Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
28 Cards in this Set
- Front
- Back
|
Impetigo
-type of infection caused by? -clinical manifestation -affects people with -Dx -Tx |
-superfical infection caused by S. Aureus or pyogenes, MRSA, and most of the time breaks in surface of skin form dermatitis-->normal flora invasion into the skin
-superficial breaks in skin, vesicles-->lare bullae or ulcerated/crusted -children/adults, immunocompromsied with systemic conditions -clinical presentations & history: pattern corresponds to scratches/breaks in skin -Tx: prevention-clean wounds and topical antibiotics(self limitin) |
|
|
Pharyngitis/tonsillitis viral
infections located where, leading to what? caused by? kind of infection? tx? |
- swollen tonsils, eryhtema of pharyneal wall with white coating, sore throat
-infections in the throat leading to infection - respiratory droplet or oral secretions - majority are viral -no Tx self-limiting |
|
|
Streptococcus:
Pharynitis/Tonsillitis: -Bacterial infection? -how common is this? -occurs mostly in? - clinicial sx - Dx -Tx |
-Group A B-hemolytic streptococcus(GAS)
-10-30% - Young children(5-15) and their parents -sore throat redness of the oropharynx and tonsil, cervical lymphadenopathy, fever..NO Vesicles-other conditions cause vesicles to erupt) -rapid direct antigen test(5-10 minutes), culture(gold standard 1-2 days) -antibiotics prevents development of complications |
|
|
Streptococcus:
Scarlet Fever -type of infection, pathogenesis -develop in which kind of patients -clinical sx: -lab studies -Tx |
-bacterial-via systemic, ERYHTROGENIC TOXIN- which attack small blood vessels
- patients with no antitoxin antibody, mostly in children. High Fever. -Exanthem: -skin: widespread rash and petechiae -fades in a week and is followed by desquamation -Enanthem -oral cavity: pharyngitis/tonsillitis, may have soft palate petechiae -tongue: hyperplastic, eryhtematous fungiform papillae against a white backround(whitestrawberry tongue) or a red background(red strawberry tongue) -Lab studies: rapid direct antigen test, culture -antibiotics |
|
|
Streptococcus:
-complications |
-autoimmune diseases: rheumatoid fever, glomerulonephritis
-antibody against M-protein cross-react with antigens present in host tissue(autoimmune). damage other tissues -patients with positive history of RF, post-therapeutic lab testing recommended after streptococcus infection |
|
|
Myobacteria types:
|
Tuberculosis: Mycobacterium tuberculosis
Leprosy: Myobacterium leprae |
|
|
Tuberculosis:
Bacteria: characteristics of bacteria: treatment? type of disease? single most important risk factor for development? often occurs in |
-Mycobacterium tuberculosis
-high lipid content in cell wall making it resistant to phagocytosis, penetration of antimicrobial agents, resistant to drying and viable in dried sputum(not blood) -drug resistance -tx: combination of antibiotics -communicable chronic granlomatous(often caseating-central necrosis) disease - macrophages cant consume something, fuse to from multinucleated giant cell -HIV-leading cause of death amongst HIV + - elderly, poor, immunocompromised |
|
|
Tubercolosis Pathogenesis:
- toxicity? -destroys tissue via? -classification? -primary? -secondary? |
- not based on inherent toxicity
- induction of a type IV hypersensitivity reaction -a proliferative and destructive granulmatous tissue(macrophages inefficient-->t cells secrete cytokines-->attract more macrophages-->giant cells) reaction(tubercles), central necrosis(caseous) common Classification: Primary: non-sensitized Secondary: reactivation or re-infection of the bacilli in a previously sensitized host |
|
|
Primary Tubercuolosis
-develops in -begins by -hypersensitivity develops when -dx |
-non-sensitized individuals
-lung by inhalation of microorganisms -hypersensitivity develops 2nd week -PPD skin test 2 weeks later-calcified nodules on x-ray |
|
|
Tubercolosis:
-how/is most TB self limiting, what may be seen? 2nd TB: Progressive primary TB -high in what kind of patients -characterized by? - conditions? |
- 95% of primary tuberculosis are arrested-self limiting
-tubercle is walled off by connective tissue and maybe calcified -not communicable even with microorganism may still be alive -tiny fibrocalcific nodule maybe seen - most of these people are infected and do not have active disease-->cannot transmit to others -infection maybe reactivated late rin life by low immune system or re-infection -progressive primary TB -high in HIV positive patients with an advanced degree of immunosuppression -continuous development of primary tb w/o interruption -proceed to conditions normally seen in 2nd TB |
|
|
Tuberculosis:
-oral lesions common? -majority seen in with what and in? -soft tissue? -jaw bones? -dx |
-uncommon
-contaminted with sputum, seen in patients with systmeic TB and/or 2ndary TB -soft tissue: chronic non-healing ulcer or swellings(granulation tissue-like) -Jaw Bones: osteomyeltitis - biopsy-usually if have non-healing ulcer/granulation tissue-->squamous cell carcinoma) |
|
|
TB:
Mantoux test -type of test -depends on what type of reaction and when? -ability to differentiate? -accuracy limited in? -best in? Culture -time -how good is the test? -allows for testing of? Stain -for..problem? PCR -used for? |
-also known as PPD or tuberculin test
-intracutaneous injection of purified protein derivative -delayed hypersensitivity reaction, peaks in 48-72 hrs -doesnt differentiate b/w infection/disease-also inaccruate against people whom have had the vaccination -not accurate on ppl that have been previously immunized -works best in large population who havent encountered the bacteria before -Culture -take a long time 3-6 weeks -gold standard: allows testing of drug susceptibility(many new cases are drug resistant) -stains acid-fast bacilli- non specific -PCR amp: quick and specific |
|
|
Leprosy:
type of disease? caused by? acquired in? incubation period? located? classification? clinical manifestation? |
- chronic granulmoatous disease
-mycobacterium leprae -childhood or young adulthood via nasal cavity -years to decades -skin, mucous membran of upper respiratory tract and peripheral nerves are the major sites of involvement in all leprosy - spread of granulomatous tissue quickly, inflammation destroys tissue in face(nasal spine, maxilla) try to repair it forming thick scar tissue -classifcation: -tuberculoid(pacibacillary-high immune response to low number of bacteria) -lepromatous(multibacillary-low immune response from high numbers of bacteria) -clinical manifestation and pronosis are related to host response |
|
|
Paucibacillary Leprosy:
in patients with? dx? oral lesions? -type of disease? clinical manifestation? -can potentially lead to? -histology? |
-high immune response
-lepromin test +( skin test to heat killed bacteria) -oral lesions are rare -localized disease: small number of well circumscribed, hypopigmented skin lesions -nerve involvement lead to loss of sensation the affected skin -histoloy: granulomatous inflammation-well formed granulomas. Paucity of organisms present, IDed by acid fast stains |
|
|
Multibacillary Leprosy:
in patients with? lepromin test? -type of disease, clinical manifestion -can involve -histology? |
- reduced immune response
- negative or positive - diffuse, numerous ill defined hypopigmented lesions with time, become thickened and loss of skin appendaes. Skin enlargement leads to facial distortion - body does not wall off spreading bacteria well-->more destruction -->scar tissue -nerve involvement spread to most of the body -histology: granulomatous inflammation with no well-formed granulomas. numerous bacteria in tissue, ided by acid-fast stains |
|
|
Multibacillary Leprosy orofacial lesions
|
-soft tissue: ulceration, necrosis and loss of tissue
-Bone: erosion and perforation of palate -Facies leprosa: resorption of anterior nasal spine and anterior maxiallry alveolar ridge |
|
|
Leprosy:
Dx Tx |
-Dx: based on caracteristic skin lesions with diminsed sensation. Demonstrate the presence of M. leprae in tissue
tx: eradicate infection with multidrug regimens -treat complication of nerve damage -reconstruction of the damae |
|
|
Treponema Pallidum:
Primary: -tx? -bacteria load Secondary: -type? -can be from? bacteria load Latent: -clinical symptoms? -30%-->? infectious in? can be treated with and when? |
-chancre-genitalis, oral cavity
-lesion heals and no permanent damage results -high systemically -macuopapular rash -mucous patch -disseminated from latent -self limiting in weeks/month, no permanenet titssue dammage -low -Latent/tertiary -30 % if untreated--> gumma(permanenent dammae) -no clinical sx otherwise -most infectious in primary/secondary -all stages can be treated with penincillin(abs) |
|
|
Syphilis:
caused by? transmission? -occurs in what kind sexual transmission? test?> recent hike from? can be complicated by? |
-treponema pallidum
- sexual contact, mother to fetus -64% in MSM, most increases in BM -oral sex and aids are main cause for recent hike -presentation complicated by AIDs -seroology-->sensitive but not accurate |
|
|
Primary Syphilis:
development? also known as? danger? clinical manifestation? healing? dx? |
-site of inoculation. develop in days(3-90)
-chancre -highly infectious -ulcer, lymphadenopathy in oral cavity or genital area -lips most common extraoral area of ulcer -heals spontaenously 3-8 weeks - seroloy-IF or dark-field microscopy + - early stages, seroloy is usually negative need more specific tests |
|
|
Secondary Syphilis
-develops when -can overlap with -clinical manifestaton -heals? -dx? |
-primary lesion not treated, patients develop 2-6 months after initial infection
-primary syphilis -systemic sx and lymphadenopathy -macuolopapular rash(skin), mucous patch(mucosa), condyloma lata(skin& mucosa) -heals spontatneous in 3-12 weeks though may relapse -dx: serology, IF/dark field microscopy |
|
|
Tertiary Syphillis:
seen in? causes? clinical manifestation? |
-aids patients, rare
-Cardiovascular CNS damage(permanent-->dementia) -Gummas -granulomatous inflammation -necrosis and ulceration -extensive tissue distruction -involves many organs:(tongue, palate(perforate) |
|
|
Congenital Syphillis:
-caused by? -clinical manifestations |
-transplacental infection with treponema pallidum during fetal development
- abortion, stillbirth, death after delivery, developmental abnormalities -hutchinsons triad -dental anomalies: hutchinsons incisor and mulberry molar -deafness(8th nerve) -blindness(interstitial keratosis) |
|
|
Bartonella Infections
-normal patients -immunocompromised patients |
-granulomatous inflammation: cat scratch disease-no TX necessary
-immunocompromised patients: -aniogenesis -bacillary angiomatosis-->need antibiotic |
|
|
Cat Scratch Disease:
-type of disease from? -clinical -affects who? -time line of disease? -scratch leads to? -dx -tx |
-benign, self limiting infection of bartonella hensellae from cat to human
-kids -1-2 weeks: primary skin lesion along scratch line -3-7 weeks: regional lymphadenopathy, fever, primary lesion resolved -scratch on face usually develop submandibular lymphadenopathy(bacteria drains to lymphnode) - clinical history, bacteria in specimen, in lymph node, positive titer of antibdoy to B. henselae |
|
|
Actinomycetes:
Actinomycosis: type of bacteria? enter tissue how? Present as an? characterized by? dx? tx? |
- gram + filanmentous anaerobic, 50% cervicofacial
-actinomyces israelii-normal oral flora -through opening via trauma -acute deep suppurative abscess with draining sinus tract(acute response) -colonies of actinomycotic organisms surrounded by neutrophils -sulfar granules: yellowish flecks seen clinically representing colonies of actinomyces dx: histology+culture tx: surgican drainage/debridement and antibiotics |
|
|
Tonsillar concretions and Tonsilloithiasis:
-clinical manifestation? -sx -tx |
-convoluted crypts filled with desquamated keratin, foreign material and 2nd colonized with bacteria(actinomycetes)
-tosillar concretions: a mass -tonsillolithiasis: calcified. noted on radiographs superimposed on midportion of mandibular ramus -most have no sx/no treatment -removal necssary if sx produced |
|
|
Noma
-type of infection frrom? -common in? -clinical manifestation -result -tx? |
-opportunistic infection from normal oral flora in severly immunodeficient
-malnourished in 3rd world -aids -necrotizin ulcerative gingivitis extends to involve adjacent soft issue and beyond -extensive necrosis and makred tissue destruction, facial disfigurement -death -tx: correct underlyin disease, debridement antibiotics |
