NBME 16 – Flashcards
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Two major theories of opioid tolerance involve:
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changes in opioid receptors. One theory purports that receptors undergo changes that result in decreased receptor activation, or desensitization, with prolonged exposure to opioids. The other line of evidence suggests that opioid receptor down-regulation is at least partially responsible for the development of tolerance. more: http://www.medscape.com/viewarticle/562216_3
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Lamelar bodies where do you find?
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Lungs! lamellar granules (otherwise known as membrane-coating granules (MCGs), lamellar bodies, keratinosomes or Odland bodies) are secretory organelles found in type II pneumocytes and keratinocytes. Lamellar granules fuse with the cell membrane and release pulmonary surfactant into the extracellular space. Epidermis!In the upper spinous layer and stratum granulosum layer of the epidermis, lamellar bodies are secreted from keratinocytes, resulting in the formation of an impermeable, lipid-containing membrane that serves as a water barrier and is required for correct skin barrier function. These granules release components that are required for skin shedding (desquamation) in the uppermost epidermal layer, the stratum corneum
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what is the 5' untranslated region (5? UTR) ?
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(also known as a Leader Sequence or Leader RNA) is the region of an mRNA that is directly upstream from the initiation codon. This region is important for the regulation of translation of a transcript by differing mechanisms in viruses, prokaryotes and eukaryotes
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The prokaryotic 5? UTR contains a ribosome binding site (RBS), also known as
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the Shine Dalgarno sequence (AGGAGGU), which is usually 3-10 base pairs upstream from the initiation codon.[5] In contrast, the eukaryotic 5? UTR contains the Kozak consensus sequence (ACCAUGG), which contains the initiation codon.[5]
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Cap-independent translation of poliovirus mRNA is conferred by sequence elements within the
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5 UTR
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which allows for translation initiation in an end-independent manner, as part of the greater process of protein synthesis?? In eukaryotic translation, initiation typically occurs at the 5' end of mRNA molecules, since 5' cap recognition is required for the assembly of the initiation complex.
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An internal ribosome entry site, abbreviated IRES, is a RNA element The location for IRES elements is often in the 5'UTR of Rna virus!, but can also occur elsewhere in mRNAs.
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the diference in risk between exposed and unexposed groups or proportion (%) of disease ocurrences that are attributable to the EXPOSURE.
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treatment rate - control rate Ie-Ine (incidence of disease/effect.. in exposed to treatment - non exposed_) if the risk of lung cancer in smokers is 21% and risk in non smokers is 1%,then 20% of lunk cancer is attributable to smoking. AR (attributable Risk) also AR %: 100x(RR-1)/RR
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the proportion of risk reduction attributable to the INTERVENTION as compared to control.
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if 2% of patients develop the flu,while 8% develop without vacine.then RR=2/8=.025 (Ie/Ine) and ...RRR= 1-RR= .75
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the diference in risk (not proportion) atributable to the INTERVENTION as compared to control
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control rate - treatment rate. (Ine-Ie) ARR if 8% receive placebo vaccine develop flu X 2% receive flu vaccine develop flu 8%-2%=6%
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presence og genetically distinct cell lines in the same individual. term and disease example
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Mosaicism Mccune Albright syndrome
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mutation affecting G ptn signaling= unilateral cafe au lai spots polyostotic fibrous dysplasia,precocious puberty multiple endocrine abnormalities. lethal if mutation occur before fertilization (affecting all cells)
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Mccune albright syndrome features
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mutations arise from mitotic errors after fertilization and propagates through multiple tissues and organs
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somatic mosaicism
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mutation only in egg or sperm cells
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gonadal mosaicism
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one gene contribute to different phenotype affecting multiple organ system
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pleiotropy (PKU)
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2 hit hypothesis remember
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loss of heterozigozity
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BRACA1 gene do not always result in breast ,ovarian cancer
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incomplete penetrance
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presence of normal and mutated mtDNA resulting in variable expressivity of mitocondrial inherited disease
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heteroplasmy
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phenotype varyes among individuasl with same phenotype (NF1)
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variable expressivity
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mutations at different LOCI can produce similar phenotype mutations at same LOCI can produce similar phenotype
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LOCUS heterogeneity: albinism allelic heterogeneity: B thalassemia
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can result is miscarriage,stillbirth and chromossomal imbalance (down,patau syndrome)
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unbalanced translocation
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Translocations can be reciprocal (balanced or unbalanced) or nonreciprocal (robertsonian)(balanced or unbalanced). give examples?
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Reciprocal translocations are usually an exchange of material between nonhomologous chromosomes. are usually harmless and may be found through prenatal diagnosis. However, carriers of balanced reciprocal translocations have increased risks of creating gametes with unbalanced chromosome translocations, leading to miscarriages or children with abnormalities.
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2 typer of chromossomal reciprocal translocations:
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chromosomal translocations occurring in gametogenesis, due to errors in meiosis, and translocations that occur in cellular division of somatic cells, due to errors in mitosis. The former results in a chromosomal abnormality featured in all cells of the offspring, as in translocation carriers. Somatic translocations, on the other hand, result in abnormalities featured only in the affected cell line, as in chronic myelogenous leukemia with the Philadelphia chromosome translocation.
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Robertsonian translocation is a type of translocation caused by
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breaks at or near the centromeres of two acrocentric chromosomes(six acrocentric chromosomes: 13, 14, 15, 21, 22 and the Y chromosome). The reciprocal exchange of parts gives rise to one large metacentric chromosome and one extremely small chromosome that may be lost from the organism with little effect because it contains so few genes. The resulting karyotype in humans leaves only 45 chromosomes, since two chromosomes have fused together
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diseases with congenital MICROscopic deletion of: short arm of 5 long arm of 7
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5: Cri du chat syndrome (46 XX or XY,5p-) 7:Williams syndrome
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microcephaly with intelectual disability,epicantal folds,cardiac abnormalities(VSD),
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Cri du chat! cat like cry!
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delected region gene of elastin, distinctive elfin fascies,intelec disab, hyper CALCEMIA (high sensitiity to vit D) WELL developed verbal skilss!!extreme friendliness with strangers! CV problems.
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williams!
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-microdeletion of chromosome -deletion of chromosome: -codon deletion -single gene deletion
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-above - turner -CF - prader/angelman
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GRAM + stain 3 divisions:
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Cocci rods(bacilli) branching filaments
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cocci next
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catalase + staph -; coagulase -; + Aureus - novobiocin sens: epidermidis X saprophyticus - strep
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rods: CCBL
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Clostridium,corynebacterium,bacillus(aerobe),listeria
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Branching filaments
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Actinomyces (A naerobe,NOT acid fast) X Nocardia
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GRAM - stain
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cocci (diplo) coccoid rods Rods curved rods
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maltose fermenter
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N meningitis
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coccoid rods HP BB
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haemophilus, pasteurela, Bordetella pertussis, Brucella
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Rods begins with -
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lactose fermenter(pink color) fast: KEE CS Klebsiella,E.coli,enteroBACTER slow: citrobacter, serratia lactose non fermenter, use oxidase because is white/colourless!
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oxidase - X +
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oxidase +: pseudomonas motile encapsuled or aeromonas hydrophila oxidase -: next TSI agar
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TSI agar (triple sugar iron) produces H2S -Black ?bacterias
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spy! Salmonella proteus Yersinia do not produce: shiiiiiiigella
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patient has burning abdominal pain that occurs 1-2 hours after patient eats. suspect:
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duodenal ulcer due arrival of acid food! usually the pain relieves when patient eats due release of pancreatic alkaline secretion
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patient has burning abdominal pain worsening when eating! fear of eat!
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stomach ulcer due increased acid secreations released
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patient wit 6 month history of burning abdominal pain that occurs 1 to 2 hours after he eats.he also has Black stools for 2 days! suspect:
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bleeding duodenal ulcer
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high grade and low grade means:
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low and high differentiation
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stage TNM
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high stage worst prognosis T: tumor size ,depth N:nodules (2 worst) M: metastasis (worst)
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lactose fermenters grow which color on Mc conkey? which color in EMB agar and specifically E.coli ?
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Mc conkey: Lactose is key! -;pink colonies EMB(eosin methilene blue|) purple/Black colonies and e.coli grows with green sheen
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which enzyme is responsible for the green color of pus and sputum in bacterial infection?
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myeloperoxidase
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a blue green heme based enzyme released from neutrophil azurophilic granules and forms hydrochlorus acid( Bleach)
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myeloperoxidase
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pigmanet producing bacteria: yellow (2) gree red
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Y: actinomyces israelli,S.aureus green: pseudomonas aeruginosa ( blue green) due production of pyocyanin Red: serratia marcescens
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condition of urine containing white blood cells or pus. Defined as the presence of 6-10 or more neutrophils per high power field of unspun, voided mid-stream urine
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piuria
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-Can be a sign of a bacterial urinary tract infection.
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piuria
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urine which contains white blood cells while appearing sterile by standard culturing techniques.
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Sterile pyuria
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sterile piuria It is often caused by:
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sexually transmitted infections, such as gonorrhea, or viruses which will not grow in bacterial cultures. Sterile pyuria is listed as a side effect from some medications such as paracetamol (acetaminophen). Its occurrence is also associated with certain disease processes, such as Kawasaki disease and genitourinary tuberculosis.[2] However, there are many known causes, including systemic or infectious disease, structural and physiological reasons, intrinsic kidney pathology, or drugs.[2]
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use monoclonal antibody TNF blockers for: name of drugs:
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PAIR reumatoid arthritis names: Adalimu/inflixi/certolizu!
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TNF decoy TNF a receptor blocker:
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Ertanecept
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main indication of ertanecept in RA
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added to metotrexate to treat mod to severe RA when Metho failed
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Sweating Shivering Headache Muscle aches Loss of appetite Dehydration General weakness
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fever symptoms (above 37 - 98.6F)
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Hallucinations Confusion Irritability Convulsions Dehydration
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High fevers between 103 F (39.4 C) and 106 F (41.1 C) may cause:
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diseases 1-liver and spleen enlargement,fibrosis and inflammation (portal hypertension) 2-chronic infection can lead to squamous cell carcinoma of the bladder and may cause KATAYAMA fever (fever,urticaria,angioedema,eosinophilia)
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1- S.mansoni (egg with lateral spine) Sjaponicum also cause intestinal disease: (diarrhea,abdominal pain,ulceration) 2-S.haematobium (egg with TERMINAL spine)
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praziquantel to treat:
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intestinal Nematodes (round) no! give bendazoles! use praz! for: -cestodes(tapeworms) except: neurocist or echinococcus both albendazole!! -trematodes(flukes)
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1.Cestodes(Tapeworms) give examples 3 2.trematodes
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1. - taenia solium -;intestinal infection (injestion of larva) X cisticercosis muscle(ingestion of eggs) or neurocisticercosis (give albendazol) -diphylobothrium latum - echinococcus granulosus give albendazole 2. schistosoma clonorchis sinensis paragommus westermani: live lung: chronic bronchitis/hemoptisis
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1.diphylobothrium latumX 2.eccinococcus granulosus X 3.clonorchis sinensis
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1/2: cestode 3. trematode 1/3 from undercooked /raw fish 1.vit B12 deficiency 3.biliary tract inflammation-; pigmented stones, may cholangiocarcinoma 2. ngestion of eggs from dogs, goes lung and liver-; hydatid cysts in the liver causing anaphylaxis if antigens released
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Nitrous oxide: blood and lipid solubility induction and potency: Isoflurane blood and lipid solubility induction and potency: relate: a) blood/gas partitition (or oil/gas) with onset of action, potency
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- Has low blood and lipid solubility and thus: - Fast Induction ; Low Potency Isoflurane - ? Lipid and Blood solubility and thus: - Slow Induction ; High Potency blood/gas is related with onset of action! and oil/gas is related to potency ? Blood solubility = ? Blood/Gas partition coefficient = ? solubility = ? Gas required to saturate blood = Slower onset of action.
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blood/gas partitition is diretly oy indirectly proportional to onset of action and recuperation?
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indirectly
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oil/gas partitition is diretly oy indirectly proportional of potency?
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directly
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is there a tendency of anesthetics with greater oil/gas have greater blood/gas partition?
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yes! higher potency with slower onset of action.
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give prophylatic penicillin daily to decrease patients´risk for infection by:
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encapsulated organisms (S.pneumo first!, H.Influenza)! due autosplenectomy (howell jolly bodies)
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drugs which Concentration in plasma decreases linearly with time. rate of elimination is constant regardless of Cp (constant amount of drug eliminated per unit time)
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zero order elimination PEA phenytoin, ETHANOL,ASPIRIN
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drugs witch decrease exponentially with time. rate of elimination is directly PROPORTIONAL to the drug concentration! is a flow dependent elimination. there a constant Proportion of drug elimined per unit time
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First Order elimination
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if first order elimination in 2hours 12,5 mg decrease to 10mg, after 2 hours which will be the concentration?
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same proportion! 20% 8mg
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bacteria mechanism of resistance for ATB 1. penicillinase in bacteria cleaves the blactam ring penicillins resistant b lactamases (oxa/methi,diclo,nafcillin)
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1. penicilli G,V amoxicillin, ampicillin(wider spectrum) Pipera/ticarcillin (anti pseudo) (may combine wit b lactamase inhibitors)
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bacteria mechanism of resistance for ATB 2. structural change in penicillin binding ptns (transpeptidases)
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cephalosporins
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bacteria mechanism of resistance for ATB 3. D ala D ala to D ala d LAC! (VRE)
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vancomycin
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bacteria mechanism of resistance for ATB 4. bacterial transferase inactivate ATB by acetylation, phosphorilation or adenylation
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aminoglycosides
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Bacteria mechanism of resistance for ATB 5. decrease or increase efflux out of the bacterial cells by plasmid encoded transport pump. production of a ptn that allows translation of bacteria to take place even when ATB is present within the bacteria.
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tetracycline
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bacteria mechanism of resistance for ATB 6. plasmid encoded acetyltransferase inactivates the drug
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chloramphenicol
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bacteria mechanism of resistance for ATB 7.point mutation of ribossomal RNA
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Linezolid
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bacteria mechanism of resistance for ATB 8. methylation of 23 S rRna binding of 50s prevents binding of drug
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macrolides
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bacteria mechanism of resistance for ATB 9.altered enzyme (bacterial dihydropteroate synthase),decreased uptake or PABA synthesis
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sulfonamides
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mechanism of resistance of mycobacteria:: mutation reduces drug binding to RNA polymerase.(mutation in gene that codes for a DNA dependent RNA polymerase)
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Rifamycin monotherapy leads to resistance
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mechanism of resistance of mycobacteria: mutation leading to underexpression of KatC
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Isoniazid KAT encodes catalase peroxidase needed to convert INH to active metabolite
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mechanism of resistance of virus for antiviral 1. mutated (thymidine) viral kinase
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cyclovirs
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mechanism of resistance of virus for antiviral 2.mutated (CMV) viral kinase
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ganciclovir
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mechanism of resistance of virus for antiviral 3. mutated DNA polymerase
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Foscarnet does not require activation by viral kinase
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characterized by acute noninflammatory encephalopathy (headache,coma) and fatty degenerative liver(hypoglycemia) decreased beta oxidation! due mitochondrial enzymes inhibition! liver failure after a viral illness, particularly an upper respiratory tract infection, influenza B, varicella, or gastroenteritis,
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Reye syndrome aspirin use!
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H1 blockers! generation? names contains 1. en/ine or en/ate 2.adine
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1. DiphENhydramINE, DimENhydrATE, chlorphENiramINE 2. lorat/fexofenadine
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H1 blockers clinical use 1generation 2generation
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both allergy! (second rhinitis! and less sedating due low penetration in CNS) but first motion sickness,sleep aid (disrupts), anaphylaxis after stabilization with epinephrine.
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expectorants think 2!:
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-N acetylcysteine mucolytic!prophylaxis against induced nephropathy if preexisting renal disease. -Guaifenesin: EXPECTORANT-thin secretions
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cough suppression:think
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-opioids:inhibits at CNS level (codeine) DEXTROmethorphan: antagonizes NMDA glutamate receptors), synthetic codeine analog! mild opioid effect if used in excess:constipation
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nasal descongestionants
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pseudoephedrine and phenylephrine (alpha adrenergic agonists) pseu used to makje methamphetamine
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AR disease: q square = prevalence q = allele frequency 2q = carrier frequency X-linked AR: Prevalence = allele frequency q square = q Carrier state for females = 2q
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the X link disease is seen in 1/100,000 males.which is the expected prevalenve of heterozygous females. Allele frequency (q) = the prevalence (q square) Thats why in this question q = 1/100000 Carrier state = 2q = 2/100000 = 1/50000
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at the initial screening evidence of clamydia tracomatis infection is founf in 500 of 2500 student .one year later evidence of C tramotis is found in an additional 200 students which of the following is anual incidence of c tracomatis infection in this population of students
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B10 % here is no info about how much students have got the treatment, so consider like a chronic disease. take out people who had the disease in people at risk! those 500 who already have it aren't at risk anymore to get it. therefore 200/2000 is the correct answer
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flow rate formula:
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- flow velocity X cross sectional area if fv:20cm/sec and cross area:2cm2 remember to convert units is L/Min
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ohms law to calculate flow resistance formula:
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- U=R.i p1-p2=R.Q(flow) Q= p1-p2/R R= viscosity/radio4 so: Q=p1-p2 x r4 /viscosity
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1. hyperproteinemia styates, polycythemia, hereditary spherocytios increases 2. anemia decreases
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viscosity
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have highest total cross sectional area and lowest flow velocity
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capillaries
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organ removal(nephrectomy) leads to
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increased TPR and decreased CO
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cm 3
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1 ml or 10 -3 L
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tanner scale I prepubertal childhood II 8-13 pubic hair ___________;breast buds________ III pubic hair _________;breast___________;penis increase________ IV penis increase__________;scrotal skin/glans, areola_; V adult; areola
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I prepubertal childhood II.pubic hair appears(pubarche);breast buds form (thelarche) III pubic hair: darkens/curly! ;breast enlarge;penis increase size/lengh IV penis increase width;scrotal skin/glans, areola raise V adult; areola are no loger raised
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irregular mestrual periods 13/14, after menarche
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anovulatory cycles
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how S pneumoniae ability to produce capsules (his major virulence factor)
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bhy transformation! SHN use this ability to take up fragments of Dna from environment (eg from cell lysis)
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transduction generalized "a packaging" event by
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litic phage infecting bacterium!cleaves bacterial DNA and parts of both DNA are packaged together in viral capside to infect another bacteria.
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transduction specialized is a "excision event" by:
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Lytic Phage! infects bacteria, its viral dna is incomporated in bacterial chromosome! when phage DNA is EXCISED, flanking bacterial genes may be excised with it, packaged into viral capside to infect another bacteria.
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which bacteria toxins are encoded by lysogenic phage: ABCDE
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Shiga Botulinum cholera diphteria erythrogenci of st pyogenes
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the condition may increase the risk for: Kidney obstruction - abnormal placement of ureter may lead to obstruction and dilation of the kidney. Kidney infections - associated with vesicoureteral reflux. Kidney stones - deviant orientation of kidneys combined with slow urine flow and kidney obstruction may lead to kidney stones. Kidney cancer - increased risk of renal cancer, especially Wilms' tumor, transitional cell carcinoma, and an occasional case report of carcinoid tumor.[3] Despite increased risk, the overall risk is still relatively low.
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While most cases of horseshoe kidneys are asymptomatic and discovered upon autops The prevalence of horseshoe kidneys in females with Turner Syndrome is about 15%. It can be associated with trisomy 18,13.[5]
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whats the LH/FSH ratio in POS?
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high LH! stimulates theca cells to produce androgens
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how insulin resistance increase androgens?
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stimulates theca cells to produce androgens
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whats does high androgens lead?
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high conversion in periphery to estrone due aromatase!
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androgens are converted to estradiolin granulosa cells?
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no, due low FSH!
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what does sex binding hormones interfere in level of strogens/androgens in blood?
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they are in low quantitity due low production by the liver leading to higher free levels of androgens and estrogens in the blood
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all are up less FSH
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POS
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consequences: 1.high estrogen 2.high androgen
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1.amenorrhea/oligo, repeated anovulatory cycles-subfertility; higher risk of endometrial hyperplasia/cancer due unoposed estrogen. 2.hirsutism,acne
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treat POS
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weight reduction OCP clomiphene ketokonazol spironolactone
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why acute alcohol intake protects for acetaminophen intake liver injury and chronic alcohol intake worse live injury?
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by inhibiting or inducing P450 enzymes to make hepatotoxic metabolites!
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oral or depot-injected contraceptive and also as the progestin component of menopausal hormone replacement therapy to prevent endometrial hyperplasia and cancer. is also used as a treatment for endometriosis, dysmenorrhea, and amenorrhea. decreases growth and increases vascularization of endometrium
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progestins (medroxyprogesterone)
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adjuvant therapy for postmenopausal women with ER+ breast cancer
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exemestane/anastrozole (aromatase inhibitors)
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selective estrogen receptor modulators
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clomiphene tamoxifen raloxifene
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antagonist at estrogen receptor in hypothalamus 1 line of infertility due anovulation prevents normal feedback inhibition and increase release of LH and FSH, which stimulates ovulation. may cause Hot flashes,ovarian enlargement,multipole pregnancies.
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clomiphene
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drug to prevent /treat breast cancer (ER+) (also agonist bone,uterus)
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tamoxifen
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drug to prevent breast cancer and mainly prevent osteoporosis *agonist bone) but antagonist at uterus!
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Raloxifene
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DX: men: Low back pain,dysuria,urgency,frequency
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prostatitis
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CD56, chromogranin, synaptophysin, and neuron-specific enolase) markers from
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neuroendocrine origin
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bacteria which causes prostatitis 35Y
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35: think UTI ( PEcKS proteus,E.COLI!!!,Klebsiella,Serratia and enterobacter
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prostatitis treat:
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fluoroquinolones,levo for ;4 weeksor TMP/SMX
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is an activator of the intrinsic coagulations cascade: Deficiency leads to increased:
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Kallikrein deficienct of kallikrein leads to defective intrinsic pathway which is measured with PTT ( is increased in dysfunction of the intrinsic pathway
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B1 selective B antagonists A to M
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Acetabulol (partial agonist),atenolol,esmolol,metoprolol
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Non selective B antagonist N to Z
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Nadolol,Pindolol(partial agonist),propranolol,Timolol
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non selective B and alpha
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labetalol and carvedilol!
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weak B1B2 agonis(partial) acts as antagonists
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acetabulol,pindolol to HTN patients with bradycardia
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non seletive irreversible X reversible Alpha blockers
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irreversible (PHEnoxbensamine! to PHEochromocytoma reversible; give to patients using MAO eating tyramine foods
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alpha 1 selective blockers (osin) to BPH
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praz,teraz,doxaz,tamsulosim
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alpha 1 selective blockers (osin) to BPH which does not lower BP!give for normotense patients
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Tamsulosin (selective for Alpha 1 a on Prostate!) does not relax vascular Alpha 1 b receptors on vessels
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alpha 2 agonist for ADHD, tourette syndrome cause CNS depression,bradycardia,hypootension,respiratory depression,miosis.
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clonidine
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alpha 2 blocher for depression but becomes asleep, fat, hungry!
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mirtazapine
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alpha 2 agonist for HTN in pregnancy diect coombs + hemolysis SLE like syndrome
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a methyldopa
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name of zone I affected first by viral hepatitis, ingested toxins
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periportal zone
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namoe of zone affected by yellow fever
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intermediate zone
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name of zone affected by ISCHEMIA! (high demant of energy by Na/Katpase)contains P450!being most sensible to metabolic toxins! and alcohol!(alcoholic hepatitis)
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pericentral vein (centrilobular)
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shows micro abscesses within the crypts and depletion of mucus from goblet cells,tenesmus and bloody diarrhea
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ulcerative colitis
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which drug upregulate LPL(lipoprotein lipase) increasing blood TG clearance increased cholesterol bile secretion by decreasing bile acid formation (inhibition of cholesterol 7 hydroxilase)
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Fibrates (high risk of cholesterol gallstones0 Myopathy (high risk with statins)
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which drug inhibits lipolysis (HSL) at adipose tissues and reduces hepatic VLDL synthesis? increases HDL perfect drug! but side effects:
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Vit B3 Niacin red,flushed face decreased by NSAIDS HyperGLYCEMIA!!:(URICEMIA:((
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caution use with statins
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ezetimibe,Fibrates
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arterial/venous supply above (superior rectum) under pectinate line (middle/inferior rectum)
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above: -superior RECTAl (a.)(v.) from IM(a.)(v.) under: -middle RECTAL (a.) from internal iliac (a.)(v.) directly! -inferior RECTAL (a.)(v.). from internal pudendal (a.) from internal iliac
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A 57 year old man comes to the physician because of a 6 month history of progressive constipation and a feeling of rectal fullness. Digital rectal examination shows no papable lesion. Test of the stool for occult blood is positive. Colonoscopy shows a mass in the sigmoid colon. A biopsy specimen of the mass shows adenocarcinoma. Metastases from this mass will most likely spread via which of the following lymph nodes?
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A) Inferior mesenteric B) Internal iliac C) Left colic D) Pararectal E) Superficial inguinal
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lymphatic drainage 1. above: (superior rectumXmiddle rectum) 2. under pectinate line
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1.above: -superior rectum: superior RECTAL nodes to IMesenteric -middle rectal nodes to internal iliac nodes 2. under -to superficial inguinal nodes
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remembre effect of partial agonist in presence of full agonist
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antagonist effect
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P450 inhibitors CRACK AMIGOS
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Cimetidine Rito NAVIR Alcohol use acute CIPROFLOXACIN KetoconaAZOLES(fluco/itra..) AMIODARONE Macrolides (EXCEP AZITRO!) Isoniazid GRAPE FRUIT juice Omeprazole SULFA Quinidine! gingko biloba
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P 450 inducers
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Phenytoin Barbiturates Chronic alcohol GRISEOFULVIN RIFANPIN St johj green vegetables/ginseng
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substrates for P450
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statins anti epilectics theophiline OCPs Ciclosporine/tacrolimus
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rouworms by ingestion EATT
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enterobius,ascaris,toxocara, trichinella
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roundworms that penetrate skin (SANd)
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Strongylois, Ancylostoma/necator
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intestinal infection causing vomiting,diahhrea,epigastric pain(fell like peptic ulcer)
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strongyloides
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intestinal infection causing anemia by sucking blood from intestinal walls
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Ancylostoma/necator (hook worms)
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At the cell surface, the binding of ligands such as hormones and neurotransmitters to a GPCR activates the receptor by causing a conformational change, which in turn activates the bound:
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G protein on the intracellular-side of the membrane. The activated receptor promotes the exchange of bound GDP for GTP
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GTP binding changes the conformation of switch regions within the alpha subunit, which allows the bound trimeric G protein (inactive) to be released fromthe receptor, and to dissociate into
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active alpha subunit (GTP-bound) and beta/gamma dimer
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the alpha subunit and the beta/gamma dimer go on to activate distinct downstream effectors, such:
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as adenylyl cyclase, phosphodiesterases, phospholipase C, and ion channels. These effectors in turn regulate the intracellular concentrations of secondary messengers, such as cAMP, diacylglycerol, sodium or calcium cations, which ultimately lead to a physiological response, usually via the downstream regulation of gene transcription
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activated receptor promotes the exchange of bound GDP for GTP in which G ptn subunit?
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G protein alpha subunit.
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The cycle is completed by the hydrolysis of
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alpha subunit-bound GTP to GDP, resulting in the re-association of the alpha and beta/gamma subunits and their binding to the receptor
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glucagon (fasting) activates which enzyme to get to gluconeogenesis
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high glucagon-;high cAMP-;high Ptn Kinase A which activates FBPase 2(fructose biphosphatase) which converts Fructose 2,6BP -;Fructose6P (less glycolysis),more gluconeogenesis.
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1.glucokinase inhibitor 2.hexokinase inhibitor 3.PFK1 inhibitor X stimuli 4.Pyruvate kinase inhibitorX stimuli 5.Fructose 1,6Bisphosphatase inhibX stimuli
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1.fructose 6P 2.glucose 6P 3.Citrate,ATP X Fructose 2,6B,AMP 4.Alanine,ATP X Fructose 1,6B 5. AMP,fructose 2,6BphosphateX AMP,ACETYL COa,Citrate
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antiviral drug ciclovirs action.inhibits
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DNA polymerase
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viral kinase (HSV/VZV) phosphorilates drug and celullar kinase also forming triphosphate which acts:
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guanosine analogs (AFV) aci,fam,valacyclovir. actsinhibiting DNA polymerase
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drug which triphosphate is formed by CMV and host cellular kinases and also inhibits DNA polymerase. also a guanosine analog
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Ganciclovir by CMV!
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incidence of neutropenia increases with coadministration of ganciclovir with
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Zidovudine or SMT TMP
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does not require virus (viral kinmase) to be activated! has also DNA and RNA polymerase inhibition action! and HIV transcriptase inhibition
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Foscarnet! a pyrophosphate analog
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also inhibits DNA polymerase also does not require virus (viral kinmase) to be activated!
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cidofovir
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use is CMV retinitis in immunocompromissed,acyclovir resistant HSV
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foscarnet or cidofovir
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prostaglandins produced by COXs
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IDE PGI2,D2,E2 ( vasodilation,increased permeability) E2 also fever and pain
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Leukotrienes produced by 5 Lipoxygenases:
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B CDE! LTC4,D4,E4 (vaso CONSTRICTION,increased permeability also., and BRONCHOSPASM! LTB4 activate neutrophil
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systemic mycosis and treat:
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Histo/blasto/coccidio/paracocci itraconazole; flucytosine w/wit ampho B
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opportunistic
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candida/aspergilus/cryptoco/mucor/pneumocystis/sporothrix candida/crypto/sporot: fluconazole aspergilus: caspogungins
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cutaneous tineas 1.corporis/pedis/ungueal: 2.capitis
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1.topical terbinafine 2.oral
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what are the Amino Acids, HC03, Phosphate and Glucose levels
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Everything decreased
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