Download Free Medical Diabetes PowerPoint Presentation

Diabetes PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Diabetes Mellits

Tags : diabetes,diabetes symptoms,diabetes diet

Published on : Sep 29, 2021 | Views : 1840 | Downloads : 12

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Pakistan Society of Chemical Pathologists Distance Learning Programme in Chemical Pathology Lesson No 4 Diabetes Mellitus (1st part) By Surg Commodore Aamir Ijaz MCPS, FCPS, FRCP (Edin) Professor of Pathology / Consultant Chemical Pathologist Bahria University Medical & Dental College / PNS SHIFA Karachi
Slide 2-

Introductions Aldehyde had carbonyl gp at end of carbon chain while it is present any where in ketone. Enol group is a structure of aldehyde in alkaline sol and having negative charge that s why act as reducing gent and reduce one e from Fe+3 and cuprric ion. Compound having identical in composition and differ in spatial composition is called stereoisomers; dextro and levorotatory Dextrorotatory is more common Ring of 5 carbon—pyranose and ring of 4—furanose When OH- gp is attach on the lower side of 1st carbon in a ring structure ----called@ configuration and when on upper side -----beta configuration HbA + Glucose-----rapid---pre-HbA1c (aldimine schiff base)------amadori rearrangement slowly----ketoamine(HbA1C)
Slide 3-

Regulation of blood glucose conc in different conditions FASTING ON BRIEF FAST by glycogenolysis and gluconeogenesis by liver and kidney b/c both contain glucose 6- PO4tase.but sketal muscle lack this enzyme.which is stimulated by counterregulatory hormone( epinephrine and glucagon-stimulatory) ON PROLONG FAST by only gluconeogenesis from glycerol and fatty acid and a.a by cortisol, GH, FED STATE Absorbed glucose is converted to glycogen and stored in liver and adipose tissue under the effect of insulin b/c insulin is inhibitory to glycogenesis and glyconegenesis Normal glucose disposal depends on the ability of pancrease to secrete insulin, the ability of insulin to promote uptake into peripheral tissue in lipogenesis and utilization by sketetal muscle and the ability of insulin to supppress hepati glucose production
Slide 4-

ppt slide no 4 content not found
Slide 5-

GLUCOSE TRANSPORT Glucose is transported in plasma and tissue in two ways by Sodium glucose co transporter and facilited glucose transporter-GLUT There are 12 different type of GLUTS They are divided into different classes.class 1-1-4, class2 (5,7,9,11) and class 3-(6,8,10,12). Significant GLUTS GLUT-4 ---skeletal muscle involve in glucose uptake under the effect of insulin---Role in IR---rate limiting .normally localised in ICF .when insulin bind with its rp ,it come of mem and causes reuptake of glucose.this action is impaired in IR GLUT-2---pancrease GLUT1,3 in neuronal tissues
Slide 6-

Role of the clinical chemistry in DM Clinical chemistry role is divided into two categories Role in diagnosis Preclinical screening Clinical Role in Management; Acute Chronic ADA which previ,ously did not support screening now advocates screening in all asymptomatic individuals over the age of 45yrs. The justification for screening is that 1.atleast 33% of type 2 D.M remained undiagnosed 2.complication are often present at the time of diagnosis 3. treatment delay the onset of complication
Slide 7-

ppt slide no 7 content not found
Slide 8-

Q 1: Essential feature for the diagnosis of Diabetes Mellitus (DM) Anti-islet cell antibodies Glucagon deficiency Hyperglycaemia Hyperinsulinaemia Insulin deficiency Best Answer: c. Hyperglycaemia
Slide 9-

By definition DM is a state of “Chronic Hyperglycaemia” Deficiency of insulin is NOT an essential feature of DM. In fact many type 2 DM patients are Hyperinsulinaemic. Definition of DM
Slide 10-

Q 2: Greater genetic predisposition is associated with: a. DM due to acromegaly b. DM due to Cushing Syndrome c. Type 1 DM d. Type 1B DM e. Type 2 DM Best Answer: e. Type 2 DM
Slide 11-

Genetics of Type 2 DM (T2DM) Family studies have revealed that first degree relatives of individuals with T2DM are about 3 times more likely to develop the disease than individuals without a positive family history of the disease. It has also been shown that concordance rates for monozygotic twins, which have ranged from 60-90%, are significantly higher than Type 1 DM 30-40% Type I A DM has much greater genetic susceptibility than Type I B DM Thus, it is clear that T2DM has a strong genetic component as compared to Type 1 DM.
Slide 12-

Q 3: Fasting Plasma Glucose (FPG) of a 48 year old senior male officer during his “Annual Check-up” was found to be 7.9 mmol/L (142 mg/dl). He was advised re-testing for DM by Glycosylated Haemoglobin (A1C). The result of A1C was found to be 6.8%. Now he wants your opinion. Keeping in view the latest recommendations by international bodies (and ignoring the social aspects for the time being, at least) which of the following you think is the best option for this patient: a. DM is confirmed b. Requires repeating of FPG c. Requires repeating of A1C d. Requires OGTT e. Requires Urinalysis Best Answer: a. DM is confirmed
Slide 13-

Criteria for the diagnosis of diabetes FPG > 7.0 mmol/l (>126 mg/dl) Repeat at interval of at least one week or when stress-free OR Two-hour plasma glucose > 11.1 mmol/l in OGTT OGTT may done due to any indication (see a subsequent slide).
Slide 14-

Criteria for the diagnosis of diabetes FPG > 7.0 mmol/l (>126 mg/dl) AND A1C > 6.5% If one of these is higher than the cut-off value repeat the same e.g. if FPG > 7.0 mmol/L and A1C < 6.5% repeat FPG to confirm. If both these tests are above these levels no need to repeat any of the two tests (as the patient in scenario of Q.3).
Slide 15-

Criteria for the diagnosis of diabetes (cont) In a patient with classic symptoms of hyperglycemia, a random plasma glucose > 11.1 mmol/L (>200mg/dl) OR A1C > 6.5% .
Slide 16-

Criteria for the diagnosis of Pre-diabetes Pre-diabetes: Categories of increased risk for diabetes Impaired Fasting Glucose (IFG) : FPG: 5.6-6.9 mmol/l (100-126 mg/dl) Impaired Glucose Tolerance (IGT) : IGT : 2-h plasma glucose in the OGTT: 7.8-11.0 mmol/l (140 – 200 mg/dl) Glycosylated Hemoglobin (Hba1c) : 5.7-6.4 %
Slide 17-

Prerequisites of OGTT Discontinue the medication that affect glucose tolerance Perform test in the morning after 03 days unrestricted diet of 150g of carbohydrates /day and activity Perform test after 10-16 hr fast only in ambulatory pt(bed rest impair glucose tolerance)
Slide 18-

Factors other than diabetes that may influence the OGTT PATIENT PREPARTION- Duration of fast, Medication (thiazides, OCP,steroid), Prior carbohydrates, Trauma, intercurrent illness, Age. Activity.weight ADMINISTRATION OF GLUCOSe-Form of glucose (anhydrous or monohydrates),quantity of glucose ingested, vol in which administered ,rate of ingestion DURING THE TEST—posture, anxiety, caffeine, smoking ,activity, time of the day
Slide 19-

Indication of OGTT Plasma Fasting glucose between 5.6 mmol/L (100 mg/dl) and 7.0 mmol/L (126 mg/dl) Patients with family history of diabetes mellitus Patients with previous history of large babies Contraindication Plasma Fasting glucose > 7.0 mmol/L (126 mg/dl)
Slide 20-

Interpretation of OGTT Based on 2 h Post Glucose Load: Normal: < 7.8 mmol/L (140 mg/dl) IGT: 7.8 – 11.1 mmol/L (140-200 mg/dl) DM: > 11.1 mmol/L (200 mg/dl)
Slide 21-

Q 4: A 42 years male has been recently diagnosed to be having DM at a state-of-the-art Karachi hospital. His medical history indicated development of typical symptoms of DM during 6 months. His BMI is 23 kg/m2. His mother has Rheumatoid Arthritis while a brother has been diagnosed as a case of glomerulonephritis. He is quite diet conscious and spends three hours in Gym per week. Which of the following investigations will be most appropriate for further elucidation of his disease: a. A1C b. Anti- GAD antibodies c. HOMA-IR d. Serum Insulin levels e. Urinary Albumin Best Answer: b. Anti- GAD antibodies
Slide 22-

Latent Autoimmune Diabetes in Adults (LADA) Rapid development of diabetic Symptoms. Positive Anti-GAD (Glutamic Acid Decarboxylase Antibodies) or Islet-cell antibodies (ICA) Do not require insulin at diagnosis but progress to insulin dependence after several months to years. Family H/O Autoimmune disorders It is Type 1 DM of adults.
Slide 23-

Q 5:. Various sampling options are available for Glucose estimation. Sample collected by which of the following options has the most STABLE glucose results: a. Arterial Whole blood collected for ABGs b. Venous plasma collected in a Lithium Heparin tube c. Venous plasma collected in a Plain Tube with gel d. Venous plasma collected in a Plain Tube without gel e. Venous plasma collected in a Sodium Fluoride tube Best Answer: e. Venous plasma collected in a Sodium Fluoride tube
Slide 24-

Q 6: An 18 years obese boy being investigated for DM had Fasting Plasma Glucose (FPG) 6.7 mmol/L (121 mg/l). He underwent OGTT which showed 2 hours post glucose load value as 9.2 mmol/L (166 mg/dl). What is the most probable diagnosis in this patient: a. Impaired Fasting Glucose (IFG) b. Impaired Glucose Tolerance (IGT) c. Normal Result d. Type 1 DM e. Type 2 DM Best Answer: b. Impaired Glucose Tolerance (IGT)
Slide 25-

Diagnosis of IGT IGT is defined as Hyperglycaemia at 2 h after glucose load. IFG is FPG between 5.6 and 7.0 mmol/L but normal 2 h after glucose load. So when IGT exists with IFG, IGT takes over and will diagnose the patient as IGT.
Slide 26-

T2DM or Pre-Diabetes in Children and Adolescence Type 2DM / Pre-Diabetes is no more a disease of adults It is due to increasing obesity and low fibre diet (fast food). Type 1DM presents with very severe hyperglycaemia and not as pre-diabetes. So the patient in the scenario of Q.6 is NOT of Type 1DM in spite of his young age.
Slide 27-

Pathogenesis of T1DM Cellular mediated autoimmune destruction—insulinitis of specificity . Beta cells by T cell and other cells are preserved,80-90% destruction leads to symptomatic type 1 DM. Antibodies against beta cells---ICAs(iselt cell cytoplasmic Antibodies 75-85% ,insulin autoantibodies(IAA)40% , antibodies to 65kD isoform of glutamic acid decarboxylase-GADs-60% .two insulinoma associated Ab Genetic susceptiabilty ---multigenetic traits—chromosome 6---HLA-DR3 AND HLA-DR4 Environmental factors ---rubella ,mumps and coxsackievirus b
Slide 28-

Q 7:. A 48 year male was diagnosed to be having IFG about 4 years ago but now his physician has informed him that he has developed Type 2 DM. His BMI is 31 and his compliance to his physician`s advice about lifestyle has always been quite poor. Which of the following pathological processes is most important in this patient leading to worsening of his disease: a. Decline in β-cell function b. Increased insulin resistance c. Increased gluconeogenesis d. Increased Glycogenolysis e. Increasing body weight Best Answer: a. Decline in β-cell function
Slide 29-

Q.7 This has very low Difficulty Index (number of students who answered correctly / number of students who answered). The details will be available in Facilitators Feedback Report Its results will not be counted in any contest or statistics. The best answer is Decline in β-cell function There were two Plausible Options in this question i.e. Insulin Resistance and Increasing Weight. Their explanation is provided in the subsequent slides.
Slide 30-

Pathogenesis of T2DM INSULIN RESISTANCE; Primary defect---Obesity ,increased nutrition, decreased exercise ,and genetic predisposition leading to increased Insulin resistance IR-in adipose tissue—increased lipolysis .there are two types of adipose tissue low turn over subcutaneous and high turnover –visceral leading to increased FFA in portal and peripherial blood thus resulting into hepatic IR and peripheral IR IR-Muscle---causes decrease uptake of glucose by GLUT-4 which not come to surface IR-LIVER---increased glucose production b/c glycogenesis is inhibited LOSS OF B-CELL FUNCTION
Slide 31-

Pathogenesis of Type 2 DM Insulin Resistance or Impaired Insulin Secretion? Most of the available evidence favors the view that the ultimate triggering event is impaired insulin secretion, which, when superimposed on a background of insulin resistance, leads to overt type 2 DM. Insulin resistance is neither necessary nor sufficient for the development of Type 2 DM but that defective insulin secretion is the primary defect responsible for unmasking overt diabetes.
Slide 32-

Pathogenesis of Type 2 DM Insulin Resistance or Impaired Insulin Secretion? (CONT) Although most patients with type 2 DM had some degree of insulin resistance, there are patients with a confirmed diagnosis of diabetes who had no evidence of insulin resistance. These individuals remain normoglycemic by compensating for the reduction in insulin sensitivity with increased insulin secretion
Slide 33-

Pathogenesis of Type 2 DM Insulin Resistance or Impaired Insulin Secretion? (CONT) In summary, insulin resistance is an early and characteristic feature of the natural history of type 2 diabetes in high-risk populations. Overt diabetes develops only when the beta cells are unable to appropriately augment their secretion of insulin to compensate for the defect in insulin action.
Slide 34-

Pathogenesis of Type 2 DM Impaired Insulin Secretion or Weight Gain? Obesity is a very important predisposing factor in the pathogenesis of Type 2 DM but studies have shown that many obese patients remain normal or with pre-diabetes (IFG or IGT) throughout their lives and never become overt diabetic. Only those obese go into Type 2 DM phase who have in-built insulin secretion defect due to one or more of the genetic and environmental factors. Obesity is a contributory factor mainly to insulin resistance. Here again the real culprit is Impaired Insulin Secretion
Slide 35-

Remember Margala Tower of Islamabad which had a construction defect. During Oct 2005 earthquake, only Margala Tower collapsed and many precious lives were lost but other buildings were unaffected or minimally damaged (IFG or IGT). But the solution is to avoid earthquake !!! Not Possible? In DM it is possible by Total Life Style Change i.e. reducing weight and physical activity. An Analogy An Analogy
Slide 36-

Q 8: A1C is a well-recognized marker used for monitoring of DM. While working in a tertiary care hospital you want to switch this test to a more sensitive and specific method. Please answer following queries in this regard: a. Name the international organization which provides technical standardization of this test b. Name the current technique widely used now for this test at many well-reputed laboratories. c. What is the ONE most important advantage of using this test for the diagnosis of DM as recently recommended? d. Name TWO major challenges for use of this test for the diagnosis in our country. e. Name one group of disorders in which the test gives poor clinical correlation even when carried out by a modern method.
Slide 37-

Suggested Answer Q.8 a International organizations which provides technical standardization The National Glycohemoglobin Standardization Programme (NGSP) certified methods and reagents having documented traceability to the Diabetes Control and Complications Trial Reference Method. International Federation of Clinical Chemistry (IFCC) Reference method of HbA1c (Mentioning either of these two was sufficient for this question)
Slide 38-

ppt slide no 38 content not found
Slide 39-

Glycosylated Haemoglobin (A1C) Assay A1C is difficult to assay as compared to Glucose or colourimetric assays. In 1993 a vary large study was published called DCCT (Diabetes Complications and Control Trial). In this study A1C was established was used as the main outcome rather than Plasma Glucose in Type 1 DM patients. In 1998 a similar study UKPDS (United Kingdom Prospective Diabetes Study) was published in Type 2 DM patients. Again A1C was the main outcome. (We will discuss these two studies in Lesson No 5-DM-2nd Part).
Slide 40-

Glycosylated Haemoglobin (A1C) Assay (Contd) So it was decided by a major International Body of Chem Path (AACC) that for A1C same methods should be used as used in DCCT or UKPDS But there was a major problem in Standardization of A1C. In 1993, data showed that there was a lot of variability among methods measuring different glycated Hb fractions i.e. measurement of Hb A or Hb A1c or other fractions. Clearly this was not acceptable for achieving specific A1C goals.
Slide 41-

Glycosylated Haemoglobin (A1C) Assay (Contd) In 1996, NGSP was formed to implement the AACC programme. Manufacturers usually give details about the traceability of their method to NGSP. But manufacture`s claim should be verified by consulting the NGSP data from their website (List attached with this ppt) Recommendation; Perform HbA1C 2times/ yr in pt who are meeting treatment goal Perform HbA1C quarteraly in pt whose therapy has changed or who are not meeting goal
Slide 42-

HbAIC Methodology Definitive methods------no Reference methods IFCC Methods-mass spectrometry, capillary elctrophoresis (Agrose gel electrophoresis but have long time of analysis and interference,so not frequently used NGSP Methods---immunoassay (TINIA), HPLC(D-10BIORAD dedicated HPLC)it is a reference method with moderate complexity ,CV<3.5% ,Time 3-5mins, and only require 5ul blood only. But it is temperature ,pH dependant, increased cost, decreased throughput ,inc TAT, most widely evaluated ,technical experties require. Commonly used method Immunoassay-TINIA
Slide 43-

TINIA HbAIC react with reagent-1 antiHbAIC and formed soluble complexes . Addition of 2nd reagent-polyhapten binds with excess Ab and form insoluble complexes which is measured turbidometry. Hb is measured separately by spectrophometric tec Result will be derived in % of Hb=(HbA1C/Hb) x 91.5 +2.15 Advantages; Highly specific ,not temperature and pH dependents, Labile and Hb variant did not interfere, rapid, CV<3% intralab and <5% interlab Disadvantages; More costly than column chromatography but lesser than HPLC .HbS and HbC can interfere and not appropriate for thalsemia
Slide 44-

Contd Traditional Methods Minicolumn(ion exchange ,and affinity chromatography )measure both labile and A1,temperture significantly affect ,pH dependent, interference with Hb F,non standarized but very fast analysis (30mins),cost effective Colorimetric-Hb bound glucose hydrolyzed and react with TBA reaction monitored at 443nm .only for A1 but not for labile, no separation req but lenghty (hrs) There are more than 30 methods used for measuring of HbA1C. Charge difference based----ion exchange chromatography, HPLC, electrophoresis , isoelectrical focussing Structural difference based ----affinity chromartography, and IA Chemical analysis--------photometry and spectrophotometry
Slide 45-

Contd Interference of minicolumn---acetylated Hb(aspirin),carbamylated-Hb, labile preHb A –fraction Labile fragment are removed by dialysis, ultrafiltration of hemosylate, incubation of RBC in saline or in buffer sol at ph 5 Pooled whole blood standard is used in NGSP method for standarization A mixture of purified Hb and HbA0 used as primary reference material for IFCC method
Slide 46-

Units of A1C NGSP Methods: HbA1c % of total Hb IFCC Methods mmol/mol of Hb
Slide 47-

The relationship between NGSP (%HbA1c) and the IFCC (mmol/mol) A master equation has been developed: NGSP = [0.09148 x IFCC] + 2.152.
Slide 48-

Estimated Average Glucose Estimated Average Glucose (eAG) is a new way to talk to patients about diabetes management. The measurement of A1C—expressed as a percentage—is usually not very clear to patients who uses gucometer or lab values. This may make A1C targets difficult for patients to translate into action. Doctors can now report A1C results to patients using the same units (mg/dl or mmol/l) that patients see routinely in blood glucose measurements.
Slide 49-

Estimated Average Glucose The relationship between Estimated Average Glucose (eAG) and HbA1c based on linear regression analysis was: eAG (mg/dl)= (28.7xA1C)-46.7 Or eAG (mmol/l)=(1.59xA1C)-2.59 You can calculate at fol link: http://professional.diabetes.org/GlucoseCalculator.aspx
Slide 50-

Estimated Average Glucose A1C% eAG (mg/dl) eAG (mmol/L) 5 97 5.4 6 126 7.0 7 154 8.6 8 183 10.2 9 212 11.8 10 240 13.4 11 269 14.9 12 298 16.5 (
Slide 51-

Suggested Answer Q.8 b Currently techniques used for this test at many well-reputed laboratories Ion-exchange HPLC TINIA
Slide 52-

Suggested Answer Q.8 c One most important advantage of using this test for the diagnosis of DM The sample can be collected at any time of the day and fasting state is not required.
Slide 53-

A1C as Diagnostic Test of DM In 2009 ADA finally recommended A1C to be used as diagnostic test. After a lot of resistance, WHO also endorsed this recommendation in 2011 and A1C is now widely used as diagnostic test. The biggest advantage is fasting state is not required. Merely dispensing with this requirement of fasting has lead to broadening of screening base and many of those patient can be screened who cant get their test done in fating state.
Slide 54-

Other Advantage of A1C for Diagnosis and Monitoring of DM Standardized and aligned to the DCCT/UKPDS while measurement of glucose is less well standardized Better index of overall glycemic exposure and risk for long-term complications Substantially less biologic variability Substantially less pre-analytic instability Relatively unaffected by acute perturbations Currently used to guide management and adjust therapy
Slide 55-

Suggested Answer Q.8 d TWO major challenges of using A1C for diagnosis in our country: 1. High cost : Several hundred per test as compared to Rs. 10-20 per test. 2. Non-Standard methods: probably our Lab persons are not even aware of the standardization etc.
Slide 56-

Contd Others disadvantages Not widely available Low sensitivity Cant seggregate IFG from IGT Non validation in third trimester of pregnancy Cant pick hypoglycemia Many factor alter its results-hemoglobinopathies
Slide 57-

Suggested Answer Q.8 e Group of disorders in which the test gives poor clinical correlation: Hemoglobinopathies Diseases with short life span of RBC leading to decreased glycosylation—falsely decreased HbA1C-like hemolytic anemia ,anaemia , pregnancy, blood loss and blood transfusion Disease which prolonged life span of RBC leading to increased glycosylation—increased HbA1C--IDA
Slide 58-

Q 9: You have conducted an interactive session on “Classification of DM” with your PG Trainees. Now you have received some queries by email form one of the PGs. Please answer her queries related to WHO Classification of DM: a. Why the older names “Insulin Dependent DM” and “Non-Insulin Dependent DM” have been replaced by new terms like Type1 DM and Type 2 DM? b. Similarly why terms like “Juvenile onset” and “Maturity Onset” have been abandoned for Type 1 and Type 2 DM, respectively? c. Why “Maturity Onset Diabetes of the Young” is placed in 3rd etiological category i.e. ‘other specific types’ and not in Type 2 DM. d. Does a patient of Type 2 DM, when on high dose of insulin, become a patient of Type 1 DM?
Slide 59-

Classification of diabetes Type 1 diabetes β-cell destruction Type 2 diabetes Progressive insulin secretary defect Other specific types of diabetes Genetic defects in β-cell function, insulin action Disease of the exocrine pancreas Drug or chemical-induced Gestational diabetes mellitus
Slide 60-

Clinical Stages of DM (WHO) Normoglycaemia Impaired Glucose Regulation Impaired Fasting Glycaemia (IFG) Impaired Glucose Tolerance (IGT) Diabetes Mellitus (DM) DM not requiring insulin DM requiring insulin for Control DM requiring insulin for Survival
Slide 61-

a. Why the older names “Insulin Dependent DM” and “Non-Insulin Dependent DM” have been replaced by new termslike Type1 DM and Type 2 DM? Diabetes mellitus is a group of metabolic disorders. Mark difference in etiology and pathophysiology leading to the hyperglycemia among patients with diabetes mellitus need different preventive, diagnostic and therapeutic strategies. Also, for example,it was difficult to correctly classify persons with NIDDM who were being treated with insulin. This confusion led to the incorrect classification of a large number of patients with diabetes mellitus, complicating epidemiologic evaluation and clinical management. So, in 1997, ADA classified diabetes according to etiologic differences rather than descriptions based upon age at onset or type of treatment. In 1999 WHO recommended the terminology of Type 1 & 2 and it holds good.
Slide 62-

B,Similarly why terms like “Juvenile onset” and “Maturity Onset” have been abandoned for Type 1 and Type 2 DM, respectively? Type 2 DM is a common disease with alarming increase incidence in children and adolescent due to increase prevalence of obesity in children so it’s no longer “maturity onset disorder”. Similar is the case with type1DM that may occur in adults (latent autoimmune diabetes in adults) and should be suspected if onset age ˂ 50 years for diabetes, BMI˂25 and family history of autoimmune disorder. Excellent answer.
Slide 63-

Why “Maturity Onset Diabetes of the Young” is placed in 3rd etiological category i.e. ‘other specific types’ and not in Type 2 DM. MODY are specific monogenetic disorders of β cells function that are characterized by onset of disease at early age i.e. before 25 years due to impaired insulin secretion but no defect in insulin action in contrast to type 2 diabetes which is characterized by insulin resistance in addition to β cell dysfunction. Good. Moreover it is monogenetic disorder while T2DM is predominantly a polygenetic disease.
Slide 64-

Q 10: A Naib Qasid, 51 y of age has been referred to you by a friend of yours for advice on humanitarian grounds. This poor chap is quite confused about his disease. The story starts with his reporting to a General Physician (GP) for early fatigability and calf pain. The GP gave some symptomatic treatment and advised Blood Glucose Random which came out to be 135 mg/dl or 7.5 mmol/L (ref range : 80-200 mg/dl). Since the value was within given range he was declared normal and no specific treatment was given. Totally unsatisfied he went to another doctor who repeated the test but this time in fasting state. The result was 115 mg/dl or 6.4 mmol/L (ref range upto 100 mg/dl). He was advised Tab Daonil (1/2 tab Daily) by the doctor. Hearing this story, plz answer these questions about this patient: a. Why there is a discrepancy between the glucose reports, assuming there is no analytical error in the tests? b. In your opinion which of the test is more reliable? c. In which category of the disease you will place this patient and what will be your exact label for this patient? d. Name a test you will like to carry out in this patient for the exact diagnosis of glucose disorder? e. Is giving a Sulfonylurea appropriate in this patient?
Slide 65-

Suggested Answer of 10 a Why there is a discrepancy between the glucose reports, assuming there is no analytical error in the tests? Random glucose estimation has very low sensitivity mainly because of its very wide ref range. It should not be done in ambulatory patients.
Slide 66-

Suggested Answer of 10 b In your opinion which of the test is more reliable? Plasma Glucose Fasting
Slide 67-

Suggested Answer of 10 c In which category of the disease you will place this patient and what will be your exact label for this patient? Pre-diabetes and IFG
Slide 68-

Suggested Answer of 10 d Name a test you will like to carry out in this patient for the exact diagnosis of glucose disorder? OGTT
Slide 69-

Suggested Answer of 10 e Is giving a Sulfonylurea appropriate in this patient? NO. Biguanide –metformin is firstline drug and sulphonylurea is 2nd line- which is most suitable for young adult and obese children b/c it causes increased insulin secretion from pancreatic beta cell(if some b-cells activity still present) by inhibiting the K-Channel of Bcell thus leading to depolarization ---ca entry inside the cells and insulin release.
Slide 70-

ppt slide no 70 content not found
Slide 71-

ppt slide no 71 content not found
Slide 72-

Thank you