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Dr Emmyoung, Juba (2026)

19/03/2026

ACUTE HEPATITIS B
Definition

Acute hepatitis B is a viral infection of the liver caused by the Hepatitis B virus (HBV), characterized by:

- Inflammation of hepatocytes
- Elevated liver enzymes
- Presence of HBsAg for < 6 months
- Possible jaundice and systemic symptoms

If HBsAg persists > 6 months → Chronic Hepatitis B

Virology

- Family: Hepadnaviridae
- DNA virus (partially double-stranded)
- Enveloped virus
- Replicates via reverse transcription
Key Antigens:
- HBsAg – surface antigen (infection marker)
- HBcAg – core antigen (not detectable in serum)
- HBeAg – marker of viral replication and infectivity

Epidemiology

- Transmitted worldwide
- Higher prevalence in:
- Sub-Saharan Africa
- East Asia
- Pacific Islands
Risk Groups:
- Healthcare workers
- IV drug users
- Multiple sexual partners
- Infants born to infected mothers
- Household contacts of infected persons

Modes of Transmission

HBV is transmitted via blood and body fluids:

1. Sexual contact
2. Parenteral exposure (needles, transfusion)
3. Perinatal (mother to child at birth)
4. Occupational exposure (needle-stick injury)

HBV is 100 times more infectious than HIV.

5. Pathophysiology

1. Virus enters bloodstream
2. Infects hepatocytes
3. Viral replication occurs inside liver cells
4. Liver injury is caused by:
- Host immune response (cytotoxic T cells)
- Not direct viral cytotoxicity
Outcomes depend on immune response:
- Strong immune response → Acute symptomatic hepatitis → Clearance
- Weak immune response → Chronic infection

Incubation Period

- 6 weeks to 6 months
- Average: 90 days

7. Clinical Features

Acute HBV has 3 phases:

A. Prodromal (Pre-icteric) Phase (3–10 days)

Non-specific symptoms:

- Fever
- Fatigue
- Malaise
- Anorexia
- Nausea and vomiting
- Right upper quadrant pain
- Arthralgia
- Rash (serum sickness–like syndrome)

B. Icteric Phase (2–6 weeks)

- Jaundice
- Dark urine
- Pale stool
- Pruritus
- Hepatomegaly
- Elevated ALT/AST

Symptoms of prodrome may improve once jaundice appears.

C. Convalescent Phase

- Gradual resolution
- Normalization of liver enzymes
- Recovery over weeks to months

Laboratory Findings
Liver Function Tests
- ALT > AST (often very high, >1000 IU/L possible)
- Elevated bilirubin
- Mildly elevated ALP
- Prolonged PT (if severe)

Serology in Acute Infection
Marker Interpretation
HBsAg Current infection
Anti-HBc IgM Acute infection marker
HBeAg High infectivity
HBV DNA Viral replication
Anti-HBs Recovery/immunity (appears later)
Diagnostic Marker of Acute HBV:
Anti-HBc IgM positive

Complications
1. Fulminant Hepatitis (Rare but fatal)
- Rapid liver failure
- Encephalopathy
- Coagulopathy
- High mortality
2. Progression to Chronic Hepatitis

Risk depends on age:

- Neonates: 90% chronic
- Children: 20–30%
- Adults: 10 mIU/mL = protective.

2. Post-Exposure Prophylaxis (PEP)

If exposed:

- HBV vaccine ± HBIG (Hepatitis B Immunoglobulin)
- Depends on vaccination status

3. Prevention of Mother-to-Child Transmission

- Screen all pregnant women
- Neonate receives:
- HBV vaccine at birth
- HBIG within 12 hours (if mother HBsAg positive)

Prognosis

Adults:
- >95% recover completely
- Lifelong immunity after recovery

Poor prognostic signs:
- INR >1.5
- Encephalopathy
- Rising bilirubin
- Severe transaminitis

Key Differences: Acute vs Chronic HBV
Feature Acute Chronic
HBsAg 6 months
Anti-HBc IgM Present Absent
ALT Markedly elevated Variable
Outcome Usually recovery Risk of cirrhosis, HCC
Clinical Pearls for Exams

- Anti-HBc IgM = acute infection
- HBsAg positive + Anti-HBs negative = active infection
- Anti-HBs positive only = vaccinated
- HBsAg > 6 months = chronic hepatitis B
- Neonates have highest risk of chronicity

07/03/2026

Shout out to my newest followers! Excited to have you onboard! William Ladu Anthony, Potor Lo Yobuta

05/03/2026

Focused Antenatal Care (FANC) – WHO Framework

Focused Antenatal Care is a goal‑oriented, individualized approach to antenatal care that emphasizes quality over quantity of visits, early detection of complications, health promotion, and birth preparedness. It was originally based on a minimum of four targeted visits, though WHO now recommends a minimum of 8 contacts to reduce perinatal mortality and improve maternal experience. Always verify with current local or national guidelines.

1. Goals of Focused Antenatal Care

1. Early detection and management of complications
2. Prevention of maternal and fetal morbidity and mortality
3. Health promotion and disease prevention
4. Birth preparedness and complication readiness
5. Establishing a continuum of care

2. WHO-Recommended Schedule (Updated Model – 8 Contacts)

1. First contact: Up to 12 weeks
2. Second contact: 20 weeks
3. Third contact: 26 weeks
4. Fourth contact: 30 weeks
5. Fifth contact: 34 weeks
6. Sixth contact: 36 weeks
7. Seventh contact: 38 weeks
8. Eighth contact: 40 weeks

(Older FANC model included 4 visits at 12, 26, 32, and 36–38 weeks.)

3. Components of Each Antenatal Visit
A. Assessment
1. History
- Obstetric history (gravidity, parity, previous complications)
- Medical history (hypertension, diabetes, cardiac disease, HIV, TB)
- Surgical history
- Family history
- Current pregnancy symptoms (bleeding, headache, edema, reduced fetal movements)
- Social history (support system, violence screening, substance use)
2. Physical Examination
- Weight
- Blood pressure
- Pallor, edema
- Fundal height
- Fetal heart rate
- Fetal lie and presentation (later visits)
3. Laboratory Investigations
At first contact:
- Hemoglobin
- Blood group and Rh factor
- Syphilis screening
- HIV testing (with consent)
- Urinalysis (protein, glucose)
- Hepatitis B (where available)

Later:
- Repeat hemoglobin
- Repeat syphilis/HIV if high-risk
- Glucose screening (24–28 weeks)
- Urine protein (preeclampsia screening)

4. Preventive Interventions
1. Nutritional Support
- Iron and folic acid supplementation
- 30–60 mg elemental iron + 400 µg folic acid daily
- Calcium supplementation (1.5–2 g/day in low-intake populations)
- Balanced diet counseling
2. Immunization
- Tetanus toxoid (or Td vaccine)
- Other vaccines per national policy (e.g., influenza, Tdap)
3. Malaria Prevention (Endemic Areas)
- Intermittent preventive treatment in pregnancy (IPTp)
- Insecticide-treated nets
4. Deworming (After First Trimester in Endemic Areas)

5. Identification and Management of Danger Signs

Educate mother to seek immediate care for:
- Vaginal bleeding
- Severe headache/blurred vision
- Convulsions
- Severe abdominal pain
- Reduced/absent fetal movements
- Fever
- Swelling of face/hands
- Leaking liquor before labor

6. Birth Preparedness and Complication Readiness

Discuss and document:
- Place of delivery
- Skilled birth attendant
- Transport arrangements
- Financial planning
- Blood donor identification (if needed)
- Postnatal care plan
- Emergency decision-making support

7. Counseling and Health Education

- Nutrition
- Breastfeeding
- Family planning/postpartum contraception
- Personal hygiene
- Rest and physical activity
- Mental health support
- Avoidance of alcohol, to***co, harmful drugs
- Recognition of labor signs

8. Management of Common Conditions in ANC

- Anemia
- Gestational hypertension/preeclampsia
- Gestational diabetes
- Urinary tract infection
- HIV and PMTCT services
- Rh incompatibility (Anti-D administration)

9. Key Principles of Focused ANC

- Individualized risk assessment
- Evidence-based interventions
- Respectful maternity care
- Continuity of care
- Woman-centered communication
- Integration with postpartum and newborn care

Summary

Focused Antenatal Care (WHO model) emphasizes:
- Early booking (before 12 weeks)
- Scheduled evidence-based contacts (now minimum 8)
- Risk detection and timely referral
- Preventive interventions (iron, immunization, malaria prevention)
- Birth preparedness
- Health education and psychosocial support

Clinical implementation should always align with updated WHO recommendations and national maternal health protocols.

23/02/2026

Lecture Notes: Angina Pectoris

Definition:
- Angina pectoris is characterized by recurrent, transient episodes of chest pain due to myocardial ischemia, typically resulting from an imbalance between myocardial oxygen demand and supply.

Epidemiology:
- Angina is a common condition, primarily affecting individuals with risk factors for coronary artery disease.

Aetiology:
- Most commonly caused by coronary artery atherosclerosis.
- Major risk factors include smoking, hypertension, diabetes, and hyperlipidemia.
- Other contributing factors: hypertension and aortic stenosis, which can lead to left ventricular hypertrophy and increased myocardial oxygen demand.

Pathogenesis:
- Myocardial ischemia occurs when myocardial oxygen demand exceeds supply, often due to significant fixed stenosis of a coronary artery.
- Episodes are often triggered by physical exertion or emotional stress.

Clinical Presentation:
- Central chest discomfort described as pressure, heaviness, tightness, or squeezing.
- Pain may radiate to the neck, jaw, shoulders, and arms.
- Associated symptoms: nausea, sweating, dyspnea, fatigue, and recurrent belching.
- Typically precipitated by exertion or stress, lasting a few minutes, and relieved by rest or medication.

Classification:
- Stable Angina: Occurs predictably with exertion and is relieved by rest.
- Unstable Angina: Occurs with minimal exertion or at rest, indicating a higher risk of myocardial infarction.
- Crescendo Angina: Increasing frequency and severity of episodes.
- Decubitus Angina: Occurs when lying flat.

Diagnosis:
- Based on history and characteristic pain description.
- Physical examination may reveal risk factors but rarely direct evidence of ischemic heart disease.
- Important to assess for signs of heart failure, peripheral vascular disease, and hypercholesterolemia.

Differential Diagnosis:
- Anxiety and hyperventilation
- Musculoskeletal chest wall pain
- Cervical or thoracic root pain
- Pneumothorax, pneumonia, or pulmonary embolism
- Gastrointestinal issues (e.g., esophageal spasm, gastritis)
- Pericarditis, aortic dissection, mitral valve prolapse

Management:
- Lifestyle modifications: smoking cessation, diet, exercise.
- Pharmacological treatment: nitrates, beta-blockers, calcium channel blockers, antiplatelet agents.
- Risk factor management: control of hypertension, diabetes, and hyperlipidemia.
- Revascularization procedures may be considered for severe cases.

Prognosis:
- Atherosclerosis is often generalized, increasing the risk for other cardiovascular events such as myocardial infarction, stroke, and peripheral vascular disease.

Conclusion:
Understanding the pathophysiology, risk factors, and clinical presentation of angina pectoris is crucial for effective management and prevention of complications. Regular monitoring and a comprehensive approach to treatment can significantly improve patient outcomes.

21/02/2026

Lecture Notes: Cholecystitis

Introduction

Cholecystitis refers to inflammation of the gallbladder, which can be acute or chronic. It is primarily associated with gallstones but can also occur without them (acalculous cholecystitis).

Types of Cholecystitis
1. Acute Calculous Cholecystitis:
- Etiology: Most common form, resulting from gallstone obstruction of the cystic duct.
- Pathogenesis: Cystic duct obstruction leads to bile stasis, gallbladder distension, and inflammation. Additional irritants like lysolecithin and infection may exacerbate inflammation.
- Clinical Manifestations: Right upper quadrant pain, fever, leukocytosis. Positive Murphy's sign on physical examination.
- Diagnosis: Abdominal ultrasound is the primary diagnostic tool; cholescintigraphy may be used if ultrasound is inconclusive.
- Complications: Gangrene, perforation, emphysematous cholecystitis, and gallstone ileus.

2. Acalculous Cholecystitis:
- Etiology: Occurs without gallstones, often in critically ill patients.
- Pathogenesis: Gallbladder stasis and ischemia lead to inflammation. Secondary infections are common.

- Clinical Manifestations: May present with unexplained fever, right upper quadrant pain, and jaundice. Often insidious and can lead to sepsis or shock.

- Diagnosis: Suspected in critically ill patients with sepsis of unknown origin. Ultrasound and CT scans are used for evaluation.
- Complications: High risk of gangrene and perforation.

3. Chronic Cholecystitis:
- Etiology: Chronic inflammation due to repeated episodes of acute cholecystitis or persistent irritation by gallstones.
- Clinical Significance: Often asymptomatic, but can lead to gallbladder fibrosis and dysfunction.
Epidemiology
- Acute cholecystitis is a common complication of gallstone disease, affecting 6-11% of patients with symptomatic gallstones.
- Acalculous cholecystitis accounts for about 10% of all acute cholecystitis cases and is more common in hospitalized, critically ill patients.
Diagnostic Approach
- Clinical Evaluation: History and physical examination, including checking for Murphy's sign.
- Laboratory Tests: Leukocytosis, liver function tests, and amylase/lipase levels to rule out other conditions.
- Imaging:
- Ultrasound: First-line imaging for detecting gallstones and gallbladder wall thickening.
- Cholescintigraphy (HIDA scan): Used if ultrasound results are inconclusive.
- CT/MRI: Considered for complications or alternative diagnoses.
Management
- Acute Calculous Cholecystitis:
- Initial management includes fasting, IV fluids, pain control, and antibiotics.
- Cholecystectomy (surgical removal of the gallbladder) is the definitive treatment, typically performed laparoscopically.

- Acalculous Cholecystitis:
- Similar initial management as calculous cholecystitis.
- Cholecystectomy or percutaneous cholecystostomy may be required, especially in unstable patients.

Conclusion
Understanding the pathophysiology, clinical presentation, and management of cholecystitis is crucial for effective diagnosis and treatment. Early recognition and appropriate intervention can prevent complications and improve patient outcomes. Always consider local guidelines and protocols when managing cholecystitis, as practices may vary based on regional healthcare resources and epidemiology.

20/02/2026

Premenstrual Syndrome (PMS) Lecture Notes
By
Mr.Emmanuel Nyong

Introduction
- Definition: Premenstrual Syndrome (PMS) encompasses a range of psychological, physical, and behavioral symptoms that occur cyclically during the luteal phase of the menstrual cycle and resolve with the onset of menstruation.
- Prevalence: Affects approximately 40% of women in the general population, with 5-8% experiencing severe symptoms.

Clinical Features
- Psychological Symptoms: Depression, anxiety, irritability, mood swings, and loss of confidence.
- Physical Symptoms: Bloating, breast tenderness (mastalgia), headaches, and fatigue.
- Behavioral Symptoms: Increased appetite, food cravings, and diminished interest in activities.

Pathophysiology
- Central Role of Ovarian Activity: Cyclical ovarian activity is a key trigger, with ovulation initiating a cascade of events.
- Neurochemical Factors: Altered responsiveness to steroids and neurotransmitters (e.g., serotonin, GABA) may contribute.
- Psychological Sensitivity: Increased sensitivity to hormonal changes may exacerbate symptoms.

Diagnosis
- Self-Diagnosis: Many women self-identify their symptoms as PMS.
- Symptom Diary: Prospective recording of symptoms over at least two consecutive menstrual cycles is essential for diagnosis. The Daily Record of Severity of Problems (DRSP) is a commonly used tool.
- Exclusion of Other Conditions: Rule out organic diseases and psychiatric disorders. Consider GnRH analogues for definitive diagnosis in complex cases.

Classification
- Physiological (Mild) Premenstrual Disorder: Symptoms are cyclical, relieved by menstruation, and do not affect quality of life.
- Core Premenstrual Disorder: Symptoms affect quality of life but are relieved by menstruation.
- Premenstrual Exacerbation: Symptoms exacerbate an existing non-menstrual condition and affect quality of life.
- Progestogen-Induced Premenstrual Disorder: Symptoms occur in women taking progesterone treatment.
- Non-Ovulatory Premenstrual Disorder: Symptoms occur without ovulation but in the presence of ovarian activity.
- Underlying Psychological Disorder: Non-cyclical symptoms with no symptom-free week, constantly affecting quality of life.

Premenstrual Dysphoric Disorder (PMDD)
- Definition: A severe form of PMS characterized by prominent symptoms of anger, irritability, and internal tension.
- Diagnostic Criteria: As per DSM-5, requires ≥5 symptoms, including at least one affective symptom, causing significant impairment.

Impact on Quality of Life
- Functional Impairment: Moderate to severe PMS can lead to decreased work productivity, increased absenteeism, and more frequent healthcare visits.
- Su***de Risk: Elevated risk of suicidal ideation in women with severe PMDD symptoms.

Natural History
- Onset and Course: Symptoms typically begin after menarche, peak in the late reproductive years, and resolve after menopause.
- Transient Resolution: Symptoms may temporarily resolve during pregnancy or any disruption of ovulatory cycles.

Evaluation and Management
- Detailed Menstrual History: Confirm the relationship between symptoms and menstrual cycle phase.
- Prospective Monitoring: Use symptom diaries like the DRSP for accurate diagnosis.
- Exclude Other Disorders: Rule out endocrine disorders and chronic mood disorders.

- Management Strategies: Lifestyle modifications, pharmacotherapy (e.g., SSRIs, hormonal treatments), and cognitive-behavioral therapy may be considered.

Conclusion
- PMS is a common condition with significant variability in symptomatology and impact on quality of life. Accurate diagnosis and tailored management are crucial for improving patient outcomes. Always consult updated guidelines specific to your region for the most appropriate management strategies.

19/02/2026

Dysmenorrhoea
By Mr. Emmanuel Nyong
At NEV.

Introduction
Dysmenorrhoea, or painful menstruation, is a prevalent condition affecting females during their reproductive years. It is categorized into two main types: primary and secondary dysmenorrhoea. Understanding the pathophysiology, clinical presentation, and management of dysmenorrhoea is crucial for medical students, as it significantly impacts the quality of life and daily functioning of affected individuals.

Types of Dysmenorrhoea
Primary Dysmenorrhoea
- Definition: Recurrent, crampy lower abdominal pain during me**es without an identifiable pelvic pathology.

Pathophysiology: Primarily due to increased prostaglandin production leading to uterine vasospasm, ischemia, and contractions.

Epidemiology: Common in adolescents and young women; prevalence decreases with age.
- Risk Factors: Younger age, smoking, stress, and familial predisposition.

Secondary Dysmenorrhoea
- Definition: Menstrual pain associated with an underlying pelvic pathology.

Common Causes: Endometriosis, adenomyosis, pelvic inflammatory disease (PID), fibroids, and pelvic adhesions.

Epidemiology: Tends to develop later in life as the underlying pathology progresses.
Clinical Presentation
Symptoms
- Pain Characteristics: Crampy, lower abdominal pain starting 1-2 days before menstruation and lasting 12-72 hours. Pain may radiate to the back or thighs.

Additional Symptoms: Nausea, diarrhea, fatigue, headache, and malaise.

Impact: Can lead to absenteeism from school or work and decreased productivity.

Examination
- Primary Dysmenorrhoea: Normal pelvic examination.
- Secondary Dysmenorrhoea: May reveal pelvic masses, tenderness, or other abnormalities.
Diagnostic Evaluation
- History: Detailed menstrual history, timing, and characteristics of pain.
- Physical Examination: To rule out pelvic pathology.

Investigations:
- STI Screening: To exclude infections.
- Ultrasound: To identify structural abnormalities like fibroids or endometriosis.
- Laparoscopy: Reserved for cases with abnormal imaging or treatment failures.

Management
Primary Dysmenorrhoea
- First-line Treatment: Nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce prostaglandin levels.
- Hormonal Therapy: Combined oral contraceptive pills (COCPs) to suppress ovulation and reduce menstrual flow.
- Supportive Measures: Heat application, TENS, vitamin B1, and magnesium supplements.

Secondary Dysmenorrhoea
- Treat Underlying Cause:
- Endometriosis: Hormonal therapy or surgery.
- PID: Antibiotics.
- Fibroids: Surgical intervention if necessary.
- Surgical Options: Therapeutic laparoscopy for diagnosis and treatment of endometriosis or adhesions.

Conclusion
Dysmenorrhoea is a common but often underdiagnosed condition that requires a comprehensive approach to diagnosis and management. Medical students should be familiar with the clinical features, evaluation, and treatment strategies to effectively manage patients and improve their quality of life. Always consider the specific needs of transgender and gender-diverse individuals in clinical practice.

29/01/2026

Nipah virus is a zoonotic virus, meaning it can spread from animals to humans. It's caused by the Henipavirus and is typically found in fruit bats, also known as flying foxes. The virus can be transmitted through direct contact with infected animals, contaminated food or drinks, or close contact with an infected person

Symptoms:

- Fever
- Headache
- Dizziness
- Muscle pain
- Vomiting
- Sore throat
- Respiratory distress
- Altered mental status and confusion

In severe cases, it can cause acute encephalitis, seizures, and coma. The fatality rate is quite high, ranging from 40% to 75%

Prevention:

- Avoid contact with bats and sick animals
- Refrain from consuming raw date palm sap or partially eaten fruits
- Practice good hand hygiene and safe food practices
- Wear protective gear in healthcare settings

There's currently no approved vaccine or treatment, but researchers are working on monoclonal antibody therapies and vaccines. Treatment is mainly supportive care, focusing on symptom management and reducing neurological and respiratory complications

20/01/2026

Part 2
Lecture Notes on Eclampsia.

Introduction
Eclampsia is a severe complication of preeclampsia characterized by the onset of seizures in a pregnant woman with no prior history of seizure disorder. It is a critical condition requiring immediate medical intervention to prevent maternal and fetal morbidity and mortality.

Pathophysiology
- Eclampsia is thought to result from endothelial dysfunction, leading to cerebral edema, vasospasm, and increased intracranial pressure.
- The exact mechanism of seizures in eclampsia is not fully understood but is associated with severe hypertension and cerebral vasculopathy.

Clinical Presentation
- Seizures: Generalized tonic-clonic seizures.
- Other symptoms: Severe headache, visual disturbances, altered mental status, and upper abdominal pain.

Diagnosis
- Clinical diagnosis based on the presence of seizures in a patient with preeclampsia.
- Laboratory tests: Proteinuria, elevated liver enzymes, thrombocytopenia, and renal impairment may be present.

Management

Magnesium Sulfate Therapy
Magnesium sulfate is the drug of choice for both the prevention and treatment of eclamptic seizures.

1. Loading Dose:
- Intravenous (IV): 4 to 6 g of magnesium sulfate administered over 15 to 20 minutes.
- Intramuscular (IM): 5 g in each buttock (total of 10 g), mixed with 1 mL of 2% lidocaine to reduce pain.

2. Maintenance Dose:
- IV Infusion: 1 to 2 g/hour. For patients with normal renal function, 2 g/hour is commonly used.
- IM: 5 g every four hours. In resource-limited settings, a lower dose of 2.5 g every four hours may be effective.

3. Monitoring:
- Clinical assessment every 1-2 hours for signs of magnesium toxicity, such as loss of deep tendon reflexes, respiratory depression, and decreased urine output.
- Serum magnesium levels are typically maintained between 4.8 to 8.4 mg/dL (2.0 to 3.5 mmol/L).

4. Toxicity Management:
- Antidote: Calcium gluconate 1 g IV to counteract magnesium toxicity.
- Monitor for hypotension, especially when used with calcium channel blockers.

Alternative Antiseizure Medications
- For patients with contraindications to magnesium sulfate (e.g., myasthenia gravis):
- Levetiracetam or Valproic Acid may be used.

Management of Recurrent Seizures
- Administer an additional bolus of 2 to 4 g magnesium sulfate IV over five minutes.
- If seizures persist, consider discontinuing magnesium sulfate and administering:
- Fosphenytoin: 20 mg PE/kg IV at 100 to 150 mg PE/min.
- Phenytoin: 20 mg/kg IV at a rate of up to 50 mg/min, with cardiac monitoring.

Delivery Considerations
- Timing: Prompt delivery is the definitive treatment for eclampsia, but maternal stabilization is prioritized.
- Mode of Delivery: Depends on gestational age, cervical status, and fetal condition. Induction of labor is reasonable for pregnancies ≥32 to 34 weeks with a favorable cervix.

Postpartum Care
- Continue magnesium sulfate therapy for 24 to 48 hours postpartum.
- Monitor for resolution of symptoms and diuresis as indicators of recovery.

Conclusion
Eclampsia is a medical emergency requiring prompt recognition and treatment. Magnesium sulfate remains the cornerstone of therapy, with careful monitoring for toxicity. Delivery is the ultimate treatment, with the timing and mode tailored to the individual clinical scenario.

19/01/2026

Lecture Notes: Pre-eclampsia
By Tutor Nyong Emmanuel

Definition:
Pre-eclampsia is a pregnancy-induced condition characterized by hypertension and proteinuria, typically occurring after 20 weeks of gestation.

Epidemiology:
- Affects approximately 5% of pregnancies.
- More common in women experiencing their first pregnancy (nulliparous women).

Aetiology and Pathogenesis:
- Abnormal Placentation: The primary underlying issue is abnormal placentation.
- Pathophysiological Mechanism:
- Shallow invasion of trophoblasts leads to inadequate transformation of spiral arteries into low-resistance vessels.
- Resultant placental ischemia causes the release of toxic substances into maternal circulation.
- These substances cause endothelial damage, leading to systemic hypertension.
- Severe progression can lead to eclampsia, characterized by widespread fibrin thrombi and risks of multi-organ failure.

Clinical Presentation:
- Symptoms: Often asymptomatic in early stages. Severe disease may present with:
- Headache
- Visual disturbances (e.g., flashing lights)
- Epigastric or right upper quadrant pain
- Nausea and vomiting
- Rapid facial edema
- Signs:
- Hypertension (BP >140/90 mmHg; severe if ≥160/110 mmHg)
- Proteinuria (Protein-Creatinine Ratio [PCR] ≥30)
- Facial edema
- Epigastric/RUQ tenderness (suggestive of liver involvement)
- Confusion or cortical blindness
- Uterine tenderness or vaginal bleeding (possible placental abruption)
- Fetal growth restriction, especially if

31/12/2025

Shout out to my newest followers! Excited to have you onboard! Aham Dizzy, Mollicier Sijali

Dr Emmyoung

19/03/2026

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