Saturday, March 29, 2025

Endocrine System

I. Structured History Taking Points

1. Chief Complaints

Weight Changes:
- Weight gain:
  - Rapid: Cushing’s syndrome, hypothyroidism.
  - Gradual: Hypogonadism, insulinoma.
- Weight loss:
  - With increased appetite: Hyperthyroidism, diabetes mellitus.
  - Without increased appetite: Addison’s disease, pituitary insufficiency, malignancy.
Temperature Intolerance:
- Heat intolerance: Hyperthyroidism.
- Cold intolerance: Hypothyroidism.
Change in Skin, Hair, Nails:
- Dry, coarse skin, brittle nails, hair fall: Hypothyroidism.
- Fine hair, hyperhidrosis: Hyperthyroidism.
- Skin hyperpigmentation: Addison’s disease.
- Striae, thin skin: Cushing’s syndrome.
Menstrual/ Sexual Dysfunction:
- Menorrhagia, amenorrhea: Hypothyroidism, PCOS.
- Oligomenorrhea: Hyperprolactinemia.
- Erectile dysfunction: Hypogonadism, DM.
Polyuria, Polydipsia:
- Diabetes mellitus, Diabetes insipidus, Hypercalcemia.
Neck Swelling:
- Goitre, thyroid nodules, thyroglossal cyst.
Growth Disorders:
- Short stature: GH deficiency, hypothyroidism.
- Tall stature: Marfan’s, acromegaly.
Lethargy, Fatigue, Myopathy:
- Hypothyroidism, Cushing’s, Addison’s.
Symptoms of Raised ICP, Vision Changes:
- Pituitary macroadenoma.
Fractures, Bone Pain:
- Osteoporosis, hyperparathyroidism.

2. Associated Symptoms

Palpitations, tremors → Hyperthyroidism.
Constipation → Hypothyroidism.
Diarrhea → Hyperthyroidism.
Polyphagia → DM, hyperthyroidism.
Hyperpigmentation → Addison’s.
Headache, galactorrhea → Prolactinoma.
Mood changes → Thyroid disorders, Cushing’s.

3. Past History

Diabetes, hypertension, autoimmune disease.
Previous neck surgeries, irradiation.
Family history of thyroid, pituitary, adrenal disorders.

4. Drug History

Steroid use, antithyroid drugs, lithium, amiodarone.

5. Lifestyle History

Diet, physical activity, stress factors.

II. Advanced Clinical Examination

A. General Examination

Build & Nutrition:
- Obesity → Cushing’s, hypothyroidism.
- Cachexia → Addison’s, pituitary insufficiency.
Facies:
- Moon face → Cushing’s.
- Myxedematous facies → Hypothyroidism.
- Acromegalic facies → Acromegaly.
- Exophthalmos → Graves’ disease.
- Pigmented lips → Addison’s.
Skin & Hair:
- Hyperpigmentation → Addison’s.
- Striae → Cushing’s (purple, broad).
- Vitiligo → Autoimmune thyroiditis.
- Dry, coarse skin → Hypothyroidism.
- Hyperhidrosis → Hyperthyroidism.
- Hirsutism → PCOS, Cushing’s.
- Alopecia → Hypothyroidism, hyperandrogenism.
Nails:
- Onycholysis (Plummer’s nails) → Hyperthyroidism.
- Brittle nails → Hypothyroidism.
Hands:
- Tremors → Hyperthyroidism.
- Palmar erythema → Hyperthyroidism.
- Carpal tunnel signs → Hypothyroidism.
- Doughy hands → Myxedema.
- Acromegalic features → GH excess.
Vitals:
- Bradycardia → Hypothyroidism.
- Tachycardia → Hyperthyroidism.
- BP: Hypertension (Cushing’s), Postural hypotension (Addison’s).
- Temperature: Low in hypothyroidism, high in thyrotoxic crisis.
Gait:
- Proximal myopathy gait → Cushing’s, hypothyroidism.

B. Systemic Examination

1. Neck Examination (Thyroid):

Inspection & Palpation:
- Goitre: Diffuse (Graves’, Hashimoto), Nodular (MNG, carcinoma).
- Surface: Smooth (physiological), nodular.
- Consistency: Soft (Graves’), firm (Hashimoto’s), hard (Malignancy).
- Tenderness: Subacute thyroiditis.
- Mobility: Moves with deglutition (thyroid), with tongue (thyroglossal cyst).
- Bruit: Graves’ disease.
- Pemberton’s sign: Retrosternal goitre.
Percussion:
- Retrosternal dullness → Substernal goitre.
Auscultation:
- Thyroid bruit → Graves’.

2. Eye Signs:

Lid retraction, lid lag → Hyperthyroidism.
Exophthalmos, chemosis → Graves’.
Periorbital edema → Hypothyroidism.

3. Chest & Cardiovascular:

Arrhythmia → Hyperthyroidism.
Hypertension → Cushing’s.
Pericardial effusion → Hypothyroidism.

4. Abdominal Examination:

Central obesity, purple striae → Cushing’s.
Hepatomegaly → NAFLD in metabolic syndrome.
Palpable adrenal mass → Pheochromocytoma.

5. Neuromuscular:

Reflexes:
- Delayed relaxation → Hypothyroidism.
- Brisk → Hyperthyroidism.
Muscle wasting → Cushing’s, thyrotoxicosis.

6. Genitalia & Secondary Sexual Characters:

Sparse axillary/pubic hair → Addison’s, hypogonadism.
Gynecomastia → Klinefelter, Cushing’s.
Clitoromegaly → Congenital adrenal hyperplasia.

III. Advanced Clinical Clues & Differential Interpretations

Hyperpigmentation + Postural hypotension + Weight loss:
- Addison’s disease.
Moon face + Buffalo hump + Central obesity + Striae:
- Cushing’s syndrome (endogenous or exogenous).
Heat intolerance, tremors, tachycardia, weight loss:
- Hyperthyroidism (Graves’, toxic MNG).
Fatigue, cold intolerance, constipation, bradycardia, weight gain:
- Hypothyroidism (Primary, secondary).
Acromegalic facies + Enlarged hands/feet + Proximal weakness:
- GH excess (Pituitary adenoma).
Bitemporal hemianopia + Galactorrhea + Amenorrhea:
- Pituitary macroadenoma (Prolactinoma).
Polyuria, polydipsia, high serum sodium:
- Diabetes insipidus (Central or Nephrogenic).
Short stature + Delayed puberty + Hyponatremia:
- Panhypopituitarism.
Neck swelling with compressive symptoms, hoarseness:
- Large goitre, carcinoma thyroid.

Friday, March 28, 2025

Cardiovascular System examination

I. History Taking Points

1. Chief Complaints:

Chest pain: Character (sharp, crushing, burning), site (retrosternal, left-sided, diffuse), radiation, severity, aggravating/relieving factors.
- Possibilities:
  - Retrosternal, crushing → MI.
  - Localized, stabbing → Pericarditis.
  - Exertional, squeezing → Angina.
  - Burning epigastric → GERD, mimicker.
Palpitations: Onset (sudden/gradual), duration, regularity, associated symptoms (syncope).
- Possibilities: Arrhythmia (AF, SVT), hyperthyroidism, anxiety.
Dyspnea: Graded (NYHA I-IV), orthopnea, paroxysmal nocturnal dyspnea.
- Possibilities: LV failure, pulmonary hypertension, pericardial disease.
Syncope/Presyncope: Circumstances (exertional, positional), duration, recovery.
- Possibilities: Aortic stenosis, arrhythmia, vasovagal.
Edema: Pitting, bilateral/unilateral, progression.
- Possibilities: Right heart failure, nephrotic syndrome, DVT (unilateral).
Fatigue, effort intolerance, dizziness.

2. Associated Symptoms:

Nocturia → CHF.
Abdominal distension → RHF, constrictive pericarditis.
Cough, hemoptysis → Pulmonary congestion, MS.
Hoarseness → Ortner’s syndrome (LA enlargement).
Claudication, cold extremities → PVD.
Constitutional symptoms → Infective endocarditis.

3. Past History:

Hypertension, diabetes, dyslipidemia, rheumatic fever, coronary artery disease, stroke, surgeries (valve replacement, angioplasty).

4. Family History:

Cardiomyopathies, sudden cardiac death, hypertension.

5. Personal & Drug History:

Smoking, alcohol, illicit drug use.
Medications: Antihypertensives, anticoagulants, statins.

6. Risk Factors:

Obesity, sedentary lifestyle, sleep apnea.

II. Clinical Examination Points (Structured)

A. General Physical Examination:

Build, nutrition: Cachexia in CHF.
Pallor: Anemia, infective endocarditis.
Cyanosis:
- Central: Congenital cyanotic heart disease, Eisenmenger syndrome.
- Peripheral: Low-output states.
Clubbing:
- Congenital cyanotic heart disease, infective endocarditis.
Edema: Pitting pedal edema in RHF.
Jaundice: Hepatic congestion.
JVP:
- Elevated: RHF, constrictive pericarditis.
- Prominent ‘a’ wave: TR, PS.
- Absent ‘a’ wave: AF.
- Cannon ‘a’ wave: Complete heart block.
- Prominent ‘v’ wave: TR.
Pulse:
- Rate, rhythm, volume, character, radio-femoral delay.
- Collapsing pulse: AR.
- Anacrotic pulse: AS.
- Pulsus alternans: Severe LV dysfunction.
- Pulsus paradoxus: Cardiac tamponade, severe asthma.
- Irregularly irregular: AF.
BP:
- Pulse pressure variations: Wide in AR, thyrotoxicosis; Narrow in AS, tamponade.
- Postural hypotension.

B. Precordial Inspection:

Shape of chest: Pectus excavatum → compressive effect.
Visible apex beat: Hyperdynamic in MR, AR; heaving in AS.
Precordial bulge: Congenital heart disease.

C. Palpation:

Apex Beat:
- Location, character:
  - Displaced laterally → LV enlargement.
  - Hyperdynamic → Volume overload (AR, MR).
  - Heaving → Pressure overload (AS).
  - Tapping → MS.
- Double apex beat → HOCM.
Parasternal heave → RV hypertrophy.
Thrills:
- Systolic → AS, VSD.
- Diastolic → MS.
Palpable P2 → Pulmonary hypertension.

D. Percussion:

Cardiac borders:
- Right border → RA enlargement.
- Left border → LV enlargement.
- Superior border → LA enlargement.
- Increased transverse dullness → Pericardial effusion.

E. Auscultation:

Heart Sounds:
- S1:
  - Loud: MS.
  - Soft: MR, LV dysfunction.
- S2:
  - Loud P2: Pulmonary hypertension.
  - Widely split: ASD.
  - Reversed split: LBBB, AS.
- S3: Volume overload (MR, CHF).
- S4: Pressure overload (HTN, AS).
Added Sounds:
- Opening snap: MS.
- Ejection click: AS, PS.
- Midsystolic click: MVP.
- Pericardial rub: Pericarditis.
Murmurs:
- Systolic:
  - Ejection: AS, PS.
  - Pansystolic: MR, TR, VSD.
- Diastolic:
  - Mid-diastolic: MS, TS.
  - Early diastolic: AR, PR.
- Continuous: PDA.
- Radiation:
  - To carotids: AS.
  - To axilla: MR.
  - To back: Coarctation.
Dynamic Auscultation:
- Murmur variation with position, respiration, handgrip, squatting.
- Maneuvers to differentiate HOCM vs AS.

F. Peripheral Vascular Examination:

Peripheral pulses: Radiofemoral delay → Coarctation.
Bruits: Carotid, renal arteries.
Capillary refill time, temperature, trophic changes → PVD.

G. Bedside Investigations:

ECG, Chest X-ray.
NT-proBNP levels in CHF.
2D-Echo.
Doppler for carotids & peripheral arteries.

III. Advanced Clinical Clues & Differential Interpretations

Elevated JVP with clear lungs: Constrictive pericarditis, RHF.
Displaced apex with S3 & MR murmur: DCM.
Heaving apex with ejection systolic murmur & slow-rising pulse: AS.
Hyperdynamic apex, collapsing pulse, early diastolic murmur: AR.
Mid-diastolic murmur with tapping apex, loud S1: MS.
Raised JVP, hypotension, muffled heart sounds: Cardiac tamponade.
Tachycardia with irregularly irregular pulse: AF.
Clubbing + continuous murmur: PDA.
Systolic murmur increasing on standing, decreasing on squatting: HOCM.
Prominent ‘v’ wave in JVP, pansystolic murmur increasing on inspiration: TR.
Midsystolic click with late systolic murmur: MVP.

Respiratory system examination

I. History Taking

A meticulous history provides invaluable clues to underlying respiratory pathologies.

A. Presenting Complaints

Breathlessness (Dyspnea)
- Onset:
  - Acute: Pneumothorax, Pulmonary Embolism (PE), Acute Asthma Exacerbation, Pneumonia.
  - Subacute: Tuberculosis (TB), Pleural Effusion, Subacute Hypersensitivity Pneumonitis.
  - Chronic: Chronic Obstructive Pulmonary Disease (COPD), Interstitial Lung Disease (ILD), Congestive Heart Failure (CHF), Pulmonary Hypertension.
- Character:
  - Exertional: COPD, ILD, CHF.
  - Orthopnea: Left Ventricular Failure (LVF), Severe Asthma.
  - Paroxysmal Nocturnal Dyspnea (PND): CHF.
  - Platypnea: Hepatopulmonary Syndrome.
  - Trepopnea: Unilateral Lung Disease.
- Severity: Utilize scales such as the New York Heart Association (NYHA) classification or the Medical Research Council (MRC) Dyspnea Scale.
- Progression: Rapid worsening may indicate PE or Acute Respiratory Distress Syndrome (ARDS); gradual progression suggests ILD or COPD.
Cough
- Onset:
  - Sudden: Aspiration, PE.
  - Gradual: Bronchiectasis, TB.
- Character:
  - Dry: ILD, Viral Infections, Medication-induced (e.g., ACE Inhibitors).
  - Productive: Bronchiectasis, COPD, TB.
  - Paroxysmal: Pertussis, Asthma.
  - Nocturnal: Asthma, Gastroesophageal Reflux Disease (GERD).
- Sputum Characteristics:
  - Mucoid: COPD, Asthma.
  - Purulent: Bacterial Infections.
  - Rusty: Pneumococcal Pneumonia.
  - Foul-smelling: Anaerobic Infections.
  - Blood-streaked: TB, Malignancy.
Chest Pain
- Site:
  - Pleuritic: Lateral Chest (e.g., Pleurisy).
  - Retrosternal: Non-pleuritic (e.g., Myocardial Ischemia).
- Character:
  - Sharp: Pleuritic Pain.
  - Dull/Aching: Malignancy.
- Severity: Severe pain may indicate PE or Pneumothorax; mild pain is common in Pleuritis.
Hemoptysis
- Quantity:
  - Streaky: Acute Bronchitis.
  - Massive (>200 mL/24 hrs): TB, Malignancy, Bronchiectasis.
- Frequency: Single episode versus recurrent episodes.
Wheezing/Stridor
- Inspiratory Stridor: Suggests Upper Airway Obstruction (e.g., Laryngeal Tumor).
- Expiratory Wheeze: Common in Asthma, COPD.
- Biphasic Stridor: Indicates Fixed Airway Obstruction (e.g., Tracheal Stenosis).
Systemic Symptoms
- Fever, weight loss, and night sweats are indicative of conditions like TB or malignancy.
- Anorexia and fatigue may accompany chronic hypoxic states.

B. Past Medical History

Previous respiratory illnesses: Childhood Asthma, TB, Pneumonia, ICU admissions.
History of ventilatory support.
Systemic diseases: Connective Tissue Disorders (CTD), Vasculitis.

C. Personal & Occupational History

Smoking history quantified in pack-years.
Substance use: Cannabis, Cocaine.
Occupational exposures: Asbestos, Silica, Organic Dusts.
Environmental exposures: Biomass fuels, Bird exposure.

D. Medication History

Drugs with pulmonary toxicity: Methotrexate, Amiodarone, Nitrofurantoin, Chemotherapy agents.

E. Family History

Genetic predispositions: Asthma, Atopy, ILD, Cystic Fibrosis.

F. Associated Comorbidities

Cardiovascular diseases, GERD, Diabetes Mellitus, CTD.

Certainly! Continuing from Physical Examination of the Respiratory System in an advanced, structured, post-PhD style with all possible clinical interpretations and variations:

II. Physical Examination (Continued)

A. General Inspection

Patient Position & Posture:
- Tripod position: Suggestive of severe airway obstruction (e.g., COPD exacerbation, severe asthma).
- Orthopnea position: Implies left heart failure, large pleural effusion.
- Unable to lie supine (Trepopnea): May occur in unilateral lung pathology.
Respiratory Rate & Pattern:
- Tachypnea: Reflective of hypoxia, metabolic acidosis, fever, pain.
- Bradypnea: Possible CNS depression, severe respiratory muscle fatigue.
- Kussmaul Breathing: Deep, labored, rapid breathing — Diabetic ketoacidosis.
- Cheyne-Stokes Respiration: Seen in CHF, CNS lesions.
- Biot’s Breathing: Brainstem injury, opioid overdose.
Use of Accessory Muscles: SCM, scalene activation → severe airway obstruction, respiratory distress.
Intercostal/Supraclavicular Retractions: Suggest increased negative intrathoracic pressure → airway obstruction.
Cyanosis:
- Central cyanosis: Hypoxemia (PaO2 < 60 mmHg) — COPD, ILD, R-L shunt.
- Peripheral cyanosis: Peripheral vasoconstriction — cold exposure, shock.
Clubbing:
- Bilateral: Bronchogenic carcinoma, bronchiectasis, ILD, cyanotic heart disease.
- Unilateral: Aneurysm, hemiplegia-related vascular changes.
Pallor, Pedal Edema: CHF, Cor Pulmonale.
Chest Wall Abnormalities:
- Barrel chest → Emphysema.
- Pectus excavatum/carinatum → May impair respiratory mechanics.
- Kyphoscoliosis → Restrictive lung disease.

B. Palpation

Tracheal Position:
- Shifted towards lesion: Lung collapse, fibrosis.
- Shifted away: Massive pleural effusion, tension pneumothorax, large mass.
- Midline: Normal or bilateral disease.
Chest Expansion:
- Unilateral reduction: Pneumothorax, consolidation, effusion.
- Bilateral reduction: COPD, ILD, NM disease.
Tactile Vocal Fremitus:
- Increased: Consolidation, cavity with patent bronchus.
- Decreased: Pleural effusion, pneumothorax, bronchial obstruction.
- Absent: Thick pleura, large effusion, pneumothorax.
Position of Apex Beat:
- Displaced: Large effusion, lung collapse, cardiomegaly.

C. Percussion

Percussion Note Variations:
- Resonant: Normal lung.
- Hyperresonant: Pneumothorax, emphysema.
- Dull: Consolidation, collapse, mass.
- Stony dull: Pleural effusion.
- Impaired resonance: Thickened pleura, small effusion.
Upper Border of Liver Dullness & Traube’s Space: Elevated in pleural effusion, diaphragmatic paralysis.

D. Auscultation

Breath Sounds:
- Vesicular: Normal.
- Bronchial: Consolidation, cavity.
- Absent: Pneumothorax, effusion, bronchial obstruction.
- Reduced: Emphysema, thickened pleura.
Adventitious Sounds:
- Crackles:
  - Fine end-inspiratory → ILD.
  - Coarse, biphasic → Bronchiectasis.
  - Basal → CHF.
- Wheezing:
  - Diffuse, expiratory → Asthma, COPD.
  - Localized → Bronchial obstruction.
- Stridor: Upper airway obstruction.
- Pleural rub: Pleurisy, pulmonary infarction.
Vocal Resonance:
- Increased (Bronchophony, Egophony, Whispering Pectoriloquy): Consolidation, cavity.
- Decreased/Absent: Effusion, pneumothorax, collapse.

E. Additional Advanced Tests (Bedside)

6-minute Walk Test: Exercise-induced desaturation.
Peak Expiratory Flow Rate: Asthma severity assessment.
Assessment of Respiratory Muscle Power: In suspected NM disorders.
Measurement of Jugular Venous Pressure (JVP): Cor pulmonale, CHF.
Oxygen Saturation Monitoring & Arterial Blood Gas Analysis: Detect hypoxia, hypercapnia.

III. Advanced Clinical Interpretation & Differential Possibilities

Tracheal Shift:
- Towards: Fibrosis, lobar collapse.
- Away: Effusion, tension pneumothorax, large mass.
- Bilateral elevation: Mediastinal mass, bilateral fibrosis.
Dull Percussion:
- Localized: Consolidation, collapse.
- Massive, stony dull: Pleural effusion.
- Diffuse: ILD.
Breath Sound Changes:
- Bronchial with crackles: Consolidation.
- Absent with dullness: Effusion.
- Absent with hyperresonance: Pneumothorax.
Fremitus & Resonance:
- Increased fremitus + bronchial breathing + dull percussion → Consolidation.
- Decreased fremitus + stony dull percussion + absent breath sounds → Effusion.
- Hyperresonance + absent fremitus + absent breath sounds → Pneumothorax.
Bilateral Basal Crackles:
- CHF, ILD.
Clubbing + Coarse Crackles + Copious Sputum:
- Bronchiectasis.
Wheezing + Prolonged Expiration + Accessory Muscle Use:
- COPD, Asthma.
Pleural Rub + Sharp Localized Pain:
- Pleurisy, PE.

Gastrointestinal System Examination

GASTROINTESTINAL SYSTEM EXAMINATION

1. HISTORY TAKING POINTS

A. Presenting Complaints

1. Abdominal Pain
Site:

Epigastric: Peptic ulcer, GERD, Pancreatitis, MI (referred)
Right hypochondrium: Cholelithiasis, Acute cholecystitis, Liver abscess
Left hypochondrium: Splenic infarct, Splenomegaly-related traction
Periumbilical: Early appendicitis, Small bowel pathology, Mesenteric ischemia
Right iliac fossa: Appendicitis, Crohn’s disease, Cecal carcinoma
Left iliac fossa: Diverticulitis, Sigmoid volvulus, Colorectal carcinoma
Suprapubic: Cystitis, Pelvic abscess, IBS

Character:

Colicky: Intestinal obstruction, ureteric colic, biliary colic
Dull aching: Chronic liver disease, malignancy, splenic pathology
Burning: GERD, PUD
Stabbing: Pancreatitis, perforation, vascular causes
Radiating to back: Pancreatitis, AAA rupture, posterior duodenal ulcer
Pain relief on bending forward: Pancreatitis

Severity:

Severe, sudden: Perforation, mesenteric ischemia, pancreatitis
Intermittent: IBS, functional dyspepsia
Nocturnal awakening: Peptic ulcer, malignancy

2. Nausea & Vomiting

Early morning vomiting: Raised ICP, Pregnancy, Alcohol gastritis
Post-prandial vomiting: Gastric outlet obstruction
Feculent vomiting: Distal small bowel obstruction
Bilious vomiting: Obstruction distal to ampulla

3. Dysphagia

Solids progressing to liquids: Malignancy, peptic stricture
Both solids and liquids from onset: Achalasia, esophageal spasm
Intermittent: Esophageal spasm, web

4. Odynophagia

Infective esophagitis (Candida, CMV, HSV), corrosive ingestion, pill esophagitis

5. Regurgitation / Heartburn

GERD, Zenker diverticulum, achalasia

6. Hematemesis / Malena / PR bleeding

Bright red vomiting: Mallory-Weiss tear, Varices
Coffee ground vomitus: Peptic ulcer
Black tarry stools: Upper GI bleed
Fresh PR bleeding: Hemorrhoids, Anal fissure, Diverticulosis, Rectal carcinoma

7. Altered Bowel Habits

Diarrhea: IBS-D, IBD, Malabsorption, Infection
Constipation: IBS-C, Hypothyroidism, Obstruction, Hirschsprung’s
Alternating diarrhea & constipation: Colonic malignancy, IBS

8. Weight Loss

With good appetite: Diabetes, Malabsorption, Hyperthyroidism
With anorexia: Malignancy, chronic infections, depression

9. Jaundice

Painful: Gallstones, cholangitis
Painless progressive: Pancreatic carcinoma, CBD obstruction
Intermittent: Hemolysis, Gilbert’s syndrome

10. Abdominal Distension

Sudden: Volvulus, Obstruction
Gradual: Ascites, Tumor, Organomegaly

11. Pruritus, Skin Changes

Cholestasis, Primary biliary cholangitis, Cirrhosis

B. Past History

Previous surgeries: Gastrectomy, Cholecystectomy
TB, Alcohol use, Hepatitis
History of similar complaints
Medications: NSAIDs, antacids, laxatives

C. Personal & Dietary History

Alcohol, Smoking
High-fat diet, Red meat intake
Recent travel, Outside food
Bowel habits

D. Family History

IBD, Colorectal carcinoma, Peptic ulcer disease, Wilson's disease

2. CLINICAL EXAMINATION POINTS

A. General Examination

Nutritional status: Cachexia, temporal wasting
Icterus: Conjunctival, generalized
Pallor: Anemia due to chronic GI bleed
Skin: Spider angioma, palmar erythema, scratch marks
Nail: Leukonychia, clubbing (IBD, Cirrhosis), koilonychia
Lymphadenopathy: Virchow node (gastric carcinoma), Sister Mary Joseph nodule (umbilical, metastasis)

B. Abdominal Examination

Inspection

Shape: Scaphoid (malnutrition), distended (ascites, obstruction)
Umbilicus: Inverted, everted, displaced
Visible peristalsis: Gastric outlet obstruction
Dilated veins: Portal hypertension (caput medusae), IVC obstruction
Surgical scars, hernia

Palpation

Superficial Palpation:

Guarding, rigidity: Peritonitis
Localized tenderness:
- RIF: Appendicitis
- LUQ: Splenic infarct
- Epigastrium: Pancreatitis, PUD

Deep Palpation:

Organomegaly:
- Liver: Surface, edge, consistency, tenderness
- Spleen: Notch, mobility
- Kidney: Bimanual palpation
Masses: Mobility, surface, pulsatility

Special Signs:

Murphy’s sign: Cholecystitis
Rovsing’s sign, Psoas sign: Appendicitis
Fluid thrill, shifting dullness: Ascites

Percussion

Liver span: Shrunk (cirrhosis), enlarged (Hepatitis)
Shifting dullness, fluid thrill: Ascites
Traube’s space dullness: Splenomegaly

Auscultation

Bowel sounds:
- Hyperactive: Obstruction, gastroenteritis
- Absent: Ileus, peritonitis
Bruits: Abdominal aorta aneurysm, renal artery stenosis

C. Per Rectal Examination

Masses: Rectal carcinoma
Tenderness: Proctitis
Melena, fresh blood
Sphincter tone

D. Other Systemic Examination

CNS: Hepatic encephalopathy signs (flap, altered sensorium)
Respiratory: Pleural effusion (hepatic hydrothorax)
CVS: High output state in chronic liver disease

3. Advanced Clinical Clues & Differential Diagnosis Pattern Recognition

Tender hepatomegaly: Hepatitis, Budd-Chiari, hepatic congestion
Firm, nodular liver: Cirrhosis, metastatic liver disease
Mass in epigastrium moving with respiration: Liver, left lobe enlargement
Shifting dullness with engorged veins: Ascites secondary to portal hypertension
Palpable gallbladder with jaundice (Courvoisier's sign): Malignancy of pancreas, CBD
Painless progressive jaundice + cachexia: Pancreatic carcinoma
Hepatosplenomegaly + pancytopenia: Portal hypertension, lymphoma
Ascites + low protein: Cirrhosis
Ascites + high protein: Malignancy, TB
Mass per rectum with bleeding: Rectal carcinoma
Visible peristalsis: Pyloric stenosis, obstruction
Generalized abdominal tenderness + rigidity: Peritonitis

CENTRAL NERVOUS SYSTEM EXAMINATION

I. HISTORY TAKING POINTS

1. Chief Complaints Analysis

When patient reports:

a) Weakness

Character: Flaccid, spastic, fatigable, episodic
- Flaccid → LMN lesion, Peripheral neuropathy, Guillain-Barré syndrome
- Spastic → UMN lesion (Stroke, MS, Myelopathy)
- Fatigable → Myasthenia Gravis
- Episodic → Periodic paralysis, Multiple sclerosis
Site:
- Hemibody → Stroke, Cortical lesion
- Quadriparesis → High cervical cord lesion, Brainstem
- Distal weakness → Peripheral neuropathy, Motor neuron disease
- Proximal weakness → Myopathy, Muscular dystrophy
Severity:
- Rapid progression → Stroke, GBS
- Slowly progressive → MND, Muscular dystrophy
- Relapsing-remitting → Multiple sclerosis

b) Sensory disturbances

Character: Numbness, tingling, burning, shooting pain
- Burning → Peripheral neuropathy (diabetes)
- Shooting → Root compression, Sciatica
- Loss of vibration/proprioception → Posterior column involvement
Site:
- Glove & stocking → Peripheral neuropathy
- Dermatomal → Nerve root lesion
- Hemisensory → Thalamic stroke
- Sensory level → Spinal cord lesion
Severity/Progression:
- Sudden onset → Infarct
- Gradual → Tumor, Degeneration

c) Headache

Character: Throbbing, dull, lancinating, band-like
- Throbbing → Migraine
- Dull, continuous → Tension headache, Tumor
- Early morning with vomiting → Raised ICP
Site:
- Unilateral → Migraine, Cluster
- Occipital → Cervical spondylosis, Posterior fossa tumor
Severity:
- Explosive onset → Subarachnoid hemorrhage
- Progressive → Tumor

d) Seizures

Character: Focal, Generalized, Myoclonic, Absence
- Focal → Structural lesion
- Generalized → Idiopathic epilepsy, metabolic
- Myoclonic → Juvenile myoclonic epilepsy
- Absence → Childhood absence epilepsy
Associated features: Aura, post-ictal confusion (Focal onset), tongue bite, incontinence

e) Gait disturbances

Type:
- Hemiplegic gait → UMN lesion
- Spastic gait → Paraplegia, Cord lesion
- Ataxic gait → Cerebellar lesion
- Festinant gait → Parkinsonism
- High-stepping → Peripheral neuropathy

f) Visual disturbances

Character: Blurring, diplopia, field defects, transient vision loss
- Blurring → Optic neuritis
- Diplopia → Brainstem lesion, CN palsy
- Field defects → Optic chiasm lesion (Bitemporal hemianopia)

g) Speech disturbances

Aphasia → Cortical (dominant hemisphere)
Dysarthria → Brainstem, CN lesion
Nasal voice → Palatal paralysis

h) Cognitive or Behavioral changes

Acute confusion → Encephalopathy
Chronic decline → Dementia, Frontal lobe lesion
Personality change → Frontal lobe tumor, Pick's disease

i) Vertigo

Peripheral: Severe, positional, with hearing loss (Labyrinthitis)
Central: Mild, persistent, with ataxia (Cerebellar stroke)

j) Autonomic dysfunction

Orthostatic hypotension → Autonomic neuropathy
Bladder dysfunction → Spinal cord involvement

2. Past History

Stroke, HTN, DM → Vascular causes
Trauma → Epidural/subdural hematoma
TB, HIV → Meningitis, Tuberculoma
Cancer → Paraneoplastic syndrome, brain metastasis

3. Family History

Huntington’s, Parkinson’s, Ataxia → Genetic predisposition
Epilepsy → Genetic or structural predisposition

4. Personal History

Alcohol → Cerebellar degeneration, Wernicke’s encephalopathy
Smoking → Vascular risk, Stroke

5. Occupational/Environmental History

Heavy metals → Encephalopathy
Rural residence → Neurocysticercosis

II. CLINICAL EXAMINATION POINTS (with diagnostic interpretation)

1. General Examination

Neurocutaneous markers:
- Café-au-lait spots → Neurofibromatosis
- Ash leaf macules → Tuberous sclerosis
Involuntary movements at rest → Parkinsonism, Chorea

2. Higher Mental Function Examination

Consciousness level

Drowsy, Comatose → Diffuse brain dysfunction (Trauma, Metabolic, Meningitis)

Orientation

Disorientation → Delirium, Dementia

Memory disturbance

Immediate → Attention deficit
Recent → Hippocampal lesion
Remote → Diffuse cortical dysfunction

Language

Fluent aphasia → Wernicke’s area lesion
Non-fluent → Broca’s area lesion
Global aphasia → Large MCA infarct

Apraxia, Agnosia

Apraxia → Dominant parietal lesion
Agnosia → Occipital/parietal lobe

Frontal lobe dysfunction

Disinhibition, impaired judgment

3. Cranial Nerve Examination

II - Optic nerve

Visual field defects:
- Bitemporal hemianopia → Pituitary tumor
- Homonymous hemianopia → Contralateral occipital/parietal lesion

III, IV, VI

Diplopia, ptosis → Brainstem lesion, raised ICP

Facial numbness → Trigeminal neuralgia, pontine lesion

VII

UMN palsy → Forehead sparing
LMN palsy → Bell’s palsy

VIII

Sensorineural deafness → Acoustic neuroma
Nystagmus → Vestibular dysfunction

IX, X

Nasal voice, dysphagia → Brainstem lesion

Shoulder droop → Accessory nerve lesion

XII

Tongue deviation → Ipsilateral LMN lesion, Contralateral UMN lesion

4. Motor System Examination

Bulk

Wasting → LMN lesion
Hypertrophy → Pseudohypertrophy in Duchenne

Tone

Spasticity → UMN lesion
Rigidity → Parkinsonism
Hypotonia → LMN, Cerebellar lesion

Power

Hemiparesis → Stroke
Distal weakness → Neuropathy
Proximal weakness → Myopathy

Involuntary movements

Tremor:
- Rest → Parkinsonism
- Intention → Cerebellar
- Postural → Essential tremor

Reflexes

Exaggerated → UMN lesion
Absent → LMN lesion
Plantar upgoing → Pyramidal tract lesion

Coordination

Dysmetria, intention tremor → Cerebellar
Dysdiadochokinesia → Cerebellar

Cranial Nerve Examination – Detailed

I – Olfactory Nerve

Tests:

Ask patient to close eyes & occlude one nostril. Present a non-irritant odor (coffee, vanilla, peppermint)
Ask to identify the smell. Repeat on both sides.

Interpretation:

Anosmia (loss of smell) → Trauma (cribriform plate fracture), Meningioma, Frontal lobe tumor
Parosmia (distorted smell) → Temporal lobe epilepsy
Hyposmia → Viral infection, aging
Hallucinations of smell → Uncinate fits

II – Optic Nerve

Tests:

A. Visual Acuity

Snellen’s chart (Distance)
Jaeger’s chart (Near vision)

B. Color Vision

Ishihara plates

C. Visual Fields

Confrontation test
Perimetry (Goldmann / Automated Humphrey)

D. Pupillary Reflexes

Direct light reflex
Consensual light reflex
Swinging flashlight test (Relative afferent pupillary defect)

E. Fundoscopy

Optic disc, Cup-disc ratio, Pallor, Papilledema, Retinal hemorrhages

F. Red Desaturation Test

Tests early optic neuritis

Interpretation:

Visual acuity ↓ → Optic neuropathy, Refractive errors
Field defects:
- Bitemporal hemianopia → Pituitary tumor
- Homonymous hemianopia → Optic tract lesion
- Central scotoma → Optic neuritis
Pupillary reflex abnormal → Optic nerve lesion

III, IV, VI – Oculomotor, Trochlear, Abducens Nerves

These are tested together

Tests:

A. Inspection

Ptosis → CN III palsy, Myasthenia

B. Eye Position

Strabismus, gaze deviation

C. Extraocular Movements (EOM)

Ask patient to follow finger in ‘H’ pattern

D. Diplopia Charting

Red-green glasses test
Hess chart

E. Convergence Test

F. Nystagmus observation

G. Pupil Size and Reactivity

Interpretation:

CN III palsy → Ptosis, ‘Down and out’ eye, Dilated pupil
CN IV palsy → Vertical diplopia, Head tilt
CN VI palsy → Medial deviation, inability to abduct

V – Trigeminal Nerve

Tests:

A. Sensory (V1, V2, V3 branches)

Light touch, pain, temperature over:
- Ophthalmic
- Maxillary
- Mandibular areas

B. Corneal Reflex

Afferent: V1
Efferent: VII

C. Motor

Palpate masseter & temporalis while clenching teeth

D. Jaw jerk reflex

Exaggerated in UMN lesion

Interpretation:

Loss of sensation in one branch → Peripheral nerve lesion
Loss in all divisions → Brainstem lesion, pontine infarct
Absent corneal reflex → CN V or VII lesion
Weak muscles of mastication → LMN lesion (pons)

VII – Facial Nerve

Tests:

A. Inspection

Facial asymmetry, forehead wrinkles, nasolabial fold

B. Motor Tests

Ask patient to:
- Raise eyebrows
- Close eyes tightly
- Show teeth
- Puff cheeks
- Whistle

C. Taste

Anterior 2/3rd of tongue: Sweet, salty

D. Stapedius reflex

Hyperacusis if impaired

E. Lacrimation test

Interpretation:

LMN lesion → Whole face affected (Bell's palsy)
UMN lesion → Forehead spared
Loss of taste → Chorda tympani lesion
Hyperacusis → Stapedius muscle involvement

VIII – Vestibulocochlear Nerve

Tests:

A. Cochlear Component

Finger rub test
Rinne’s test: AC > BC (normal)
Weber’s test: Lateralization in conductive loss
Audiometry (Pure tone)
Otoacoustic emissions

B. Vestibular Component

Dix-Hallpike maneuver → BPPV
Head impulse test → Vestibular hypofunction
Romberg’s test
Caloric test (COWS – Cold Opposite, Warm Same)

Interpretation:

Sensorineural loss → Acoustic neuroma, Labyrinthitis
Vertigo with nystagmus → Vestibular neuronitis, Cerebellar stroke

IX & X – Glossopharyngeal & Vagus Nerves

Tests:

A. Palatal Movement

Ask patient to say “Ah”
Observe uvula deviation

B. Gag Reflex

Afferent: IX
Efferent: X

C. Phonation

Hoarseness, nasal voice

D. Swallowing

E. Cough reflex

Interpretation:

Absent gag reflex → IX or X nerve lesion
Uvula deviated away from lesion → Unilateral vagus lesion
Nasal regurgitation → Palatal palsy

XI – Spinal Accessory Nerve

Tests:

A. Sternocleidomastoid strength

Ask patient to turn head against resistance

B. Trapezius strength

Shrug shoulders against resistance

Interpretation:

Weakness → LMN lesion in posterior triangle (surgical injury) or brainstem lesion

XII – Hypoglossal Nerve

Tests:

A. Tongue Inspection

Atrophy, fasciculations

B. Tongue Protrusion

Deviation → Towards side of LMN lesion

C. Tongue movement

Lateral movement, speed

Interpretation:

Deviation towards side of lesion → LMN palsy
UMN lesion → Contralateral weakness without atrophy

5. Sensory System Examination

Primary sensations

Loss of vibration/proprioception → Posterior column disease
Loss of pain/temp → Spinothalamic tract lesion
Sensory level → Spinal cord compression

Cortical sensations

Astereognosis → Parietal cortex lesion

6. Cerebellar Examination

Nystagmus, Dysarthria, Ataxia → Cerebellar lesion
Romberg positive → Sensory ataxia

7. Gait Examination

Spastic → UMN lesion
Ataxic → Cerebellar lesion
High stepping → Peripheral neuropathy
Parkinsonian → Basal ganglia disease

8. Meningeal Signs

Neck stiffness, Kernig’s, Brudzinski’s → Meningitis, SAH

9. Autonomic Nervous System

Orthostatic hypotension → Autonomic failure
Bladder dysfunction → Spinal cord lesion

10. Psychiatric Evaluation

Apathy, Disinhibition → Frontal lobe
Delirium → Acute diffuse dysfunction
Dementia → Alzheimer’s, Vascular, Lewy body

LOCOMOTOR SYSTEM EXAMINATION

I. HISTORY TAKING POINTS

1. Patient Profile

Name, Age, Gender, Occupation, Hand dominance (right/left-handed)
Residence (rural/urban; relevance in trauma, infection)
Socioeconomic status
Risk factors in occupation (repetitive stress, vibration exposure, heavy lifting)

2. Chief Complaints

Record in the patient’s own words, along with:

Duration of symptoms
Site of complaint (joint, bone, muscle, back)
Pattern: Single joint / multiple joints / generalized
Main symptom(s):
- Pain
- Swelling
- Stiffness
- Deformity
- Weakness
- Difficulty in movement / gait abnormalities
- Numbness / Paresthesia

3. History of Present Illness

A. Pain Analysis

Onset: Acute / Subacute / Insidious
Location: Joint / Bone / Muscle / Periarticular
Character: Dull, aching, sharp, throbbing, burning
Severity and grading
Radiation: Nerve distribution pattern (sciatica, brachialgia)
Aggravating factors: Activity, rest, cold, weight-bearing, specific movements
Relieving factors: Rest, analgesics, position
Diurnal variation:
- Morning stiffness (inflammatory arthritis)
- Night pain (neoplasm, infection)
Nocturnal awakening: Suggests mechanical or malignant cause

B. Swelling Analysis

Site, onset, progression
Associated redness, warmth, fluctuation, consistency
Relation to joint movement

C. Stiffness

Duration of stiffness (minutes to hours)
Morning stiffness: Inflammatory conditions
Stiffness after rest: Osteoarthritis
Improvement with activity or rest

D. Deformity

Onset, progression
Functional limitation
Cosmetic concerns

E. Instability

Sensation of joint giving way, locking, catching

F. Functional Limitations

Difficulty in Activities of Daily Living (ADLs)
Gait disturbance, imbalance, claudication
Difficulty in specific movements

G. Neurological Symptoms

Paresthesia, numbness, weakness
Radicular pain, spinal cord symptoms

H. Systemic Features

Fever, weight loss, malaise
Skin rash, photosensitivity, oral ulcers
Eye involvement (uveitis, scleritis)
Respiratory symptoms (restrictive lung disease in connective tissue disorders)
GI symptoms (IBD-related arthritis)

4. Past History

Previous trauma, fractures, joint dislocations
Previous episodes of joint complaints
History of tuberculosis, infections
Chronic systemic illness (Diabetes, Gout, Psoriasis)
Any malignancy

5. Family History

Inflammatory arthritis (RA, AS, Psoriatic arthritis)
Congenital musculoskeletal disorders
Metabolic bone disease

6. Personal History

Dietary habits (Calcium, Vitamin D intake)
Smoking, Alcohol consumption (risk factors for osteoporosis, AVN)
Physical activity level
Menstrual & obstetric history in females (osteoporosis risk)

7. Drug History

Steroid usage
Antiepileptics (bone demineralization)
Statins (myopathy)
Anti-TB drugs (arthropathy)
Recent fluoroquinolone usage (tendon rupture risk)

8. Occupational and Environmental History

Repetitive joint use, heavy lifting, sports injury
Exposure to zoonotic infections (Brucellosis, TB)

9. Psychosocial and Quality of Life Impact

Impact on daily activities
Mental health impact: Depression, anxiety
Sleep disturbance due to pain
Work productivity impairment

II. CLINICAL EXAMINATION POINTS

General Guidelines:
Always examine in a systematic, comparative manner. Examine all four limbs, axial skeleton, joints, bones, muscles, and neural components in an integrated approach.

1. General Physical Examination

General appearance: Cachexia, obesity, muscle wasting
Pallor, icterus, cyanosis
Clubbing (hypertrophic osteoarthropathy)
Lymphadenopathy
Nail changes (psoriasis, SLE)
Skin examination: Rashes, nodules, ulcers
Eye examination: Scleritis, Uveitis
Vitals: Especially fever, BP

2. Local Examination (Systematic Approach)

A. Inspection

Attitude and posture
Gait analysis:
- Antalgic gait
- Trendelenburg gait
- Waddling gait
- High-stepping gait
- Hemiplegic / Spastic gait
- Ataxic gait
Alignment and symmetry:
- Scoliosis, kyphosis, lordosis
- Deformities: Varus, valgus, swan neck, boutonniere, Z-thumb
Swelling
- Site, extent, shape
- Skin changes over swelling (redness, atrophy, ulceration)
Muscle bulk
- Wasting
- Hypertrophy
- Fasciculations
Scars, Sinuses, Discharging fistulas
Bony prominences

B. Palpation

Local temperature
Tenderness
- Pinpoint, diffuse, deep-seated
Swelling characteristics
- Consistency, fluctuation, mobility, reducibility, compressibility
Joint line tenderness
Crepitus on movement
Synovial thickening
Effusion
Muscle tone
Bony irregularities
Peripheral pulses (in trauma)
Neurological palpation (nerve thickening, tenderness)

C. Movements Assessment

Assess both Active and Passive movements:

Range of motion: Flexion, extension, abduction, adduction, rotation
Restriction of movement: Painful, mechanical block, muscle spasm
Instability testing
Special tests for specific joints (see below)

D. Measurements

Limb length discrepancy
Muscle girth comparison
Joint line distance

E. Functional Assessment

Power grading of affected muscles (MRC scale)
Joint stability tests
Functional performance tests:
- Squat test
- Sit-to-stand test
- Stairs climbing

3. Examination of Specific Joints and Regions

Shoulder

Drop arm test
Neer’s impingement test
Hawkin’s test
Apprehension test

Elbow

Carrying angle assessment
Cozen’s test (Tennis elbow)
Valgus and varus stress test

Wrist and Hand

Finkelstein’s test
Tinel’s sign
Phalen’s test
Bunnel-Littler test
Grind test for CMC arthritis

Spine

Inspection for scoliosis, kyphosis, lordosis
Schober’s test (lumbar flexibility)
Adam’s forward bending test
Palpation of spinous processes
Straight leg raising test
Femoral nerve stretch test

Hip

Trendelenburg test
Telescoping test
Patrick’s test
Thomas test (Flexion deformity)

Knee

Effusion tests: Patellar tap, Fluctuation test
Ligamentous instability: Anterior/Posterior drawer, Lachman’s test, Varus/Valgus stress test
Meniscal tests: McMurray’s, Apley’s grind test

Ankle and Foot

Anterior drawer test
Talar tilt test
Thompson test (Achilles tendon rupture)

4. Neurological Examination (Locomotor relevance)

Sensory examination: Touch, pain, temperature, vibration, proprioception
Motor power examination
Reflexes
Upper motor neuron signs: Clonus, Babinski sign
Lower motor neuron signs: Hypotonia, fasciculations

5. Vascular Examination

Peripheral pulses
Capillary refill time
Ankle-brachial index (if vascular insufficiency suspected)

6. Systemic Examination

Cardiovascular: Aortic regurgitation (seen in AS)
Respiratory: Fibrosis in Ankylosing Spondylitis
Abdominal: Hepatosplenomegaly (SLE, Felty syndrome)
Skin, Eye, Nail examination (as earlier described)

Optional Advanced Techniques

Dynamic gait analysis using software
Pressure plate analysis
Musculoskeletal Ultrasound examination
Thermography for inflammatory focus
Electromyography / Nerve conduction study
Bone densitometry
Functional Outcome Scores: DASH, Oxford Knee Score, HAQ

LOCOMOTOR SYSTEM EXAMINATION

1. HISTORY TAKING – Subheadings & Points

A. Chief Complaints

Pain (site, onset, duration, character, aggravating & relieving factors, radiation, diurnal variation)
Swelling (location, onset, duration, progression)
Stiffness (morning, evening, continuous)
Weakness (focal/generalized, proximal/distal)
Deformity (congenital/acquired)
Gait disturbance
Joint instability or giving way
Functional impairment

B. History of Present Illness

Onset: Acute/Chronic, sudden/insidious
Course: Progressive, intermittent, relapsing-remitting
Pattern: Monoarticular, oligoarticular, polyarticular
Associated symptoms:
- Fever (Infective, autoimmune)
- Skin rash (Psoriatic arthritis, SLE)
- Eye symptoms (Uveitis – Ankylosing spondylitis)
- Oral/genital ulcers (Behçet’s disease)
- Urinary complaints (Reiter’s syndrome)
- Weight loss, malaise
Morning stiffness: Duration (>1 hour → Inflammatory; <30 min → Mechanical)
Joint involvement sequence (Additive, migratory, intermittent)
Diurnal variation: Worse in morning → Inflammatory; worse at end of day → Osteoarthritis
Functional limitation: Bedridden, joint restriction, activities of daily living (ADLs)
Deformities: Onset, progression
Neurological symptoms: Tingling, numbness, bowel/bladder involvement

C. Past History

Trauma
Infections (TB, septic arthritis)
Previous surgeries or joint injections
History of similar illness
Fractures

D. Drug History

Steroid use → Avascular necrosis
Quinolones → Tendinopathy
Anticonvulsants → Osteomalacia

E. Family History

Rheumatoid arthritis, Ankylosing spondylitis, Osteoporosis

F. Personal History

Occupation (Repetitive stress injury)
Smoking, Alcohol (Gout, osteoporosis)
Diet (Calcium/Vitamin D intake)

G. Menstrual/Obstetric History

Early menopause → Osteoporosis

H. Systemic Review

Skin, Respiratory, Cardiovascular, CNS symptoms

2. PHYSICAL EXAMINATION – Subheadings & Points

A. General Physical Examination

Pallor
Edema
Clubbing
Cyanosis
Lymphadenopathy
Skin lesions (Psoriasis, SLE rash, nodules)
Muscle wasting
Deformities (Genu valgum, varum, kyphosis)

B. Vitals

Fever (Septic arthritis, autoimmune disease)
Tachycardia (Systemic illness)
BP (Vasculitis)
Respiratory rate (Restrictive lung disease in SLE)

3. LOCAL EXAMINATION – Systematic Approach

I. Inspection

Swelling
- Site, size, shape, skin over swelling, sinuses, scars
Deformity
- Angular (valgus, varus), rotational, length discrepancy
Muscle wasting
Joint alignment & posture
Scars/sinuses
Gait observation
- Antalgic, Trendelenburg, High-stepping, Spastic, Scissor gait

II. Palpation

Temperature over joint
Tenderness
- Localized, diffuse, specific anatomical point
- Grading: Grade 1-4
Swelling consistency
- Bony, cystic, fluctuant, soft
Synovial thickening
- Slippage sign
Crepitus
- Fine (Degenerative), Coarse (Inflammatory)
Muscle tone
- Hypotonia (LMN), Hypertonia (UMN)
Bony irregularities

III. Movement

Assess active and passive movements

Range of motion (ROM) in all planes
Painful/restricted/free movement
Crepitus during movement
Stability tests
- Stress tests
- Anterior drawer, Lachman’s test (Knee instability)
- Varus-valgus stress

Types of Movement Limitation:

Painful → Inflammatory/infective
Mechanical block → Loose body, bony block
Spasticity/Contracture → Neurological

IV. Measurements

Length of limb (True, apparent)
Circumference of muscles (atrophy/hypertrophy)
Joint angles
Leg length discrepancy

V. Special Tests (Joint specific)

Shoulder

Neer’s Impingement test
Hawkins-Kennedy test
Apprehension test (instability)
Drop arm test (Supraspinatus tear)

Elbow

Valgus/Varus stress
Tinel’s sign

Wrist & Hand

Phalen’s test, Tinel’s sign (Carpal Tunnel)
Finkelstein test (De Quervain’s)
Allen test (Vascular supply)

Hip

Trendelenburg test
Thomas test (Hip flexion contracture)
FABER (Flexion, Abduction, External Rotation)

Knee

Anterior drawer test, Lachman test (ACL)
Posterior drawer test (PCL)
McMurray’s test (Meniscus)
Varus/Valgus stress

Ankle & Foot

Anterior drawer test (ATFL injury)
Talar tilt test

4. SYSTEMIC EXAMINATION

To rule out systemic involvement:

Cardiovascular (Rheumatic disease, Vasculitis)
Respiratory (SLE, RA lung)
Abdominal (Hepatosplenomegaly)
Neurological (Myopathy, Neuropathy)

5. FUNCTIONAL ASSESSMENT

Activities of Daily Living (ADL) – Dressing, bathing, ambulation
Gait analysis
Balance tests

6. CLINICAL CORRELATION & DIFFERENTIAL POINTS

Pain

Inflammatory: Morning stiffness >1 hour, improves with activity
Mechanical: Worsens with use, relieved by rest

Swelling

Soft: Effusion
Firm: Synovial thickening
Hard: Bony overgrowth

Deformity

Acute: Dislocation
Chronic: Rheumatoid deformity, OA

Weakness

Proximal: Myopathy
Distal: Neuropathy

Joint Pattern

Monoarthritis: Gout, septic arthritis
Oligoarthritis: Spondyloarthropathy
Polyarthritis: RA, SLE

History Taking in Skin Disorders

SKIN, HAIR & NAIL EXAMINATION

I. HISTORY TAKING

A. Chief Complaints (Detailed with possibilities)

Skin Lesions
- Site: Localized (e.g., face → acne, butterfly rash), Generalized (e.g., drug rash, viral exanthem)
- Onset: Sudden (urticaria, drug rash), Gradual (psoriasis, vitiligo)
- Duration: Acute (<6 weeks → urticaria), Chronic (>6 weeks → psoriasis, lichen planus)
- Progression: Static (mole), Progressive (psoriasis)
- Character:
  - Maculopapular rash: Viral exanthem, Drug rash
  - Vesicular: Herpes, Chickenpox
  - Pustular: Acne, Bacterial infection
  - Scaly: Psoriasis, Pityriasis rosea
  - Pigmented: Melasma, Post-inflammatory
  - Depigmented: Vitiligo, Pityriasis versicolor
Itching (Pruritus)
- Character: Localized (Scabies, dermatitis), Generalized (Uremia, cholestasis, lymphoma)
- Severity: Mild (xerosis), Severe (Atopic dermatitis, scabies)
- Aggravating factors: Night-time (scabies), after bath (eczema)
- Relieving factors: Cold (eczema), scratching (psychogenic)
Burning / Pain
- Possibilities: Herpes zoster (burning pain), Contact dermatitis, Staphylococcal infections
Ulceration
- Site & Cause: Leg (venous ulcer, arterial ulcer, neuropathic ulcer), Mouth (Aphthous, Behçet’s)
Swelling/Nodule/Lump
- Single (sebaceous cyst), Multiple (neurofibroma)
Discharge from lesion
- Purulent (bacterial), Serous (viral), Bloody (malignancy)
Photosensitivity
- SLE, Porphyria, Drug-induced
Hair Loss
- Pattern: Diffuse (Telogen effluvium), Patchy (Alopecia areata), Frontal recession (Androgenic alopecia)
- Onset: Sudden (Telogen effluvium), Insidious (Androgenic)
- Associated symptoms: Itching, scaling
Nail Changes
- Discoloration (Onychomycosis, Psoriasis)
- Deformity (Koilonychia, Clubbing)
- Fragility, Brittleness
Systemic Associations
- Weight loss (Lymphoma, HIV)
- Fever (Viral exanthem, Drug rash)
- Joint pain (Psoriasis, SLE)
- Diarrhea (Dermatitis herpetiformis, Zinc deficiency)

B. Past History

Similar lesions in past
Chronic systemic illness (Diabetes, HIV)
Drug intake (Antibiotics, Anticonvulsants, NSAIDs)
Allergies

C. Family History

Psoriasis, Atopy, Vitiligo, Alopecia areata

D. Personal History

Occupation (Chemical exposure → Contact dermatitis)
Hygiene
Sexual history (STDs with skin manifestations)
Stress (Alopecia areata, Psoriasis flare)

II. PHYSICAL EXAMINATION

1. General Examination

Pallor (Chronic infection, malignancy)
Icterus (Cholestasis causing pruritus)
Lymphadenopathy (Cutaneous lymphoma, secondary infection)
Clubbing (Pulmonary disease with hypertrophic osteoarthropathy)
Edema

2. LOCAL EXAMINATION – SKIN

A. Inspection

Points to Note:

Site: Specific patterns
- Sun-exposed areas → SLE, Photosensitive dermatitis
- Flexural → Atopic dermatitis
- Extensor surfaces → Psoriasis
- Pressure points → Callosities, Decubitus ulcers
Distribution
- Symmetrical → Psoriasis, Drug rash
- Asymmetrical → Fungal infections
- Dermatomal → Herpes zoster
- Linear → Lichen striatus, Koebner phenomenon
Type of Primary Lesion:
- Macule (Vitiligo, Pityriasis alba)
- Papule (Lichen planus)
- Vesicle (Herpes, Chickenpox)
- Bulla (Pemphigus vulgaris)
- Pustule (Impetigo, Acne)
- Nodule (Leprosy)
- Plaque (Psoriasis)
- Wheal (Urticaria)
- Cyst (Sebaceous cyst)
Secondary Changes:
- Crusting (Impetigo)
- Scaling (Psoriasis, Dermatophytosis)
- Ulceration (Pyoderma gangrenosum, Vasculitis)
- Lichenification (Chronic eczema)
Color Changes
- Hyperpigmentation → Addison’s disease, Lichen planus
- Hypopigmentation → Vitiligo, Tinea versicolor
- Erythema → Acute dermatitis
Surface
- Smooth, rough, verrucous
Margins
- Well-defined (Psoriasis, Fungal infection)
- Ill-defined (Eczema)
Shape
- Annular, polycyclic, linear, serpiginous
Hair & Nail involvement
- Psoriasis, Lichen planus

B. Palpation

Temperature
Tenderness
Consistency (Soft → Lipoma, Firm → Fibroma)
Mobility (Cystic, Fixed)
Induration
Sensation over lesion (Leprosy)

C. Special Tests (Bedside)

Diascopy: Blanchable lesions (Urticaria), non-blanchable (purpura)
Nikolsky sign: Positive in Pemphigus vulgaris
Bulla spread sign
Koebner phenomenon: Psoriasis, Lichen planus
Dermographism: Physical urticaria
Sensory testing over lesions: Leprosy

3. HAIR EXAMINATION

A. Inspection

Distribution:
- Diffuse (Telogen effluvium)
- Localized (Alopecia areata)
- Androgenic pattern
Quality:
- Thin, thick, brittle, dry
Shaft Abnormalities:
- Pili torti, Trichorrhexis nodosa
Color Changes:
- Premature greying
- Poliosis (Vitiligo)

B. Palpation

Texture
Fragility

C. Specific Tests

Hair pull test (Anagen/Telogen shedding)
Tug test
Hair microscopy (Shaft abnormality)

4. NAIL EXAMINATION

A. Inspection

Shape & Curvature
- Koilonychia (Iron deficiency)
- Clubbing (Systemic disease)
Surface
- Pitting (Psoriasis, Alopecia areata)
- Beau’s lines (Systemic illness)
- Longitudinal ridges (Lichen planus)
Color
- Leukonychia (Hypoalbuminemia)
- Yellow nails (Yellow nail syndrome)
- Subungual hyperkeratosis (Psoriasis)
- Splinter hemorrhages (Endocarditis)
Periungual Changes
- Paronychia
- Pterygium (Lichen planus)

B. Palpation

Tenderness (Paronychia, ingrown nail)
Texture

III. SYSTEMIC EXAMINATION

To detect systemic disease with skin manifestations:

CVS: Vasculitis, Endocarditis (Janeway lesions)
Respiratory: Sarcoidosis, Clubbing
Gastrointestinal: Dermatitis herpetiformis, Porphyria
Endocrine: Acanthosis nigricans, Addison’s pigmentation
Neurology: Sensory loss in Hansen’s disease
Rheumatology: SLE, Psoriasis-related arthritis

IV. CLINICAL CLUES & DIFFERENTIAL POSSIBILITIES BASED ON FINDINGS

When examining the skin, a primary lesion’s morphology immediately directs the clinical gaze toward certain pathophysiological categories. For instance, if one observes well-defined, erythematous, scaly plaques with silvery white scales predominantly over extensor surfaces, the morphological clue suggests a papulosquamous disorder; the sharply demarcated plaques and the presence of Auspitz sign make Psoriasis vulgaris the leading possibility, although tinea corporis and pityriasis rosea must be considered and excluded by distribution, scale pattern, and scraping for fungal elements.

Macular hypopigmentation over the face, particularly in children, without sensory loss and with fine scaling favors pityriasis alba; however, if the margins are well defined, with complete depigmentation and no scaling, vitiligo becomes more likely. Should hypo- or depigmented patches show sensory loss, hair loss, or peripheral nerve thickening, suspicion must shift toward Hansen’s disease, particularly borderline or tuberculoid leprosy.

Vesicular lesions clustered unilaterally along a dermatome prompt immediate consideration of Herpes zoster; burning pain preceding the eruption clinches the diagnosis. If vesicles are generalized, involve mucosa, and appear in crops, the leading differential becomes varicella infection. Conversely, if vesicles are widespread but pruritic, with predilection for flexural areas and excoriation marks, the differential tilts towards scabies.

The presence of lichenification, excoriation, and pigmentation over flexural surfaces points to chronic eczema, especially in atopic individuals. However, the clinician must differentiate this from lichen simplex chronicus, where a single area is repeatedly scratched leading to lichenification, and from lichen planus, characterized by violaceous flat-topped papules with Wickham striae.

Generalized pruritus without primary skin lesions demands systemic evaluation. The possibility of chronic renal failure (uremic pruritus), cholestasis (bile salt deposition), hematologic malignancies (Hodgkin’s lymphoma, polycythemia vera), or HIV-related pruritus must be considered based on associated systemic features like lymphadenopathy, splenomegaly, jaundice, or anemia.

In hair examination, diffuse non-scarring hair loss with positive pull test, history of febrile illness, childbirth, or stress suggests telogen effluvium. If hair loss is in well-defined patches without inflammation or scarring, and exclamation mark hairs are seen, alopecia areata is the likely diagnosis. However, when hair loss is scarring, with loss of follicular ostia, the differentials narrow to discoid lupus erythematosus, lichen planopilaris, or folliculitis decalvans.

Hypertrichosis or hirsutism necessitates differentiation: when excessive terminal hair is distributed in a male pattern in females, associated with menstrual irregularities or virilization, polycystic ovarian syndrome, androgen-secreting tumors, Cushing’s syndrome, or congenital adrenal hyperplasia are considered. Diffuse non-androgenic hypertrichosis may result from medications (phenytoin, minoxidil), porphyria, or systemic illnesses.

Nail findings also yield systemic clues. Clubbing, when identified, prompts evaluation for pulmonary (bronchiectasis, lung carcinoma), cardiac (cyanotic congenital heart disease, infective endocarditis), or gastrointestinal (ulcerative colitis, cirrhosis) causes. Koilonychia demands iron studies to evaluate for iron deficiency anemia but also triggers consideration of Plummer-Vinson syndrome. Beau’s lines reflect systemic stressors such as high-grade fever, chemotherapy, or severe malnutrition during the period of nail matrix insult.

Pitting of nails typically suggests psoriasis, especially when accompanied by onycholysis, subungual hyperkeratosis, or oil drop sign. However, it may also occur in alopecia areata and, less commonly, in eczema. Leukonychia may be due to trauma, hypoalbuminemia, or systemic illnesses like cirrhosis. Splinter hemorrhages require careful evaluation for infective endocarditis, vasculitis, or trauma.

Yellow nail syndrome characterized by slow-growing, thickened, yellow nails, is often associated with lymphoedema, pleural effusion, and bronchiectasis — a key paraneoplastic and systemic clue.

Generalized hyperpigmentation particularly involving mucosa, palmar creases, and pressure areas suggests Addison’s disease; associated hypotension and hyponatremia may confirm this. In contrast, hyperpigmentation with weight loss and hepatosplenomegaly warrants evaluation for hemochromatosis or chronic liver disease.

If one encounters cutaneous nodules that are non-tender, shiny, and multiple over cooler parts of the body (ears, elbows, face), and associated peripheral nerve thickening with glove-and-stocking anesthesia, the possibility of lepromatous leprosy becomes evident.

In ulcer examination, the character of edges provides diagnostic clues. Punched out edges point towards trophic or neuropathic ulcers (diabetes, leprosy). Undermined edges suggest tuberculous ulcers. Raised everted edges immediately prompt concern for squamous cell carcinoma, while rolled edges make basal cell carcinoma more probable.

Livedo reticularis with purpuric lesions is a vascular clue, possibly pointing to antiphospholipid syndrome, cryoglobulinemia, or vasculitis.

Butterfly-shaped facial erythema sparing nasolabial folds with photosensitivity is a strong pointer toward systemic lupus erythematosus; however, if the rash is papular, scaly, and involves nasolabial folds, seborrheic dermatitis is considered.

Erythema nodosum, presenting as tender, erythematous subcutaneous nodules over the shins, leads to evaluation for streptococcal infection, tuberculosis, sarcoidosis, inflammatory bowel disease, or drug reaction.

Targetoid lesions with central dusky zone, erythematous middle ring, and peripheral pale ring suggest erythema multiforme, which is often related to herpes simplex virus infection, medications, or Mycoplasma infection.

In examining generalized dryness of skin (xerosis), especially in elderly or renal failure patients, the clinician considers senile xerosis, ichthyosis vulgaris, hypothyroidism, or chronic renal disease.

Friday, March 21, 2025

MOVEMENTS OF ALL JOINTS

MOVEMENTS OF ALL JOINTS

Contents:

Joint Overview – Type and structure of the joint.
Possible Movements – Detailed movements with mechanism.
Components Involved – Bones, muscles, ligaments, and tendons.
Sports Scenarios – Different scenarios where these movements occur.

✅ 1. Head and Neck Joints

A. Atlanto-Occipital Joint (C0-C1)

Type: Condyloid Joint
Movements: Flexion, Extension, Lateral Flexion
Components: Occipital bone, Atlas, Sternocleidomastoid, Splenius Capitis
Mechanism: The occipital condyles glide over the Atlas facet.

Sports Examples:

A swimmer tilting the head to breathe during freestyle (lateral flexion).
A footballer scanning the field (extension).
A gymnast performing a forward roll (flexion).

B. Atlanto-Axial Joint (C1-C2)

Type: Pivot Joint
Movements: Rotation
Components: Atlas, Axis, Sternocleidomastoid, Obliquus Capitis Inferior
Mechanism: The dens (odontoid process) of the Axis acts as a pivot.

Sports Examples:

A cricket fielder turning to catch a ball.
A tennis player watching the ball during a serve.
A referee looking left and right on the field.

✅ 2. Spine and Back Joints

A. Intervertebral Joints

Type: Cartilaginous Joint
Movements: Flexion, Extension, Lateral Flexion, Rotation
Components: Vertebrae, Intervertebral Discs, Rectus Abdominis, Erector Spinae
Mechanism: Vertebrae slide and compress the disc.

Sports Examples:

A gymnast performing a backbend (extension).
A wrestler twisting to avoid an opponent (rotation).
A basketball player bending forward to pick up the ball (flexion).

✅ 3. Upper Limb Joints

A. Shoulder (Glenohumeral Joint)

Type: Ball-and-Socket Joint
Movements: Flexion, Extension, Abduction, Adduction, Rotation, Circumduction
Components: Humerus, Scapula, Deltoid, Pectoralis Major, Rotator Cuff
Mechanism: Humerus moves in the glenoid cavity with rotator cuff stabilization.

Sports Examples:

A volleyball player spiking the ball (abduction).
A swimmer doing a backstroke (circumduction).
A cricket bowler delivering a ball (internal rotation).

B. Elbow Joint

Type: Hinge Joint
Movements: Flexion, Extension, Pronation, Supination
Components: Humerus, Radius, Ulna, Biceps Brachii, Triceps Brachii
Mechanism: The ulna moves around the humeral trochlea.

Sports Examples:

A weightlifter performing a bicep curl (flexion).
A tennis player executing a forehand stroke (supination).
A boxer extending the arm for a punch (extension).

C. Wrist Joint

Type: Condyloid Joint
Movements: Flexion, Extension, Radial Deviation, Ulnar Deviation
Components: Radius, Carpal Bones, Flexor Carpi Radialis, Extensor Carpi Ulnaris
Mechanism: Radius moves over carpal bones.

Sports Examples:

A badminton player flicking the shuttlecock (extension).
A golfer bending the wrist during a backswing (flexion).
A baseball pitcher throwing a curveball (radial deviation).

✅ 4. Lower Limb Joints

A. Hip Joint

Type: Ball-and-Socket Joint
Movements: Flexion, Extension, Abduction, Adduction, Rotation, Circumduction
Components: Femur, Pelvis, Gluteus Maximus, Iliopsoas
Mechanism: The femoral head rotates within the acetabulum.

Sports Examples:

A soccer player kicking a ball (flexion).
A dancer doing a side leg lift (abduction).
A sprinter pushing off the ground (extension).

B. Knee Joint

Type: Hinge Joint
Movements: Flexion, Extension, Rotation (Slight when flexed)
Components: Femur, Tibia, Patella, Quadriceps, Hamstrings
Mechanism: The femoral condyles glide on the tibial plateau.

Sports Examples:

A runner taking a stride (extension).
A basketball player squatting before a jump (flexion).
A football goalkeeper diving (rotation when flexed).

C. Ankle Joint

Type: Hinge Joint
Movements: Dorsiflexion, Plantarflexion, Inversion, Eversion
Components: Tibia, Fibula, Talus, Gastrocnemius, Tibialis Anterior
Mechanism: The talus moves within the tibiofibular mortise.

Sports Examples:

A sprinter pushing off from the blocks (plantarflexion).
A gymnast landing on their toes (dorsiflexion).
A footballer changing direction quickly (inversion).

✅ 5. Small Joints

A. Finger Joints (Interphalangeal Joints)

Type: Hinge Joint
Movements: Flexion, Extension
Components: Phalanges, Flexor Digitorum Profundus, Extensor Digitorum
Mechanism: The phalanges hinge like a door.

Sports Examples:

A cricketer gripping the ball (flexion).
A basketball player releasing a shot (extension).
A guitarist strumming strings (flexion and extension).

B. Toe Joints (Metatarsophalangeal Joints)

Type: Condyloid Joint
Movements: Flexion, Extension, Abduction, Adduction
Components: Metatarsals, Phalanges, Flexor Digitorum Longus, Extensor Hallucis Longus
Mechanism: Movement occurs at the joint between the toes and metatarsals.

Sports Examples:

A sprinter pushing off the toes (flexion).
A dancer balancing on tiptoes (extension).
A footballer adjusting foot position to kick (abduction).

Thursday, March 20, 2025

ENDOCRINE SYSTEM

I. ANATOMY OF THE ENDOCRINE SYSTEM

✔ Definition & Importance

The Endocrine System consists of ductless glands that secrete hormones directly into the bloodstream.
Works in coordination with the nervous system to regulate growth, metabolism, reproduction, homeostasis, and stress responses.

1. Hypothalamus (Master Regulator of Endocrine System)

✔ Location:

Situated in the diencephalon, just above the pituitary gland.
✔ Structure:
Composed of specialized neurosecretory cells that regulate hormone secretion from the pituitary gland.
✔ Hormones Secreted:
Corticotropin-releasing hormone (CRH) → Stimulates ACTH secretion.
Thyrotropin-releasing hormone (TRH) → Stimulates TSH secretion.
Gonadotropin-releasing hormone (GnRH) → Stimulates FSH & LH secretion.
Growth hormone-releasing hormone (GHRH) → Stimulates GH release.
Dopamine (Prolactin-inhibiting factor, PIF) → Inhibits Prolactin secretion.

2. Pituitary Gland (Master Gland of the Endocrine System)

✔ Location:

Lies within the sella turcica of the sphenoid bone.
✔ Divisions & Hormones:
Anterior Pituitary (Adenohypophysis)
- TSH → Thyroid stimulation.
- ACTH → Adrenal cortex stimulation.
- FSH & LH → Gonadal function.
- GH → Growth & metabolism.
- Prolactin → Milk secretion.
Posterior Pituitary (Neurohypophysis)
- ADH (Vasopressin) → Water retention.
- Oxytocin → Uterine contraction & lactation.

3. Thyroid Gland

✔ Location:

Anterior to the trachea, below the larynx, consisting of two lobes connected by an isthmus.
✔ Structure:
Made of follicular cells (secrete T3 & T4) and parafollicular cells (C cells) (secrete calcitonin).
✔ Hormones:
T3 (Triiodothyronine) → More active, regulates metabolism.
T4 (Thyroxine) → Less active, converted to T3 in peripheral tissues.
Calcitonin → Lowers serum calcium levels.

4. Parathyroid Glands

✔ Location:

Four small glands located behind the thyroid gland.
✔ Hormone Secreted:
Parathyroid Hormone (PTH) → Increases blood calcium by stimulating osteoclasts, increasing renal calcium reabsorption, and activating Vitamin D.

5. Adrenal Glands

✔ Location:

Situated above each kidney, consisting of cortex & medulla.
✔ Structure & Hormones:
Adrenal Cortex (Outer layer):
- Zona Glomerulosa → Secretes Aldosterone (Mineralocorticoid) for sodium retention.
- Zona Fasciculata → Secretes Cortisol (Glucocorticoid) for stress response & metabolism.
- Zona Reticularis → Produces Androgens (DHEA) for secondary sexual characteristics.
Adrenal Medulla (Inner layer):
- Produces Epinephrine & Norepinephrine (Catecholamines) for the fight-or-flight response.

6. Pancreas (Mixed Exocrine & Endocrine Gland)

✔ Location:

Lies retroperitoneally in the upper abdomen (head, body, and tail).
✔ Endocrine Function (Islets of Langerhans):
β-cells → Secrete Insulin (lowers blood glucose).
α-cells → Secrete Glucagon (raises blood glucose).
δ-cells → Secrete Somatostatin (inhibits insulin & glucagon).

7. Gonads (Testes & Ovaries)

✔ Location:

Testes (Scrotum) → Male gonads.
Ovaries (Pelvic cavity) → Female gonads.
✔ Hormones:
Testosterone → Male reproductive function.
Estrogen & Progesterone → Female reproductive function.

II. PHYSIOLOGY OF THE ENDOCRINE SYSTEM

✔ General Functions of Hormones

Maintain homeostasis (e.g., glucose, calcium levels).
Regulate growth & development (GH, IGF-1).
Modulate metabolism & energy balance (Thyroid hormones).
Control reproduction & sexual differentiation (FSH, LH, Estrogen, Testosterone).

1. Hypothalamic-Pituitary Axis (HPA System)

✔ Hypothalamus regulates pituitary secretion via releasing & inhibiting hormones.
✔ Negative feedback loops control hormone levels.

2. Thyroid Hormones & Metabolism

✔ T3/T4 regulate basal metabolic rate (BMR) by increasing mitochondrial activity.
✔ Effects:

Increases oxygen consumption & heat production.
Stimulates protein synthesis & glucose utilization.

3. Cortisol & Stress Response

✔ Effects of Cortisol:

Increases blood glucose via gluconeogenesis.
Suppresses immune system.
Promotes lipolysis & muscle catabolism.

4. Insulin & Glucagon (Glucose Homeostasis)

✔ Insulin (Secreted after meals) → Lowers blood glucose by promoting glucose uptake & glycogenesis.
✔ Glucagon (Secreted during fasting) → Raises blood glucose by stimulating glycogenolysis & gluconeogenesis.

5. Growth Hormone (GH) & IGF-1

✔ Functions:

Stimulates bone growth & muscle anabolism.
Increases lipolysis & protein synthesis.

6. ADH & Water Regulation

✔ Effects:

Promotes water reabsorption in kidneys.
Regulates blood pressure & osmolarity.

7. Reproductive Hormones

✔ Testosterone → Promotes spermatogenesis & secondary male characteristics.
✔ Estrogen & Progesterone → Regulate ovulation & menstrual cycle.

CONCLUSION

The Endocrine System regulates growth, metabolism, reproduction, and homeostasis via hormonal feedback mechanisms.
Understanding endocrine physiology is critical for diagnosing and managing hormonal disorders.
Dysfunctions result in diseases like Diabetes, Thyroid Disorders, Cushing’s, Addison’s, and Pituitary Disorders.

PATHOLOGY OF THE ENDOCRINE SYSTEM

I. GENERAL PATHOLOGY OF THE ENDOCRINE SYSTEM

✔ Endocrine Disorders Classification

Hypofunction → Hormone deficiency due to autoimmune destruction, infection, infarction, genetic defects.
Hyperfunction → Excess hormone secretion due to tumors, autoimmune stimulation, ectopic production.
Receptor Defects → Target tissue resistance to hormones (e.g., Insulin resistance in Type 2 Diabetes).

II. PATHOLOGY OF INDIVIDUAL GLANDS

1. Hypothalamic-Pituitary Disorders

✔ Pituitary Adenomas (Most common)

Prolactinoma → Causes galactorrhea, amenorrhea, infertility.
GH-secreting adenoma → Causes Acromegaly (adults) / Gigantism (children).
ACTH-secreting adenoma → Causes Cushing’s disease.

✔ Hypopituitarism (Panhypopituitarism)

Causes: Sheehan’s Syndrome (postpartum infarction), pituitary apoplexy (hemorrhage), tumors, radiation.
Symptoms: Fatigue, infertility, cold intolerance, growth retardation.

✔ Diabetes Insipidus (ADH Deficiency)

Polyuria, polydipsia, hypernatremia, low urine osmolality.
Central DI → Lack of ADH from pituitary.
Nephrogenic DI → Renal resistance to ADH.

✔ SIADH (Syndrome of Inappropriate ADH Secretion)

Causes hyponatremia, low serum osmolality, concentrated urine.
Causes: Lung cancer (paraneoplastic), CNS disorders, drugs (carbamazepine, SSRIs).

2. Thyroid Disorders

✔ Hyperthyroidism (Thyrotoxicosis)

Graves’ Disease (Autoimmune, TSH receptor stimulation).
Toxic Multinodular Goiter.
Thyroid Storm (Life-threatening emergency).
Symptoms: Heat intolerance, weight loss, tachycardia, exophthalmos, tremors.

✔ Hypothyroidism

Hashimoto’s Thyroiditis (Autoimmune, anti-TPO antibodies).
Iodine Deficiency (Endemic goiter).
Symptoms: Cold intolerance, weight gain, bradycardia, lethargy, dry skin.

✔ Thyroid Nodules & Cancer

Papillary Carcinoma → Most common, good prognosis.
Follicular Carcinoma → Hematogenous spread.
Medullary Carcinoma → Associated with MEN 2, produces calcitonin.
Anaplastic Carcinoma → Poor prognosis, rapidly growing.

3. Parathyroid Disorders

✔ Hyperparathyroidism

Primary → Parathyroid adenoma.
Secondary → Chronic kidney disease.
Symptoms: Hypercalcemia (bones, stones, abdominal groans, psychic moans).

✔ Hypoparathyroidism

Causes: Surgery, autoimmune disease.
Symptoms: Hypocalcemia (tetany, Chvostek’s & Trousseau’s signs, seizures, arrhythmias).

4. Adrenal Disorders

✔ Cushing’s Syndrome (Hypercortisolism)

Causes: Pituitary ACTH tumor, adrenal adenoma, ectopic ACTH (small cell lung cancer).
Symptoms: Moon face, buffalo hump, striae, osteoporosis, hypertension, hyperglycemia.

✔ Addison’s Disease (Adrenal Insufficiency)

Causes: Autoimmune destruction, TB, metastases.
Symptoms: Hyperpigmentation, hypotension, weight loss, hyponatremia, hyperkalemia.

✔ Pheochromocytoma (Adrenal Medulla Tumor)

Symptoms: Episodic hypertension, palpitations, sweating, headaches.
Diagnosed by elevated metanephrines & catecholamines.

5. Pancreatic Disorders (Diabetes Mellitus)

✔ Type 1 DM (Autoimmune destruction of β-cells)

Insulin deficiency → Hyperglycemia, weight loss, DKA risk.

✔ Type 2 DM (Insulin resistance)

Associated with obesity, metabolic syndrome.
Can cause hyperosmolar hyperglycemic state (HHS).

✔ Diabetic Complications

Macrovascular: Stroke, MI, PAD.
Microvascular: Retinopathy, Nephropathy, Neuropathy.

III. CLINICAL EXAMINATION OF THE ENDOCRINE SYSTEM

✔ General Inspection

Obesity (Cushing’s, Hypothyroidism), Cachexia (Addison’s, DM-1).
Skin changes: Hyperpigmentation (Addison’s), Myxedema (Hypothyroidism), Vitiligo (Autoimmune).
Hair distribution: Hirsutism (PCOS, Cushing’s), Loss of outer eyebrows (Hypothyroidism).

✔ Head & Neck Examination

Goiter (Thyroid enlargement, Graves’, Iodine deficiency).
Exophthalmos (Graves’ disease).

✔ Cardiovascular Examination

Tachycardia (Hyperthyroidism, Pheochromocytoma).
Bradycardia (Hypothyroidism, Addison’s).

✔ Neurological Examination

Tremors (Hyperthyroidism, Pheochromocytoma).
Hyporeflexia (Hypothyroidism), Hyperreflexia (Hyperthyroidism).

✔ Special Tests

Chvostek’s Sign (Facial spasm in Hypocalcemia).
Trousseau’s Sign (Carpopedal spasm in Hypocalcemia).

IV. DIFFERENTIAL DIAGNOSIS & CONFIRMATORY DIAGNOSIS

✔ Hyperthyroidism

Graves’ Disease → Diffuse goiter, exophthalmos, low TSH, high T3/T4.
Toxic Multinodular Goiter → Nodular thyroid, no eye signs.

✔ Hypothyroidism

Hashimoto’s Thyroiditis → Anti-TPO antibodies, goiter.
Iodine Deficiency → Low T3/T4, goiter.

✔ Diabetes Mellitus

Type 1 → Autoimmune, low insulin, GAD antibodies.
Type 2 → Insulin resistance, obesity, metabolic syndrome.

✔ Cushing’s Syndrome

Pituitary ACTH tumor (Cushing’s Disease) → High ACTH, suppresses with dexamethasone.
Adrenal Adenoma → Low ACTH, no suppression with dexamethasone.

✔ Pheochromocytoma

Diagnosed by 24-hour urine metanephrines, plasma catecholamines.

CONCLUSION

Endocrine disorders present with systemic manifestations due to hormone imbalances.
Clinical examination is crucial in differentiating conditions like thyroid disorders, diabetes, adrenal insufficiency, and pituitary abnormalities.
High-yield diagnostic tools include hormonal assays, imaging, and stimulation/suppression tests.
Mastering pathology, clinical examination, and diagnosis is essential for both entrance exams and clinical practice.