Final Exam Flashcards
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| Rhinitis |
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| URT -Cold. -Viral: Rhinovirus & coronavirus -cilliated epithelial cells of nose |
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| Pharyngitis & Tonsilitis |
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| URT -Sore throat and tonsilitis -Infected mucosa and lymphoid tissue -Cytomegalovirus(CMV) blood to placenta -EBV. -S. pyogenes/N. gonorrhoeae/C. diptheria |
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| Otitis media and sinusitis |
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| URT -Ear & sinus -50% viral & 50% bacteria -Respiratory syncytial virus (RSV)/Influenza/parainfluenza/rhinovirus/adenovirus -S. pneumoniae/Haemophilus influenzae/Moraxella |
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| Epiglottitis |
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| URT -H. influenzae type B(vaccine Hib) -Ages 2-7 -Symptoms: Drooling/dysphagia/respiratory distress -Life threatening if severe inflammation |
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| Laryngitis & tracheitis |
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| LRT -Virus:Parainfluenza(croup=barking seal) RSV, Influenza, Adenovirus -Bacteria: GAS, H. influenzae, S. Aureus -C. diptheria(life threatening but vaccine-DaPT) |
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| Whooping Cough/Pertussis |
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| LRT -Bordetella pertusis -Attach to ciliated mucosa in trachea (fimbriae & hemagglutinin-prevents cilliary movement) -Toxic factors: 1.Pertussis toxin-Prod mucoid secretions 2.Adenylate cyclase toxin-Inhibits chemotaxis,phagocytosis, & killing 3.Tracheal Cytotoxin-Kills tracheal epitherlia cells 4.Endotoxin 90-95% rate of infection if exposed to unvaccinated |
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| Acute Bronchitis |
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| LRT -Inflammation of the tracheal/bronchial tree -P. pathogens: Rhino corona, adeno, influenze viruses & Mycoplasma pneumoniae -Secondary invaders-S. pneumoniae, H. influenzae |
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| Influenza |
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| LRT-The flu -Influenza virus types A, B, C,; A segmented RNA, 3 HA types, 2NA types -Antigenic epitopes change from yr-yr(drift and shift) -Airborne droplets |
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| Influenza Colonization |
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| -Attaches via HA to sialic acid receptors on ciliated epithelium of trachea/bronchi -RME |
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| Pathology of Influenza |
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| -Incubation 1-3 days -Impair mucociliary clearance, tacheobronchitis, bronchospasms;cytokines released from damaged cells & WBC |
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| Presentation of Influenza |
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| -Fever of 102-104 -Chills -Severe headache w/retro-orbital pain -Muscular aches -Dry cough -Weakness Resolves in 1-2 weeks |
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| Complications of Influenza |
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| Primary influenza-1% of cases but 30% fatal. Pregnant women at increased risk Secondary Bacterial pneumonia-H. influenzae, S. pneumonia, S. aureus, S. pyogenes |
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| How many cases are required for influenza to be considered epidemic? |
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| 10,000-50,000 DEATHS |
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| Bronchiolitis |
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| LRT -Children <2 -Necrosis of epithelial cells lining bronchioles -75% RSV (Respiratory Syncytial Virus) Colonization:Nasopharynx-surface spikes are fusion proteins that fuse host cells to cause syncytia. Virus invades LRT by surface spread in secretions. -Maternal Ab in infants react w/virus -Presentaion:bluish ashy lips/cough/rapid respiration -25% Other viruses |
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| RSV |
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| Respiratory Syncytial Virus Paramyxovirus(RNA), enveloped Humans only reservoir Transmission:Resp. droplets to hands |
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| Pneumonia |
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| LRT -Pathogen clinically indistinguishable Transmission: Inhalation of rep. droplets or aspration from UR Colonization: Attach to rep. epithelium Pathology: Respdistress from the interference of gas exchange in lungs, Children: Viral maybe bacterial Adults: Bacterial |
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| Bacterial Pneumonia |
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| Acute onset, high fever Typicals: S. pneumoniae, H. influenzae, S. aureus, Klebsiella, E. coli, Pseudomonas Atypical: M. pneumoniae, Chlamydia pneumoniae, Legionella pneumophila, Coxiella burnetii -Chest Exam for: Rales(abnormal crackles)/Evidence of consolidation/Chest X-ray |
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| Viral Pneumonia |
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| Transmission: Inhaled or from blood Colonization: Attach specifically Orgs: RSV-Chlidren Parainfluenza virus-Children; hemagglutinin & neuraminidase & fusion proteins Adenovirus Influenzavirus |
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| Fungal Infections of LRT |
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| Chronic -Aspergaillus fumigatus: predisposing condition or immunosuppressed individuals. 45 degree branching septate hyphae present -Histoplasma Capsulatum-Histoplasmosis -Coccidiodes immitis-San Joaquin Valley Fever -Blastomyces dermititidis-blastomycosis -Pneumocystis jiroveci-pneumocystis pneumonia |
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| Cystic Fibrosis |
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| Very Viscous bronchiol secretions leads to fluid stasis in the lungs & infections w/P. aeruginosa (S. auresus, H influenzae, B. cepacia CF patients over reactive inflammatory response= too many PMNs, too much secretion=damage to mucosal epithelium, fluid stasis=bacteria are not removed |
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| NK cells |
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| viruses & I.C. bacteria |
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| Interferon |
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| Viruses |
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| Phagocytosis |
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| PMN, E.C. bacteria |
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| Complement Activation |
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| E.C. bacteria |
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| Steps for Infectous Microbes |
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| 1. Entry 2. Spread 3. Multiplication 4. Evasion 5. Transmission 6. Pathology |
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| Gram Positive vs. Gram Negative Cell Wall |
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| GP: LTA Thick peptidoglycan resists activity of bile Digested by lysozyme which targets beta 1-4 glycosidic linkages GN: Thin peptidoglycan LPS-Carbs: Stimulates immune response Lipid A: Endotoxin that induces fever, ^vascular permeability |
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| Importance of Capsule |
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| -Attach to a wide variety of surfaces -More resistant to engulfment by host defense cells |
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| Importance of Flagella |
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| -Movement -Proteins are stongly antigenic/immune simulating |
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| Importance of Fimbriae |
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| -aka common pili -Attachment(adhesins target cell membranes) |
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| Importance of Pili |
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| -Exchange genetic info, including antibiotic resistance |
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| Entry of bacteria into host |
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| -Direct contact -Ingestion -Fomites(inanimate objects) |
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| Clinical significance of normal microbiota |
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| -Common contaminants of clinical specimens -Opportunistic pathogens |
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| Opsonin |
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| Molecule that attaches to cells; providing a bridge to receptors on phagocytic cells and enhances the rate of phagocytosis |
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| Edema |
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| Excess accumulation of serous fluid in connective tissue or in a serous cavity |
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| Erythema |
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| Abnormal redness of the skin due to capillary congestion (as in inflammation) |
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| Inflammation |
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| locall response to cellular injury Marked by: Capillary dilation, leukocytic infiltration, redness, heat, pain, swelling, & often loss of function -Serves as a mechanism initiating the elimination of noxious agents and damaged tissue |
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| Non-specific Physical Defenses |
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| -Overlapping epithelial cells -Turbulence in nose that makes it hard for MOs to attach -Shedding, scrapping, flushin(saliva, urine, tears)-Shear force -Muco-ciliary clearance-goblet & ciliary cells |
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| Non-Specific Chemical Defenses |
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| 1. Acids 2. Enzymes(lysozymes) 3.Microbiciidal chemicals (zinc & dermicidin) |
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| Non-Specific Biological Defenses |
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| 1. Normal microbiota-Physical, competition, inhibitory substances 2. Immune defense cells and molecules |
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| 2nd line NS Defense |
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| Inflammation -phagocytic cells -cytolytic cells -acute phase proteins: CRP, interferon, and complement |
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| Signs of acute inflammation |
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| 1. Erythema-redness 2. Edema-swelling 3. Heat 4. Pain (sensitivity to area) |
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| Triggers of accute inflammation |
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| 1. IM 2. Peptidoglycan, LTA, LPS |
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| Roles of phagocytes |
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| -Engulf & destroy foreign matter -Secrete chemicals (cytokines) |
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| Types of phagocytic cells |
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| -PMN=neutrophils -mononuclear leukocytes |
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| PMN |
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| -Dominant in beginning of inflammatory response -Contains cytoplasmic granules loaded with antimicrobial chemicals -Best with extracellular pathogens |
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| Mononuclear Leukocyte |
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| -Later in inflammatory response -Concentrated in lung, liver, lymph nodes and spleen -live longer than PMNs -APC -Best with intracelular pathogens |
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| Which type of phagocyte is best against extracellular pathogens? |
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| PMNs |
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| Microbe-PAMP to PRR-Phagocyte |
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| Allows microbe and phagocyte to overcome negative-negative charge repulsion since both have exterior negative charges. |
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| NK cells |
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| -Target viruses -attach to infected to cells via glycoproteins -release perforins & granzyme to kill cell |
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| Th1, Th2, Tregs |
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| CD4 |
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| Tc |
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| Cytotoxic T cells CD8 Kills cells infected w/intracellular pathogens |
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| Which MHC class do Th cells recognize? |
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| MHC class 2 |
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| What MHC do Tc recognize? |
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| MHC class 1 |
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| Activation of T lymphocytes |
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| 1. Receive cytokines from APC(IL-1) 2. ^ of IL-2 Received adn secrete/receive Il-2=proliferation 3. Differentiation into: effector Th1 cells(activate macrophages=NK & Tc) & Th2 (activates B cells to make antibodies) Memor Tcells |
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| IL-2 |
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| -Secreted by Th1 -Stimulates Tc proliferation & maturation |
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| IL-4 |
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| -Secreted by Th2 -Stimulates B cell proliferation & differentiation into plasma cells |
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| gamma-interferon |
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| -Secreted by Th1 cells -Activates effector Tc, macrophages and NK to kill intracellular pathogens |
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| Opsonizing agents |
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| C3b CRP IgG |
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| What is a neutralizing antibody? |
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| IgA |
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| Rheumatic Heart Disease |
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| Delayed sequela of URT infection with group A beta-hemolytic strep Abs that target strep bind to heart tissue due to similarity in receptors. IS cross reacts w/heart and kidneys |
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| Antigenic Drift |
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| Caused by single base mutations in RNA. Slight changes in hemagglutinin (H) of influenza virus Seasonal Epidemics |
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| Antigenic Shift |
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| Major changes in surface proteins caused by recomvinationg of genes b/w 2 different strains of virus. Pandemic |
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| What MO produce IgA protease? |
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| Nice STriP of Ham Neisseria Streptococcus pneumoniae Haemophilus influenzae |
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| Which cytokines are responsible for fever? |
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| IL-1 & TNF |
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| Physiological cause of fever |
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| Hypothalamus secretes PG upon binding of IL-1 or TNF. PG then self activates the hypothalamus |
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| Type 1 Hypersensitivity |
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| IgE rapid onset |
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| Type 2 Hypersensitivity |
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| IgG activated mins to hrs |
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| Type 3 Hypersensitivity |
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| Response to Ag-Ab complex IgM & IgG stick to blood vessels or tissue activating C & neutrophils Activated 3-8 hrs |
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| What type of hypersensitivity is the reaction to tuberculosis? |
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| Type 4 mediated by t-cells & macrophages |
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| Steps in a clinical encounter |
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| 1. Patient History 2. Physical Examination 3. Investigation plan 4. Management plan |
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| What is the UUT? LUT? |
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| Upper Urinary Tract=kiney & ureter Lower Urinary Tract= Urinary bladder & urethra |
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| Common community acquired UTI pathogens |
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| 1. E. coli 2. S. Saprophyticus 3. Proteus miravilis 4. Klebsiella, Enterobacter, Serratia, Pseudomonas aeruginosa |
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| Hospital acquired UTI pathogens |
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| 1. E. coli 2. Klebsiella, enterobacter, serratia, Pseudomonas aeurinosa 3. GPC 4. Proteus mirabilis |
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| Predisposing factors for UTI |
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| Anything that Disrupts of urine flow Preventscomplete emptying of bladder Promotes microbial access |
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| Virulence factors of UTI E. coli |
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| O & K serotypes -Pathogenicity island -P fimbriae -Capsular acid polysaccharid to resist phagocytosis -Membran active cytotoxins |
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| VF of S. saprophyticus |
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| Adherence to uroepithelium Microbistatic to GP & GN Urease-ultimately increases pH cause stone formation allowing more attachment sites for pathogens |
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| P. mirabilis |
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| Flagella Urease |
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| Urethritis |
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| LUT -Dysuria(painful urination) |
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| Cystitis |
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| LUT Bladder -Rapid onset of dysuria;^urgency/frequency -Cloudy urine(pus or bacteria);blood |
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| Prostatitis |
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| LUT Prostate -dysuria, ^frequency, low back pain, fever |
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| Pyelonephritis |
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| UUT Renal parencyma -Cystitis+more sever FEVER -Septicemia, loss of renal function |
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| How to collect urine samples |
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| Voiding(midstream) Urinary catheter Suprapubic bladder aspiration |
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| How do you distinguish cystitis from pyelonephritis? |
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| Pyelonephritis includes sever fever |
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| What is consider clinically significant bacteriuria? |
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| 10^5 cells |
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| What MO helps protect the vagina & how? |
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| Lactobacili because it secretes acid=lower pH=barrier against infection |
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| Incurable STD's |
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| HumanPapillomavirus Herpes Simplex Virus HIV Haemophilus ducreyi |
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| Human Papilloma Virus |
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| HPV-Genital warts -Attach via capsid protein, enter via RME Pathology-Dyplasia(abnormal growth) -Associated with cervical neoplasia |
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| Reading HPV PAP |
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| -Less cytoplasm=more sever dysplasia -Mildly ^nuclear to cytoplasm ratio |
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| Chlamydia trachomatis |
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| Non-gonococcal urethritis E-Abrasions A-Receptors on host cell, parasite-induced endoytosis S-asymptomatic or urethritis C-infertility also PID, ectopic pregnancy txt-tetracycline etc |
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| Candida albicans |
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| Yeast infection -Part of normal microbiota T-disruptions to bacterial vagina community results in overgrowth with yeast S-UTI, burning/cottage cheesy discharge Balanitis(inflammation of glans penis) txt-antifungal |
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| Trichomonas vaginalis |
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| Vaginitis-Protozoa E-Vagina in women; Urethra/Prostate in men S-Vaginitis, yellow/green frothy discharge. Rise in vaginal pH txt-metranidazole |
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| Herpes Simplex Virus types 1 & 2 |
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| Genital Herpes E-Membrane fusion P-Causes host cells to fuse together forming giant cells. S-Genital lesion vesicles->ulcer w/tender, swolen nodes, fever, headache, malaise -Remains latent in root ganglion -Can reactivate due to stress, trauma or sun |
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| Neisseria gonorrhoea |
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| Gonorrhea -Women have 20% chance of passing; Men 50-90% E-Mucous membranes A-Common pilus, Opa proteins. Invade non-ciliated e cells P-LPS & Enzymes -Neonatal blindness TXT-Treat for gonorrhea (Cefixime & Ciprofloxacin) & Chlamydia |
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| AIDS/HIV |
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| Disease of immune cells-CD4(Macrophages & Th) |
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| Treponema pallidum |
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| Syphilis E-abrasions S- Chancre 2-4 weeks postinfct Primary-bacteria multiply in nodes causing swelling Seconary- Bacteria multiply causing lesions. Most cured some become latent Tertiary-Host cell-mediated response causes progressive destruction of neuro-, cardio-, skin, and joints Txt-arsenic, penicillin, |
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| Gastritis |
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| -Inflammation of the stomach -Pain in upper abdomen -Bleeding |
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| Gastroenteritis |
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| -Inflammation of stomach & intestines -Diarrhea, nausea, vomiting, crampy abdominal pain |
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| Colitis |
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| Intestinal syndrome that primarily involves the colon or large intestines |
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| Enterocolitis |
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| Inflammation of mucosa of both large & small intestine=dysentery-diarrhea often contains blood & mucus |
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| Hepatitis |
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| Caused by liver damage Patients become jaundiced due to bilirubin build up in the body |
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| How do pathogens cause disease in the GI tract? |
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| 1) Action of toxins 2) Adherence to & effacement of microvilli=>inflammation 3) Invasion of intestinal epithelial cells |
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| Enterotoxin |
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| Results in net secretion w/out intestinal damage |
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| Cytoskeleton-altering toxin |
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| Alters cell shape, may injure cells but not lethal |
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| Cytotoxin |
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| Causes cell damage and ultimately cell death |
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| Neural toxin |
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| Alters smooth muscle activity in intestines |
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| What causes bacterial food poining? |
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| Ingesting preformed toxins; not infections |
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| Bacteria responsible for food poisoning |
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| Clostridium botulinum-botulism. Staphylococcus aureus-most common. Starts 30 mins-8hrs post ingestion. Resolves in 24 hrs. Bacillus cereus-Emetic. Starts 1-5hrs after ingestions. Lasts 1-6 hrs |
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| Pathology of Vibrio cholera |
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| S-Contaminate water P-1. Ingest large numbers>10^8 2. Flagella allows Vibrio to reach epithelial cells 3. Attachment by way of fimbriae to receptors on brush border & crypt cells of small intestine 4. Damage due to production of CXT(A & B subunits). Disrupts adenylate cyclase. CXT=enterotoxin, neurotoxin, & cytotoxin 5.Secretion of large quatities of Cloride ion ino intestine. Water and sodium ion follow=hypersecretion of fluids & electrolytes |
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| Symptoms of Cholera |
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| Extreme diarrhea, rice water stool Dehydration & electrolyte imbalance=cardiac failure Txt-Fluid & electrolyte replacement |
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| What mechanism do ETEC(Enterotoxigenic E. coli) and B. cereus use to cause disease? |
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| Both colonize epithelial surfaces of small intestine & then release toxins. Do not enter cells. |
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| What mechanism does Shigella use to cause disease? |
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| Atrach to and enter epithelial cells. Multiply intracellularly & destroy(efface) mirovilli of epithelial cells and induce diarrhea |
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| Pathology of Shigella |
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| S- Contact w/feces from infected person P-1. descending infection of intestine. Small intestine then colon. 2. Capsule, secretes enterotoxin=watery diarrhea 3. Adhere to cells of colon using Outer membrane proteins 4. Use M cells of GALT and enterocytes to transport Shigella across intestinal epithelium using endocytosis. 5.Escape from phagolysosome 6. Triggers macs to produce IL-1 also triggers apoptosis 7. IL-1 induce inflammation & stimulates edema & extravasation of neutrophis across epithelial barrier 8. Movement of PMNs destroys barrier allowing shigella to move across in mass 9. Further prod. of cytokines & intense inflammation w/destruction of epithelium=>ulcerations=>blood in stool |
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| Symptoms of Shigella infection |
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| Blood and pus filled diarrhea Self limiting 2-3 days |
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| What other baacteria share the disease mechanism of Shigella? |
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| EHEC Yersinia enterocolitis Entamoeba histolytic Rotavirus/Norwalk virus |
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| Salmonella enteritidis, S. typhmuium Salmonella typhi, paratyphi |
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| Salmonellosis Typhoid fever Pathology: 1. Ingest lots of cells 2. Attach to fibronectin of epithelial cells of small intestine 3. Transported by M cells to GALT 4. Invade gut wall=ulcers adn hemorrhage. Spread to intestinal lymphatics & are phagocytized by macs 5. Produces toxin that ^cAMP & fluid secretion=loose, watery diarrhea & nausea 6. Causes influx of PMN that confines infection to GI 7. OR influx of macrophages which resuls in systemic spread. |
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| What mechanism do S. enteritidis & S. typhi use to cause disease in the GI? |
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| Attaches, enters & multiplies in deep tissues that are normally sterile-submucosal or subepithelial tissues sometimes will spread systemically |
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| What mechanism do Hepatitis A virus, Reoviruses & Enteroviruses use to cause disease in the GI? |
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| Attaches, enters & multiplies in deep tissues that are normally sterile-submucosal or subepithelial tissues sometimes will spread systemically |
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| Character of Meningitis |
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| High fever, headache, stiff neck |
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| How do MO get to the CNS? |
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| 1. From the bloodstream-cross the BBB (Bacterial meningitis) 2. From peripheral nerves (Herpes, VZV, rabies) 3. Invasion from bone/sinuses/middle ear 4. Trauma |
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| Encephalitis |
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| Acute febrile illness Changes in mental state consciousness behavior |
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| Bacterial Meningitis |
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| Acute-nearly always fatal Neonates: E.coli, Group B strep 1mo to 5 yrs: Haemophilus influenzae type B 5 to 40 yrs: Neisseria meningitidis 30 and over:S. pneumoniae |
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| Viral meningitis |
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| Self-limiting/non-fatal 1. Enteroviruses 2. Arboviruses 3. HIV 4. HSV-2 |
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| CSF of bacterial meningitis vs viral |
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| Bacterial-elevated:neutrophils, protein. Decreased: glucose Virus Elevated:lymphocytes, protein. Normal glucose |
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| Viral encephalitis |
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| Very severe 1. Arboviruses 2. HSV-1 3. Eneroviruses, mumps 4. Rabies(Rhabodovirus) |
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| Protozoan encephalitis |
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| Amebic encephalitis-Naegleria fowleri African Sleeping Sickness-Trypanosoma |
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| Abscess |
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| Localized collection of pus |
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| Why are MOs in abscesses difficult to treat with antimicrobial agents? |
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| 1. Microbes aren't multiplying 2. Chemical nature of pus interferes with action of some antibiotics 3. Hard to reach site due to lack of vessel penetrations |
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| Scalded skin syndrome |
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| Strains of S. aureus with lysogenic phages Causes splitting in deep layers=40% of outer skin layers are lost=loss of body fluid, high fever, and bacteremia |
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| Nectrotizing fasciitis/Flesh eating Strep |
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| GAS infected by phage Subdermal tissues 2 toxins-Pyrogenic toxin A: superantigen-IL2 Exotoxin B-destroys tissues by breaking down protein 1in/hr |
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| Exanthems |
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| Viral diseases resulting in skin rashes |
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| Measles |
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| Rubeola virus |
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| Scarlet Fever |
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| s. PYOGENES |
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| German measles |
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| Rubella virus |
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| Disease 5/Erythema infectiosum |
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| Parovirus B19 |
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| Diseae 6/Roseola infantum |
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| Human Herpesvirus 6 |
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| Most dangerous pathogen of burn damaged skin |
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| P. aeruginosa GNR/Ox+ |
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| Sites of action of antimicrobials |
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| 1. Cell wall synthesis 2. Cell membrane function 3. Nucleic acid synthesis or replication 4. Bacterial ribosome and protein synthesis 5. Metabolic pathways |
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| Ciprofloxacin |
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| Quinolline DNA replication |
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| Sulfamethoxazole |
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| Sulfonamide Antimetabolites |
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| Tetracycline |
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| Tetracyline Protein synthesis |
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| Gentamicin |
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| Aminoglycoside Protein synthesis |
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| Cephalothin |
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| Beta Lactam cell wall synthesis |
