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MoD Respiratory

respiratory pathology, pharmacology, pathophysiology

QuestionAnswer
asthma immune response Th2, il4, il13-->bcell-->IgE-->mast cells-->histamine, LKTs, IL5, GMCSF, eosinophils, smooth muscle, neutrophils
diff asthma vs bronchitis asthma reversible by bronchodilators
bronchitis immune response CD8 tcells, macrophages (^bc of smoking)
inflam from smoking macrophages, neutrophils-->oxidants, proteases (>>antiproteases), IL8, TNFa, IL1, IL6-->remodeling, mucous, destruction
clinical hallmarks of emphysema dyspnea, cachectic, pursed lip breathing, decreased breath sounds, hyperresonant to percussion, distant heart sounds
clinical hallmarks of chronic bronchitis chronic cough, dyspnea, wheezing, ^AP diameter, decreased breath sounds, wheezing, cyanosis, edema, poss loud P2
clinical hallmarks of asthma dyspnea, chest tightness, wheezing, cough (Sx=episodic, may be persistent), use of accessory muscles, prolonged expiratory phase, wheezing
apthous canker common, recurrent, painful, shallow hyperemic ulcer covered by thing exudate
HSV infection of mouth cold sore, grouped clear fluid filled vesicles in area innervated by nerve fiber, person to person transmission
oral candidiasis immunosuppressed, superficial curdy white membrane easily scraped off
glossitis beefy red tougue
irritation fibroma nodular mass of fibrous tissue on buccal mucosa
pyogenic granuloma highly vascular pedunculated gingival lesion, pregnancy tumor, erythematous
hairy leukoplakia immunosuppressed, white confluent patches, lateral tongue, hyperkeratosis, acanthosis, baloon cells
leukoplakia white plaque that can't be removed by scraping, varying dysplasia, from acanthosis/hyperkeratosis to carcinoma in situ
white plaques-can be scraped vs. can't candidiasis can be scraped, leukoplakia cannot be scraped off easily
erythroplakia red velvety plaque, less commonrelated to tobacco, etoh, hpv
squamous cell carcinoma of oral cavity 95% of oral cavity cancersassoc w/ tobacco, etohlocation: ventral tongue, mouth floor, lower lip, soft palate, gingivalooks like plaque/mass, starts as dysplasia, may invade then metast
kaposi sarcoma caused by KSHV (HHV8), intraoral purple nodular lesions
nasopharyngial carcinoma assoc w/EBV, can be keratinizing squamous, non, undiff
what is most common tumor of oral cavity? squamous cell carcinoma
paraganglioma carotid body tumor, cluster of neuroendocrine cells, rare, usually sporadic, may metast
branchial cleft cyst benign, anterolateral neck, remnant of branchial arch, squamous/columnar lining
thyroglossal duct cyst resp/squamous epith, has lymphoid, thyroid tissue
sialadenitis saliv gland inflametio: viral, bac, autoimmune (SLE, sjorgen's)may be secondary to obstruction, impaction, injury
mucocele common lesion of saliv glandsblock/rupture fo duct-->mucous spills into stroma=bluish swelling
benign lymphoepithilial lesion nonneoplastic enlarged saliv gland, dense lymphoid prolif in gland, ducts invaded by lympocytes
diff b/w sialadenitis and benign lymphoepithelial lesion lymphocytes invade ducts in BLL, not sialadenitis
benign lymphoepithelial cyst asso w/HIV, EBVduct destruction due to lymphoid hyperplasia, epith lined cyst w/lympoid infiltration
most common benign saliv gland neoplasms 1.pleomorphic adenoma 2. warthin's
most common malignant saliv gland 1. mucoepidermoid2. adenocarcinoma
pleomorphic adenoma ^in parotid, slow growing, epith/mesench diff, plus myoepitheliod cells
warthin's tumor papillary cystadenoma lymphatosumusually in parotid, cleft like cystic mass lined by oncocytic cells surrounding lymphocytes
mucoepidermoid most common salivary malig tumoradmixture of squamous, goblet, intermediate cellsnon encapsulated, infiltrative
most common tumor of minor saliv glands adenoid cystic carcinoma
most common benign saliv gland neoplasms 1.pleomorphic adenoma 2. warthin's
most common malignant saliv gland 1. mucoepidermoid2. adenocarcinoma
pleomorphic adenoma ^in parotid, slow growing, epith/mesench diff, plus myoepitheliod cells
warthin's tumor papillary cystadenoma lymphatosumusually in parotid, cleft like cystic mass lined by oncocytic cells surrounding lymphocytes
mucoepidermoid most common salivary malig tumoradmixture of squamous, goblet, intermediate cellsnon encapsulated, infiltrative
most common tumor of minor saliv glands adenoid cystic carcinoma
corticosteroids mechanism of action cytoplasmic receptor to GRE=affect transcription/translation, TFs, broad spectrum of action
effects of corticosteroids (desired) decrease: recruitment of inflam cells, activation of inlfam, cytokine synth, airway edema, vascular permincreases: response to bronchodilators
side effects of steroids metabolic/mineralcortoid effects: fat deposition, osteoperosis, hyperglycemia, HTN, muscle wasting, bruisability, cataracts, immune suppression, adrenal axis supression
inhibitors of leukotriene synth zileuton-5LO blockerhepatotoxic
LTK receptor blockers monteleukast, zafrileukastused as controller/preventor
anti IgE omalizumabbinds Fc portion so IgE can't bind/activate mast cells
short acting beta agonists albuterol, pirbuterolrapid onset, use for acute asthma in all asthma patientsADR: tachycardia, tremors, tolerance
long acting beta agonists salmeterol, formoterolcontroller/preventors
cholinergic bronchodilators ipotropium, tiotropiumblock muscarinic (ip3-Ca-smooth muscle contrac)tio=better, selective for m1, m3 receptors=1st line therapy for COPD
theophylline xanthine, controller/preventor, ^side effects, narrow theraputic index
nonpulm restrictive neuromuscular, chest wall, pleural spaceno diffusion defect, RV is normal because no process to hold airways open
Idiopathic pulm fibrosis restrictive process, decreased lung compliance, diffusion impairedCXR-peripheral reticular markingsfibroblastic foci (collagen deposition), heterogeneousetio: poss lung injury and abnl repair, related to TGFbeta
sarcoid granulomatous, non caseating, poss immune originhilar adenopathy-->parenchymal infiltrates-->advanced fibrosis/destruction
desquamative IP smoking assoc, macrophages in airspaces
respiratory bronchiolitis smoking, macrophages
actue IP ARDS but without discernable cause
Cryptogenic organizing pneum protrusions of granulation tissue into distal airspaces
nonspecific interstitial pneum doesn't look like others
lymphocytic IP lymphoproliferative, ^in HIV
hypersensitivity pneumonitis gradual or acute, due to environmental exposureactive inflamation, giant cells, granulomatous inflam
asbestos causes: asbestosis, methothelioma, pleural plaques
most lobar pneumonia caused by Strep Pneum
bronchopneum vs lobar bronch=patchy, diffuse, lobar=only 1 lobe, whole lobe affected
CA PNA usually strep pneumonia Hflu, staph Aur, Pseud, Klebs, Legio^in CHF, COPD, diabetes
course Strep Pneum congestion: 1-2 days, heavy, red boggy, vascular congestion, bacteria, prot fluidred hepat: 2-4 days, neutrophils, RBCs, fibrinGrey hepat: RBCs lysed, neutrophils/fibrin exudateresolution: organizing PNA, connective tissue
CA PNA complications abscess, empyema, scarring, bacteremia
staph aureuous PNA 2nd to viral resp infec, ^complic, assoc w/right sided IE in IVDU
Klebsiella Pneum ^common G- bac PNA, chronic etoh, currant jelly sputum
Pseudamonas pna vasculitis/bacteremia, infarcts
legionella pna aquatic env=humidifier
atypical pna acute, afebrile, distress out of proportion with signsmycoplasma pneum=^ commoninflam confined to septa=thickened-inflam infiltrateNO alveolar exudate=no productive cough
nosocomial severe disease, immunosuppG- (enterobac, psued), staphy aureus
aspiration pna necrotizing, abnl gag reflex, subsequent abscess
lung abscess local area of supperative necrosis-->cavitationanaerobic bac from oral cavity, ^ on rightcan rupture, cause bronch obstructhick fibrous wall, necrotic debris inside
pna in immunocompromised host pseud, mycobac, legio, listeria monocyt, CMV, HSV, PCP, candida, aspergilla, cryptococcus
CMV PNA cells=giant, mononuc, ^ in immunosupp, hyaline membranes, edema/inflam, CMV owl's eye halo inclusions
PCP fungal, PNA in immunosuppdry cough, dysp, feverbilat perihilar shadowingcup shaped cysts, foamy pink staining exudate, thickened septaecan be with CMV
Diffuse alveolar damage ARDS-rapid onset resp insuff, hypoxinjury to alv capillary endoth/epith-->pulm edema, hyaline membrane formation, eventually organization/fibrosis
pulm TB chronic infec of lung
Created by: bsilver