosed by Kayser- fleischar rings, dec ceruloplasmin
SPE for MI
dec albumin; inc alpha globulins(AAT and Hp)