diabetes mellitus
DESCRIPTION
TRANSCRIPT
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BYTIKAL KANSARA
BARODA MEDICAL COLLEGE (BMC)
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DIABETES MELLITUS
• Diabetes Mellitus (DM) refers to a group of common metabolic disorders that share the common phenotye of hyperglycemia
• Depending on etiology, factors contributing to hyperglycemia includes:– Reduced insulin secretion– Decreased glucose utilization– Increased glucose production
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CLASSIFICATION• Type I DM • Type II DM• Other specific types:– Genetic deficiency of B- cell functions• Hepatocyte nuclear transcriptioon factor 4 alfa (MODY 1)• Glucokinase (MODY 2)• HNF – 1alfa (MODY 3)• Insulin promoter factor 1 (MODY 4)• HNF 1beta (MODY 5)• neuroD1 (MODY 6)
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– Genetic defects in insulin action• Type A insulin resistance• Leprechaunism• Lipodystrophy syndromes
– Dieases of exocrine pancreas: pancreatitis, pancreatectomy, neoplasia, cystic fibrosis, hemochromatosis
– Endocrinopathies: Acromegaly, Cushing Syndrome, pheochromocytoma, hyperthyroidism
– Drug or chemical induced: pentamitice, nicotinic acid, glucocorticoids, thyroid hormones, phenytion, protease inhibitors, clozapine
– Infections: congenital rubella, CMV, Coxsachie– Uncommon forms: anti-insulin receptor antibodies– Other genetic conditions associated with Diabetes: Down
Syndrome, Klinefelter Syndrome, Turner’s Syndrome, Friedrich’s Ataxia, Huntington’s Chorea, Porphyria
– Gestational Diabetes Mellitus
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SPECTRUM OF GLUCOSE HOMEOSTASIS & DM
TYPE OF DIABETES
NORMAL GLUCOSE
TOLERANCE
HYPERGLYCEMIA
PRE-DIABETES DIABETES MELLITUS
Impaired fasting glucose or
impaired glucose tolerance
Not insulin requiring
Insulin required for
control
Insulin required
for survival
TYPE 1
TYPE 2
OTHER SPECIFIC TYPESGRSTATIONAL DIABETESTIME (Years)
FPG <100 mg/dl 100-125 mg/dl 126 mg/dl
2-HR PG 140 mg/dl 140-199 mg/dl/ 200 mg/dl
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NORMAL PHYSIOLOGY OF INSULIN ACTION
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RISK FACTORS FOR DIABETES MELLITUS
• Family history of diabetes (parent or sibling)• Obesity (BMI > 25)• Habitual physical inactivity• Race/ethinicity• Previously identified IFG or IGT• History of GDM or delivery of baby > 4 kg• Hypertension ( BP > 140/90 mmHg )• HDL cholestrol level < 35 mg/dl &/or a TG level > 250 mg/dl• PCOD or Acanthosis nigricans• History of vascular disease
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PATHOGENESIS OF DM 1
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http://ocw.tufts.edu/Content/14/lecturenotes/265878/133132_medium.jpg
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http://ocw.tufts.edu/data/51/673764/674515_xlarge.jpg
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http://img.medscape.com/slide/migrated/editorial/cmecircle/2001/145/prato/slide02.gif
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METABOLIC ABNORMALITIES OF DM TYPE DEUX
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MAIN INSULIN RESISTANCE SYNDROMES
• The main insulin resistance syndromes include– The Metabolic Syndrome (Syndrome X)– Polycystic Ovary Syndrome (PCOS)
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METABOLIC SYNDROME
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http://kardiol.com/wp-content/uploads/2011/01/metabolic-syndrome-2.jpg
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COMPLICATIONS
ACUTE
Diabetic Ketoacidosis
Hyperglycemic hyperosmolar state
CHRONIC
MicrovascularEye
disease
Neuropathy
Nephropathy
MacrovascularCoron
ary
Peripheral
Cerebrovascu
lar diease
s
Others
GI & GU
Dermatologic
Infections
Periodontal
diseases
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DIABETIC KETOACIDOSISSYMPTOMS
Nausea/Vomitting Thirst/Polyuria Abdominal Pain Shortness Of Breath
PHYSICAL SIGNS Tachycardia Dehydration/Hypotension Tachpnea/Kussmaul Respiration/Respiratory Distress Abdominal Tenderness Lethargy/Obtundation/Cerebral Oedema/Possibly Coma
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http://www.bestsyndication.net/images_com/2010/02_february/04/20100204_diabetic_ketoacidosis-lg01.jpg
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PATHOPHYSIOLOGY OF DK
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DKA HHS
GLUCOSE 250-600 600-1200
SODIUM 125-135 135-145
POTASSIUM N / Increased N
MAGNESIUM N N
CHLORINE N N
CREATININE Slightly reduced Moderately increased
OSMOLALITY 300-320 330-380
PLASMA KETONES ++++ +/-
BICARBONATE < 15 mEq/L N / Slightly reduced
ARTERIAL pH 6.3 – 7.3 > 7.3
ANION GAP Increased N / Slightly Increased
COMPARATIVE LABORATORY IN DK & HHS
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http://pmj.bmj.com/content/80/943/253/F1.large.jpg
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TREATMENT OF DKINITIAL EVALUATION
History & physical examinationLaboratory Tests: ABG, CBC, Urinalysis, RBS, BUN,
creatinine.ECG & CXRStart IV fluids … 1 L of 0.9% NaCl /hr initially (15 – 20
ml/kg/hr)DIAGNOSTIC CRITERIA
RBS > 250 mg/dlpH < 7.3S. bicarbonate < 15 mEq/LModerate ketonuria & ketonemia
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FLUID REPLACEMENT
• 2 – 3 L of 0.9% NaCl over first 1 – 3 hrs (10-15 ml/kg/hr);
• Followed by: 0.45% NaCl @ 150 – 300 ml/hr• Change to 5% glucose & 0.45% NaCl when
glucose level reaches 250 mg/dl
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SHORT ACTING INSULIN
• IV (0.1 U/kg) or IM (0.3 U/kg) stat• Then, 0.1 U/kg/hr continuous infusion;
increase to 2 to 3 times, if no response by 2 – 4 hrs
• If initial potassium < 3.3 mEq/L, do not administer insulin till potassium corrected to > 3.3 mEq/L
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ELECTROLYTE CORECTIONSPOTASSIUM
10 mEq/L when K+ < 5.5 mEq/L, ECG normal, urine flow & creatinine documented;
40 – 80 mEq/L, when initial K+ < 3.5 mEq/L or bicarbonate given
BICARBONATE If pH = 6.9 – 7.0 after initial hydration, HCO3 50
mEq/L in 200 ml sterile water with 10 mEq/L KCl If pH < 6.9, 100 mEq/L HCO3 with 20 mEq/L KCl
over 2 hrs in 400 ml sterile water
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• Monitor glucose, BP, pulse, respiratory rate, mental status, fluid intake & output every 1 – 4 hrs.
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CHRONIC COMPLICATIONS OF DM
• MICROVASCULAR– Eye disease• Retinopathy• Macular oedema
– Neuropathy• Sensory• Motor• Autonomic
– Nephropath
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• MACROVASCULAR– Coronary artery disease– Peripheral artery disease– Cerebrovascular disease
• OTHERS– Gastrointestinal– Genitourinary– Dermatologic– Infections– Cataracts– Glaucoma– Periodontal disease
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MECHANISM OF COMPLICATIONS
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1. Advanced glycosylated end-products2. Increased metabolism by sorbitol pathway
Alters redox potential Increases cellular osmolality Generated reactive oxygen free radicals
3. Diacylglycerol activating protein kinase C4. Increases flux through hexoseamine pathway.
PROPOSED THEORIES
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OPHTHALMIC COMPLICATIONS
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TREATMENT OF OPHTHALMIC COMPLICATIONS
• Prevention• Prophylactic photocoagulation
Laser photocoagulation– Panretinal– focal
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RENAL COMPLICATIONS OF DM
• Causes ESRD
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Necrotising papillitis
http://missinglink.ucsf.edu/lm/IDS_106_DM_Complications/ASSETS/DMrenalNPgross.jpg
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TREATMENT OF RENAL COMPLICATIONS
• Maintain blood glucose level• Maintain BP to < 130/80 mmHg• Use ACE-I & ARBs• CCBs, B-blockers, Diuretics• Protein restriction 0.8 g/kg/day in
microalbunemia & <0.8 g/kg/day in macroalbunemia
• Renal transplantation
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NEUROPATHY
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TREATMENT OF NEUROPATHY
• Improve glycemic control• Reduce chances of hypertension &
hypertriglyceridemia• Avoid smoking, alcohol• Supplement vitamins• Daily care of foot wear• For chronic painful neuropathy – use
antidepressants, anticonvulsant
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GI/GU COMPLICATIONS• Delayed gastric emptying• Altered small & large bowel motility• Nocturnal diarrhoea• Oesophageal dysfunction
• Erectile dysfunction• Reduced sexual desire• Dysparenuria• Reduced vaginal lubrications• Diabetic cystopathy
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TREATMENT OF GI/GU COMPLICATIONS• Small frequent meals• Metoclopromide• Domperidone• Erythromycin– Interacts eith motilin receptors
• Loperamide• Octreotide • Diabetic cystopathy – self cathaterisation• Sildenafil (Viagra) for erectile dysfunction
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CARDIOVASCULAR COMPLICATIONS
• Absence of chest pain (“Silent ischemia”) is common
• One of the risk factors for atherosclerosisTREATMENT
Same as per the cardiac complication
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LOWER EXTREMITY COMPLICATIONS
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DERMATOLOGIC COMPLICATIONS
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NECROTISING LIPOIDICA
DIABETICORUM
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NECROBIOSIS DIABETICORUM: Atrophy of skin
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DIAGNOSISCRITERIA FOR DIAGNOSIS OF DIABETES MELLITUS
•Symptoms of Diabetes plus random blood glucose concentration >= 200 mg/dl or•Fasting plasma glucose >= 126 mg/dl or•Two-hour plasma glucose >= 200 mg/dl during an oral glucose tolerance test
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SCREENING TESTS
• Widespread use of FPG for screening is recommended because:– Large number of people who meet the criteria are
unaware of their problem & are asymptomatic– Epidemiological studies show that type 2 DM may
be present for a decade before the diagnosis– As many as 50 % of individuals with DM have one or
more of the complications– Treatment of DM has favorably altered the natural
history of the disease
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• Individuals >45 years of age are to be screened every 3 years
• Individuals who are overweight (BMI > 25) and have an additional risk factor for the disease should also be screened
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LONG TERM TREATMENTTRETMENT GOALS FOR ADULTS WITH DIABETES MELLITUS
GLYCEMIC CONTROLHb A1C < 7.0
Preprandial capillary plasma glucose level
90 – 130 mg/dl
Peak postprandial capillary plasma glucose
< 180 mg/dl
BLOOD PRESSURE < 130/80 mmHg
LIPIDSLow density lipoproteins < 100 mg/dl
High density lipoproteins > 40 mg/dl
Triglycerides < 150 mg/dl
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BEFORE GIVING MEDICATIONS
• Diabetic education• Nutrition (Medical Nutrition Therapy, MNT)• Exercise
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PATIENT EDUCATION
• Self-monitoring of blood glucose• Urine ketone monitoring• Self insulin administration• Foot & skin care• Management of hypoglycemia
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MEDICAL NUTRITION THERAPY• FATS
– 20 – 35% of total calories– Saturated fats < 7% of total calories– < 200 mg/day of dietary cholesterol– Two or more servings of fish/week– Minimal trans fats consumption
• CARBOHYDRATES– 45 - 65% of total calorie intake– Type & amount of carbohydrate is important– Sucrose containing food must be consumed with adjustments in insulin
• PROTEINS– 10 – 35% of total calorie intake
• OTHER COMPONENTS– Fibre containing food may reduce postprandial glucose excrusions– Nonnutrient sweeteners
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EXERCISE
• Around 150 mins/week
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ASSESSMENT OF LONG TERM GLYCEMIC CONTROL
• GLYCATED HAEMOGLOBIN (HbA1C)– Non-enzymatic glycation of hemoglobin– Keep less than 7%– That is around < 170 mg/dl– Status of around last 3 months
• FRUCTOSEAMINE ASSAY– For prior 2 weeks
• Other method is : 1,5 anhydroglucitol assay
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TREATMENT OF DM
• Type I DM– Give insulin primarily
• Type II DM– Give oral hypoglycemic drugs, primarily
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TREATMENT OF TYPE I DM
PREPARATION ONSET PEAK EFFECTIVE DURATION
SHORT ACTING, SC (Lispro, Aspart, Glulisine) <0.25 0.5 – 1.5 3 – 4
SHORT ACTING, SC (regular) 0.5 – 1.0 2 – 3 4 – 6
SHORT ACTING, INHALED (inhaled regular insulin) < 0.25 0.5 – 105 4 – 6
LONG ACTING (NPH, Detemir, Glargine)
1 – 4 6 – 10 10 – 16 Glargine up to 24 hrs
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http://img.medscape.com/fullsize/migrated/501/976/smj501976.fig3.gif
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• Other agent that can improve glucose control are:– Pramlintide– Insulin pumps
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TREATMENT OF TYPE II DMDRUGS MECHANISM OF ACTION
AGENT – SPECIFIC
ADVANTAGESAGENT – SPECIFIC DISADVANTAGES
BIGUANIDES (Metformin)
Reduce hepatic glucose production & insulin resistance, weight loss,
Weight loss Lactic acidosis, diarrhoea, vomitting
Alfa-Glucosidase inhibitors (Acarbose, Miglitol)
Reduce glucose absorption
Reduce postprandial hypoglycemia
GI flatulence, LFT elevated
Dipeptidyl Peptidase IV inhibitors (Sitgliptin)
Prolongs endogenous GLP-1 action
Do not cause hypoglycemia
Insulin secretagogues
Increase insulin secretion
Lower fasting blood glucose
Hypoglycemia, weight gain
Thiazolidinediones (Rosiglitazone, Pioglitazone)
Reduce insulin resistance, increase glucose utilisation
Lower insulin requirements
Peripheral edema, CHF, weight gain, fractures, macular edema
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DRUGS MECHANISM OF ACTION
AGENT – SPECIFIC ADVANTAGES
AGENT – SPECIFIC DISADVANTAGES
INSULIN Increase glucose utilisation & other anabolic actions
Known safety profile
Weight gain, hypoglycemia
GLP-1 AGONIST (EXENATIDE)
Increase insulin, reduce glucagon, slow gastric emptying
Weight loss Increased risk of hypoglycemia with insulin secretogogues
AMYLIN AGONISTS (PRAMLINTIDE)
Slow gastric emptying, reduce glucagon
Reduce postprandial glycemia, weigh loss
Increased risk of hypoglycemia with insulin secretogogues
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TIKAL KANSARAINTERN
CIVIL HOSPITALAHMEDABAD