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Most modern theorists also accept Williams’ ideas: the evolutionary disadvantage of aging must be effectively zero; aging must convey an evolutionary advantage that compensates for its individual disadvantage; therefore aging must be linked to symptoms viral infection buy cheap bimat 3ml online an individually advantageous trait or traits symptoms 7 days post iui order bimat 3 ml with visa. This evolutionary mechanics concept leads to medications an 627 cheap bimat 3 ml with amex the conclusion that programmed aging can only exist in special circumstances medicine sans frontiers order bimat 3 ml overnight delivery. Modern programmed aging theories are based on more recent mechanics theories to the effect that non-individual benefit can offset individual disadvantage and lead to the conclusion that purposely limited lifespan has a general evolutionary benefit specifically including mammals. Programmed aging theories suggest that the mechanisms responsible for diverse agerelated diseases and conditions such as cancer and heart disease have common elements. Pharmaceutical agents can therefore be sought that alter these common elements and result in simultaneously delaying or ameliorating multiple agerelated diseases and conditions. Regulated programmed aging theories even more strongly suggest commonality and suggest existence of sensing and signaling mechanisms that offer additional targets for intervention. Non-programmed theories suggest that aging is the result of deficiencies in a potentially large number of independent maintenance and repair mechanisms and that therefore there is little or no commonality between mechanisms responsible for the different age-related diseases and conditions. Medical research efforts consequently should be directed toward each disease or condition separately. Williams) consider anti-aging medicine to be theoretically impossible based on their non-programmed theories. Special Journal Issue – Programmed vs Non-programmed Aging 2009 In December 2008, eighteen scientists active in the field of biological aging theory received an interesting invitation. Other commonly used ways of stating this same question: Is aging an adaptation in that the deteriorative effects serve some purpose and therefore are the result of evolved organism design featuresfi Is aging the result of an active, pro-aging mechanism in the organism’s design or is aging entirely the passive result of forces acting upon the organismfi Does an organism’s design fight aging, cause (or purposely allow) aging, or do both at different times in the organism’s life (as proposed here)fi Scientists representing both sides of the “programmed” argument were invited to participate in the project. I submitted a pro-programmed article titled the Case for Programmed Mammal Aging[48] in response to the invitation. Because the special issue is read by a diverse audience the article avoided arcane terminology and included substantial background material. The request specified rather long articles and the journal is published in both Russian and English. This could provide major impetus toward finally resolving an issue with potentially major medical and public health implications. Homo Sapiens Liberatus Workshop, Moscow 2010 In May 2010, a workshop titled Homo Sapiens Liberatus was conducted at Moscow State University. One of the assigned tasks of this workshop was to develop arguments regarding the evolutionary mechanics whereby an individually-adverse organism design characteristic having 164 the Evolution of Aging a non-individual benefit. I presented two arguments, either of which, if correct, would support various programmed aging theories[49]: the linkage argument suggests that linkage between an individually beneficial trait and an individually adverse trait could protect the individually adverse trait from being selected out. Williams in support of his 1957 antagonistic pleiotropy theory of (non-programmed) aging. The argument was now made that linkage works better for programmed aging because it only has to withstand the evolutionary process (acting to separate benefit from adverse side effect) for a relatively short time as opposed to indefinitely in the case of Williams’ proposal. This linkage allows a long-term group benefit to trade off against a short-term individual cost and supports group selection and evolvability considered as a group benefit. According to a sort of beneficiary or cui bono analysis, evolvability traits benefit the group, species, or even future species and therefore opponents conflate an evolvability benefit with long-term group benefit and some use the same arguments they historically used against group selection. The evolvability argument suggests that the propagation mechanics of evolvability are completely different from group selection. Where group selection is trading a future group benefit against a current individual disadvantage, an evolvability trait contributes to a precondition that is necessary for the evolution process to operate and consequently is effective on the same time-scale as natural selection. Therefore an evolvability benefit can trade off against an individual disadvantage. I have not seen specific counter-arguments against either of these arguments, either of which support generally applicable programmed aging. Programmed Aging in 2011 Tom Kirkwood, author of the 1975 non-programmed disposable soma theory, is predictably a vocal opponent of programmed aging theories. By 2011, programmed theories of aging had acquired a significant following in the scientific community and Kirkwood felt a need to make formal arguments against programmed aging as opposed to merely denouncing such theories without any scientific rationale for doing so. In 2011, Kirkwood published a paper On the programmed/ non-programmed nature of aging within the life history[50] (with Simon Melov) attacking programmed aging theories and their authors and citing papers written by me and V. Their paper makes the case that mammal programmed aging is not supported by traditional individual-benefit-only evolutionary mechanics theory, a position that most adaptive programmed aging proponents already concede. Although it notes the existence of group and evolvability (non-individual benefit) theories it makes no specific arguments against them and even concedes they could be applicable in certain circumstances. Nor does it make arguments against any of the specific mammal programmed aging theories based on group selection or evolvability. Even more favorably, their paper concludes that, considering only individual benefit, the net evolutionary disadvantage of aging must be “effectively zero” beyond some species165 the Evolution of Aging specific age. They have therefore set up a situation in which they have to argue that the evolutionary advantage of limiting life beyond that critical age cannot even minutely exceed the zero disadvantage of death and result in the evolution of a lifespan limiting mechanism, a very difficult case that they do not even attempt to make. Instead, they contend that interpretation of empirical evidence should be biased in favor of nonprogrammed aging because of their evolutionary mechanics concepts. I wrote a paper On the programmed/ non-programmed aging controversy[51] responding to the Kirkwood-Melov paper. Vladimir Skulachev also published a responding paper Aging as a particular case of phenoptosis, the programmed death of an organism (A response to Kirkwood and Melov "On the programmed/non-programmed nature of ageing within the life history")[52]. Proponents of programmed aging considered this exchange a definitive “win” for their side. Serious students of aging theory should read these three papers and also see Aging by Design[53] for a longer discussion of this exchange. Biochemistry (Moscow) Phenoptosis Vladimir Skulachev has initiated publication of a journal dedicated to aging and especially programmed aging called Phenoptosis as a periodic special issue of the existing journal Biochemistry (Moscow) published in English and Russian. Phenoptosis means programmed organism death as an extension of the term apoptosis or programmed cell death. Recent Scientific Opposition to Programmed Aging Theories “The way evolution works makes it impossible for us to possess genes that are specifically designed to cause physiological decline with age or to control how long we live. In recent years, I have had extensive interactions with many, sometimes very senior, proponents of passive, non-adaptive, non-programmed aging theories. Here are the four main lines of reasoning they presented as supporting their view that aging in humans is the result of passive non-programmed aging. I have not used their names because the following position statements are composites of several scientists with similar positions and/or contain material from private communications. Evolution makes it impossible: Scientist “A” accepts and promotes the view quoted above to the effect that orthodox evolutionary mechanics theory makes active programmed aging “impossible” regardless of any amount of purported supporting observational evidence. He suggests that as a very outspoken and longtime proponent of passive aging, he would have to reconsider his position only if and when a single new programmed-aging-compatible evolutionary mechanics theory was to become “generally accepted. In the meantime he suggests that I am trying to single-handedly overthrow 150 years of scientific 166 the Evolution of Aging tradition. He ostentatiously ignores the existence of the other programmed aging proponents as well as all those having issues with orthodox mechanics and multiple published non-individual mechanics theories. He further suggests that I might be some sort of closet Intelligent Design proponent merely for voicing any uncertainty regarding the absolute truth of orthodox evolutionary mechanics! They ignore both observational evidence and developments that affect evolutionary mechanics theory. Some merely ignore proponents of programmed theories in the hope (so far futile) that they will eventually go away. Others write articles criticizing programmed aging theorists based on the given that evolution makes it impossible. For “A” to change his mind on aging would be like an Episcopal bishop deciding to start over as an entry-level Methodist seminarian. People who believe that it is impossible that orthodox mechanics theory could be less than perfectly comprehensive will also understandably believe extremely improbable orthodox explanations for apparently conflicting observations. Evolution makes it functionally impossible: Scientist “B” accepts that there are issues with evolvability, group selection, and so forth that affect evolution theory on some intellectual level but contends that it is functionally impossible for these factors to affect evolved mammal aging mechanisms.

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Information about the child’s educational abilities and extracurricular activities need to symptoms diagnosis buy 3ml bimat amex be available to medications grapefruit interacts with buy discount bimat 3ml line the child’s welfare caseworker and caregivers in order to medications narcolepsy buy generic bimat 3ml on-line ensure some feeling of continuity medicine ubrania generic 3ml bimat with visa, predictability, and access to esteem-building activities. The therapist may need to negotiate with the child welfare caseworker to have a psychiatric evaluation conducted if the child’s emotional state or behavior warrants medication or hospitalization, a psychological evaluation if additional diagnostic information is necessary, or a medical evaluation if any physical problems seem to interfere with the child’s stability and well-being. The child welfare caseworker should always be notified if the child is a danger to self or others. Any suicidal or homicidal ideation or plans need to be passed on to the child welfare caseworker who has responsibility for the child. However, in such instances, the therapist has responsibility for facilitating hospitalization of the child (when appropriate) and for continuing involvement in the case. Visitation the therapist is often asked to make recommendations regarding visitation with noncustodial parents or caretakers. The child’s concerns regarding safety and protection, feelings about the parent and the visits, and the child’s interest and willingness to interact with the parent seeking visitation need to be considered. Again, a multidisciplinary approach that elicits information from the parents, the parents’ attorneys, the parents’ advocate or therapist if possible, and the child welfare agency is important. Reunification When reunification with the parents is a consideration, the therapist needs to be in close contact with the child welfare caseworker in order to relay information about the child’s progress in treatment and to gain information to help prepare the child for changes in visitation or living arrangements. Recommendations regarding reunification, including information about the child’s ability to trust the parent and feel safe and protected, need to be relayed to the child welfare caseworker. The therapist should advocate for appropriate departure from the foster home and a reasonable transition to termination of child welfare services. During these sessions, the course of events can be reviewed, changes discussed, and parental responsibility verbalized and processed. The sessions also offer a forum for the child to share his/her concerns and for the parents to make a commitment to protect the child from further harm. It is often useful to continue the child’s therapy through the reunification process in order for the child to have a place to discuss adjustment to living with his/her family again and explore solutions to any problems that may arise. Law Enforcement When the child is involved in a criminal investigation, it is often helpful to advocate for timely and sensitive intervention with law enforcement personnel. The therapist can help the child feel comfortable about the interview by providing some pertinent details about the experience. Providing the officer’s name and time of visit can help the child feel the officer is a somewhat familiar figure. Identifying the officer as a friend and a person who helps children can also ease some of the child’s discomfort. Educating officers regarding developmental considerations, including the use of language, skills that facilitate memory and recall, as well as personal skills that help the child feel comfortable and safe are important. For more information on the law enforcement officer’s role, the interested reader is referred to the Role of Law Enforcement in the Response to Child Abuse and Neglect, another manual in this series. Prosecution Testifying in criminal court can be such a stressful experience that it keeps the child focused on the outcome of the criminal proceeding and deters resolution of the issues related to the abuse or neglect. Schetky and Green 222 note that the fears expressed by child witnesses include: fi the fear of retaliation by the defendant, particularly if the defendant has made threats to the child in the past; fi the fear that he/she will not be believed; fi feeling as if he/she (the child) is on trial, often reinforced by aggressive cross-examination, or guilt if the child blames him/herself for what happened; and fi humiliation and embarrassment from the nature of questions asked and the presence of the jury and press. The child and family need to develop coping responses that ameliorate these fears. The therapist can help the family remain realistic about the criminal proceedings and can prepare them for the possible outcomes. Praising the child’s effort, without emphasizing the content or outcome of the criminal court proceedings, can enhance the child’s self-esteem and positive feelings about the experience. The therapist may need to advocate with the attorney prosecuting the case for the child who is expected to participate in a criminal proceeding. For a description of preparing a child for testifying in court, the reader is referred to another manual in this series entitled Working With the Courts in Child Protection. Clinicians must develop, organize, and use all the resources available to help children. Parents and family members, school, law enforcement, and child welfare personnel are all striving to protect children from trauma generated by abuse and neglect. A comprehensive and cooperative effort that builds on the skills and services in the community will improve the condition of abused and neglected children. Kazdin, “Developmental Psychopathology: Current Research, Issues, and Directions,” American Psychologist 44(1989):180-187. James, Psychology (New York: Fawcett, 1963 [Original work published in 1892]); and C. Jewett, Helping Children Cope with Separation and Loss (Boston: the Harvard Common Press, 1982). Kegan, the Evolving Self: Problems and Process in Human Development (Boston: Harvard University Press, 1982). Garbarino, Children and Families in the Social Environment (New York: Aldine Publishing Company, 1982). Crittenden, “Abusing, Neglecting, Problematic, and Adequate Dyads: Differentiating By Patterns of Interactions,” Merrill-Palmer Quarterly 27(1981):1-18. Helfer, “The Developmental Basis of Child Abuse and Neglect: An Epidemiological Approach,” in R. Galdston, “Violence Begins at Home: the Parents Center for the Study and Prevention of Child Abuse,” Journal of the American Academy of Child Psychiatry 10(1971):336-350. Green, “Psychiatric Treatment of Abused Children,” Journal of American Academy of Child Psychiatry 17(1978):356-371. Sheaff, “Neurological Manifestations of the Battered Child Syn-drome,” Pediatrics 45(1970):1003-1007. Caffey, “On the Theory and Practice of Shaking Infants: Its Potential Residual Affects of Permanent Brain Damage and Mental Retardation,” American Journal of Diseases of Childhood 124(1972): 161-169. Gregg, “Developmental Characteristics of Abused Children,” Pediatrics 40(1967): 596602. Martin, the Abused Child: A Multidisciplinary Approach to Developmental Issues and Treatment. Ryan, “Victim to Victimizer: Rethinking Victim Treatment,” Journal of Interpersonal Violence 4(1989):325-341. Russell, the Politics of Rape: the Victims Perspective (New York: Stein and Day, 1975). Gutierres, “Escape/Aggression Incidence in Sexually Abused Juvenile Delin quents,” Criminal Justice and Behavior 6(1979):239-243. Courtois, “The Incest Experience and Its Aftermath,” Victimology: An International Journal 4(1979):337-347. Meiselman, Incest: A Psychological Study of Causes and Effects With Treatment Recommendations (San Francisco: Jossey Bass, 1979). Canavan, “Sexual Abuse of Boys,” American Journal of Diseases in Children 134(1980):255-257. Sgroi, “Kids with Clap: Gonorrhea as an Indicator of Child Sexual Assault,” Victimology: An International Journal 2(1977):251-267. American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, 3rd ed. Beilke, “Behavior Problems in Sexually Abused Young Children,” Journal of Pediatric Psychology 11(1986):47-57. Tufts New England Center, “Sexually Exploited Children: Service and Research Project. Luecke, “Young School-Age Sexually Aggressive Children,” Professional Psychology: Research and Practice 19(1988):155-164. Conger, “Family Interaction Patterns Related to Child Abuse and Neglect: Preliminary Findings,” Child Abuse and Neglect 1(1977): 269-277. Norberta, “Sexual Disturbance in Young Children,” the American Journal of Maternal Child Nursing (May-June 1976):187-194. Groth, “Sexual Trauma in the Life Histories of Rapists and Child Molesters,” Victimology: An International Journal 4(1979):10-16. Lanyon, “Theory and Treatment of Child Molestation,” Journal of Consulting and Clinical Psychology 54(1986):176-182. Friedrich, Urquiza, and Beilke, “Behavior Problems in Sexually Abused Young Children. Urquiza, “Behavior Problems in Young Sexually Abused Boys,” Journal of Interpersonal Violence 3(1988):1-12. Beilke, “Children from Sexually Abusive Families: A Behavioral Comparison,” Journal of Interpersonal Violence 2(1987):391-402. Tufts’ New England Medical Center, “Sexually Exploited Children: Service and Research Project.

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The relationship of the extra Y to treatment shingles cheap bimat 3ml with mastercard behavior is controversial symptoms hypoglycemia generic bimat 3 ml on line, but these individuals do have problems with motor and language development medicine jar order bimat 3 ml on line. Multi-X females are normal medicine vial caps purchase bimat 3ml on-line, except there is an increased tendency toward mental retardation that is proportional to the number of X chromosomes that are present. Ductal sex depends on the presence of derivatives of the Mullerian or Wolffian ducts. True hermaphroditism refers to the presence of both ovarian and testicular tissue. Female pseudohermaphroditism results from excessive exposure General Pathology Answers 123 to androgens during early gestation; most often this is the result of congenital adrenal hyperplasia. Male pseudohermaphroditism results from defective virilization of the male embryo, most commonly caused by complete androgen insensitivity syndrome, also called testicular feminization. Kallmann’s syndrome results from a lack of embryonic migration of cells from the olfactory bulb to the hypothalamus and is characterized by primary amenorrhea, lack of secondary sex characteristics, and decreased sense of smell (hyposmia). Mixed gonadal dysgenesis consists of one well-defined testis and a contralateral streak ovary. The first definable stage of B cell maturation occurs as the cell begins the process of producing immunoglobulin (Ig). The heavy chain genes, which are located on chromosome 14, are first rearranged, but because this occurs before the rearrangement of the light chain genes, complete immunoglobulin is not yet expressed on the cell surface. Instead µ heavy chain genes are rearranged first, and are found within the cytoplasm. If something goes wrong in this process, then the fi light chain genes on chromosome 22 are rearranged; otherwise they stay in their germline configuration. The synthesized light chains then combine with the intracytoplasmic µ heavy chains to form complete IgM, which is then transported to the surface, forming surface IgM (sIgM). Next these developing B cells produce IgD, which is also expressed on the cell surface (sIgD). They 124 Pathology are also called “virgin” B cells because these cells have not encountered any foreign antigen. Before B cells become plasma cells, there may be a class switch (isotype switch) to a particular surface immunoglobulin that the plasma cell will then secrete. This activation occurs within germinal centers, where morphologically B cells are classified as being small cleaved lymphocytes, large cleaved lymphocytes, small noncleaved lymphocytes (with prominent nucleoli), or large noncleaved lymphocytes (with prominent nucleoli). Prior to forming plasma cells, these activated B lymphocytes are called B immunoblasts. In contrast, memory B lymphocytes, which histologically look like unremarkable small lymphocytes, have surface immunoglobulin of the IgG, IgA, or IgE type. Igs are composed of light chains and heavy chains, each of which are composed of a variable region and a constant region. The variable regions of both of these chains form the antigenbinding region of Ig, which is called the Fab portion. Not only can the Fc portion of Ig bind to complement, but it can bind to cells that have Fc receptors. The two light chains are the fi chain, the genes of which are located on chromosome 2, and the fi chain, the genes of which are located on chromosome 22. The heavy chains are M, D, A, E, and G, the genes of all of these being on chromosome 14. The combination of one type of light chain with a particular heavy chain forms each of the five types of immunoglobulin. It is secreted in the second response to certain antigens, but it does not predominate early during the first response. IgG can cross the placenta, and it is the major protective immunoglobulin in the neonate. IgM, which conGeneral Pathology Answers 125 stitutes about 5 to 10% of the Ig in the serum, is secreted in the first exposure to antigen (primary immune response). The monomeric form of IgM is found on the surface of some B cells, while the pentameric form is found in the serum and cannot cross the placenta. IgD, which forms less than 1% of serum Ig, is found on the cell surface of some B cells and functions in the activation of these B cells. IgE, also known as reaginic antibody, is found on the plasma membrane of mast cells and basophils and participates in type I hypersensitivity reactions, such as allergies, asthma, and anaphylaxis. IgA, which constitutes about 10 to 15% of serum Ig, exists as a monomer in the serum and a dimer in glandular secretions. It is secreted as a dimer bound to a secretory piece that stabilizes the molecule against proteolysis. This stage of development occurs prior to the migration of the developing cell to the thymus and is called the prethymus stage. These mature thymocytes, which are single-positive cells, make up about 15% of the thymus thymo126 Pathology cytes. That is, about 40% of peripheral lymphocytes are helper cells and 20% of peripheral lymphocytes are cytotoxic T cells. Products of lymphocytes are called lymphokines, while products of monocytes or macrophages are called monokines. Interferon fi is an antiviral interferon, while interferon fi is an immune interferon. In general these class I molecules bind to proteins synthesized within the cell; one example is the cellular production of viral antigens. Macrophages and neutrophils are active phagocytes and have receptors for the Fc portion of IgG and C3b; both of these substances are important opsonins. Ankylosing spondylitis is one type of spondyloarthropathy that lacks the rheumatoid factor found in rheumatoid arthritis. Other seronegative spondyloarthropathies include Reiter’s syndrome, psoriatic arthritis, and enteropathic arthritis. Ankylosing spondylitis, also known as rheumatoid spondylitis or Marie-Strumpell disease, is a chronic inflammatory disease that primarily affects the sacroiliac joints of adult males. They are classified into four different cat128 Pathology egories based on the immune mechanisms involved. Type I hypersensitivity reactions involve IgE (reaginic) antibodies that have been bound to the surface of mast cells and basophils. This IgE then attaches to mast cells and basophils, because these cells have cell surface receptors for the Fc portion of IgE. When these “armed” mast cells or basophils are reexposed to the allergen, the antigen bridges two IgE molecules and causes mast cells to release preformed (primary) mediators. This antigen-to-antibody binding also causes these cells to synthesize secondary mediators. The reactions that occur as a result of the primary mediators of type I hypersensitivity are rapidly occurring, since the mediators have already been made and are present within the granules of mast cells. These substances include biogenic amines, such as histamine, chemotactic factors, enzymes, and proteoglycans. Histamine causes increased vascular permeability, vasodilation, and bronchial smooth muscle contraction. Mast cells also produce new products (secondary mediators) via a series of reactions within the cell membrane that lead to the generation of lipid mediators and cytokines. Membrane receptors bound to IgE activate phospholipase A2, which then cleaves membrane phospholipids into arachidonic acid. These last three leukotrienes are the most potent vasoactive and spasmogenic agents known. Prostaglandin D2, which is produced via the enzyme cyclooxygenase, is abundant in lung mast cells. Local reactions include urticaria (hives), angioedema, allergic rhinitis (hay fever), conjunctivitis, food allergies, and allergic bronchial asthma. Systemic reactions usually follow parenteral administration of antigen, such as with drug reactions (penicillin) or insect stings. Symptoms include vomiting, cramps, diarrhea, itching, wheezing, and shortness of breath, and death may occur within minutes. Complement-mediated cytotoxicity occurs when IgM or IgG binds to a cell surface antigen with complement activation and consequent cell membrane damage or lysis. Blood transfusion reactions and autoimmune hemolytic anemia are examples of this form. Systemic anaphylaxis is a type I hypersensitivity reaction in which mast cells or basophils that are bound to IgE antibodies are reexposed to an allergen, which leads to a release of vasoactive amines that causes edema and bronchoand vasoconstriction.

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It is characterized by the binding of these antibodies to administering medications 6th edition order bimat 3 ml with mastercard antigens on vascular endothelial cells symptoms hyperthyroidism bimat 3 ml discount. Acute rejection (days-weeks post-transplant) (T cell mediated) involves direct cytotoxicity and cytokine mediated pathways treatment 6th nerve palsy 3ml bimat free shipping. Acute rejection is the most common and the primary target of immunosuppressive agents medicine x xtreme pastillas buy bimat 3ml low cost. Chronic rejection is (>1year post-transplant) has unknown causes, but an acute rejection is a strong predictor. Reference: Robbins Basic Pathology 8th ed page 1207 Q2: What is the pattern of inheritance in polycystic kidney diseasefi A: Autosomal dominant B: Autosomal recessive Answer: A Explanation: the gene involved is in chromosome 17q11. A: Point mutation B: Deletion Answer: A Explanation: a point mutation in the sixth codon of fi-globin that leads to the replacement of a glutamate residue with a valine residue. The abnormal physiochemical properties of the resulting sickle hemoglobin (HbS) causes the disease. B: 4 normal beta chain genes, abnormal 2 alpha chain genes C: 2 abnormal beta chain genes, normal 4 alpha chain genes Answer: C Reference:sickle. A: Tunica Intima B: Tunica media C: Tunica adventitia Answer: C Explanation: Tunica adventitia is the most prominent layer. The macula densa cells, the juxtaglomerular cells (renin secreting), and the extraglomerular mesangium (structural support). A: Alveolar phase B: Calanicular phase C: Saccular phase Answer: C Explanation: In the third trimester, sacs form at the level of terminal bronchioli, and the septa between them develops capillary networks to connect them with blood vessels Reference. A: Follicular cells of the thyroid gland B: Parafollicular cells of the thyroid gland (C cells) Answer: B Reference: en. A: duodenum B: jejunum C: ileum D: esophagus Answer: D Reference: histologyolm. A: melanocytes B: Somatotrophs C: Corticotrophs Answer: A Explanation: Corticotrophs mainly secrete melanocyte-stimulating hormone. Some other cells sometimes secrete melanin (retina, neurons, adipocytes) Reference: eknygos. Explanation: Mostly associated with chronic kidney disease due to diabetes and hypertension. A: Tunica adventitia B: Muscularis externa Answer: B Explanation: Taenia coli are formed by outer longitudinal muscles, it is absent in the appendix and the rectum. Answer: In acute phase, periportal necrosis, hepatocyte apoptosis, and lobular inflammation (mimics cholestasis). A: Neutrophils B: Lymphocytes C: Eosinophils D: Basophils Answer: A Explanation: In descending order, Never Let Monkeys Eat Bananas (Neutrophil, Lymphocytes, Eosinophils, Basophils) Reference. A: Chief cells B: G cells (gastrin producing) C: Parietal cells Answer: B Explanation: Specific products of H. This effect inhibits platelet generation of thromboxane A2, resulting in an antithrombotic effect. Answer: Levodopa Clonidine affects Levodopa by inhibiting its antiparkinsonism effect. These differences in mechanism influence both the onset and reversibility of treatment. Answer: Phocomelia Exposure to the drug during early embryonic development resulted in severe and a range of damage never seen together before nor since. Indeed, arguably the most striking damage the drug caused is phocomelia, which still is not fully understood. Phocomelia occurs through a severe shortening of the limb/s, due to proximal elements (long bones) being reduced or missing and leaving distal elements (handplate) in place. Phocomelia ranges in severity, from severe, where long bones are missing with just a flipperfi like structure consisting of digits/handplate articulating with the body, to less severe forms exhibiting a shortening of the long bones and normal distal bones. Answer: Infection with poliovirus causes IgM and IgG responses in the blood, but mucosal IgA is vital for blocking infection. This antibody can neutralize poliovirus in the intestine, the site of primary infection. The live attenuated Sabin poliovirus vaccine is effective because it elicits a strong mucosal IgA response and provide intestinal immunity. In contrast, the injected (Salk) polio vaccine does not produce intestinal immunity, and therefore is less effective at preventing spread of poliovirus in a population. Adecrease cholesterol BIncrease satiety Cdecrease pancreatic enzymes Answer: C Gastric and pancreatic lipases are enzymes that play a pivotal role in the digestion of dietary fat. Orlistat, a semisynthetic derivative of lipstatin, is a potent and selective inhibitor of these enzymes, with little or no activity against amylase, trypsin, chymotrypsin and phospholipases. Blurred vision Answer: C Dry mouth, urinary retention, constipation, blurred vision, toxic-confusional states. Which of the following medications used in treating osteoporosis and can cause heartburn sensationfi Inhibit replication Answer: C Inhaled antiviral (Zanamivir; A neuraminidase inhibitors) is used for prevention and treatment of influenza A and B. It inhibits influenza neuraminidase lead to decrease the release of progeny virus and inhibit virus replication. AThromboxane A2 Answer: A Aspirin irreversibly inhibits platelet cyclooxygenase 1 preventing the formation of prostaglandin H2, and therefore thromboxane A2. Aspirin can be used as an antipyretic but why does it cause hyperthermia if given in high dosesfi Osteoporosis drug causes retrosternal pain or heart pain: ARaloxifene BDenosumab Answer: A It causes chest pain Reference. This activity produces inhibition of the effects of this leukotriene on bronchial smooth muscle resulting in the attenuation of bronchoconstriction and decreased vascular permeability, mucosal edema, and mucus production. Aspirin side effect: ADry mouth BConstipation CDiarrhea Answer: C Reference: uptodate 22. Man got a bee sting then his wife trying look for the epinephrine what it is going to inhibitfi ALeukotriene release from macrophages BCross reactivity with the cardiac CInhibit immunocomplex formation Answer: B In patients with anaphylaxis, epinephrine has potent life-saving alpha-1 adrenergic vasoconstrictor effects on the small arterioles and precapillary sphincters in most body [1] organ systems. Through vasoconstriction, it decreases mucosal edema, thereby preventing and relieving upper airway obstruction and increases blood pressure, thereby preventing and relieving shock. Its beta-1 adrenergic effects lead to increased rate and force of cardiac contractions. Its beta-2 effects lead to increased bronchodilation and decreased release of histamine, tryptase, and other mediators of inflammation from mast cells and basophils. Clozapine had significantly less use of antiparkinson medication than risperidone. CMan got a bee sting then his wife trying look for the epinephrine what it is going to inhibitfi The mechanism of respiratory depression involves a reduction in the responsiveness of the brain stem respiratory centers to increases in carbon dioxide tension and to electrical stimulation. AAcarbose Answer: Certainly not Acarbose, in case if two oral agents didn’t control hyperglycemia, switch to Insulin! Patient diagnosed with duodenal ulcer he was prescribed medication 1 month ago now he have gynecomastia which medicationfi Clinically, these effects can cause galactorrhea in women and gynecomastia, reduced sperm count, and impotence in men. The antiviral is likely to be Oseltamivir or Zanamivir, thus the answer will be neuraminidase inhibitor (Flu virus surface protein). APhenytoin Answer: A the major systemic side effects of phenytoin are gingival hypertrophy, body hair increase, rash, folic acid depletion, and decreased bone density. Pseudoephedrine Answer: the side effect that we are concerned about here is Peptic Ulcer Disease. Antacid causing constipation: ASodium chloride BCalcium Answer: Aluminium Hydroxide. Most common side effect of Atropine: (No Dry Mouth in options) Answer: Decrease secretions (Sweating, salivary, bronchial). Effects in order of increasing dose are: Decreased secretions > Mydriasis and Cycloplegia > Hyperthermia with resulting vasodilation > Tachycardia > Sedation > Urinary retention and constipation > Behavioral excitation and hallucination. Melasma presents as symmetrically distributed hyperpigmented macules, which can be confluent or punctate.

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