NBME 12 – Flashcard
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IL 2 agonist for
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melanoma and renal cell carcinoma
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hep C therapy
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Ribavirin Simeprevir Sofosbuvir
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induces lethal hypermutation, inhibits Rna polimerase (inhibits synthesis of G (guanine) nucleotides by competitively inhibiting IMP dehydrogenase. Use for Chronic Hep C and RSV (palivisumab)
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Ribavirin causes hemolytic anemia, severe teratogen
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limbs defects(phocomelia,micromelia-flipper limbs)
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thalidomide
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encapsuled bacteria
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SHiNE SKs vaccines for SHiN Streptococcus pneumoniae, Haemophilus influenxae type B, Neisseria meningitidis,E.coli, Salmonella,Klebsiella pneumoniae and group B Strep
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drug combination of sulfapyridine (antibacterial) and 5 ASA aminosalicyclic acid (anti-inflammatory) activated by colonic bacteria.
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sulfasalazine for IBD toxicity:malaise/nausea sulfonamide toxicity,reversible oligospermia.
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IBD treatment: drugs for MILD and SEVERE disease and acute exacerbation as curative therapy.
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MILD: 5 ASA agents (mesalamine, sulfazalazine) SEVERE: -Immunosupressants! azathioprine/6 mercatopurine,MTX or -Anti TNF (infliximab), adalimumab if arthritis ACUTE exacerbation: -ATB and glucorticoids CURATIVE: colectomy for Ulcerative colitis
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the trueness oif test measurement (validity).The absence of systematic error or bias in a test.
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accuracy obs: systematic error decrease accuracy in a test
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the consistency and reproducibility of a test (reliability,confiance)
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precision obs: random error decrease precision in a test high precision=low SDeviation and high statistical power(1-B)
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tetracyclines VACUM THe BRazil!
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Vibrio c, Acne Chlamydia Ureaplasma urealyticum Mycoplasma pneumo Tularemia Helicobacter Borrelia Burgdor Rickettsia
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30 S inhibitors
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AT! aminoglicosides(cidal) tetracyclines
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50S
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LMCC linezolid macrolides chloramphenicol clindamycin
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use ceftriaxone for
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meningitis, gonorrhea, disseminated lyme disease
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use ceftazidime
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pseudomonas
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cephalosporins are lame agsinst
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listeria Atypicals MRSA enterococci obs: in PNM give Ceftriazone for G- and macrolides for atypicals
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supra scapular inervates
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infraspinatus m supraspinatus m
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Km reflects the
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***affinity of the enzymes*** for its substrate... obs:Km shows the ability of enzymes to bind to receptor,in the other words Km value is an intrinsic property of enzyme-substrate system and can not be altered by changing the [enzyme] or[substrate]. km and Vmax are independent of each other...they measure two different values:affinity versus concentration The Km cannot be predicted based solely on the value of Vmax.
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Vmax reflex the
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***enzyme concentration directly *** and it can be changed by [enzyme
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prostate cancer drugs 2
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leuprolide: GnRH antagonist if used in continuous fashion flutamine: competitive inhibitor of androgen receptors
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COPD,Asthma drugs (muscarinic antagonists)
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Tio/Ipra tropium
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why amenorrhea by stress??
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the stress system is comprised of the hypothalamic-pituitary-adrenal (HPA) axis, arousal, and the autonomic system.18 The main chemical mediators of stress include CRH, glucocorticoids, and beta-endorphins. CRH has receptors in many different tissues including ovary, endothelium, hypothalamus, and inflammatory tissues. Produced in the hypothalamus, CRH and arginine vasopressin stimulate adrenocorticotropic hormone (ACTH) production in the pituitary. This increases cortisol production in the adrenal glands. Cortisol is a glucocorticoid that acts on multiple body systems and reduces LH, estradiol, and progesterone effects. Beta-endorphins are secreted from nerve terminals in response to CRH and produce the initial euphoria of acute stress, necessary for survival. Elevated levels of CRH and cortisol suppress GnRH secretion and consequently decrease ovulation.15 Stress is a common problem in patients undergoing fertility workup and treatment.
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factitious hyperthyroidism
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There is no goiter. The thyroid gland is usually small. The eyes do not bulge, as they do in Graves disease (the most common type of hyperthyroidism). The skin over the shins does not thicken, as it sometimes does in people who have Graves disease.
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Tests used to diagnose factitious hyperthyroidism include:
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Free T4 Radioactive iodine uptake Thyroglobulin Total T3 Total T4 TSH
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Radioactive iodine uptake
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Radioactive iodine uptake (RAIU) is a test of thyroid function. It measures how much radioactive iodine is taken up by the thyroid gland in a certain time period. Higher-than-normal uptake may be due to an overactive thyroid gland caused by:
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Higher-than-normal uptake may be due to an overactive thyroid gland caused by:
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-Graves disease -An enlarged thyroid gland that contains nodules producing too much thyroid hormone (toxic nodular goiter) -A single thyroid nodule that is producing too much thyroid hormone These conditions often result in normal uptake, but the uptake is concentrated into a few (hot) areas while the rest of the thyroid gland does not take up any iodine (cold areas).
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Lower-than-normal uptake may be due to:
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Factitious hyperthyroidism Iodine overload Subacute thyroiditis Silent (or painless) thyroiditis Amiodarone
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OR RR AR RR R AR R NNT NNH
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RR: Ie/Ine AR: proportio of diseases attributable to EXPOSURE! (Ie-Ine) or 100(RR-1/RR) (%)! RR R: (relative is proportion) proportion of risck reduction due INTERVENTION! as compared to control. (1-RR) AR R: diference in risk atributable to the INTERVENTION! (Ine-Ie) =(event control -event treatment) (%)! attention if 6% is .06! NNT=1/AR R NNH= 1/AR
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characterized by significant difficulties in social interaction and nonverbal communication, along with restricted and repetitive patterns of behavior and interests.[1] As a milder autism spectrum disorder (ASD), it differs from other ASDs by relatively normal language and intelligence.[2] Although not required for diagnosis, physical clumsiness and unusual use of language are common.[3][4] Symptoms usually begin before two years old and typically last for a person's entire life.[1]
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Asperger syndrome (AS), also known as Asperger's, is a developmental disorder. Interventions may include social skills training, cognitive behavioral therapy, physical therapy, speech therapy, parent training, and medications for associated problems such as mood or anxiety.[7] Most children improve as they grow up, but social and communication difficulties usually persist.
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shows normal development and he/she acquires "normal development of age-appropriate verbal and nonverbal communication, social relationships, motor, play and self-care skills"[citation needed] comparable to other children of the same age. However, between the ages of 2 and 10, skills acquired are lost almost completely in at least two of the following six functional areas:
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hildhood disintegrative disorder (CDD), also known as Heller's syndrome and disintegrative psychosis, is a rare condition DD, especially in cases of later age of onset, has also been associated with certain other conditions, particularly the following: Lipid storage diseases: In this condition, a toxic buildup of excess fats (lipids) takes place in the brain and nervous system. Subacute sclerosing panencephalitis: Chronic infection of the brain by a form of the measles virus causes subacute sclerosing panencephalitis. This condition leads to brain inflammation and the death of nerve cells. Tuberous sclerosis (TSC): TSC is a genetic disorder. In this disorder, tumors may grow in the brain and other vital organs like kidneys, heart, eyes, lungs, and skin. In this condition, noncancerous (benign) tumors, hamartomas, grow in the brain. Leukodystrophy: In this condition, the myelin sheath does not develop in a normal way causing white matter in the brain to disintegrate.
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genetic postnatal neurological disorder of the grey matter of the brain[2] that almost exclusively affects females but has also been found in male patients. The clinical features include small hands and feet and a deceleration of the rate of head growth (including microcephaly in some). Repetitive stereotyped hand movements, such as wringing and/or repeatedly putting hands into the mouth, are also noted. prone to gastrointestinal disorders and up to 80% have seizures.[4] They typically have no verbal skills, and about 50% of affected individuals do not walk. Scoliosis, growth failure, and constipation are very common and can be problematic.
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Rett syndrome (RTT), originally termed cerebroatrophic hyperammonemia,[1] disorder are most easily confused with those of Angelman syndrome, cerebral palsy and autism.
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drug which hyperstabilize polymerized microtubules in M phase so that mitotic spindle cannot break down (anaphase cannot occur). (bind b tubulin and increase polymerization!) "taxes to stabilize society" for breast and ovarian cancers!
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PacliTAXEL
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paclitaxel side effects
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myelosuppression,hypersensitivity,alopecia
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which drug?? vinca alkaloids that bind b tubulin and inhibits polymerization into microtubules-; prevent mitoric spindle (M phase arrest)
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VIn cristine, VINblastine for solid tumors, Leukemias, hodgkin (vin Blastine) non Hodgkin (cristine) wilms tumor ewing sarcoma choriocarcinoma cristine causes neurotoxicity (arreflexia, peripheral neuritis blastine, Blasts!!bone! bone marrow suppression!
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gelatinous appearance tumor, benign mesenchimal.most common primary cardiac tumor in adults
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Myxoma, pedunculated mass in lef atrium
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benign hamartoma of cardiac muscle. most common primary tumor in children! associated with:
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rhabdoMYOMA associated with tuberous sclerosis. usually arises in ventricle
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more common than primary tumors in the heart
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metastasis from Breast and lung melanoma, lymphoma-->involves pericardium with pericardial effusion
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rash on palms and soles (use to drive Cars)
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Coxsackie A Rocky mountains s f Syphilis 2 meningococcus kawasaki
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treatment for Rickettsial diseases and Vector borne illness
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doxycycline
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rickettsial diseases-; disease 1:by Rickettsia rickettsii (dog Tick)remember classical triat:
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rocky mountains spotted fever: headache,fever, RASH(vasculitis) common in palms and soles!!
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rickettsial diseases -; disease 2
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Typhus
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Typhus 2 types:
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endemic (fleas) R.Typhi Epidemic (human body louse) R prowazekii rash starts centraly (trunk) abd spreads out (spare palms and soles)
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other vector borne illness - Tick!
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Ehrlichiosis:(tick lone star)- monocyte with morulae.(febrile symptoms with nos specific symptoms) Anaplasmosis (ixodes tick) isso! anaplasma!
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coxiella burnetti disease name: spores from:
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Q fever! no arthropode vetor! from aerosols from cattle/sheep aminiotic fluid. most commom cause of - culture endocarditis
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Q fever apresentation:
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acute flu like illness oftem with PNM Chronic Q fever is rare bur fatal if not treated
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antileukotrienes
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Zileuton Monterlukast, zafirlukast
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Zileuton action
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5 lipoxygenase pathway inhibitor blocks conversion of arachidonic acid to leukotrienes (hepatotoxic)
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Lukasts action
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Blocks leukotriene receptor (good for aspirin induced asthma
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monoclonal anti IgE antibody
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bind mostly unbound serum IgE and blocks binding Fc receptor. used to asthma resistant to inhaled steroids!' and long acting b2 agonists!
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Type of crigler najjar syndrome which respondes to phenobarbital and so is less severe
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type 2 (similar do gilbert) type 1 there is complete absence of UDPG
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treatment of crigler najar
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plasmapheresis, phototeraphy to liver transplant
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leptin action: decreases and increases the production of: mutations in leptin gene or receptor result in:
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decrease NEUROPEPTIDE Y (potent stimulus to appetite) and increases production of: POMC in arcuate nucleus. Alpha melanocyte stimuling hormone (alpha MSH) fom cleavage of PONC and inhibits food intake. mutation results in: hyperphagia and profound obesity.
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GLP 1 secreted by: in response to: function:
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-intestinal cells -in response to food intake -decreases glucose by decreasing gastric emptying, increasing insuline release.
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Tocolitics names: inhibits:
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Nifedipine-calcium channel bocker - inhibits myosin light chain Terbutaline- Beta sympathico mimetic - increases cAMP inhibiting also myosin light chain kinase!
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testicular tumor types
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germ cell tumors (95%) sex cord stroma
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germ cell tumors testicular: risk factors:
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-seminoma and non seminomas - cryptorchidism and klinefelter syndrome
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seminomas: sensibility for radiotherapy?metastasis late or early?prognosis
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- sensible! metastasis late and excelemnt prognosis!
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germ cell tumor ovarian:
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(oocyte)dysgerminomas, (fetal tissue)teratomas and embryonal carcinoma,(placenta tissue)choriocarcinoma, (yolk sac) tumor
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germ cell tumor testicular types
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seminomas (same as dysgerminoma) non seminomas (same as others germ cell ovarian tumors)
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seminoma histology
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malignante tumor comprised of large cells with clear cytoplasm and central nuclei(resemble spermatogonia) and ovarian dysgerminoma!
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non seminomas:
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teratomas,embryonal carcinoma,choriocarcinoma,yolk sac tumor
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testicular tumors:(non seminomas) 1.immature primitive cells,produce glands, forms hemorrhagic mass with necrosis.agressive with early hematogenous spread,chemotherapy may diferentiate in another type of type of germ cell tumor(teratoma); increased AFP or bhCG.
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1.Embryonal carcinoma
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2. most common testicular tumor in children, Shiller duval bodies "glomerulus".AFP elevated!
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2.Yolk sac tumor(endodermal sinus tumor)
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3.b hCG elevated, may lead to hyperthyroidism! or gynecomastia in testicular tumor due:
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in Choriocarcinoma.subunit of bHcG is similar to LH,FSH and THS
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4. malignante in males!Xfemales. AFP or BHcg elevated mature fetal tissue derived from 2/3 layers
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teratoma testicular MALIGNANT!here
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5.prognosis based in the worst component
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micex germ tumor
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sex cord stromal tumors testiculi sex cord stromal tumors ovarian (3!)
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Leydig , sertoli ovarian add Fibroma! (associated pleural effusions and ascitis -Meigs syndrome)
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Reinke crystals characteristic on hystology in testicular tumor called
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Leydig
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most common cause testicular mass males>60 y
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diffuse large B cell Lymphoma!
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high glucocerebrosidase activity due
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accumulation in gauchers disease
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lysosomal storage diseases: deficient enzyme: 1.a-galactosidase A 2.Gluco cerebrosidase 3.Sphingo myelinase 4.hexoaminidase A 5.galacto cerebrosidase 6.Arylsulfatase
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1. Fabry disease 2.Gaucher 3.Niemann pick 4.tay sachs 5.Krabbe 6.metachromatic (leukodystrophy)
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fundoscopic examination shows copper wiring and arteriovenous nicking
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Hypertensive retinopathy
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tumor wich leads to hematuria, flank pain.palpable mass(minority), 4 paraneoplastic syndroms: gene deletion on chromossome:
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RCC renal cell carcinoma. chromosome 3 - EPO,ACTH,PTHrP,prolactin release -rarely with left varicolele due left renal vein invasion.
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RCC risk factors
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smoking! obesity! 50-70y
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dopaminergic pathways
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mesocortical/mesolimbic ( both behavior) nigrostriatal (moviment) tuberoinfundibular (endocrine)
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results of dopaminergic pathway inhibition:
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mesocortical:increase negative symptoms mesolimbic: decrease positive symptoms of schizophrenia nigrostriatal: parkinson symptoms tuberoinfundibular: higher prolactin secretion
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A partial agonist at dopamine D(2) receptors therefore offers an attractive option for the treatment of schizophrenia. why? which drug is?
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aririprazole -act as a functional antagonist in the mesolimbic dopamine pathway, where excessive dopamine activity is thought to cause positive symptoms, -but show functional agonist activity in the mesocortical pathway, where reduced dopamine activity is thought to be associated with negative symptoms and cognitive impairment. - In addition, it should avoid the complete blockade of the nigrostriatal or tuberoinfundibular pathways, associated with extrapyramidal symptoms (EPS) and elevated prolactin levels, respectively.
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aririprazole
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partial agonist activity at D(2) receptors and serotonin 5-HT(1A) receptors, and antagonist activity 5-HT(2A) recepto.
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aririprazole againt haloperidol
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showing a low liability for EPS and hyperprolactinemia, a lack of QTc prolongation, and minimal weight gain or sedation.
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drug for roundworms: 1.intestinal 2.tissue
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bendazoles! intestinal!
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roundworms intestinal 5
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EAT SAN Enterobius Ascaris Trichinella Strongyloides (and ivermectin) Ancylostoma duodenale,Necator (and pyrantel pamoate)
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how BPH may cause confusion?
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uremia
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budding reprodution: 1.broad base budding (same size as RBC)
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blastomycosis (systemic)
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2.multiple budding yeast with captains´s wheel formation (much larger than RBC)
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paracoco (systemic)
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3.budding yeast at 20C and pseudohyphae
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candida (oportunistic).germ tubes at 37C
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4. inequal Round or oval budding of yeast
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cryptococcus (oportunistic)
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cryptococcus stains 1.mucicarmine colour 2.methenamine 3.India ink
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1.red capsule 2.stain tissue 3.wide capsular halos
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endospore formation
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coccidioides imitis spores are formed by fragmentation of hyphae(mold form 25C)(multicelular)(mycelia )(artroconidio), once inside lung (body temperature 37C) they become spherules that contains endospores which disseminate in organs
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action of hydroxylurea in SCD
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increase HbF
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how eithroblastosis fetalis occurs (FC and Fab portions of antibodies)
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anti Rh antibodies, i,e Anti D-IgG antibodies. These then cross the placenta. The Fab portion of this antibody (which is the antigen binding site)goes and attaches to the fetal Rh positive cells. The fetal splenic macrophages then go and attach to the Fc portion of the maternal antibody and phagocytose the RBCs leading to anemia.
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In a patient with chronic peripheral neuropathy, enzyme histochemical staining of a muscle biopsy shows fiber grouping. whats cause this finding?
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Reinnervation takes place in the chronic neuropathies......type grouping is a feature of reinnervation .
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the most common changes in dennervation are
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atrophic muscle fibers and fiber grouping.
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What is type grouping?
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-muscle has type I and II fibers .normally arrange like Checkerboard" pattern of type I (Light) and II (Dark) fibers -in type grouping Type I and type II muscle fibers are clustered in large groups (Type I together and Type II together )...
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reflex grading
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Grade Description 0 Absent 1+ or + Hypoactive 2+ or ++ "Normal" 3+ or +++ Hyperactive without clonus 4+ or ++++ Hyperactive with clonus
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fracture at neck of fibula injuries which nerve?
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common peroneal nerve
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1.year history of progressive ringing in her right ear 2.dizzy while exercising. Neurologic examination shows dysmetria of the right upper and lower extremities 3.Audiometry shows moderate hearing loss in the right ear An MRI of the brain is most likely to show a mass compressing which of the following labeled structures in the photograph of a cross section of the brain stem?name the disease??
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- its an ipsilateral lesion as you know cerebellar signs are ipsilateral - The right side of the pt.is affected. - the inferior cerebellar peduncle is associated with schwannoma and VIII
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acoustic neuroma.The tumor mass of Rt. vestibulocochlear nerve will compress cerebellopontine angle if it's large enough where there in which peduncle?
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inferior cerebellar peduncle
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substitution of an alanine residue for the serine residue normally present on position 127 in the enzyme, this mutation is most likely to reduce the activity of the enzyme by preventing which of the following:
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- phosphorylation of serine residues in cytoplasmic enzymes (EX: Glycogen phosphorylase) so here mutation has replaced serine with alanine so no serine no phosphorylation no activation of that enzyme. - serine is usually the phosphorylation site for lots of signaling pathway. like MAPK
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C difficile DX
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Stool assay for toxin
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how helmet can worse acne
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due hypoxia inducible factor leading to growing og anaerobic propineobacterium
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7 days newborn with swelling of the eyelids and copious purulent eye discharge bilaterally. Giemsa stain shows blue-stained intracytoplasmic inclusions. Culture grows no pathogens. What is the most likely infectious agent?
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Ophthalmia neonatorum (MCC is Chlamydia trachomatis)
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bone pain with hypercalcemia (neoplastic cells activate RANK receptor on osteoclasts leading to bone destruction (vertebra,skull)); increased risk of infection due monoclonal antibody; rouleaux formation primry AL amyloidosis; proteinuria of freelight chains! risk kidney failure
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multiple myeloma
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increased serum protein with M spike, other features of MM absent! we call:
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Monoclonal gammopathy of undertemined significance(1% become MM)in elderly
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B cell Lymphoma with monoclonal IgM production (M spike! also)call:
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Waldenstrom macroglobulinemia
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Waldenstrom macroglobulinemia features:
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-generalized lymphadenopathy but absent lytic bone lesions - visual and neurologic deficits (IgM large pentamer!-;viscosity) bleeding due defective PTL aggregation due viscosity! treat? plasmapheresis
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which kind of mediated immune response we have against C.pnumoniae? cell or humoral??
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this agent is an obligate intracellular infectious agent, and the kind of immunity agaist this type of infections is cell mediated immunity, and to be more specific CD8+ T cytotoxic cell.
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nervous system responsible to erection ejaculation
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erection: parasymp ejaculation: sympathetic if nervous loose erection, ejaculate early! give paroxetin!
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Ondasetron action
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is a serotonin 5-HT3 receptor antagonist used mainly as an antiemetic (to treat nausea and vomiting), often following chemotherapy. It affects both peripheral and central nerves. Ondansetron reduces the activity of the vagus nerve, which deactivates the vomiting center in the medulla oblongata, and also blocks serotonin receptors in the chemoreceptor trigger zone. It has little effect on vomiting caused by motion sickness,
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IL-10 and TGF beta X inhibit NF-kB (as coricosteroid)
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Inhibition of NF KB inhibit cytokines release IL10 and TGF B it will decrease inflammatory response response
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splitting defense is commonly associated in which type of personality disorder?
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bordeline
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fasting: Gluconeogenisis enzymes increases, Glycolysis enzymes decrease. how is gonna be Fructose 2,6 bisphosphate.
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Fructose 2,6 Bisphosphate should be low to keep PFK1 low
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splice site mutation leads to correct splicing.How? which disease example?
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have to look at a point of exon intron binding 5'GU splice donor site 3'AG acceptor site -B thalassemia!
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Causes of thrombocytopenia in cirrhosis
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Portal hypertension-induced splenic sequestration Alterations in thrombopoietin Bone marrow suppression mediated by toxins (eg, alcohol, hepatitis B and C) Consumptive coaguloapathy (eg, low-grade disseminated intravascular coagulation, acquired intravascular coagulation and fibrinolysis) Increased blood loss (eg, hemorrhage)
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organism cause painful ulcer in penis. culture with chocolate agar grows a small, oxidase positive,G-,bacillus that expresses b-lactamase.
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Haemophilus ducrey
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bacteria (4) exotoxins with inhibit ptn synthesis:
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Corynebacterium Diphtheriae Pseudomonas aeroginosa Shigella spp EHE
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toxins and actions of: Corynebacterium Diphtheriae Pseudomonas aeroginosa Shigella spp EHE
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diph toxin Exotoxin A both inactivate EF-2 shiga toxin Shiga like Toxin both inactivate 60S ribosome by removing ADENINE from rRNA.
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toxin which enhance cytokine release, causing Hemolytic uremic syndrome (HUS)
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ST SLT
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mucosal damage by invasion of bacteria(dysentery) X does not invade!
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shigella X EHEC
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toxin which enhance cytokine release, causing Hemolytic uremic syndrome (HUS)
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ST SLT by serotype 157:H7
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bacteria (3) exotoxins which increase fluid secretion: (EBV) watery diarrhea!
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ETEC (2) Bacillus anthacis (edema border) V.cholerae
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ETEC 2 types
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Heat Labile Toxin(LT) (overactivate adenilate cyclase (increase cAMP)by activating Gs -; high Cl secretion in gut and h2O efflux heat stable Toxin(ST) (overactivate cGMP)-;less reabsorption of NaCl/H2O in Gut
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name of B.anthracis toxin
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Edema toxin
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Edema toxin does:
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mimics adenylate cyclase
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cholera toxin does:
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=LT
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bacteria exotoxin which inhibit phagocytic ability (1) perimiting survival of microbe
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similar to LT, overactivating adenylate cyclase (increase cAMP) but DISABLING Gi!!
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bacteria exotoxins which inhibit release of neurotransmitter (2)
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Clostridium tetani C.Bolulinum
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actions of Clostridium T and B olulinum:
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proteases that cleave SNARE, set of ptn required for neurotransmitter release via vesicular fusion.
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spastic paralysis,ridus sardonicus,lockjaw! toxin prevent release of:
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release of inhibitory (GABA and GLYCINE) neurotransmiter from renshaw cells in spinal cord (tetani)
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Flaccid paralysis,floppy baby, toxin prevents release of:
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stimulatory ACH signals at neuromuscular junctions!-;flaccid paralysis.
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AB toxins bacteria
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all! 2 component of toxins (and 3 for anthrax)
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B component is responsible for
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BBinding!!and triggering uptake (endocytosis)
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A component of toxin responsible for
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active function! are ADp ribosyltransferases with enzymatic activities described before.
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bacteria with exotoxin lyse cell membranes (2)
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Clostridium also Perfringens! Streptococcus pyogenes
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toxin with lyse cell membranes from clostridium
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Phospholipase (lecithinase) that degrades tissue and cell membranes. Degradation of phospholipids leads to myonecrosis (gas gangrenbe) and hemolysis (double zone of hemolysis on blood agar).
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toxin with lyse cell membranes from Strep Pyogenes
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Streptolysin O lyses RBCs,contributing to B hemolysis (total). host antibodies agains this toxin called ASO (used to DXrheumatic fever)
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bacterias with exotoxin acting as superantigens causing shock!
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Staphylococcus aureus Strep pyogenes (again)
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superantigens (exotoxins) of Staphylococcus aureus Strep pyogenes (again) mechanism of action:
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binds to MHC II and TCR outside of antigen binding site to cause overwhelming release of IL1,2 and INF gamma and TNF alpha-;shock!
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manifestation of exotoxins (superantigens) in S aureus and Pyogenes:
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TOXIC SHOCK syndrome: fever/rash,shock
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others exotoxins of S. Aureus:
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Exfoliative toxin (scalded skin syndrome) enterotoxin (food poisoning)
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endotoxin 3 main effects:
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-macrophage activation-;Il1/6-fever ;TNF alpha fever/hypotension;nitric oxide: hypo tension also -complement activation (C3a/C5a) -tissue factor activation-;DIC
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CATCH Individuals with a 22q11.2 deletion
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Cardiac abnormality (particularly conotruncal malformations : interrupted aortic arch/ truncus arteriosus and tetralogy of Fallot) Abnormal facies Thymic aplasia (immunodef) Cleft palate Hypocalcemia/Hypoparathyroidism
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substance that increase release of dopamine in the nucleus accumbens
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nicotine
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how is gonna be the parathyropid hormone in end stage renal disease?
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high, due low excretion of phosphate!stibulates PTH secretion!
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where glycosilation of ptns to be exported occurs?
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inside RER
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cells with densely basophilic granules with histamine and heparine originating from the same precursor cell:
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basophils and mast cells!
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besides heparin and histamin, synthesize and release on demand leukotrienes (SRSA)
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Basophils
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SRSA
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slow reacting substance od anaphylaxis is a mixture of leukotrienes that cause amage to epithelial cells
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highly phagocytic for antigen-antibody complexes produces histaminase major basic protein
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eosinophil
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eosinophilia canadaP
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Collagen vascular disease(panmdermatomyositis) Atopic diseases (allergy,asthma,churg strauss,allergic broncopulmonary aspergilosis0 neoplasms Adrenal insufficiency(addison) drugs(NSADS,penicillin,cephalo) acute interstitial nephritis parasitis (strongyloides,ascaris-;Loeffler eosinophilic pneumonitis)
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major basic ptn causes damage to parasites but also to:
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epithelial cells(host celldamage)--> bronchial epithelial cells in patients with atopic asthma.
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anti IgE monoclonal antibody called:
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Omalizumab
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Omazilumab action
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binds to IgEinhibiting its action of IgE receptor on mas cells and basophils decreasing alergic response
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patient with heavy mestrual blleding,intermittent gingival hemorrhages,multiple bruises. peripheral blod smear: mormochromic normocytic erythrocytes without anisopoikilocytosis. bone marrow aspirate: increased megacariocytes
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ITP!
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LOW platelet only think 2 diseases:
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ITP/TTP with high BT obs:rare Bernard soulier may be low also!Large PTL with lor Gp1b
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TTP is thrombotic disease due:
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overactivation of PTL-;trmbosis-;thrombocytopenia leading to symptoms! (HUS)+neuro,fever symptoms
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TTP due to deficiency of
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ADAM13 (vWF metalloprotease)-;low degradation of vWF multimers)
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TTP lab differentiation from ITP
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schistocytes,high LDH X increased megacariocytes in bone marrow of ITP
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defect in Gpiib/IIIa disease
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Glanzmann thrombastenia
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anti Gpiib/IIIa antibodies disease
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Immune thrombocytopenia! with splenic macrophage consumption of platelet antibody complex.commonly after VIRAl illness
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treat difference TTP X ITP both corticosteroids but:
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TTP:plasmaferesis ITP:immunoglobulin
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abnormal behavior during the sleep phase with rapid eye movement (REM) sleep
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Rapid eye movement sleep behavior disorder (RBD) is a sleep disorder (more specifically a parasomnia)
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only abnormal feature of RBD is
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loss of muscle atonia (i.e., the loss of paralysis) during otherwise intact REM sleep (during which paralysis is not only normal but necessary). REM sleep is the stage of sleep in which most vivid dreaming occurs. The loss of motor inhibition leads to a wide spectrum of behavioral release during sleep. This extends from simple limb twitches to more complex integrated movement, in which sufferers appear to be unconsciously acting out their dreams. These behaviors can be violent in nature and in some cases will result in injury to either the patient or their bed partner.
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gens for the following 5 bacterial toxins are encoded in a lysogenic phage: ABCDE
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A shigA like Toxin Botulinum Cholerae Diphteria Erythrogenic toxin of Strep pyogenes
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ability to take up naked DNA(from lysis cells) from environment and incorporate to its own DNA but do not pass to progenity. we call this process as: used by:
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transformation SHiN S;pneumo,H.Flu B,neisseria
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which bacteria use transfer of plasmid (containing genes) for sex pilus and conjugation
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E.coli
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small segments of DNA (transposons) that can carry ATB resistance or virulence factors can jump (self excise and relocate) from one location to another(from plasmid to chromossome,vice versa) in a process by:
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transposition obs:when excision occur may iclude some flanking chromossomal DNA,which can be incorporated into plasmid and transferred to another bacteria via conjugation (eg: van A gene from vancomycin resistant enterococcus to S.aureus- a conjugative transposon)
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fungal cell structure
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cell wall cell membrane nucleus
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antifungal therapy: 1. cell wall 2. cell membrane: (3) 3. Nucleic acid sinthesis
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1. echinocandins:caspo/micafungins 2.lanosterol synthesis : terbinafine ergosterol synthesis: Azoles cell ergosterol membrane pores: AmphoB/Nystatin 3.Flucytosine (with ampho!) to penetrate!
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UTI G- pek G+ es
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G-E.coli 80%!!!, proteus,Klebsiela G+ enterococcus faecalis Staphilo saprophyticus 2 most common cause!
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muscle spindle control function:
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monitor muscle length
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muscle spindle fibers. 2 types:
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- extrafusal muscle fibers: functional unit of muscle -intrafusal fibers: regulate length
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how intrafusal fibers work?
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when muscle is streched, fiber is streched also,stimulating Ia afferent-;dorsal horn-;alpha motor neuron causing reflex muscle contraction. help you pick up a heavy case
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how golgi tendons work?
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monitor tension rather than length provide inhibitory Ib!afferent feedback! -cue you to drop a heavy suitcase
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but who regulates the sensivity of reflex??
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GAMMA LOOP from CNS-;the gamma motor neuron-;contracts intrafusal fiber-;decreases sensitivity of reflex
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patient without superior control leads to higher reflexes, spasticity! what we can do to reduce spasticity.drug!
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activation of GABA receptors in muscle spindle afferents. baclofene!
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sinovial fluid rheumatoid arthritis: complement,neutrophils,IL1,TNF
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only low complement!
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at fasting 2 year age patient has hypoglycemia, ketonemia,lactic acidosis,hypercholesterolemia disease?
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Von Gierge disease deficincy of Glucose 6 phosphatase
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if RBC deficient in Carbonic anhydrase leads to increased venous blood level of which ion?
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cloride due impaired shift
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Most individuals appear normal at birth. If newborn screening fails, progressive developmental delay is the most common presentation. Other findings in untreated children in later infancy and childhood may include vomiting, musty/mousy odor, eczema, seizures, self-mutilation, and severe behavioral disorders. Older individuals who cease dietary treatment in childhood may have evidence of demyelination on MRI. Occasionally, deterioration of cognitive performance or motor skills also may be present. Intelligence quotients (IQs) may drop by 10 points or more if the diet is stopped in midchildhood.
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phenylketonuria (PKU)
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Older individuals who cease dietary treatment in childhood may have evidence of demyelination on MRI. Occasionally, deterioration of cognitive performance or motor skills also may be present. Intelligence quotients (IQs) may drop by 10 points or more if the diet is stopped in midchildhood.
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phenylketonuria (PKU)
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what does lyonization means?
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X-inactivation (also called lyonization) is a process by which one of the copies of the X chromosome present in female mammals is inactivated