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;
107 Cards in this Set
- Front
- Back
What drug has the following MOA? Inhibits transcription of IL-2 -> inhibition of T-cell activation
|
(Calcineurin inhibitors) Cyclosporine
|
|
What drug's absorption is very erratic (pka issue), so we must do therapeutic drug monitoring?
|
Cyclosporine
|
|
What drug has the following MOA? Binds to FKBP-12 --> binding and inhibition of mTOR --> inhibition of G1-S phase progression? (CELL CYCLE ARREST), cells are then not responsive to IL-2
|
(Antimetabolite class) Sirolimus/Rapamycin
|
|
What drug is used for prophalaxis of organ rejection in patients receiving renal transplants?
|
Sirolimus/Rapamycin
|
|
What drug has the following MOA? The active metabolite MPA inhibits inosine monophosphate (IMPDH) --> inhibition of de novo guanosine nucleotide synthesis --> inhibition of T and B lymphocyte proliferation
|
(Antimetabolite class) Mycophenolate Mofetil
|
|
Which drug is used therapeutically for -prophylaxis of organ rejection concomitantly with Cyclosporine and corticosteroids in patients receiving allogeneic renal (CellCept, Myfortic), cardiac (CellCept), or hepatic (CellCept) transplants
|
(Antimetabolite class) Mycophenolate Mofetil
|
|
Which immunopharm drug has adverse effects on bone marrow?
|
Mycophenolate mofetil
|
|
Which drug has the following MOA? Binds to the CD3 cell surface receptor on thymocytes and T cells --> disruption of IL-2 signaling?
|
Muromonab-CD3
|
|
Which drug has the following MOA? A composition of cytotoxic antibodies directed against T-cells and inhibits lymphocyte function and direct cytotoxicity of lymphocytes?
|
Anti-thymocyte globin (Thymoglobulin)
|
|
What is another name for lesions that produce purpura (small hemorrhages) in skin?
|
Petechiae
|
|
Discontinuities in skin; complete loss of epidermis & often depressed in center (e.g. chancre of primary syphilis)
|
Ulcers
|
|
Large, blister-like, fluid filled vesicles
|
Bullae (bullous impetigo lesions)
|
|
Nodules consisting of lumpy & swollen accumulations of tissue
|
Nodular eruptions (e.g. some disseminated fungal diseases)
|
|
Proliferations of epithelial tissue caused by HPV
|
Warts
|
|
What is the causative agent of Pityriasis (Tinea)Versicolor?
|
Malassezia furfur
|
|
What condition is diagnosed by visualization of yeast cells and short hyphae "spaghetti and meatballs" in KOH-treated scrapings from lesion? (Lesions fluoresce yellow on exposure to UV light)
|
Pityriasis (Tinea) Versicolor (Malassezia furfur)
|
|
What pathogen leads to irregular pigmented (brown-black) lesions, usually on the palms or soles?
|
Tinea Nigra (Hortaea wernecki)
|
|
While still rare what is the only common subcutaneous mycosis in the US?
|
Sporotrichosis: Sporothrix schencki
|
|
What is a common name for the most common cutaneous mycoses?
|
Tinea or ring worm infections dermatophyte fungi ; Most important genera: Trichophyton & microsporum
|
|
With microscopic evaluation of tinea infections what are you looking for?
|
Septate fungal hyphae in KOH-treated scraping from lesion
|
|
What are the 7 types of tinea infections.
|
1. Tinea corporis 2. Tinea capitis (scalp) 3. Tinea Unguium 4. tinea pedis (athletes foot). 5. Tinea barbae (reingworm of the face and/or neck
|
|
What is the term for sloughing of the epidermal tissue?
|
Positive Nikolsky sign
|
|
What virulence factors are serine proteases that cleave desmoglein 1? They disrupt intercellular bridges in stratum granulosum epidermis (destabilizing epithelium)
|
ETA, ETB (Exfoliative toxins) of S. Aureus
|
|
Abrupt onset of perioral erythema that spreads over entire body within 2 days. Bullae form, desquamation of epithelium. ETB mostly, What is the causative pathogen and what is the syndrome called?
|
SSSS (staphylcoccal scaled skin syndrome) Ritter disease
|
|
Localized form of SSSS, mostly associated with ETA,
|
Bullous impetigo
|
|
LasA & LasB are enzymes that degrade elastin, cause hemorrhagic lesions(ecthyma gangrenosum) that develop in disseminated infections
|
Pseudomonas Aeruginosa
|
|
Hot tub folliculitis, fingernail infections, osteochondritis
|
Pseudomonas Aeruginosa
|
|
External otitis (swimmers ear), malignant external otitis**
|
Pseudomonas Aeruginosa
|
|
P. Aeruginosa
|
Aztreonam, 4th gen pens (Ticarcillin, piperacillin)
|
|
Pathogen grows in sebaceous follicles, secretes peptides that attract leukocytes, local inflammatory response
|
Acne Vulgaris/ Propionibacterium acnes
|
|
What are 2 forms of leprosy?
|
Tuberculoid and Lepromatous
|
|
Associated with strong cellular immune response, erythematous or hypopigmented plaques on skin, peripheral nerve damage and sensory loss, low infectivity, confirmed by skin test
|
Tuberculoid leprosy
|
|
What is confirmed by a skin test to Lepromin?
|
M. Leprae
|
|
Which type of immune response is predominate in Tuberculoid leprosy?
|
Th1 cells (granuloma formation, disease progresses slowly)
|
|
Which type of immune response is predominate in
|
Th2 cells predominate (depressed cell-mediated) growth of bacteria in macrophages
|
|
Associated with strong antibody response, erythematous macules, papules, nodules on skin, patchy sensory loss Histo: "Foamy" macrophages, few lymphocytes, NUMEROUS acid-fast rods HIGH infectivity
|
M. Leprae, lepromatous leprosy
|
|
Which drug has the following MOA? Competitive antagonist of PABA --> inhibition of folic acid synthesis
|
Dapsone
|
|
What anti-Tb drug has agranulocytosis and hemolysis as adverse effects?
|
Dapsone
|
|
What are the 2 pathogens of the spotted fever diseases and their disease names?
|
Rickettsia Rickettsii - Rocky Mountain Spotted Fever Rickettsia Akari - Rickettsialpox
|
|
Which disease starts with a rash on the wrists, arms, ankles then moves into the trunk?
|
Rocky Mountain spotted Fever (Rickettsia Rickettsii)
|
|
What pathogen/disease is associated with a "cosmopolitan" disease?
|
Rickettsial Pox/ Rickettsia akari
|
|
Papulovesicular rash, eschars*
|
Rickettsial Pox/ Rickettsia akari
|
|
What type of extrachromosomal elements sometimes occasionally incorporate into the chromosome?
|
Episomes
|
|
What are the 5 main things plasmids code for?
|
1. Resistance to heavy metals (Hg, Cr, etc) 2. Ability to degrade complex organic compounds 3. Pili that aid in attachment to tissue surfaces 4. Toxins & other virulence factors (e.g. anthrax) 5. Antibiotic resistance and multiple resistance
|
|
This type of bacteriophage can replicate in the bacterial cell, eventually causing the cell to lyse
|
Lytic infection
|
|
This type of bacteriophage integrates into the host cell's chromosome w/o killing the host cell
|
Lysogenic infection
|
|
What are mobile genetic elements?
|
transposons "jumping genes"
|
|
What are clusters of genes that code for virulence factors that can move within the chromosome or into the plasmid and be transferred to other cells?
|
Pathogenicity (virulence) islands
|
|
The uptake of naked DNA from the environment, can acquire plasmids, drug-resistant genes, etc
|
Transformation
|
|
What are the 4 clinically important bacteria that transfer genes by transformation?
|
1. H. Influenzae (meningitis, otitis media), 2. S. Pneumoniae, 3. Bacillus spp (Anthrax, etc.), 4. Neisseria spp (gonorrhea, meningitis)
|
|
Direct one-way transfer of DNA from cell to cell
|
Conjugation
|
|
Cells with F plasmid & F pilus
|
F+ cells (donor cell)
|
|
Cells without F plasmid
|
F- cells (recipient cell)
|
|
F plasmid integrates into chromosome of host cell -> Single strand of HFR chromosome mobilized and starts to move into recipient cell (Only part of chromosome transferred in typical conjugation event
|
Hfr cell (High freq. of recombination)
|
|
Why does an F- cell stay F-?
|
Only part of the F plasmid is transferred because the conjugation bridge is fragile
|
|
Genetic transfer mediated by bacteriophages
|
Transduction
|
|
What are the 3 ways bacteria develop resistance?
|
1. Decrease access of drug to target site 2. Export of drug from bacterial cell 3. Modify drug target in bacterial cell
|
|
Modification in 30S subunit of bacterial ribosome leads to resitance to:
|
Aminoglycosides
|
|
Modification in Replacement of alanine with lactate in bacterial peptidoglycan leads to resitance to:
|
Vancomycin
|
|
Modification in DNA gyraseleads to resitance to:
|
Quinolones
|
|
Modification in RNA polymeraseleads to resitance to:
|
Rifampin
|
|
Modification in catalase peroxidase leads to resitance to:
|
Isoniazid
|
|
Modification in penicillin-binding proteins leads to resitance to:
|
Penicillins
|
|
Chickenpox, shingles (What is the common viral name and classification?)
|
HHV3, Varicella-zoster
|
|
Mononucleosis, lymphomas, carcinoma
|
HHV4, EBV
|
|
Congenital & opportunistic infections
|
HHV5, CMV
|
|
Roseola, mono-like syndrome, etc
|
HHV6, Herpes lymphotophic virus
|
|
Roseola, mono-like syndrome, etc
|
HHV7
|
|
Kaposi sarcoma
|
HHV8
|
|
Cold sores/Fever blisters, lesions around and/or throughout mouth
|
HSV-1 (most) or HSV-2
|
|
Massive outbreak of cold sores in mouth area (primarily in children or immunocompromised)
|
Gingivostomatitis (HSV-1 &2)
|
|
Infection of finger, nurses, physicians, thumb sucking childrend
|
Herpetic Whitlow(HSV-1 &2)
|
|
Infection of the body, often acquired during wresting or playing rugby
|
Herpes Gladiatorum (HSV-1 &2)
|
|
Occurs in children with active eczema; relatively rare in adults
|
Eczema Herpaticum (HSV-1 &2)
|
|
Lesions typically involve a single dermatone
|
Shingles/ HHV3 (Varicella-Zoster)
|
|
Latent infection can be established in dorsal root or cranial nerve ganglia and be reactivated later in life , transmission is by droplet infection with skin vesicles
|
Shingles/ HHV3 (Varicella-Zoster)
|
|
Leads to chronic pain syndrome in older people who develop shingles, what is the prevention for?
|
Postherpetic Neuralgia, vaccinate (Zostavax)
|
|
Sudden fever (high 103-106), rash numerous pale, pink, almond-shaped macules, fade in few hours to 2 days (no scaling)
|
Roseola Infantum (HHV-6& HHV-7)
|
|
Large brick-shaped nucleocapsides, only DNA viruses that replicate in cytoplasm of host cells
|
Poxviruses
|
|
Virus with 2-8 wk incubation period, papules, pearl-like or wart-like nodules, easily expressed central plug, more common in children than adults
|
Molluscum Contagiosum (Poxvirus)
|
|
Non-enveloped virus, icosahedral capsids and DS DNA genome, warts, mucous membrane infections
|
Papillomaviridae
|
|
Causative agent, family of Rubella (german measles), transmitted by respiratory droplet
|
Rubella virus, togaviridae, enveloped, icosahedral capsid, (+) ssRNA
|
|
Virus has a prodromal period, can cross the placenta and infect fetus
|
Rubella virus, togaviridae
|
|
Fever, sore throat, pain on swallowing, vomiting, ulcerated lesions around soft palate and uvula, self limiting, viral
|
Herpangina (Coxsackie A)
|
|
Vesicular lesions on hands, feet, mouth and tongue, self resolves in a few days
|
Hand-Foot-and mouth disease (Coxsackie virus A15)
|
|
"Slapped Cheek" appearance
|
Fifth Disease (Erythema infectiosum) Parovirus B19
|
|
What viral infection can cause a sudden aplastic crisis in patients with sickle cell anemia, proxsomal nocturnal hemoglobinuria, etc?
|
Parovirus B19
|
|
What is the difference between German measles and regular measles?
|
German measles: Rubella Regular measles: rubeola
|
|
Rash developsbehind the patient’s ears, spread to the forehead, and then rapidly covers the rest of the body with high fever
|
Measles - Rubeola
|
|
Poor hygiene, papules, crusty, honey-comb like crust,
|
Non-bullous impetigo (Strep pyogenes, staph aureus)
|
|
causes a skin disease with rapidly enlarging, blister-like lesions that break down and leave paper thin crusts
|
Bullous impetigo (staph. Aureus)
|
|
What is the causative agent of cellulitis?
|
Strep pyogenes and Staph Aureus >90% of cases
|
|
What produces a superficial, expanding, erythematous, warm rash on the skin that looks like, but is not, cellulitis? Differ from cellulitis in that they are indurated with elevated margins, and their margins generally are sharply demarcated from the surrounding unaffected skin
|
Erysipelas caused by Strep pyogenes
|
|
Tinea Capitis (ringworm of the scalp)
|
Griseofulvin (Oral)
|
|
Tinea Pedis treament (athletes foot)
|
Terbinafine & Naftifine
|
|
Tinea Corporis
|
Oral terbinifine, itraconazole, or fluconazole
|
|
Tinea Cruris
|
Most topical antifungals nystatin is not effective
|
|
SSSS (MSSA)
|
Naficillin or Oxacillin
|
|
SSSS (MRSA)
|
Vancomycin
|
|
Bullous Impetigo
|
Topical: Mupirocin; MSSA: dicloxacillin or cephalexin; MRSA: TMP-SMX or Clindamycin or Minocycline
|
|
Erysipelas cellulitis
|
IV: Pen G or Oxacillin or Nafcillin or Cefazolin or Oral Dicloacillin
|
|
Facial erysipelas cellulitis or where MRSA is a concern
|
IV: Vanco or Dapto or Linezolid
|
|
Acne
|
Topical retinoids, topical antimicrobials
|
|
Mycobacterium leprae
|
Dapsone, rifampin
|
|
Rickettsia Rickettsii
|
Doxy, Chloramphenicol
|
|
Rickettsia Akari
|
Mild illness - don't treat
|
|
VSV Shingles
|
Oral: Acyclovir, Valacyclovir & Famciclovir Topical: Penciclovir & Acyclovir
|