Sunday, November 30, 2025

SERIES 3- GIT DISORDERS



Gastrointestinal Diseases 


1. Gastroesophageal Reflux Disease (GERD)

Early

  • Occasional retrosternal burning after meals
  • Sour taste in mouth
  • Worse on lying down

Progression

  • Frequent heartburn
  • Regurgitation of acidic fluid
  • Nocturnal cough / throat irritation

Advanced

  • Dysphagia (esophagitis, stricture)
  • Hoarseness
  • Dental enamel erosion

Classical Feature: Heartburn after meals + relief on antacids

Special: Symptoms worsen on bending forward (water brash)


2. Peptic Ulcer Disease (Gastric & Duodenal)

Early

  • Epigastric burning pain

Progression

  • Gastric ulcer: Pain worsens after meals
  • Duodenal ulcer: Pain relieved by meals, worsens 2–3 hours later

Advanced

  • Hematemesis, melena
  • Anemia

Special: Nocturnal pain common in duodenal ulcer


3. Acute Gastritis

Early

  • Epigastric discomfort
  • Nausea, bloating

Progression

  • Vomiting
  • Mild hematemesis

Advanced

  • Erosive gastritis → brisk bleeding

Classical: History of NSAID/alcohol use


4. Chronic Atrophic Gastritis

Early

  • Vague dyspepsia
  • Early satiety

Progression

  • Vitamin B12 deficiency → paresthesia
  • Fatigue (anemia)

Advanced

  • Achlorhydria

Special: Associated with autoimmune thyroid disease (Type A)


5. Acute Pancreatitis

Early

  • Acute severe epigastric pain radiating to back

Progression

  • Vomiting
  • Fever
  • Abdominal distension

Advanced

  • Hypotension, shock
  • Grey-Turner & Cullen signs

Peculiar: Pain relieved by leaning forward


6. Chronic Pancreatitis

Early

  • Recurrent epigastric pain

Progression

  • Steatorrhea
  • Weight loss

Advanced

  • Diabetes mellitus (pancreatic)

Classical: Calcifications on imaging


7. Acute Appendicitis

Early

  • Periumbilical pain

Progression

  • RLQ pain (McBurney’s point)
  • Fever, vomiting

Advanced

  • Guarding, rebound tenderness
  • Perforation → generalized peritonitis

Special: Rovsing, Psoas, Obturator signs


8. Irritable Bowel Syndrome (IBS)

Early

  • Recurrent abdominal pain

Progression

  • Altered bowel habits (constipation/diarrhea)
  • Bloating

Advanced

  • Mucus in stools
  • Relief of pain after defecation

Special: No red-flag signs (weight loss, fever)


9. Inflammatory Bowel Disease (Ulcerative Colitis)

Early

  • Bloody diarrhea

Progression

  • Tenesmus
  • Lower abdominal pain

Advanced

  • Weight loss
  • Extra-intestinal features (uveitis, arthritis)

Classic: Continuous lesion from rectum


10. Crohn's Disease

Early

  • Intermittent abdominal pain

Progression

  • Chronic diarrhea (non-bloody early)
  • Weight loss

Advanced

  • Perianal fistula
  • Malabsorption

Classical: Skip lesions + cobblestone mucosa


11. Acute Cholecystitis

Early

  • RUQ pain

Progression

  • Fever
  • Vomiting

Advanced

  • Murphy's sign positive
  • Empyema / perforation

Special: Pain after fatty meals


12. Chronic Cholecystitis

Early

  • Recurrent RUQ discomfort

Progression

  • Bloating, indigestion

Advanced

  • Porcelain gallbladder

Classical: History of repeated gallstone attacks


13. Cholangitis (Ascending)

Early

  • Fever + RUQ pain

Progression

  • Jaundice

Advanced

  • Hypotension + Confusion (Reynold's pentad)

Classic: Charcot’s triad

Special: Rapid deterioration


14. Hepatitis A/B/C (Acute Viral Hepatitis)

Early

  • Fatigue
  • Nausea
  • Anorexia

Progression

  • Jaundice
  • Dark urine, pale stools
  • RUQ discomfort

Advanced

  • Coagulopathy

Classical: ALT/AST > 10x normal


15. Cirrhosis (Any Etiology)

Early

  • Fatigue, anorexia

Progression

  • Jaundice
  • Ascites
  • Edema

Advanced

  • Hepatic encephalopathy
  • Variceal bleeding

Special: Spider nevi + palmar erythema


16. Portal Hypertension

Early

  • Splenomegaly

Progression

  • Ascites

Advanced

  • Esophageal varices
  • Caput medusae

Special: Hematemesis from variceal rupture


17. Gastroenteritis (Infective)

Early

  • Nausea
  • Vomiting

Progression

  • Diarrhea
  • Abdominal cramps

Advanced

  • Dehydration
  • Electrolyte imbalance

Classical: History of contaminated food/water


18. Colorectal Cancer

Early

  • Change in bowel habits

Progression

  • Occult GI bleeding → iron deficiency anemia

Advanced

  • Weight loss
  • Obstructive symptoms

Left-sided: Constipation + pencil-thin stool

Right-sided: Occult bleeding + anemia


19. Celiac Disease

Early

  • Diarrhea
  • Bloating

Progression

  • Steatorrhea
  • Weight loss

Advanced

  • Dermatitis herpetiformis

Special: Symptoms resolve on gluten-free diet


20. Intestinal Obstruction

Early

  • Colicky abdominal pain

Progression

  • Vomiting
  • Distension

Advanced

  • Obstipation
  • Dehydration

Classical: High-pitched tinkling bowel sounds



SERIES 2 - RESPIRATORY DISEASES

 



🌬️  COMMON RESPIRATORY DISEASES 


1. Acute Bronchitis

Stage 1: Early Viral Phase

  • Sore throat, runny nose
  • Dry cough
  • Mild fever
  • Chest discomfort

Stage 2: Progressive Bronchial Inflammation

  • Harsh barking cough
  • Burning sensation behind sternum
  • Mild wheeze

Stage 3: Productive Phase

  • Cough with mucoid sputum
  • Diffuse wheeze + rhonchi

Classical Features

  • Cough > 5 days
  • Normal chest X-ray

2. Community-Acquired Pneumonia (CAP)

Stage 1: Infection Onset

  • Sudden fever
  • Shaking chills
  • Malaise

Stage 2: Consolidation

  • Productive cough → rust-colored sputum (classical for pneumococcal)
  • Pleuritic chest pain
  • Breathlessness

Stage 3: Severe CAP

  • High fever
  • Confusion (elderly)
  • Hypoxia

Classical Signs

  • Bronchial breathing
  • Dull percussion
  • Increased vocal fremitus / resonance

3. Tuberculosis (Pulmonary TB)

Stage 1: Early Infection (Subclinical)

  • No symptoms or mild dry cough
  • Fatigue

Stage 2: Active Disease

  • Chronic cough (>2–3 weeks)
  • Evening rise of temperature
  • Night sweats (classical)
  • Weight loss
  • Hemoptysis

Stage 3: Advanced TB

  • Chest pain
  • Breathlessness
  • Loss of appetite

Peculiar Features

  • Cavitary lesions (upper lobe)
  • Post-tussive crepitations

4. COPD (Chronic Bronchitis + Emphysema)

Stage 1: Early COPD

  • Chronic productive cough
  • Morning “smoker’s cough”

Stage 2: Moderate

  • Breathlessness on exertion
  • Wheezing
  • Frequent infections

Stage 3: Severe

  • Dyspnea at rest
  • Barrel-shaped chest
  • Pursed-lip breathing

Classical Phenotypes

  • Blue Bloater (Chronic Bronchitis): cyanosis + edema
  • Pink Puffer (Emphysema): breathless, thin, no cyanosis

5. Asthma

Stage 1: Prodrome

  • Itchy throat
  • Chest tightness
  • Mild wheeze

Stage 2: Exacerbation

  • Cough (worse night/early morning)
  • Wheezing
  • Dyspnea

Stage 3: Severe Asthma Attack

  • Silent chest
  • Tachypnea
  • Accessory muscle use

Special Features

  • Reversible airway obstruction
  • Wheezing + episodic pattern
  • Cough variant asthma – cough only

6. Pleural Effusion

Stage 1: Small Effusion

  • Mild dyspnea
  • Chest pressure

Stage 2: Moderate

  • Stony dull percussion
  • Decreased breath sounds
  • Reduced chest expansion

Stage 3: Large Effusion

  • Orthopnea
  • Tracheal shift (away from side)

Classical Sign

  • Pleural rub (early stage)

7. Pneumothorax

Stage 1: Small Pneumothorax

  • Mild chest pain
  • Slight dyspnea

Stage 2: Moderate

  • Sudden sharp unilateral chest pain
  • Hyperresonant percussion
  • Decreased breath sounds

Stage 3: Tension Pneumothorax

  • Severe dyspnea
  • Tracheal shift (opposite side)
  • Distended neck veins
  • Hypotension → shock

Classical Feature

  • Hyperresonant percussion

8. Pulmonary Embolism (PE)

Stage 1: Early

  • Sudden chest pain
  • Tachypnea
  • Anxiety

Stage 2: Progressive

  • Dyspnea
  • Palpitations
  • Non-productive cough
  • Hemoptysis (in infarction)

Stage 3: Massive PE

  • Hypotension
  • Syncope
  • Right heart failure

Classical Feature

  • Sudden unexplained dyspnea + clear lungs

9. Interstitial Lung Disease (ILD)

Stage 1: Early

  • Dry cough
  • Progressive breathlessness

Stage 2: Moderate

  • Velcro-like fine inspiratory crackles
  • Fatigue
  • Clubbing

Stage 3: Advanced ILD

  • Severe dyspnea at rest
  • Cyanosis
  • Pulmonary hypertension

Classical Feature

  • Velcro crackles

10. Bronchiectasis

Stage 1: Early

  • Chronic productive cough
  • Foul-smelling sputum

Stage 2: Progressive

  • Recurrent infections
  • Fever
  • Wheezing
  • Hemoptysis

Stage 3: Advanced

  • Clubbing
  • Coarse crepitations
  • Large-volume purulent sputum

Classical Feature

  • Copious purulent sputum in 3 layers

11. Pneumoconiosis (Silicosis / Asbestosis / Coal worker’s)

Stage 1: Early

  • Chronic dry cough
  • Fatigue

Stage 2: Progressive Fibrosis

  • Breathlessness
  • Chest tightness

Stage 3: Late

  • Clubbing (asbestosis)
  • Recurrent infections
  • Cor pulmonale

Classical Features

  • Silicosis – Eggshell calcification of lymph nodes
  • Asbestosis – Pleural plaques

12. Lung Cancer

Stage 1: Early

  • Persistent cough
  • Chest pain
  • Hoarseness

Stage 2: Progressive

  • Hemoptysis
  • Weight loss
  • Fatigue
  • Recurrent pneumonia

Stage 3: Metastatic / Locally Advanced

  • Bone pain
  • Neurological deficits
  • Superior vena cava obstruction → face swelling, dilated chest veins

Peculiar Signs

  • Pancoast tumor → shoulder/arm pain + Horner syndrome
  • Clubbing

13. Acute Respiratory Distress Syndrome (ARDS)

Stage 1: Early

  • Acute dyspnea
  • Tachypnea
  • Hypoxia

Stage 2: Progressive

  • Pink frothy sputum
  • Severe breathlessness
  • Cyanosis

Stage 3: Severe ARDS

  • Diffuse crackles
  • Respiratory failure
  • Multiorgan dysfunction

Classical Feature

  • Refractory hypoxemia

14. Obstructive Sleep Apnea (OSA)

Stage 1: Early

  • Loud snoring
  • Daytime fatigue

Stage 2: Progressive

  • Morning headaches
  • Non-restorative sleep
  • Choking at night

Stage 3: Advanced

  • Hypertension
  • Personality changes
  • Poor concentration

Classical Feature

  • Witnessed apneic episodes

15. Cystic Fibrosis (in children/young adults)

Stage 1: Early

  • Persistent cough
  • Salty sweat (peculiar finding)
  • Poor weight gain

Stage 2: Moderate

  • Recurrent chest infections
  • Large-volume sputum
  • Nasal polyps

Stage 3: Advanced

  • Clubbing
  • Bronchiectasis
  • Respiratory failure

Special Feature

  • Salty skin test (sweat chloride ↑)


SERIES 1-CARDIOVASCULAR DISEASES

 



COMMON CARDIOVASCULAR DISEASES – PROGRESSIVE CLINICAL PRESENTATION


1. Coronary Artery Disease → Angina → Myocardial Infarction

Stage 1: Early Atherosclerosis (No symptoms)

  • No complaints
  • Fatigue on heavy exertion
  • Mild breathlessness

Stage 2: Stable Angina

  • Chest tightness with exertion
  • Relieved by rest
  • Radiation to arm/jaw
  • Mild sweating

Stage 3: Worsening (Crescendo) Angina

  • Pain with less exertion
  • More frequent episodes
  • Temporary relief with nitrates

Stage 4: Unstable Angina

  • Pain at rest
  • Severe squeezing pressure
  • Pre-infarction stage

Stage 5: Myocardial Infarction

  • Severe crushing pain
  • Not relieved by rest/nitrates
  • Profuse sweating
  • Breathlessness
  • Shock in extensive MI

2. Heart Failure (LHF → RHF → CHF)

Stage 1: Early Left-Sided Failure

  • Exertional dyspnea
  • Fatigue
  • Orthopnea
  • Palpitations

Stage 2: Pulmonary Congestion

  • PND (sudden night breathlessness)
  • Pink frothy sputum
  • Tachycardia
  • Cold extremities

Stage 3: Right-Sided Failure

  • Pedal edema
  • Hepatomegaly
  • Right hypochondriac pain
  • Distended neck veins

Stage 4: Congestive Heart Failure

  • Ascites
  • Anasarca
  • Cyanosis
  • Low urine output
  • Confusion, drowsiness (brain hypoperfusion)

3. Hypertension (Primary) – Silent → Complicated

Stage 1: Early

  • Usually asymptomatic
  • Occasional headache
  • Mild fatigue

Stage 2: Progressive

  • Early morning headache
  • Palpitations
  • Dizziness
  • Blurred vision

Stage 3: Target Organ Damage

  • Retinopathy → visual changes
  • LVH → exertional breathlessness
  • CKD → nocturia, swelling
  • TIA → transient weakness

Stage 4: Hypertensive Crisis

  • Severe headache
  • Vomiting
  • Seizures
  • Chest pain
  • Acute pulmonary edema
  • Stroke symptoms

4. Rheumatic Heart Disease (Post-RF → Valve Damage)

Stage 1: Post-Strep Infection

  • Fever
  • Throat infection history
  • Migratory joint pains

Stage 2: Acute Rheumatic Carditis

  • Tachycardia
  • Chest discomfort
  • New murmurs
  • Breathlessness

Stage 3: Chronic Mitral Valve Disease

Mitral Stenosis

  • Progressive dyspnea
  • Palpitations (AF)
  • Hemoptysis
  • Malar flush

Mitral Regurgitation

  • Fatigue
  • Dyspnea
  • Palpitations
  • Pansystolic murmur

Stage 4: Advanced RHD

  • Congestive heart failure
  • Edema
  • Ascites
  • Thromboembolism

5. Aortic Aneurysm & Dissection

Stage 1: Silent Aneurysm

  • Usually asymptomatic
  • Mild back discomfort
  • Pulsatile abdominal mass (AAA)

Stage 2: Expanding Aneurysm

  • Constant deep back pain
  • Abdominal bloating
  • Early satiety
  • Leg pain (nerve compression)

Stage 3: Aortic Dissection – Sudden

  • Tearing, ripping chest/back pain
  • Radiation between shoulder blades
  • Unequal arm BP
  • Syncope

Stage 4: Rupture

  • Severe pain
  • Shock
  • Collapse
  • High mortality

6. Atrial Fibrillation (AF)

Stage 1: Paroxysmal AF

  • Occasional palpitations
  • Mild shortness of breath
  • Anxiety
  • Irregular heartbeat sensation

Stage 2: Persistent AF

  • Palpitations more frequent
  • Fatigue
  • Exertional dyspnea
  • Mild ankle swelling

Stage 3: Chronic AF

  • Irregularly irregular pulse
  • Reduced exercise capacity
  • Dizziness

Stage 4: Complications

  • Stroke (clots form in left atrium)
  • Heart failure
  • Syncope

7. Peripheral Arterial Disease (PAD)

Stage 1: Early

  • Leg fatigue on walking
  • Foot coldness
  • Mild numbness

Stage 2: Intermittent Claudication

  • Calf pain after walking fixed distance
  • Relieved by rest
  • Weak dorsalis pedis pulse

Stage 3: Rest Pain

  • Pain even at rest
  • Worse at night
  • Relieved by hanging leg down

Stage 4: Critical Limb Ischemia

  • Ulcers
  • Black discoloration
  • Gangrene
  • Limb-threatening stage

8. Deep Vein Thrombosis (DVT)

Stage 1: Early

  • Mild calf discomfort
  • Tightness in leg

Stage 2: Progressive

  • Unilateral leg swelling
  • Warmth and redness
  • Tender calf
  • Homan’s sign +

Stage 3: Severe

  • Severe swelling
  • Severe pain
  • Cyanosis of limb

Stage 4: Complication

  • Pulmonary embolism → sudden dyspnea, chest pain, syncope

9. Infective Endocarditis

Stage 1: Early

  • Low-grade fever
  • Fatigue
  • Joint pains

Stage 2: Progressive

  • High spiking fever
  • Sweating
  • New/changed murmur
  • Weight loss

Stage 3: Embolic Phenomena

  • Splinter hemorrhages
  • Osler nodes
  • Janeway lesions
  • Petechiae

Stage 4: Severe

  • Heart failure
  • Stroke (emboli)
  • Renal failure
  • Septic shock

10. Pericarditis → Pericardial Effusion → Tamponade

Stage 1: Acute Pericarditis

  • Sharp chest pain
  • Worse lying down
  • Relieved by sitting forward
  • Pericardial friction rub

Stage 2: Effusion Formation

  • Reduced chest pain
  • Dyspnea
  • Feeling of chest heaviness
  • Distant heart sounds

Stage 3: Cardiac Tamponade

  • Severe breathlessness
  • Hypotension
  • Tachycardia
  • Raised JVP
  • Pulsus paradoxus
  • Shock


Saturday, November 15, 2025

Diabetes Mellitus (DM)

Diabetes Mellitus (DM)


1. INTRODUCTION

Diabetes Mellitus (DM) is a chronic metabolic disease characterized by persistent hyperglycemia.
Hyperglycemia means abnormally high glucose levels in blood, usually because of:

  1. Impaired insulin secretion (pancreas not producing enough insulin)
  2. Impaired insulin action (body cells not responding to insulin – called insulin resistance)
  3. Both combined

Diabetes is a multisystem disorder affecting blood vessels, nerves, kidneys, eyes, heart, and immunity.


2. NORMAL PHYSIOLOGY OF GLUCOSE REGULATION

2.1 Pancreatic Structure & Insulin Synthesis

Pancreas has clusters of endocrine cells called Islets of Langerhans:

  • β-cells (beta cells) – produce insulin
  • α-cells (alpha cells) – produce glucagon
  • δ-cells (delta cells) – produce somatostatin
  • PP cells – produce pancreatic polypeptide

Insulin is synthesized as: Preproinsulin → Proinsulin → Insulin + C-peptide

C-peptide reflects the body’s natural insulin production.


2.2 Mechanism of Insulin Secretion

Insulin release occurs when blood glucose rises after a meal.

Sequence:

  1. Glucose enters β-cells via GLUT-2 transporter
  2. Glucose undergoes metabolism → increases ATP
  3. ATP closes K⁺ channels on β-cell membrane
  4. Cell depolarizes → Calcium enters
  5. Insulin-containing vesicles fuse → Insulin is released into blood

2.3 Actions of Insulin

Insulin is an anabolic hormone (builds tissues).

Effects on major tissues

Liver

  • Inhibits gluconeogenesis (producing glucose from non-carbohydrate sources)
  • Inhibits glycogenolysis (breakdown of glycogen)
  • Promotes glycogenesis (formation of glycogen)
  • Promotes lipogenesis (fat formation)

Muscle

  • Increases GLUT-4 translocation → more glucose uptake
  • Increases protein synthesis

Adipose tissue

  • Promotes fat storage
  • Inhibits lipolysis (breakdown of fat)

2.4 Role of Glucagon

Secreted when blood sugar falls.

Actions:

  • Stimulates glycogenolysis
  • Stimulates gluconeogenesis
  • Raises blood glucose levels

Thus, INSULIN and GLUCAGON work as a balanced system.


3. PATHOPHYSIOLOGY OF DIABETES MELLITUS

3.1 Type 1 Diabetes Mellitus (T1DM)

Autoimmune destruction of β-cells → absolute insulin deficiency.

Mechanisms:

  • Immune system produces autoantibodies against β-cell antigens
  • Gradual β-cell destruction
  • No insulin → glucose cannot enter cells → severe hyperglycemia

Common before age 20, but may occur anytime.

Clinical signs:

  • Sudden weight loss
  • Polyuria (excess urination)
  • Polydipsia (excess thirst)
  • Polyphagia (excess hunger)
  • Diabetic ketoacidosis (DKA)

3.2 Type 2 Diabetes Mellitus (T2DM)

Most common type.
Characterized by:

  1. Insulin resistance – cells do not respond to insulin
  2. β-cell dysfunction – gradual decline in insulin production

Causes:

  • Obesity
  • Abdominal fat (visceral fat)
  • Physical inactivity
  • Genetics
  • Chronic inflammation

Mechanisms:

Insulin receptor signaling fails → GLUT-4 fails to move → glucose cannot enter cells
• Liver continues producing glucose even when blood sugar is already high
• Pancreas tries to compensate → hyperinsulinemia
• β-cells eventually fatigue → insulin levels fall


3.3 Gestational Diabetes Mellitus (GDM)

Diabetes first detected during pregnancy.

Mechanism:

  • Pregnancy hormones (human placental lactogen, estrogen, progesterone) cause insulin resistance
  • Pancreas cannot compensate → hyperglycemia

3.4 Secondary Diabetes

Due to:

  • Pancreatic diseases (pancreatitis, pancreatic cancer)
  • Endocrine excess (Cushing’s, acromegaly)
  • Drugs (steroids, antipsychotics)
  • Genetic disorders

4. WHY DOES HYPERGLYCEMIA DAMAGE ORGANS?

(Pathogenesis of Complications)**

Chronic hyperglycemia leads to:

4.1 Advanced Glycation End Products (AGEs)

High glucose attaches to proteins → forms AGEs
These cause:

  • Vessel wall thickening
  • Inflammation
  • Oxidative stress

4.2 Polyol Pathway Activation

Glucose converted into sorbitol
Sorbitol accumulates → cell swelling → nerve & lens damage
→ leads to neuropathy and cataracts


4.3 Protein Kinase C Activation

Causes:

  • Vasoconstriction
  • Retinal damage
  • Renal damage

4.4 Oxidative Stress

Excess glucose produces free radicals
Damages:

  • Endothelium
  • DNA
  • Mitochondria

5. CLINICAL FEATURES OF DIABETES

5.1 Classic Features

  • Polyuria
  • Polydipsia
  • Polyphagia
  • Weight loss (mainly in T1DM)
  • Fatigue
  • Blurred vision
  • Recurrent infections

5.2 Complications

Acute

  • DKA (ketoacidosis)
  • HHS (hyperosmolar hyperglycemic state)
  • Severe hypoglycemia

Chronic

Microvascular:

  • Retinopathy
  • Nephropathy
  • Neuropathy

Macrovascular:

  • Coronary artery disease
  • Stroke
  • Peripheral vascular disease

6. INVESTIGATIONS IN DIABETES

6.1 Blood Glucose Tests

Fasting Plasma Glucose (FPG)

Measured after 8 hours of fasting.
High fasting glucose = impaired hepatic glucose regulation.


Postprandial Plasma Glucose (PPG)

Measured 2 hours after food.
Reflects ability of pancreas to handle a glucose load.


Random Plasma Glucose

Useful for symptomatic patients.


6.2 Oral Glucose Tolerance Test (OGTT)

Patient drinks 75 g glucose.
Blood glucose measured fasting & after 2 hours.
Shows how efficiently the body clears glucose.


6.3 HbA1c (Glycated Hemoglobin)

Represents average blood glucose for last 3 months.

Mechanism: Glucose binds to hemoglobin in RBCs → forms HbA1c
Higher glucose = higher HbA1c

Useful for diagnosis and monitoring.


6.4 Urine Investigations

Urine glucose

Appears when blood sugar > renal threshold (180 mg/dL)

Urine ketones

Indicates fat breakdown; important in suspected DKA.

Microalbuminuria

Very early marker of diabetic kidney disease.


6.5 Tests for Complications

Kidney

  • Serum creatinine
  • eGFR
  • Urine albumin-creatinine ratio

Eyes

  • Fundus examination
  • OCT (when needed)

Nerves

  • Monofilament test
  • Vibration sense
  • Nerve conduction studies (advanced)

Cardiovascular

  • Lipid profile
  • ECG
  • Carotid Doppler (if needed)

6.6 Immunological Tests (Type 1 DM)

Presence of autoantibodies:

  • GAD (Glutamic acid decarboxylase) antibody
  • IA-2 antibody
  • ZnT8 antibody
  • Islet cell antibody (ICA)

These confirm autoimmune destruction of β-cells.


7. DIABETIC KETOACIDOSIS (DKA) – PATHOPHYSIOLOGY IN SIMPLE TERMS

Occurs mainly in Type 1 diabetes.

Sequence:

  1. No insulin → cells cannot take up glucose
  2. Body thinks it is starving → breaks fat rapidly
  3. Fat breakdown produces ketone bodies
  4. Ketones accumulate → blood becomes acidic
  5. Dehydration + acidosis = dangerous, life-threatening condition

Clinical features:
Fruity breath, Kussmaul breathing, abdominal pain, vomiting.


8. HYPEROSMOLAR HYPERGLYCEMIC STATE (HHS)

Typical of T2DM in elderly.

Mechanism:

  • Severe hyperglycemia
  • Extreme dehydration
  • No significant ketoacidosis

Very high mortality.


9. SUMMARY  

Diabetes = chronic hyperglycemia due to insulin defect.
Type 1 = absolute insulin deficiency.
Type 2 = insulin resistance + β-cell failure.
Chronic high glucose causes vascular, neural, renal & retinal damage.
Diagnosis uses FPG, PPG, OGTT, HbA1c.
Monitoring includes checking for kidney, eye, nerve & heart involvement.



Sunday, November 9, 2025

Parameter of a Full-Body Laboratory Check-up

 

🔬 The Pathophysiological Basis of a Full-Body Check-Up

— Understanding Health Through Laboratory Parameters

A complete health check-up is more than a screening exercise; it is a systematic assessment of physiology in action. Each test reflects how the body maintains equilibrium and how that equilibrium is disturbed in disease.
Let us explore the major test groups one by one, linking physiology → pathology → clinical interpretation.


🩸 1. Hematological Parameters

Complete Blood Count (CBC):
The bone marrow is responsible for producing red cells, white cells, and platelets.

  • RBC indices (MCV, MCH, MCHC) reveal whether hemoglobin synthesis and erythrocyte maturation are normal.
    • ↓ MCV, ↓ MCH → iron-deficiency anemia (defective hemoglobin synthesis).
    • ↑ MCV → megaloblastic anemia (impaired DNA synthesis due to B₁₂ or folate deficiency).
  • Leukocyte count and differential show immune activity.
    • Neutrophilia → bacterial infection; lymphocytosis → viral illness; eosinophilia → allergy or parasitic infestation.
  • Platelet count reflects megakaryocytic function and hemostasis.
    • Thrombocytopenia → bleeding tendency; thrombocytosis → inflammation or myeloproliferation.

Thus, the CBC converts the physiology of blood formation into a tool for detecting hematologic and infectious pathology.


🩺 2. Hemoglobin Estimation

Hemoglobin carries oxygen from lungs to tissues. Adequate Hb ensures tissue oxygenation; reduction causes hypoxia and compensatory tachycardia or fatigue.
Low Hb can result from:

  • Decreased production (iron/B₁₂ deficiency, marrow suppression)
  • Increased loss (bleeding)
  • Increased destruction (hemolysis)

Hence, Hb links oxygen transport physiology with anemia pathogenesis.


🧬 3. Erythrocyte Sedimentation Rate (ESR)

Inflammation increases plasma fibrinogen and globulins, reducing the negative charge (zeta potential) of RBCs and promoting their stacking (rouleaux formation).
A faster sedimentation rate therefore signals the presence of inflammatory proteins—a nonspecific but valuable pointer toward chronic infection, autoimmune disease, or malignancy.


⚙️ 4. Blood Glucose and HbA1c

Glucose homeostasis depends on hepatic glycogen storage, pancreatic insulin secretion, and cellular uptake.

  • Fasting glucose represents basal hepatic output.
  • Post-prandial glucose reflects insulin efficiency.
  • HbA1c measures long-term glycemic control, correlating with average glucose over 8–12 weeks.

Persistent hyperglycemia injures endothelium, kidneys, retina, and nerves—pathological sequelae of diabetes mellitus, illustrating how disordered metabolism translates into multisystem disease.


🧪 5. Liver Function Tests (LFT)

The liver performs metabolic, synthetic, and detoxifying roles.

  • ALT, AST rise with hepatocellular injury (viral hepatitis, toxins).
  • ALP, GGT elevate when bile flow is obstructed (cholestasis).
  • Bilirubin fractions distinguish pre-hepatic (hemolytic), hepatic, and post-hepatic (obstructive) jaundice.
  • Albumin & Prothrombin time assess synthetic capacity.

Thus, LFTs bridge hepatocyte physiology with patterns of hepatic pathology—injury, obstruction, or failure.


⚡ 6. Kidney Function Tests (KFT)

Kidneys regulate filtration, reabsorption, secretion, and electrolyte balance.

  • Urea & creatinine reflect glomerular filtration rate.
  • Electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻) reveal tubular function and acid-base status.
  • Uric acid indicates purine metabolism and renal excretory ability.

Abnormal results pinpoint nephron dysfunction, dehydration, or metabolic disorders—linking excretory physiology with renal pathology.


🧠 7. Thyroid Profile (T₃, T₄, TSH)

The hypothalamic-pituitary-thyroid axis maintains basal metabolic rate.

  • Primary hypothyroidism: low T₃/T₄, high TSH (thyroid failure).
  • Hyperthyroidism: high T₃/T₄, suppressed TSH (excess hormone output).
    Clinically manifests as altered weight, pulse, and energy levels—direct reflections of metabolic regulation gone awry.

💉 8. Lipid Profile

Lipids circulate as lipoproteins.

  • LDL/VLDL deposit cholesterol in arteries → atherogenesis.
  • HDL removes cholesterol → anti-atherogenic.
    The profile quantifies the balance between deposition and clearance, connecting fat metabolism physiology to cardiovascular pathology.

💧 9. Calcium and Phosphorus

Bone serves as a reservoir regulated by parathyroid hormone (PTH), vitamin D, and renal handling.

  • ↓ Calcium → vitamin D deficiency or hypoparathyroidism.
  • ↑ Calcium → bone resorption, hyperparathyroidism, or malignancy.
    They reveal mineral metabolism disorders underlying bone or endocrine disease.

⚙️ 10. Serum Electrolytes

Sodium governs extracellular volume, potassium maintains membrane potential, chloride and bicarbonate maintain acid–base equilibrium.
Abnormalities disturb neuromuscular excitability and cardiac rhythm, providing a biochemical mirror of systemic homeostasis.


🧫 11. Urine Routine and Microscopy

Urine analysis reflects nephron function directly:

  • Proteinuria → glomerular damage.
  • Casts → tubular involvement.
  • Crystals → lithiasis risk.
    It translates renal physiology into visible evidence of renal pathology.

⚕️ 12. Stool Examination

Normal digestion leaves no blood, fat, or parasites in stool.
Detection of occult blood signals ulcer or carcinoma; fat globules indicate malabsorption; ova/cysts denote infection.
Hence, stool study reveals intestinal and pancreatic pathophysiology.


🩸 13. Iron Studies (Serum Iron, Ferritin, TIBC)

Iron balance depends on absorption, storage, and utilization.
Low ferritin with high TIBC → depletion; high ferritin → chronic inflammation or overload.
These parameters elucidate mechanisms of anemia and iron metabolism disorders.


🦴 14. Vitamins D and B₁₂

  • Vitamin D enables calcium absorption; deficiency causes osteomalacia or rickets.
  • Vitamin B₁₂ is essential for DNA synthesis and myelin maintenance; deficiency causes megaloblastic anemia and neuropathy.
    They exemplify how micronutrient physiology supports structural and neurological integrity.

💉 15. C-Reactive Protein (CRP)

CRP is an acute-phase protein synthesized by the liver under IL-6 stimulation.
It rises rapidly during infection or inflammation, embodying the molecular link between cytokine release and systemic response.


⚕️ 16. Rheumatoid Factor (RF)

An autoantibody (IgM) against IgG Fc portion—its presence signifies loss of self-tolerance and immune complex-mediated inflammation in joints, typical of rheumatoid arthritis.


🦠 17. HBsAg, HIV, VDRL

These serological tests illustrate pathogen-specific immune responses: antigen detection (HBsAg), antibody detection (HIV), or reagin antibodies (VDRL).
They reveal infectious pathologies and enable early preventive intervention.


🧫 18. Urine Microalbumin

Early leakage of albumin before overt proteinuria indicates glomerular basement-membrane damage, especially in diabetes.
It is the biochemical harbinger of incipient nephropathy.


💉 19. Amylase and Lipase

Produced by pancreatic acinar cells; leakage into blood reflects pancreatic inflammation or ductal obstruction.
A rise parallels enzyme escape from damaged tissue, a key concept in clinical biochemistry.


⚙️ 20. LDH (Lactate Dehydrogenase)

Present in all cells; elevated levels mean cell destruction—from hemolysis to myocardial infarction.
LDH exemplifies the principle that cytoplasmic enzymes in plasma = tissue necrosis.


⚡ 21. Cortisol

Secreted by adrenal cortex under ACTH control.
Excess → Cushing’s syndrome (protein catabolism, hypertension); deficiency → Addison’s disease (hypotension, pigmentation).
Demonstrates stress physiology and its derangements.


🫀 22. Cardiac Enzymes (CK, CK-MB, Troponin)

Cardiomyocyte necrosis releases these enzymes. Their timed elevation confirms myocardial infarction, directly translating cellular injury into a diagnostic biomarker.


💊 23. Homocysteine and Insulin Studies

  • Homocysteine: Elevated when B-vitamins are low; promotes endothelial injury → atherothrombosis.
  • Insulin and HOMA Index: Quantify insulin resistance—the earliest metabolic disturbance in obesity and type 2 diabetes.

These reflect biochemical precursors of vascular and metabolic disease.


🧬 24. Serum Proteins (Albumin/Globulin Ratio)

Albumin indicates hepatic synthesis and nutritional status; globulins rise in chronic inflammation or plasma-cell disorders.
An inverted ratio points to liver disease or immunoproliferative pathology.


⚕️ 25. Uric Acid

Final product of purine metabolism. Overproduction or reduced excretion causes crystal deposition in joints and kidneys—gout.
Links metabolic excess with inflammatory arthropathy.


🧬 26. Blood Grouping and Rh Typing

Based on RBC surface antigens (A, B, Rh).
Understanding agglutination physiology prevents hemolytic transfusion reactions and Rh-incompatibility hemolytic disease of the newborn—a classic immune-hematologic pathology.


🩻 Integration and Interpretation

Together, these tests form a physiological map of the human body:

  • Hematology → marrow and immune function
  • Biochemistry → metabolism, detoxification, excretion
  • Serology → infection and immunity
  • Endocrine assays → hormonal control
  • Microscopy → direct evidence of organ damage

By interpreting deviations from normal, the student learns how homeostasis fails in disease—the essence of pathology.


🩺 Summary Insight

A full-body check-up, when understood physiologically, is not mere data collection. It is a functional dissection of life’s chemistry, demonstrating how:

  • Structure (cells, organs) sustains function (physiology), and
  • Functional derangement manifests as disease (pathology).


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