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621 Cards in this Set
- Front
- Back
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5 bugs that causes heart block
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"LSD Loves Company"
Lyme Salmonella Diptheria legionella Chagas |
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treatment for legionella
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macrolide (azithomycin, erythromycin)
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what are the bugs that can cause Reiter's Syndrome
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"ICCCYS"
IBD Crohn's Chlamydia Campylobacter Yesernia Shigella |
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bugs that cause low complement?
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"I AM HE"
Influenza Adenovirus Mycoplasma Hep B and C EBV |
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drug induce SLE
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"HIPPPE"
Hydralazine INH Phenytoin Penicillamine Procainamide Ethosuximide |
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drug that blast the BM
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"ABCV"
AZT Benzene Chloramphencol Vinblastin |
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comma shaped bugs
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HaLV-C
H.pylori listeria vibrio campylobacter |
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chinese letters
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corneybacterium
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crescent shaped protozoa and Tx
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giardia lamblia
Tx. metronidazole |
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TB treatments
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RESPI
Rifampin, ethambutol, streptomycin, pyrazinamide, INH |
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6 low complement associated with nephrotic syndromes
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"PMS in Salt Lake City"
serum sickness, Lupus (SLE), SBE, PSGN, MPGN II, Cryoglobulinemia |
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drugs that induce P450
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"Queen Barb StealS Phen-phen And Then Refuses Greasy Carbs"
Quinidine, barbiturates, st jhon's worth/spirololactones, phenytoin, alcohol, Tetracyclines, rifampin, griseofulvin, carbamazepine |
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drugs that inhibit P450
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I'D SMACK Quin
INH, dapsone, sulfa drugs, macrolides, amiodranone, cimetidine, ketoconazole, quinolones |
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drugs that are P450 dependent
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"WEPTeD"
warfarin, estrogen, phenytoin, theophylline, digoxin |
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SE of statins
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myositis, hepatitis, increased liver enzymes
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painful genital lesions
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herpes, chancroid (H. ducreyi), L.venereum, L. inguinale
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Disulfide bonds
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"PIGI"
prolactin inhibin GH Insulin |
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Hookworms
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"NEAT ASs"
Nicatur americanus, enterobius vermicularis, ankylostoma duodenale, trichuris trichurium, ascaris lumbricoides, strongyloides |
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treatment for the hookworms?
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mebendazole
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second line treatment for ascaris lumbricoides?
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pyantel pamoate
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treatment for strongyloides?
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thiabendazole
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X-linked enzyme deficiencies
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"Fabry and Lesh Go Huntin for Candy and Pie"
Fabry's, lesch-nyhan, G6PD, hunter's, CGD, Pyruvate DH |
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screen newborns
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"Please Check Before Going Home"
PKU, CAH, Biotinase/beta thalessemia, Galactosemia, Hypothyroidism/homocytenuria |
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Action of Steroids
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"KIIISS"
kills T-cells and eosinophils inhibits macrophage migration inhibits phospholipase A inhibits mast cell degranulation stabilizes endothelium stimulates protein synthesis |
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cause of severe monocytosis
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"STELS"
salmonella, TB, EBV, Listeria, Syphillis |
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macrolides
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"ACE"
Azithromycin Clarithromycin Erythromycin |
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1 dose treatment for chlamydia
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azithromycin
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4 big mama anaerobes
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strep. bovis
c. difficil c. melanogo-speticus bacteriodes fragilis |
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If blood culture show s.bovis or c. melanogo-speticus what should be ruled out?
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colon cancer
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3 treatments for big mama anaerobes
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metronidazole, clindamycin, cefoxitin
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serum values for low volume state on the ff
K+, Na+, Cl-, pH, BP |
K⇩, Na⇩, Cl⇩, pH⇧, BP⇧
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1 dose tx for gonorrhea
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"TRI to FIX the FOX with FLOX"
ceftriaxone, cefixime, cefoxitin, ciprofloxacin |
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tx for gonorrehea with allergy
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macrolides
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why don't we give fluoroquinolones anymore for gonorrehea?
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due to resistance
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psammoma bodies
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"PSAMMoma bodies"
papillary CA of thyroid, serous cystadenoma of the ovary, meningioma, mesothelioma |
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2 drugs that cause cardiac fibrosis
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adriamycin, phen-phen
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indications for PUD surgery
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"IHOP"
Intractable pain, hemorrage, obstruction, perforation |
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urease positive bacteria
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"PPUNCHS"
proteus, pseudomonas, ureplasma urealyticum,nocardia, crytococcus neoformans, H.pylori, s. sprofyticus |
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drug that can cause pulmonary fibrosis
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"MC BBAT"
bleomycin, busulfan, amiodranone, tocainide, methotrexate and carmustine |
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5 salmonella typhi signs and symptoms
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high fever, rose spots, intestinal fire, moncytosis, heart block
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drugs that can cause myositis
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"RIPS"
rifampin, INH, prednisone (all steroids), statins |
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encapsulated bacterias
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"Some Strange Killers Have Pretty Nice Capsules"
s. pneumo (gram +), salmonella, klebsiella, H. Influenza B, pseudamonas, neisseria, citrobacter |
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encapsulated yeast
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cryptococcus
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jones criteria
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"JONES"
Polyarthritis (joints), carditis (heart like and "O"), nodules subcutaneous, erythema marginatum, sydenham chorea |
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3 IgA nephropathies
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henoch-schoenlein purpura (HSP), Berger's, alport's
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massive eosinophillia
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"NAACP"
neoplasm, allergies/asthma, addison's, collagen vascular disease, parasites |
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Risk factors for primary liver cancer
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"VIndiCATe"
Virus: Hep B and C Infections:schistomiasis Congenital: hemochromatosis Added: smoking, alcohol Toxins: vinyl chloride, carbon tertrachloride, anyline dyes |
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9 live vaccines
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ROBY'S live Vaccine was MMR
Rotavirus, oral polio,BCG, yellow fever,small pox, varicella, measels mumps, rubella. |
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autoimmune hemolytic anemias
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"PAD PACS"
penicillin, anti-malarias, dapsone, PTU, α-methyldopa, cephalosporins, sulfa-drugs |
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3 things that can cause autoimmune thrombocytopenia:
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aspirin, heparin, quinidine
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pansystolic murmurs
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mitral regurge, tricuspid regurge,ventricular septal defect
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name 3 Dihydrofolate Reductase Inhibitors
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pyremethamine/sulfadiazine, triemethroprim/sulfmethoxazole, methotrexate
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sulfa containing drugs
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sulfonamides, sulfonylureas, celecoxib (COX 2 inhibitor)
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5 silver staining bugs
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legionella, pneumocystis, H.pylori, bartonella henelae, candida
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Blood gas of restrictive lung disease
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tachypnea, ⇩pCO₂, ⇩pO₂,⇧pH
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Blood gas with obstructive lung disease
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⇧ or normal pO₂,⇧ pCO₂,⇩pH
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MI-Enzymes
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Troponin I, CK-MB, LDH
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Troponin I: when does it appears, peaks and goes away
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appears: 2 hrs
peaks: 2 days gone: 7 days |
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CK-MB: when does it appears, peaks and goes away
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appears: 6 hrs
peaks:12 hrs gone: 2 days |
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LDH: when does it appears, peaks and goes away
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appears: 1 hrs
peaks: 2 days gone: 3 days |
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Macrophage deficiency
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chediak-higashi, NADPH-oxidase deficiiency
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2 medications for 1 dose tx for H. ducreyi
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Azithromycin-1 gram
Ceftriaxone 250mg |
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1 dose tx for gardnerella
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metronidazole
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SE of thiazides and loop diuretics
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hyperglycemia
hyperuricemia hypovolemia hypokalemia |
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Macrophages in various tissues: brain
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microglia
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Macrophages is various tissues: lung
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Type I pneumocytes
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Macrophages is various tissues: liver
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kupper cells
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Macrophages is various tissues: spleen
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RES cells
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Macrophages is various tissues: kidney
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mesangial cells
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Macrophages is various tissues: Lymph nodes
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dendritic
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Macrophages is various tissues: skin
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langerhans
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Macrophages is various tissues: skin
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langerhans
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Macrophages is various tissues: bone
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osteoclasts
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Macrophages is various tissues: Connective Tissues
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histiocytes, giant cells ,epithelioid
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Rashes of palm and soles
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"TRICKSSSS"
TSS (toxic shock) Rocky Mt. Spotted Fever Coxcasckie A (hand and foot mouth disease) Kawasaki Scarlet fever 2ndary Syphilis Staph. scaled skin Streptobacillus moniliformis |
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4 sources of renal acid
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plasma RTA
ammonia production in the collection duct- 10% of urea cycle glutaminase carbonic anhydrase |
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5 hormones produced by small cell CA of lung
which one is the most common? |
ACTH (most common), ADH, PTH, TSH, ANP
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1 dose tx-candidiasis
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ketoconazole 150mg
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1 dose tx-vaginal candidiasis
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diflucan-1 pill
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1 dose tx- trichomonas
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metronidazole
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Viruses related to Cancer: HPV
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cervical cancer
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Viruses related to Cancer: EBV
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lymphoma
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Viruses related to Cancer: HVB
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liver carcinoma
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Viruses related to Cancer: HVC
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liver carcinoma
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Viruses related to Cancer: HIV
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kaposi sarcoma
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NM disease ABG's
pO₂ pCO₂ pH RR risk of seizures pulmonary capillary wedge pressure |
restrictive blood gas
⇩pO₂, ⇩pCO₂, ⇧pH,⇧RR,⇧risk of seizures, ⇩pulmonary capillary wedge pressure |
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5 pathogens that can cause PIE Syndrome (pulmonary infiltrate with eosinophillia)
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"NASSA"
necator americanus ascaris lumbricoides schistosomiasis strongyloides ankylostoma |
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Enzymes used by B12
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methyl malonyl CoA mustase, homocystine methyl transferase
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4 risk factors of Increased suceptibility to pseudomonas and S. aureus
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diabetics, CF, burned paitients, neutropenics
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Crohn's disease clues
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"GIFTS"
Granulomas Ileum Fistulas Transmural Skip lesions |
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Causes of Widened S2
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⇧pO₂,⇧volume right ventricle, blood transfusion, supplemental O₂, Right sided heart failure, pregnancy, I.V fluids, ASD (fixed), Deep breathing. Concept:⇧O2 dilates vessels, breathing in streches the arteries-->increase volume-->delayed closure of pulmonic valve--> widened S₂
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8 cavities of blood loss:
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pericardium, intracranial, mediastinum, pleural cavity, thighs, Retroperoteneum, abdominal, pelvis.
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how long is the prodromal period of a negative stranded RNA before the patient get symptoms? and why?
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>>1-3 week prodromal period before symptoms
>>must switch to positive stranded before it can replicate |
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how long is the prodromal period for a positive stranded RNA?
why? what are the 3 exceptions? |
>>symptoms occur within 1 week or less
>> don't have to switch before replicating >>exceptions: hanta, ebola, and yellow fever which are negative stranded |
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cyanotic heart diseases
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"Hi PEAT₁₋₅"
Hypoplastic heart syndrome, Pulmonic Atresia, Aortic atresia, Ebstein's anomaly, (1) truncus arteriosus (has one trunk) (2) transposition of great vessels (2 vessels involved) (3)TRIcuspid atresia (4) TETRAlogy of fallot (5) Total anomalous pulmonary venous return (has five words) |
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what ions would make a cell "least likely" to depolarize?
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hypermagnesemia,
hypercalcemia (except the atrium) hypokalemia (early) hyponatremia (early) |
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what are the ions that would make a cell "most likely" depolarize?
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hypomagnesemia
hypocalcemia (except atrium) hyperkalemia (early) hypernatremia (early) |
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what are the 6 hormones produced by placenta
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hCG, Inhibin, human placental lactogen, oxytoxin, progesterone, estrogen
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uses for pilocarpine
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CF, closed angle glucoma
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give 4 example of things that can cause dysgeuzia
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metronidazole, clarithomycin, zinc deficiency, lithium?
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carcinoid triad
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flushing, wheezing, diarreah
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carcinoid syndrome diagnosis
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measuring 5-HIAA in urine
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carcinoid syndrome: most common location
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appendix
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carcinoid syndrome: most common metastatic location
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pancreas and illeum
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AVM: machinery murmur in the Heart
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PDA
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AVM: machinery murmur in the elbow
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dialysis fistula
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AVM: machinery murmur in the brain
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von-hipple-lindau
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AVM: machinery murmur in the lung
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osler-weber-rendu
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Hemophilus Influenza clues (3)
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gram negative rods, pleomorphic, "school of fish".
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Hemophilus Influenza: Type A clues (3)
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>>non-encapsulated
>> non-invasive >> MCC of sinusitis, otitis, bronchitis |
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Hemophilus Influenza: Type B clues (4) and Tx:
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>>encapsulated
>>invasive >>IgA protease >>MCC of epiglottitis Tx: cefuroxamine |
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Rust Colored Sputum
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Strep. Pneumoniae (aka pneumococcus)
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Staph. Epidermiditis is most common infection of what?
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shunts and central lines
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how do you tell catalase positive staphylococci apart (by pigment)
S.aureus |
gold
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how do you tell catalase positive staphylococci apart (by pigment)
S. epidermidis |
white
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how do you tell catalase positive staphylococci apart (by pigment)
S. saprophyticus |
no pigment
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strep. pyogenes is the most common cause of what diseases (5)
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all throat infections: "LINES"
lymphaginitis, impetigo, necrotizing faceitis, erysipelas, scarlet fever |
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strep. pyogenes is the second most common cause of what diseases
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all other skin infections
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name 4 neutrophil deficiencies
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job-buckley syndrome, neutropenia, myeloperoxidase defieciency, NADPH oxidase deficiency
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compartment syndrome: what is always firs? last?
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pain (always first), pallor, polkiothermia, parthesia, pulselessness (always last)
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4 itchiest rashes
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scabies
lichen planus utricaria dermatitis hepatiformis |
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6 Oddities about listeria
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>>only gram positive with endotoxin, lipid A is toxic part
>>crosses placenta, cause sepsis in neonate,cause granulomas >>raw cabbage, spoiled milk |
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what are the B vitamins (B₁ to B₁₂)
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(B₁) Thiamine, (B₂) Riboflavin, (B₃) Niacin, (B₄) lipoic acid, (B₅) Pantothenic acid, (B₆) Pyridoxine, (B₉) Folate, (B₁₂) cobalamine
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what does (B₁) Thiamine deficiency cause
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beriberi, weirnickes, korsakoff
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What does (B₂) Riboflavin defieciency cause?
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angular stomatitis
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what does (B₃) Niacin deficiency cause?
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pellegra: diarrhea, dermatitis, death, dementia
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what does (B₄) lipoic acid and (B₅) Pantothenic acid causes?
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none
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what does (B₆) Pyridoxine defieciency causes?
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seizures
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what does (B₉) Folate defieciency causes? (6)
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fatigue, pallor, diarrhea, loss of appetite and headaches (no neuropathy)
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what does (B₁₂) cobalamine deficiency causes?
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pernicious anemia and neuropathy
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what are periods of rapid growth
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birth to 2-months
4-7 years puberty |
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only immune deficiency with low calcium
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DiGeorge syndrome
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bugs with IgA Protease, which one is resistant to IgA
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S. pneumonia, H. influenza, Neisseria (are resistant to IgA)
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Secretions of Mast cells
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histamine
SRSA (slow reacting substance of anaphylaxis) ECFA (eosinophil chemotactic factor of anaphylaxis) |
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secretions of eosinophil
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histaminase, arylsulfatase, heparin
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function of E.coli in the gut (5)
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secretes vitamin K, biotin,folate, panthothenic acid, aids in absorption of B12
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heart block clue
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>>increase body temparature with a normal heart rate
>>HR should increase by 10bmp for every degree increase in temparature |
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what do macrophages release?
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releases MHC II
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TH1 secrete
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IL-2, IF-γ
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TH2 secrete
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IL-4, IL-5, IL-6, IL-10
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TH0 secrete
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TH1, TH2
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T-cytotoxic cells
markers negative markers recognition |
CD8 positive, CD4 negative, recognize MHC I, also have markers CD2 and CD3
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T-Helper cells
markers negative markers recognition |
CD4 positive, CD8 negative, recognizes MHCII, also have marker CD2 and CD3
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elevated cholesterol
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xanthomas on extensor surfaces and increase risk for CAD
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elevated triglycerides
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xanthelesmas on eyelid and face and increase risk of pancreatitis
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4 causes of severe pain
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pancreatitis (ETOH)
kidney stones (bloody urine) AAA (riping tearing pain) Ischemic bowel (bloody diarrhea) |
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5 causes of SIADH
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"SIADH"
small cell carcinoma, increase intracranial pressure, a pain, drugs, hypoxia |
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cells of neural crest origin
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"POT CLAMPS"
parafollicular cells, odontoblast, tracheal cartilage, chromafin cells, laryngeal cartilage, all ganglion cells, melanocytes, pseudounipolar cells, spiral membrane |
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Ions and the EKG
P wave QRS complex S-T interval T wave U wave |
P wave = Calcium
QRS complex = sodium S-T interval = Calcium T wave = potassium U wave = sodium |
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maximum sinus rate
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220-age in years
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tri-nucleotide repeats (4)
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huntington's, fragile x, myotonic dystrophy, spinal/bulbar muscular atrophy (rare)
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low volume states with acidosis (not alkalosis)
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RTA, diarrhea
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4 MCC of croup and bronchiolitis (in order)
which is #1 in the ER? |
parainfluenza
RSV (ER this is #1) adenovirus influenza |
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4D's of pellegra
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dermatitis, diarreah, dementia, death
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5 Types of kidney stones:
which one is most common? |
calcium oxalate (80%),struvite, uric acid, cysteine, oxalate
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pseudogout:
composition shape who is at risk Tx |
Calcium pyrophosphate, + bifringent crystals
rhomboid crystals MC older patients, seen equally in both genders. Tx: colchicine |
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4 most common non-cyanotic congenital heart disease
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VSD, ASD, PDA, coarctation of the aorta
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4 enzymes NEVER seen in glycolysis
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pyruvate carboxylase
PEP carboxykinase fructose-1,6-phosphatase glucose-6-phosphatase. |
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3 enzymes ONLY seen in glycolysis
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hexokinase
phosphofructokinase-1 (PFK-1) pyruvate kinase |
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3 acid fast organisms
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mycoplasma
nocardia (partially gram +) cryptosporidium (partially protozoa) |
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microsteatosis can be caused by 3 things
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acetamenophen, reye syndrome, pregnancy
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macrosteatosis cause
|
alcohol
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bacteria with elastase
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staph aureus, pseudomonas
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bacteria with toxins that inhibit EF-2
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pseudomonas, diptheria
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phage medicated toxins
|
"Oh BED"
"O" antigen (salmonella) Botulinum Erythrogenic toxin Diptheria |
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segmented viruses
|
"BOAR"
Bunyaviridae Orthoviridae Arenaviridae Reoviridae |
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3 Functions of adhesion molecules
|
lymphocytes homing, inflammation, cell-cell interaction
|
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esophageal/gastric CA Risk Factors
|
smoking, alcohol, nitrates, japanese
|
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bladder CA risk factors
|
"TICCS"
Toxins: analine dyes, benzene, aflatoxin Infection: schistomiasis Congenital: Von-hippel-lindau, Tubular sclerosis C: cyclophosphomide S: smoking |
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structure with no known function
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appendix, epithalamus, palmaris longus, pancreatic polypeptide
|
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4 progressing to RPGN:
which one is #1 |
goodpastures (#1), diabetes melitis, hypertension, wagener's
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cause of papillary necrosis
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vasculites, AIDS
|
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drugs that cause extravascular hemolysis
|
"HIPPPE AND PAD PACS"
SAD: Sulfa, methyldopa, dapsone, Anti malarials HIPPPE: hydralazine, INH Phenytoin, Penicillamine, Procainamide, Ethoxusimide PCP: penicillins, cephalosporins, PTU |
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3 gram positive spore formers
|
bacillus anthracis, clostridium perfringens, clostridium tetani
|
|
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used for cold agglutinin testing
|
strep. salivarus
|
|
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drugs that cause disulfram reaction
|
"CLAM"
chlorpropamide, lactams, antabuse, metranidazole |
|
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3 toxins of bacillus
|
lethal factor, protective factor and edema factor
|
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beta blockers (2 types)
|
B1 selective: A-M (except C-L)
B2 selective: N-Z, C,L |
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Fanconi's syndrome
location of defect what happens cause by? |
defect in proximal
can't reabsorb, low energy state can be caused by old teracycline |
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glutaminase
location function what can it cause? |
In collecting duct
absorbs ammonia from the liver cause of hepato-renal syndrome |
|
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3 anatomical narrowings of ureter
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hilum, pelvic brim, entrance of bladder
|
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fanconi's syndrome
|
can be cause by old tetracyline, defect in the proximal tuble, cannot reabsorb -->low energy state
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Odd MCC of death in SLE, endometrial and cervical cancer
|
renal failure
|
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methotraxate uses
Dx Tx (3) |
to Dx fragile X
Tx: molar preganacy, fast growing cancers, steroid resistant diseases |
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what are the 5 group D streptococcus bacterias
|
bovis, mutans, sanguinis, salivaris and viridans
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what group D streptococcus bacteria give out green pigment and causes SBE
|
viridans
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what are the group D strptococcus bacteria that cause cavities
|
mutans
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Nephritic syndrome presentation (3)
|
hypertension, hematuria, RBC casts
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Nephrotic syndrome presentation (6)
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edema, hyperlipedemia, hypercholesterolemia, hypercoagubility, decrease serum albumin, increase urine albumin
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3 MCC of airway infection
what are the bugs that causes this (in order) |
Sinusitis, bronchitis, pneumonia
#1 S.pneumonia #2 H. influenza #3 N. meningitis |
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Gastroenteritis within 8 hours of eating, what type of toxin is used?
|
The preformed toxins
>>S. aureus (potato salads) >>C. perfringens (holiday turkey/ham) >>B. cerus(fried rice) |
|
|
citrobacter
|
causes multiple cerebral abscesses in newborns
|
|
|
MCC cause of UTI (in order)
|
#1 E.coli
#2 proteus #3 klebsiella |
|
|
most frequent UTI in females 5-10 yrs and 18-24
|
S. saprophyticus because they stick things inside themselves
|
|
|
what 2 things that S.aureus most commonly cause
|
MCC of osteomyelitis
MCC of infection in burn patients |
|
|
MCC of newborn meningitis
|
"baby BEL"
Group B strep E. coli Listeria |
|
|
bacterias associated with colon cancer
|
C. melanogosepticus
S.bovis |
|
|
gram (-) that are strict anaerobes
|
H. flu and neisseria
|
|
|
labs of pre-renal failure
serum BUN, Serum Cr , FeNa |
serum BUN >20
Serum Cr > 40 FeNa <1% |
|
|
labs of renal failure: serum BUN, Serum Cr ,FeNa
|
serum BUN 10 to 15
Serum Cr <20 FeNa >2% |
|
|
what are the 4 steps of extravasation?
|
pavementing, margination, diapedesis and migration
|
|
|
If a patient has cell mediated deficiency, what 6 infections should you treat for?
|
"Very Foolish to Meet Parents Post Nuptally"
viral, fungal, mycobacterium, protozoa, parasite, neoplasm |
|
|
Herpes Virus I
|
oral herpes
|
|
|
Herpes Virus II
|
genital herpes
|
|
|
Herpes Virus III
|
varicella zoster
|
|
|
Herpes Virus IV
|
EBV
|
|
|
Herpes Virus V
|
CMV
|
|
|
Herpes Virus VI
|
roseola
|
|
|
Herpes Virus VII
|
pityriasis rosea
|
|
|
Herpes Virus VIII
|
kaposi's sarcoma
|
|
|
5 diseases that are picked up by the baby during delivery.
|
group B strep, s. pneumonia, herpes, N. gonorrhea, chlamydia
|
|
|
name 6 diseases that are both T and B-cell deficiencies?
|
WAS (wiskott-aldrich syndrome)
SCID CVID HIV (HTLV-1) job buckley syndrome |
|
|
WAS (wiskott-aldrich syndrome):
type of deficiency presentation (3) what IL association |
T and B-cell deficiencies
thrombocytopenia, Eczema, decrease IgM IL-4 |
|
|
SCID
type of deficiency enzyme deficiency which part of the immune system is more affected type of mutation(s) presentation (2) |
T and B-cell deficiencies
adenosine deaminase deficiency T>B frameshift and nonsense mutation increase bacterial and fungal infection |
|
|
CVID (common variable immunodeficiency)
type of deficiency enzyme deficiency onset type of mutation(s) |
T and B-cell deficiencies
tyrosine kinase deficiency late onset frameshift/ missense mutation |
|
|
HIV (HTLV-1)
type of deficiency what 5 areas of body does it affect the most and why? which part of the immune system is affected the most? |
T and B-cell deficiencies
effects CD4 rich tissues (brain, testicles, cervix, rectum, blood vessels) T>B |
|
|
Job-buckley syndrome
type of deficiencies presentation enzyme deficiency |
T and B-cell deficiencies
red headed female tyrosine kinase deficiency |
|
|
B-cell deficiencies
name 5 diseases enzyme deficiency of bruton's |
bruton's agammaglobulinemia- tyrosine kinase deficiency
leukemias lymphomas and other diseases with overlap (SCID, HIV) |
|
|
name 3 T-cell deficiencies
|
DiGeorge's, HIV and SCID
|
|
|
DiGeorge's syndrome
type of deficiency pathogenesis and lab chromosome |
T-cell deficiencies:
problem with 3rd and 4th pharyngeal pouches, hypokalemia deletion of chromosome 22 |
|
|
what are the 3 things that stops Electron transport Chain from working?
|
poisons
chemical uncouplers physical uncouplers |
|
|
name 2 Chemical uncouplers of the electron transport chain:
|
DNP and free fatty acids
|
|
|
name 1 physical uncoupler of the electron transport chain:
|
aspirin
|
|
|
name 2 Electron transport chain complex I poisons:
|
amytal
rotenone |
|
|
Electron transport chain complex II: poisons
|
malonate
|
|
|
Electron transport chain complex III: poisons
|
antimycin
|
|
|
name 3 poisons of electron transport chain complex IV:
|
CN, CO, chroramphenicol
|
|
|
Electron transport chain complex V: poisons
|
oligomycin
|
|
|
3 aa feed in/out of the TCA cycle: pyruvate
|
gly, ala, ser
|
|
|
6 feed in/out of the TCA cycle: acetyl CoA
|
Phe, Iso, Thr, Tyr, Lys, Leu
|
|
|
name 2 aa feed in/out of the TCA cycle: alpha ketoglutarate
|
Glu, Gln
|
|
|
aa feed in/out of the TCA cycle: succinyl CoA
|
Phe, Trp, Tyr
|
|
|
places where aa feed in/out of the TCA cycle: fumarate
|
Pro
|
|
|
2 aa feed in/out of the TCA cycle: oxaloacetate
|
Asp, Asn
|
|
|
PKU
type of deficiency enzyme deficiency |
AA deficiencies
Phenylalanine hydroxylase deficiency needed to make tyrosine, leads to a lack of dopamine, epi and norepi, melanin |
|
|
AA deficiencies: maple urine syrup disease
|
deficiency in branched aa (leu,lys, val), defective transport in the kidneys
|
|
|
cystinuria
type of deficiency enzyme deficiency presentation |
AA deficiency
cystathionase syntase deficiency "COLA" :cysteine, onrnithine, lysine and arginine end up in urine, stones |
|
|
AA abbreviations: rule
|
the first 3 letters of the aa is its short cut form. (ie. GLYcine, ALAnine) EXCEPT:GLutamiNe and ASparagiNe
|
|
|
AA subgroups: acidic
|
Asp, glu
|
|
|
AA subgroups:basic
|
Arg, Lys
|
|
|
AA subgroups: sulfur bonds:
|
cys and met
|
|
|
AA subgroups: O-bonds
|
ser, Thr, Trp
|
|
|
AA subgroups: N-bonds
|
Asn, Gln
|
|
|
AA subgroups: branched
|
leu, Iso, val
|
|
|
AA subgroups: bulky (aromatic)
|
phe, Thr, Trp
|
|
|
AA subgroups:smallest
|
Gly
|
|
|
AA subgroups: responsible for bends
|
pro
|
|
|
AA subgroups: ketogenic
|
lys, leu
|
|
|
AA subgroups: gluco-& ketogenic
|
"PITT"
phe, Iso, Thr, Trp |
|
|
AA subgroups: Glucogenic
|
all the rest
arg,asp,asn, ala, cys, his, pro, met gly, glu, gln, tyr,val |
|
|
Essential AA
what becomes essential when Phe or Met is deficient? |
PVT TIM HALL
Phe, val, thr, trp, iso, met, his, arg, leu, lys (if there is a deficiency with Phe then tyr is and essential amino acid, if met then cys becomes essential) |
|
|
Restriction Enzymes: trypsin
|
cuts to the right of Arg and lys
|
|
|
Restriction Enzymes: chymotrypsin
|
cuts to the right Phe, tyr, trp
|
|
|
Restriction Enzymes: elastase
|
cuts to the right gly, ser, ala
|
|
|
Restriction Enzymes: mercaptoethanol
|
cuts to the right met and cys
|
|
|
Restriction Enzymes: aminopeptidase
|
cuts to the right amino terminal
|
|
|
Restriction Enzymes: cyanobromide
|
cuts to the right met
|
|
|
Restriction Enzymes: carboxypeptidase
|
cuts to the Left carboxy terminal
|
|
|
2nd messangers: cAMP
system metabolism what pituitary pathway uses cAMP |
sympathetic
catabolic CRH |
|
|
2nd messangers: cGMP
autonomic system metabolism |
parasympathetic
anabolic |
|
|
2nd messangers: IP3 and DAG
function what hypothalamic hormones use this pathway? |
>>smooth muscle contraction by hormone or NT.
>>all hypothalamic hormones (except CRH) |
|
|
2nd messangers: Ca-calmodulin
function |
smooth muscle contraction by distention
|
|
|
2nd messangers: Ca++
|
gastrin
|
|
|
2nd messangers: Tyrosine Kinase
|
Insulin and all grow factors
|
|
|
2nd messangers: NO (4)
|
Nitrates, Viagra, ANP and LPS
|
|
|
Autoimmune antibodies: SLE
which one is specific? |
anti-smith (specific), anti-DS DNA, anti-cardiolipin
|
|
|
Autoimmune antibodies:drug induce SLE
|
anti-histones
|
|
|
Autoimmune antibodies: progressive systemic sclerosis
|
anti-topisomerase
|
|
|
Autoimmune antibodies: Graves
|
anti-TSH receptor
|
|
|
Autoimmune antibodies: CREST
|
anti-centromere
|
|
|
Autoimmune antibodies: Goodpasture's
aka: collagen |
anti-glomerular basement membrane (aka. Type IV collagen)
|
|
|
Autoimmune antibodies: primary biliary cirrhosis
|
anti-mitochondria
|
|
|
Autoimmune antibodies: alopecia areata
|
anti-hair follicle
|
|
|
Autoimmune antibodies: Rheumatoid Arthritis
|
anti-IgG
|
|
|
Autoimmune antibodies: Multiple Sclerosis
|
anti-myelin receptors
|
|
|
Autoimmune antibodies: Celiac sprue
|
anti-gliaden/gluten
|
|
|
Autoimmune antibodies: Type I diabetes
|
anti- islet cell receptor
|
|
|
Autoimmune antibodies: vitiligo
|
anti-melanocytes
|
|
|
Autoimmune antibodies: mixed connective tissue
|
anti-ribonuclear protein
|
|
|
Autoimmune antibodies: pernicious anemia (aka)
|
anti-parietal cell receptor (aka. Intrinsic factor)
|
|
|
Autoimmune antibodies: pemphigus vulgaris
aka |
anti-epidermal anchoring protein receptor
(aka. intercellular junctions of epidermal cells) |
|
|
Autoimmune antibodies: bullous pemphigoid
|
anti-epidermal basement membrane protein
|
|
|
2 Autoimmune antibodies: Hashimoto's
|
anti-thyroglobulin
anti-microsomal |
|
|
2 Autoimmune antibodies: Scleroderma
|
anti-smooth muscle
anti-scl70 |
|
|
Autoimmune antibodies: autoimmune hepatitis
|
anti-smooth muscle
|
|
|
4 Autoimmune antibodies: sjogren's
|
anti-Rho, anti-La, anti-SSA, anti-SSB
|
|
|
2 Autoimmune antibodies: Wegener's
|
anti-proteinase
anti-C-ANCA |
|
|
Autoimmune antibodies: Polyarteritis Nodosa
|
anti-P-ANCA
|
|
|
Autoimmune antibodies: Idiopathic thrombocytic Purpura
aka |
anti-platelet (aka glycoprotien IIb/IIIa)
|
|
|
What are the 5 co-factors for pyruvate DH, α-ketogluterate DH & branched chain DH?
|
"TLC for Nana"
TPP, Lipoic acid, CoA, FAD, NAD |
|
|
What are the vitamins that are associated with the co-factors for pyruvate DH, α-ketogluterate DH & branched chain DH?
|
vitamins B1 to B5:
TPP needs B₁ (thiamine) Lipoic Acid (B₄) CoA needs pantothentic acid (B₅) FAD need riboflavin (B₂) NAD need Niacin (B₃) |
|
|
what are the x-linked recessive diseases?
|
"Fabry and Lesh Can't Go Hunting for Pie Because they are Blind Have a Disease "
Fabry's, lesch-Nyhan, Hunter's, G6PD, CGD (NADPH Oxidase Def.), Pyruvate DH deficiency, Bruton's Agammaglobulinemia, Hemophillia, Color blindness and Duchenne's Muscular Dystrophy |
|
|
what are the x-linked dominant diseases?
|
PDH and vitamin D resistant rickets
|
|
|
Nephrotic patterns of vasculitis: Renal artery stenosis
|
clot in front of the renal artery
|
|
|
Nephrotic patterns of vasculitis: renal failure
|
clot off entire renal artery
|
|
|
Nephrotic patterns of vasculitis: GN
|
Inflammed glomeruli
|
|
|
Nephrotic patterns of vasculitis: Papillary necrosis
|
clot of papilla
|
|
|
Nephrotic patterns of vasculitis: Interstitial Nephritis
|
clot of medulla
|
|
|
Nephrotic patterns of vasculitis: Focal segmental GN
|
Clot off pieces of nephron
|
|
|
Nephrotic patterns of vasculitis: Rapidly Progressive GN
|
Clot off lots of nephrons
|
|
|
most common nephrotic disease in Adults
|
membranous glomerulonephritis
|
|
|
most common renal disease in blacks/hispanics
|
focal segmental glomerulonephritis
|
|
|
most common renal disease in HIV/drug users
|
focal segmental glomerulonephritis
|
|
|
most common renal mass
|
cyst
|
|
|
most common malignant renal tumor in adults
|
adenocarcinoma
|
|
|
most common malignant renal tumor in kids
|
wilm's tumor
|
|
|
most common cause of RPGN
|
goodpasture's
|
|
|
most common cause of nephrotic disease in kids
|
minimal change disease
|
|
|
what would you see in a biopsy of RPGN
|
crescent formation
|
|
|
minimal change disease happens after what kind of infection?
|
2 weeks post URI
|
|
|
thrombolytic rescues: tPa
|
aminocaproic acid
|
|
|
thrombolytic rescues: streptokinase
|
amioncaproic acid
|
|
|
thrombolytic rescues: warfarin
|
vitamin K
|
|
|
thrombolytic rescues: heparin
|
protamine sulfate
|
|
|
what do you give if there is active hemmorage?
|
fresh frozen plasma (FFP)
|
|
|
Rashes Associated with cancer: urticaria (hives)
|
any, but especially lymphoma
|
|
|
Rashes Associated with cancer: Paget's disease
|
intraductal carcinoma
|
|
|
Rashes Associated with cancer: seborrheic keratosis
what if a patient suddenly have a high increase in seborrheic keratosis, Dx? |
colon cancer
HIV if there is a sudden increase |
|
|
Rashes Associated with cancer: Actinic Keratosis
|
squamous cell carcinoma of skin
|
|
|
Rashes Associated with cancer: Dermatomyosistis (heliotropic, malar)
|
colon cancer
|
|
|
Rashes Associated with cancer: akathosis nigricans
|
visceral cancer and end organ damage
|
|
|
Rashes Associated with cancer: erythema nodosum
|
granulomatous (non-bacterial)
|
|
|
cancer grading
|
severity of microscopic changes
|
|
|
cancer staging
|
degree of dissemination of tumor
|
|
|
tumor markers/oncogenes: L-myc
|
small cell carcinoma of the lung
|
|
|
tumor markers/oncogenes: c-myc
|
burkitt's lymphoma
|
|
|
tumor markers/oncogenes: n-myc
|
neuroblastoma
|
|
|
tumor markers/oncogenes: c-abl (2 diseases)
|
CML, ALL
|
|
|
name 2 diseases with tumor markers/oncogenes: c-myb
|
colon, AML
|
|
|
give 3 diseases that has tumor markers/oncogenes: c-sis
|
osteosarcoma, glioma, fibrosarcoma
|
|
|
give 2 syndromes with "ret" tumor markers/oncogenes
|
MEN II, MEN III
|
|
|
give 2 diseases with "k-ras" tumor markers/oncogenes:
|
lung, colon
|
|
|
tumor markers/oncogenes: bcl-2
note |
follicular lymphoma ( can show up in burkitt's -pick follicular first)
|
|
|
tumor markers/oncogenes: Rb
|
retinoblastoma
|
|
|
give 2 diseases with "CEA" tumor markers/oncogenes:
|
colon, pancreas
|
|
|
tumor markers/oncogenes: S-100
|
melanoma
|
|
|
name 6 tumor markers/oncogenes for breast cancer
|
HER-II
Neu Erb BRCA-I & II p53 CSF-1 |
|
|
Translocations: 9:22
name of chromosome disease |
philadelphia chromosome (CML)
|
|
|
Translocations: 8:14
|
burkitt's lymphoma
|
|
|
Translocations: 14:18
|
follicular lymphoma
|
|
|
Translocations: 15:17
|
promyelblastic leukemia
|
|
|
Translocations: 11:14
|
mantel cell lymphoma
|
|
|
Translocations: 11:22
|
ewing's sarcoma
|
|
|
Translocations: 17:22
|
neurofibromatosis
|
|
|
what are the 4 enzymes needed to make glycogen?
|
glycogen synthase
branching enzymes >>>glycogen α-1,4 glycosyl transferase >>>glycogen α-1,6 glycosyl transferase |
|
|
what are the 4 enzymes needed to breakdown glycogen?
|
phosphorylase
debranching enzyme A-1,6-glucosidase phosphatase |
|
|
lipoprotein transport: chylomicrons
|
takes triglycerides fom GI to liver and endothelium
|
|
|
lipoprotein transport: VLDL
|
takes triglycerides from liver to adipose
|
|
|
Lipoprotein transport: VLDL
|
takes triglycerides from liver to adipose
|
|
|
Lipoprotein transport: IDL
|
takes triglycerides from adipose to tissue
|
|
|
Lipoprotein transport: LDL
|
only one to carry cholesterol
|
|
|
where is VLDL made?
|
only make in the liver
|
|
|
Lipoprotein transport: IDL +LDL
|
break down products of VLDL
|
|
|
3 Most common cause of meningitis from 0 months - 2 months?
|
"baby BEL"
group B strep E.coli Listeria |
|
|
what are the Tx of meningitis from 0 months - 2 months?
|
>>vanco + gen + amp
>>vanco + cefotaxime + amp |
|
|
2 Most common cause of meningitis from 2 months - 10 months?
|
S. pneumoniae
N. meningitides |
|
|
what is the Tx of meningitis from 2 months - 10 months?
|
vanco + ceftriaxone/cefotaxime +/- steroids
|
|
|
Most common cause of meningitis from 10 years - 21 years?
|
N. meningitides
|
|
|
most common cause of meningitis over 21 years? and Tx
|
S. pneumo
Tx: vanco + ampi + ceftriaxone |
|
|
Indications for pneumovax (4)
what does it cover? |
>>covers most common 23 strains
>>given at 2,4,6 months >>given to anyone over 65 >>anyone who is asplenic >>anyone with end organ damage (CF,RF, nephrotic) |
|
|
HIV: most common infection
|
CMV
|
|
|
HIV: most common cause of death
|
PCP
|
|
|
HIV: P41
|
just a surface marker
|
|
|
HIV: GP120
|
attachment to CD4
|
|
|
HIV: Pol
|
trascription
|
|
|
HIV: Reverse trascriptase
|
intergration
|
|
|
HIV: p17 and p24 antigens
|
assembly
|
|
|
HIV: Normal CD4 count in adults? kids?
|
800-1200 in adults (up to 1500 in kids)
|
|
|
HIV:
CD4 count <500 in adults: Tx CD4 count <750 in kids: Tx |
2 nucleotide inhibitors and 1 protease inhibitor (HAART therapy)
|
|
|
HIV: CD4 count <200.
Dx Tx |
pt has AIDS, add treatment for PCP
|
|
|
HIV: CD4 count <100. Tx
|
add treatment for MAC
|
|
|
Characteristics of autosomal dominant Inheritance:
1) male/female 2) manefestation 3) onset 4) transmission 5) mutation occurance 6) how is it exhibited 7) defects |
>>affects male = female
>>can manifest as a heterozygous state >>often delayed onset (adult dx) >>vertical transmission >>new mutations occur in germ cells of older fathers >>can exhibit reduced penetrance and variable expressivity >>usually structural defects |
|
|
Characteristics of autosomal recessive Inheritance
1) parent 2) who has it? 3) onset 4) when does it present on an offspring? 5) transmission 6) defects |
>>ususlly does not affect parents
>>disease is seen in siblings and uncles >>often early onset (early dx) >>only present when both alleles are present >>horizontal transmission >>enzyme defects (inborn errors of metabolism) |
|
|
characteristic of mitochondrial inheritance
1) how is it passed on? 2) who is affected? 3) what part of the body does it affects? 4) what is it caused by? |
⇒ONLY females will pass on the disease
⇒ALL offsprings are affected ⇒often affects CNS, heart and skeletal muscle ⇒caused by uneven cytokenesis during meiosis/oogenesis |
|
|
Immune System Timeline:
< 24 hours |
swelling
|
|
|
Immune System Timeline:
what shows up at 24 hours? |
neutrophils show
|
|
|
Immune System Timeline:
Day 3 |
neutrophils peak
|
|
|
Immune System Timeline:
day 4 |
T-cells and macrophages show up
|
|
|
Immune System timeline:
day 7 |
fibroblasts show up
|
|
|
Immune System timeline:
1 month |
fibroblast peak
|
|
|
Immune System timeline:
3-6 months |
fibroblast are gone
|
|
|
mitochondrial diseases (2)
|
leigh's disease
Leber's Disease |
|
|
mitochondrial diseases: leigh's disease
presentation (4) deficiency |
subacute necrotizing encephalopmyelopathy
progressive decrease of IQ, seizures, ataxia cytochrome oxidase deficiency. |
|
|
mitochondrial diseases: leber's Disease
|
hereditary optic atrophy
|
|
|
Tx and MoA of Hypercholesterolemia
|
statins. Inhibits HMG CoA reductase. It is most active around 8pm. Must take at night for maximum efficiency.
|
|
|
Tx of Hypercholesterolemia: statin that is renally excreted?
|
Provostatin
|
|
|
Tx of Hypercholesterolemia:
what should you check for when putting a patient on statins? give examples |
check liver enzymes every 3 months
ie: atrovostatin, lovastatin, simvastatin |
|
|
Tx of Hypercholesterolemia:
MoA mechanism of action (MOA) how should it be taken. |
MoA inhibits HMG CoA reductase. It is most active around 8pm and therefore must be taken at night for maximum efficiency
|
|
|
Atrial action potential:
phase 0 |
depolarization
|
|
|
Atrial action potential:
phase 1 |
no name
|
|
|
Atrial action potential:
phase 2 |
plateau (A-V node)
|
|
|
Atrial action potential:
phase 3 |
repolarization
|
|
|
Atrial action potential:
phase 4 |
automaticity (S-A node)
|
|
|
4 pathogens that causes Pneumonia: 6 wks-18yrs
which one is infants only? |
RSV (infants only),
mycoplasma chlamydia pneumonia strep. pneumonia. |
|
|
3 pathogens that causes Pneumonia in 18 yrs.-40 yrs
|
mycoplasma
chlamydia pneumonia strep. pneumonia |
|
|
5 pathogens that causes Pneumonia in 40 y/o-65 y/o
in order |
s.pneumonia
H. influenza anaerobes viruses mycoplasma |
|
|
5 pathogens that causes Pneumonia in Elderly
|
S. pneumonia
viruses anaerobes H. influenza gram negative rods. |
|
|
Oxalate stones in 3 yo white female. Dx
|
cystic fibrosis.
|
|
|
Oxalate stones in 5 y/o black female
|
celiac sprue.
|
|
|
Oxalate stones in adult female
|
whipple's disease
|
|
|
Oxalate stones in adult male or female
|
crohn's
|
|
|
what are the anterior pituitary acidophillic hormones?
|
GH, prolactin
|
|
|
what are the anterior pituitary basophillic hormones?
|
TSH, ACTH, LH, FSH
|
|
|
what are the posterior pituitary hormones and nucleus
|
ADH from the supraoptic nucleus
oxytoxin from the paraventricular nucleus |
|
|
most common bacteria of sub-acute bacterial endocarditis:
|
strep. viridans
|
|
|
6 Physical Exam clues for sub-acute bacterial endocarditis:
|
"clots everywhere"
⇒roth spots (eye) ⇒osler's nodes (fingers) ⇒janeway lesions (toes) ⇒splintter hemorrages ⇒endocarditis ⇒mycotic aneurysm (septic emboli) |
|
|
Emphysema types:
what microbe is bullous emphysema due to (top 2) |
#1 S. aureus
#2 pseudomonas |
|
|
Emphysema types:
what is centroacinar emphysema due to? |
smoking
|
|
|
Emphysema types:
what is distalacinar emphysema due to? |
aging
|
|
|
Emphysema types:
what is panacinar emphysema due to? |
α₁-antitrypsin deficiency
|
|
|
where does erythropoesis happen during 4 months of gestation?
|
yolk sac
|
|
|
3 areas of erythropoesis during 6 months of gestation?
|
spleen, liver, flat bones
|
|
|
where does erythropoesis happen during 8 months of gestation?
|
long bones
|
|
|
where does erythropoesis happen during 1 months of gestation?
|
long bones
|
|
|
Erythropoeisis: if long bone gets damaged what takes over?
what would you see on PE? |
spleen -->splenomegally
|
|
|
diptheria:
1) MOA of toxin 2) what does the toxin do? 3) type of bacteria 4) how does it aquire its exotoxin? 5) why should one not scrape the membrane? 6) name one complication |
⇒toxin ADP ribosylates EF-2
⇒leads to stop cell synthesis ⇒gram + ⇒acquire exotoxin from a virus by transduction ⇒never scrape the membrane because its highly vascular so it will bleed and it will also release toxin. ⇒causes heart block |
|
|
Cystic Fibrosis: diagnostic tests
normal homozygoous heterozygous |
sweat test:
>60 definitive positive <20 Normal 30-60 Heterozygous |
|
|
Cystic Fibrosis: 2nd messanger
|
IP3/DAG
|
|
|
Cystic Fibrosis: what gene is it on
|
deletion on the chromosome 7
|
|
|
Cystic Fibrosis: teatment
|
pilocarpine
|
|
|
Inclusion bodies:
howell-Jolly |
Sickle Cell
|
|
|
Inclusion bodies:
heinz |
G-6PD
|
|
|
Inclusion bodies:
zebra |
neimann pick
|
|
|
Inclusion bodies:
donovan |
leishmaniasis
|
|
|
Inclusion bodies:
mallory (2) |
alcoholism and wilson's disease
|
|
|
Inclusion bodies: negri
|
Inclusion bodies: rabies
|
|
|
Inclusion bodies:
councilman |
yellow fever
|
|
|
Inclusion bodies:
call-exner |
ovarian tumors
|
|
|
Inclusion bodies:
lewy |
parkinsons
|
|
|
Inclusion bodies:
pick bodies |
pick disease
|
|
|
Inclusion bodies:
barr bodies |
female
|
|
|
Inclusion bodies:
aschoff |
rheumatic fever
|
|
|
Inclusion bodies:
cowdry type A |
herpes
|
|
|
Inclusion bodies:
auer rods |
AML
|
|
|
Inclusion bodies:
globoid |
krabbe's disease
|
|
|
Inclusion bodies:
russell |
multiple myeloma
|
|
|
Inclusion bodies:
schiller-duvall |
yolk sac tumor
|
|
|
Inclusion bodies:
basal bodies |
smooth muscle
|
|
|
what are the 3 Primary Allergic Response:
for each, answer the ff. when they show up peak gone |
1) neutrophils work in the first 3 days
2) B cells produce IgM ⇒shows up at 3 days ⇒peaks in 14 days ⇒gone in 2 months 3) IgG ⇒show up at 2 weeks ⇒peak in 2 months ⇒gone in 1 year |
|
|
Secondary Allergic Response: Memory
1) what shows up, when does it show up and at what concentration. 2) affinity 3) peaks 4) stays for how long |
IgG shows up at day 3 with 5x the concentration
⇒ highest affinity for antigen ⇒peaks in 5 years ⇒stays for 10 years |
|
|
Amyloidosis:
AL describe associations (2) |
It is a portion homologous with Ig Light chain.
associated with primary amyloidosis and multiple myeloma |
|
|
Amyloidosis:
AA describe associations (2) |
It is a unique N terminal sequence.
associated with chronic active disease and hodgekin's disease |
|
|
Amyloidosis:
Pre-albumin/transthyretin describe associations |
It is a single amino acid substitution.
associated with hereditary neuropathy, nephropathy and cardiopathy |
|
|
Amyloidosis:
AB describe associations (3) |
It is a B₂ microglobulin.
It is associated with cerebral artery amyloid, alzheimers, downs |
|
|
Amyloidosis:
AE describe associations |
"Endocrine"
Associated with Aging, medullary thyroid cancer |
|
|
Amyloidosis: AP
associations |
universally associated with all amyloids
|
|
|
Chelaytors: methylene blue
|
methemaglobinemia
|
|
|
Chelaytors: sodium thiosulfate
|
cyanide
|
|
|
Chelaytors: CaEDTA, what is it used for?
|
lead (to test)
|
|
|
Chelaytors: penicillamine, what is it used for?
|
lead (in plasma)
|
|
|
Chelaytors: dimercapterol, what is it used for?
|
lead (in bone marrow)
|
|
|
Chelaytors: tx. for cyanide poisoning
|
⇒Amyl Nitrate
⇒sodium thiosulfate ⇒methylne blue ⇒transfusion |
|
|
Renal Tubular acidosis causes what to the electrolytes.
|
acidosis and hypokalemia
|
|
|
RTA type I
urine pH patient is acidotic/alkalotic associations (2) presentaion in babies |
⇒high urine pH
⇒acidosis ⇒frequent UTI ⇒stones ⇒babies die <1 year |
|
|
RTA type II
urine pH hyper/hypokalemia deficiency |
⇒low urine pH (2)
⇒hypokalemia ⇒No carbonic anhydrase |
|
|
RTA type III
describe urine pH hyper/hypokalemia |
⇒combo type of RTA type I and II
⇒normal urine pH ⇒hypokalemia |
|
|
RTA type IV
who is at risk hyper/hypokalemia etiology |
⇒diabetics
⇒hyperkalemia ⇒No aldosterone (infracted JG apparatus) |
|
|
Hemolytic Properties of Streptococcus: α-, β-, γ-
|
α- partial hemolysis, green zone
β- complete hemolysis, clear zone γ- no hemolysis, red zone |
|
|
tranduction
what bug uses tranduction to acquires its exotoxin? |
bacteria becomes deadly when a virus injects its DNA
diptheria acquires its exotoxin this way |
|
|
where does bacteria uses transformation to become deadly:
|
In a hospital or nursing home the bacteria has become deadly by this mechanism
|
|
|
conjugation
|
only occurs if bacteria has PILI
|
|
|
Coumadin: describe the ff.
Pathway location evaluation factors affected route time contraindication |
Pathway: extrinsic
location: tissues evaluation: PT factors affected: 2,7,9,10 route: PO time: 8-10 hrs. delay contraindication: pregnancy |
|
|
coumadin: mechanism of action
|
Inhibits vitamin K dependant factor
|
|
|
Heparin: describe the ff.
pathway location PT/PTT factors affected route time C/I DOC |
Heparin: describe the following
Pathway: Intrinsic location: blood PTT factors affected: factor 3 route: IV time: immediate not contraindicated in pregnancy DOC for DVT |
|
|
Rashes: Erythyma marginatum
describe association |
small red spots with bright red margins, sand papery, Rheumatic fever
|
|
|
Rashes: Erythyma chronium migrans
describe disease |
target lesion, bulls eye, lyme disease
|
|
|
measles
describe is presentation |
morbiliform rash, preceded by cough and conjunctivitics
|
|
|
roseola
describe its presentation pathogen |
fever for 2 days then rash pops up ( rash only after fever is gone), HHV6
|
|
|
describe erythyma nodosum
|
tender nodules and redness on the anterior aspect of the legs
|
|
|
erythyma multiforme:
what is the second most common cause? describe how it looks like (2) and what causes it? (2) Mild: moderate: severe: |
red macules, target lesions, caused by allergy and viruses
⇒mild-most common cause is viral (2nd is drugs) ⇒moderate - stevens Johnson syndrome ⇒severe - toxic epidermal necrolysis |
|
|
seborrheic dermatitis
|
scaly skin with oily skin on the hairline
|
|
|
seborrheic keratosis
|
stuck on wart appearance
|
|
|
psoriasis
|
silvery white plaques on extensor surfaces, scaly skin, pitted nails
|
|
|
varicella zoster
type of herpes progression describe its presentation |
red macules, papules, vesicles, pustules then scabs:
different stages at the same time HHV3 |
|
|
dermatitis herpetiformis
describe association |
rash/blisters on anterior thigh,
associated with diarrhea due to celiac sprue flare up. |
|
|
typhoid fever
describe pathogen |
rose spots associated with " intestinal fire", salmonella typhi
|
|
|
dermatomyositis
|
heliotropic rash
|
|
|
erysipelas
|
reddened area with raised borders, does not blanch
|
|
|
tinea cruris
|
redness, itchy groin
|
|
|
tinea cruris
|
redness, itchy groin
|
|
|
pityriasis rosea
describe and pathogen |
herald patch: dry skin patched that follow skin lines.
HHV7 |
|
|
tinea versicolor
|
hypo-pigmented macules on the upper back in a "V" pattern
|
|
|
scabies
|
linear excoriations on belt line and finger webs
|
|
|
Hepatitis B
incubation: acute disease: convalescence: recovery: |
incubation: 4-26 weeks (8 wk avg)
acute disease: 4-12 weeks convalescence: 4-20 weeks recovery: year |
|
|
acute recent infection (3)
|
HBcAg+, HBsAg+, (HBcAb+/-)
|
|
|
recent immunization (within previous 2 weeks)
|
HBsAg+ only
|
|
|
immunization (more than 2 weeks previous)
|
HBsAb+ only
|
|
|
previous infection, now immune (3)
|
HBcAb+,HBsAb+,HBsAg-
|
|
|
infectious
|
HBeAg+
|
|
|
non-infectious
|
HBeAg-
|
|
|
chronic carrier (2)
|
HBsAg+ for more than 6 months (HBsAb+/-)
|
|
|
window period (3)
|
HBeAb+, HBcAb+, HBsAg-
|
|
|
HLA markers: DR-2
|
"2 itchy sheep (mary and sarah), sleep in a good pasture"
Narcolepsy, allergy, good pasture, MS |
|
|
HLA markers: DR-3
|
"3 S's and chronic active hepatitis"
Sjogren's, SLE, celiac sprue, chronic active hepatitis |
|
|
HLA markers: DR-3 & 4
|
IDDM type 1
|
|
|
HLA markers: DR-4
|
"RAP"
Rheumatioid arthritis, pemphigus vulgaris |
|
|
HLA markers: DR-5
|
"JRAP"
Juvenille Rheumatoid arthritis, Pernicious Anemia |
|
|
HLA markers: DR-7
|
steroid Induced nephrotic syndrome
|
|
|
HLA markers: DR-3 & B-8
|
celiac disease
|
|
|
HLA markers: A-3
|
hemochromatosis
|
|
|
HLA markers: B-3
|
myathenia gravis
|
|
|
HLA markers: B-13
|
psoriasis w/o arthritis
|
|
|
HLA markers: B-27
|
"2PAIR"
psoriasis w/ arthritis and postgonococcal arthritis ankylosing spondylitis IBD Reiter's |
|
|
HLA markers: BW-47
|
21-α-hydroxylase deficiency (vitamin D)
|
|
|
Immunoglobulins: IgA
form in blood form in secretions function |
⇨monomer in blood
⇨dimer in secretions ⇨protects the mucoscal surfaces and body secretions |
|
|
Immunoglobulins: IgD
function |
only known function is as a surface marker on mature B-cells
|
|
|
Immunoglobulins: IgE
hypersensitivity function: advantage and disadvantage what does it bind to complement activation |
⇨Mediator of type I hypersensitivity (anaphylaxis)
⇨parasite defense ⇨responsible for allergies ⇨Fc portion binds to mast cells and basophills ⇨does not fix complement |
|
|
Immunoglobulins: IgG
primary response secondary response (2) types |
⇨second to be produced during the primary immune response
⇨only one to be produced during the secondary immune response ⇨has memory (secondary) response ⇨ has 4 subclasses( antigenic differences in heavy chains and with disulfide bonds) |
|
|
Immunoglobulins: IgG memory (secondary) response
when does it show up and concentration, peak and remain in cirulation |
It show up in 3 days with 5x the concentration of primary response
peaks around 5 years remain in cirulation for 10 years |
|
|
Immunoglobulins: what are the 4 IgG subclasses?
|
IgG₁ to IgG₄
|
|
|
Immunoglobulins:
which Ig croses the placenta? how does it do this? |
IgG₁:
it can cross the placenta due to it Fc portion. |
|
|
Immunoglobulins:
which IgG is involved in a Ig deficiency what are they suceptible to? |
IgG₂:
most common deficiency, suceptible to encapsulated organisms |
|
|
Immunoglobulins:
which Ig is involved in memory antibodies? |
IgG₃
|
|
|
Immunoglobulins:
the only IgG that does NOT fix complement |
IgG₄
|
|
|
Immunoglobulins: IgM
primary or secondary immune response when is it most effective (2) function |
⇨present only in the primary immune response
⇨most effective in agglutination and complement fixation ⇨defense against bacteria and viruses |
|
|
Which type of hyperlipedemias is the most common in general population?
|
Type II Hyperlipidemia
|
|
|
Which type of hyperlipedemias is the associated with DM?
|
Type V hyperlipidemia
|
|
|
what is the deficiency in Hyperlipidemia type I?
|
lipoprotein Lipase- defect in liver type only.
|
|
|
what component is increase in Hyperlipidemia type I?
|
chylomicrons
|
|
|
what is Type II Hyperlipidemia deficiency?
|
receptor or receptor enzyme--IIa, IIb, or B100
|
|
|
what component is increased in Hyperlipidemia Type II
|
LDL
|
|
|
what is type III Hyperlipidemia deficiency?
|
APO E receptor
|
|
|
what component is elevated in type III Hyperlipidemia?
|
IDL
|
|
|
what is type IV Hyperlipidemia deficiency?
|
lipoprotein lipase defect of the adipose type only
|
|
|
what component is elevated in Type IV Hyperlipidemia?
|
VLDL
|
|
|
what is type V Hyperlipidemia deficiency?
|
enzyme-receptor defect -- APO CII
|
|
|
what 2 component is elevated in hyperlipedemia type V?
|
chylomicrons & VLDL
|
|
|
IL-1:
secreted by side effects function |
⇨secreted by macrophages
⇨causes FEVER and other non-specific symptoms of illness ⇨RECRUITS T HELPER CELLS |
|
|
IL-2:
secreted by function what must be done prior to transplantation |
⇨secreted by T cells
⇨MOST POTENT ⇨ most powerful chemotactic factor (RECRUITS EVERYONE) ⇨must be inactivated prior to transplantation |
|
|
IL-3
secreted by function labeled by |
⇨secreted by T cells
⇨cause B CELL PROLIFERATION ⇨labeled by thymidine |
|
|
IL-4
who secretes it? function: (2) |
⇨screted by T cells
⇨causes B cell differentiation ⇨responsible for class switching to IgG and IgE |
|
|
IL-5
who secretes it function |
⇨secreted by T cells
⇨responsible for CLASS SWITCHING TO IgA |
|
|
IL-8
|
NEUTROPHILLIC CHEMOTACTIC FACTOR
|
|
|
IL-10
funtions (2) |
⇨SUPPRESES CELL MEDIATED RESPONSE
⇨tells macrophages and T-cells to stay away if there is a bacterial infection |
|
|
IL-12
over all function recruits, activates, inhibits and switches what? |
⇨PROMOTES CELL MEDIATED RESPONSE
⇨if infection in non-bacteria it is released to recruit macrophages and T cells ⇨activates NK cells to secrete IF-γ ⇨inhibits IL-4 induced IgE secretions ⇨changes T helper cells in TH1 cells |
|
|
IF-α
who secretes it? what does it inhibit? 2 things that it increases? what does it interfere with? |
⇨secreted by leukocytes
⇨inhibits viral replication and tumor growth ⇨increases NK activity ⇨increases MHC (class I and II) expression ⇨interferes with protein sythesis |
|
|
IF-β
secreted by inhibition (2) increases (2) interferes with |
same function as IF alpha but secreted by a different cell
⇨secreted by fibroblast ⇨inhibits viral replication and tumor growth ⇨increase NK activity ⇨increases MHC (class I and II) expression ⇨interferes with protein synthesis. |
|
|
IF-γ
secreted by (2) Increases (3) co-stimulation decreases (1) |
⇨secreted by Tcells and NK cell
⇨increases NK activity ⇨increases MHC (class I and II) activity ⇨Increase macrophage activity ⇨co-stimulates B-cell growth and differentiation ⇨decreases IgE secretion |
|
|
TNF-α
aka secreted by (2) what interleukin does it induce? increases (2) side effect describe (2) |
⇨aka cachectin
⇨secreted by monocytes and macrophages ⇨induces IL-1 ⇨increases adhesion molecules and MHC class I on endothelial cells ⇨is a pyogen ⇨induces secretion IFγ ⇨cytotoxic/cytostatic |
|
|
TNF-β
aka secreted by cytotoxic/cytostatic? |
⇨aka lymphotoxin
⇨secreted by T-cells ⇨cytotoxic |
|
|
TGF-α
secreted by (3) what does it induce (4) |
⇨secreted by solid tumors (carcinoma<sarcoma) and monocytes
⇨induces agiogenesis, keratinocyte proliferation, bone resorption and tumor growth |
|
|
TGF-β
secreated by (5) induces (3) inhibits (5) enhances (2) |
⇨secreted by platelets, placenta, kidney,bone, T-cell and B-cells
⇨induces fibroblast proliferation, collagen synthesis and fibronectin synthesis ⇨inhibits NK, lymphokine activated killer cells, cytotoxic T lymphocytes, T cell & B cell proliferation ⇨ENHANCES WOUND HEALING AND ANGIOGENESIS |
|
|
what portion of the EKG is phase 0?
|
p wave
|
|
|
what are the 5 portion of the EKG is phase 2?
|
PR interval, Q wave, R-upstroke, S-downstroke, S-T interval
|
|
|
what portion of the EKG is phase 3?
|
T wave
|
|
|
what portion of the EKG is phase 4?
|
U wave
|
|
|
what portion of the Heart and EKG is phase 0?
|
atrium, p wave
|
|
|
what portion of the Heart and EKG is phase 2?
|
PR interval: AV node
Q-wave: septum R-upstroke: anterior wall S-downstroke: posterior wall S-T "interval" ventricle |
|
|
what portion of the Heart and EKG is phase 3?
|
ventricle: T wave
|
|
|
Adhesion molecules:
IgCAM function and examples |
they are the BINDING PROTEINS.
Example ICAM-1, ICAL-2, ICAM-3, LFA-3, LFA-2 (CD2) |
|
|
Adhesion molecules: ICAM-1, ICAL-2, ICAM-3
FUNCTION where are the found (3) |
⇨HOMING OF LYMPHNODES TO SITE OF INFLAMMATION
⇨found on T-cells, endothelial cells, dendridic cells |
|
|
Adhesion molecules: LFA-3
FUNCTION where are they found (2) |
⇨MEDIATE T CELL INTERACTIONS
⇨found on lymphocytes, APC |
|
|
Adhesion molecules: LFA-2 (CD2)
where are they found |
⇨found on T cells, NK cells
|
|
|
Adhesion molecules: what are the integrins and function
|
Integrins STOP THE LEUKOCYTES.
They are the VLA-1 (β₁), LFA-1 (β₂), CR3 (β₂), CR4(β₂) |
|
|
adhesion molecules: VLA-1 (β1)
FUNCTION |
⇨MIGRATION thru extracellular matrix
⇨widely distributed |
|
|
adhesion molecules: LFA-1 ((β2)
FUNCTION where are they found? |
⇨TIGHT BINDING TO ENDOTHELIUM
⇨found on lymphocytes |
|
|
adhesion molecules: CR 3 (β2)
function (2) receptors (3) |
⇨TIGHT BINDING TO ENDOTHELIUM, PHAGOCYTOSIS, MAC1
⇨CD11/CD18 |
|
|
adhesion molecules: CR4 (β2)
FUNCTION(2) |
⇨PHAGOCYTOSIS AND OPSONIN RECEPTOR
|
|
|
adhesion molecules: what are the selectins and function
|
selectins are the carbohydrate binders that mediates "rolling" (SLOWS DOWN LEUKOCYTES). examples E-selectins, L-selectins, P-selectins
|
|
|
adhesion molecules: E-selectins
function where are they found? |
⇨LEUKOCYTE MIGRATION AND HOMING
⇨found on activated Endothelium |
|
|
adhesion molecules: L-selectins
function where are they found |
⇨INITAL BINDING TO ENDOTHELIUM
⇨found on Leukocytes |
|
|
adhesion molecules: P-selectins
function where are they found |
⇨LEUKOCYTE MIGRATION to inflammatory sites
⇨found on activated endothelium and Platelets |
|
|
Hypersensitivities: what are the 4 hypersensitivities?
|
Type I: anaphylaxis
Type II: Cytotoxic (humoral) Type III: Immune complex mediated Type IV: Delayed (cell mediated) |
|
|
Hypersensitivities: Type I:
anaphylaxis pathogenesis (2) |
⇨IgE binds to mast cells-degranulates mast cells
⇨IgA activates IP3 cascade-degrades mast cells |
|
|
Type II Hypersensitivities:
Cytotoxic (humoral) 3 examples |
goodpasture, autoimmune, hemolytic anemia
|
|
|
Hypersensitivities:Type III:
Immune complex mediated 2 examples |
rheumatoid arthritis, SLE
|
|
|
Hypersensitivities:Type IV:
delayed (cell mediated) 3 examples |
TB skin test, contact dermatitis, transplant rejection
|
|
|
Drug MOA: 5-FU
|
Inhibit thymidylate
|
|
|
Drug MOA: methotrexate
|
inhibits dihydrofolate reductase
|
|
|
Drug MOA:
Hydroxyurea |
Inhibits ribonucleotide reductase
|
|
|
Drug MOA:
vincristine/vinblastin |
inhibits microtuble formation
|
|
|
Drug MOA:
paclitaxel |
inhibits microtubles from migrating
|
|
|
Drug MOA:
levamisole |
stimulates natural killer cells
|
|
|
Drug MOA:
steroids |
⇨kill Tcell and eosinophils
⇨inhibits macrophage migration ⇨inhibits phospholipase A ⇨inhibits mast cell degranulation ⇨stabilizes endothelium |
|
|
Drug MOA:
statins |
inhibits HMG CoA reductase
|
|
|
Drug MOA:
niacin |
decreases VLDL production in the liver
|
|
|
Drug MOA:
1st generation sulfonylureas |
blocks potassium channels in the islet cells promotes insulin release
|
|
|
Drug MOA:
2nd generation sulfonylureas |
promotes insulin release and inhibit gluconeogenesis in the liver
|
|
|
Drug MOA:
miglitol/ascarbose |
inhibit glucose absorption from GI
|
|
|
Drug MOA:
metformin |
stops gluconeogenesis in the liver
|
|
|
Drug MOA:
troglitazone |
increases sensitivity of insulin receptors
|
|
|
Drug MOA:
anti-psychotics |
block dopamine receptors
|
|
|
Drug MOA:
aspirin |
irreversible inhibitor of cyclo-oxygenase
|
|
|
Drug MOA:
K+ sparing diuretics |
competitive aldosterone receptor antagonist
|
|
|
Drug MOA:
topical anesthetics |
block Na+ channels
|
|
|
Drug MOA:
quinalones |
block topisomerase (supercoils)
|
|
|
Drug MOA:
aminoglycosides |
block initiation factor (IF) 2 on the 30s subunit
|
|
|
Drug MOA:
tetracyclines |
blocks tRNA biinding on the 30s subunit
|
|
|
Drug MOA:
rifampin |
block beta subunit of RNA polymerase
|
|
|
Drug MOA:
sulfa drugs |
blocks para-amino benzoic acid (PABA)
|
|
|
Drug MOA:
cephalosporins |
inhibit the cell wall
|
|
|
Drug MOA:
penicillins |
block transPeptidase
|
|
|
Drug MOA:
chroramphenicol |
blocks peptydyl transferase on the 50s subunit
|
|
|
Drug MOA:
clindamycin/lincomycin |
blocks translocase on the 50s subunit
|
|
|
Drug MOA:
macrolides |
blocks translocase on the 50s subunit.
|
|
|
Drug MOA:
metronidazole |
increases production of free radicals
|
|
|
Drug MOA:
vancomycin |
blocks cell wall (phospholipid)
|
|
|
Drug MOA:
benzodiazepine |
increase the frequency of the GABA receptors via Chloride channels
|
|
|
Drug MOA:
barbiturates |
increase the duration of the GABA channels via Chloride channels
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3 Drug MOA:
TCA |
blocks reuptake of catecholamines, AV conduction and alpha receptors
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Drug MOA:
SSRIs |
block reuptake of serotonin
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Drug MOA:
MAOIs |
inhibit MAO
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Drug MOA:
lithium |
MOA is unknown but is suspected to be related to it mimicking the sodium
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Drug MOA:
valproic acid |
blocks sodium and sometimes calcium
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Drug MOA:
carbamazapene |
block sodium and calcium
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Drug MOA:
epinephrine |
blocks beta (2>1) receptors and then alpha receptors
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Drug MOA:
1st generation antihistamines |
blocks H1 and H2 receptors (H1>H2)
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Drug MOA:
2nd generation antihistamines |
blocks H2 only
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Drug MOA:
decongestants |
alpha agonist
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antibiotic coverage: gram + (4)
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"PC+S"
penicillins, cephalosporins, tetracyclines, sulfa drugs |
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antibiotic coverage:
gram + and s. aureus (5) |
"MC QVC"
quinolones, macrolides, chloramphenicol, clindamycin, vancomycin |
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antibiotic coverage: simple gram - only (H.Flu and e.coli)
name 6 MOA for each |
"Triple MUT"
MacroLides: blocks transLocase sUlfa drugs: blocks PABA Tetracyclines block TRNA binding on 30S subunit ChloramPhenicol: block Peptidly transferase on a 50S subunit CLindamycin: blocks transLocase on 50S subunit Cephalosporins: inhibit Cell wall |
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antibiotic coverage:
all gram - and pseudomonas (2) MOA |
quinolones: blocks topoisomerase supercoils
aminoglycosides: block IF2 on 30S subunit |
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antibiotic coverage: atypicals (chlamydia, mycoplasma, ureaplasma and legionella) name 3 and MOA
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" 4 (tetra) Queens eating Mac and cheese is Atypical"
quinolones: blocks topoisomerase Tetracycline: blocks TRNA binding on 30S subunit macroLides: blocks transLocase on 50S subunit |
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antibiotic coverage: anaerobes (simple only no "big mama anaerobes) name 2 and its MOA
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" simPle Coverage of Anaerobes"
Cephalosporins: Cell wall inhibitor Penicillins: blocks transPePtidase |
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antibiotic coverage: anaerobes (4)
MOA |
chloramPhenicol: block Peptidyl transferase on 50S subunit
cLindamycin: blocks transLocase on 50S subunit vancomycin: cell wall inhibitor metronidazole: increases free radicals |
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antibiotic coverage: ricketsia and its mechanism of action
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Tetracyclines: block TRNA on a 30S subunit
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antibiotic coverage: pseudomembranous colitis, MRSA and enterococcis
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vancomycin: inhibits cell wall synthesis
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antibiotic coverage: protozoa
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metronidazole: increases free radicals
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antibiotic coverage: TB
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rifampin: block beta subunit of RNA polymerase
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Name the 7 Nephrotic patterns of vasculitis in order and what each one means in laymans terms:
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1) Renal artery stenosis: clot in front of renal artery
2) renal failure: clot of the whole renal artery 3) Glomerulonephritis: inflammed glomeruli 4) papillary necrosis: clot in papilla 5) Interstitial nephritis: clot in the medulla 6) Focal segmental glomerulonephritis: clot off pieces of the nephron 7) Rapidly progressive GN: clot off lots of nephrons |
