Dr Emmyoung

16/06/2026

11/06/2026

Diabetes Mellitus – Comprehensive Lecture

1. Definition

Diabetes mellitus (DM) is a group of metabolic disorders characterized by chronic hyperglycemia resulting from:

- Defects in insulin secretion
- Defects in insulin action (insulin resistance)
- Or both

Persistent hyperglycemia leads to long-term damage, especially to:

- Eyes (retinopathy)
- Kidneys (nephropathy)
- Nerves (neuropathy)
- Heart and blood vessels (macrovascular disease)

2. Classification of Diabetes
1. Type 1 Diabetes Mellitus (T1DM)
- Autoimmune destruction of pancreatic beta cells
- Absolute insulin deficiency
- Risk of diabetic ketoacidosis (DKA)
- Usually younger onset, but can occur in adults
- Includes latent autoimmune diabetes in adults (LADA)
2. Type 2 Diabetes Mellitus (T2DM)
- >90% of adult cases
- Insulin resistance + progressive beta-cell dysfunction
- Often associated with obesity
- May be asymptomatic initially
3. Gestational Diabetes Mellitus (GDM)
- Diabetes diagnosed during pregnancy
- Increases future risk of T2DM
4. Other Specific Types
- Monogenic diabetes (MODY)
- Pancreatic disease
- Drug-induced (e.g., steroids)
- Endocrinopathies

3. Epidemiology

- Rapidly increasing worldwide
- Strongly linked to obesity and sedentary lifestyle
- Higher risk in:
- Asian
- Hispanic
- African descent
- Native American populations

4. Pathophysiology
Type 1 DM
- Autoimmune beta-cell destruction
- Absolute insulin deficiency
- Increased glucagon
- Lipolysis → ketone production → DKA risk
Type 2 DM
Core defects:
1. Insulin resistance (muscle, liver, adipose tissue)
2. Progressive beta-cell failure

Additional mechanisms:
- Increased hepatic glucose production
- Decreased incretin effect
- Increased glucagon secretion
- Renal glucose reabsorption
- Chronic inflammation

5. Risk Factors for Type 2 Diabetes
Non-modifiable
- Age ≥35 years
- Family history
- High-risk ethnicity
- History of gestational diabetes
- Genetic susceptibility
Modifiable
- Obesity (strongest risk factor)
- Sedentary lifestyle
- Unhealthy diet
- Smoking
- Hypertension
- Dyslipidemia
- Polycystic o***y syndrome

6. Clinical Presentation
Type 1
- Polyuria
- Polydipsia
- Weight loss
- Fatigue
- DKA in ~25% at diagnosis
Type 2
- Often asymptomatic
- Incidental hyperglycemia
- Classic symptoms:
- Polyuria
- Polydipsia
- Nocturia
- Blurred vision
- Severe cases:
- Hyperosmolar hyperglycemic state (HHS)

7. Diagnostic Criteria (Non-pregnant Adults)

Diagnosis requires one of the following:
A. Symptomatic hyperglycemia
- Random plasma glucose ≥200 mg/dL (11.1 mmol/L)
B. Asymptomatic (confirm on separate day)

1. Fasting plasma glucose (FPG) ≥126 mg/dL
(≥7.0 mmol/L)

2. 2-hour plasma glucose ≥200 mg/dL
during 75g OGTT

3. HbA1c ≥6.5%

If two different tests are discordant, repeat the abnormal test.

Always verify against local/regional diabetes guidelines.

8. Prediabetes (High-Risk State)
Impaired Fasting Glucose (IFG)
- FPG 100–125 mg/dL
Impaired Glucose Tolerance (IGT)
- 2-hour OGTT 140–199 mg/dL
HbA1c
- 5.7–6.4%

Risk increases progressively with higher values.

Annual monitoring recommended.

9. Screening Recommendations

Screen:
- Adults ≥35 years
- BMI ≥25 kg/m² (≥23 in Asian populations) + ≥1 risk factor
- History of gestational diabetes

Repeat:
- Every 2–3 years if normal
- Annually if prediabetes

10. Complications
Acute
1. Diabetic Ketoacidosis (DKA)
- Hyperglycemia
- Metabolic acidosis
- Ketones
- Common in T1DM
2. Hyperosmolar Hyperglycemic State (HHS)
- Severe hyperglycemia
- Severe dehydration
- Minimal ketosis
- More common in T2DM

Chronic Complications
Microvascular
- Retinopathy
- Nephropathy
- Neuropathy
Macrovascular
- Coronary artery disease
- Stroke
- Peripheral arterial disease

Risk correlates with duration and glycemic control.

11. Prevention of Type 2 Diabetes
Goals
- Prevent/delay diabetes onset
- Preserve beta-cell function
- Prevent complications
- Reduce healthcare burden
Lifestyle Intervention (First-line)

For IFG, IGT, or HbA1c 5.7–6.4%:

- Weight loss (5–10%)
- Moderate-intensity exercise ≥150 min/week
- Dietary modification
- Smoking cessation

Lifestyle intervention has sustained benefits.
Pharmacologic Prevention

Consider metformin in high-risk individuals:
- Age

29/05/2026

Early detection helps save the mother

24/05/2026

Dysfunctional Uterine Bleeding (DUB)

1. Definition

Dysfunctional uterine bleeding (DUB) refers to abnormal uterine bleeding (AUB) without identifiable structural, systemic, or pregnancy-related causes after appropriate evaluation.

It commonly occurs at the extremes of reproductive life:

Shortly after menarche

During the perimenopausal period

2. Normal Menstrual Parameters

Parameter Normal Range

Cycle length 21–35 days
Duration of flow 2–7 days
Blood loss Approximately 30–40 mL (≤80 mL)

3. Clinical Presentation

Symptoms

Heavy menstrual bleeding (menorrhagia)

Prolonged menstrual bleeding

Irregular menstrual cycles

Passage of blood clots

Flooding episodes

Dysmenorrhoea

Intermenstrual bleeding (IMB)

Post-coital bleeding (PCB)

Symptoms of anaemia:

Fatigue

Dizziness

Dyspnoea

Significant impairment in quality of life

4. Important History

Key areas to assess include:

Menstrual history:

Frequency

Duration

Volume of bleeding

Onset of symptoms:

Since menarche?

Recent changes?

Contraceptive history:

Hormonal contraception

Intrauterine devices (IUD)

Cervical screening history

Obstetric history

Drug history:

Anticoagulants

Hormonal therapy

History of systemic disease:

Thyroid disorders

Coagulopathies

Sexual history

Risk factors for endometrial cancer

5. Physical Examination

General Examination

Pallor indicating anaemia

Body Mass Index (BMI)

Obesity increases the risk of endometrial hyperplasia and malignancy

Features of endocrine disorders

Abdominopelvic Examination

Findings may be normal in DUB.

Possible abnormal findings:

Enlarged uterus → consider fibroids

Cervical lesions → exclude malignancy

Adnexal masses

6. Differential Diagnosis (PALM–COEIN Classification)

Structural Causes (PALM)

Letter Condition

P Polyp
A Adenomyosis
L Leiomyoma (fibroid)
M Malignancy / Hyperplasia

Non-Structural Causes (COEIN)

Letter Condition

C Coagulopathy
O Ovulatory dysfunction
E Endometrial
I Iatrogenic
N Not otherwise classified

DUB most commonly corresponds to:

AUB-O (Ovulatory dysfunction)

AUB-E (Endometrial causes)

7. Investigations

1. Exclude Pregnancy

Always perform:

Urine β-hCG

Serum β-hCG if necessary

2. Blood Tests

Full blood count (FBC)

Ferritin level

Thyroid function tests (TSH) if indicated

Coagulation profile if bleeding disorder suspected

3. Cervical Screening

Required if:

Screening is not up to date

Presence of IMB or PCB

4. Imaging

Pelvic Ultrasound Scan (USS)

First-line imaging modality.

Used to:

Assess endometrial thickness

Detect fibroids or polyps

Evaluate uterine morphology

5. Endometrial Assessment

Indications

Age ≥45 years with AUB

Age

09/05/2026

Paracetamol (Acetaminophen) – Mode of Action

Paracetamol is an analgesic and antipyretic with minimal anti‑inflammatory activity. Its mechanism is primarily central (within the CNS) and differs from traditional NSAIDs.
Central Cyclooxygenase (COX) Inhibition
- Inhibits prostaglandin synthesis in the brain and spinal cord.
- Reduces PGE₂ production in the hypothalamus, lowering the thermoregulatory set point → antipyretic effect.
- Provides analgesia by decreasing central prostaglandin-mediated pain sensitization.
- Has little peripheral COX inhibition because high peroxide levels in inflamed tissues limit its activity.
Modulation of Descending Serotonergic Pathways
- Enhances activity of descending inhibitory serotonergic pathways in the spinal cord.
- Contributes to central analgesic effect.
Endocannabinoid System Involvement
- Metabolized in the CNS to AM404, which:
- Inhibits reuptake of endogenous cannabinoids
- Activates TRPV1 receptors
- This contributes to analgesic effects.

Key Clinical Implications
- Effective for mild–moderate pain and fever
- Minimal anti-inflammatory effect
- Lacks significant peripheral COX inhibition → fewer GI and platelet effects compared with NSAIDs

09/05/2026

Superfetation is an extremely rare reproductive phenomenon in which a second conception occurs during an ongoing pregnancy, resulting in embryos of different gestational ages developing simultaneously in the uterus.
Key Concepts

- Normal physiology: During pregnancy, ovulation is suppressed by hormonal changes (primarily progesterone and hCG), and the uterine environment becomes unfavorable for additional implantation.
- Superfetation requires three unlikely events:
1. Continued or resumed ovulation during pregnancy
2. Fertilization of the second o**m
3. Successful implantation in an already pregnant uterus

Because these conditions are biologically suppressed in normal pregnancy, true superfetation is considered extremely rare in humans.
Clinical Features

- Fetuses show different gestational ages, with measurable differences in size and developmental stage.
- The gestational age gap is typically weeks apart, not just a few days.
- Often suspected on ultrasound when there is a persistent and significant size discrepancy that cannot be explained by growth restriction.
Differentiation from Similar Conditions

- Superfecundation: More common; involves fertilization of two ova from the same cycle by s***m from separate acts of in*******se (sometimes different fathers). Gestational ages are the same.
- Intrauterine growth restriction (IUGR): Can mimic superfetation but involves growth lag, not true difference in conception timing.
Obstetric Implications

- Management usually follows twin pregnancy protocols.
- Delivery timing is generally based on the more advanced fetus, balancing risks of prematurity for the younger fetus.
- Outcomes depend on the gestational age gap and overall maternal–fetal health.