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Their pathophysiological importance ment discount diovan 80mg with amex arterial network, but not to a change in the net water content discount diovan 80mg with visa blood pressure medication make you cold. However discount 160 mg diovan with amex arrhythmia tutorial, if some residual is isoosmotic discount 40 mg diovan with mastercard blood pressure keeps changing, caused by breakdown of the blood– blood flow persists, water is taken up from the blood, brain barrier, and accumulates in the extracellular and the net tissue water content increases. Apoptosis With the evolution of tissue necrosis and the deg- Apoptosis is an evolutionarily conserved form of pro- radation of basal lamina, the blood–brain barrier grammed cell death that in multicellular organisms breaks down [81], and after 4–6 hours serum proteins matches cell proliferation to preserve tissue homeo- begin to leak from the blood into the brain. It is an active process that requires intact disturbance initiates a vasogenic type of edema which energy metabolism and protein synthesis, and it is further enhances the water content of the tissue. Both pathways tissue may be so pronounced that transtentorial involve a series of enzymatic reactions and converge herniation results in compression of the midbrain. An endstage brain infarction is by far the most dangerous compli- of this process is the ordered disassembly of the cation of stroke and an indication for decompressive genome, resulting in a laddered pattern of oligonu- craniectomy [82]. The matrix shows possible combinations between nuclear and cytoplasmic morphologies near or at the terminal stages of degeneration [35]. Although apoptosis is mainly involved in physio- Apoptosis, an active form of programmed cell logical cell death, it is widely assumed to contribute to death, may contribute to a certain extent to ische- the pathogenesis of diseases, including cerebral ische- mic cell death. In the context of stroke this is difficult to understand because in areas with primary cell death the obvious cause is energy failure, and in regions Ischemic pre- and postconditioning with delayed injury protein synthesis is irreversibly The molecular signaling cascades initiated by brain suppressed (Figure 1. However, ischemia induces a ischemia are not solely destructive but may also multitude of biochemical reactions that are reminis- exert a neuroprotective effect. This effect is called manipulation or pharmacological interventions reduces “ischemic preconditioning” and can be differenti- the volume of brain infarcts. It has, therefore, been ated into three phases: during the induction phase suggested that ischemic cell death is a hybrid of necrosis molecular sensors which respond to the precondi- 20 and apoptosis, appearing on a continuum with the tioning stimulus are activated by transcription two forms of cell death at its poles [86](Figure 1. After stroke, neurogenesis increases in these phase proteins with a protective impact are switched areas, and some of the newly formed cells migrate on [87]. The increase in ischemia tolerance appears 2–3 to the infarct penumbra, differentiate into glia and days after the preconditioning stimulus, and it slowly mature neurons, and survive for at least several weeks disappears after 1 week. Neurogenesis may also occur within cerebral An important preconditioning pathway is the up- cortex, but this finding is debated. The tive mechanism is the endoplasmic reticulum stress functional consequences of spontaneous or drug- response. As the latter contributes to delayed ische- not yet been achieved, and further research is neces- mic injury (see above) its reduction may have a neu- sary to explore the actual potentials of stroke regen- roprotective effect. Recently, evidence has been provided that ische- Several brain regions may provide lifelong supply mic injury can also be alleviated by repeated mechan- of newly generated neurons. The possibility of influencing about brain physiology and the pathophysiology of ischemic injury after the primary impact is challen- brain disorders, but the transfer of this knowledge ging but it remains to be shown for which kind of into clinical application is difficult and often lags clinical situation this finding is of practical relevance. One of the reasons is the differences between the brains of experimental animals and man with Short episodes of ischemia can improve the toler- respect to evolutionary state (non-gyrencephalic vs. The other problem arises from the inves- ingly irresolvable, in agreement with Cajal’s classic tigative procedures, which cannot be equally applied statement that in the adult brain “everything may in animals and patients. This dogma was pathophysiological changes obtained by invasive pro- reversed by the discovery of three permanently neuro- cedures in animals, e. Similar results applied extensively for studies in patients with acute, were obtained in ischemia models of baboons. The introduction of scanners with high ous tissue compartments within an ischemic territory: resolution (2. With time, can be used as markers of neuronal integrity as they Chapter 1: Neuropathology and pathophysiology of stroke Figure 1. If reperfusion is achieved after this therapeutic window, tissue cannot be salvaged (right cat, right patient). This method yields sinuses or veins and are often accompanied by more reliable results than the determination of mis- edema, hemorrhagic transformation and bleeding. Delayed neuronal death can occur after 23 Section 1: Etiology, pathophysiology and imaging 7. Compensatory enlargement of human nuclear fragmentation and development of apop- atherosclerotic coronary arteries. Thrombus formation on atherosclerotic which usually reflect only certain aspects of ischemia plaques: pathogenesis and clinical consequences. From these experimental models prin- ciples of regulation of cerebral blood flow and flow 9. As the energy requirement of the brain is very high, decreases of blood supply lead 10. Cerebral miliary aneurysms in to potentially reversible disturbance of function and, if hypertension. Pathology, complex cascade of electrophysiological disturbances, Pathogenesis, and Computed Tomography. The progression of ischemic injury is fur- Stroke – Pathophysiology, Diagnosis, and Management. Stroke – into clinical application and management of stroke Pathophysiology, Diagnosis, and Management. The Harvard Cooperative Stroke Chapter 1: Neuropathology and pathophysiology of stroke Registry: A prospective registry. Brott T, Broderick J, Kothari R, Barsan W, Tomsick T, A new experimental model of cerebral embolism in Sauerbeck L, et al. Early hemorrhage growth in rats in which recirculation can be introduced in the patients with intracerebral hemorrhage. Recurrent primary cerebral volume after permanent and transient middle cerebral hemorrhage: frequency, mechanisms, and prognosis. Basic Neurochemistry: changes in apparent diffusion coefficient during focal Molecular, Cellular, and Medical Aspects, 6th ed. New York: oxide in the pathophysiology of focal cerebral Marcel Dekker; 2007: 77–92. Dynamics of regional brain þ milieu: the emerging role of Zn2 in ischemic neuronal metabolism and gene expression after middle cerebral injury. Dependence of vital cell function on endoplasmic reticulum calcium levels: implications 61. Ischemic penumbra: evidence from for the mechanisms underlying neuronal cell injury functional imaging in man [Review]. J Cereb Blood Flow Metab 2007; permanent and temporary middle cerebral artery 27:875–93. Interleukin I in the brain: ischaemic stroke: a systematic review of the evidence to biology, pathology and therapeutic target [Review]. Neurochem Int 2007; pathways mediating inflammatory responses in brain 50:1028–41. Effects of stroke on local cerebral metabolism basal lamina in ischemic brain injury. J Cereb Blood Flow Metab diffusion coefficient, diffusion-weighted, and T2- 1989; 9:723–42.
Reduced fertility among Finnish schizophrenics is not compensated for by higher fertility among their siblings cheap diovan 40mg on line blood pressure chart poster. Feeley & O’Shea diovan 160mg low cost blood pressure kit cvs, 2001) Indeed 40mg diovan otc blood pressure medication parkinson's, there is Danish evidence that suggests that autoimmune disorders may be more common in schizophrenia sufferers than in the general population proven diovan 40mg arterial nephrosclerosis. The apparent decline in the frequency of some subtypes, such as 961 catatonia (Cf later), has been noted with interest, although some authors contest the validity of this decline on methodological grounds. Season of birth effect is small, with differences of only 5-10% from expected rates. A survey of Norwegian psychiatric inpatients born from 1866 to 1939 revealed a striking excess of winter births, a tendency which was less marked in patients from the higher social classes. Being born or reared in urban areas may add to the risk of viral infection in utero. Research on urban/rural place of birth, the relevance of being male/female, and the time of year when one is born is on-going. Finnish work on birth cohorts suggest a move from rural to urban births over time, but there are still clusters that suggest possible genetic isolation. Van Os ea (2003, 2004) found both level of urbanicity and familial liability independently and synergistically increased risk for psychotic disorder. If both parents have schizophrenia the risk for their child is about 45%, compared to 1% in the general population. Various 968 969 loci have been highlighted by research as possibly being important in schizophrenia. These results should be approached with caution until there is much more in the way of replication. It has also been implicated in bipolar disorder, especially when accompanied by psychosis. Mood incongruent psychotic features in bipolar patients may be linked to 13q21-33. However, Williams ea (2004) using Cardiff and Dublin samples, produced evidence that variations in the dysbindin gene confers susceptibility to schizophrenia. Fanous ea (2005) found that a haplotype for dysbindin may predispose to psychosis with high levels of negative symptoms. Kishimoto ea (2008) found preliminary evidence that the dysbindin gene is associated with risk of metamphetamine psychosis. Schizophrenia, like criminality (Mednick & Finello, 1983), may have a genetic input but environmental influences are also important (see van Os ea, 2009). Up to one- 976 third of schizophrenics have no known family history of schizophrenia. Also, schizophrenia may be 977 associated with a far wider range of mental disorders than we have been apt to think, a fact that may influence studies of risk factors. Nonfamilial cases may have an environmental aetiology because they were more likely to show cerebral abnormalities such as enlarged cerebral 978 ventricles. McGuffin ea, 1994) suggest that schizophrenia can be explained entirely by genes or that non-genetic phenocopies account for very few cases. Crow (1990) favoured a ‘continuum of psychosis’ and suggested that we failed to genetically demarcate schizophrenia from affective disorder. Other authors have also reported overlap between affective disorders and schizophrenia in the families of patients with schizophrenia. However, there is evidence (Kasckow ea, 2009) that adding citalopram to antipsychotic medication in schizophrenia patients with subsyndromal depression does seem to improve their social and mental functioning as well as their quality of life. Overlap between schizophrenia and bipolar affective disorder may be linked to 2p11-q14. Humans (diploid) usually have 2 copies of each chromosomal region, one per chromosome. A very large (more than 2 million nuclear families) Swedish study (Lichtenstein ea, 2009), using a multi- generation register the hospital discharge register, found evidence that schizophrenia and bipolar disorder partly share a common genetic aetiology – 63% of the co-morbidity between disorders was due to additive genetic effects common to these two conditions. This research shows that the first-degree relatives of probands with schizophrenia or bipolar disorder are at increased risk for both disorders, a slap in the face for Emil Kraepelin! Niemi ea (2004) followed up all women born between 1916 and 1948 and treated for schizophrenia spectrum disorders in Helsinki psychiatric hospitals and looked at their offspring born 1960-4 and at controls. The cumulative incidences of schizophrenia and schizophrenia spectrum disorders among the offspring were similar to those in first degree relatives of probands with schizophrenia and adoptees whose biological mothers had schizophrenia. Children of schizophrenic mothers were also at increased risk for non-psychotic disorders, especially mood and substance use disorders, and the fathers of these high risk 983 offspring had increased rates of psychiatric disorders, especially alcohol and substance use disorders. This was published in 1916 and reported an increased rate of dementia praecox among siblings of probands over the general population. Shur (1982) did a retrospective study from the case notes (and item sheets filled out by psychiatrists dealing with the subjects) of hospitalised schizophrenics. Those with relatives with psychiatric diagnoses other than schizophrenia were significantly more likely to have been diagnosed as schizoaffective. The author wondered if there was a constitutional trait in the parents of those patients with a family history of psychiatric disorders delaying child bearing. Family studies: Lifetime expectancy of an individual in the general population for schizophrenia is about 1% but far higher figures are reported among relatives of schizophrenics. If both parents are schizophrenic the chance of one of their children developing the illness is about 25%; if there is only one schizophrenic parent the risk falls to around 12%. Critics point out that twins share an intrauterine environment and may share perinatal hazards. If schizophrenic adoptive parents adopt the child of non-schizophrenic biological parents he carries the same risk for schizophrenia as anyone else (1%). Critics suggest that adoption agencies seek adoptive families resembling families of origin. The type of rearing a person genetically at risk receives in the adoptive home has a bearing on the likelihood of expression of schizophrenia spectrum disorder. A meta-analysis of 32 genome-wide linkage studies of schizophrenia (Ng ea, 2008) suggested that future work might concentrate on chromosomes 1, 2q, 3q, 4q, 5q, 8p, and 10q. Large scale studies using big patient numbers are needed to further our knowledge and this necessitates the combined efforts of many investigators. Narrowly defined schizophrenia with a constellation of physical abnormalities, and a piece of chromosome 5 on chromosome 1, thus giving a partial trisomy of chromosome 5, has been reported. So-called ‘mirror neurones’ in this part of the brain help us to read the intended actions of others. He suggests that the basic problem in schizophrenia relates to a sense of detachment and disembodiment from the social self and social world. This concept receives support from the work of Schürmann ea (2007) with twins discordant for schizophrenia. There are cleft lip/palate, congenital heart defects, thymic dysplasia, hypocalcaemia, nasal speech, intellectual disability (in almost half – of various degrees of severity), long facies, bullous nasal tip, and an increased 998 incidence of schizophrenia-like and bipolar disorder-like disorders.
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An atmosphere mittee will be chaired by the Vice Dean who of mutual respect purchase diovan 80mg with visa blood pressure medication breastfeeding, collegiality buy 160mg diovan otc blood pressure chart diastolic, fairness 40mg diovan mastercard blood pressure pictures, and will vote only in the case of a tie purchase 40mg diovan overnight delivery blood pressure for women. Although both teachers ciate Dean/Registrar, the Associate Dean for and learners bear signifcant responsibility Student Affairs, and the Assistant Dean for in creating and maintaining this atmosphere, Minority Affairs will be non-voting ex-offcio teachers also bear particular responsibility members. The student will be asked to pro- with respect to their evaluative roles relative vide information regarding the grounds for the to student work and with respect to modeling grade appeal and will be given an opportunity appropriate professional behaviors. After con- sideration, the Committee will advise the Vice Responsibilities in the Teacher/Learner Dean for Education of any changes merited. Relationship Two standards will be employed by the Com- Responsibilities of Teachers mittee in evaluating the appeal which could lead to a recommended amendment: • Treat all learners with respect and fairness. The student may appeal an adverse deci- Responsibilities of Learners sion to the Dean of the Medical School by notifying him/her in writing within 7 days of • Treat all fellow learners and teachers with the decision. Students must take Step 1 by September 15 of their third year and receive a passing score • Be on time for didactic, investigational, and in order to proceed with core clerkships. Guidelines for Conduct Behaviors Inappropriate to the Teacher- Learner Relationship in Teacher/Learner These behaviors are those which demon- Relationships strate disrespect for others or lack of profes- sionalism in interpersonal conduct. Although Statement of Philosophy there is inevitably a subjective element in the The Johns Hopkins University School of witnessing or experiencing of such behaviors, Medicine is committed to fostering an envi- certain actions are clearly inappropriate and ronment that promotes academic and profes- will not be tolerated by the institution. These sional success in learners and teachers at all include, but are not limited to, the following: levels. Avenues for Addressing Inappropriate • If the person reporting the behavior is a Behavior in the Teacher/Learner Context research fellow: The trainee should speak with the Associate Dean for Postdoctoral Learners’ Concerns Affairs. Learners may address situations in which they feel that they have been the object of Teachers’ Concerns inappropriate behavior at various levels. At If a teacher feels that a learner has engaged the most basic level, the most effective way in inappropriate behavior, it is likewise most to handle a situation may be to address effective to address the situation immediately it immediately and non-confrontationally. If the matter is not Oftentimes, a person is simply unaware that resolved satisfactorily, the teacher should his/her behavior has offended someone, or contact the course director, program director, even if aware, will correct the behavior appro- or laboratory mentor to discuss the matter. If priately if given the opportunity to do so in a the teacher wishes to make a formal allega- way that is not threatening. The way to raise tion of misconduct, they should contact the such an issue is to describe the behavior following members of the administration: factually (“When you said... Students may also elect to speak to tact the Associate Dean for Postdoctoral their respective Associate or Assistant Deans Affairs. These individuals may offer addition- ing to established School of Medicine poli- al suggestions for resolving the matter infor- cies published elsewhere. The student may also attention of the School of Medicine admin- directly contact that offce. Indi- days of the allegation as follows: viduals who believe that action has been • If the complaint is lodged against a faculty taken against them in retaliation for raising member, the Vice Deans for Education and concerns under this policy, may address Faculty will be notifed. Other than those those concerns through the procedures matters referred to the Offce of Institu- described in this policy. If the will be referred for disciplinary action under complaint is lodged against a research fel- the appropriate University procedures which low, the Vice Dean for Education and the are described elsewhere. Other than those matters referred to the Offce of Institutional Equity, Procedures Relating to if based on the written report, those Deans Student Discipline decide that a formal investigation is mer- ited, they will convene an ad hoc commit- The following procedures will govern com- tee to investigate the complaint and will plaints regarding the conduct of a student notify the complainant, the respondent and enrolled in the School of Medicine. The ad Medicine will contain documentation refect- hoc committee will be composed of three ing conduct during the period of enrollment. A faculty members from departments other student will have access to his School record, than those of the complainant or respon- including those documents, if any, refecting dent. The committee will be responsible for conduct, in accordance with the standards set gathering information and interviewing the forth in the Family Educational Rights to Pri- complainant, respondent, and other indi- vacy Act and applicable University policy. Based University’s policy on access to and release upon information gathered and their delib- of student records is published annually and erations, the committee will submit a writ- a copy may be obtained from the Offce of the ten report to the Deans involved within thirty Registrar of the School of Medicine. When information reaches the School indi- will include their fndings and recommenda- cating that a student has engaged in behavior tions for dismissal of the complaint or for unbeftting a physician and/or a medical sci- disciplinary action(s). The senior Deans entist, the student will be requested to confer will then communicate to the complainant with the Associate Dean for Student Affairs. If the committee fnds cannot be resolved to the satisfaction of the against a post-graduate trainee, the fnd- Associate Dean for Student Affairs, or where ings will be communicated to the appropri- the gravity of the acts with which the student ate Department Chair and Program Direc- is charged appears to warrant further atten- tor and sanctions will be determined and tion, the Dean of the Medical Faculty will enforced according to the policy on Pro- appoint an ad hoc committee of the Adviso- bation, Suspension, and Termination of ry Board of the Medical Faculty to hear the Post-Doctoral Fellows published elsewhere charge of misconduct. Suspension for a specifed time or until mittee and may vote when the ad hoc com- explicit* conditions are met. Unconditional Expulsion given written notice of the charges and of the date and time of the Committee hearing. Prior *Explicit conditions are to be unambiguous to the hearing an accused student shall be and as objective as the conditions allow. An accused stu- sion to the Dean of the School of Medicine, dent may request an opportunity to consult or, in the absence of the Dean, appeal may with the Dean, Vice Dean, or an Associate be made to the Vice Dean or an Associate Dean prior to a hearing. A student may be accompanied to the calendar days of the date of the committee hearing by a faculty member or student advi- decision. A student may attend classes pending or the accusing party at the hearing by attor- the proceedings before the ad hoc commit- neys will not be permitted. In the course of the hearing, a student will Vice Dean, or Associate Dean to be a danger be given the opportunity to present evidence to himself or others. A student must seek the and witnesses in his behalf, to question all permission of the Dean, Vice Dean, or Asso- witnesses, and to make statements to the ciate Dean in order to continue the education- Committee. Members of the ad hoc committee may ask questions of the student charged and of wit- nesses appearing before the Committee. A hearing before the ad hoc committee will be closed and persons other than Deans Preclinical Curriculum appearing as witnesses will be asked to Among the goals of the Scientifc Founda- absent themselves before and after their tes- tions of Medicine and the Genes to Society timony. Parents of the accused student will be courses are to develop a sense of profes- permitted to accompany a student throughout sionalism, to promote collegiality, to engage the hearing, and, if they should wish to do so, students in teaching one another, and to give to make a statement. A hearing shall be recorded but the delib- different backgrounds and expertise are rep- erations of the ad hoc committee shall not resented. Following the hearing, the student to be actively engaged, therefore accused student shall be permitted to listen attendance is mandatory at all group learn- to the recording upon request, but all copies ing and teamwork activities including activi- of the recording shall remain in the School’s ties in the Simulation Center and workshops. All parties, witnesses, and representa- that involve patients and/or guests, such as tives shall be excused at the conclusion of clinical correlations. Videofles of large group the hearing and the ad hoc committee shall lectures where attendance is not required deliberate privately. The Committee shall are available online via course management make fndings as to the truth or falsity of the software. Unexcused attendance below 80% the Committee decide that the student’s will affect the student’s performance in the behavior warrants discipline, will include, but course and will be considered a breach of will not necessarily be limited to the following: the standards of professionalism expected by a. Probation for a specifed time period or Group Discussions), attendance at 80% of until explicit* conditions are met. Students Excused absences may be granted in should make every effort to leave as late as cases of illness, religious observance, fam- possible and return as early as possible when ily emergency, presentations at scientifc interviewing to minimize time lost from a core conferences, or required legal activity (e. On 6-9 week clerkships, students will be whenever feasible) with the section director, allowed to miss 3 full days of responsibili- course director, and/or Associate Dean for ties as excused absences for interviews. Students must inform course directors Attendance Policy of any such absences in advance of the The School of Medicine recognizes the pri- beginning of the clerkship when possible. Atten- be considered unexcused and will impact dance rules are governed by the School of on the student’s fnal grade.
The bladder is a mucous rough terrain due to thickening of the muscle fibers in its wall cheap diovan 80 mg arrhythmia vs atrial fibrillation. Both lateral ventricles are severely dilated purchase diovan 40 mg mastercard blood pressure 300200, forming a cavity among the brain tissue with total 12 / 8 order diovan 40mg online pulse pressure 56. Part of the liver highly variegated cut surface due to the presence of numerous dark brown-red small and large spots discount diovan 40mg line arterial blood gas, which merge in places surrounded by grayish yellow fields. Section of brain, with a clearly visible distinct, rounded, brownish-red area in the white brain matter demarcated from the surrounding tissue - hematoma. Its shear surface is showing well-delimited areas airless triangular-shaped, dark red-brown, slightly protruding. Visceral pleura is smooth and evenly stretched, fireplace, dim the sections above infarctions. In view of the upper part of the preparation, over the thrombotic mass, the aorta intima is covered with complicated atherosclerotic plaques. Preparation of the heart, including incoming tract of the left ventricle, mitral valve and left ventricle. Valves layers are thickened, gray-white, with an uneven surface, deformed, shortened and fused with each other - a combined heart defect - stenosis and insufficiency, predominantly stenosis. Left ventricle is significantly enlarged with hypertrophic myocardium and endocardium is thickened and whitish. The left ventricle is small (atrophy by inactivity) and appears as an appendage of the atrium. Guide to diagnosis is lung organ chilus, which is visible at the rear of the preparation. The cut surface shows that both lobes are evenly diffuse greyish with fine granular structure. Density creates an impression that the edges between the two cut surfaces are very well defined (stage of gray ‘hepatization’). Head brain with polished edge - the folds are broad and flat and gyri between them were shallow. By convexity there is a heavy white purulent exudate, located subarachnoidal, filling gyri and spreading on the folds. Organ diagnosis is made in view of the rear surface of the preparation, where a partially removed Glisson’s capsule shows the hepatic parenchyma. Inside, thin cystic structure with a milky color soft and friable - chitin membrane of Hydatid cyst. In the area of the apex, the heart myocardium is whitish, sealed and significantly taper - chronic aneurysm. In endocardium in this area there is mural lobular gray-brown mass with whitish stripes - thrombus. Top shows a large tumor formation - 7,5 / 6 cm, whitish, poorly demarcated, with a central fission of tissue originating from the wall of the main broncus - mostly exophytic bronhogenic cancer. In the field of small curvature, a rounded tumor formation is seen with sunken central part and raised, not better contouring soft edges. The bottom is colorful - showing necrotic areas, hemorrhage, inflammatory deposits. Part of the colon with available exophytic, nodular, tumor formation, increasing broad-based, measuring 3. The bottom was unequal, with a whitish color, and the raised edges with the color of environmental mucosa. Organ diagnosis is made by the presence of smooth fibrous capsule and preserved nodular array. In the middle of the preparation is clearly visible distinct bluish-black area with a spongy structure - a cavernous haemangioma. Material from liver, cut surface on which are visible numerous large rounded foci with dark brown to black, sharply contrasting with preserved liver parenchyma - metastatic malignant melanoma. Unicameral cystic formation with traces of ‘porridge- like’ content, , brownish in color about 1 cm in diam. The surface is uniformly as "grain" sizes are 1-2 mm which correspond to hypertrophic (regenerative) nephrons. Papillary muscles are massive, rounded and with prominant trabeculae in the cavity. The intima is a colorful and grossly unequal because of outbreaks and prominent yellowish thick whitish areas that narrow and deform lumens. Distally, there is mural thrombotic deposition (uneven dark brownish-red mass above bifurcation). Visible extensive area of irregular shape, deleted fascicular structure and clay-yellow (coagulation necrosis), with distinct peripheral dark red stripe (hyperemic-haemorrhagic area). Preparation of the heart, including incoming tract of the left ventricle, mitral valve and left ventricle. Valves layers are thickened, gray-white, with an uneven surface, deformed, shortened and fused with each other. Left Учебна програма за специалност “Медицина” 225 ventricle is significantly enlarged with hypertrophic myocardium and endocardium thickened and whitish in color. One of the sails of the aortic valve with ulceration and another with thrombotic deposits that have polypoidal appearance. The visceral pericardial sheet (epicardium) shows grayish-whitish, sometimes ‘velvet’-like coating with a thickness of 2-3 mm, covering the whole heart. Thin bodies with transparent walls, filled with air (bullae) are seen in the upper and lower lobe. The background ispale gray-pink to gray-white parenchyma showing abundant deposits of anthracotic pigment, imparting a characteristic mosaic variegation on the surface. Lung, covered with smooth, slightly dim, intense visceral pleura, showing numerous airless areas with dense grayish color and texture - lobular pneumonia. The cut surface is diffusely airless, compact, grayish, covered with small whitish nodules or fields the size of ‘millet’ grains. Lung, in which chilus a nodular tumor formation is seenwith a size about 10 cm emanating from a wall of the bronchus and sprouting into the surrounding lung tissue. Preparation of the esophagus, the upper half of which shows saccular extension of its wall, with communicating lumens – pulsating diverticulitis. Shown are several shallow ulcers with a round shape, sizes from 1 mm to 2 cm, with slightly raised edges and a smooth hollow bottom with black color. In the small gastric curvature seen ulcerative defect with irregular oval, raised, solid and well- contouring edges. Part of the stomach wall which is engaged by exophytic tumor with rounded shape, gray-whitish in color and shaped with a central ulcerative defect. Diffusely scattered nodules with a size of lentil to a pea stand out above the hepatic parenchyma. A single rounded concretion with a brownish color and uneven surface is presented in its lumen.
