ABCD MEDICAL

MBBS Medical
Questions
Diabetes

Dr. Jason Smith (MBBS)

Dr. Sumeet Pratap (MBBS)
MBBS Questions and Answers on
Diabetes
Q1.

What are the primary types of diabetes, and how do they differ in terms of pathophysiology,
clinical presentation, and management?

The primary types of diabetes mellitus are type 1 diabetes, type 2 diabetes, and gestational
diabetes mellitus (GDM). Each type differs in terms of pathophysiology, clinical presentation,
and management:

1. Type 1 Diabetes Mellitus:

Pathophysiology:

Type 1 diabetes is characterized by autoimmune destruction of pancreatic beta cells, resulting in

absolute insulin deficiency. This autoimmune process is believed to be triggered by genetic
predisposition and environmental factors.

Clinical Presentation:

● Typically presents in childhood or adolescence, although it can occur at any age.

● Patients often present with symptoms of hyperglycemia, such as polyuria, polydipsia,
polyphagia, weight loss, fatigue, and blurred vision.
● Onset is usually abrupt, with rapid progression of symptoms.

Management:

● Requires lifelong exogenous insulin therapy to replace the deficient insulin secretion.
● Multiple daily injections of insulin or insulin pump therapy are commonly used.
● Close monitoring of blood glucose levels, carbohydrate intake, and insulin doses is
essential.
● Education on insulin administration, blood glucose monitoring, and hypoglycemia
management is crucial.

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2. Type 2 Diabetes Mellitus:

Pathophysiology:

Type 2 diabetes is characterized by insulin resistance and relative insulin deficiency. Insulin
resistance occurs when target tissues (e.g., liver, muscle, adipose tissue) become less
responsive to insulin action, leading to impaired glucose uptake and utilization.

Clinical Presentation:

● Typically occurs in adults, but increasingly diagnosed in children and adolescents due to
rising obesity rates.
● Often asymptomatic initially, with many cases detected incidentally through routine
screening.
● Symptoms of hyperglycemia may develop gradually and include polyuria, polydipsia,
fatigue, and blurred vision.

Management:

● Initial management focuses on lifestyle modifications, including diet, exercise, and

weight loss.
● Oral antidiabetic medications (e.g., metformin, sulfonylureas, DPP-4 inhibitors, SGLT2
inhibitors) may be prescribed to improve glycemic control.
● Insulin therapy may be required if oral medications are inadequate in controlling blood
glucose levels.
● Regular monitoring of blood glucose levels, HbA1c, lipid profile, blood pressure, and
kidney function is essential.

3. Gestational Diabetes Mellitus (GDM):

Pathophysiology:

GDM occurs during pregnancy and is characterized by glucose intolerance that develops or is
first recognized during gestation. It is thought to result from hormonal changes during pregnancy
that increase insulin resistance.

Clinical Presentation:

● Often asymptomatic and diagnosed through routine screening during pregnancy.

● Some women may experience symptoms of hyperglycemia, such as increased thirst,
urination, and fatigue.

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Management:

● Lifestyle modifications, including diet and exercise, are the primary interventions for
managing GDM.
● Blood glucose monitoring and glycemic control are crucial to reduce the risk of adverse
outcomes for both the mother and the fetus.
● Insulin therapy may be necessary if dietary and lifestyle interventions are insufficient to
maintain target blood glucose levels.
● Close monitoring of fetal growth and maternal health is essential throughout pregnancy.

Type 1 diabetes is characterized by autoimmune destruction of pancreatic beta cells and

requires lifelong insulin therapy. Type 2 diabetes involves insulin resistance and relative insulin
deficiency and is managed initially with lifestyle modifications and may progress to require oral
antidiabetic medications or insulin therapy. Gestational diabetes mellitus occurs during
pregnancy and is managed through lifestyle modifications and, if necessary, insulin therapy to
optimize maternal and fetal health.

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Q2.

Describe the diagnostic criteria used to establish a diagnosis of diabetes mellitus. How are
these criteria applied in clinical practice?

The diagnostic criteria for diabetes mellitus are established by various organizations such as the
American Diabetes Association (ADA) and the World Health Organization (WHO). These criteria
are based on measurements of blood glucose levels and are used to identify individuals with
diabetes.

1.) Fasting Plasma Glucose (FPG) Test:

Criteria:

Diabetes: Fasting plasma glucose level ≥ 126 mg/dL (7.0 mmol/L) on two separate occasions.
Impaired Fasting Glucose (IFG): Fasting plasma glucose level between 100-125 mg/dL (5.6-6.9
mmol/L), indicating an increased risk for diabetes.

Application:

● FPG test is performed after an overnight fast (usually 8 hours).

● If the initial FPG level is ≥ 126 mg/dL, a repeat test is recommended to confirm the
diagnosis.
● Diagnosis of diabetes is made if the FPG level is ≥ 126 mg/dL on two separate
occasions.

2.) Oral Glucose Tolerance Test (OGTT):

Criteria:

Diabetes: 2-hour plasma glucose level ≥ 200 mg/dL (11.1 mmol/L) during an OGTT.
Impaired Glucose Tolerance (IGT): 2-hour plasma glucose level between 140-199 mg/dL
(7.8-11.0 mmol/L), indicating increased risk for diabetes.
Application:

● OGTT involves administering a standardized glucose solution (75 g) orally, followed by

blood glucose measurements at baseline and 2 hours post-ingestion.
● Diagnosis of diabetes is made if the 2-hour plasma glucose level is ≥ 200 mg/dL during
the OGTT.

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 3.) Hemoglobin A1c (HbA1c) Test

Criteria:

Diabetes: HbA1c level ≥ 6.5% (48 mmol/mol).

Prediabetes: HbA1c level between 5.7-6.4% (39-47 mmol/mol).

Application:

● HbA1c test measures the average blood glucose level over the past 2-3 months.
● Diagnosis of diabetes is made if the HbA1c level is ≥ 6.5% on two separate occasions.
● HbA1c test does not require fasting and can be performed at any time of the day.

4.) Random Plasma Glucose Test:

Criteria:

Diabetes: Random plasma glucose level ≥ 200 mg/dL (11.1 mmol/L) in a patient with classic
symptoms of hyperglycemia.

Application:

A random plasma glucose test is performed without regard to the time since the last meal.
Diagnosis of diabetes is made if the random plasma glucose level is ≥ 200 mg/dL in a patient
with symptoms such as polyuria, polydipsia, and unexplained weight loss.

Clinical Application:

● Healthcare providers use a combination of clinical symptoms, risk factors, and diagnostic
test results to diagnose diabetes mellitus.
● The choice of diagnostic test may vary depending on factors such as patient's age,
clinical presentation, comorbidities, and convenience.
● Diagnosis is confirmed based on repeat testing or a combination of different diagnostic
criteria to minimize false positives.

Once diagnosed, patients are stratified into different categories based on glycemic control and
risk for complications to guide management decisions.

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Q3.

Discuss the role of insulin in glucose metabolism and regulation. How does insulin deficiency or
resistance contribute to the development of diabetes?

Insulin plays a central role in glucose metabolism and regulation by facilitating the uptake,
utilization, and storage of glucose in various tissues throughout the body. Its actions are
essential for maintaining normal blood glucose levels and ensuring adequate energy supply to
cells.

Role of Insulin in Glucose Metabolism

1.) Glucose Uptake: Insulin promotes the uptake of glucose into cells, particularly muscle,
adipose (fat), and liver cells, by facilitating the translocation of glucose transporter
proteins (GLUTs) to the cell membrane. This increases the rate of glucose uptake into
cells, lowering blood glucose levels.

2.) Glycolysis: Once inside the cell, glucose undergoes glycolysis, a series of enzymatic
reactions that break down glucose into pyruvate, generating ATP (adenosine
triphosphate), the primary energy currency of cells. Insulin indirectly stimulates glycolysis
by promoting the synthesis and activity of enzymes involved in this process.

3.) Glycogen Synthesis: Insulin stimulates glycogen synthesis in the liver and muscle cells
by activating glycogen synthase, the enzyme responsible for linking glucose molecules
into glycogen, a branched polymer that serves as a storage form of glucose. This helps
to lower blood glucose levels by removing excess glucose from circulation and storing it
for future energy needs.

4.) Inhibition of Gluconeogenesis: Insulin inhibits gluconeogenesis, the process by which

the liver produces glucose from non-carbohydrate precursors such as amino acids and
glycerol. By suppressing gluconeogenesis, insulin helps prevent excessive glucose
production and release into the bloodstream.

5.) Lipogenesis: Insulin promotes lipogenesis, the synthesis of fatty acids from glucose and
other precursors, primarily in adipose tissue. This process is important for storing excess
glucose as triglycerides, which are then stored in adipose tissue for long-term energy
storage.

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Contribution to Diabetes

Insulin Deficiency (Type 1 Diabetes)

In type 1 diabetes, autoimmune destruction of pancreatic beta cells leads to an absolute

deficiency of insulin production. Without sufficient insulin, glucose uptake into cells is impaired,
resulting in hyperglycemia (high blood glucose levels). Cells are unable to use glucose for
energy, leading to increased breakdown of fats and proteins for fuel, resulting in weight loss,
ketosis, and metabolic acidosis.

Insulin Resistance (Type 2 Diabetes)

In type 2 diabetes, cells become resistant to the effects of insulin, leading to reduced glucose
uptake and utilization despite normal or elevated insulin levels. This insulin resistance primarily
affects muscle, liver, and adipose tissue. As a compensatory mechanism, the pancreas
increases insulin secretion to overcome insulin resistance. Over time, however, pancreatic beta
cells may become exhausted and unable to produce sufficient insulin, leading to relative insulin
deficiency. Insulin resistance also contributes to dyslipidemia, inflammation, and endothelial
dysfunction, increasing the risk of cardiovascular complications associated with type 2 diabetes.

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Q4.

What are the acute and chronic complications associated with diabetes mellitus? How can these
complications be prevented or managed effectively?

Diabetes mellitus is associated with a wide range of acute and chronic complications that can
affect various organ systems throughout the body.

Acute Complications

1.) Diabetic Ketoacidosis (DKA)

Description: DKA is a life-threatening condition characterized by severe hyperglycemia, ketosis,

and metabolic acidosis.

Prevention and Management: Regular monitoring of blood glucose levels, adherence to insulin
therapy, hydration, correction of electrolyte imbalances, and early recognition and treatment of
precipitating factors (e.g., infection, insulin omission).

2.) Hyperosmolar Hyperglycemic State (HHS)

Description: HHS is a severe complication characterized by profound hyperglycemia,

dehydration, and altered mental status, often occurring in elderly patients with type 2 diabetes.

Prevention and Management: Similar to DKA, focusing on fluid replacement, correction of

electrolyte imbalances, insulin therapy, and identification and treatment of underlying triggers
(e.g., infections, medications).

Chronic Complications

1.) Microvascular Complications

Description: Microvascular complications include diabetic retinopathy (leading cause of

blindness), diabetic nephropathy (leading cause of end-stage renal disease), and diabetic
neuropathy (nerve damage leading to sensory, motor, and autonomic dysfunction).

Prevention and Management: Tight glycemic control, blood pressure control, regular eye and
foot exams, renal function monitoring, lifestyle modifications (e.g., smoking cessation, regular
exercise), and medications (e.g., ACE inhibitors/ARBs for nephropathy, neuropathic pain
medications for neuropathy).

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 2.) Macrovascular Complications

Description: Macrovascular complications include cardiovascular diseases such as coronary

artery disease, stroke, and peripheral arterial disease, which are major causes of morbidity and
mortality in individuals with diabetes.

Prevention and Management: Aggressive management of cardiovascular risk factors, including

blood pressure control, lipid management (e.g., statin therapy), smoking cessation, regular
physical activity, healthy diet, and antiplatelet therapy (e.g., aspirin).

3.) Diabetic Foot Complications

Description: Diabetic foot complications include neuropathic ulcers, infections, and peripheral
arterial disease, which can lead to foot amputations if not managed promptly.

Prevention and Management: Daily foot care, regular foot exams, appropriate footwear,
glycemic control, smoking cessation, early detection and treatment of foot ulcers or infections,
and multidisciplinary foot care teams for high-risk individuals.

Other Complications

1.) Gastroparesis: Delayed gastric emptying leading to gastrointestinal symptoms.

Management includes dietary modifications, medications to improve gastric motility, and
insulin therapy adjustments.

2.) Hypoglycemia: Abnormally low blood glucose levels that can lead to neuroglycopenic
symptoms and impaired consciousness. Prevention involves individualized glycemic
targets, appropriate insulin dosing, carbohydrate counting, and recognition of
hypoglycemia symptoms.

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Q5.

Explain the pathophysiology of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic

state (HHS). What are the key clinical features and management principles for these acute
complications of diabetes?

Pathophysiology of Diabetic Ketoacidosis (DKA)

1. Insulin Deficiency: DKA typically occurs in individuals with type 1 diabetes or in those
with type 2 diabetes who have profound insulin deficiency. Insufficient insulin levels lead
to uncontrolled lipolysis and increased free fatty acid release from adipose tissue.
2. Increased Lipolysis: In the absence of adequate insulin, free fatty acids are converted
into ketone bodies (acetoacetate and β-hydroxybutyrate) in the liver through
ketogenesis.
3. Ketone Accumulation: The overproduction of ketone bodies overwhelms the buffering
capacity of the body, leading to ketonemia and ketonuria. This results in metabolic
acidosis as ketones are acidic compounds.
4. Hyperglycemia: Insulin deficiency also leads to uncontrolled hepatic gluconeogenesis
and glycogenolysis, contributing to severe hyperglycemia.
5. Dehydration and Electrolyte Imbalance: Hyperglycemia induces osmotic diuresis, leading
to dehydration, electrolyte loss (particularly potassium), and intravascular volume
depletion.

Clinical Features of Diabetic Ketoacidosis (DKA)

● Polyuria, Polydipsia, Polyphagia: Classic symptoms of hyperglycemia.

● Nausea, Vomiting, Abdominal Pain: Common gastrointestinal symptoms.
● Kussmaul Respirations: Deep, rapid breathing as a compensatory mechanism to
decrease blood acidity (acidosis).
● Fruity Breath Odor: Due to the presence of acetone in exhaled breath.
● Dehydration: Manifested by dry mucous membranes, decreased skin turgor, and
orthostatic hypotension.
● Altered Mental Status: Ranging from confusion to coma, reflecting the severity of
metabolic derangements.

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Management Principles for Diabetic Ketoacidosis (DKA)

1. Fluid Resuscitation: Rapid intravenous infusion of isotonic saline to restore intravascular

volume and correct dehydration.
2. Insulin Therapy: Continuous intravenous insulin infusion to suppress lipolysis, promote
glucose uptake, and reduce ketone production. Transition to subcutaneous insulin when
ketosis resolves and patient can tolerate oral intake.
3. Electrolyte Replacement: Correction of electrolyte imbalances, particularly potassium,
phosphorus, and magnesium, based on frequent monitoring of serum levels.
4. Correction of Acidosis: Administration of sodium bicarbonate may be considered in
severe acidosis (pH <7.0), although controversial due to potential adverse effects.
5. Identification and Treatment of Precipitating Factors: Address underlying triggers such
as infection, noncompliance with insulin therapy, or other medical conditions.

Pathophysiology of Hyperosmolar Hyperglycemic State (HHS)

1. Severe Hyperglycemia: HHS typically occurs in individuals with type 2 diabetes and is
characterized by extreme hyperglycemia (>600 mg/dL) due to insulin resistance and
relative insulin deficiency.
2. Hyperosmolarity: Hyperglycemia induces osmotic diuresis, leading to significant
dehydration and intravascular volume depletion.
3. Absence of Ketosis: Unlike DKA, HHS is characterized by the absence of significant
ketosis and metabolic acidosis. Instead, there is marked hyperosmolarity due to
hyperglycemia.

Clinical Features of Hyperosmolar Hyperglycemic State (HHS)

● Profound Dehydration: Severe dehydration with profound thirst, dry mucous membranes,
decreased skin turgor, and signs of hypovolemic shock.
● Altered Mental Status: Neurological symptoms ranging from confusion to stupor or coma,
reflecting the severity of hyperosmolarity.
● Neurological Symptoms: Seizures, focal deficits, and hemiparesis may occur in severe
cases.

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Management Principles for Hyperosmolar Hyperglycemic State (HHS)
1. Fluid Resuscitation: Aggressive intravenous fluid replacement with isotonic saline to
correct dehydration and restore intravascular volume.
2. Insulin Therapy: Initiation of continuous intravenous insulin infusion to promote glucose
uptake and reduce hyperglycemia. Transition to subcutaneous insulin when patient can
tolerate oral intake.
3. Electrolyte Replacement: Correction of electrolyte imbalances, particularly potassium,
phosphorus, and magnesium, based on frequent monitoring of serum levels.
4. Gradual Correction of Hyperglycemia: Avoid rapid reduction of blood glucose to prevent
cerebral edema and other complications. Aim for gradual reduction in blood glucose
levels (~50-75 mg/dL/hour) until target range is achieved.
5. Identification and Treatment of Precipitating Factors: Address underlying triggers such
as infection, medication noncompliance, or other medical conditions contributing to
hyperglycemia and dehydration.

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Q6.

Discuss the importance of lifestyle modifications, including diet, exercise, and weight
management, in the prevention and management of diabetes mellitus.

Lifestyle modifications, including dietary changes, regular physical activity, and weight
management, play a crucial role in both the prevention and management of diabetes mellitus.
These interventions are fundamental components of comprehensive diabetes care and can
significantly improve glycemic control, reduce the risk of complications, and enhance overall
health and well-being.

Prevention of Diabetes Mellitus

Dietary Modifications

● Consuming a balanced diet rich in whole grains, fruits, vegetables, lean proteins, and
healthy fats can help prevent the development of type 2 diabetes.
● Emphasizing high-fiber foods and limiting refined carbohydrates and added sugars can
help regulate blood glucose levels and reduce the risk of insulin resistance.
● Portion control and mindful eating practices can prevent overeating and excessive
calorie intake, which are risk factors for obesity and insulin resistance.

Regular Physical Activity

● Engaging in regular physical activity, such as brisk walking, jogging, cycling, or

swimming, improves insulin sensitivity and glucose uptake by muscle cells.
● Aim for at least 150 minutes of moderate-intensity aerobic exercise per week, along with
resistance training exercises to build muscle mass and enhance metabolic health.
● Incorporating daily physical activity into routine tasks, such as taking the stairs instead of
the elevator or walking instead of driving short distances, can contribute to overall fitness
and weight management.

Weight Management

● Maintaining a healthy weight through proper diet and regular exercise is essential for
preventing obesity, a major risk factor for type 2 diabetes.
● Achieving and maintaining a modest weight loss (5-10% of body weight) can significantly
reduce the risk of developing diabetes in high-risk individuals, such as those with
prediabetes or a family history of diabetes.

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Focus on sustainable lifestyle changes rather than short-term restrictive diets, emphasizing
long-term behavior modifications and healthy habits.

Management of Diabetes Mellitus

Dietary Management

● Following a balanced meal plan that includes carbohydrates, proteins, and fats in
appropriate proportions helps regulate blood glucose levels and prevent postprandial
hyperglycemia.
● Monitoring carbohydrate intake, spacing meals evenly throughout the day, and avoiding
large fluctuations in blood glucose levels can help optimize glycemic control.
● Consulting a registered dietitian or diabetes educator for personalized dietary
recommendations and meal planning strategies tailored to individual needs and
preferences.

Regular Physical Activity

● Incorporating regular exercise into daily routines helps improve insulin sensitivity, lower
blood glucose levels, and reduce cardiovascular risk factors in individuals with diabetes.
● Aim for a combination of aerobic exercise, strength training, and flexibility exercises, with
guidance from healthcare professionals to ensure safety and effectiveness.
● Monitoring blood glucose levels before, during, and after exercise, and adjusting insulin
doses or carbohydrate intake as needed to prevent hypoglycemia or hyperglycemia.

Weight Management

● Achieving and maintaining a healthy weight through diet, exercise, and behavior
modifications is essential for managing diabetes and preventing complications.
● Weight loss in overweight or obese individuals with diabetes can improve glycemic
control, reduce the need for diabetes medications, and lower the risk of cardiovascular
events.
● Setting realistic weight loss goals, adopting sustainable lifestyle changes, and seeking
support from healthcare providers, dietitians, and support groups can facilitate
successful weight management.

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Q7.

What are the pharmacological treatment options available for managing diabetes mellitus? How
do these medications work, and what are their respective indications, contraindications, and
adverse effects?

Pharmacological treatment options for managing diabetes mellitus include various classes of
medications that target different aspects of glucose metabolism and regulation.

1. Insulin

Mechanism of Action: Insulin replacement therapy replaces deficient endogenous insulin and
promotes glucose uptake by peripheral tissues, inhibits hepatic glucose production, and
facilitates glucose storage as glycogen.

Indications: Used in type 1 diabetes and advanced type 2 diabetes when oral medications are
inadequate in achieving glycemic control.

Contraindications: Hypoglycemia, hypersensitivity to insulin or its components.

Adverse Effects: Hypoglycemia, weight gain, injection site reactions, allergic reactions.

2. Metformin (Biguanide)

Mechanism of Action: Decreases hepatic glucose production, enhances insulin sensitivity in

peripheral tissues, and reduces intestinal glucose absorption.

Indications: First-line treatment for type 2 diabetes, particularly in overweight or obese

individuals.

Contraindications: Renal impairment (creatinine clearance <30 mL/min), liver disease, acute or
chronic metabolic acidosis, alcohol abuse, contrast dye exposure.

Adverse Effects: Gastrointestinal side effects (diarrhea, nausea, abdominal discomfort), lactic
acidosis (rare), vitamin B12 deficiency.

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3. Sulfonylureas (e.g., Glipizide, Glyburide)

Mechanism of Action: Stimulate insulin secretion from pancreatic beta cells by binding to
sulfonylurea receptors on the cell membrane.

Indications: Used in type 2 diabetes when lifestyle modifications and metformin fail to achieve
glycemic control.

Contraindications: Hypersensitivity to sulfonylureas, type 1 diabetes, severe renal or hepatic

impairment.

Adverse Effects: Hypoglycemia, weight gain, gastrointestinal disturbances, skin reactions, rare
cases of hematologic and hepatic toxicity.

4. Dipeptidyl Peptidase-4 (DPP-4) Inhibitors (e.g., Sitagliptin, Linagliptin)

Mechanism of Action: Inhibit the enzyme DPP-4, which degrades incretin hormones (GLP-1 and
GIP), leading to increased insulin secretion and decreased glucagon secretion.

Indications: Used as monotherapy or in combination with other antidiabetic agents in type 2

diabetes.

Contraindications: Hypersensitivity to DPP-4 inhibitors, history of pancreatitis.

Adverse Effects: Upper respiratory tract infections, headache, nasopharyngitis, pancreatitis

(rare).

5. SGLT2 Inhibitors (e.g., Canagliflozin, Empagliflozin)

Mechanism of Action: Inhibit sodium-glucose cotransporter 2 (SGLT2) in the proximal renal

tubules, leading to increased urinary glucose excretion and decreased blood glucose levels.

Indications: Used as monotherapy or in combination with other antidiabetic agents in type 2

diabetes.

Contraindications: Severe renal impairment (eGFR <30 mL/min/1.73m^2), end-stage renal

disease, ketoacidosis, type 1 diabetes.

Adverse Effects: Genital mycotic infections, urinary tract infections, polyuria, hypotension,
volume depletion, euglycemic diabetic ketoacidosis (rare).

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6. Thiazolidinediones (e.g., Pioglitazone, Rosiglitazone)

Mechanism of Action: Activate peroxisome proliferator-activated receptor gamma (PPAR-γ)

receptors, leading to improved insulin sensitivity in adipose tissue, skeletal muscle, and liver.
Indications: Used as second- or third-line therapy in type 2 diabetes.

Contraindications: Heart failure, liver disease, active bladder cancer, hypersensitivity to

thiazolidinediones.

Adverse Effects: Edema, weight gain, increased risk of heart failure, bone fractures,
hepatotoxicity (rare).

7. GLP-1 Receptor Agonists (e.g., Liraglutide, Exenatide)

Mechanism of Action: Mimic the action of GLP-1 incretin hormones, stimulating insulin
secretion, inhibiting glucagon secretion, delaying gastric emptying, and promoting satiety.

Indications: Used as adjunctive therapy in type 2 diabetes, particularly in overweight or obese

individuals.

Contraindications: History of medullary thyroid carcinoma or multiple endocrine neoplasia

syndrome type 2, pancreatitis, severe gastrointestinal disease.

Adverse Effects: Nausea, vomiting, diarrhea, constipation, injection site reactions, pancreatitis
(rare).

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Q8.

How does gestational diabetes mellitus (GDM) differ from other types of diabetes? What are the
implications for both the mother and the fetus during pregnancy and childbirth?

Gestational diabetes mellitus (GDM) is a type of diabetes that develops during pregnancy and
usually resolves after childbirth.

It differs from other types of diabetes in several key ways:

Differences from Other Types of Diabetes

Onset: GDM typically develops during the second or third trimester of pregnancy, whereas type
1 and type 2 diabetes occur outside of pregnancy.

Pathophysiology: GDM results from hormonal changes during pregnancy that increase insulin
resistance, particularly in the third trimester. In contrast, type 1 diabetes is caused by
autoimmune destruction of pancreatic beta cells, and type 2 diabetes is characterized by insulin
resistance and relative insulin deficiency.

Risk Factors: While obesity and a family history of diabetes are risk factors for both GDM and
type 2 diabetes, GDM is also influenced by pregnancy-related factors such as maternal age,
gestational weight gain, and previous history of GDM or macrosomia (large birth weight baby).

Implications for the Mother and Fetus

Maternal Complications

● Women with GDM are at increased risk of developing pregnancy-related complications,

including preeclampsia (hypertension and proteinuria), gestational hypertension, and
cesarean delivery.
● GDM also increases the long-term risk of developing type 2 diabetes mellitus in the
mother, highlighting the importance of postpartum screening and follow-up care.

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Fetal Complications

● Infants born to mothers with GDM are at higher risk of macrosomia (large birth weight),
which can lead to birth trauma, shoulder dystocia, and cesarean delivery.
● Neonatal hypoglycemia may occur in infants born to mothers with GDM due to fetal
hyperinsulinemia in response to maternal hyperglycemia during pregnancy.
● Other fetal complications associated with GDM include neonatal jaundice, respiratory
distress syndrome, and an increased risk of developing obesity and type 2 diabetes later
in life.

Management and Treatment

1. Screening: Pregnant women are routinely screened for GDM between 24 and 28 weeks
of gestation using oral glucose tolerance tests (OGTT) or other screening methods.

2. Lifestyle Modifications: Women diagnosed with GDM are advised to make dietary
modifications, engage in regular physical activity, and monitor blood glucose levels to
maintain optimal glycemic control during pregnancy.

3. Medical Treatment: Insulin therapy may be initiated if lifestyle modifications alone are
insufficient in achieving glycemic targets. Oral antidiabetic medications such as
metformin or glyburide may also be used in select cases.

4. Fetal Monitoring: Close monitoring of fetal growth and well-being is essential in

pregnancies complicated by GDM, with regular ultrasound scans to assess fetal growth
and amniotic fluid volume.

5. Delivery Planning: Management of GDM often involves early delivery at term (39-40
weeks gestation) to reduce the risk of stillbirth and macrosomia while minimizing the risk
of neonatal complications associated with prematurity.

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Q9.

Describe the principles of diabetic foot care and the management of diabetic foot ulcers. What
strategies can be implemented to prevent foot complications in patients with diabetes?

Diabetic foot care is crucial for individuals with diabetes to prevent the development of foot
ulcers, infections, and other complications that can lead to serious consequences, including
lower limb amputations.

Principles of Diabetic Foot Care

1.) Daily Foot Inspection:

● Inspect feet daily for any signs of injury, blisters, redness, swelling, or changes in skin
color.
● Use a mirror or seek assistance if unable to visualize the entire foot.

2.) Proper Foot Hygiene:

● Wash feet daily with mild soap and lukewarm water, ensuring thorough drying, especially
between the toes.
● Avoid soaking feet, as it can lead to maceration of the skin.

3.) Moisturizing and Skin Protection:

● Apply moisturizer to keep skin hydrated and prevent dryness, but avoid applying
between the toes.
● Use a protective barrier cream to prevent skin breakdown and friction injuries.

4.) Nail Care:

● Trim toenails straight across and file sharp edges to prevent ingrown toenails and
injuries.
● Avoid cutting nails too short to prevent nail bed injuries.

5.) Footwear:
● Wear properly fitting, supportive shoes with a wide toe box to prevent pressure points
and rubbing.
● Avoid high heels, open-toed shoes, and shoes with pointed toes.
● Inspect shoes regularly for foreign objects, rough edges, or signs of wear and tear.

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 6.) Foot Protection:

● Use protective footwear, such as diabetic shoes or custom orthotic inserts, to reduce
pressure and friction on the feet.
● Wear clean, dry socks made of moisture-wicking materials and change them daily.

Management of Diabetic Foot Ulcers

Wound Assessment:

● Assess the size, depth, and appearance of the ulcer, as well as signs of infection or
ischemia.
● Measure and document ulcer dimensions and characteristics regularly to monitor healing
progress.

Wound Cleansing

● Cleanse the ulcer with mild soap and water or a wound cleanser solution to remove
debris and bacteria.
● Use sterile saline or an antiseptic solution for heavily contaminated wounds.

Debridement:

● Remove necrotic tissue and calluses to promote wound healing and prevent infection.
● Debridement methods include sharp debridement, enzymatic debridement, or autolytic
debridement with dressings.

Infection Management:

● Treat infections promptly with appropriate antibiotics based on culture and sensitivity
results.
● Monitor for signs of systemic infection and escalate treatment if necessary.

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Offloading:

● Offload pressure from the ulcerated area using specialized footwear, total contact casts,
or removable cast walkers.
● Minimize weight-bearing on the affected foot to facilitate healing.

Dressings and Wound Care:

● Select appropriate dressings based on wound characteristics, moisture levels, and

healing trajectory.
● Change dressings regularly according to the wound care plan and monitor for signs of
complications.

Prevention Strategies for Foot Complications

1. Glycemic Control: Maintain optimal blood glucose levels to reduce the risk of peripheral
neuropathy and impaired wound healing.
2. Regular Foot Exams: Schedule regular foot exams with a healthcare provider, podiatrist,
or diabetes care team to detect early signs of foot complications.
3. Education and Self-Care: Educate patients about foot care principles, including daily foot
inspections, proper hygiene, and footwear selection.
4. Encourage patients to seek prompt medical attention for any foot problems or injuries.
5. Smoking Cessation: Advise patients to quit smoking, as smoking impairs circulation and
increases the risk of foot complications.
6. Peripheral Circulation Assessment: Assess peripheral vascular status regularly, and
refer patients for further evaluation if signs of peripheral arterial disease are present.
7. Footwear Modification: Provide guidance on proper footwear selection and recommend
customized orthotic inserts or diabetic shoes when necessary.

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Questions prepared by Dr. Jason Smith and Dr. Sumeet Pratap for Year 1 MBBS Physiology
(Tutorial)

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