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1013 Cards in this Set
- Front
- Back
5 Heart Block
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(LSD Loves Company) Lyme Dz; Salmonella; Chagas; Legionella; Diphtheria
|
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Reiter's Syndrome
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Shigella, Yersinia, Crohn's, IBD, Chlamydia
|
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Low Complement Bugs
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(I AM HE) = Influenza, Adenovirus, Mycoplasma, Hep B & C, EBV
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Drugs Induced SLE
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HIPPPE) = Hydralazine, INH, Penicillamine, Procainamide, Phenytoin, Ethosuximide
|
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Drugs that blast the BM
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(ABC-V) = AZT, Benzene, Chloramphenecol, Vinblastin
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Comma Shaped Bugs
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Vibrio, Campylobacter, Listeria, H. pylori
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Chinese letters
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Corynbacter
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Crescent Shaped Protozoa
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Giardia lambdia
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TB Treatments
|
(PRISE) = Pyrazinamide, Rifampin, INH, Streptomycin, Ethambutol
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6 low complement associated nephrotic syndromes
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serum sickness, SLE, SBE, PSGN, MPGN II, Cryoglobulinemia
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Induce P450
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(BAG for CPR QTS) Barbiturates, Alcohol, Griseofulvin, Carbamazepine, Phenytoin, Rifampin, Quinidine, Tetracyclines, Spironolactones
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Inhibit P450
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(I'D SMACK Quin) INH, Dapsone, Sulfa drugs, Macrolides, Amiodarone, Cimetadine, Ketoconazole, Quinolones
|
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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, incr Liver enzymes
|
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Painful Genital lesions
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Herpes, Chancroid (H.ducreyi), Lymphogranuloma venerum, Lymphomuloma 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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Necatar Americanis, Enterobius Vermicularis, Ankylostoma Duodenale, Trichuris Trichurium, Ascaris Lumbroicoides, Strongyloides
|
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X-linked Enzyme Deficiencies
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(Fabry & Lesh go Hunting for Candy, Pie and Gum) G6PD, CGD (NADPH), Fabry's, Hunter's, Lesh-Nyhan
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Screen Newborns
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(Please Check Before Going Home) PKU, Congenital Adrenal, Hyperplasia, Biotidinase, Galactosemia, Hypothyroidism
|
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Action of Steroids
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(KIIISS) = Kills T-cells and Eosinophils; Inhibit macrophage migration; Inhibit Phospholipase A; Inhibit mast cell degranulation; Stabilizes endothelium; Stimulates protein synthesis
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Causes of Severe Monocytosis
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(STELS) = Salmonella, TB, EBV, Listeria, Syphilis
|
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Macrolides
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(MACE) = macrolides; Azithromycin, Clarithromycin, Erythromycin
|
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1 dose Tx for Chlamydia
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Azithromycin
|
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"""Big Mama"" Anaerobes"
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Strep. Bovis; Bacteriodes fragilis, C. melango-septicus; C. difficile. ---R/O colon cancer if positive S. bovis or C. melango-septicus
|
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"Tx for ""Big Mama"" anaerobes"
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Methronidazole, Clindamycin, Cefoxitin
|
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Serum Values for Low Volume State
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Decrease -->K, Na, Cl, Increase --> pH, BP
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1 dose Tx for Gonorrhea
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Ceftrioxone, Cefixime, Cefoxitin; Ciprofloxacin, Ofloxacin, Gatifloxicin
|
|
Psammoma bodies
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Papillary CA of Thyroid; Serous Cystadenoma of ovary; Meningioma; Mesothelioma
|
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Drugs that cause Cardiac fibrosis
|
Adriamycin (Doxorubycin); Phen-Fen
|
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Indications for Peptic Ulcer Dz
|
(IHOP) = Intractable Pain, Hemorrhage, Obstruction, Perforation
|
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Urease +ve Bacteria
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(PPUNCHeS) = Proteus, Pseudomonas, Ureaplasma urealyticum, Norcardia, Cryptococcus neoformans, H. pylori, S. saprofiticus
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Drugs that cause Pulmonary Fibrosis
|
(BBAT) = Bleomycin, Busulfan, Amiodarone, Tocainide; methotrexate, cormustine
|
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Salmonella Typhi
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High fever, Rose spots, Intestinal fire, Monocytosis, Heart block
|
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Drugs that cause Myositis
|
(RIPS) = Rifampin, INH, Prednisone (steroids), Statins
|
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Encapsulated Bacteria
|
(Some Strange Killers Have Pretty Nice Capsules); Strep. Pneumonia, Salmonella, Klebsiella, H. Flu B, Pseudomonas, Neisseria, Citrobacter
|
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Encapsulated Yeast
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Cryptococcus
|
|
Jones Criteria
|
(JONES) = Polyarthritis (Joints), Carditis, Nodules subcutaneous, Erythema marginatum, Sydenham chorea
|
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IgA Nephropathies
|
Henoch-Schoenlein Purpura (HSP); Berger's; Alport's
|
|
Massive Eosinophilia
|
(NAACP) = Neoplasms, Allergies/ Asthma, Addison's, Collagen Vascular Dz, Parasites
|
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Risk Factors for Primary Liver Cancer?
|
Hep B and C, Aflatoxin, Vinyl Chloride, Alcohol, Carbon Tetrachloride, Anyline dyes, Smoking, Hemochromatosis, Benzene, Schistosomiasis
|
|
9 Live Vaccines
|
Measles, Mumps, Rubella, Oral Polio, Rotavirus, Small Pox, BCG, Yellow Fever, Varicella
|
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Autoimmune Hemolytic Anemia
|
PTU, Cephalosporins, alpha-methyldopa, Sulfa drugs, Anti-malarials, Penicillin
|
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Autoimmune Thrombocytopenia
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Aspirin, Heparin, Quinidine
|
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Pansystolic Murmurs
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Mitral Regurg., Tricuspid Regurg., Ventrical Septal Defect
|
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Dihydrofolate Reductase Inhibitors
|
Pyremethamine/Sulfadiazine; Triamethroprim/ Sulfamethoxazole; Methotrexate
|
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Sulfa Containing Drugs
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Sulfonamides, Sulfonylureas, Celecoxib (COX-2 inhibitor)
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Silver Staining Bugs
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Legionella, Pneumocystis, H. pylori, Bartonella henselae, Candida
|
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Blood Gas with RESTRICTIVE lung disease
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Tachypnea, decr CO2, decr O2, incr pH
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Blood Gas with OBSTRUCTIVE lung disease
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Incr or normal pO2, incr pCO2, decr pH
|
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MI- enzymes
|
Troponin I = appears 2hrs; peaks 2 days, gone 7 days == CKMB = appears 6 hrs; peaks 12hrs, gone 2 days == LDH = appears 1 day; peaks 2 days, gone 3 days
|
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Macrophage deficiency
|
Chediak Higashi; NADPH-Oxidase def. (CGD)
|
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1 dose tx for H. ducreyi
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Azithromycin - 1 gram; Ceftriaxone - 250 mg IM
|
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1 dose tx for Gardnerella
|
Metronidazole
|
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SE of Thiazides and Loop diuretics
|
Hyperglycemia; Hyperuricemia; Hypovolemia; Hypokalemia
|
|
Macrophages in Brain?
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Microglia
|
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Macrophages in Lung?
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Type I Pneumocytes
|
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Macrophages in Liver?
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Kupffer cells
|
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Macrophages in Spleen?
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RES cells
|
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Macrophages in Kidney?
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Mesangial cells
|
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Macrophages in Lymph nodes?
|
Dendritic cells
|
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Macrophages in Skin?
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Langerhans
|
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Macrophages in Bone?
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Osteoclasts
|
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Macrophages in Connective tissue?
|
Histiocytes, Giant cells, Epitheloid
|
|
Rashes of Palm and Soles
|
(TRiCKSSSS) = TSS - toxic shock; Rocky Mt. Spotted Fever; Coxsackie A (Hand Foot & Mouth dz); Kawasaki; Scarlet Fever; Syphilis; Staph. Scalded Skin; Streptobacillus moniliformis
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4 sources of Renal Acid
|
Plasma (RTA); Ammonia production in collecting ducts - 10% urea cycle; Glutaminase; Carbonic Anhydrase
|
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Hormones Produced by Small Cell CA of Lung
|
ACTH (mc), ADH, PTH, TSH, ANP
|
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1 dose tx for Candidiasis
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Ketoconazole - 150mg
|
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1 dose tx for Vaginal Candidiasis
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Diflucan - 1 pill
|
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1 dose tx for Trichomonas
|
Metronidazole
|
|
Viruses Related to CA
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HPV = Cervical cancer; EBV = Lymphoma/ Nasopharyngeal carcinoma; HVB and HCV = Liver carcinoma; HIV = Kaposi
|
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NM disease concept
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Restrictive Blood Gas; decr pO2 and pCO2; incr pH, RR; Incr risk for seizures; Decr Pulmonary Capillary Wedge pressure
|
|
PIE Syndrome (Pulmonary Infiltrates with Eosinophilia)
|
(NASSA) = Necatar Americanus, Ascaris Lumbriocoides, Schistosomiasis, Strongyloides, Ankylostoma
|
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Enzymes used by B12
|
Methyl Malonyl CoA mutase; Homocysteine methyl transferase
|
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Increased succeptibility to pseudomonas and S. aureus
|
Burn patients; Cystic Fibrosis; Diabetes; Neutropenias
|
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Crohn's Disease
|
(GIFTS) = Granuloma, Illeum, Fistula, Transmural, Skip lesions
|
|
Causes of Widened S2
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incr pO2; incr volume Right ventricle; Blood transfusion; Supplemental O2; Right sided heart failure; Pregnancy; I.V. Fluids; ASD (fixed); Deep breathing
|
|
Cavities of Blood loss
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Pericardium, Intracranial, Mediastinum, Pleural cavity, Thighs, Retroperitoneum, Abdominal, Pelvis
|
|
Negative Stranded RNA
|
1-3 week prodromal period before sxms; Must switch to positive stranded before it can replicate
|
|
Positive Stranded RNA
|
Sxms occur within 1 week or less; Don't have to switch before replicating; === Exceptions: Hanta, Ebola and Yellow Fever which are negative stranded
|
|
Cyanotic Heart Diseases
|
Transposition of great vessels; Tetralogy of Fallot; Truncus Arterious; Tricuspid Atresia; Total Anomalous Pulmonary Venous Return; Hypoplastic Left Heart syndrome: Ebstein's Anomaly; Aortic Atresia; Pulmonic Atresia
|
|
Less likely to depolarize
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Hypermagnesia; Hypercalcemia (except Atrium); Hypokalemia
|
|
More likely to depolarize
|
Hypomagnesia; Hypocalcemia (except atrium); Hyperkalemia; Hypernatremia; Hyponatremia (Ca++ effect)
|
|
Hormones produced by the Placenta
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hCG; Inhibin: Human Placental Lactogen: Oxyctocin: Progesterone: Estrongen
|
|
Uses of Pilocarpine
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Cystic fibrosis dx; Closed angle Glaucoma
|
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Causes of Dusguzia
|
Metronidazole; Clarithromycin: Zinc deficiency
|
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Carcinoid Triad
|
Flushing, Wheezing, Diarrhea --- Dx by measuring 5-HIAA in urine
|
|
Where is carcinoid tumor’s primary location
|
Appendix
|
|
Most common metastatic location of carcinoid tumor?
|
Pancreas and Ileum
|
|
Give 4 examples of AVMs
|
Heart = PDA; Elbow = dialysis fistula; Brain = Von Hippel Lindau; Lung = Osler Weber Rendu
|
|
Hemophilus Influenza
|
Gram negative rods; Pleomorphic “school of fish”; Type A = non encapsulated, non invasive, MCC of sinusitus, otitis, bronchitis; Type B = encapsulated, invasive, IgA protease, MCC of epiglotitis
|
|
Rust Colored Sputum
|
Strep. Pneumoniae (aka. pneumococcus)
|
|
Staph. Epidermidis
|
MC infection of shunts and central lines at the hospital
|
|
How do you tell Catalase positive Staphylococi apart?
|
Aureus = gold; Epidermidis = white; Saprophyticus = none
|
|
Strep. pyogenes
|
MCC of all throat infections, lymphangitis, impetigo, necrotizing facitis, erysipelas, Scarlet fever; 2nd MCC of all other skin infections
|
|
Neutrophil Deficiencies
|
Job-Buckley Syndrome; NADPH Oxidase deficiency; Neutropenia; Myeloperoxidase deficiency
|
|
Compartment Syndrome
|
Pain (always first); Pallor; Polkiothermia; Paresthesia; Pulseless (always last)
|
|
Itchiest Rashes
|
Scabies; Lichen planus; Urticaria; Dermatitis herpatiformis
|
|
Oddities About Listeria
|
Only gram positive with endotoxin; Crosses placenta; Lipid A is toxic part; Causes granulomas; Causes sepsis in neonates; Raw cabbage, spoilded milk
|
|
Vitamin B1?
|
Thiamine; Beriberi Wernickes Encephalopathy; Karsacoff
|
|
Vitamin B2?
|
Riboflavin; Angular chelosis/stomalitis
|
|
Vitamin B3?
|
Niacin; Pellegra; 4D’s
|
|
Vitamin B4?
|
Lipoic acid
|
|
Vitamin B5?
|
Pantothenic acid
|
|
Vitamin B6?
|
Pyridoxine; seizures
|
|
Vitamin B9?
|
Folate
|
|
Vitamin B12?
|
Cobalamine; perinicious anemia; neuropathy
|
|
Periods of rapid growth
|
Birth-2months; 4-7 years; Puberty
|
|
Only Immune deficiency with low calcium?
|
DiGeorge’s Syndrome
|
|
Bugs with IgA Protease
|
(Resistant to IgA) = S. Pneumonia; H. Influenza; Neisseria
|
|
Secretions of Mast Cells
|
Histamine; Slow Reacting Substance of Anaphylaxis; Eosinophil Chemotactic factor of anaphylaxis
|
|
Secretions of Eosinophil
|
Histamine; Arylsulfatase; Herparin
|
|
Actions of E. coli
|
Secrete Vitamin K, Biotin, Folate, panthothenic acid and absorption of B12
|
|
Heart Block Clue
|
Increased body temp with a normal heart rate; HR should increase by 10bpm for every 1 degree increase in temperature
|
|
Macrophages
|
Release MHC II
|
|
TH1 Secrete
|
IL-2, IF-gamma
|
|
TH2 Secrte
|
IL-4, IL-5, IL-6, IL-10
|
|
TH0 Secrte
|
TH1 and TH2
|
|
T-Cytotoxic Cells
|
CD-8 positive; CD-4 negative; Recognize MHC 1; Have CD-2 and CD-3 markers
|
|
T-Helper Cells
|
CD-4 positive; CD- 8 negative; Recognize MHC II; Have CD-2 and CD-3 markers
|
|
Elevated Cholesterol
|
Xanthanthomas on extensor surfaces; incr risk for CAD
|
|
4 Causes of Severe Pain
|
Pancreatitis (EtOH); Kidney Stones (bloody urine); AAA (ripping, tearing pain radiating to back); Ischemic Bowel (blood diarrhea)
|
|
5 Causes of SIADH
|
Small Cell Carcinoma; incr intracranial pressure; A Pain; Drugs (eg. Carbamazepine); Hypoxia (Restrictive Lung Dz)
|
|
Cell of Neural Crest Origin
|
(POT CLAMPS) = Parafollicular cells; Ondontocytes; Tracheal cartilage; Chromaffin Cells; Laryngeal cartilage; All Ganglion cells/ Adrenal Gland; Melanocytes; Pseudounipolar cells/ Parafollicular cells; Spiral membrane
|
|
Ions and the EKG
|
P-wave = Ca++ ; QRS = Na+ ; ST interval = Ca++ ; T-wave = K+ and U-wave = Na+
|
|
Maximum Sinus Rate
|
220 - age in years
|
|
Tri-Nucleotide Repeats
|
Huntington’s; Fragile X; Myotonic dystrophy; Spinal/bulbar muscular atrophy; Prader Willi Syndrome; Frederick Ataxia
|
|
Low volume states with acidosis (not alcolosis)
|
Renal Tubular Acidosis; Diarrhea; Diabetes Ketoacidosis
|
|
MCC Croup & Bronchiolitis
|
Parainfluenza; RSV (ER this is #1); Adenovirus; Influenza
|
|
4 D’s of Pellegra
|
Dermatitis; Diarrhea; Dementia; Death
|
|
Types of Kidney Stones
|
Calcium oxalate (80%); Struvite (proteus); Uric Acid (radiolucent); Cysteine; Oxalate
|
|
Pseudogout
|
Ca++ pyrophosphate; positive birefringent crystals; Rhomboid crystals; MC older patients; equal in both genders; Tx = Colchicine
|
|
MC Non-cyanotic Congenital Heart Dz
|
VSD; ASD; PDA: Coarctationof aorta
|
|
Enzymes NEVER in Glycolysis
|
Pyruvate carboxylase; PEP carboxykinase; Fructose-1,6-phosphatase; Glucose-6-phosphatase
|
|
Enzymes ONLY in Glycolysis
|
Hexokinase/Glucokinase; Phosphofructokinase-1, Pyruvate kinase
|
|
Acid Fast Organisms
|
Mycoplasma; Norcardia (partially gram +ve); Cryptosporidium (partially, protozoa)
|
|
Microsteatosis causes
|
Acetaminophen; Reye Syndrome; Pregnancy)
|
|
Macrosteatosis causes
|
Alcohol
|
|
Bacteria with Elastase
|
Staph aureus and Pseudomonas
|
|
Bacteria with toxins that inhibit EF-2
|
Pseudomonas and Diphtheria
|
|
Viruses Related to CA
|
HPV = Cervical cancer; EBV = Lymphoma/ Nasopharyngeal carcinoma; HVB and HCV = Liver carcinoma; HIV = Kaposi
|
|
NM disease concept
|
Restrictive Blood Gas; decr pO2 and pCO2; incr pH, RR; Incr risk for seizures; Decr Pulmonary Capillary Wedge pressure
|
|
PIE Syndrome (Pulmonary Infiltrates with Eosinophilia)
|
(NASSA) = Necatar Americanus, Ascaris Lumbriocoides, Schistosomiasis, Strongyloides, Ankylostoma
|
|
Enzymes used by B12
|
Methyl Malonyl CoA mutase; Homocysteine methyl transferase
|
|
Increased succeptibility to pseudomonas and S. aureus
|
Burn patients; Cystic Fibrosis; Diabetes; Neutropenias
|
|
Crohn's Disease
|
(GIFTS) = Granuloma, Illeum, Fistula, Transmural, Skip lesions
|
|
Causes of Widened S2
|
incr pO2; incr volume Right ventricle; Blood transfusion; Supplemental O2; Right sided heart failure; Pregnancy; I.V. Fluids; ASD (fixed); Deep breathing
|
|
Cavities of Blood loss
|
Pericardium, Intracranial, Mediastinum, Pleural cavity, Thighs, Retroperitoneum, Abdominal, Pelvis
|
|
Negative Stranded RNA
|
1-3 week prodromal period before sxms; Must switch to positive stranded before it can replicate
|
|
Positive Stranded RNA
|
Sxms occur within 1 week or less; Don't have to switch before replicating; === Exceptions: Hanta, Ebola and Yellow Fever which are negative stranded
|
|
Cyanotic Heart Diseases
|
Transposition of great vessels; Tetralogy of Fallot; Truncus Arterious; Tricuspid Atresia; Total Anomalous Pulmonary Venous Return; Hypoplastic Left Heart syndrome: Ebstein's Anomaly; Aortic Atresia; Pulmonic Atresia
|
|
Less likely to depolarize
|
Hypermagnesia; Hypercalcemia (except Atrium); Hypokalemia
|
|
More likely to depolarize
|
Hypomagnesia; Hypocalcemia (except atrium); Hyperkalemia; Hypernatremia; Hyponatremia (Ca++ effect)
|
|
Hormones produced by the Placenta
|
hCG; Inhibin: Human Placental Lactogen: Oxyctocin: Progesterone: Estrongen
|
|
Uses of Pilocarpine
|
Cystic fibrosis dx; Closed angle Glaucoma
|
|
Causes of Dusguzia
|
Metronidazole; Clarithromycin: Zinc deficiency
|
|
Carcinoid Triad
|
Flushing, Wheezing, Diarrhea --- Dx by measuring 5-HIAA in urine
|
|
Where is carcinoid tumor’s primary location
|
Appendix
|
|
Most common metastatic location of carcinoid tumor?
|
Pancreas and Ileum
|
|
Give 4 examples of AVMs
|
Heart = PDA; Elbow = dialysis fistula; Brain = Von Hippel Lindau; Lung = Osler Weber Rendu
|
|
Hemophilus Influenza
|
Gram negative rods; Pleomorphic “school of fish”; Type A = non encapsulated, non invasive, MCC of sinusitus, otitis, bronchitis; Type B = encapsulated, invasive, IgA protease, MCC of epiglotitis
|
|
Rust Colored Sputum
|
Strep. Pneumoniae (aka. pneumococcus)
|
|
Staph. Epidermidis
|
MC infection of shunts and central lines at the hospital
|
|
How do you tell Catalase positive Staphylococi apart?
|
Aureus = gold; Epidermidis = white; Saprophyticus = none
|
|
Strep. pyogenes
|
MCC of all throat infections, lymphangitis, impetigo, necrotizing facitis, erysipelas, Scarlet fever; 2nd MCC of all other skin infections
|
|
Neutrophil Deficiencies
|
Job-Buckley Syndrome; NADPH Oxidase deficiency; Neutropenia; Myeloperoxidase deficiency
|
|
Compartment Syndrome
|
Pain (always first); Pallor; Polkiothermia; Paresthesia; Pulseless (always last)
|
|
Itchiest Rashes
|
Scabies; Lichen planus; Urticaria; Dermatitis herpatiformis
|
|
Oddities About Listeria
|
Only gram positive with endotoxin; Crosses placenta; Lipid A is toxic part; Causes granulomas; Causes sepsis in neonates; Raw cabbage, spoilded milk
|
|
Phage Mediated Toxins (Oh BED)
|
O antigen of salmonella
|
|
|
Botulinum
|
|
|
Erythrogenic Toxin
|
|
|
Diptheria
|
|
|
|
|
Segmented viruses
|
Orthoviridae
|
|
|
Bunya
|
|
|
Arena
|
|
|
Reo
|
|
|
|
|
Functions of adhesion molecules
|
Lymphocyte homing
|
|
|
Inflammation
|
|
|
Cell-cell interaction
|
|
|
|
|
Espphageal/Gastric cancer risk factors
|
Smoking
|
|
|
Alchohol
|
|
|
Nitrates
|
|
|
Japanese
|
|
|
|
|
Bladder Cancer risk factors
|
Smoking
|
|
|
Aniline dyes
|
|
|
Benzene
|
|
|
Aflatoxin
|
|
|
Cyclophosphamide
|
|
|
Schistosomiasis
|
|
|
VHL syndrome
|
|
|
Tuberous Sclerosis
|
|
|
|
|
Structures with no known function
|
Appendix;
Epithalamus; Palmaris longus; Pancreatic Polypeptide |
|
|
Epithalamus
|
|
|
Palmaris Longus
|
|
|
Pancreatic Polypeptide
|
|
|
|
|
Progression to RPGN
|
Goodpatures (#1)
|
|
|
Diabetes
|
|
|
Hypertension
|
|
|
Wegeners Granulomatosis
|
|
|
|
|
Causes of Papillary Necrosis
|
Vasculities
|
|
|
AIDS
|
|
|
|
|
Gram + spore formers
|
Bacillus
|
|
|
Clostridium perfringes
|
|
|
Clostridium tetani
|
|
|
|
|
Used for Cold Agglutinin testing
|
Strep salivarius
|
|
|
|
|
Drugs w/ disulfiram like reaction
|
Chlorpropamide
|
|
|
Lactams
|
|
|
Antabuse
|
|
|
Metronidazole
|
|
|
|
|
3 toxins of bacillus
|
Lethal factor
|
|
|
Edema factor
|
|
|
Protective factor
|
|
|
|
|
Beta Blockers
|
A-M : Cardioselective
|
|
|
N-Z : non selctive
|
|
|
C/L : agonist/antagonist
|
|
|
|
|
Fanconi syndrome
|
Defect in PCT
|
|
|
Cant reabsorb
|
|
|
Low energy state
|
|
|
Can be caused by old tetracycline
|
|
|
|
|
Glutaminase
|
In collecting ducts
|
|
|
Absorbs ammonia in liver
|
|
|
cause of hepato-renal syndrome
|
|
|
|
|
3 anatomin narrowings of ureter
|
Hilum
|
|
|
Pelvic Brim
|
|
|
Entrance of Bladder
|
|
|
|
|
Odd MCC of death
|
SLE, endometrial and cervical cancer
|
|
|
RENAL FAILURE
|
|
|
|
|
Methotrexate uses
|
Dx fragile X;
Tx Molar Pregnancy Tx. Fast growing CA Tx. Steroid resistant disease |
|
|
TX molar pregnancy
|
|
|
TX fast growing cancer
|
|
|
TX steriod resistant disease
|
|
|
|
|
Group D strep
|
Viridans (green pigment) causes SBE
|
|
|
Mutans - cavities
|
|
|
Sanguis
|
|
|
Salivarius
|
|
|
Bovis
|
|
|
|
|
Nephritic Syndrome
|
HTN
|
|
|
Hematuria
|
|
|
RBC casts
|
|
|
|
|
Nephrotic Syndrome
|
Edema
|
|
|
Hyperlipidemia
|
|
|
Hypercholesterolemia
|
|
|
Hypercoagulable
|
|
|
decrease serum Albumin
|
|
|
increase urine Albumin
|
|
|
|
|
MCC of airway infection(sinusitis, otitis, bronchitis, pneumo)
|
1) strep pneumo
|
|
|
2) H influenza
|
|
|
3) N meningitidis
|
|
|
|
|
Gastroenteritis within 8 hours of eating (pre formed toxins)
|
Staph Aureus (potato salad)
|
|
|
C perfringes ( holiday ham/turkey)
|
|
|
B cereus ( reheated fried rice)
|
|
|
|
|
Citrobacter
|
Multiple cerebral abscess in newborns
|
|
|
|
|
MCC of UTI
|
1) Ecoli
|
|
|
2)proteus
|
|
|
3) Klebsiella
|
|
|
|
|
MCC infection of females age 5-10 and 18-24
|
S. saprophyticus (sticking things in themselves)
|
|
|
|
|
S Aureus
|
MCC osteomyelitis
|
|
|
MCC infection in burn patients
|
|
|
|
|
MCC newborn Meningitis
|
Group B strep
|
|
|
E Coli
|
|
|
Listeria
|
|
|
|
|
Bacteria associated with colon cancer
|
C Melanogosepticus
|
|
|
S bovis
|
|
|
|
|
Strict anaerobis gram -
|
H influenza
|
|
|
Niesseria
|
|
|
|
|
Pre renal failure
|
serum BUN above 20
|
|
|
serum Creatanine above 40
|
|
|
fractional Na exc. Above 2%
|
|
|
|
|
Renal Failure
|
BUN 10-15
|
|
|
Creatinine less than 20
|
|
|
Fractional Na exc. Greater then 2%
|
|
|
|
|
Extravasation
|
Pavementing
|
|
|
Margination
|
|
|
Diapedesis
|
|
|
Migration
|
|
|
|
|
If cell mediated imm is defective - TX for
|
Viral
|
|
|
Fungal
|
|
|
Mycobacterium
|
|
|
Protozoa
|
|
|
Parasite
|
|
|
Neoplasm
|
|
|
|
|
Herpes virus types
|
I - oral
|
|
|
II genital
|
|
|
III varicella zoster
|
|
|
IV EBV
|
|
|
V CMV
|
|
|
VI Roseola
|
|
|
VII Pityriasis Rosea
|
|
|
VIII Kaposi
|
|
|
|
|
Dz piced up during delivery
|
Group B Strep
|
|
|
S Pneumo
|
|
|
Herpes
|
|
|
N gonorrhea
|
|
|
Chlamydia
|
|
Page 6
|
PPclue Flash Cards
|
|
T & B-cell Deficiencies
|
WAS – Thrombocytopenia, IL-4, Eczema, ↓ IgM --|-- SCID – Adenosine deaminase deficiency, T> B, frameshift/nonsense mutation, ↑ bacterial & fungal infx. --|-- CVID – Tyrosine kinase deficiency, Late onset, frameshift/missense mutation --|-- HIV (HTLV-1) – Effects CD-4 rich tissues (brian, testicles, cervix, rectum, blood vessels), T>B --|-- Job-Buckley Syndrome – red headed female, Tyrosine kinase deficiency
|
|
B-Cell Deficiencies
|
Bruton’s Agammaglobulinemia – Tryosine kinase deficiency --|-- Leukemias --|-- Lymphomas --|-- See above for those with T-cell overlap --|-- HIV (HTLV-1) – Effects CD-4 rich tissues (brian, testicles, cervix, rectum, blood vessels), T>B --|-- SCID – Adenosine deaminase deficiency, T> B, frameshift/nonsense mutation, ↑ bacterial & fungal infx.
|
|
T-Cell Deficiencies
|
DiGeorge’s – hypokalemia, problem with 3rd and 4th pharyngeal pouches, deletion of chromosome 22 --|-- HIV --|-- See above for those with B-cell overlap --|-- HIV (HTLV-1) – Effects CD-4 rich tissues (brian, testicles, cervix, rectum, blood vessels), T>B --|-- SCID – Adenosine deaminase deficiency, T> B, frameshift/nonsense mutation, ↑ bacterial & fungal infx.
|
|
Electron Transport Chain Poisons, Chemical Uncouplers, Physical Uncouplers
|
Electron Transport Chain --|-- Poisons --|-- Complex I…….Amytal, Rotenone --|-- Complex II……Malonate --|-- Complex III…..Antimycin --|-- Complex IV…..CN, CO, Chloramphenicol --|-- Complex V……Oligomycin --|-- --|-- Chemical Uncouplers --|-- DNP --|-- Free Fatty Acids --|-- --|-- Physical Uncouplers - Aspirin
|
|
Electron Transport Chain Poisons
|
Poisons --|-- Complex I…….Amytal, Rotenone --|-- Complex II……Malonate --|-- Complex III…..Antimycin --|-- Complex IV…..CN, CO, Chloramphenicol --|-- Complex V……Oligomycin --|--
|
|
Electron Transport Chain Chemical Uncouplers
|
Chemical Uncouplers --|-- DNP --|-- Free Fatty Acids --|--
|
|
Electron Transport Chain Physical Uncouplers
|
Physical Uncouplers - Aspirin
|
|
Places where Amino Acids feed in/out of TCA Cycle
|
Pyruvate…………..Gly, Ala, Ser --|-- Acetyl CoA……….Phe, Iso, Thr, Tyr, Lys, Leu --|-- α-ketogluterate……Glu, Gln --|-- Succinyl CoA…….Phe, Trp, Tyr --|-- Fumerate………….Pro --|-- Oxaloacetate………Asp, Asn
|
|
Amino Acid Deficiencies
|
PKU – Phenylalanine hydroxylase deficiency, needed to make tyrosine, leads to a lack of Dopamine, Epi and Norepi, melanin --|-- Maple Syrup Urine Disease – deficiency in branched amino acids (Leu, Lys, Val), defective transport in the kidneys --|-- Cystinuria – Cystathione synthase deficiency; cysteine, ornithine, lysine and Arginine end up in urine, stones --|-- --|-- --|-- --|-- --|--
|
|
Thr – (Amino Acid Abbreviation stands for : )
|
Threonine
|
|
Cys – (Amino Acid Abbreviation stands for : )
|
Cysteine
|
|
Tyr – (Amino Acid Abbreviation stands for : )
|
Tyrosine
|
|
Asn – (Amino Acid Abbreviation stands for : )
|
Asparagine
|
|
Gln – (Amino Acid Abbreviation stands for : )
|
Glutamine
|
|
Asp – (Amino Acid Abbreviation stands for : )
|
Aspartic Acid
|
|
Glu – (Amino Acid Abbreviation stands for : )
|
Glutamic Acid
|
|
Lys – (Amino Acid Abbreviation stands for : )
|
Lysine
|
|
Arg – (Amino Acid Abbreviation stands for : )
|
Arginine
|
|
His – (Amino Acid Abbreviation stands for : )
|
Histidine
|
|
Gly – (Amino Acid Abbreviation stands for : )
|
Glycine
|
|
Ala – (Amino Acid Abbreviation stands for : )
|
Alanine
|
|
Val – (Amino Acid Abbreviation stands for : )
|
Valine
|
|
Leu – (Amino Acid Abbreviation stands for : )
|
Leucine
|
|
Iso – (Amino Acid Abbreviation stands for : )
|
Isoleucine
|
|
Met – (Amino Acid Abbreviation stands for : )
|
Methionine
|
|
Phe – (Amino Acid Abbreviation stands for : )
|
Phenylalanine
|
|
Trp – (Amino Acid Abbreviation stands for : )
|
Tryptophan
|
|
Pro – (Amino Acid Abbreviation stands for : )
|
Proline
|
|
Ser – (Amino Acid Abbreviation stands for : )
|
Serine
|
|
Give the amino acid in this subgroup - Acidic:
|
Asp Glu
|
|
Give the amino acid in this subgroup - Basic
|
: Arg Lys
|
|
Give the amino acid in this subgroup - Sulfur Bonds:
|
Cys Met
|
|
Give the amino acid in this subgroup - O-Bonds:
|
Ser Thr Trp
|
|
Give the amino acid in this subgroup - N-Bonds
|
: Asp Gln
|
|
Give the amino acid in this subgroup - Branched:
|
Leu Iso Val
|
|
Give the amino acid in this subgroup - Bulky (Aromatic):
|
Phe Thr Trp
|
|
Give the amino acid in this subgroup - Smallest
|
: Gly
|
|
Give the amino acid in this subgroup - Responsible for Bends:
|
Pro
|
|
Give the amino acid in this subgroup - Ketogenic
|
: Lys Leu
|
|
Give the amino acid in this subgroup - Glucogenic & Ketogenic:
|
Mr. PITT = Phe Iso Thr Trp
|
|
Give the amino acid in this subgroup - Glucogenic His
|
Arg Glu Asp Gln Asn Tyr Cys Pro Met Val Ala Gly
|
|
Essential Amino Acids
|
Essential Amino Acids --|-- (PVT TIM HALL) --|-- Phe Trp His --|-- Val Iso Arg --|-- Thr Met Leu --|-- Lys --|-- --|-- *****If there is a deficiency in Phe then Tyr becomes essential (like in PKU). If there is a deficiency in Met then Cys becomes essential***** --|--
|
|
If there is a deficiency in Phe (Phenylalanine) what amino acid becomes essential?
|
--|-- --|--
|
|
If there is a deficiency in Met (Methionine) what amino acid becomes essential?
|
If there is a deficiency in Met then Cys becomes essential --|-- *****If there is a deficiency in Phe then Tyr becomes essential (like in PKU). ***** --|-- Essential Amino Acids --|-- (PVT TIM HALL) --|-- Phe Trp His --|-- Val Iso Arg --|-- Thr Met Leu --|-- Lys --|--
|
|
Give a list of the restriction enzymes (in the body)
|
Restriction Enzymes --|-- (Cut to the right unless otherwise specified) --|-- Trypsin…………………………………………….Arg, Lys --|-- Chymotrypsin…………………………….…..Phe, Tyr, Trp --|-- Elastase…………………………………..……Gly, Ser, Ala --|-- Mercaptoethanol…………………………………...Met, Cys --|-- Aminopeptidase……………………………..amino terminal --|-- Carboxypeptidase………………….Left of carboxy terminal --|-- Cyanobromide......……………...……………………….Met
|
|
What do the different restriction enzymes cut?
|
Restriction Enzymes --|-- (Cut to the right unless otherwise specified) --|-- Trypsin…………………………………………….Arg, Lys --|-- Chymotrypsin…………………………….…..Phe, Tyr, Trp --|-- Elastase…………………………………..……Gly, Ser, Ala --|-- Mercaptoethanol…………………………………...Met, Cys --|-- Aminopeptidase……………………………..amino terminal --|-- Carboxypeptidase………………….Left of carboxy terminal --|-- Cyanobromide......……………...……………………….Met
|
|
Restriction Enzymes – what/where does this cut? - (Cut to the right unless otherwise specified) --- Trypsin
|
Arg, Lys
|
|
Restriction Enzymes – what/where does this cut? - (Cut to the right unless otherwise specified) --- Chymotrypsin
|
Phe, Tyr, Trp
|
|
Restriction Enzymes – what/where does this cut? - (Cut to the right unless otherwise specified) --- Elastase
|
Gly, Ser, Ala
|
|
Restriction Enzymes – what/where does this cut? - (Cut to the right unless otherwise specified) --- Mercaptoethanol
|
Met, Cys
|
|
Restriction Enzymes – what/where does this cut? - (Cut to the right unless otherwise specified) --- Aminopeptidase
|
amino terminal
|
|
Restriction Enzymes – what/where does this cut? - (Cut to the right unless otherwise specified) --- Carboxypeptidase
|
Left of carboxy terminal
|
|
Restriction Enzymes – what/where does this cut? - (Cut to the right unless otherwise specified) --- Cyanobromide
|
Met
|
|
Pg7
|
PPclues
|
|
Name the major second messengers (7)
|
2nd Messangers ; -cAMP……………Sympathetic, catabolic, CRH ; -cGMP………..…..Parasympathetic, anabolic ; -IP3/DAG……..…..Smooth muscle contraction by horm./NT ; -…………All hypothalamic hormones (except CRH) ; -Ca:Calmodulin…..Smooth muscle contraction by distention ; -Ca++…………….Gastrin ; -Tyrosine Kinase…Insulin and all growth factors ; -NO…………….…Nitrates, Viagra, ANP and LPS ; -
|
|
What is the main sympathetic second messenger?
|
cAMP……………Sympathetic, catabolic, CRH ; -
|
|
What is the main Parasympathetic second messenger?
|
cGMP………..…..Parasympathetic, anabolic ; -
|
|
What is the main second messenger for .Smooth muscle contraction by hormone./NT?
|
IP3/DAG……..…..Smooth muscle contraction by horm./NT ; -…………All hypothalamic hormones (except CRH) ; -
|
|
What is the main second messenger for .Smooth muscle contraction by distension?
|
Ca:Calmodulin…..Smooth muscle contraction by distention ; -
|
|
What is the main hypothalamic hormone second messenger?
|
IP3/DAG……..…..Smooth muscle contraction by horm./NT ; -…………All hypothalamic hormones (except CRH) ; -
|
|
What is the main Gastrin second messenger?
|
Ca++…………….Gastrin ; -
|
|
What is the main Insulin and all growth factors second messenger?
|
Tyrosine Kinase…Insulin and all growth factors ; -
|
|
What is the main Nitrates, Viagra, ANP and LPS second messenger?
|
NO…………….…Nitrates, Viagra, ANP and LPS ; -
|
|
What is the exception to the rule for the main hypothalamic hormone second messenger?
|
IP3/DAG……..…..Smooth muscle contraction by horm./NT ; -…………All hypothalamic hormones (except CRH) ; -
|
|
SLE (give the Autoimmune Antibodie(s) ; -For this Disease )
|
; - Smith ; - Double stranded DNA ; - Cardiolipin ; -
|
|
Drug Induced SLE - (give the Autoimmune Antibodie(s) ; -For this Disease )
|
; - Histone ; -
|
|
Progressive Systemic Sclerosis (give the Autoimmune Antibodie(s) ; -For this Disease )
|
; - Topoisomerase ; -
|
|
Graves (give the Autoimmune Antibodie(s) ; -For this Disease )
|
; - TSH Receptor ; -
|
|
CREST (give the Autoimmune Antibodie(s) ; -For this Disease )
|
; - Centromere ; -
|
|
Goodpasture’s (give the Autoimmune Antibodie(s) For this Disease )
|
; - Glomerular Basement Membrane ; - (aka. Type IV Collagen) ; -
|
|
Primary Biliary Cirrhosis (give the Autoimmune Antibodie(s) For this Disease )
|
; - Mitochondria ; -
|
|
Alopecia Areata (give the Autoimmune Antibodie(s) For this Disease )
|
; - Hair follicle ; -
|
|
Rheumatoid Arthritis (give the Autoimmune Antibodie(s) For this Disease )
|
; - IgG ; -
|
|
Multiple Sclerosis (give the Autoimmune Antibodie(s) For this Disease )
|
; - Myelin Receptors ; -
|
|
Celiac Sprue (give the Autoimmune Antibodie(s) For this Disease )
|
; - Gliaden/gluten ; -
|
|
Type I Diabetes (give the Autoimmune Antibodie(s) For this Disease )
|
; - Islet cell receptor ; -
|
|
Vitiligo (give the Autoimmune Antibodie(s) For this Disease )
|
; - Melanocyte ; -
|
|
Myathenia Gravis (give the Autoimmune Antibodie(s) For this Disease )
|
; - Acetylcholine receptor ; -
|
|
Mixed Connective Tissue Disease (give the Autoimmune Antibodie(s) For this Disease )
|
; - Ribonuclear protein ; -
|
|
Pernicious anemia (give the Autoimmune Antibodie(s) For this Disease )
|
; - Parietal cell receptor ; - (aka. Intrinsic factor) ; -
|
|
Pemphigus vulgaris (give the Autoimmune Antibodie(s) For this Disease )
|
; - Epidermal anchoring protein receptor ; - (aka. Intercellular junctions of epidermal cells ; -
|
|
Bullous pemphigoid (give the Autoimmune Antibodie(s) For this Disease )
|
; - Epidermal basement membrane protein ; -
|
|
Hashimoto’s (give the Autoimmune Antibodie(s) For this Disease )
|
; - Thyroglobulin ; - Microsomal ; -
|
|
Scleroderma (give the Autoimmune Antibodie(s) For this Disease )
|
; - Smooth Muscle ; - SCL-70 ; -
|
|
Sjogren’s (give the Autoimmune Antibodie(s) For this Disease )
|
; - Rho ; - La ; - SSA ; - SSB ; -
|
|
Wegener’s (give the Autoimmune Antibodie(s) For this Disease )
|
; - Proteinase ; - C-ANCA ; -
|
|
Polyarteritis Nodosa (give the Autoimmune Antibodie(s) For this Disease )
|
; - P-ANCA ; -
|
|
Idiopathic Thrombocytic Purpura (give the Autoimmune Antibodie(s) For this Disease )
|
; - Platelet ; - (aka glycoprotein IIb/IIIa) ; -
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? ; - Smith ; - Double stranded DNA ; - Cardiolipin ; -
|
SLE
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Histone ; -
|
Drug Induced SLE
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Topoisomerase ; -
|
Progressive Systemic Sclerosis
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - TSH Receptor ; -
|
Graves
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Centromere ; -
|
CREST
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Glomerular Basement Membrane ; - (aka. Type IV Collagen) ; -
|
Goodpasture’s
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Mitochondria ; -
|
Primary Biliary Cirrhosis
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Hair follicle ; -
|
Alopecia Areata
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - IgG ; -
|
Rheumatoid Arthritis
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Myelin Receptors ; -
|
Multiple Sclerosis
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Gliaden/gluten ; -
|
Celiac Sprue
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Islet cell receptor ; -
|
Type I Diabetes
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Melanocyte ; -
|
Vitiligo
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Acetylcholine receptor ; -
|
Myathenia Gravis
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Ribonuclear protein ; -
|
Mixed Connective Tissue Disease
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Parietal cell receptor ; - (aka. Intrinsic factor) ; -
|
Pernicious anemia
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Epidermal anchoring protein receptor ; - (aka. Intercellular junctions of epidermal cells ; -
|
Pemphigus vulgaris
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Epidermal basement membrane protein (desmosome); -
|
Bullous pemphigoid
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Thyroglobulin ; - Microsomal ; -
|
Hashimoto’s
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Smooth Muscle ; - SCL-70 ; -
|
Scleroderma
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Rho ; - La ; - SSA ; - SSB ; -
|
Sjogren’s
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Proteinase ; - C-ANCA ; -
|
Wegener’s
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - P-ANCA ; -
|
Polyarteritis Nodosa
|
|
What autoimmune disease is most likely associated with these autoimmune antibodies? - Platelet ; - (aka glycoprotein IIb/IIIa) ; -
|
Idiopathic Thrombocytic Purpura
|
|
What are the cofactors for Pyruvate DH, α-ketogluterate DH & Branched Chain DH (dehydrogenase); -
|
Co-factors for Pyruvate DH, α-ketogluterate DH & Branched Chain DH ; -(TLC For Nanna) ; - TPP……Thiamin (B1) ; - Lipoic Acid………..B4 ; - CoA……..Pantothentic Acid (B5) ; - FAD………….Riboflavin (B2) ; - NAD……...Niacin (B3) ; -[All of these vitamins help MAKE this associated compound (ie, niacin helps make NAD, or B2 helps make FAD2) or are transformed or included in the structure or is analogous to their associated compound-FA]; -
|
|
Give the vitamins associated with these cofactors for Pyruvate DH, α-ketogluterate DH & Branched Chain DH - TPP ; - Lipoic Acid ; - CoA ; - FAD; - NAD ; -
|
Co-factors for Pyruvate DH, α-ketogluterate DH & Branched Chain DH ; -(TLC For Nanna) ; - TPP……Thiamin (B1) ; - Lipoic Acid………..B4 ; - CoA……..Pantothentic Acid (B5) ; - FAD………….Riboflavin (B2) ; - NAD……...Niacin (B3) ; -[All of these vitamins help MAKE this associated compound (ie, niacin helps make NAD, or B2 helps make FAD2) or are transformed or included in the structure or is analogous to their associated compound-FA]; -
|
|
TPP……Thiamin (B1) is in a group of cofactors for which three dehydrogenases? (name the three)
|
Co-factors for Pyruvate DH, α-ketogluterate DH & Branched Chain DH ; -(TLC For Nanna) ; - TPP……Thiamin (B1) ; - Lipoic Acid………..B4 ; - CoA……..Pantothentic Acid (B5) ; - FAD………….Riboflavin (B2) ; - NAD……...Niacin (B3) ; -[All of these vitamins help MAKE this associated compound (ie, niacin helps make NAD, or B2 helps make FAD2) or are transformed or included in the structure or is analogous to their associated compound-FA]; -
|
|
Lipoic Acid………..B4 is in a group of cofactors for which three dehydrogenases? (name the three)
|
Co-factors for Pyruvate DH, α-ketogluterate DH & Branched Chain DH ; -(TLC For Nanna) ; - TPP……Thiamin (B1) ; - Lipoic Acid………..B4 ; - CoA……..Pantothentic Acid (B5) ; - FAD………….Riboflavin (B2) ; - NAD……...Niacin (B3) ; -[All of these vitamins help MAKE this associated compound (ie, niacin helps make NAD, or B2 helps make FAD2) or are transformed or included in the structure or is analogous to their associated compound-FA]; -
|
|
CoA……..Pantothentic Acid (B5) is in a group of cofactors for which three dehydrogenases? (name the three)
|
Co-factors for Pyruvate DH, α-ketogluterate DH & Branched Chain DH ; -(TLC For Nanna) ; - TPP……Thiamin (B1) ; - Lipoic Acid………..B4 ; - CoA……..Pantothentic Acid (B5) ; - FAD………….Riboflavin (B2) ; - NAD……...Niacin (B3) ; -[All of these vitamins help MAKE this associated compound (ie, niacin helps make NAD, or B2 helps make FAD2) or are transformed or included in the structure or is analogous to their associated compound-FA]; -
|
|
FAD………….Riboflavin (B2) ; -is in a group of cofactors for which three dehydrogenases? (name the three)
|
Co-factors for Pyruvate DH, α-ketogluterate DH & Branched Chain DH ; -(TLC For Nanna) ; - TPP……Thiamin (B1) ; - Lipoic Acid………..B4 ; - CoA……..Pantothentic Acid (B5) ; - FAD………….Riboflavin (B2) ; - NAD……...Niacin (B3) ; -[All of these vitamins help MAKE this associated compound (ie, niacin helps make NAD, or B2 helps make FAD2) or are transformed or included in the structure or is analogous to their associated compound-FA]; -
|
|
NAD……...Niacin (B3) is in a group of cofactors for which three dehydrogenases? (name the three)
|
Co-factors for Pyruvate DH, α-ketogluterate DH & Branched Chain DH ; -(TLC For Nanna) ; - TPP……Thiamin (B1) ; - Lipoic Acid………..B4 ; - CoA……..Pantothentic Acid (B5) ; - FAD………….Riboflavin (B2) ; - NAD……...Niacin (B3) ; -[All of these vitamins help MAKE this associated compound (ie, niacin helps make NAD, or B2 helps make FAD2) or are transformed or included in the structure or is analogous to their associated compound-FA]; -
|
|
Diseases with X-linked Recessive Inheritance ; -(10); -
|
Diseases with X-linked Recessive Inheritance ; -(10); -- • Burton’s Agammaglobulinemia ; -- • CGD (NADPH Oxidase deficiency) ; -- • Duchenne’s Muscular Dystrophy ; -- • Color Blindness ; -- • Hemophilia ; -- • G6PD ; -- • Lesch-Nyhan ; -- • Pyruvate DH deficiency ; -- • Fabry’s ; -- • Hunter’s - X linked Dominant :; -• Huntington’s ; -- • Vitamin D resistant Rickets
|
|
What is the mode of inheritance of: Burton’s Agammaglobulinemia
|
Diseases with X-linked Recessive Inheritance ; -(10); -
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|
What is the mode of inheritance of: CGD (NADPH Oxidase deficiency)
|
Diseases with X-linked Recessive Inheritance ; -(10); -
|
|
What is the mode of inheritance of: Duchenne’s Muscular Dystrophy
|
Diseases with X-linked Recessive Inheritance ; -(10); -
|
|
What is the mode of inheritance of: Color Blindness
|
Diseases with X-linked Recessive Inheritance ; -(10); -
|
|
What is the mode of inheritance of: Hemophilia
|
Diseases with X-linked Recessive Inheritance ; -(10); -
|
|
What is the mode of inheritance of: G6PD
|
Diseases with X-linked Recessive Inheritance (10); -
|
|
What is the mode of inheritance of: Lesch-Nyhan
|
Diseases with X-linked Recessive Inheritance (10)
|
|
What is the mode of inheritance of: Pyruvate DH deficiency
|
Diseases with X-linked Recessive Inheritance (10)
|
|
What is the mode of inheritance of: Fabry’s
|
Diseases with X-linked Recessive Inheritance (10)
|
|
What is the mode of inheritance of: Hunter’s
|
Diseases with X-linked Recessive Inheritance (10)
|
|
Name two diseases that can show x linked dominant inheritance
|
X linked Dominant :; -• Huntington’s ; - - • Vitamin D resistant Rickets; -Diseases with X-linked Recessive Inheritance ; -(10); -- • Burton’s Agammaglobulinemia ; -- • CGD (NADPH Oxidase deficiency) ; -- • Duchenne’s Muscular Dystrophy ; -- • Color Blindness ; -- • Hemophilia ; -- • G6PD ; -- • Lesch-Nyhan ; -- • Pyruvate DH deficiency ; -- • Fabry’s ; -- • Hunter’s -
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Nephrotic Patterns of Vasculitis - name the clue to look for in this pathology: Renal Artery Stenosis
|
Clot in front of renal artery
|
|
Nephrotic Patterns of Vasculitis - name the clue to look for in this pathology: Renal Failure
|
Clot off entire renal artery
|
|
Nephrotic Patterns of Vasculitis - name the clue to look for in this pathology: GN
|
Inflamed glomeruli
|
|
Nephrotic Patterns of Vasculitis - name the clue to look for in this pathology: Papillary Necrosis
|
Clot in papilla
|
|
Nephrotic Patterns of Vasculitis - name the clue to look for in this pathology: Interstitial Nephritis
|
Clot of medulla
|
|
Nephrotic Patterns of Vasculitis - name the clue to look for in this pathology: Focal Segmental GN
|
Clot off pieces of nephron
|
|
Nephrotic Patterns of Vasculitis - name the clue to look for in this pathology: Rapidly Progressive GN
|
Clot off lots of nephrons
|
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MC Nephrotic Disease in Adults
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Membranous GN
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MC Renal Dis. in Blacks/Hispanics
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Focal Segmental GN
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MC Renal Disease in HIV/drug users
|
Focal Segmental GN
|
|
MC Renal Mass
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Cyst
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|
MC Malignant Renal tumor in adults
|
adenocarcinoma
|
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MC Malignant Renal tumor in kids
|
Wilm’s tumor
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|
MCC of Rapidly Progressive GN
|
Goodpasture’s
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MC Nephrotic Disease in kids
|
Minimal Change Disease
|
|
What formations do you see in RPGN?
|
crescent formations (rapidly progressive “crescentic” glomerulonephritis)
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|
What is a common etiology association with Minimal Change Disease
|
2 weeks post URI
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A child 2 weeks post URI can have what kind of benign kidney syndrome?
|
Minimal change disease
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|
Give the rescue drugs to use if needed after administering thrombolytic or anticoagulant therapy (their “antidotes”)
|
Thrombolytics and Rescues ; - tPa………………………………..Amioncaproic acid ; - Streptokinase…………………….Aminocaproic acid ; - Warfarin………………………………..…Vitamin K ; - Heparin…………………………….Protamine Sulfate --- If active hemorrhage give Fresh Frozen Plasma (FFP) -
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|
What is the rescue/antidote for this thrombolytic/anticoagulant? tPa
|
Amioncaproic acid
|
|
What is the rescue/antidote for this thrombolytic/anticoagulant? Streptokinase
|
Aminocaproic acid
|
|
What is the rescue/antidote for this thrombolytic/anticoagulant? Warfarin
|
Vitamin K
|
|
What is the rescue/antidote for this thrombolytic/anticoagulant? Heparin
|
Protamine Sulfate - If active hemorrhage give Fresh Frozen Plasma (FFP) ; -
|
|
What is the rescue/antidote for this thrombolytic/anticoagulant? tPa
|
Amioncaproic acid
|
|
Amioncaproic acid is the rescue/antidote for what thrombolytic/anticoagulant drug therapy?
|
tPa
|
|
Aminocaproic acid is the rescue/antidote for what thrombolytic/anticoagulant drug therapy?
|
Streptokinase
|
|
Vitamin K is the rescue/antidote for what thrombolytic/anticoagulant drug therapy?
|
Warfarin
|
|
Protamine Sulfate is the rescue/antidote for what thrombolytic/anticoagulant drug therapy?
|
Heparin - If active hemorrhage give Fresh Frozen Plasma (FFP) ; -
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|
Page 8
|
Ppclues
|
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What are the Rashes Associated with Cancer?
|
Urticaria (hives)………..any, but especially lymphoma ; - Paget’s Disease……………….....intraductal carcinoma ; - Seborrheic keratosis……colon cancer (HIV is sudden ↑) ; - Actinic keratosis……...squamous cell carcinoma of skin ; - Dermatomyositis (heliotropic, malar)...……colon cancer ; - Akanthosis nigricans....visceral CA & end organ damage ; - Erythema nodosum………granulomatous (nonbacterial) ; -
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|
This rash is associated with which cancer or other pathology? Urticaria (hives
|
any, but especially lymphoma
|
|
This rash is associated with which cancer or other pathology? Paget’s Disease
|
intraductal carcinoma
|
|
This rash is associated with which cancer or other pathology? Seborrheic keratosis
|
colon cancer (HIV is sudden ↑)
|
|
This rash is associated with which cancer or other pathology? Actinic keratosis
|
squamous cell carcinoma of skin
|
|
This rash is associated with which cancer or other pathology? Dermatomyositis (heliotropic, malar
|
colon cancer
|
|
This rash is associated with which cancer or other pathology? Akanthosis nigricans
|
visceral CA & end organ damage
|
|
This rash is associated with which cancer or other pathology? Erythema nodosum
|
granulomatous (nonbacterial)
|
|
What is the major factor in cancer grading?
|
Cancer Grading – Severity of microscopic changes - (Cancer Staging – Degree of dissemination of tumor ); -
|
|
What is the major factor in cancer staging? - ; -
|
Cancer Staging – Degree of dissemination of tumor - (Cancer Grading – Severity of microscopic changes ) -
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|
Name which neoplasm is associated with this tumor marker/oncogene -- l-myc
|
Small cell carcinoma of the lung ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
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|
Name which neoplasm is associated with this tumor marker/oncogene -- c-myc
|
Burkitt’s Lymphoma ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which neoplasm is associated with this tumor marker/oncogene -- n-myc
|
Neuroblastoma ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
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|
Name which neoplasm is associated with this tumor marker/oncogene -- c-abl
|
CML, ALL ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
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|
Name which neoplasm is associated with this tumor marker/oncogene -- c-myb
|
Colon, AML ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which neoplasm is associated with this tumor marker/oncogene -- c-sis
|
Osteosarcoma, glioma, fibroscarcoma ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which neoplasm is associated with this tumor marker/oncogene -- ret
|
MEN II, MEN III ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
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|
Name which neoplasm is associated with this tumor marker/oncogene -- k-ras
|
Lung, Colon ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which neoplasm is associated with this tumor marker/oncogene -- bcl-2
|
Follicular lymphoma (can show up in Burkitts – pick follicular ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -first)
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|
Name which neoplasm is associated with this tumor marker/oncogene -- Rb
|
Retinoblastoma ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which neoplasm is associated with this tumor marker/oncogene -- CEA
|
Colon, Pancreas ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which neoplasm is associated with this tumor marker/oncogene -- S-100
|
Melanoma ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which neoplasm is associated with this tumor marker/oncogene -- HER-II, Neu, Erb, ; -BRCA-I & II, p53, CSF-1
|
Breast ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which tumor marker/oncogene is associated with this neoplasm -- Small cell carcinoma of the lung
|
l-myc ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which tumor marker/oncogene is associated with this neoplasm -- Burkitt’s Lymphoma
|
c-myc ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which tumor marker/oncogene is associated with this neoplasm -- Neuroblastoma
|
n-myc ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which tumor marker/oncogene is associated with this neoplasm -- CML, ALL
|
c-abl ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which tumor marker/oncogene is associated with this neoplasm -- Colon, AML
|
c-myb ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which tumor marker/oncogene is associated with this neoplasm -- Osteosarcoma, glioma, fibroscarcoma
|
c-sis ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which tumor marker/oncogene is associated with this neoplasm -- MEN II, MEN III
|
ret ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which tumor marker/oncogene is associated with this neoplasm -- Lung, Colon
|
k-ras ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which tumor marker/oncogene is associated with this neoplasm -- Follicular lymphoma (can show up in Burkitts – pick follicular first)
|
bcl-2 ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which tumor marker/oncogene is associated with this neoplasm -- Retinoblastoma
|
Rb ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease (loss of heterozigosity)
-Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; - |
|
Name which tumor marker/oncogene is associated with this neoplasm -- Colon, Pancreas
|
CEA ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which tumor marker/oncogene is associated with this neoplasm -- Melanoma
|
S-100 ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Name which tumor marker/oncogene is associated with this neoplasm -- Breast
|
HER-II, Neu, Erb, - BRCA-I & II, p53, CSF-1 ; -Tumor Suppressor Gene - Loss of function of tumor suppressor --> cancer; both alleles must be lost for expression of disease.; -Oncogene - Gain of function of onco-gene (“cancer”-gene)--> cancer. Need damage to only I allele.; -Tumor marker - Theses have elevated presence in blood when certain cancers are present in the body Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to confirm diagnosis, to monitor for tumor recurrence, and to monitor response to therapy.; -
|
|
Give the associated disease/translocation: -- 9:22
|
Philadelphia Chromosome (CML)
|
|
Give the associated disease/translocation: -- 8:14
|
Burkitt’s Lymphoma
|
|
Give the associated disease/translocation: -- 14:18
|
Follicular Lymphoma
|
|
Give the associated disease/translocation: -- 15:17
|
Promyeloblastic leukemia (AML)
|
|
Give the associated disease/translocation: -- 11:14
|
Mantle Cell Lymphoma
|
|
Give the associated disease/translocation: -- 11:22
|
Ewing’s Sarcoma
|
|
Give the associated disease/translocation: -- 17:22
|
Neurofibromatosis
|
|
Give the associated disease/translocation: -- 8:14
|
Burkitt’s Lymphoma (follicular is 14:18)
|
|
Give the associated disease/translocation: -- 9:22
|
Philadelphia Chromosome (CML)
|
|
Give the associated disease/translocation: -- 14:18
|
Follicular Lymphoma (Burkitt is 8:14)
|
|
Give the associated disease/translocation: -- Philadelphia Chromosome (CML)
|
9:22
|
|
Give the associated disease/translocation: -- Burkitt’s Lymphoma
|
8:14
|
|
Give the associated disease/translocation: -- Follicular Lymphoma
|
14:18
|
|
Give the associated disease/translocation: -- Promyeloblastic leukemia (AML)
|
15:17
|
|
Give the associated disease/translocation: -- Mantle Cell Lymphoma
|
11:14
|
|
Give the associated disease/translocation: -- Ewing’s Sarcoma
|
11:22
|
|
What are the enzymes needed to make glycogen (4)
|
Enzymes Needed to Make Glycogen ; - Glycogen synthase ; - Branching enzymes ; -o glycogen α-1,4 glycosyl transferase ; -o glycogen α-1,6 glycosyl transferase ; -Enzymes Needed to Break Down Glycogen ; - Phosphorylase ; - Debranching enzyme ; - Α-1,6-Glucosidase ; - Phosphatase ; -
|
|
What are the enzymes needed to break down glycogen (4)
|
Enzymes Needed to Make Glycogen ; - Glycogen synthase ; - Branching enzymes ; -o glycogen α-1,4 glycosyl transferase ; -o glycogen α-1,6 glycosyl transferase ; -Enzymes Needed to Break Down Glycogen ; - Phosphorylase ; - Debranching enzyme ; - Α-1,6-Glucosidase ; - Phosphatase ; -
|
|
What are the different lipoproteins involved in fatty acid metabolism? (give 4-5, their functions and unique characteristics)
|
Lipoprotein Transport
Chylomicrons: takes triglycerides from GI to liver & endothelium ; VLDL: takes triglycerides from liver to adipose ; VLDL: only made in the liver IDL: takes triglycerides from adipose to tissue ; LDL: only one to carry cholesterol ; IDL + LDL: break down products of VLDL; HDL |
|
What is the function of this lipoprotein? Chylomicrons:
|
takes triglycerides from GI to liver & endothelium
|
|
What is the function of this lipoprotein? VLDL:
|
takes triglycerides from liver to adipose
|
|
What is the function of this lipoprotein? IDL:
|
takes triglycerides from adipose to tissue
|
|
Where is this lipoprotein only made? VLDL:
|
only made in the liver
|
|
These lipoproteins are breakdown products of? IDL + LDL:
|
break down products of VLDL
|
|
What are the most common causes of meningitis?
|
Meningitis (MCC) ; -0 months - 2 months……Group B strep ; -……E. coli ; -……Listeria - 2 months - 10 years……S. pneumoniae ; -……Neisseria meningitides - 10 years – 21 years……Neisseria meningitides - Over 21 years…………S. pneumoniae ; -remember – neonate less than 1 month, Infant less than one year old
|
|
What are the most common causes of meningitis in patients 0 months - 2 months?
|
0 months - 2 months……Group B strep ; -……E. coli ; -……Listeria - remember – neonate less than 1 month, Infant less than one year old; -
|
|
What are the most common causes of meningitis in patients 2 months - 10 years?
|
; -2 months - 10 years……S. pneumoniae ; -……Neisseria meningitides ; -
|
|
What are the most common causes of meningitis in patients 10 years – 21 years?
|
10 years – 21 years……Neisseria meningitides ; -
|
|
What are the most common causes of meningitis in patients Over 21 years?
|
Over 21 years…………S. pneumoniae ; -
|
|
What are the indications for Pneumovax? Name at least 3-4
|
Indications for Pneumovax ; - Covers MC 23 strains ; - Given at 2, 4 & 6 months ; - Given to anyone over 65 years old ; - Anyone who is asplenic ; - Anyone with end organ damage (CF, RF, Nephrotic) ; -
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|
Explain important things to note of the CD4 count in an HIV+ patient at 500, 200, and 100 in terms of treatment. What is a normal CD4 count?
|
Normal CD4 count: 800-1200 in adults (up to 1500 in kids) ; - <500: begin treating with 2 nucleotide inhibitors and 1 protease inhibitor (750 in kids) ; - <200: is AIDS, add treatment for PCP ; - <100: add treatment for MAC ; -
|
|
What CD4 count is considered AIDS in an HIV+ patient?
|
Normal CD4 count: 800-1200 in adults (up to 1500 in kids) ; - <500: begin treating with 2 nucleotide inhibitors and 1 protease inhibitor (750 in kids) ; - <200: is AIDS, add treatment for PCP ; - <100: add treatment for MAC
|
|
What is a normal CD4 Count?
|
Normal CD4 count: 800-1200 in adults (up to 1500 in kids) ; - <500: begin treating with 2 nucleotide inhibitors and 1 protease inhibitor (750 in kids) ; - <200: is AIDS, add treatment for PCP ; - <100: add treatment for MAC
|
|
In an HIV+ patient , what is the Most Common Infection
|
CMV
|
|
In an HIV+ patient , what is the Most Common Cause of death
|
PCP
|
|
In an HIV+ patient , what is the purpose of p41
|
just a surface marker
|
|
In an HIV+ patient , what is the purpose of GP120
|
attachment to CD4
|
|
In an HIV+ patient , what is the purpose of Pol
|
transcription
|
|
In an HIV+ patient , what is the purpose of Reverse transcriptase
|
integration
|
|
In an HIV+ patient , what is the purpose of p17 and p24 antigens
|
assembly
|
|
What is the most common cause of infection in HIV+ Patient? The MCC of death ?
|
Most Common Infection.…...…….……………….…..CMV ; -Most Common Cause of death...……………..…………PCP ; -Normal CD4 count: 800-1200 in adults (up to 1500 in kids) ; - <500: begin treating with 2 nucleotide inhibitors and 1 protease inhibitor (750 in kids) ; - <200: is AIDS, add treatment for PCP ; - <100: add treatment for MAC
|
|
Explain the function of the Pol gene, GP120, and p17, p24 antigens in an HIV infection
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p41.……………………………………just a surface marker ; -GP120…..……………………………….attachment to CD4 ; -Pol….……………………….………………….transcription ; -Reverse transcriptase….………...……………….integration ; -p17 and p24 antigens….…………..……………….assembly ; -
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Name some characteristics of autosomal dominant inheritance (8)
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Characteristics of Autosomal Dominant Inheritance ; - Affects males and females equally ; - Manifests in heterozygous state ; - Can be transmitted by either parent ; - Often delayed onset (adult dx) ; - Vertical transmission ; - New mutations occur in germ cells of older fathers ; - Can exhibit reduced penetrance & variable expressivity ; - Usually structural defects ; -(if one parent is has one diseased allele{has the disease}– chances of child having it are 50%, if both parents have one, 75%) ; -
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Name some characteristics of autosomal recessive inheritance (6)
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Characteristics of Autosomal Recessive Inheritance ; - Disease usually does not effect parents ; - Disease may be seen in siblings and uncles ; - Often early onset (early dx) ; - Disease only present when both alleles are mutant ; - Horizontal transmission ; - Usually enzyme defects (Inborn errors of metabolism) -
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The following are all characteristics of what mode of inheritance? Can be transmitted by either parent ; - Often delayed onset (adult dx) ; - Vertical transmission ; -
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Characteristics of Autosomal Dominant Inheritance ; - Affects males and females equally ; - Manifests in heterozygous state ; - Can be transmitted by either parent ; - Often delayed onset (adult dx) ; - Vertical transmission ; - New mutations occur in germ cells of older fathers ; - Can exhibit reduced penetrance & variable expressivity ; - Usually structural defects ; -(if one parent is has one diseased allele{has the disease}– chances of child having it are 50%, if both parents have one, 75%); -+---- ----+ ; -Characteristics of Autosomal Recessive Inheritance ; - Disease usually does not effect parents ; - Disease may be seen in siblings and uncles ; - Often early onset (early dx) ; - Disease only present when both alleles are mutant ; - Horizontal transmission ; - Usually enzyme defects (Inborn errors of metabolism) ; -
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The following are all characteristics of what mode of inheritance? Affects males and females equally ; - New mutations occur in germ cells of older fathers ; - Usually structural defects ; -
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Characteristics of Autosomal Dominant Inheritance ; - Affects males and females equally ; - Manifests in heterozygous state ; - Can be transmitted by either parent ; - Often delayed onset (adult dx) ; - Vertical transmission ; - New mutations occur in germ cells of older fathers ; - Can exhibit reduced penetrance & variable expressivity ; - Usually structural defects
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The following are all characteristics of what mode of inheritance? - Often delayed onset (adult dx) ; - Vertical transmission ; - Can exhibit reduced penetrance & variable expressivity ; -
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Characteristics of Autosomal Dominant Inheritance ; - Affects males and females equally ; - Manifests in heterozygous state ; - Can be transmitted by either parent ; - Often delayed onset (adult dx) ; - Vertical transmission ; - New mutations occur in germ cells of older fathers ; - Can exhibit reduced penetrance & variable expressivity ; - Usually structural defects
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The following are all characteristics of what mode of inheritance?; - Affects males and females equally ; - Manifests in heterozygous state ; - Can be transmitted by either parent ; - New mutations occur in germ cells of older fathers ; - Can exhibit reduced penetrance & variable expressivity ; -
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Characteristics of Autosomal Dominant Inheritance ; - Affects males and females equally ; - Manifests in heterozygous state ; - Can be transmitted by either parent ; - Often delayed onset (adult dx) ; - Vertical transmission ; - New mutations occur in germ cells of older fathers ; - Can exhibit reduced penetrance & variable expressivity ; - Usually structural defects
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The following are all characteristics of what mode of inheritance?; - Affects males and females equally ; - New mutations occur in germ cells of older fathers ; - Can exhibit reduced penetrance & variable expressivity ; - Usually structural defects ; -
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Characteristics of Autosomal Dominant Inheritance ; - Affects males and females equally ; - Manifests in heterozygous state ; - Can be transmitted by either parent ; - Often delayed onset (adult dx) ; - Vertical transmission ; - New mutations occur in germ cells of older fathers ; - Can exhibit reduced penetrance & variable expressivity ; - Usually structural defects
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The following are all characteristics of what mode of inheritance?; - Disease usually does not effect parents ; - Disease may be seen in siblings and uncles ; - Often early onset (early dx) ; -
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Characteristics of Autosomal Recessive Inheritance ; - Disease usually does not effect parents ; - Disease may be seen in siblings and uncles ; - Often early onset (early dx) ; - Disease only present when both alleles are mutant ; - Horizontal transmission ; - Usually enzyme defects (Inborn errors of metabolism) ; -+---- ----+ - Characteristics of Autosomal Dominant Inheritance ; - Affects males and females equally ; - Manifests in heterozygous state ; - Can be transmitted by either parent ; - Often delayed onset (adult dx) ; - Vertical transmission ; - New mutations occur in germ cells of older fathers ; - Can exhibit reduced penetrance & variable expressivity ; - Usually structural defects ; -(if one parent is has one diseased allele{has the disease}– chances of child having it are 50%, if both parents have one, 75%); -
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The following are all characteristics of what mode of inheritance?; - Disease only present when both alleles are mutant ; - Horizontal transmission ; - Usually enzyme defects (Inborn errors of metabolism) ; -
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Characteristics of Autosomal Recessive Inheritance ; - Disease usually does not effect parents ; - Disease may be seen in siblings and uncles ; - Often early onset (early dx) ; - Disease only present when both alleles are mutant ; - Horizontal transmission ; - Usually enzyme defects (Inborn errors of metabolism) ; -
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The following are all characteristics of what mode of inheritance?; - Disease usually does not effect parents ; - Disease may be seen in siblings and uncles ; - Usually enzyme defects (Inborn errors of metabolism) ; -
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Characteristics of Autosomal Recessive Inheritance ; - Disease usually does not effect parents ; - Disease may be seen in siblings and uncles ; - Often early onset (early dx) ; - Disease only present when both alleles are mutant ; - Horizontal transmission ; - Usually enzyme defects (Inborn errors of metabolism) ; -
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The following are all characteristics of what mode of inheritance?; - Disease may be seen in siblings and uncles ; - Horizontal transmission ; - Usually enzyme defects (Inborn errors of metabolism) ; -
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Characteristics of Autosomal Recessive Inheritance ; - Disease usually does not effect parents ; - Disease may be seen in siblings and uncles ; - Often early onset (early dx) ; - Disease only present when both alleles are mutant ; - Horizontal transmission ; - Usually enzyme defects (Inborn errors of metabolism) ; -
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Characteristics of mitochondrial inheritance:
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All females will pass on the disease
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no males will pass on the disease
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all offsprings of affected females will be affected
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often affects CNS, heart and skeletal muscle
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due to uneven cytokinesis during meiosis/oogenesis
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Immune system timeline:
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< 24 hrs -----> swelling
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at 24 hrs -----> neutrophils show up
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day 3 ----->neutrophils peak
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day 4 ----->T-cells and Macrophages show up
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Day 7 -----> Fibroblasts show up
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1 month -----> fibroblasts peak
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3-6 months -----> fibroblasts are gone
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Mitochondrial diseases:
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Leigh's Disease
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subacute necrotizing encephalopmyelopathy,
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progressive decrease in IQ
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seizures
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ataxia
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cytochrome oxidase deficiency
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Leber's Disease
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hereditary optic atrophy
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TX for hypercholesterolemia:
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Statins: PALS
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P-Provostatin (only one renally excreted)
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A-Atorvastatin (lover enzymes every 3 months)
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"L-Lovastatin ("" "")"
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"S-Simvastatin ("" "")"
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MoA:
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Inhibit HMG CoA reductase
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most active around 8pm
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must take at night for maz efficiency
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atrial action potential: Phases-
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Phase 0-depolarization
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phase 1- no name
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phase 2- plateau (A-V Node)
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phase 3- repolarization
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phase 4 automaticity (S-A Node)
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Pneumonia (MCC):
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6 weeks- 18 yrs:
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RSV (infants only)
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mycoplasma
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chlamydia pneumonia
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strep. Pneumonia
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18 yrs- 40 yrs:
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mycoplasma
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chlamydia pneumonia
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strep. Pneumonia
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40yrs- 65 yrs:
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strep. Pneumonia
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H. influenza
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anaerobes
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viruses
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mycoplasma
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elderly:
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strep. Pneumonia
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viruses
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anaerobes
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H. influenza
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Gram negative rods
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Oxalate stones:
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in 3 y.o white female-
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Cystic Fibrosis
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in 5 y.o black female-
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Celiac sprue
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in adult female-
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Whipple's Disease
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in Adult male or female-
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crohn's disease
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Pituitary Hormones:
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Anterior:
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GH- acidophilic
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Prolactine- acidophilic
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TSH- basophilic
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ACTH- basophilic
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LH- basophilic
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FSH- basophilic
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Posterior:
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ADH (supraoptic nucleus)
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Oxytocin (paraventricular nucleus)
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Sub-Acute Bacterial Endocarditis:
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MC bateria is strep veridans
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roth spots
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janeway lessions (toes)
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osler's nodes (fingers)
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splinter hemorrhages
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endocarditis
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mycotic aneurysm (septic emboli)
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Emphysema Types:
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Bullous
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Due to #1 = staph. Aureus
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due to #2= pseudomonas
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centroacinar
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due to smoking
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distalacinar
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due to normal aging
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panacinar
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due to alpha 1 antitrypsin deficiency
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Erythropoiesis:
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4 months gestation
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Yolk sac
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6 months gestation
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spleen, liver, flat bones
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8 months gestation
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long bones
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1 yr of age
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long bones
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* if long bones become damaged the spleen can take over,
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resulting in splenomegaly
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Diphtheria:
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its toxin ADP ribosylated EF 2
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stops cell synthesis
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gram positive
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acquired exotoxin from a virus via transduction
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causes heart block
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never scrap the membrane b/c it is highly vascular so
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it will bleed and it will also release toxin
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Cystic Fibrosis:
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sweat test
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>60 - definitive positive
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<20 - normal
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30-60 - heterozygous
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second messenger is
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IP3/ DAG
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gene is on Chromosome
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Chromosome 7
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treatment
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pilocarpine can be used to treat
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howell- jolly
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sickle cell
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heinz
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G6PD
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zebra
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niemann pick
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donovan
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leishmaniasis
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mallory
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alcoholism
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negri
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rabies
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councilman
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yellow fever
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call-exner
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ovarian tumors
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lewy
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parkinsons
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pick
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pick's disease
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barr bodies
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female
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aschoff
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rheumatic fever
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cowdry type A
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herpes
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Auer rods
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AML
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Globoid
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Krabbe's disease
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Russell
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multiple myeloma
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schiller-duvall
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yolk sac tumor
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basal bodies
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smooth muscle
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Allergic Response-Primary: CONTACT
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neutrophils work in the first 3 days
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then B-cells produce IgM:
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*shows up at 3 days
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*peaks at 14 days
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*gone in 2 months
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IgG:
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*show up at 2 weeks
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*peaks in 2 months
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*gone in 1 year
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Allergic response-secondary: MEMORY
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IgG shows up at day 3 with 5x the concentration
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*highest affinity for antigen
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*peaks in 5 years
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*stays for 10 years
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Amyloidosis-AL
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portion homologous with Ig light chain
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Primary amyloidosis, Multiple myeloma
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Amyloidosis-AA
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Unique N- terminal sequence
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Chronic active disease, Hodgkin's disease
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Amyloidosis-Pre-albumin/transthyretin
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single amino acid, substitution
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hereditary neuropathy, nephropathy, cardiopathy
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amyloidosis-AB
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b2 microglobin
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cerebral artery amyloid, alzheimers, downs
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amyloidosis-AE
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endocrine
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aging
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amyloidosis-AP
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universally associated with all amyloids
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methylene blue
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methemaglobinemia
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sodium thiosulfate
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cyanide
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CaEDTA
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lead (to test)
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penicillamine
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lead (in plasma)
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dimeraprol
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lead (in bone marrow)
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Tx for cyanide poisoning
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amyl nitrate
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sodium thiosulfate
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methylene blue
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transfusion
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Renal tubular Acidosis- type 1
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high urine pH
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acidosis
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freq UTI
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stones
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babies die <1 yr
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Renal tubular Acidosis- type 2
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low urine pH (2)
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hypokalemia
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no carbonic anhydrase
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renal tubular acidosis-type 3
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combo of type 1 and 2
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normal urine pH
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hypokalemia
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renal tubular acidosis-type 4
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diabetics
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hyperkalemia
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no aldosterone (infarcted JG apparatus)
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hemolytic properties of streptococcus
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alpha-partial hemolysis with green zone
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beta- complete hemolysis with clear zone
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Gamma- no hemolysis with red zone
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transduction
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bacteria becomes deadly when a virus injects its DNA
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transformation
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in a hospital or nursing home the bacteria has become deadly by this mechanism
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conjugation
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only occurs if bacteria has PILI
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Coumadin
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Extrinsic
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tissue
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PT
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Factors 2,7,9,10
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p.o
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8-10 hrs delay
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C/I in preg
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inhib vit k dependant factors
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heparin
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intrinsic
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blood
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PTT
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factor 3
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i.v
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immediate
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ok to preg.
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DOC for DVT
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What disease is this HLA Marker associated with: DR-2
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Narcolepsy, Allergy, Goodpasture, MS --- Mnemonic - 2 Itchy Sheep (Mary and Sarah), Sleep in a Goodpasture
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What disease is this HLA Marker associated with: DR-3
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Sjogren’s, SLE, Celiac Sprue, Chronic Active Hepatitis --- Mnemonic - 3 S’s and Chronic Active Hepatitis
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What disease is this HLA Marker associated with: DR-3 & 4
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IDDM Type I - Insulin-Dependent Diabetes Mellitus
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What disease is this HLA Marker associated with: DR-4
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Rheumatoid Arthritis, Pemphigus vulgaris --- Mnemonic - RAP
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What disease is this HLA Marker associated with: DR-5
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Juvenille Rheumatoid Arthritis, Pernicious Anemia --- Mnemonic - JRAP
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What disease is this HLA Marker associated with: DR-7
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Steroid Induced Nephrotic Syndrome
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Celiac Disease
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What disease is this HLA Marker associated with: A-3
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Hemochromotosis
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What disease is this HLA Marker associated with: B-8
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Myathenia Gravis
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What disease is this HLA Marker associated with: B-13
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Psoriasis w/o arthritis
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What disease is this HLA Marker associated with: B-27
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Psoriasis w/ arthritis, Ankylosing Spondylitis, IBD, Reiter’s, Postgonococcal arthritis --- Mnemonic - 2PAIR
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What disease is this HLA Marker associated with: BW-47
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21-α-Hydroxylase deficiency (Vitamin D)
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What HLA marker are these diseases associated with ? -- Narcolepsy, Allergy, Goodpasture, MS
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DR-2 --- Mnemonic - 2 Itchy Sheep (Mary and Sarah), Sleep in a Goodpasture
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What HLA marker are these diseases associated with ? -- Sjogren’s, SLE, Celiac Sprue, Chronic Active Hepatitis -
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DR-3 -- Mnemonic - 3 S’s and Chronic Active Hepatitis
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What HLA marker are these diseases associated with ? -- IDDM Type I (Insulin-Dependent Diabetes Mellitus)
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DR-3 & 4
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What HLA marker are these diseases associated with ? -- Rheumatoid Arthritis, Pemphigus vulgaris
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DR-4 --- Mnemonic - RAP
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What HLA marker are these diseases associated with ? -- Juvenille Rheumatoid Arthritis, Pernicious Anemia -
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DR-5 -- Mnemonic - JRAP
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What HLA marker are these diseases associated with ? -- Steroid Induced Nephrotic Syndrome
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DR-7
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What HLA marker are these diseases associated with ? -- Celiac Disease
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DR-3 & B-8
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What HLA marker are these diseases associated with ? -- Hemochromotosis
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A-3
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What HLA marker are these diseases associated with ? -- Myasthenia Gravis
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B-8
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What HLA marker are these diseases associated with ? -- Psoriasis w/o arthritis
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B-13
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What HLA marker are these diseases associated with ? -- Psoriasis w/ arthritis, Ankylosing Spondylitis, IBD, Reiter’s, Postgonococcal arthritis
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B-27 --- Mnemonic - 2PAIR
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What HLA marker are these diseases associated with ? -- 21-α-Hydroxylase deficiency (Vitamin D)
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BW-47
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; -Give some important characteristics about this immunoglobulin -- : IgA (3)
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; - Monomer in the blood ; - Dimer in secretions ; - Protects the mucoscal surfaces and body secretions ; -
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Give some important characteristics about this immunoglobulin -- : IgD
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; - Only known function is as a surface marker on mature B-cells ; -
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Give some important characteristics about this immunoglobulin -- : IgE (5)
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; - Mediator of Type I hypersensitivity (anaphylaxis) ; - Parasite defense ; - Responsible for allergies ; - Fc portion binds to mast cells and basophils ; - Does not fix complement ; -
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Give some important characteristics about this immunoglobulin -- : IgG (7)
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; - Second to be produced during the primary immune response ; - Only one to be produced during the secondary immune response ; - In memory (secondary) response ; -o Shows up a 3 days with 5x the concentration of primary response ; -o Peaks around 5 years ; -o Some remain in circulation for 10 years ; - Has 4 subclasses (antigenic differences in heavy chains and with disulfide bonds) ; -o IgG1 – crosses the placenta due to Fc portion ; -o IgG2 – most common deficiency, susceptible to encapsulated organisms ; -o IgG3 – Most memory antibodies ; -o IgG4 – Only one that does not fix complement ; -
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Give some important characteristics about this immunoglobulin -- : IgM (3)
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; - Present only in the primary immune response ; - Most effective in agglutination and complement fixation ; - Defense against bacteria and viruses ; -
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These Characteristics go with what immuno globulin?; - Monomer in the blood ; - Dimer in secretions ; - Protects the mucoscal surfaces and body secretions ; -
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; -IgA
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These Characteristics go with what immuno globulin? - Only known function is as a surface marker on mature B-cells ; -
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IgD
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These Characteristics go with what immuno globulin? - Mediator of Type I hypersensitivity (anaphylaxis) ; - Parasite defense ; - Responsible for allergies ; - Fc portion binds to mast cells and basophils ; - Does not fix complement ; -
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IgE
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These Characteristics go with what immuno globulin? - Second to be produced during the primary immune response ; - Only one to be produced during the secondary immune response ; - In memory (secondary) response ; -o Shows up a 3 days with 5x the concentration of primary response ; -o Peaks around 5 years ; -o Some remain in circulation for 10 years ; - Has 4 subclasses (antigenic differences in heavy chains and with disulfide bonds) ; -
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IgG o - IgG1 – crosses the placenta due to Fc portion ; -o IgG2 – most common deficiency, susceptible to encapsulated organisms ; -o IgG3 – Most memory antibodies ; -o IgG4 – Only one that does not fix complement ; -
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These Characteristics go with what immuno globulin? - Present only in the primary immune response ; - Most effective in agglutination and complement fixation ; - Defense against bacteria and viruses ; -
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IgM
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How many hyperlipidemias are there?
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5 different types ; -I - Lipoprotein Lipase – defect of the liver type only - Chylomicrons - ; -II - Receptor or receptor enzyme – IIa, IIb, or B100 - LDL - Most common in general population ; -III - APO E receptor - IDL - ; -IV - Lipoprotein Lipase – defect of the adipose type only - VLDL - ; -V - Enzyme and receptor defect – APO CII - Chylomicrons & VLDL - Associated with diabetes melitis; -
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What is the deficiency found in hyperlipidemia type I
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Lipoprotein Lipase – defect of the liver type only
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What is the deficiency found in hyperlipidemia type II
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Receptor or receptor enzyme – IIa, IIb, or B100
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What is the deficiency found in hyperlipidemia type III
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APO E receptor
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What is the deficiency found in hyperlipidemia type IV
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Lipoprotein Lipase – defect of the adipose type only
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What is the deficiency found in hyperlipidemia type V
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Enzyme and receptor defect – APO CII
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What is the lipid component involved in hyperlipidemia type I
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Chylomicrons Lipoprotein Lipase – defect of the liver type only
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What is the lipid component involved in hyperlipidemia type II
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LDL Receptor or receptor enzyme – IIa, IIb, or B100
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What is the lipid component involved in hyperlipidemia type III
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IDL APO E receptor
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What is the lipid component involved in hyperlipidemia type IV
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VLDL Lipoprotein Lipase – defect of the adipose type only
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What is the lipid component involved in hyperlipidemia type V
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Chylomicrons & VLDL Enzyme and receptor defect – APO CII
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Which hyperlipidemia is Most common in general population
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Type II - Receptor or receptor enzyme – IIa, IIb, or B100 - LDL - Most common in general population
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Which hyperlipidemia is Associated with diabetes melitis
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Type V - Enzyme and receptor defect – APO CII - Chylomicrons & VLDL - Associated with diabetes melitis
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Name important associations with this cytokine (role, cell that produces it etc... ) IL-1
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; - Secreted by macrophages ; - Causes fever and other non-specific symptoms of illness ; - Recruits Thelper cells ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) IL-2 ---- **IL = Interleukin** **IF = Interferon** **TNF = Tumor Necrosis Factor** **Transforming Growth Factor**
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; - Secreted by T cells ; - Most potent ; - Most powerful Chemotactic factor (recruits everyone) ; - Must be inactivated prior to transplantation ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) IL-3
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; - Secreted by T cells ; - Causes B cell proliferation ; - Labeled by Thymidine ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) IL-4
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; - Secreted by T cells ; - Causes B cell differentiation ; - Responsible for class switching to IgG and IgE ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) IL-5 ---- **IL = Interleukin** **IF = Interferon** **TNF = Tumor Necrosis Factor** **Transforming Growth Factor**
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; - Secreted by T cells ; - Responsible for class switching to IgA ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) IL-8
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; - Neutrophil Chemotactic factor ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) IL-10
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; - Suppresses cell mediated response ; - Tells macrophages and T-cells to stay away if there is a bacterial infection ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) IL-12
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; - Promotes cell mediated response ; - If infection in non-bacterial it is released to recruit macrophages and T cells ; - Activates NK cells to secrete IF-γ ; - Inhibits IL-4 induced IgE secretions ; - Changes TH cells into TH1 cells ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) IF-α
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; - Secreted by Leukocytes ; - Inhibits viral replication and tumor growth ; - Increases NK activity ; - Increases MHC (class I and II) expression ; - Interferes with protein synthesis ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) IF-β ---- **IL = Interleukin** **IF = Interferon** **TNF = Tumor Necrosis Factor** **Transforming Growth Factor**
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; - Secreted by fibroblast ; - Inhibits viral replication and tumor growth ; - Increases NK activity ; - Increases MHC (class I and II) expression ; - Interferes with protein synthesis ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) IF-γ
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; - Secreted by T-cells and NK cells ; - Increases NK activity ; - Increases MHC (class I and II) activity ; - Increases macrophage activity ; - Co-stimulates B-cell growth and differentiation ; - Decreases IgE secretion ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) Name important associations with this cytokine (role, cell that produces it etc... ) TNF-α ---- **IL = Interleukin** **IF = Interferon** **TNF = Tumor Necrosis Factor** **Transforming Growth Factor**
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; - 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 IF-γ ; - Cytotoxic/Cytostatic ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) TNF-β
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; - aka Lymphotoxin ; - Secreted by T-cells ; - Cytotoxic ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) TGF-α
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; - Secreted by solid tumors (carcinoma<sarcoma) and monocytes ; - Induces angiogenesis, keratinocyte proliferation, bone resporption and tumor growth ; -
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Name important associations with this cytokine (role, cell that produces it etc... ) TGF-β ---- **IL = Interleukin** **IF = Interferon** **TNF = Tumor Necrosis Factor** **Transforming Growth Factor**
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; - Secreted by platelets, placenta, kidney, bone, T-cells 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 ; -
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What cytokine do these characteristics most likely match? ; - Secreted by macrophages ; - Causes fever and other non-specific symptoms of illness ; - Recruits Thelper cells ; -
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IL-1
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What cytokine do these characteristics most likely match? - Secreted by T cells ; - Most potent ; - Most powerful Chemotactic factor (recruits everyone) ; - Must be inactivated prior to transplantation ; -
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IL-2
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What cytokine do these characteristics most likely match? - Secreted by T cells ; - Causes B cell proliferation ; - Labeled by Thymidine ; -
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IL-3 ---- **IL = Interleukin** **IF = Interferon** **TNF = Tumor Necrosis Factor** **Transforming Growth Factor**
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What cytokine do these characteristics most likely match? - Secreted by T cells ; - Causes B cell differentiation ; - Responsible for class switching to IgG and IgE ; -
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IL-4
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What cytokine do these characteristics most likely match? - Secreted by T cells ; - Responsible for class switching to IgA ; -
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IL-5
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What cytokine do these characteristics most likely match? - Neutrophil Chemotactic factor ; -
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IL-8
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What cytokine do these characteristics most likely match? - Suppresses cell mediated response ; - Tells macrophages and T-cells to stay away if there is a bacterial infection ; -
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IL-10 ---- **IL = Interleukin** **IF = Interferon** **TNF = Tumor Necrosis Factor** **Transforming Growth Factor**
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What cytokine do these characteristics most likely match? - Promotes cell mediated response ; - If infection in non-bacterial it is released to recruit macrophages and T cells ; - Activates NK cells to secrete IF-γ ; - Inhibits IL-4 induced IgE secretions ; - Changes TH cells into TH1 cells ; -
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IL-12
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What cytokine do these characteristics most likely match? - Secreted by Leukocytes ; - Inhibits viral replication and tumor growth ; - Increases NK activity ; - Increases MHC (class I and II) expression ; - Interferes with protein synthesis ; -
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IF-α ---- **IL = Interleukin** **IF = Interferon** **TNF = Tumor Necrosis Factor** **Transforming Growth Factor**
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What cytokine do these characteristics most likely match? - Secreted by fibroblast ; - Inhibits viral replication and tumor growth ; - Increases NK activity ; - Increases MHC (class I and II) expression ; - Interferes with protein synthesis ; -
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IF-β
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What cytokine do these characteristics most likely match? - Secreted by T-cells and NK cells ; - Increases NK activity ; - Increases MHC (class I and II) activity ; - Increases macrophage activity ; - Co-stimulates B-cell growth and differentiation ; - Decreases IgE secretion ; -
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IF-γ ---- **IL = Interleukin** **IF = Interferon** **TNF = Tumor Necrosis Factor** **Transforming Growth Factor**
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What cytokine do these characteristics most likely match? - 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 IF-γ ; - Cytotoxic/Cytostatic ; -
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TNF-α
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What cytokine do these characteristics most likely match? - aka Lymphotoxin ; - Secreted by T-cells ; - Cytotoxic ; -
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TNF-β ---- **IL = Interleukin** **IF = Interferon** **TNF = Tumor Necrosis Factor** **Transforming Growth Factor**
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|
What cytokine do these characteristics most likely match? - Secreted by solid tumors (carcinoma<sarcoma) and monocytes ; - Induces angiogenesis, keratinocyte proliferation, bone resporption and tumor growth ; -
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TGF-α
|
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What cytokine do these characteristics most likely match? - Secreted by platelets, placenta, kidney, bone, T-cells 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 ; -
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TGF-β ---- **IL = Interleukin** **IF = Interferon** **TNF = Tumor Necrosis Factor** **Transforming Growth Factor** ; -
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Give the different parts of the EKG and the corresponding portion of the heart and phase in the action potential
|
P-wave - Atrium - 0 ; -P-R interval - AV node - 2 ; -Q-wave - Septum - 2 ; -R-upstroke - Anterior wall - 2 ; -S-downstroke - Posterior wall - 2 ; -S-T interval - Ventricle - 2 ; -T-wave - Ventricle - 3 ; -U-wave - Ventricle - 4
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What portion of the heart does this part of the ECG /EKG represent? P-wave
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Atrium 0
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What portion of the heart does this part of the ECG /EKG represent? P-R interval
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AV node 2
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What portion of the heart does this part of the ECG /EKG represent? Q-wave
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Septum 2
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What portion of the heart does this part of the ECG /EKG represent? R-upstroke
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Anterior wall 2
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What portion of the heart does this part of the ECG /EKG represent? S-downstroke
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Posterior wall 2
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What portion of the heart does this part of the ECG /EKG represent? S-T interval
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Ventricle 2
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What portion of the heart does this part of the ECG /EKG represent? T-wave
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Ventricle 3
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What portion of the heart does this part of the ECG /EKG represent? U-wave
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Ventricle 4
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What is the general function of this type of adhesion molecule -- IgCAM
|
These are binding proteins - - ICAM-1, ICAL-2, ICAM-3 - ; -• Homing of lymph nodes to site of inflammation ; -• Found on T-cells, endothelial cells, dendritic cells - ; -LFA-3 - ; -• Mediate T-cell interactions ; -• Found on lymphocytes, APC - ; -LFA-2 (CD2) - ; -• Found on T-cells, NK cells -
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What is the general function of this type of adhesion molecule -- Integrins
|
These stop the leukocytes ... ; -VLA-1 (β1) - ; -• Migration thru extracellular matrix ; -• Widely distributed - ; -LFA-1 (β2) - ; -• Tight binding to endothelium ; -• Found on lymphocytes - ; -CR3 (β2) - ; -• Tight binding to epithelium ; -• Phagocytosis ; -• Mac-1 ; -• CD11/CD18 - ; -CR4 (β2) - ; -• Phagocytosis ; -• Opsonin receptor -
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What is the general function of this type of adhesion molecule -- Selectins
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BIND CARBOHYDRATES ; -MEDIATES “ROLLING” (slows leukocytes) - E-selectins - ; -• Leukocyte migration and homing ; -• Found on activated endothelium - ; -L-selectins - ; -• Initial binding to endothelium ; -• Found on leukocytes - ; -P-selectins - ; -• Leukocyte migration to inflammatory sites ; -• Found on activated endothelium and platelets -
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Describe theses adhesion molecules, what do they specifically do, and/or where are they found, what is important to know about them? ICAM-1, ICAL-2, ICAM-3 - ; -
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ICAM-1, ICAL-2, ICAM-3 - ; -• Homing of lymph nodes to site of inflammation ; -• Found on T-cells, endothelial cells, dendritic cells - Major Group – IgCAM’s – Binding proteins [ICAM-1, ICAL-2, ICAM-3, LFA-3, LFA-2 (CD2)]; -
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Describe theses adhesion molecules by giving the major group they belong to and the function of that group. ICAM-1, ICAL-2, ICAM-3 - ; -
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Major Group – IgCAM’s – Binding proteins [ICAM-1, ICAL-2, ICAM-3, LFA-3, LFA-2 (CD2)] - ; -ICAM-1, ICAL-2, ICAM-3 - ; -• Homing of lymph nodes to site of inflammation ; -• Found on T-cells, endothelial cells, dendritic cells ; -
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Describe theses adhesion molecules by giving the major group they belong to and the function of that group. LFA-3 - ; -
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Major Group – IgCAM’s – Binding proteins [ICAM-1, ICAL-2, ICAM-3, LFA-3, LFA-2 (CD2)] - LFA-3 - ; -• Mediate T-cell interactions ; -• Found on lymphocytes, APC ; -
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Describe theses adhesion molecules, what do they specifically do, and/or where are they found, what is important to know about them? LFA-3 - ; -
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LFA-3 - ; -• Mediate T-cell interactions ; -• Found on lymphocytes, APC - Major Group – IgCAM’s – Binding proteins [ICAM-1, ICAL-2, ICAM-3, LFA-3, LFA-2 (CD2)] - ; -
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Describe theses adhesion molecules by giving the major group they belong to and the function of that group. LFA-2 (CD2) -
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Major Group – IgCAM’s – Binding proteins ; -[ICAM-1, ICAL-2, ICAM-3, LFA-3, LFA-2 (CD2)] - ; -LFA-2 (CD2) - ; -- • Found on T-cells, NK cells
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Describe theses adhesion molecules, what do they specifically do, and/or where are they found, what is important to know about them? LFA-2 (CD2) -
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LFA-2 (CD2) - ; -• Found on T-cells, NK cells ; -Major Group – IgCAM’s – Binding proteins; -[ICAM-1, ICAL-2, ICAM-3, LFA-3, LFA-2 (CD2)]; -
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Describe theses adhesion molecules by giving the major group they belong to and the function of that group. VLA-1 (β1) - ; -
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Major Group: Integrins – Role: Stop the leukocytes [Examples - VLA-1 (β1), LFA-1 (β2), CR3 (β2), CR4 (β2)] - VLA-1 (β1) - ; -• Migration thru extracellular matrix ; -• Widely distributed - ; -
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Describe theses adhesion molecules, what do they specifically do, and/or where are they found, what is important to know about them? VLA-1 (β1) - ; -
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; -VLA-1 (β1) - ; -• Migration thru extracellular matrix ; -• Widely distributed - - Major Group: Integrins – Role: Stop the leukocytes [Examples - VLA-1 (β1), LFA-1 (β2), CR3 (β2), CR4 (β2)]
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Describe theses adhesion molecules by giving the major group they belong to and the function of that group. LFA-1 (β2)
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Major Group: Integrins – Role: Stop the leukocytes [Examples - VLA-1 (β1), LFA-1 (β2), CR3 (β2), CR4 (β2)] - LFA-1 (β2) - ; -• Tight binding to endothelium ; -• Found on lymphocytes - ; -
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Describe theses adhesion molecules, what do they specifically do, and/or where are they found, what is important to know about them? LFA-1 (β2)
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- LFA-1 (β2) - ; -• Tight binding to endothelium ; -• Found on lymphocytes - ; -Major Group: Integrins – Role: Stop the leukocytes [Examples - VLA-1 (β1), LFA-1 (β2), CR3 (β2), CR4 (β2)]
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Describe theses adhesion molecules by giving the major group they belong to and the function of that group. CR3 (β2)
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Major Group: Integrins – Role: Stop the leukocytes [Examples - VLA-1 (β1), LFA-1 (β2), CR3 (β2), CR4 (β2)] - CR3 (β2) - ; -• Tight binding to epithelium ; -• Phagocytosis ; -• Mac-1 ; -• CD11/CD18 - ; -
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Describe theses adhesion molecules, what do they specifically do, and/or where are they found, what is important to know about them? CR3 (β2)
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; -CR3 (β2) - ; -• Tight binding to epithelium ; -• Phagocytosis ; -• Mac-1 ; -• CD11/CD18 - - ; -Major Group: Integrins – Role: Stop the leukocytes [Examples - VLA-1 (β1), LFA-1 (β2), CR3 (β2), CR4 (β2)]
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|
Describe theses adhesion molecules by giving the major group they belong to and the function of that group. CR4 (β2)
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Major Group: Integrins – Role: Stop the leukocytes [Examples - VLA-1 (β1), LFA-1 (β2), CR3 (β2), CR4 (β2)] - CR4 (β2) - ; -• Phagocytosis ; -• Opsonin receptor - -
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Describe theses adhesion molecules, what do they specifically do, and/or where are they found, what is important to know about them? CR4 (β2)
|
; -CR4 (β2) - ; -• Phagocytosis ; -• Opsonin receptor - - Major Group: Integrins – Role: Stop the leukocytes [Examples - VLA-1 (β1), LFA-1 (β2), CR3 (β2), CR4 (β2)]
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Describe theses adhesion molecules by giving the major group they belong to and the function of that group. E-selectins
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Major Group : Selectins --- BIND CARBOHYDRATES ; -MEDIATES “ROLLING” (slows leukocytes) --- [Examples, E-selectins, L-selectins, P-selectins] - E-selectins - ; -• Leukocyte migration and homing ; -• Found on activated endothelium - -
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Describe theses adhesion molecules, what do they specifically do, and/or where are they found, what is important to know about them? E-selectins
|
- E-selectins - ; -• Leukocyte migration and homing ; -• Found on activated endothelium - - ; -Major Group : Selectins --- BIND CARBOHYDRATES ; -MEDIATES “ROLLING” (slows leukocytes) --- [Examples, E-selectins, L-selectins, P-selectins]; -
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Describe theses adhesion molecules by giving the major group they belong to and the function of that group. L-selectins
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Major Group : Selectins --- BIND CARBOHYDRATES ; -MEDIATES “ROLLING” (slows leukocytes) --- [Examples, E-selectins, L-selectins, P-selectins] - ; -L-selectins - ; -• Initial binding to endothelium ; -• Found on leukocytes - ; -
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Describe theses adhesion molecules, what do they specifically do, and/or where are they found, what is important to know about them? L-selectins
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; -L-selectins - ; -• Initial binding to endothelium ; -• Found on leukocytes - - - Major Group : Selectins --- BIND CARBOHYDRATES ; -MEDIATES “ROLLING” (slows leukocytes) --- [Examples, E-selectins, L-selectins, P-selectins]; -
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|
Describe theses adhesion molecules by giving the major group they belong to and the function of that group. P-selectins - ; -
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Major Group : Selectins --- BIND CARBOHYDRATES ; -MEDIATES “ROLLING” (slows leukocytes) --- [Examples, E-selectins, L-selectins, P-selectins] - P-selectins - ; -• Leukocyte migration to inflammatory sites ; -• Found on activated endothelium and platelets - -
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Describe theses adhesion molecules, what do they specifically do, and/or where are they found, what is important to know about them? P-selectins - ; -
|
- P-selectins - ; -• Leukocyte migration to inflammatory sites ; -• Found on activated endothelium and platelets - - ; -Major Group : Selectins --- BIND CARBOHYDRATES ; -MEDIATES “ROLLING” (slows leukocytes) --- [Examples, E-selectins, L-selectins, P-selectins]; -
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Describe the different hypersensitivities and the mnemonic for them.
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(ACID) ; -Type I - Anaphylaxis ; -• IgE binds to mast cells – degranulates mast cells ; -• IgA activates IP3 cascade – degrades mast cells - Type II - Cytotoxic (humoral) – Goodpasture, Autoimmune hemolytic anemia ; -Type III - Immune Complex mediated – Rheumatoid arthritis, SLE ; -Type IV - Delayed (cell mediated) – TB skin test, contact dermatitis, transplant rejection - A- Anaphylaxis (type 1) --- C – Cytotoxic (type 2) --- I-Immune Complex (Type 3) ---- D-Delayed (cellmediated, type 4)
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Describe type 1 Hypersensitivity (give the general name or term in the Mnemonic ACID, and describe the area of the immune system related, and any major diseases associated)
|
Type I - Anaphylaxis ; -• IgE binds to mast cells – degranulates mast cells ; -• IgA activates IP3 cascade – degrades mast cells; -A- Anaphylaxis (type 1) --- C – Cytotoxic (type 2) --- I-Immune Complex (Type 3) ---- D-Delayed (cellmediated, type 4)
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Describe type 2 Hypersensitivity (give the general name or term in the Mnemonic ACID
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Type II - Cytotoxic (humoral) – Goodpasture, Autoimmune hemolytic anemia - A- Anaphylaxis (type 1) --- C – Cytotoxic (type 2) --- I-Immune Complex (Type 3) ---- D-Delayed (cellmediated, type 4)
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Describe type 3 Hypersensitivity (give the general name or term in the Mnemonic ACID
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Type III - Immune Complex mediated – Rheumatoid arthritis, SLE; -A- Anaphylaxis (type 1) --- C – Cytotoxic (type 2) --- I-Immune Complex (Type 3) ---- D-Delayed (cellmediated, type 4)
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Describe type 4 Hypersensitivity (give the general name or term in the Mnemonic ACID
|
type IV - Delayed (cell mediated) – TB skin test, contact dermatitis, transplant rejection ; -A- Anaphylaxis (type 1) --- C – Cytotoxic (type 2) --- I-Immune Complex (Type 3) ---- D-Delayed (cellmediated, type 4)
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Goodpasture, Autoimmune hemolytic anemia are associated with what kind of hypersensitivity?
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Type II - Cytotoxic (humoral) – Goodpasture, Autoimmune hemolytic anemia - A- Anaphylaxis (type 1) --- C – Cytotoxic (type 2) --- I-Immune Complex (Type 3) ---- D-Delayed (cellmediated, type 4)
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|
Rheumatoid arthritis, SLE ; -are associated with what kind of hypersensitivity?
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Type III - Immune Complex mediated – Rheumatoid arthritis, SLE; -A- Anaphylaxis (type 1) --- C – Cytotoxic (type 2) --- I-Immune Complex (Type 3) ---- D-Delayed (cellmediated, type 4)
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TB skin test, contact dermatitis, transplant rejection are associated with what kind of hypersensitivity?
|
type IV - Delayed (cell mediated) – TB skin test, contact dermatitis, transplant rejection ; -A- Anaphylaxis (type 1) --- C – Cytotoxic (type 2) --- I-Immune Complex (Type 3) ---- D-Delayed (cellmediated, type 4)
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Anaphylaxis is associated with what kind of hypersensitivity?
|
Type I - Anaphylaxis ; -• IgE binds to mast cells – degranulates mast cells ; -• IgA activates IP3 cascade – degrades mast cells; -A- Anaphylaxis (type 1) --- C – Cytotoxic (type 2) --- I-Immune Complex (Type 3) ---- D-Delayed (cellmediated, type 4)
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IgE and IgA are associated with what kind of hypersensitivity?
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Type I - Anaphylaxis ; -• IgE binds to mast cells – degranulates mast cells ; -• IgA activates IP3 cascade – degrades mast cells; -A- Anaphylaxis (type 1) --- C – Cytotoxic (type 2) --- I-Immune Complex (Type 3) ---- D-Delayed (cellmediated, type 4)
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Give the mechanism of this drug and/or drug class -- ; -5FU
|
Inhibits thymidylate
|
|
Give the mechanism of this drug and/or drug class -- ; -Methotrexate
|
Inhibits dihydrofolate reductase
|
|
Give the mechanism of this drug and/or drug class -- ; -Hydroxyurea
|
Inhibits ribonucleotide reductase
|
|
Give the mechanism of this drug and/or drug class -- ; -Vincristine/Vinblastin
|
Inhibit microtubule formation
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|
Give the mechanism of this drug and/or drug class -- ; -Paclitaxel
|
Inhibits microtubules from migrating
|
|
Give the mechanism of this drug and/or drug class -- ; -Levamisole
|
Stimulates Natural Killer (NK) cells
|
|
Give the mechanism of this drug and/or drug class -- ; -Steroids
|
; -1. Kills T-cell and Eosinophils ; -2. Inhibits macrophage migration ; -3. Inhibits phospholipase A ; -4. Inhibits mast cell degranulation ; -5. Stabilizes endothelium ; -
|
|
Give the mechanism of this drug and/or drug class -- ; -Statins
|
Inhibit HMG CoA reductase
|
|
Give the mechanism of this drug and/or drug class -- ; -Niacin
|
Decreases VLDL production in the liver
|
|
Give the mechanism of this drug and/or drug class -- ; -Sulfonylureas
|
1st generation - Block potassium channels in the islet cells increasing insulin release ;
2nd generation – Promote insulin release and inhibit gluconeogenesis in the liver |
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Give the mechanism of this drug and/or drug class -- ; -Miglitol/Ascarbose
|
Inhibit glucose absorption from the GI
|
|
Give the mechanism of this drug and/or drug class -- ; -Metformin
|
Stops gluconeogenesis in the liver
|
|
Give the mechanism of this drug and/or drug class -- ; -Troglitazone
|
Increases the sensitivity of insulin receptors
|
|
Give the mechanism of this drug and/or drug class -- ; -Anti-psychotics
|
Block dopamine receptors
|
|
Give the mechanism of this drug and/or drug class -- ; -Aspirin
|
Irreversible inhibitor of cyclo-oxygenase
|
|
Give the mechanism of this drug and/or drug class -- ; -K+ Sparing Diuretics
|
Competitive aldosterone receptor antagonist
|
|
Give the mechanism of this drug and/or drug class -- ; -Topical Anesthetics
|
Block Na+ channels
|
|
Give the mechanism of this drug and/or drug class -- ; -Quinalones
|
Block topoisomerase (supercoils)
|
|
Give the mechanism of this drug and/or drug class -- ; -Aminoglycosides
|
Blocks Initiation Factor (IF) 2 on the 30S subunit
|
|
Give the mechanism of this drug and/or drug class -- ; -Tetracyclines
|
Blocks tRNA binding on the 30S subunit
|
|
Give the mechanism of this drug and/or drug class -- ; -Rifampin
|
Blocks beta subunit of RNA polymerase
|
|
Give the mechanism of this drug and/or drug class -- ; -Sulfa Drugs
|
Blocks Para-Amino Benzoic Acid (PABA)
|
|
Give the mechanism of this drug and/or drug class -- ; -Cephalosporins
|
Inhibit the cell wall
|
|
Give the mechanism of this drug and/or drug class -- ; -Penicillins
|
Block transpeptidase
|
|
Give the mechanism of this drug and/or drug class -- ; -Chloramphenicol
|
Blocks peptidyl transferase on the 50s subunit
|
|
Give the mechanism of this drug and/or drug class -- ; -Clindamycin/Lincomycin
|
Blocks translocase on the 50s subunit
|
|
Give the mechanism of this drug and/or drug class -- ; -Macrolides
|
Blocks translocase on the 50s subunit
|
|
Give the mechanism of this drug and/or drug class -- ; -Mitronidazole
|
Increases production of free radicals
|
|
Give the mechanism of this drug and/or drug class -- ; -Vancomycin
|
Blocks cell wall (phopholipid)
|
|
Give the mechanism of this drug and/or drug class -- ; -Benzodiazepine
|
Increase the frequency of the GABA receptors via Cl- channels
|
|
Give the mechanism of this drug and/or drug class -- ; -Barbiturates
|
Increase the duration of the GABA channels via Cl- channels
|
|
Give the mechanism of this drug and/or drug class -- ; -TCAs
|
Block reuptake of catacholamines, AV conduction and alpha receptors
|
|
Give the mechanism of this drug and/or drug class -- ; -SSRIs
|
Block reuptake of Serotonin
|
|
Give the mechanism of this drug and/or drug class -- ; -MAOIs
|
Inhibit MAO
|
|
Give the mechanism of this drug and/or drug class -- ; -Lithium
|
MOA is unknown but is suspected to be related to it mimicking of Na+
|
|
Give the mechanism of this drug and/or drug class -- ; -Valproic Acid
|
Blocks Na+ and sometimes Ca2+
|
|
Give the mechanism of this drug and/or drug class -- ; -Carbamizapine
|
Blocks Na+ and Ca2+
|
|
Give the mechanism of this drug and/or drug class -- ; -Epinephrine
|
Blocks Beta (2>1) receptors and then Alpha receptors
|
|
Give the mechanism of this drug and/or drug class -- ; -Antihistimines
|
1st generation – blocks H1 and H2 receptors (H1>H2) ; -2nd generation – blocks H2 only
|
|
Give the mechanism of this drug and/or drug class -- ; -Decongestants
|
Alpha agonists ; -
|
|
Give the name of an important drug that: Inhibits thymidylate
|
5FU
|
|
Give the name of an important drug that: Inhibits dihydrofolate reductase
|
Methotrexate
|
|
Give the name of an important drug that: Inhibits ribonucleotide reductase
|
Hydroxyurea
|
|
Give the name of an important drug that: Inhibit microtubule formation
|
Vincristine/Vinblastin
|
|
Give the name of an important drug that: Inhibits microtubules from migrating
|
Paclitaxel
|
|
Give the name of an important drug that: Stimulates Natural Killer (NK) cells
|
Levamisole
|
|
What class of drugs likes to KIIIS? ; -1. Kills T-cell and Eosinophils ; -2. Inhibits macrophage migration ; -3. Inhibits phospholipase A ; -4. Inhibits mast cell degranulation ; -5. Stabilizes endothelium ; -
|
Steroids
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|
Name the class of drugs that: Inhibit HMG CoA reductase
|
Statins
|
|
Give the name of an important drug that: Decreases VLDL production in the liver
|
Niacin
|
|
What class of drugs would these descriptions belong to - 1st generation - Block potassium channels in the islet cells preventing insulin release ; -2nd generation – Promote insulin release and inhibit gluconeogenesis in the liver
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Sulfonylureas
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Give the name of an important drug that: Inhibit glucose absorption from the GI
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Miglitol/Ascarbose
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Give the name of an important drug that: Stops gluconeogenesis in the liver
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Metformin
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Give the name of an important drug that: Increases the sensitivity of insulin receptors
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Troglitazone
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What class of drugs: Block dopamine receptors
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Anti-psychotics
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Give the name of an important drug that: Irreversible inhibitor of cyclo-oxygenase
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Aspirin
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What class of drugs are: Competitive aldosterone receptor antagonist
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K+ Sparing Diuretics
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Give a class of drugs that have this mechanism - Block Na+ channels
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Topical Anesthetics
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Give a class of drugs that have this mechanism - Block topoisomerase (supercoils)
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Quinalones
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Give a class of drugs that have this mechanism - Blocks Initiation Factor (IF) 2 on the 30S subunit
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Aminoglycosides
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Give a class of drugs that have this mechanism - Blocks tRNA binding on the 30S subunit
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Tetracyclines
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What drug Blocks beta subunit of RNA polymerase (DNA dependent) and is used in special treatment.?
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Rifampin
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Give a class of drugs that have this mechanism - Blocks Para-Amino Benzoic Acid (PABA)
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Sulfa Drugs
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Give a class of drugs that have this mechanism - Inhibit the cell wall
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Cephalosporins
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Give a class of drugs that have this mechanism - Block transpeptidase
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Penicillins
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Give a class of drugs that have this mechanism - Blocks peptidyl transferase on the 50s subunit
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Chloramphenicol
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Give a class of drugs that have this mechanism - Blocks translocase on the 50s subunit
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Clindamycin/Lincomycin
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Give a class of drugs that have this mechanism - Blocks translocase on the 50s subunit
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Macrolides
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Give a name of a drug that have this mechanism - Increases production of free radicals
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Mitronidazole
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Give a class of a drug that have this mechanism - Blocks cell wall (phopholipid)
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Vancomycin
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Give a class of drugs that have this mechanism - Increase the frequency of the GABA receptors via Cl- channels
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Benzodiazepine
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Give a class of drugs that have this mechanism - Increase the duration of the GABA channels via Cl- channels
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Barbiturates
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Give a class of drugs that have this mechanism - Block reuptake of catacholamines, AV conduction and alpha receptors
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TCAs
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Give a class of drugs that have this mechanism - Block reuptake of Serotonin
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SSRIs
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Give a class of drugs that have this mechanism - Inhibit MAO
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MAOIs
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What is this drug: MOA is unknown but is suspected to be related to it mimicking of Na+ (hint, used in a mood disorder)
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Lithium
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Give an antiepileptic drug that is also used as a mood stabilizing drug and Blocks Na+ and sometimes Ca2+
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Valproic Acid
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What is the name of a drug used to treat severe stabbing shooting pain, and Blocks Na+ and Ca2+
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Carbamizapine
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Give the drug that Blocks Beta (2>1) receptors and then Alpha receptors
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Epinephrine
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Give a class of drugs that have this mechanism – - 1st generation – blocks H1 and H2 receptors (H1>H2) ; -2nd generation – blocks H2 only
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Antihistimines
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Alpha agonists are commonly used as what kind of drug
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Decongestants
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Give some of the main classes of drugs used to treat infections caused by: Gram+
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Tetracyclines ; -Cephalosporins ; -Penicillins; -Sulfa Drugs
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Give some of the main classes of drugs used to treat infections caused by: Gram+ & S.aureus -
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Quinolones ; -Macrolides ; -Chloramphenicol ; -Clindamycin ; -Vancomycin
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Give some of the main classes of drugs used to treat infections caused by: Simple Gram- only – (includes H.Flu (not B) and E. coli) ; -
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Tetracyclines ; -Cephalosporins ; -Macrolides ; -Sulfa Drugs ; -Chloramphenicol ; -Clindamycin
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Give some of the main classes of drugs used to treat infections caused by: All Gram- & pseudomonas -
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Quinolones ; -Aminoglysides
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Give some of the main classes of drugs used to treat infections caused by: Atypicals (Includes chylmydia, Mycoplasma, ureaplasma and legionella)
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Quinolones ; -Tetracyclines ; -Macrolides
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Give some of the main classes of drugs used to treat infections caused by: Anaerobes -
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Cephalosporins -- Simple only (no “Big Mama”); -Penicillins-- Simple only (no “Big Mama”) - Chloramphenicol ; -Clindamycin ; -Vancomycin ; -Metronidazole
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Give some of the main classes of drugs used to treat infections caused by: Richetisia -
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Tetracyclines
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Give some of the main classes of drugs used to treat infections caused by: pseudomembranous colitis, MRSA and enterococcis
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Vancomycin
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Give some of the main classes of drugs used to treat infections caused by: protozoa
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Metronidazole
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Give some of the main classes of drugs used to treat infections caused by: TB (deals with RNA enzyme)
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Rifampin
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Name the microorganisms that this drug targets mostly: Quinolones
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Gram+ & S.aureus ; -All Gram- & pseudomonas ; -Atypicals (Includes chylmydia, Mycoplasma, ureaplasma and legionella)
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Name the microorganisms that this drug targets mostly: Aminoglysides
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All Gram- & pseudomonas
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Name the microorganisms that this drug targets mostly: Tetracyclines
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Gram+ ; -Simple Gram- only (H.Flu (not B) and E. coli)); -Atypicals1 ; -Richetisia
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Name the microorganisms that this drug targets mostly: Cephalosporins
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Gram+ ; -Simple Gram- only (H.Flu (not B) and E. coli)); -Anaerobes - Simple only (no “Big Mama”)
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Name the microorganisms that this drug targets mostly: Penicillins
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Gram+ ; -Anaerobes - Simple only (no “Big Mama”); -
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Name the microorganisms that this drug targets mostly: Macrolides
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Gram+ & S.aureus ; -Simple Gram- only (H.Flu (not B) and E. coli)); -Atypicals (Includes chylmydia, Mycoplasma, ureaplasma and legionella)
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Name the microorganisms that this drug targets mostly: Sulfa Drugs
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Gram+ ; -Simple Gram- only (H.Flu (not B) and E. coli)); -
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Name the microorganisms that this drug targets mostly: Chloramphenicol
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Gram+ & S.aureus ; -Simple Gram- only (H.Flu (not B) and E. coli)); -Anaerobes Simple only (no “Big Mama”)
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Name the microorganisms that this drug targets mostly: Clindamycin
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Gram+ & S.aureus ; -Simple Gram- only3 ; -Anaerobes Simple only (no “Big Mama”)
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Name the microorganisms that this drug targets mostly: Vancomycin
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Gram+ & S.aureus ; -Anaerobes - Simple only (no “Big Mama”); -
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Name the microorganisms that this drug targets mostly: Metronidazole
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Anaerobes
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Name the microorganisms that this drug targets mostly: Rifampin
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TB- tuberculosis
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