This document contains summaries of three patient cases. The first case involves an 18-year-old female presenting with recurrent thrush, boils, tiredness, obesity, and other signs and symptoms. The second case is about a 15-year-old girl with frequent urination problems. The third case does not provide many details but mentions differential diagnoses of diabetes types.
MODY is the name given to a collection of different types of inherited forms of diabetes that usually develop in adolescence or early adulthood.
MODY stands for “Maturity-onset diabetes of the young” and was given that name in the past because it acted more like the adult type of diabetes (Type 2 Diabetes) but was found in young people.
MODY limits the body’s ability to produce insulin, but is different than the juvenile type of diabetes (Type 1 Diabetes).
When our bodies don’t produce enough insulin, it can increase blood glucose levels. High blood glucose levels lead to diabetes.
MODY is the name given to a collection of different types of inherited forms of diabetes that usually develop in adolescence or early adulthood.
MODY stands for “Maturity-onset diabetes of the young” and was given that name in the past because it acted more like the adult type of diabetes (Type 2 Diabetes) but was found in young people.
MODY limits the body’s ability to produce insulin, but is different than the juvenile type of diabetes (Type 1 Diabetes).
When our bodies don’t produce enough insulin, it can increase blood glucose levels. High blood glucose levels lead to diabetes.
October is the global awareness month of Niemann-Pick Disease (NPD), a fatal inherited metabolic disorder. Hence, I am sharing a presentation I made on NPD in 2013 in this month of 2016.
October is the global awareness month of Niemann-Pick Disease (NPD), a fatal inherited metabolic disorder. Hence, I am sharing a presentation I made on NPD in 2013 in this month of 2016.
This student "cheat sheet" is designed to provide medical students with basic information regarding the diagnosis and treatment of type 2 DM. It includes Questions to Ask, what to look for on a Physical Exam, Labs to Order, and basic Treatment Plans.
These guides are particularly designed for first and second-year medical students as an introduction to ambulatory care medicine and attempts to tie in the basic pathophysiology that is high-yield for USMLE Step 1.
Any and all feedback is very welcomed.
Teaching Clinical Pathology of Disorders of RBC covered using a clinical case of Anemia. Pathology lecture and tutorials are delivered through short video clips covering parts of topic. this is the first part with overview of whole topic and clinical case. Each powerpoint is screen recorded using camtasia studio and saved as MP4 video.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
3. CPC 3.1: Molly 15y.. Wee problem. Molly is a 15 year old Y10 student comes to ED with her Aunty Ada, community health worker. Ada says Molly has ‘wee’ problem. Molly : ‘I’m going to the toilet often to pass wee and it is sore and itchy afterwards’ ? Key points: ? Differential Diagnosis: ? Further questions ? DM type ? How to confirm Investigations? ? Complications Prognosis? ? Management
8. “Nothing great in the world has ever been accomplished without passion” - - CHRISTIAN FRIEDRICH HEBBEL
9. Most likely .. What type of DM ? 56 year male obese 30 year female following pregnancy 8 year old boy, poor growth, DKA. 24 year female Cushing’s sy 68 Year male following Ca. pancreas. 32 male, DM, BMI 18, Anti-GAD +ve. 34 year male, extensive tuberculosis. 12 year old female following viral fever 41y DM2, BMI 17.1, HbA1c 14.1, DKA 15y male, BMI 16.2, recurrent infect. II NIDDM II GDM I IDDM Sec IDDM Sec IDDM I LADA Sec IDDM I IDDM LADA MODY
10. The foundation of lasting self-confidence and self esteem is excellence, mastery of your work.- Brian Tracy
16. Diabetes Mellitus - Definition 2nd Century, Greek physician, Aretus named Diabetes from diabainein, “to flow through or siphon & Mellitus meaning sweet/Honey. * insipidus tasteless – dilute urine. Disorder of metabolism (Carb, Prot & Fat) Absolute/Relative deficiency of insulin. Characterized by hyperglycemia. Polyuria, Polydypsia, Polyphagia.
17. Criteria for the Diagnosis of Diabetes A random blood glucose concentration of 11mmol/L or higher, with classical signs and symptoms. or A fasting glucose concentration of 7mmol/L or higher on more than one occasion. or An abnormal oral glucose tolerance test (OGTT, done for borderline 5.5-6.9 mmol/L ), in which the glucose concentration is >11mmol/L at 2 hours after a standard carbohydrate load (75 gm of glucose).
30. Diabetes Classification: (not a single disease) Primary DM Type I – IDDM / Juvenile – 5-10%. Type II – NIDDM /Adult onset – 90-95%. MODY – 5% Maturity Onset Diabetes of Youth Genetic, sub types MODY 1–6, LADA – Latent Autoimmune Diabetes in Adults (LADA) Gestational Diabetes Mellitus. Other. Secondary DM Excess hyperglycemic stimulus. Cushings, Phaeochromocytoma, acromegaly, Steroid therapy. Beta cell destruction: Pancreatitis/tumors/Hemochromatosis Infectious – congenital rubella, CMV, TB, Endocrinopathy, Downs Sy.
31. Metabolic Syndrome (X) - IDF criteria Central Obesity >90cm male, >80 fem – Asian, chinese, Jap. >94cm male, >80 fem – Europ, Africa, Arab. + Any two of the following. Raised triglycerides >1.7mmol/l or treat. Reduled HDL-C <1.03mmol/l or treat. Hypertension 130/85 or treat. Fasting plasma glucose >5.6mmol/l or DM2. Australia prevalence 2005 – 30.7% 10 Year CVD risk - 23.4%
32. LADA: Late onset Autoimmune DM Features of both type 1 and type 2. Younger, Rapid onset & progression to insulin dependency. Immune markers like type 1 diabetes, may lack ketoacidosis symptoms. Incidence: - 6-10% (UK). Diagnosis: Elevated pancreatic autoantibodies Risk factors: Metabolic Syndrome LADA + Metabolic syndrome = DM Type 1.5. Complications of both type 1 & 2. (metabolic, Macro & Microangiopathy etc).
33. MODY: Maturity Onset Diabetes of Young. 5% of DM, Young*, non obese, insulin release defect* Like DM2, non-ketotichyperglycemia, no DM Antibodies. Auto. Dom. - Monogenic – Genetic testing*. Treatment is specific to type. Unline type 1 or 2 Also known as Type 1.5 (MODY + LADA) Subtypes: 1,2,3,4,5,6 – type 3 & 2 common. 1,3,4,5,6 – Insulin transcription defect HNF. Type 2 – Enzyme glucokinase, defective β cell response.
34. One machine can do the work of fifty ordinary men. No machine can do the work of one extraordinary man.- - Elbert Hubbard
46. DM2 Islets:Normal early amyloid late: Normal. Loss of ß cells (only in late stage) replaced by Amyloid protein deposit (hyalinization).
47. Type-I Type-II Less common (10%) Children < 25 Years Insulin- Dependent Duration: Weeks Acute Metabolic complications Autoantibody: Yes Family History: No Insulin levels: low Islets: Insulitis 50% in twins More common (90%) Adult >25 Years NIDDM* Months to years Chronic Vascular complications. No Yes Normal or high * Normal / Exhaustion ~100% in twins
48. Type-I Type-II Insulitis: Lymphocytic infiltrate within islets. Islet Hyalinization: Central hyaline deposits replacing dead beta cells (only in late stage…!)
49. Being a good human is maintaining complete harmony between thought, word and deed. Divergence between thought, word and deed is the cause of all our problems…!- BABA.
50. DM Complications: Glucose is highly reactive - damages tissues. Glucose absorption, storage & use – Timely Insulin release - critical. Diabetes is state of insulin deficiency. Absolute/Delayed/inappropriate insulin response Glucose excess – Hyperglycemia. Neo-glucogenesis – Proteolysis, lipolysis Clinical symptoms & signs are mainly due to complications. Complications: Acute Metabolic & Chronic Vascular. Damage to BV, Kidney, CNS & immune system.
51. Diabetes Complications: Short term Complications: (metabolic) Hypoglycemia Diabetic Ketoacidosis Non Ketotic hyperosmolar diabetic coma Lactic acidosis Long term Complications: (Angiopathy) Microngiopathy - Retinopathy, Nephropathy, Neurophathy, dermatopathy. Macroangiopathy – Atherosclerosis.
80. Retinopathy: Non Proliferative Microaneurysms, Dots & blots Hard and soft exudates Cotton wool – infarcts Macular edema. Proliferative. Neovascularization Large hemorrhages Retinal detachment.
81. Non Proliferative Retinopathy Venous dilation and small red dots posterior retinal pole - capillary micro-aneurysms. Dot and blot retinal hemorrhages and deep-lying edema and lipid exudates impair macular function. Cotton-wool spots (soft exudates) - microinfarcts due to ischemia. They are white and obscure underlying vessels. Hardexudates are caused by chronic edema. They are yellow and generally deep to retinal vessels. Late generalized diminution of vision due to ischemia and macular edema - common cause of visual defect (best detected by fluorescein angiography)
82. Proliferative Retinopathy Neovascularization – new capillaries grow into the vitreous cavity. hemorrhages may lead to sudden severe loss of vision. In advanced disease, neovascular membranes can occur, resulting in a traction & retinal detachment. Leading to permanent blindness. Panretinal photocoagulation may diminish or eliminate proliferative retinopathy
87. You must learn to distinguish between good and bad, truth and untruth. You must use your education for the purpose of serving community. - Sai - Summer Showers, 1973.
93. Cataract – Sorbitol.. Polyol..osmotic.. Lens epithelium (Insulin independent) is exposed to Hyperglycaemia, excessive flux of glucose to sorbitol by the polyol pathway. The accumulation of intracellular sorbitol exerts osmoprotection and prevents cell shrinkage. The excessive accumulation of sorbitol, causes an increased osmotic load within the lens causing swelling, fibre breakdown, and opacification (the osmotic hypothesis). Other mechanisms, including glycation and oxidative stress, may also be responsible for lens opacification.
94.
95. Pathogenesis of Infections in DM: Multifactorial: Impaired inflammation – BV thickening – Decreased immune function: WBC, chemical mediator glycosylation. Glycosylation of immune mediators. Abs. Tissue damage: Ischemia & infarctions. Decreased metabolism – low immunity. Increased glucose (alone is not the cause*)
96. Laboratory Diagnosis: Urine glucose - dip-stick –Screening Fasting > 7mmol, Random >11mmol If Fasting level is 5.5 to 7 OGTT HbA1c - for follow-up, not for diagnosis Fructosamine – similar to HbA1c - long term maintenance. Antibodies – Type-1 Gene testing: MODY
97. “It's not that I'm so smart, it's just that I stay with problems longer”…! --Albert Einstein
98. CPC-3.2– END–DM2 Pathology – Major Core Learning Issues: Pathology of Diabetes Overview & Classification. Pathological basis of clinical features. Details of Type 1 & 2 (Etiology, pathogenesis, morphology, clinical features) Complications of Diabetes: Micro & Macroangiopathy. Retinopathy, nephropathy, neuropathy, dermatopathy.. etc.. & Metabolic complications (ketoacidosis, coma etc) Laboratory diagnosis of diabetes. (GTT, HBA1c, etc) Pathology – Minor CLI: Metabolic Syndrome (Syndrome X). MODY, LADA, Gestational, childhood type 2, Secondary diabetes, Bronze diabetes. Hyperglycemia Syndromes: Cushings, drugs, etc. Hypoglycemia syndromes, Insulinoma. New research & developments
99. Case 1 A 29y woman BMI = 33 kg/m2. complains of declining visual acuity since 6 months. Fundoscopic examination shows peripheral retinal microaneurysms. Urinalysis reveals 3+ proteinuria and 3+ glucosuria. Serum albumin is low & cholesterol is high. These clinicopathologic findings are best explained by which of the following pathologic mechanisms of disease
102. 50y, male DM2, kidney biopsy. Likely nature of feature shown by arrow? Amyloid protein. AGE protein Basement mem protein. Fibrinoid necrosis. Inflammatory cells.
104. Thickening of small BV in this patient is most likely related which pathologic mechansim? Glycosylation of hemoglobin. Inadequate inflammtion resp. Insulin resistance in tissues. Increased Atherosclersis. Microvascular disease.
113. 56y Fem, Anterior wall MI. 3+ proteinuria & FBG 19mmol/L. Image shows her pancreas. What complication she may develop? Gall stones. Chronic pancreatitis. Uric acid stones. Gangrene of foot. Pancreatic carcinoma
114. A 65y man, BMI 40, peripheral neuropathy, retinopathy and abdominal aortic aneurysm is now developing renal failure. His FBS is 18.3 mmol/L, microscopic examination of his renal biopsy. What is the microscopic feature shown? Renal papillary necrosis. Nodular glomerulosclerosis. Hyaline artereolosclerosis. Atrophy + Amyloid deposition. Diffuse glomerular sclerosis. What is the chemical nature of nodular deposit within glomerulus? Briefly describe steps in the Pathogenesis of nodular glomerulosclerosis? What other renal pathology are commonly seen in diabetic patients?
115. A 47 year old man, Hypertensive & DM2 since 6 years for checkup. Complains of his vision as spectacles recently made does not seem to help. Image shows his fundoscopy. What is the most likely diagnosis ? Normal fundus. Mild Hypertensive retinopathy. Non proliferative retinopathy. Proliferative retinopathy. Retinal detachment. Retinopathy – Differences between Hypertensive & Diabetic retinopathy? Briefly describe steps in the Pathogenesis of diabetic retinopathy? Differentiate soft & hard exudates, dots & blots, proliferative & non-proliferative.?
116. A 65y man, BMI 40, Diabetes since 18 years. His FBS is 18.3 mmol/L, is now developing hypertension since 3 years (BP 186/98 mm of Hg) . Image shows microscopic appearance of his renal biopsy. What microscopic feature shows pathogenesis of high blood pressure? Hyperplasticartereosclerosis Protein cast within tubule. Artereolosclerosis. Nodular glomerulosclerosis. Both A & C. What is the pathogenesis of feature A (hyperplasticarterosclerosis) in the image? Briefly describe feature B and its clinical presentation? What is seen in the interstitium of this kidney? Pathogenesis? Clinical feature?
117. A 42 year female presents with recent onset polyuria, polydypsia and decreasing vision. HbA1c was 16.1%. She is chronic alcoholic with past history of jaundice. Image shows her pancreatic biopsy compared with normal. What is the most likely diagnosis ? Secondary diabetes. Late onset Type 2 diabetes. Chronic cholecystitis. Cushing’s syndrome. Type 1 diabetes. Normal Patient Briefly describe features of LADA? What further investigations can be done to confirm the diagnosis? List & briefly describe other types of Diabetes ?
118. 70y man brought from nursing home with progressive confused & disoriented status since 2 weeks. Not eating or drinking well. On steroid therapy for COPD. What is the most likely diagnosis ? Diabetic ketoacidosis. Non-ketotichyperosmolar coma. Diabetic lactic acidosis. Respiratory acidosis. Diabetic nephropathy. Lab tests: List & briefly discuss common metabolic complications of Diabetes? ? ?
119. The most splendid achievement of all is the constant striving to surpass yourself and to be worthy of your own approval.- - Denis Waitley
134. Case 2 – 58y Fem Asymptomatic. She has a BMI of 29 and is on enalapril for hypertension. She has no symptoms of diabetes. A fasting glucose is 6.5mmol/L. Mother had DM type2. Should she be tested for DM? Indications? Yes. (IGTT, IFG, Aboriginals, High risk immig, Obese fem+, cardiac event, >45y+ BMI>30, FH of DM2 or HPTN). Diagnosis? next investigation for this patient? IFG, oGTT (FG 5.5-7, RG 7-11 mmol/L) How do you manage a IGT patient? Advice about Diet & excercise.
136. Summary Abnormal metabolic state characterised by glucose intolerance due to inadequate insulin action. Type I (juvenile onset) Autoimmune destruction of β-cells (Genetic + ? Virus + Autoimmunity); insulin-dependent – Treat by Insulin. Type II (maturity onset) - defective insulin action – peripheral resistance to insulin. treatment by life style change & oral hypoglycaemic agents. Complications: accelerated atherosclerosis, susceptibility to infections, and microangiopathy (retinopathy, neuropathy, dermatopathy, nephrophathy)
137. Points to remember/review: Diabetes is a state of hyper ketabolism. Increased fat & protein breakdown, wt loss. Blood vessel damage – arteriosclerosis is central to chronic complications. Increased Infections – why?. Glucose control is critical * why? Hypoglycemia is more dangerous. Not hyper FBS, GTT & HbA1C – interpretation.
138. Questions.. How – Ketoacidosis? How – hypoglycemia ? Macro Angiopathy ? – (atherosclerosis) Micro Angiopathy “Pathy” (arteriolosclerosis) Retinopathy – types, morphology, Nephropathy – types, morphology. Dermatopathy – morphology. Diabetic Amyotrophy - What is Diabetes insipidus ?
139. 56y woman, nocturia 56y Fem, 3/12 nocturia excessive thirst and polyuria(1-4 times) disturbing her sleep. Recently noticed blurring of vision, & tingling sensation in her toes on both sides. Weight 94kg & height 1.71m. BMI 32. Hypertensive for several years. Mother diabetic type2. Glucometer capillary BS is 15mmol/L. What further Investigations? Ans: Twice..Lab RBS/FBS, GTT. Why not HbA1c for diagnosis? 60% of new diabetics have normal HbA1c. What other investigations should be done? Retina, urine, Lipid profile, Cardiac exam.
140. It is a matter of great satisfaction if you are educated on the right lines, become an example to others and accept positions of responsibility. In all these things, always keep “Truth & Love for all” as your goal.Then only you will get the Grace of God….!- Sai - Summer Showers, 1973.
144. DECODE: increased 2-hour glucose is associated with increased mortality rate (adjusted for age, center, and gender).
145. Cumulative incidence of diabetes mellitus (based on American Diabetes Association criteria) according to study group in the DPP. * The incidence of diabetes differed significantly among the 3 groups (p <0.001 for each comparison. Reprinted with permission from Knowler et al.13
146. Endocrinology Other : (Brief notes) Tumours – adenomas of endocrine gl. Cushings disease. Pheochromocytoma. Zollinger Ellison syndrome. MEN Syndromes – MEN type 1 & 2.