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