Diabetes and RHD

Name of the Speaker

Dr. Rama Shankar
Associate Professor
Community Medicine
Date: 28/04/25
 Introduction to Diabetes

Diabetes is a group of metabolic disorders.

Characterized by hyperglycaemia in the absence of treatment.

Results from:
• Defects in insulin secretion.
• Defects in insulin action.
• Or both.
 Metabolic Disturbances in Diabetes

Disturbances in the metabolism of:

• Carbohydrates
• Fats
• Proteins

Diabetes has a heterogeneous aetio-pathology.

 Long-term Specific Effects of Diabetes

Microvascular complications:
•Retinopathy (eye)
•Nephropathy (kidneys)
•Neuropathy (nerves)
 Increased Risk of Other Diseases

People with diabetes are at higher risk

of:
•Heart disease
•Peripheral arterial disease
•Cerebrovascular disease (e.g., stroke)
 Other Associated Conditions

Obesity

Cataracts

Erectile dysfunction

Non-alcoholic fatty liver disease (NAFLD)

 Change from Previous
Type of Diabetes Brief Description
Classification

β-cell destruction (mostly immune-mediated) and absolute Type 1 sub-classes

Type 1 diabetes
insulin deficiency; common in childhood and early adulthood removed

Most common type; β-cell dysfunction and insulin resistance; Type 2 sub-classes
Type 2 diabetes
associated with overweight and obesity removed

Hybrid forms of
New type of diabetes
diabetes
Slowly evolving, Nomenclature changed
Similar to type 1 in adults but retains β-cell function; features of
immune-mediated (previously referred as
metabolic syndrome; single GAD autoantibody present
diabetes of adults LADA)

Presents with ketosis and insulin deficiency but later does not
Ketosis-prone type 2
require insulin; common episodes of ketosis; not immune- No change
diabetes
mediated
 Change from Previous
Type of Diabetes Brief Description
Classification
Other specific types

Monogenic diabetes (defects of β- Caused by gene mutations; Updated nomenclature for

cell function) neonatal period or early adulthood onset specific genetic defects
Caused by gene mutations;
Monogenic defects in insulin Updated nomenclature for
severe insulin resistance without obesity;
action specific genetic defects
β-cells fail to compensate
Conditions like trauma, tumor, inflammation affecting the
Diseases of the exocrine pancreas No change
pancreas, resulting in hyperglycemia

Diseases causing excess secretion of hormones acting as

Endocrine disorders No change
insulin antagonists
Drug- or chemical-induced Some medicines and chemicals impair insulin secretion or
No change
diabetes destroy β-cells
Infection-related diabetes Some viruses associated with direct β-cell destruction No change

Uncommon specific forms of

Associated with rare immune-mediated diseases No change
immune-mediated diabetes
Other genetic syndromes Genetic disorders and chromosomal abnormalities
No change
associated with diabetes increasing diabetes risk
 Change from Previous
Type of Diabetes Brief Description
Classification

Diabetes that does not clearly fit into other categories;

Unclassified diabetes New type of diabetes
used temporarily especially close to time of diagnosis

Hyperglycemia first detected

during pregnancy

Type 1 or type 2 diabetes first diagnosed during

- Diabetes mellitus in pregnancy No change
pregnancy

Hyperglycemia below diagnostic thresholds for diabetes Defined by 2013 diagnostic

- Gestational diabetes mellitus
but detected during pregnancy criteria

- Fasting plasma glucose ≥ 7.0 mmol/L or 2-hour post-load

Diagnostic Criteria for Diabetes
plasma glucose ≥ 11.1 mmol/L or HbA1c ≥ 48 mmol/mol

- Fasting plasma glucose 5.1–6.9 mmol/L or 1-hour post-

Diagnostic Criteria for Gestational
load plasma glucose ≥ 10.0 mmol/L or 2-hour post-load
Diabetes
plasma glucose 8.5–11.0 mmol/L
 Insulin Resistance Syndrome (Syndrome X)
• In obese type 2 diabetics, hyperglycaemia, hyperinsulinaemia, dyslipidaemia,
and hypertension are commonly associated.
• May result from a genetic defect producing insulin resistance, worsened by
obesity.
• Insulin resistance predisposes to hyperglycaemia, leading to
hyperinsulinaemia.
• Excess insulin:
• Increases triglyceride levels.
• Causes sodium retention by renal tubules → induces hypertension.
• High insulin levels stimulate endothelial proliferation, initiating
atherosclerosis.
 Natural History and Epidemiological
Determinants of Diabetes

Main cause: Insulin deficiency

• Absolute in type 1 diabetes

• Partial in type 2 diabetes

Leads to reduced glucose utilization →

Hyperglycaemia with Glycosuria
 Agent Factors
Pancreatic disorders (e.g., cystic fibrosis, inflammation, neoplasm)

Defects in insulin formation (e.g., abnormal insulin molecules)

Destruction of β-cells (e.g., viral infections, chemical agents)

Decreased insulin sensitivity (↓ insulin receptors in adipocytes/monocytes)

Genetic defects (e.g., mutations in insulin gene)

Auto-immunity (attack on insulin-producing cells)

Genetic control over insulin response to glucose

 Host Factors — Age

Diabetes can occur at any age

Prevalence rises steeply with age

Type 2 diabetes:
• Common in middle-aged and older adults
• Malnutrition-related diabetes in younger populations

Worse prognosis in young diabetics

 Host Factors — Sex and Genetics

Sex:
• Some countries: Male = Female prevalence
• South-East Asia: Slight male predominance
Genetic Factors:
• Strong genetic basis
• Type 2 diabetes: ~90% concordance in identical twins
• Type 1 diabetes: ~50% concordance
 Host Factors — Genetic Markers, Immune
Mechanisms

Genetic Markers:
• Type 1 diabetes associated with HLA-B8, B15, DR3, DR4
• Type 2 diabetes not HLA-associated

Immune Mechanisms:
• Cell-mediated and humoral autoimmunity against islet cells
• Environmental "triggers" may activate autoimmunity
 Host Factors — Obesity and Maternal
Diabetes
Obesity:
• Central (visceral) obesity is a major risk for type 2 diabetes
• Related to BMI, waist circumference, waist-hip ratio
• Voluntary weight loss improves insulin sensitivity
• Obesity does not play a major role in type 1 diabetes

Maternal Diabetes:
• Offspring of diabetic mothers (especially gestational diabetes) at high risk
• Threefold higher risk if mother develops diabetes before pregnancy
 Environmental Risk Factors for Diabetes

Susceptibility to diabetes may be unmasked by environmental factors in

genetically predisposed individuals.

Key risk factors include

• Sedentary lifestyle,
• Diet,
• Alcohol intake,
• Infections,
• Chemical agents,
• Stress, and
• Social class.
 Sedentary Lifestyle and Diet

Sedentary Lifestyle:
• Important risk factor for type 2 diabetes.
• Lack of exercise alters insulin and receptor interaction → insulin resistance.

Diet:
• High saturated fat intake → impaired glucose tolerance, hyperglycaemia,
and insulin resistance.
• Unsaturated and polyunsaturated fats (vegetable sources) reduce risk.
• Total fat intake >37% of energy → little benefit from changing fat quality.
 Dietary Fibre and Malnutrition

Dietary Fibre:
• High intake reduces blood glucose and insulin levels.
• Recommended intake: 20g/day of dietary fibre (whole grains,
vegetables, fruits).
Malnutrition:
• Early malnutrition leads to β-cell failure.
• Associated with impaired glucose tolerance later in life.
 Alcohol and Viral Infections

Alcohol:
• Excessive intake damages pancreas and liver.
• Promotes obesity, increasing diabetes risk.
Viral Infections:
• Viruses like rubella, mumps, coxsackievirus B4 implicated.
• May trigger β-cell destruction in genetically susceptible
individuals.
 Chemical Agents and Stress

Chemical Agents:
• Toxins like alloxan, streptozotocin, VALCOR damage β-cells.
• Cyanide-producing foods ( certain beans) can also be harmful.
Stress:
• Surgery, trauma, or emotional stress may trigger onset of
diabetes.
 Other Factors - Social Class

Other Factors:
•Socioeconomic status, occupation, education,
urbanization influence diabetes risk.
•Lower social classes now show higher
diabetes prevalence compared to the past.
 Symptoms and Signs of Diabetes

Symptoms of Diabetes:
• Thirst
• Frequent urination
• Blurred vision
• Fatigue
• Unintentional weight loss

Signs of Diabetes:
• Acute metabolic deterioration: Severe dehydration, Kussmaul’s respiration, vomiting, altered
consciousness
• Chronic complications: Acute coronary disease, stroke, kidney disease, vision loss, diabetic
foot
Diagnostic Criteria for Diabetes

Fasting venous or capillary plasma glucose:

• Diagnostic cut-off: ≥7.0 mmol/L (126 mg/dL)
• Comment: Least costly but difficulties ensuring a fasting state
2-hour post-load venous plasma glucose:
• Diagnostic cut-off: ≥11.1 mmol/L (200 mg/dL)
• Comment: Cumbersome, costly, and difficulties ensuring fasting
2-hour post-load capillary plasma glucose:
• Diagnostic cut-off: ≥12.2 mmol/L (220 mg/dL)
• Comment: Similar difficulties as with venous testing
 Diagnostic Criteria for Diabetes

Random plasma glucose:

• Diagnostic cut-off: ≥11.1 mmol/L (200 mg/dL)
• Comment: To be used only if symptoms are present
HbA1c:
• Diagnostic cut-off: 6.5% (48 mmol/mol)
• Comments:
• Less variability than plasma glucose
• No need for fasting, but costly and indirect
• Can be inaccurate in certain conditions (haemoglobinopathies, renal failure,
anaemias)
 Glycaemic Index (GI)
• Definition: The Glycaemic Index (GI) is a ranking system for
carbohydrates based on how quickly they raise blood glucose levels
after consumption.
• GI Scale:
• Low GI (≤55): Foods that cause a slow, gradual rise in blood glucose (e.g.,
lentils, apples).
• Medium GI (56-69): Foods that cause a moderate increase in blood glucose
(e.g., bananas, whole wheat bread).
• High GI (≥70): Foods that cause a rapid spike in blood glucose (e.g., white
bread, sugary snacks).
 Screening Methods
1. Urine Examination:
• Glucose tested 2 hours after a meal.
• Glycosuria suggests diabetes unless proved otherwise.
• Problems:
• Low sensitivity (10–50%) → many false negatives.
• High specificity (>90%) but occasional false positives.
• Not reliable for epidemiological surveys.

2. Blood Sugar Testing:

• Standard oral glucose test = cornerstone for diagnosis.
• Fasting, postprandial, or random blood samples used.
• Random samples are not reliable for epidemiological use.
• Fasting values alone are less reliable.
• 2-hour value after 75g oral glucose is preferred.
 Target Population for Screening

Whole population screening is not recommended.

High-risk groups to screen:

• Age ≥ 40 years.
• Family history of diabetes.
• Obese individuals.
• Women with babies >4.5 kg (or >3.5 kg in small populations).
• Women with excess weight gain during pregnancy.
• Patients with premature atherosclerosis.
Prevention and Care — Primary Prevention

Two strategies:
•Population strategy.
•High-risk strategy.
 Population Strategy for Primary Prevention

Limited scope for primary prevention of type 1 diabetes.

Focus on type 2 diabetes by addressing environmental risk

factors.

Emphasis on primordial prevention:

• Prevent emergence of risk factors before they appear.
 Preventive Measures
Maintain normal body weight.

Adopt healthy nutritional habits:

• Adequate protein intake.
• High intake of dietary fibre.
• Avoidance of sweet foods.

Promote physical exercise.

Eliminate factors like protein deficiency and food toxins.

Integrate preventive measures into broader non-communicable disease programs (e.g., for
coronary heart disease).
 High-Risk Strategy

No high-risk prevention strategy for type 1 diabetes.

For type 2 diabetes (NIDDM):

• Correct sedentary lifestyle, overnutrition, and obesity.
• Avoid alcohol and diabetogenic drugs (e.g., oral contraceptives).
• Control smoking, blood pressure, cholesterol, and triglyceride
levels.
• Focus on high-risk groups for maximum effectiveness.
Secondary Prevention — Goals

Maintain blood glucose levels close to normal.

Maintain ideal body weight.

Treatment options:
• (a) Diet alone: small balanced meals.
• (b) Diet + oral antidiabetic drugs.
• (c) Diet + insulin.
 Secondary Prevention — Management

Routine checks:
• Blood sugar, urine proteins/ketones, blood pressure, visual acuity, weight.
• Feet examination (doppler ultrasound for circulation, sensation check).

Importance of primary health care in management.

Glycosylated Hemoglobin (HbA1c):

• Measured every 6 months.
• Reflects average glucose over past 2–3 months.
 Secondary Prevention — Self-care
Diabetic patient responsibilities:
• Adherence to diet and drugs.
• Monitoring urine and blood glucose.
• Self-administration of insulin.
• Abstain from alcohol, maintain optimum weight.
• Attend periodic checkups.
• Recognize symptoms of glycosuria and hypoglycemia.

Home blood glucose monitoring:

• Immediate, accurate readings with capillary blood samples.

Carry an identification card with personal and treatment details.

 Tertiary Prevention

Aim: Prevent disability from diabetes complications (e.g.,

blindness, kidney failure, coronary thrombosis, gangrene).

Strategies:

• Establish specialized diabetic clinics and management units.

• Clinics in large towns and cities.
• Engage in basic, clinical, and epidemiological research.
• Establish local and national registries for diabetics.
 Rheumatic Heart Disease (RHD)
• Rheumatic Fever (RF) and Rheumatic Heart Disease (RHD) are closely linked
epidemiologically.

• Rheumatic fever is a febrile disease affecting connective tissues, especially the heart
and joints.

• Caused by infection of the throat with Group A β-haemolytic streptococci.

• RF is not a communicable disease, but results from a communicable infection

(streptococcal pharyngitis).

• RF can lead to RHD, a crippling disease.

 Rheumatic Heart Disease (RHD)

Consequences of RHD include:

• Continuing heart damage
• Increasing disabilities
• Repeated hospitalization
• Premature death (often by age 35 or earlier)

RHD is one of the most readily preventable chronic diseases.

 Epidemiological Factors (Agent)

Group A streptococcus is the causative agent.

Not all strains cause RF; strains with "rheumatogenic potential" are responsible.

Serotype M type 5 frequently associated with RF.

All Group A streptococci are sensitive to penicillin.

Virus like Coxsackie B4 may act as conditioning agent.

 Host and Environmental Factors
Age:
• RF typically affects children and adolescents (5–15 years).
• Also occurs in adults (20% of cases).
Sex:
• Disease affects both sexes equally.
• Prognosis is worse in females.
Immunity:
• Toxic–immunological hypothesis:
• Group A streptococcal products and host tissue components have antigenic cross-reaction.
• Leads to immune response resulting in RF.
 Host and Environmental Factors

Socio-economic Status:
• Linked to poverty, overcrowding, poor housing, inadequate health services,
and low disease awareness.
• Disease declines with improved standard of living but persists even in affluent
areas.

High-Risk Groups:
• Children aged 5–15 years.
• Slum dwellers.
• Those living in closed communities (e.g., barracks).
Determinants Effects Impact on RF and RHD Burden

- Higher incidence of acute

Socio-economic and environmental - Rapid spread of group A streptococcal streptococcal-pharyngitis and
factors (poverty, undernutrition, strains suppurative complications
overcrowding, poor housing) - Difficulties in accessing health care - Higher incidence of acute RF
- Higher rates of recurrent attacks

Health-system related factors: - Inadequate diagnosis and treatment of - Higher incidence of acute RF and its
- Shortage of resources for health care streptococcal pharyngitis recurrence
- Inadequate expertise of health-care - Misdiagnosis or late diagnosis of acute - Patients unaware of the first RF episode
providers RF - More severe evolution of disease

- Untimely initiation or lack of secondary

prophylaxis
- Higher rates of recurrent attacks with
- Inadequate secondary prophylaxis
Low-level awareness of the disease in more frequent and severe heart valve
and/or non-compliance with secondary
the community involvement
prophylaxis
- Higher rates of repeated hospital
admissions and expensive surgical
interventions
 Clinical Features of Rheumatic Fever

Fever:
• Present at onset of acute illness.
• May last for ~12 weeks or longer, with tendency to recur.
• Often accompanied by profuse sweating.

Polyarthritis:
• Seen in 90% of cases.
• Affects large joints (ankles, knees, elbows, wrists); occasionally small joints.
• Pain and swelling subside spontaneously within 5–7 days.
• No residual joint damage.
 Clinical Features (Continued)

Carditis:
• Occurs in 60–70% of cases.
• Involves all heart layers (pericardium, myocardium, valves).
• May start early without clinical signs.
• Manifestations: Tachycardia, murmurs, cardiac enlargement, pericarditis, heart
failure.
• First-degree AV block is the most common ECG finding.

Subcutaneous Nodules:
• Appear ~4 weeks after RF onset.
• Small, painless, non-tender, disappear without residual damage.
 Clinical Features (Continued)

Brain Involvement:
• Abnormal, jerky, purposeless movements (chorea).
• Gradually resolves without residual damage.
Skin:
• Various types of rashes may occur.
• Except carditis, other manifestations of RF do not cause
permanent damage.
 Diagnosis of Rheumatic Fever

Based on 2015 WHO Criteria and Revised Jones

Criteria.

Identification of low, medium, and high-risk

populations:
• Low-risk:
• Acute RF cases ≤2 per 100,000 school-age children per year.
• RHD cases ≤1 per 1,000 patients at any age per year.
 Modifications in Jones Criteria (2015)
Major Criteria:
• Low-risk population:
• Clinical/subclinical carditis (Doppler echocardiography recommended even without clinical
signs).
• Medium/High-risk population:
• Clinical/subclinical carditis and arthritis (monoarthritis/polyarthritis/possible polyarthralgia).

Minor Criteria:
• Low-risk population:
• Precisely defined parameters of inflammation and fever.
• Medium/High-risk population:
• Monoarthralgia plus defined inflammatory parameters and fever.
Criteria Low Risk Population High Risk Population

- Carditis (clinical or subclinical)

- Carditis (clinical or subclinical) - Arthritis (monoarthritis or
- Arthritis (only polyarthritis) polyarthritis)
Major Criteria - Chorea - Polyarthralgia
- Erythema marginatum - Chorea
- Subcutaneous nodules - Erythema marginatum
- Subcutaneous nodules

- Polyarthralgia - Monoarthralgia
- Hyperpyrexia (≥ 38.5°C) - Hyperpyrexia (≥ 38.0°C)
- ESR ≥ 60 mm/h and/or CRP ≥ 3.0 - ESR ≥ 30 mm/h and/or CRP ≥ 3.0
Minor Criteria mg/dl mg/dl
- Prolonged PR interval (after - Prolonged PR interval (after
accounting for age differences; if accounting for age differences; if
no carditis as a major criterion) no carditis as a major criterion)
 Diagnosis of Rheumatic Fever

First episode:
• Evidence of antecedent Group A β-hemolytic streptococcal infection.
• Confirmation of 2 major or 1 major + 2 minor or 3 minor criteria.

Subsequent episodes:
• Confirmation of 2 major or 1 major + 2 minor or 3 minor criteria.

Subclinical carditis:
• Detected only by Doppler echocardiography, not by auscultation.
 Echocardiographic (Doppler) Criteria

Pathological Mitral Regurgitation (all 4 criteria must be met):

• Visible in at least 2 projections.
• Regurgitation jet length ≥ 2 cm in 1 projection.
• Regurgitation peak velocity > 3 m/s.
• Pansystolic regurgitation.

Pathological Aortic Regurgitation (all 4 criteria must be met):

• Visible in at least 2 projections.
• Regurgitation jet length ≥ 1 cm in 1 projection.
• Regurgitation peak velocity > 3 m/s.
• Pandiastolic regurgitation.
 Pathological Mitral Regurgitation

[Link] in at least 2 views:

1. When we scan the heart, the leaking mitral valve should be clearly seen from two
different angles.
[Link] (jet) is big enough (≥ 2 cm):
1. The backflow of blood (the leak) must be at least 2 centimeters long in one view.
[Link] is fast (> 3 meters/second):
1. The speed of the blood leaking backward is very fast (more than 3 meters per second).
[Link] happens throughout heart pumping (pansystolic):
1. The leak is constant during the entire time when the heart is squeezing (systole).
 Pathological Aortic Regurgitation
[Link] in at least 2 views:
1. The leak at the aortic valve must be seen from two different angles.
[Link] (jet) is big enough (≥ 1 cm):
1. The backflow of blood here needs to be at least 1 centimeter long.
[Link] is fast (> 3 meters/second):
1. The speed of the leak is very fast (over 3 meters per second).
[Link] happens throughout heart filling (pandiastolic):
1. The leak is continuous when the heart is relaxing and filling (diastole).
 Prevention Strategies for Rheumatic Fever

Primary Prevention:
• Identify and treat streptococcal sore throat cases with penicillin.
• High-risk group focus: school-age children.
• Treatment options:
• Benzathine penicillin injection or
• Oral penicillin for 10 days.
• Alternatives for allergy: cephalosporins, erythromycin,
azithromycin.
 Challenges in Primary Prevention

Difficult in many developing countries due to:

• High number of infections.
• Inadequate healthcare services.
• Need for reliable laboratory confirmation.

Hence, secondary prevention becomes the focus.

 Secondary Prevention

Goal: Prevent recurrences of RF.

Approach:
• Regular intramuscular benzathine penicillin every 3 weeks.

Duration:
• Minimum 5 years or until 21 years of age.
• 10 years or until 40 years if there is a history of carditis.
• Life-long treatment for severe valvular disease.
 Non-Medical Measures

Improve living conditions (housing, sanitation).

Break the poverty–disease–poverty cycle.

Only penicillin prophylaxis is not sufficient without socioeconomic

improvement.

Socioeconomic upliftment can significantly reduce incidence.

 Evaluation of Rheumatic Heart Disease
Control Program
Best indicator: Prevalence of RHD among school children.

Method:
• Random surveys among children aged 6–14 years.
• Surveys every 5 years.
Sample size:
• 20,000 to 30,000 children depending on expected prevalence.
Thank You!!