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;
219 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
Commonly occurring causative agents for intoxications
|
STAn's Intoxicated (ignore) Bowels Crap Creamy Poop (creamy poop = diarrhea.)
§ Staphylococcus aureus STAn's § Bacillus cereus Bowell's Crap § Clostridium perfringens Creamy Poop |
|
|
|
Commonly Occurring Causative Agents for Non-Inflammatory Infectious Gastroenteritis
|
§ Bacteria (Bacteria Eat Colon)
□ Enterotoxigenic Escherichia coli (ETEC): Montezuma's Revenge (the "T" in ETEC stands for Traveler…) □ Vibrio cholerae: curved gram negative rod with a polar flagellum; Rice Water Stool § Viruses (Viruses ARC) □ Rotaviruses □ Enteric adenoviruses (40-41) □ Caliciviruses (noroviruses, Sapporo-like viruses) § Parasites (protozoa) (Parasites Guard Crypts In Cycles) □ Giardia lamblia □ Cryptosporidium parvum & Cryptosporidium hominis □ Cyclospora cayetanensis □ Isospora belli |
|
|
|
Commonly Occurring Causative Agents Inflammatory Infectious Gastroenteritis
|
§ Bacteria (EHEC Shakes ViPer Salmon Close to Yer (your) Camp)
□ Enterohemorrhagic Escherichia coli (EHEC) (a more serious form) □ Shigella spp. □ Salmonella enterica □ Campylobacter jejuni □ Vibrio parahaemolyticus □ Yersinia enterocolitica □ Clostridium difficile § Parasites (protozoa) (Parasites Enter Balls) □ Entamoeba histolytica □ Balantidium coli |
|
|
|
Causative agents of penetrating infections
|
Salmonella typhi
Yersinia entercolitica |
|
|
|
Vibrio cholera serotypes that cause cholera
|
O1 & O139
|
|
|
|
Staph Aureus Virulence Factors
|
○ Virulence Factors (TCCEEE)
§ Cell envelope components (facilitate invasion of host, avoidance of host defenses, etc.) § Cytolytic toxins (kill various types of host cells) § Exfoliative toxins (→ certain skin diseases) § Toxic shock syndrome toxin TSST-1 (→ toxic shock) § Enzymes (abscess formation, enhance invasiveness) Enterotoxins (→ food poisoning) |
|
|
|
EHEC (STEC) dangerous strain
|
O157:H7
|
|
|
|
Ivermectin is the best treatment for...
|
Onchocerca volvulus
Strongyloidiasis |
|
|
|
Albendazole is the best treatment for...
|
Neurocysticercosis
Echinococcus granulosus |
|
|
|
Praziquantel is the best treatment for...
|
Trematodess and Cestodes
|
|
|
|
Diethylcarbamazepine is the best treament for...
|
lymphatic filariasis
|
|
|
|
Oxamniquine is used as an alternative treatment for...
|
Schistosoma mansoni
|
|
|
|
Pyrantel pamoate is effective against...
|
ascariasis, enterobiasis, trichostrongylus, and hookworm infections (PATHE)
|
|
|
|
Nitrazoxanide is used to treat X and Y, but also has activity against Z
|
X = Cryptosporidiosis (in children)
Y = Giardiasis (in children) Z = Ascaris |
|
|
|
Entecavir can be used in cases in which the patient has...
|
decompensated cirrhosis
|
|
|
|
Entecavir is used to treat what?
|
Primary HBV not Lamicudine-resistant HBV.
|
|
|
|
Telbivudine is slightly more potent than which drugs?
|
Lamivudine and Adefovir
|
|
|
|
Tenofovir is used as a treatment option for whom?
|
1st line agent for treatment-naive patients and patients withLamivudine, Telbivudine, or Entecavir resistance hepatitis.
|
|
|
|
Hepatitis C, the C stands for what?
|
chronic...70% of the cases of HCV progress to a chronic stage.
|
|
|
|
What do you use to treat HCV?
|
Ribavirin and Interferon
|
|
|
|
Ribavirin is also used to treat what sort of infection?
|
influenza
|
|
|
|
Post-Exposure Prophylaxis for HAV guidelines:
|
if you have not yet been vaccinated, then:
1 yr - 40 yrs: single antigen HAV vaccine immunocompromised or <1 or > 40 yrs: Ig is preferred |
|
|
|
Describe the HBV vaccine.
|
recombinant vaccine with subunit of HBV surface antigen.
Requires 3 doses. |
|
|
|
HBe is shed when?
|
when the virus is replicating; not the best marker for determining if the infection has resolved or not.
|
|
|
|
HBs is present when?
|
for a long period of time
|
|
|
|
HBc is what?
|
a core antigen that is not exposed to the exterior and is therefore not helpful for immunological recognition.
|
|
|
|
HAV serology:
IgM anti-HAV: IgG anti-HAV: |
IgM anti-HAV: diagnostic of acute infection, detectable before symptoms (used for early infection, b/c it disappears later)
IgG anti-HAV: appears early in fection and remains for lifetime. Can be used as a marker to see if you have been infected in the past. |
|
|
|
HBV serology looks at what?
|
HBe/s/c
|
|
|
|
anti-HBc:
IgM: IgG: |
IgM anti-HBc = acute/late acute
IgG anti-HBc = late acute/chronic |
|
|
|
HBsAg and HBeAg are what?
|
These are antigens on the surface of the HBV. They can be used as serological markers indicated the presence and stage of the infection.
HBs: present at all disease stages HBe: present in early acute/acute and chronic stages. |
|
|
|
Only exposed to HBc when?
|
during an active infection
|
|
|
|
Do HCV-HEV have vaccines?
|
No
|
|
|
|
dacryoadenitis
|
lacrimal gland infection
|
|
|
|
Dacryocystitis
|
lacrimal sac infection
|
|
|
|
Blepharitis
|
eyelid infection
|
|
|
|
External Hordeolum
|
infection of Zeiss/Moll tear glands in the eyelid margin
|
|
|
|
Internal Hordeolum
|
infection of the meibomian gland in the tarsal plate.
|
|
|
|
Orbital Cellulitis
|
Eyelid/Sinus Infections
Treat with Vancomycin, Clindamycin, Cefotaxime |
|
|
|
Conjunctivitis
|
Viral: often preceded by a URI
infection of the conjunctiva |
|
|
|
Keratitis with dendrite lesion is caused by what?
|
Herpese Simplex Virus
|
|
|
|
Keratitis is what?
|
infection of the cornea
|
|
|
|
Endophthalmitis
|
infection of the globe of the eye
|
|
|
|
Endemic trachoma is transmitted how?
|
eye to eye by Serotypes A, B, C
|
|
|
|
Inclusion conjunctivitis (trachoma)
|
sexually transmitted Chlamydia trachoma serotypes D-K
Not as severe (b/c adapted to STI infections style) |
|
|
|
Trachoma (Chlamydia infection)
|
Arlt Line
|
|
|
|
Bacterial dacryoadenitis.
|
○ Organisms
§ most commonly due to viral (mumps, Epstein-Barr virus) or bacterial infection (staphylococcus, and n. gonorrhoeae) |
○ Rx:
§ Bacterial - systemic antibiotics § Viral - warm compresses & rest |
|
|
• Dacryocystitis: lacrimal sac infection
|
○ Organisms
§ Staphylococcus & streptococcus sp. § Diphtheroids, Klebsiella pneumoniae, Haemophilus influenzae, Pseudomonas aeruginosa, Actinomyces and fungi (Candida) |
○ Rx:
§ systemic antibiotics and topical antibiotics § needle aspiration if needed, surgery to reestablish patent drainage system. □ Drain this structure with a needle |
|
|
• Blepharitis
|
○ Organisms
§ primarily staphylococcus, less commonly streptococcus; § also hsv, molluscum (immunocompromised) |
○ Therapy
§ lid scrubs (with Johnson's Baby shampoo), antibacterial antibiotics (erythromycin, gentamicin, sulfa) |
|
|
• Stye & Chalazion
|
○ Organisms
§ Primarily staphylococcus & streptococcus, normal flora |
○ Therapy
§ Hot compresses, antibacterial antibiotics (erythromycin, gentamicin, sulfa), surgical drainage |
|
|
• Orbital Cellulitis
|
○ Organisms
§ Staphylococcus aureus, Streptococcus or Haemophilus influenzae |
○ Rx:
§ systemic antibiotics (Vancomycin -MRSA, Clindamycin, Cefotaxime) |
|
|
• Conjunctivitis
|
○ Organisms
§ Bacterial (Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus sp, Chlamydia trachomatis, Neisseria gonorrhoeae) § Viral (adenovirus) |
○ Therapy
§ Antibacterials, hygiene (viral) |
|
|
• Keratitis
|
○ Organisms
§ wide range of fungal, bacterial, protozoa (acanthamoeba), viral (herpes) |
○ Therapy
§ Antimicrobial drops |
|
|
• Retinitis
|
○ Organisms
§ viral (herpetic), parasitic (toxoplasmosis, toxocariasis), fungal (candida) |
○ Therapy
§ systemic antimicrobials |
|
|
• Endophthalmitis
|
○ Organisms
§ bacterial □ staphylococcus, streptococcus – surgical □ Pseudomonas, E. coli, enterococcus – penetrating |
○ Therapy
§ intraocular & systemic antimicrobials § surgical debridement |
|
|
IgM anti-HBc test:
|
This is the most reliable test for diagnosing acute HBV infection.
|
|
|
|
S. Pyogenes
|
Pen G +/- Clindamycin (Bad MC)
Prompt aggressive debridement of infected tissue |
|
|
|
Clostridium Perfringens
|
Pen G +/- Clindamycin (Bad MC)
2nd Line - ceftriaxone, Erythromycin Prompt aggressive debridement of infected tissue. Hyperbaric Oxygen |
|
|
|
M. Tuberculosis
|
RIPE, Streptomycin
|
|
|
|
S. Aureus
|
High, daily dose of IV antibiotic therapy for 4-6 weeks. Use antistaphylococcal penicillin (NOD), 1st generation cephalosporin -cefazolin,
|
|
|
|
Chlamydia trachomatis
|
AZ/DC?
Since it is due to the immune response… perhaps no treatment? |
|
|
|
S. Epidermidis
|
Removal of prosthetic joint
High doses of parenteral antibiotics for 4-6 weeks |
|
|
|
S. Aureus
|
SSSS - NOD (MSSA) or Vancomycin (MRSA)
Bullous Impetigo - Mupirocin (Topical, PS Inhibitor), Dicloxacillin or Cephalexin (MSSA), TMP-SMX, or Clindamycin, or Minocycline (MRSA) |
|
|
|
S. Pyogenes
|
Uncomplicated Cellulitis: IV - Pen G, Nafcillin, Oxacillin, Cefazolin.
Oral Dicloxacillin. If MRSA - Vancomycin, Daptomycin, Linezolid |
|
|
|
M. Leprae
|
Preferred: Dapsone, Rifampin.
Alternative - Ofloxacin, Levofloxacin, Minocycline, clarithromycin. "Dr. CLOM has Leprosy |
|
|
|
Rickettsia Rickettsii
|
Doxycycline - preferred
Chloramphenicol - Alternative "Ritzy Rickettsi likes to treat herself at DC. |
|
|
|
Rickettsia Akari
|
Self limiting
|
|
|
|
Propionibacterium
P. acnes P. propionicum |
1. Topical Retinoids, Topical Antimicrobials - Benzoyl Peroxide, Erythromycin, Sulfacetamide, dapsone
|
|
|
|
N. Gonorrhoeae
|
"Greek Cefs"
Ceftriaxone (IV or IM every 24 hrs) or Cefotaxime (IV every 8 hours) for 7-14 days |
|
|
|
Parvovirus B19
|
Nothing
|
|
|
|
Rubeola (Measles) Virus
|
Vaccine - MMR (Live attenuated)
|
|
|
|
Streptococcus Pyogenes, Staphylococcus Aureus
|
Mupirocin
|
|
|
|
VZV
|
Vaccine - Zostavax
Oral - Acyclovir, Valacyclovir, Famciclovir Topical- Acyclovir, penciclovir |
|
|
|
Rubella
|
MMR Vaccine (live attenuated)
|
|
|
|
Tinea Infection
|
Tinea Capitis - Griseofulvin superior to terbinafine, itraconazole, fluconazole
Tinea Pedis - terbinafine and Naftifine Tinea Corporis - Oral terbinafine, Itraconazole, fluconazole Tinea Cruris - Topical antifungal Oral Griseofulvin |
|
|
|
Anaerobic Cocci/ Pepto-streptococcus
|
Broad spectrum therapy
|
|
|
|
Rickettsia Akari
|
Self limiting
|
|
|
|
Propionibacterium
P. acnes P. propionicum |
1. Topical Retinoids, Topical Antimicrobials - Benzoyl Peroxide, Erythromycin, Sulfacetamide, dapsone
|
|
|
|
N. Gonorrhoeae
|
"Greek Cefs"
Ceftriaxone (IV or IM every 24 hrs) or Cefotaxime (IV every 8 hours) for 7-14 days |
|
|
|
Parvovirus B19
|
Nothing
|
|
|
|
Rubeola (Measles) Virus
|
Vaccine - MMR (Live attenuated)
|
|
|
|
Streptococcus Pyogenes, Staphylococcus Aureus
|
Mupirocin
|
|
|
|
VZV
|
Vaccine - Zostavax
Oral - Acyclovir, Valacyclovir, Famciclovir Topical- Acyclovir, penciclovir |
|
|
|
Rubella
|
MMR Vaccine (live attenuated)
|
|
|
|
Tinea Infection
|
Tinea Capitis - Griseofulvin superior to terbinafine, itraconazole, fluconazole
Tinea Pedis - terbinafine and Naftifine Tinea Corporis - Oral terbinafine, Itraconazole, fluconazole Tinea Cruris - Topical antifungal Oral Griseofulvin |
|
|
|
Anaerobic Cocci/ Pepto-streptococcus
|
Broad spectrum therapy
|
|
|
|
What is contained in mast cell granules?
|
1) Enzymes (neutral proteases, acid hydrolases, cathepsin G, carboxypeptidases)
2) TNF-alpha 3) Histamine, Heparin |
|
|
|
Type 1 Late Phase: Lipid Mediators
|
1) Prostaglandin D2: Vasodilation, bronchoconstriction, neutrophil chemotaxis
2) Leukotriene (C4, D4, E4): prolonged vasoconstriction, mucus secretion, increasesd vascular permeability 3) Platelet-Activating Factor: Chemotaxis and activation of leukocytes, broncho constriction, increased vascular permeability Late Phase Cytokines: Production of IgE and attraction of Eosinophils |
|
|
|
Glucocorticoid modification:
methyl group on 6 or 16 |
decrease mineralcorticoid activity
|
|
|
|
Glucocorticoid modification:
hydroxyl group on 16 |
decrease mineralcorticoid activity
|
|
|
|
Glucocorticoid modification:
double bond between 1 and 2 |
increase in anti-inflammatory activity
|
|
|
|
Glucocorticoid modification:
fluoride between the 6 and 9 |
increase in anti-inflammatory activity
|
|
|
|
How does cortisol inhibit leukocyte action?
|
Cortisol binds to CBG --> Enters the nucleus --> modulates transcription
|
|
|
|
Cortisol effects on metabolism
|
§ Effects on metabolism
□ Carbohydrates and Proteins: ® stimulate gluconeogenesis in the liver: the production of glucose from glycerol and amino acids ® stimulate glycogenesis in the liver ® diminish peripheral glucose utilization ® increase protein breakdown ® Lipids: activate lipolysis in the periphery |
|
|
|
Cortisol anti-inflammatory effects
|
§ Anti-inflammatory effects
□ suppress activation of T lymphocytes □ suppress production of cytokines by activated helper T cells □ prevent release of inflammatory mediators (histamine, prostaglandins, leukotrienes) by mast cells, basophils, and eosinophils □ stabilize lysosomal membranes and prevent release of catabolic enzymes stimulate vasoconstriction and decrease capillary permeability both directly and indirectly by inhibiting the actions of kinins, bacterial toxins and other mediators |
|
|
|
Anti-Inflammatory Corticosteroids
|
Prednisones and Dexamethasone
|
|
|
|
Mineral Corticosteroids
|
Fludrocortisone
|
|
|
|
Rhogam
|
Prevents Hemolytic Disease of Newborn (HDN); Anti-D Gamma globin that mops of fetal RBCs in the maternal circulation so maternal Rh antibodies will not be produced (prevents B cell activation and memory formation)
|
|
|
|
Goodpasture's syndrome
|
antibodies against glomerular basement membrane ('G' oodpasture ~ 'G' lomerular)
|
|
|
|
Myastenia gravis
|
Antibodies reactive with acetylcoline receptos in the motor end plates of skeletal muscles block neuromuscular transmission and therefore muscle weakness
|
|
|
|
Graves disease (hyperthyroidism)
|
Antibodies against the thyroid-stimulating hormone receptor on thyroid epithelial cells stimulates cell function
|
|
|
|
Antibodies deposited on fixed tissues stimulate what?
|
1) Complement activation
2) Release or generation of prostaglandins, vasodilator peptides, and chemotactic substances 3) Production of other substances that damage tissues (re-structure tissues) 4) Binding to the Fc receptor and phagocytosis |
|
|
|
Arthus reaction
|
Type 3 hyper sensitivity reaction due to subcutaneous administration of antigen
|
|
|
|
What are the two types of Type 4 hypersensitivity reactions?
|
1) Delayed-type hypersensitivity
2) Contact hypersensitivity |
|
|
|
How does contact hypersensitivity occur (Type 4)?
|
1) agent penetraes skin and binds to self proteins
2) self proteins are then taken up, processed, and presented on APCs 3) activation of Th1 cells which secrete IFN-y 4) Keratinocytes secrete inflammatory cytokines to attract macrophages 5) Macrophages that arrive at the site are further stimulated to secrete inflammatory mediators |
|
|
|
Treatment of type 4 hypersensitivity reactions
|
1) Relieve the pruritis: calamine, anti-histamines
2) topical glucocorticoids for early stages 3) 2-3 weeks of oral glucocorticoids |
|
|
|
What causes Type 1 Necrotizing Fasciitis?
|
Streptococcus
Penicillin G +/- Clindamycin |
|
|
|
What causes Type 2 Necrotizing Fasciitis?
|
Clostridium
Penicillin G +/- Clindamycin |
|
|
|
What causes Type 3 Necrotizing Fasciitis?
|
Polymicrobial
Carbapenems or Ampicillin +/- Sulbactam +/- Clindamycin +/- Metronidazole |
|
|
|
What causes Type 4 Necrotizing Fasciits?
|
MRSA
Vancomycin +/- Daptomycin plus Carbapenems or Ampicillin +/- Sulbactam +/- Clindamycin +/- Metronidazole |
|
|
|
Three Protozoan GI pathogens
|
1) Cryptosporidium: watery stool
2) Giardia: fatty stool 3) Entamoeba: bloody stool |
|
|
|
Target for Staph Aureus exfoliative toxins.
|
desmoglein 1; disrupts intercellular bridges in the stratum granulosum
|
|
|
|
Which contains bacteria in lesions? SSSS or Bullous Impetigo
|
Bullous Impetigo
|
|
|
|
Mupirocin
|
Topical protein synthesis inhibitor; used to treat Bullous Impetigo
|
|
|
|
S. pyogenes skin disorders
|
1) erysipelas
2) cellulitis 3) necrotizing fasciitis |
|
|
|
Psuedomonas, think...
|
oxidase positive
puncture wounds burn wounds folliculitis finger nail infections osteocondritis of foot external otitis |
|
|
|
Pseudomonas skin infection
|
Las A and Las B damage elastin containing tissues are result in Ecthyma Gangrenosum (develop in disseminated infections)
|
|
|
|
Sulfacetamide is used for what disease and what does it do/
|
Used to treat acne
interferes with folic acid synthesis |
|
|
|
Tuberculoid Leprosy (Hansen's Leprosy) histology
|
many lymphocytes and granulomas (typical of mycobacterium infections)
Primarily a Th1 response few or no visible bacteria diagnosis is confirmed by a skin test (reactivity to lepromin) |
|
|
|
Th1 cytokine profile
|
IFN-y
IL-2 TNF-B |
|
|
|
Lepromatous Leprosy histology
|
foamy macrophages, feew lymphocytes, lack of langerhans cells numerous acid-fast rods
|
|
|
|
Lepromatous Leprosy
|
depressed cell-mediated immunity
strong antibody response growth of bacteria in macrophages (lots of bacteria present) Th2 response (B-cells): IL-10 suppresses macrophage activation |
|
|
|
Th2 cytokine profile
|
IL-4
IL-5 IL-10 |
|
|
|
IL-10
|
suppresses macrophage activation
|
|
|
|
IFN-y
|
activates macrophages
|
|
|
|
Two medications that cause Agranulocytosis.
|
Dapsone and Primaquin
(this results in a decrease in the number of granulocytes and therefore the immune system is impaired) |
|
|
|
Intracellular parasite bacteria that move from cell to cell without leaving the intracellular environment.
|
Chlamydia
Ricketsia (OmpA) Shigella |
|
|
|
Erysipelothrix rhusiopathiae
|
inflammatory, painful and pruritic lesions (erysipeloid)
|
|
|
|
Capnocytophaga
|
filamentous, Gram-negative rod; infections related to cat and dog bites
|
|
|
|
Pasteurella multocida
|
gram-negative coccobacillus' infections related to animal bites
|
|
|
|
Bacillus anthracis
|
Gram-positive, spore-forming rod; cutaneous anthrax
|
|
|
|
HHV3
|
vericella-zoster virus
|
|
|
|
Isoniazad,Ethambutol, Streptomycin and FQN, absorption?
|
delayed absorption with Al anti-acids
|
|
|
|
What vaccine is used to prevent shingles and postherpatic neuralgia?
|
Zostavax
|
|
|
|
HHV-6/7 cause...
|
Roseolum Infantum
|
|
|
|
Some of the diseases caused buy pathogens in which humans are the only known hosts
|
German measles
Shigella Salmonella Typhi |
|
|
|
Rubella vaccine
|
MMR
Meruvax is the rubella component that is a live attenuated virus |
|
|
|
Diseases that are more serious in adults than children
|
Mumps, Hepatitis, Rubella (German Measles)
|
|
|
|
Herpangia
|
sore throat, painful swallowing, vomiting
ulcerated lesions on the soft palate and uvula. Coxsackie A: herp'A'ngia |
|
|
|
Which Coxsackie virus causes hand-foot-mouth disease?
|
coxsackie A15
|
|
|
|
Clostridium perfringens produces its fast-acting enterotoxin when...
|
it sporulates in the alkaline conditions of the intestine
|
|
|
|
Two main dermatophyte genera:
|
Trichophyton and Microsporum
|
|
|
|
CTL granules contain:
|
1) perforin (makes pores)
2) granzymes (initiate apoptosis) |
|
|
|
Prevention/Treatment of Acute GVHD
|
Methotrexate and Cyclosporine
|
|
|
|
Prevention/Treatment of Chronic GVHD
|
Prednisone, Cyclosporin, Tacrolimus, Mycophenolate Mofetil
|
|
|
|
Prevention/Treatment of Uncomplicated, Chronic GVHD
|
Prednisone
|
|
|
|
Prevention/Treatment of Chronic GVHD
|
Thalidomide
|
|
|
|
New agents for prevention/treatment of GVHD
|
anti-CD20 monoclonal antibody Rituximab
Pentostatin (nucleoside analog) |
|
|
|
Epstein-Barr Virus is which Herpes virus?
|
HHV-4
|
|
|
|
Epstein Barr Virus can cause which cancers?
|
1) Burkitt's Lymphoma (B-cell Lymphoma)
2) Hodgkin lymphoma 3) Nasopharyngeal Carcinoma |
|
|
|
HBV and HCV can cause what cancer?
|
hepatocellular carcinoma
|
|
|
|
GM-CSF
|
can be injected into tumor cells to attract and activate dendritic cells that will lead to their destruction
|
|
|
|
Bevacizumab function
|
neutralizes VEGF (vascular endothelial growth factor)
anti-angiogenic |
|
|
|
What are the four diseases/lesions caused by nocardia?
|
1) Bronchopulmonary disease
2) Lymphocutaneous disease 3) Cellulitis subcutaneous subcutaneous 4) Brain abscess Nocardia is exogenous and lives in nitrogen rich soils |
|
|
|
Parvovirus B19 presentation in adults
|
anemia, arthralgias, arthritis, usually no rash
reticulocytopenia for 7 to 10 days (length of time for the immune response) |
|
|
|
What are the dangers for a seronegative mother that gets infected with Parvovirus B19 during her pregnancy?
|
anemia, congestive heart failure (hydrops fetalis) for the baby
|
|
|
|
Distinguishing feature of early measles...
|
conjunctivitis with lacrimation
|
|
|
|
Koplick spots are unique to...
|
Measles
|
|
|
|
Members of the paramyxoviridae family
|
1) measles
2) mumps 3) respiratory syncytial virus |
|
|
|
3 Diseases that can result in crusted skin lesions:
|
1) Nonbulous Impetigo
2) Oral Herpes 3) Vericella |
|
|
|
NonBullous Impetigo is caused by what pathogens?
|
Initiated by Strep. pyogenes and then a secondary infection occurs with Staph. aureus.
|
|
|
|
Two most common causative agents of cellulitis:
|
1) Staph. aureus
2) Strep Pyogenes |
|
|
|
Anaerobe infection characteristics
|
foul smelling, crepitant, due to fermentative processes
Tissue samples must be obtained such that the bacteria is not exposed to O2. |
|
|
|
Clostridium perfringens toxin:
|
alpha toxin (phospholipase C) lyses erythrocytes, platelets, endothelial cells and other human cells
|
|
|
|
Involucrum
|
layer of new bone that is formed around sequestre in osteomylietes.
|
|
|
|
Predisposing factor to Reiter's syndrome
|
HLA-B27
|
|
|
|
Reiter's syndrome is seen with:
|
Chlamydia
and GI infections like: 1) Yersinia enterocolitica 2) Campyobacter jejuni 3) Salmonella |
|
|
|
Treatment of nongonococcal bacterial arthritis:
Gram (+) Cocci |
Vancomycin
|
|
|
|
Treatment of nongonococcal bacterial arthritis:
Gram (-) bacilli |
3rd Generation Cephalosporin
plus Aminoglycoside (if pseudomonas is likely) |
|
|
|
TORCH
|
Toxoplasmosis
Other (Group B Strep {Strep Agalactiae}, Listeria monocytogenes, HIV, Hepititis B, Syphilis) Rubella Cytomegalovirus (CMV) Herpes Simplex Virus |
|
|
|
4 pathogens acquired normally in utero and the birth defects they cause.
|
Toxoplamosis and CMV: neurological defects
Rubella: cataracts, deafness, retardation Syphilis: noticable hydrops |
|
|
|
Strep. pyogenes
|
aka Group A Strep
|
|
|
|
Strep. agalactiae
|
aka Group B Strep
|
|
|
|
What is the only Gram Positive Rod that does not produce spores?
|
Listeria
|
|
|
|
Listeria virulence factors
|
1) Internalin
2) Listeriolysin O 3) Phospholipases |
|
|
|
What causes Granulomatosis Infantiseptica?
|
Listeria monocytogenes
(Early Onset Neonatal Disease) |
|
|
|
Late Onset Neonatal Disease (Listeria)
|
2-3 weeks post partum
Meningitis |
|
|
|
Lack of MAC (C5-C8)
|
susceptible to Neisseria
|
|
|
|
Lack of C3
|
more infections by encapsulated bacteria (Staph)
|
|
|
|
Lack of DAF (Decay Accelerating Factor)
|
Nocturnal Hemoglobinuria
|
|
|
|
CD-19 and CD-20 are proteins found on the surface of what cell?
|
B cell
|
|
|
|
CD-3 is found on the surface of what cell?
|
T cell
|
|
|
|
X-linked Agammaglobulinemia
|
(Bruton's agammaglobulinemia)
Defect in Btk, a tyrosine kinase to survival of progenitor B cells after H chain gene rearrangement, and survival of mature B cells |
|
|
|
No IgA, what infections will be common?
|
lung, sinus
|
|
|
|
Characteristic of lymph nodes in patients with hyper IgM syndromes
|
no germinal centers
|
|
|
|
CD 56 is a surface protein for which cells?
|
NK cells
|
|
|
|
CD-25 is a receptor for what?
|
IL-2
|
|
|
|
GM-CSF attracts what cells?
|
leukocytes
|
|
|
|
How to treat X-linked hyper IGM syndrome
|
IgG and GM-CSF supplementation
|
|
|
|
Bruton's agammaglobulinemia has low levels of what?
|
Mature B cells (there are plenty of pre-B cells) and few IgG, IgA, IgM, IgD, IgE
|
|
|
|
Hyperr IgM patients have lots of what types of infections?
|
sinopulmonary and GI infections
|
|
|
|
DiGeorge's syndrome
|
Congenital malformation in development of hte third and fourth pharyngeal pouches --> hypoplasia of the thymus --> deficient T cell maturation
Sometimes absent parathyroid gland results in abnormal caclcium homeostasis and tetany |
|
|
|
Ig's that activate complement
|
IgM, IgG1, IgG3
|
|
|
|
Main Ig's for Opsonnization
|
IgG1/3
|
|
|
|
Main Ig's for sensitizing NK cells
|
IgG1/3
|
|
|
|
Clinically important competent bacteria:
|
Competent: capable of taking up free DNA
1)Haemophilus influenza 2) Strepotococcus pneumoniae 3) Bacillus (anthrax) 4) Neisseria |
|
|
|
Bacterial Drug Resistance Mechanisms: Porin Mutations confer resistance to...
|
1) Penicillins
2) Aminoglycosides (Gentamycin, Streptomycin) |
|
|
|
Bacterial Drug Resistance Mechanisms: Efflux Pumps confer resistance to...
|
1) Tetracyclines
2) Sulfonamides 3) Quinolones |
|
|
|
Bacterial Drug Resistance Mechanisms: Mutation in catalase-peroxidase
|
Isoniazid
|
|
|
|
Bacterial Drug Resistance Mechanisms: Replacement of alanine with lactate in bacterial peptidoglycan
|
Vancomycin
|
|
|
|
Vector for sylvanic plague
|
Xenopsylla (rat flea)
|
|
|
|
Mallory Bodies
|
Alcoholic hepatitis
Accumulations of proteins in cells |
|
|
|
Gaucher's Disease
|
Accumulations of complex lipids and carbohydrates in cells
|
|
|
|
dystrophic calcifications
|
dead or dying tissue; normal Ca2+ levels
|
|
|
|
metastatic calcifications
|
normal tissue; hypercalcemia (ie calcium deposits
|
|
|
|
Coagulative necrosis
|
characterized by the preservation of cell and tissue architecture for up to several days. The “ghosts” of the pre-existing cells remain identifiable for up to several days.
This type of necrosis is that which is seen in ischemia (deprivation of blood supply). Denaturation of protein predominates in this pattern of necrosis |
|
|
|
Liquefactive necrosis
|
takes its name from the fact that the affected tissue become “liquid”.
It is often the result of bacterial infections which result in the formation of an abscess [a localized collection of pus (necrotic cellular debris and pmn’s)] Enzymatic digestion of tissue predominates in this pattern of necrosis primarily as the result of the degradative action of PMN’s • Coagulative necrosis may ultimately come to look like liquefactive necrosis due to the action of the PMN’s on the dead tissue as part of the inflammatory response elicited by the dead tissue |
|
|
|
Caseous necrosis
|
named for its gross appearance-which is like cheese
Often results from infection with Mycobacterium tuberculosis. • In reality it is a distinctive form of coagulative necrosis (denaturation of structural proteins) Gross appearance: Yellow-white, dry and friable Microscopic appearance: Eosinophilic amorphous debris often times associated with a “giant-cell” reaction |
|
|
|
Enzymatic fat necrosis
|
much like caseous necrosis, is a subset of coagulative necrosis.
Typically it is a focal process resulting in the death of adipose tissue often the result of injury to the pancreas which results in release of lipase and destruction of the adipocytes This is an example of dystrophic calcification Triglycerides from the fat cells unite with calcium from local circulation to become “soaps” (dystrophic calcification) which gives these lesion their characteristic appearance Gross: White chalky appearance typically involving abdominal or retroperitoneal fat Microscopic: One sees the outline or “ghosts” of the adipocyte without a nucleus (coagulative necrosis) associated with calcium deposits (which typically have a blue smudgy appearance on H&E sections) |
|
|
|
Fibrinoid necrosis
|
another example of a subset of coagulative necrosis.
typically it involves small vessels and is not visible macroscopically Microscopically it looks like packed fibrin (deeply eosinophilic and homogeneous). Hence the name “fibrin-oid” (fibrin like). Often associated with autoimmune disorders which result in inflammation of the vascular walls (vasculitis) |
|
|
|
Necrosis is characterize by:
|
Loss of membrane integrity, Enzymatic digestion of cells, Leakage of cellular contents, Frequently eliciting an inflammatory response
|
|
|
|
Apoptosis is characterized by:
|
Cell shrinkage (in most other forms of cell injury cell swelling predominates), Loss of mitochondrial function, Disruption of the cytoskeleton, Chromatin condensation, Fragmentation without loss of membrane integrity, Little if any inflammatory response, Rapid phagocytosis
|
|
|
|
Pyknosis
|
Nuclear Shrinkage. The nucleus becomes a small dark ball
|
|
|
|
Karyolysis
|
Fading of the nucleus
|
|
|
|
Karyorrhexis
|
The nucleus breaks up into little pieces (so-called nuclear dust)
|
|
|
|
Guillain-Barre syndrome
|
Type 2 hypersensitivity directed against GM1 gangliosides and is associated with C. jejeuni infections
|
|
|
|
Examples of Type 4 Hypersensitivities
|
1) Type 1 diabetes (insulin dependent diabetes mellitus)
2) Rheumatoid arthritis 3) Multiple Sclerosis |
|
|
|
Examples of type 2 hyper sensitivities
|
1) Autoimmune hemolytic anemia
2) Godd pastures syndrome 3) Guillain-Barre Syndrome |
|
|
|
rituximab
|
monoclonal antibody that targets CD20 cells (B cells ) for destruction by NK cells
Treatment of Rheumatoid Arthritis. |
|
|
|
TH17 cell
|
T cells that specifically interact with myelin glycoprotein and cause MS
|
|
