Appendiceal mucocele is an obstructivedilatation of the appendix caused byintraluminal accumulation of mucoid material.It is a rare disease. The incidence is 0.2%to 0.3% of all appendectomied specimens.The brush size to 3 cm are considered to besmall, up to 6 cm - average and more than9 cm - giantCases: the patient 50 years old, man,place of residence: the city of UB songinokhairkhan duureg. Specialists of the driver,in the year immediately 2015,02,02 wasoperated with the diagnosis of acuteappendicitis. Complaints on admission:pain on the right side of the abdomen, anagging pain when moving and walking,stomach rumbling. History of the disease:the pain started with 2015,01,31 at 8 pmfrom the bottom of the abdomen. tookhome chloramphenicol but not helpedso 2015,02,02 year at 9 o’clock enteredvia ambulance. Medical examination: thesatisfactory condition of the active position,the skin clean, moist, blood pressure160/110, pulse 98 beats per minute Spo298%. 10*7,7*5,5 см size /Fig.1-2/ , white /Fig. 3-4/ , smooth surface /Fig.1-4/, insideslimy gray mucinous /Fig. 5-6/ bag /Fig. 5/above listed items on a standard attached,aims to study the histology. The result ofthe following: Mucocele of the appendixwith hyalinized wall and with the additionof acute inflammation with microabscesses.

Regardless the possession of any graduation and qualifications anywhere in order to train the doctors and medical professionals with the capabilities to work in any places there are the needs of the knowledgeable mentors to teach their knowledge, abilities and trends to the students in national, regional and international levels. This survey was started to determine the needs of the skills development of the mentors of the Mongolian National University of Medical Sciences under the mission to make it as one of the best 100 medical universities in the Asia-Pacific region and in order to create the favorable environment to accelerate the development of the university and creating a team consists from qualified mentors and researchers by improving the trainings, researches and clinical favorable environment including the quality improvement of the activities.The total of 333 mentors from the 5 structures and 3 branches of the Mongolian National University of Medical Sciences were surveyed to be developed by the University of Michigan including the use of the widely used questionnaires in the universities consisting from 7 groups and 81 questions to determine the needs of the mentors.The working range of the best medical mentors including their needs of the skills was studied. The 55.7% (50.4-61.0%) of the mentors included in the survey were told that the facilitation of the learning needed, 82.4% (78.3-86.5%) as the role models needed, 79.9% (75.6-84.2%) as the provision of the information is needed, 76.3% (71.7-80.9%) as 82.8% (78.8-86.9%) as the planning needed and 81.0% (76.8-85.2%) as the assessment of the training is needed.There is a need to develop the skills related to the 6 frameworks as the learning facilitation for the mentors, role model providers, information providers, resource developers, planners and assessors.

Hemochromatosis is a common inherited disorder of iron metabolism in which an inappropriate increase in intestinal iron absorption results in deposition of excessive amounts of iron in parenchymal cells with eventual tissue damage and impaired organ function. The human HFE gene was identified as the most common form of hemochromatosis in 1996. A homozygous G A mutation resulting in a cysteine to tyrosine substitution at position 282 (C282Y) is the most common mutation. It is identified in 85–90% of patients with hereditary hemochromatosis in populations of northern European descent. A second relatively common HFE mutation (H63D) results in a substitution of histidine to aspartic acid at codon 63. Homozygosity for H63D is not associated with clinically significant iron overload. Some compound heterozygotes (e.g., one copy each of C282Y and H63D) have moderately increased body iron stores but develop clinical disease only with cofactors such as heavy alcohol intake or hepatic steatosis. Thus, HFE-associated hemochromatosis is inherited as an autosomal recessive trait; heterozygotes have no, or minimal, increase in iron stores. However, this slight increase in hepatic iron can act as a cofactor that modifies the expression of other diseases such as porphyria cutanea tarda (PCT) and nonalcoholic steatohepatitis. Mutations in other genes involved in iron metabolism are responsible for non-HFE-associated hemochromatosis, including juvenile hemochromatosis, which affects persons in the second and third decade of life. Mutations in the genes encoding hepcidin, transferrin receptor 2 (TfR2), and hemojuvelin result in clinicopathologic features indistinguishable from HFE-associated hemochromatosis. However, mutations in ferroportin, responsible for the efflux of iron from enterocytes and most other cell types, result in iron loading of reticuloendothelial cells and macrophages, as well as parenchymal cells.

Autosomal dominant PKD (ADPKD) is the most common monogenic genetic disease, and affects one in 500–1000 humans. Approximately half of all affected patients develop end-stage renal disease in the fifth to sixth decade of life. In a majority of cases (80-85%), the gene involved is PKD1, which is located on chromosome 16 (16q13.3) and encodes polycystin-1, a large receptor-like integral membrane protein that contains several extracellular mo-tifs indicative of cell-cell and cell-matrix interaction. In the remaining (10-15%) cases, the disease is milder and is caused by mutational changes in another gene (PKD2), which is located at chromosome 4 (4q21-23) and encodes polycystin-2, a transmembrane protein, which acts as a nonspecific calcium-permeable channel. ADPKD is gener¬ally a late-onset multisystem disorder characterized by bilateral renal cysts; cysts in other organs including the liver, seminal vesicles, pancreas, and arachnoid membrane; vascular abnormalities including intracranial aneurysms, dilatation of the aortic root, and dissection of the thoracic aorta; mitral valve prolapse; and abdominal wall hernias. Renal manifestations include hypertension, renal pain, and renal insufficiency. PKD1 and PKD2 gene mutations result in similar extra-renal manifestations, including PLD and intracranial aneurysms. Autosomal recessive polycystic kidney disease (ARPKD) is an important cause of childhood renal- and liver-related morbidity and mortality with variable disease expression. While most cases manifest peri-/neonatally with a high mortality rate in the first month of life, others survive to adulthood. ARPKD is caused by mutations in the Polycystic Kidney and Hepatic Disease 1 (PKHD1) gene on chromosome 6p12. PKHD1 is an exceptionally large gene (470 kb) with a longest open reading frame transcript of 67 exons predicted to encode a 4,074-amino acid (aa) (447 kDa) multidomain integral membrane protein (fibrocystin/polyductin) of unknown function.

In our country for developing these services closer to the population, providing home care and treatment can be conducted in order to get the patient’s health care refer to the family and sum based health centers should be carried out. At the family and sum hospitals are working graduators of medical university, who assisting health care of Community based rehabilitation. In those cases adoctor have a role to give health care services, and to mediate between disabled people and other health care services as physical therapy, speech therapy, prosthesis and orthotics care, disability surgery and other professional cares. Therefore, there is needs to determine training needs of Community based rehabilitation and to accommodate with study curriculum.To evaluate the curriculum content, retrospective databases and descriptive research method were used and research data was collected by previous data analysis, interview and surveillance.In the result, contents of the “Community based rehabilitation” curriculum in different medicaluniversities are generally the same. But the curriculum was more attached to the disease and its drug medications rather than reflecting to proper guidance and advice for patients and main idea of “Community based rehabilitation”. Availability of specific textbooks and handbooks is limited, hence the trainings are held using international declaration, annual report or guidelines. Also the specialists who teach the subject were inadequate. Relating the due subjects, teaching methods were various, such as problem solving and small group discussion, case study etc., and students were evaluated bytest, case solving, essay writing and for School of Medicine, MNUMS they use OSCE. In conclusion, content of the “Community based rehabilitation” curriculum in undergraduate medical education is not adequate, indefinite, and discordant and there is lack of specialized teachers. Additionally, the curriculum content was not applied to the WHO guidance. Therefore we developed“Community based rehabilitation” curriculum in each medical disciplines, available to be used in undergraduate medical education in further.

Introduction: Leading cause of mortality was cardiovascular disease alone last two decade and occurs5500-6000 deaths annually in Mongolia. Familial hypercholesterolemia is the most common inheritedmetabolic disorders and is characterized by severely elevated LDL-cholesterol levels. The prevalenceof the heterozygous state has been estimated at 1 in 200 to 1 in 500 and of the homozygous state from1 in 160,000 to 1 in 1,000, 000.Goal: To identify Heterozygous Familial hypercholesterolemia among the patients with cardiovasculardisease and study clinical features.Materials and Methods: After view medical examination patients with coronary heart disease andcerebral vascular disease, we selected 183 patients among 26 family who possible to have HeterozygousFamilial hypercholesterolemia. We analyzed family history, clinical examination and lipid parameters.And identifi ed Heterozygous Familial hypercholesterolemia by diagnostic criteria of Netherlands.Results: The mean age for males was 42.3±14, for females was 45.8±15 and gender distribution was42.6% (78) male, 57.4% (105) female. Hypertension occurred in 80.9% (148). BMI was increasedwith age in both sexes (P<0.001). The frequency of tendon xanthoma was 26.8% (49) and cornealarcus was 36.6% (67). The level of total cholesterol and LDL-C were signifi cantly elevated in patients.Identity Heterozygous Familial hypercholesterolemia by criteria of Netherlands was certain-36.1%,probable-42.6%, possible-18.6%, unlikely FH-2.7%.Conclusion: Identifi cation of these individuals at an early age and an aggressive treatment of all knownrisk factors are important for reduce mortality of cardiovascular disease. The Netherland’s criteria issuitable for diagnosing Familial hypercholesterolemia in the Mongolian population, although it does notdiagnose the condition at the genetic level.

Goal: The aim of the study was to identify economic burden from hypertention in Ulaanbaatar and develop some recommenadations. Material and Method: The top down approach was used to calculate direct costs of hypertension in five hospitals of the secondary and tertiary levels. To calculate cost of hypertension financial reports and cost centres data were used. A self-administered questionnaire was used to calculate indirect costs from the disease. Patients, admitted to six UB district and three tertiary level hospitals due to hypertension filled in the questionnaire. Data was analysed using SPSS 15 programme.Results: Some 114 patients were surveyed. The average cost of hypertension was 143914 ± 38189.5 (average bed days 8.7) and 264756 ± 40760.4¥ (average bed days 9.5) in the selected district and tertiary level hospitals respectively. The average cost for per out-patient visit was 4237 ± 2123.5¥ in the selected district hospitals and 3,162 ± 308.3¥ in the selected tertiary level hospitals. The indirect costs included transport cost to and from hospital, food, transport cost of relatives to visit them, cost of medications, and some other expenses related to their admission. Average indirect cost of an admission of patients with the hypertension was 253,395 and 212,717.44¥ in district and tertiary level hospitals respectively. Economic burden from temporary loss of working ablility due to hypertension was 177.1 millions tugrigs. National average wage was 300500¥ in 2009. Some 65.8% of respondents used antihypertension drugs at least once a day and average cost was 653.4¥ per patient per day. Annual and 10 years drug use estimates were 238491 and 2.3 million tugrigs per patient respectively (Inflation and price changes were not counted).Conclusion: Indirect and direct costs for admission were 1.1 billion (49.6%) and 939 million (42.5%) tugrigs respectively. Cost of hypertension in Ulaanbaatar was 2.2 billion tugrigs in 2009 and it is 1.1% of total health sector financing.

Introduction: Studies have shown that hepatitis C virus (HCV) infection not only causes hepatitis, but also pathological changes in other organ systems. Therefore, it is necessary to study the relationship between chronic HCV and chronic kidney disease. Objective : To determine the factors influencing renal glomerular function in chronic hepatitis C patients Materials and methods: Patients with chronic hepatitis C virus were referred to Third Central Hospital, Tegsh Huslen Medical Center, two regional 2020 from August to October. Data on morbidity of patients with chronic hepatitis C were analyzed. The results were processed using SPSS-23 software. Statistical probabilities were determined by checking whether there were statistically significant differences between the groups, using logistic regression analysis and chi-square methods. Results : There were 54 (46.9%) individuals whose renal glomerular filtration rate was reduced to less than 90 ml/min. In a linear regression analysis, a decrease in renal glomerular filtration rate with age was a significant correlation. Renal glomerular filtration rate is decreased in 37% patients by age-related manner (r2 = 0.37). To determine other causes, no significant correlations were observed when grouped by diabetes, cirrhosis, BMI, and hepatic steatosis (p>0.005). The older age of the patient and the high blood pressure were at 6.4 times higher risk to decrease the glomerular filtration rate in patients with chronic hepatitis C (OR 6.4 (95% CI 1.3-31.4), p=0.021) than the patients who have young age and normal blood pressure by multiple logistic regression analysis. Conclusion The age of the patient and high blood pressure are contributing factors to the decline in the incidence of low glomerular filtration rate in patients with chronic hepatitis C.

Background and Purpose Liver disease that caused by iron metabolism failure is called Hemochromatosis (clinically “Bronze diabetes”, “Over spotted liver cirrhosis”). The two types of hemochromatosis are primary and secondary. Primary hemochromatosis is caused by a defect in the genes that control how much iron the human body absorb from food. Secondary hemochromatosis usually is the result of another disease or condition that causes iron overload. According to the study there is a real need to study the clinical reveals of hemachromatosis in Mongolian patients. The purpose of the study to determine the hemachromatosis in patients with liver cirrhosis and cancer.Methods and Materials: The study involved 68 patients with diagnosis Liver cirrhosis and HCC (1st stage) who were hospitalized in Clinic of Gastroenterology of Shastin clinical hospital and “Shagdarsuren” Hepatic hospital from April to July, 2011. All patients were increased blood iron and iron compounded proteins (ferritin, transferrin). DNA analyze have made in Molecular Biological Laboratory of Institute of Biology, Mongolia. Sequencing assay has made in Molecular Biological Laboratory of Humboldt University, Germany.Results. The patient’s age was 25-86, the mid aging – 55.42±1.7. The allele frequencies of the C282Y, H63D, and S65C mutation (which in chromosome 6) were 16/136, 11.7% (heterozygous 7, homozygous 2), 9/136, 6.6% (heterozygous 0, homozygous 9), 3/136, 2.2% (heterozygous 0, homozygous 3), equally 28/136, 20.5% (heterozygous 7, homozygous 14). Conclusions. In conclusion, the occurrence of the C282Y, H63D, and S65C mutation within HFE in this studied cohort of hereditary hemochromatosis. Therefore, these data incline that other factors than the HFE gene may play a role in determining hereditary hemochromatosis in Mongolians.

Background and purpose: Liver disease that caused by iron metabolism failure is called Hemochromatosis (clinically "Bronze diabetes", "Over spotted liver cirrhosis"). The two types of hemochromatosis are primary and secondary. Primary hemochromatosis is caused by a defect in the genes that control how much iron the human body absorb from food. Secondary hemochromatosis usually is the result of another disease or condition that causes iron overload. According to the study there is a real need to study the clinical reveals of hemachromatosis in Mongolian patients. The purpose of the study to determine the hemachromatosis in patients with liver cirrhosis and cancer.Materials and Methods: The study involved 50 patients with diagnosis liver cirrhosis and cancer (1st stage) who were hospitalized in Clinic of gastroenterology of Shastin clinical hospital and "Shagdarsuren" hepatic hospital from April to July, 2011. The special questionnaire was used in the study. The biochemical laboratory examinations were taken and analyzed in lab "MED ANALYTIC". Biochemical tests performed on HumaStar 80 fully automatic analyzer. Determination of Iron level was performed by Photometric colorimetric test for iron with lipid clearing factor (normality 37-148ug/dl), transferring level by Turbidimetric monoreagent for the quantitative determination of transferring (normality 170-340ug/dl), glucose level by (GOD-PAP method) Enzymatic colorimetric test for glucose method without Deproteinisation (normality 75-115ug/dl). The ferritin level performed by ELISA analyzer (normality 15-240ng/ml).Results: The patient's age was 25-86, the mid aging-55.42. From all patients (29 male and 21 female) who were participated in the study, the 25 were with diagnosis liver cirrhosis and 18 of them clinically has the Child Pugh "B" cirrhosis, 7 has Child Pugh "A". The other 25 patients were with diagnosis liver cancer first stage.According to biochemical analyzes iron (n=35;70%); ferritin (n=41;82%); transferring (n=27; 54%); sugar (n=21;42%) levels were elevated.During the liver disease caused by iron overloading the following clinical symptoms were observed:- Skin spotting, n=48 (98%)- Hepatomegaly, n=33 (66%)- Splenomegaly, n=28 (56%)- Diabetes mellitus symptoms, n= 30 (60%)- Cardiovascular disease, n=16 (32%)- Respiratory system disorders, n=11 (22%)- Gonadotrophy, n= 2 (4%)The average serum iron level in case of livercirrhosis was 189.84+18.5mg/dl, in liver cancer 160.4±13.91 mg/ dl, ferritin level in case of liver cirrhosis was 407.69+50.08ng/ml, transferrin 375.68±47.38mg/dl, glucose 121.1±7.15mg/dl, ferritin level in liver cancer was 391.67±47.79ng/ml, transferring 388.76±47.38mg/dl, glucose 114.59±5.78mg/dl.