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Dyspepsia & Gastrointestinal Syndromes — Comprehensive Review

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1. Classification of Dyspepsia & Differences Between Functional and Organic Forms

Classification

Dyspepsia (uninvestigated)
        │
        ├─── ORGANIC DYSPEPSIA (identifiable structural/biochemical cause)
        │
        └─── FUNCTIONAL DYSPEPSIA (no organic cause on investigation)
                    ├─ Postprandial Distress Syndrome (PDS) — meal-related
                    └─ Epigastric Pain Syndrome (EPS) — meal-unrelated

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2. Main Reasons for Development of Dyspeptic Syndrome

Organic causes:

• Peptic ulcer disease (PUD) — most common organic cause (~15–25%)
• GERD — second most common organic cause
• Gastric/esophageal malignancy
• Biliary tract disorders — cholelithiasis, cholecystitis
• Pancreatic disease — chronic pancreatitis, pancreatic cancer
• Medications — NSAIDs, aspirin, iron, antibiotics, bisphosphonates, opioids
• Other systemic diseases — diabetes (gastroparesis), thyroid disease, chronic kidney disease, ischemic heart disease, connective tissue disease

Functional dyspepsia pathophysiology:

1. Impaired gastric accommodation (~40% of FD patients) — failure of proximal stomach to relax after eating → early satiation, postprandial fullness
2. Visceral hypersensitivity — abnormally enhanced perception of gastric distension (~37%)
3. Delayed gastric emptying (~30%)
4. Low-grade duodenal mucosal inflammation — increased mast cells and eosinophils
5. Altered duodenal sensitivity to lipids and acid
6. H. pylori infection — eradicating H. pylori provides modest benefit in some FD patients
7. Psychosocial factors — anxiety, depression, somatization

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3. Diagnostic Criteria for Gastric Dyspepsia

• Epigastric pain or burning — often worsened or relieved by food
• Postprandial fullness / heaviness
• Early satiation — unable to complete a normal meal
• Nausea ± vomiting
• Belching, regurgitation
• Anorexia, weight loss in severe cases

• ≥1 of: bothersome postprandial fullness, early satiation, epigastric pain, or epigastric burning
• Symptoms present for ≥6 months, active for last 3 months
• No structural disease on upper endoscopy to explain symptoms

• PDS (Postprandial Distress Syndrome): meal-induced fullness, early satiation; may overlap with gastroparesis
• EPS (Epigastric Pain Syndrome): intermittent epigastric pain/burning not exclusively postprandial

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4. Diagnostic Criteria for Intestinal Dyspepsia

• Lower abdominal bloating and distension (especially postprandial)
• Flatulence and excessive gas
• Borborygmi (audible bowel sounds)
• Altered bowel habits — diarrhea or constipation (or alternating)
• Loose, bulky, greasy, or foul-smelling stools (steatorrhea in malabsorption)
• Cramping or colicky abdominal pain relieved by defecation
• Nausea without prominent epigastric pain

• Lactase deficiency / lactose intolerance
• Small intestinal bacterial overgrowth (SIBO)
• Celiac disease
• Inflammatory bowel disease (Crohn's, UC)
• Irritable bowel syndrome (IBS)
• Parasite infestation (Giardia)
• Carbohydrate malabsorption (fructose, sorbitol)

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5. Diagnostic Criteria for Pancreatic Dyspepsia

• Epigastric/periumbilical pain radiating to the back (band-like or boring)
• Steatorrhea — bulky, pale, greasy, foul-smelling stools (steatorrhea appears when >90% exocrine function lost)
• Flatulence, bloating, meteorism
• Weight loss (due to malabsorption)
• Postprandial aggravation of pain (especially fatty meals)
• Nausea, vomiting
• Possible new-onset diabetes mellitus (endocrine insufficiency)
• Jaundice (if biliary obstruction from pancreatic head involvement)

• Pain radiates to the back
• Steatorrhea with fat-soluble vitamin deficiencies
• History of alcoholism or gallstones
• Elevated serum amylase/lipase (acute exacerbations)
• Low fecal elastase-1 (<200 μg/g)
• Pancreatic calcifications on imaging

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6. Diagnostic Criteria for Hepatic Dyspepsia

• Right upper quadrant or epigastric dull ache/heaviness
• Anorexia and early satiety (often profound)
• Nausea, bitter taste in the mouth
• Bloating, flatulence
• Intolerance to fatty, fried foods and alcohol
• Constipation alternating with loose stools
• Jaundice, dark urine, acholic stools (in cholestatic disease)

• Signs of chronic liver disease: spider angiomas, palmar erythema, jaundice, hepatomegaly/splenomegaly
• Elevated transaminases (ALT, AST), bilirubin, ALP, GGT
• Decreased albumin, prolonged PT (advanced disease)
• Esophageal varices (portal hypertension)
• Ascites

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7. Diagnostic Criteria for Biliary Dyspepsia

• Biliary colic: episodic right upper quadrant or epigastric pain, often severe, typically begins 30–60 min after eating fatty foods, lasts 1–5 hours, may radiate to right shoulder/scapula
• Nausea and vomiting accompanying pain episodes
• Intolerance to fats, fried foods, eggs, spices
• Bloating and belching postprandially
• Bitter taste in the mouth
• Murphy's sign positive on examination (acute cholecystitis)

• Typical timing: postprandial onset, right-sided
• Ultrasound: gallstones, thickened gallbladder wall, pericholecystic fluid
• Pain lasts hours (vs. minutes in peptic pain, vs. days in pancreatitis)
• Elevated bilirubin, ALP, GGT if bile duct obstruction
• Normal amylase/lipase (unless complicated by pancreatitis)

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8. Main Aggressive and Protective Factors of the Gastric Mucosa

Aggressive Factors (promote mucosal injury):

Protective Factors (maintain mucosal integrity):

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9. Diagnostic Criteria for Chronic Cholecystitis

1. Symptoms:
   • Recurrent episodes of right upper quadrant or epigastric pain (biliary colic), typically lasting 1–5 hours
   • Postprandial nausea, vomiting, bloating
   • Intolerance to fatty foods
   • Symptoms may be more subtle than acute cholecystitis
   • No fever or leukocytosis between attacks (unlike acute cholecystitis)
2. Physical examination:
   • Right upper quadrant tenderness
   • Murphy's sign may be absent or mild
3. Laboratory findings:
   • Usually normal between episodes
   • Mild elevations of ALP/GGT if biliary involvement
4. Imaging:
   • Ultrasound (first-line): gallstones + gallbladder wall thickening (>3 mm), pericholecystic fluid; gallbladder may be shrunken/contracted
   • HIDA scan: reduced gallbladder ejection fraction (<35%) indicates dysfunction (chronic acalculous form)
   • CT/MRI: confirms stones, wall thickening, excludes complications
5. Histopathology (definitive): lymphocytic infiltrate in muscularis, fibrosis, mucosal atrophy — but biopsy is rarely needed clinically

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10. Diagnostic Criteria for Chronic Pancreatitis

1. Symptoms consistent with pancreatitis:
   • Chronic or recurrent epigastric pain radiating to the back
   • Steatorrhea (malabsorptive diarrhea, fatty/greasy stools)
   • New-onset diabetes mellitus (type 3c)
   • Weight loss, malnutrition, fat-soluble vitamin deficiencies
2. Imaging evidence (CT, MRI/MRCP, EUS):
   • Pancreatic ductal dilation (>3 mm main duct)
   • Pancreatic calcifications (pathognomonic when present)
   • Pancreatic atrophy, irregular contour, pseudocysts
   • CT: calcifications, ductal dilation
   • MRCP/MRI: best for ductal morphology
   • EUS (Rosemont criteria): most sensitive for early disease
3. Laboratory evidence:
   • Fecal elastase-1 <200 μg/g stool (exocrine insufficiency)
   • 72-hour fecal fat >7 g/day
   • Serum amylase/lipase may be normal in established disease (burned out)
   • HbA1c, fasting glucose (endocrine insufficiency)
4. Risk factors to support diagnosis:
   • Chronic heavy alcohol use (most common cause in adults)
   • Recurrent acute pancreatitis
   • Genetic mutations (PRSS1, SPINK1, CFTR)
   • Autoimmune pancreatitis (elevated IgG4)
   • Tropical pancreatitis (malnutrition)

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11. Diagnostic Criteria for Enteritis (Small Intestinal Inflammation)

1. Symptoms:
   • Diffuse periumbilical or right lower quadrant cramping pain
   • Watery, loose, or mucoid diarrhea (>3 stools/day)
   • Nausea and vomiting
   • Fever (infectious enteritis)
   • Malabsorption symptoms in chronic forms: steatorrhea, weight loss, bloating, flatulence
   • Edema (hypoalbuminemia from protein-losing enteropathy)
2. Signs:
   • Borborygmi, diffuse abdominal tenderness
   • Signs of dehydration
   • Pallor, glossitis, angular cheilitis (vitamin/mineral deficiencies)
3. Laboratory:
   • Stool culture, ova & parasites (infectious)
   • Complete blood count (eosinophilia, anemia)
   • Albumin, pre-albumin (malnutrition)
   • Anti-tTG IgA, anti-endomysial antibodies (celiac)
   • ESR, CRP (inflammation)
   • Fecal calprotectin (mucosal inflammation)
   • Fecal fat (malabsorption)
4. Imaging/Endoscopy:
   • Small bowel follow-through or CT enterography (Crohn's, structural lesions)
   • Capsule endoscopy (mucosal inflammation, bleeding)
   • Small bowel biopsy (villous atrophy in celiac, granulomas in Crohn's)

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12. Diagnostic Criteria for Colitis (Large Intestinal Inflammation)

1. Symptoms:
   • Bloody or mucoid diarrhea (key feature distinguishing from small bowel disease)
   • Frequent small-volume stools with tenesmus
   • Left lower quadrant or diffuse crampy pain
   • Urgency and incontinence
   • Fever, malaise, anorexia in severe cases
2. Signs:
   • Tenderness (often left-sided in UC, variable in Crohn's)
   • Rebound/guarding (if fulminant/toxic megacolon)
   • Pallor, tachycardia in severe cases
3. Laboratory:
   • CBC: leukocytosis, anemia, thrombocytosis
   • CRP, ESR elevated
   • Albumin low (severe disease)
   • Stool cultures (to exclude infectious colitis)
   • Stool C. difficile toxin
   • Fecal calprotectin (elevated in inflammatory colitis)
4. Endoscopy (colonoscopy is gold standard):
   • Continuous mucosal inflammation starting from rectum (UC)
   • Segmental/patchy inflammation with rectal sparing (Crohn's)
   • Pseudomembranes (C. difficile)
   • Biopsy: crypt abscesses, goblet cell depletion (UC); granulomas (Crohn's)

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13. Differential Diagnosis: Crohn's Disease vs. Ulcerative Colitis

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14. Laboratory and Instrumental Methods for Diagnosing Pancreatitis

Acute Pancreatitis

1. Acute onset epigastric pain ± radiation to back
2. Serum amylase and/or lipase ≥3× upper limit of normal
   • Lipase preferred (more specific, stays elevated longer)
   • Amylase rises within 2–12 hours, normalizes in 3–5 days
   • Lipase rises within 4–8 hours, normalizes in 8–14 days
3. Radiologic imaging consistent with pancreatitis

• CBC: leukocytosis, hemoconcentration (Hct >44% → predicts severity)
• CRP >150 mg/L at 48h → severe pancreatitis
• BMP: BUN, creatinine (renal failure), calcium (hypocalcemia), glucose
• LFTs: ALT >3× → gallstone etiology
• Triglycerides (if hypertriglyceridemia suspected)
• Ranson's criteria (11 parameters at admission and 48h)
• APACHE-II score

Chronic Pancreatitis

• Serum amylase/lipase: often normal in advanced disease ("burn-out")
• Fecal elastase-1 <200 μg/g (exocrine insufficiency — most useful functional test)
• 72-hour fecal fat collection (>7g/day = steatorrhea)
• Fasting glucose / HbA1c (endocrine insufficiency)
• IgG4 (autoimmune pancreatitis)
• CA 19-9 (to exclude pancreatic cancer)

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15. Complications of Gastric Ulcer and Duodenal Ulcer

Major complications:

• Gastric ulcers: higher malignancy risk → always biopsy; bleed from posterior wall (left gastric or splenic artery)
• Duodenal ulcers: bleed from posterior wall (gastroduodenal artery); most common cause of upper GI bleeding; perforate anteriorly

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16. Basic Methods of Instrumental Diagnostics of Peptic Ulcer Disease

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17. Basic Approaches to Treatment of Gastric Dyspepsia

Uninvestigated Dyspepsia (initial management):

1. Test and treat H. pylori (in populations with >10% prevalence) — eradication benefits ~8% of FD patients (NNT ~15)
2. Empirical PPI trial (4–8 weeks) if H. pylori negative or post-eradication
3. EGD if alarm features or age >55, or failure of empirical therapy

Functional Dyspepsia Treatment:

• Small, frequent, low-fat meals
• Avoid NSAIDs, alcohol, smoking
• Identify and avoid trigger foods
• Stress management

• Cognitive-behavioral therapy (CBT)
• Hypnotherapy
• Psychotherapy — for refractory cases with anxiety/depression

Organic Dyspepsia:

• PUD: H. pylori eradication + PPI; discontinue NSAIDs
• GERD: PPI + lifestyle modification
• Malignancy: surgical/oncologic management
• Biliary: cholecystectomy

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18. Basic Approaches to Treatment of Intestinal Dyspepsia

• Antispasmodics (mebeverine, hyoscine butylbromide) for cramping
• Loperamide for diarrhea-predominant symptoms
• Bulking agents/osmotic laxatives for constipation
• Simethicone/activated charcoal for excessive gas/bloating
• Elimination diets based on individual food triggers

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19. Principles of Treatment of Dyspeptic Syndrome in Pancreatitis and Cholecystitis

In Chronic Pancreatitis:

• Analgesics stepwise: paracetamol → tramadol → strong opioids (morphine as last resort)
• Celiac plexus block (EUS-guided) for refractory pain
• Pancreatic enzyme supplements may reduce pain (via feedback inhibition of pancreatic secretion)
• Endoscopic therapy: pancreatic duct stone removal, ESWL (extracorporeal shock wave lithotripsy), stenting
• Surgery (Frey/Beger procedure) for severe ductal obstruction

• Pancreatic enzyme replacement therapy (PERT): lipase ≥40,000–75,000 Ph.U. per main meal (e.g., Creon®)
• Take with meals (not before/after); enteric-coated microspheres
• Add PPI to reduce gastric acid (prevents enzyme inactivation)
• Low-fat diet (but not excessively restricted — calories are needed)
• Fat-soluble vitamin supplementation (A, D, E, K) + B12

• Dietary management
• Insulin therapy when needed (pancreatogenic diabetes type 3c is insulin-deficient but also lacks glucagon → hypoglycemia risk)

• High-calorie, high-protein diet (≥35 kcal/kg/day)
• Medium-chain triglycerides (absorbed without lipase)
• Enteral/parenteral nutrition in severe malnutrition

• Alcohol cessation (paramount — slows progression)
• Treat hyperlipidemia, hyperparathyroidism
• Autoimmune pancreatitis: corticosteroids

In Chronic Cholecystitis:

• Low-fat diet, small frequent meals
• Avoid fatty/fried foods, eggs, whole dairy, spices, alcohol
• Maintain hydration

• Antispasmodics/anticholinergics (hyoscine butylbromide, mebeverine): relieve biliary colic
• NSAIDs (diclofenac, ketorolac): analgesic and anti-inflammatory for biliary colic attacks — superior to opioids for biliary spasm
• Opioids (meperidine preferred over morphine — less Oddi sphincter spasm): for severe pain
• Antacids/PPIs: for coexisting dyspeptic symptoms
• Prokinetics: for nausea and motility impairment
• Ursodeoxycholic acid (UDCA): 8–10 mg/kg/day — dissolves small cholesterol stones; used in non-surgical candidates; takes months to years; effective only for small (<5 mm), non-calcified cholesterol stones

• Laparoscopic cholecystectomy — gold standard, curative
  • Elective for chronic calculous cholecystitis
  • Also for symptomatic acalculous cholecystitis with reduced ejection fraction
• Open cholecystectomy: for complicated cases

• Not indicated for uncomplicated chronic cholecystitis
• Required for acute exacerbation: cephalosporin (ceftriaxone) ± metronidazole

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Quick Navigation Guide

Cardialgia & Chest Pain — Comprehensive Review (Questions 83–102)

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83. Classification of Cardialgia Depending on Their Origin

I. Ischemic (Coronary) Cardialgia

• Stable angina pectoris
• Unstable angina
• NSTEMI
• STEMI
• Silent (painless) myocardial ischemia
• Vasospastic (Prinzmetal) angina
• Microvascular angina (cardiac syndrome X)

II. Non-Ischemic Cardiogenic Cardialgia

• Pericarditis — inflammation of pericardial sac
• Myocarditis — myocardial inflammation
• Hypertrophic cardiomyopathy (HCM) — LVOT obstruction + diastolic dysfunction
• Dilated cardiomyopathy — relative ischemia, wall stress
• Aortic stenosis — subendocardial ischemia from LVH + impaired diastolic filling
• Mitral valve prolapse — usually atypical/benign pain
• Aortic dissection — tearing pain from aortic wall
• Pulmonary hypertension — right ventricular ischemia

III. Non-Cardiogenic Chest Pain (see Q.92)

• Pulmonary (pleuritis, PE, pneumonia, pneumothorax)
• Gastrointestinal (GERD, esophageal spasm, peptic ulcer, pancreatitis)
• Musculoskeletal (osteochondrosis, costochondritis, Tietze syndrome)
• Neurological (intercostal neuralgia, herpes zoster, nerve root compression)
• Psychogenic (neurocirculatory dystonia, panic disorder, anxiety)

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84. Differential Diagnosis of Cardiogenic and Non-Cardiogenic Chest Pain

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85. Differences in Clinical Picture: Cardiogenic vs. Non-Cardiogenic Chest Pain

Cardiogenic (Ischemic) Pain — Classic Presentation:

• Onset: gradual, builds over minutes
• Quality: pressure, constriction, "vise-like," suffocating; patients clench fist over sternum (Levine sign)
• Location: midsternal/retrosternal, may be precordial
• Radiation: left shoulder → ulnar aspect of left arm, jaw, neck, throat (throat tightness is a key anginal equivalent); occasionally to right arm or epigastrium
• Duration: stable angina 2–10 min, resolves with rest; ACS >20 min, not relieved by rest
• Provocation: physical effort, emotion, cold exposure, sexual activity, heavy meals
• Associated: diaphoresis, pallor, dyspnea, nausea/vomiting, sense of impending doom, palpitations
• Relief: rest (stable angina); sublingual nitroglycerin within 3–5 min
• Atypical presentations (especially women, elderly, diabetics): exertional dyspnea only, nausea, fatigue, epigastric pain — "anginal equivalents"

Non-Cardiogenic Pain — Features Suggesting Alternative Cause:

• Sharp, stabbing, pleuritic (worse with inspiration or cough) → pleural/pericardial
• Reproduced precisely by palpation of chest wall → musculoskeletal
• Burning, worse postprandially, relieved by antacids → GERD/esophageal
• Dermatomal distribution, vesicular rash → herpes zoster
• Positional (worse supine, better sitting forward) → pericarditis
• Constant, present at rest, lasts for days → not ischemic
• "Tearing" or "ripping," maximal at onset, radiating to back → aortic dissection
• Brief episodes lasting seconds → not ischemic

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86. Classification of Coronary Heart Disease (CHD) — WHO

1. Angina Pectoris

• Stable (effort) angina — predictable, provoked by exertion, relieved by rest/GTN; Canadian Cardiovascular Society (CCS) classes I–IV
• Unstable angina — new onset, crescendo (progressive worsening), rest angina without troponin rise
• Vasospastic (Prinzmetal) angina — ST elevation at rest; coronary spasm

2. Acute Myocardial Infarction

• STEMI (ST-elevation MI) — full-thickness (transmural) necrosis; Q-wave MI
• NSTEMI (Non-ST-elevation MI) — subendocardial necrosis; non-Q-wave MI

3. Postmyocardial Infarction (Post-MI) Syndrome

• Dressler's syndrome
• Post-infarction cardiosclerosis

4. Heart Failure Due to IHD

• Ischemic cardiomyopathy / chronic heart failure

5. Cardiac Arrhythmias as a Form of IHD

• Chronic arrhythmias on ischemic basis

6. Silent (Painless) Myocardial Ischemia

• ECG/imaging evidence of ischemia without anginal symptoms (~85% of ambulatory ischemic episodes are silent)

7. Sudden Cardiac Death (Coronary)

• Death within 1 hour of symptom onset, presumed coronary in origin

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87. Characteristics of Pain Syndrome in Ischemic Heart Disease

1. Character

• Pressure, heaviness, squeezing, constricting, vise-like, suffocating, crushing
• Some describe burning (easily confused with GERD) or numbness
• Rarely described as "sharp" — if sharp, question the diagnosis

2. Site and Distribution

• Central substernal or retrosternal (most common)
• May be precordial
• Radiation: left neck/shoulder → left arm (ulnar surface); jaw; throat (throat tightness is a highly specific anginal equivalent); less commonly right arm; occasionally epigastric

3. Provocation and Relief

• Provoked by: physical exertion, emotional stress, cold, sexual activity, large meals, tachycardia
• Relieved by: rest (within 2–5 min), sublingual nitroglycerin (within 3–5 min)
• Rest/nocturnal angina or angina on minimal exertion = unstable; indicates possible plaque rupture

4. Duration

• Stable angina: typically 2–10 minutes; resolves with rest or GTN
• ACS: >15–20 minutes; not fully relieved by rest or GTN

CCS Angina Classification:

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88. Differential Diagnosis: Angina Pectoris vs. Myocardial Infarction

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89. Main Symptoms of Cardiogenic Pain in Pericarditis

Cardinal Pain Characteristics:

• Quality: sharp, stabbing, or knifelike — distinctly different from ischemic pressure
• Location: retrosternal or precordial
• Radiation: to trapezius ridge / left shoulder / back — radiation to the trapezius is a pathognomonic feature strongly suggesting pericarditis
• Aggravating factors: inspiration (pleuritic), lying flat/supine, swallowing, movement, coughing
• Relieving factors: sitting upright and leaning forward (reduces pericardial contact with diaphragm)
• Onset: sudden or gradual; may wax and wane
• Duration: persistent (hours to days), unlike angina

Associated Clinical Features:

• Pericardial friction rub — classic finding; triphasic scratchy sound best heard at left sternal border, patient leaning forward in full expiration; evanescent and intermittent
• Fever, malaise, myalgias (especially in viral pericarditis)
• Dyspnea (if pericardial effusion develops)
• ECG: diffuse saddle-shaped ST elevation (concave upward) in multiple leads; PR segment depression; no reciprocal changes (unlike MI); evolution: ST elevation → T-wave inversion → normalization
• Pulsus paradoxus if cardiac tamponade develops

Etiology (Box 68.3, Rosen's):

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90. Role of Hypertrophic Cardiomyopathy in Development of Cardialgia

Mechanisms of Chest Pain in HCM:

1. Subendocardial ischemia — massively hypertrophied LV has increased oxygen demand, while the compressed intramural coronary arteries (small vessel disease, arteriolar remodeling) have reduced oxygen supply → demand-supply mismatch without epicardial CAD
2. LVOT obstruction — dynamic obstruction creates a pressure gradient → increased wall stress → ischemia
3. Diastolic dysfunction — impaired ventricular relaxation → elevated filling pressures → subendocardial ischemia
4. Microvascular dysfunction — abnormal coronary microcirculation independent of macrovascular disease
5. Mitral valve abnormalities — SAM (systolic anterior motion) of mitral valve → increased MR → increased wall stress

Pain Characteristics in HCM:

• Exertional chest pain — indistinguishable from angina pectoris
• Often accompanied by exertional dyspnea and pre-syncope/syncope (triad)
• Pain may occur at rest (in obstructive forms)
• Worsened by maneuvers that reduce preload (standing, Valsalva) or afterload (vasodilators)
• Worsened by tachycardia (reduced diastolic filling time)

Key Clinical Findings:

• Harsh crescendo-decrescendo systolic murmur at LLSB/apex; decreases with squatting (↑ preload), increases with standing/Valsalva (↓ preload) — distinguishes from AS
• Bifid carotid pulse (spike-and-dome pattern)
• ECG: LVH, deep septal Q waves in I, aVL, V5–V6
• Echo: asymmetric septal hypertrophy (septum:posterior wall ratio >1.3), SAM, LVOT gradient

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91. Principles of Treatment of Cardiogenic Chest Pain in Acute Conditions

Acute Coronary Syndrome (Angina/MI):

1. Position — rest, semi-recumbent; O₂ if SpO₂ <90%
2. Sublingual nitroglycerin (GTN) — 0.4 mg SL q 5 min × 3; reduces preload, dilates coronary arteries; contraindicated if SBP <90, bradycardia, recent PDE5 inhibitor use, RV infarction
3. Aspirin — 162–325 mg chewed immediately (antiplatelet)
4. P2Y12 inhibitor — ticagrelor 180 mg loading, or clopidogrel 300–600 mg, or prasugrel
5. Morphine — 2–4 mg IV for unresponsive severe pain (use cautiously — may mask symptoms, ↓ gut absorption of antiplatelet agents)
6. IV beta-blocker (metoprolol 5 mg IV) — reduces HR, O₂ demand; avoid if acute LV failure, bradycardia, hypotension
7. Anticoagulation — UFH, LMWH (enoxaparin), or fondaparinux
8. STEMI: emergency reperfusion — primary PCI within 90 min (preferred); thrombolysis if PCI unavailable within 120 min

Acute Pericarditis:

• NSAIDs (aspirin 750–1000 mg TID or ibuprofen 600 mg TID) — first-line
• Colchicine 0.5 mg BID × 3 months — reduces recurrence
• Corticosteroids only if NSAIDs contraindicated (e.g., post-MI, pregnancy)
• Restrict physical activity until pain-free and CRP normalized
• Avoid NSAIDs in post-MI pericarditis (aspirin preferred)

Aortic Dissection:

• Immediate IV beta-blockade (labetalol, esmolol) — target HR <60 bpm and SBP <120 mmHg
• Opioid analgesia — morphine IV for pain
• Type A (ascending): emergency surgery
• Type B (descending): medical management ± endovascular stenting

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92. Classification of Non-Cardiogenic Chest Pain

By Origin:

• Pleuritis (pleurisy)
• Pulmonary embolism
• Pneumothorax
• Pneumonia / pleuropneumonia
• Lung cancer
• Pulmonary hypertension (RV ischemia)

• Gastroesophageal reflux disease (GERD)
• Esophageal spasm (diffuse esophageal spasm)
• Esophagitis
• Peptic ulcer (gastric/duodenal)
• Acute pancreatitis
• Acute cholecystitis

• Osteochondrosis (cervicothoracic)
• Costochondritis (Tietze syndrome)
• Intercostal myalgia / fibromyalgia
• Rib fractures
• Thoracic vertebral fractures

• Intercostal neuralgia
• Herpes zoster (postherpetic neuralgia)
• Cervical/thoracic radiculopathy
• Nerve root compression (disc herniation)
• Spinal cord lesions

• Neurocirculatory dystonia (Da Costa syndrome / functional cardiovascular disorder)
• Panic disorder / anxiety
• Somatoform disorder
• Depression

• Mediastinitis
• Thoracic aortic aneurysm
• Breast pathology

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93. Causes of Non-Cardiogenic Chest Pain Associated with Lung Diseases

1. Pleuritis (Pleurisy)

• Inflammation of the pleura → friction of roughened pleural surfaces
• Sharp, stabbing pain strictly worsened by inspiration and coughing
• Pleural friction rub on auscultation
• Causes: pneumonia, TB, viral (Bornholm disease), PE, autoimmune (SLE, RA)

2. Pulmonary Embolism (PE)

• Acute onset pleuritic chest pain (if peripheral PE/pulmonary infarction) or anginal-type (if massive PE causing RV strain)
• Associated: dyspnea (most common), tachycardia, hypoxia, hemoptysis (pulmonary infarction)
• Risk factors: DVT, immobilization, malignancy, oral contraceptives
• ECG: sinus tachycardia; S1Q3T3 pattern; right heart strain

3. Spontaneous Pneumothorax

• Sudden, sharp, unilateral chest pain + acute dyspnea
• Absent breath sounds + hyperresonance on affected side
• Tracheal deviation (tension pneumothorax)
• Common in tall, thin young males (primary); secondary to COPD, Marfan's

4. Pneumonia / Pleuropneumonia

• Pleuritic chest pain + fever, productive cough, consolidation
• Friction rub or reduced breath sounds + bronchial breathing

5. Pulmonary Hypertension

• Exertional chest pain resembling angina (RV subendocardial ischemia)
• Associated: dyspnea, syncope, signs of right heart failure
• Loud P2, parasternal heave, raised JVP

6. Lung Cancer / Mesothelioma

• Persistent, dull, aching chest wall pain (from pleural invasion)
• Weight loss, hemoptysis, clubbing

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94. Nature of Pain in Acute Diseases of the GI Tract

GERD / Esophagitis:

• Burning retrosternal/epigastric pain
• Worsened by lying down, bending, large meals, alcohol, coffee
• Relieved by antacids, PPIs, upright posture
• Associated: acid regurgitation, waterbrash, hoarseness

Esophageal Spasm (Diffuse Esophageal Spasm / Nutcracker Esophagus):

• Severe squeezing/gripping substernal pain — can mimic angina exactly
• May radiate to back, arms, jaw
• Triggered by: cold liquids, hot drinks, emotional stress
• May be relieved by nitroglycerin (smooth muscle relaxation) — a dangerous diagnostic pitfall
• Associated: dysphagia to solids and liquids

Peptic Ulcer (Gastroduodenal):

• Epigastric/lower chest burning, gnawing pain
• Gastric ulcer: worsened by eating; duodenal ulcer: relieved by eating (food buffers acid), worsened 2–3 hours postprandially; nocturnal pain
• Perforated ulcer: sudden severe epigastric → generalized rigid abdomen

Acute Pancreatitis:

• Severe epigastric/left upper quadrant pain radiating to the back (band-like)
• Worsened lying flat, relieved by sitting forward (pancreatic position)
• Associated: nausea/vomiting, fever, elevated amylase/lipase

Acute Cholecystitis / Biliary Colic:

• Right upper quadrant → right shoulder/scapula radiation
• Episodic, severe (biliary colic), triggered by fatty meals
• Murphy's sign positive

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95. Signs and Symptoms of Non-Cardiogenic Chest Pain in Neurological Pathologies

Intercostal Neuralgia:

• Burning, shooting, or stabbing pain along the course of an intercostal nerve (dermatomal)
• Continuous or paroxysmal; follows specific dermatome (band around the chest)
• Allodynia — even light touch of the skin in that dermatome causes pain
• Percussion of the spine or pressure at the paravertebral point triggers/aggravates pain
• Causes: disc herniation, osteochondrosis, herpes zoster, trauma, post-thoracotomy

Herpes Zoster:

• Prodromal phase: burning/tingling pain in dermatomal distribution (T1–T10 common), before rash appears (may last days–weeks → diagnostic challenge)
• Active phase: grouped vesicular rash on erythematous base in dermatome + severe burning pain
• Post-herpetic neuralgia: persistent severe neuropathic pain after rash heals; allodynia
• Diagnosis: clinical + PCR or DFA from vesicle; Tzanck smear

Cervicothoracic Radiculopathy (C6–T2 radiculopathy):

• Arm pain + paresthesia (numbness/tingling) in a specific nerve root distribution
• May radiate to chest/shoulder
• Worsened by neck movement, Valsalva, Spurling's test positive

Thoracic Outlet Syndrome:

• Compression of brachial plexus/subclavian vessels → chest/shoulder/arm pain + neurological symptoms

Psychogenic / Panic Disorder:

• Sudden onset chest tightness, palpitations, dyspnea, derealization
• All normal investigations
• Associated: anxiety, hyperventilation, paresthesia of hands/lips (from hypocarbia)

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96. Role of Osteochondrosis in Non-Cardiogenic Chest Pain

Mechanisms:

1. Disc herniation → compression of thoracic nerve roots → intercostal neuralgia
2. Osteophyte formation → direct nerve/vascular compression
3. Vertebral instability → muscle spasm of paravertebral muscles → chest wall pain
4. Sympathetic chain compression → referred chest pain that may mimic cardiac pain
5. Discogenic pain — pain from the disc annulus itself

Clinical Features of "Vertebrogenic" Chest Pain:

• Pain follows a dermatomal pattern (girdle-like, one-sided, or bilateral)
• Worsened by: movement of the spine, deep breathing, coughing, prolonged sitting/standing, lifting
• Worsened by: neck or trunk rotation, extension
• Relieved by: change of position, rest, local warming, analgesics
• NOT relieved by nitroglycerin; NOT triggered by exertion alone
• Tenderness on percussion of spinous processes (T1–T8) or paravertebral pressure
• Pain on passive movements of the thoracic spine
• Associated: radicular pain into arm, numbness, paresthesia
• May have long history of "back problems"

Differential from Angina:

• Reproducible by palpation/movement — angina is not
• No autonomic features (no diaphoresis, pallor)
• Normal ECG and cardiac biomarkers
• X-ray/MRI spine: osteophytes, disc narrowing, spondylosis

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97. Neurocirculatory Dystonia — Laboratory and Instrumental Diagnostics

Diagnostic Criteria (clinical):

• Multiple cardiovascular symptoms: chest pain, palpitations, dyspnea, fatigue
• Emotional lability, anxiety, asthenic syndrome
• Labile blood pressure (hypertonic, hypotonic, or normotonic forms)
• Symptoms disproportionate to objective findings
• Young age, predominantly females

Laboratory Investigations:

Instrumental Diagnostics:

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98. Treatment of Non-Cardiogenic Chest Pain in Gastroesophageal Reflux Disease (GERD)

Step 1 — Lifestyle Modifications:

• Elevate head of bed 15–20 cm
• Avoid eating 2–3 hours before lying down
• Weight reduction (obesity is primary risk factor)
• Eliminate triggers: caffeine, alcohol, tobacco, chocolate, fatty/spicy foods, citrus, tomatoes, carbonated drinks
• Small, frequent meals; chew food thoroughly

Step 2 — Pharmacological Treatment:

• Omeprazole 20–40 mg/day, esomeprazole 20–40 mg, lansoprazole, pantoprazole
• Take 30 min before the first meal
• Initial course: 4–8 weeks; maintain for 3–6 months in erosive esophagitis
• Diagnostic trial: symptom relief with PPI strongly supports GERD as cause

• Famotidine 20–40 mg at night
• Less effective than PPIs for erosive esophagitis

• Immediate symptom relief (calcium carbonate, magnesium hydroxide)
• Not disease-modifying

• Domperidone, metoclopramide — ↑ LES tone and gastric emptying; useful in gastroparesis-associated reflux
• Use for ≤12 weeks (metoclopramide: tardive dyskinesia risk with long-term use)

• Form raft over gastric contents → reduces reflux

Step 3 — Refractory/Severe GERD:

• Increase PPI dose (BID dosing)
• Add H2-blocker at night (for nocturnal acid breakthrough)
• Baclofen (GABA-B agonist) — reduces transient LES relaxations
• Nissen fundoplication — laparoscopic surgical anti-reflux procedure (for PPI-refractory or structural defect)

• Low-dose tricyclic antidepressants (amitriptyline 10–25 mg at night) — reduce visceral pain perception
• SSRIs (sertraline, paroxetine) — for patients with anxiety-associated esophageal hypersensitivity

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99. Diagnostic Methods for Cardiogenic and Non-Cardiogenic Chest Pain

Cardiogenic:

Non-Cardiogenic:

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100. Laboratory Diagnostics of Myocardial Infarction

Cardiac Biomarkers:

Rapid Diagnosis (0h/1h or 0h/2h ESC Protocol):

• 0h hs-cTn + 1h hs-cTn: if both low (below LOD) + no symptoms → rule out MI; if rise >3 ng/L in 1h → rule in MI

Other Blood Tests:

• CBC: leukocytosis (reactive neutrophilia) within hours; elevated WBC correlates with infarct size
• ESR, CRP: rise 24–48h after onset (acute phase reactants); peak 3–5 days
• BNP/NT-proBNP: elevated if LV dysfunction complicates MI; predicts prognosis
• Blood glucose: hyperglycemia (stress response); predicts worse outcome
• Lipid profile: measure within 24h (falsely lowered after 24h due to acute phase reaction)
• Coagulation studies: before thrombolysis/PCI (INR, aPTT, platelets)
• Creatinine, eGFR, electrolytes: baseline before contrast for PCI; hypokalemia/hypomagnesemia predispose to arrhythmias

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101. Instrumental Diagnostics of Myocardial Infarction — ECG Signs

ECG — Cornerstone of MI Diagnosis

STEMI — ECG Criteria:

• New ST elevation at the J-point in ≥2 contiguous leads:
  • ≥1 mm in all leads except V2–V3
  • ≥2 mm in V2–V3 (men ≥40 years); ≥2.5 mm (men <40 years); ≥1.5 mm (women)
• Left bundle branch block (LBBB) — new LBBB = STEMI equivalent until proven otherwise
• Posterior MI: tall R waves + ST depression in V1–V2 (mirror of inferior STEMI)

Evolution of STEMI on ECG (Temporal Stages):

Localization of MI by ECG Leads:

NSTEMI / Unstable Angina — ECG:

• No persistent ST elevation
• May show: ST depression (≥0.5 mm), T-wave inversion, nonspecific ST-T changes, or normal ECG
• Persistent ST depression + elevated troponin = NSTEMI

Other Instrumental Methods for MI Diagnosis:

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102. Principles of Treatment of Acute Myocardial Infarction

STEMI — Emergency Reperfusion is Priority:

1. O₂ — only if SpO₂ <90% (hyperoxia may worsen ischemia)
2. Nitroglycerin SL/IV — pain relief, preload reduction; contraindicated if SBP <90, RV infarct, PDE5i use
3. Morphine 2–4 mg IV (pain relief; use cautiously)
4. Aspirin 162–325 mg chewed (irreversible COX-1 inhibitor)
5. P2Y12 inhibitor loading — ticagrelor 180 mg or prasugrel 60 mg (preferred) or clopidogrel 600 mg
6. Anticoagulation — UFH (70–100 U/kg IV bolus) or enoxaparin; bivalirudin for primary PCI

• Beta-blockers (metoprolol, carvedilol) — reduce mortality; start oral within 24h if stable; reduce infarct size, arrhythmias; avoid if cardiogenic shock, bradycardia, severe LV failure acutely
• ACE inhibitors / ARBs — within 24h in anterior STEMI, EF <40%, hypertension, diabetes; reduce LV remodeling; reduce mortality
• Aldosterone antagonist (eplerenone) — start within 3–14 days if EF <40% + either HF or diabetes; reduces mortality
• Statins (high-intensity) — atorvastatin 80 mg or rosuvastatin 20–40 mg; start immediately; plaque stabilization + long-term CV benefit; target LDL <55 mg/dL
• Dual antiplatelet therapy (DAPT): aspirin + P2Y12 inhibitor for 12 months

NSTEMI / Unstable Angina:

• Same antiplatelet/anticoagulant therapy as above
• Risk stratification: GRACE score, TIMI score → determines timing of invasive strategy
• High-risk NSTEMI: early invasive strategy (coronary angiography within 2–24h)
• Lower-risk: conservative or semi-elective (within 72h)
• Ongoing medical therapy: same as post-STEMI (beta-blockers, ACE-I, statins)

Monitoring and Complication Management:

• Continuous ECG monitoring (arrhythmia surveillance)
• Reperfusion arrhythmias: accelerated idioventricular rhythm (AIVR) — benign; VF/VT → defibrillation
• Cardiogenic shock: IV inotropes (dobutamine, norepinephrine), IABP or LVAD, urgent PCI
• Acute LV failure / pulmonary edema: IV diuretics, nitroglycerin, CPAP; avoid beta-blockers acutely
• Mechanical complications (VSD, mitral regurgitation, free wall rupture) → urgent surgical repair

Secondary Prevention (long-term after MI):

• DAPT ×12 months → then aspirin monotherapy lifelong
• High-intensity statin lifelong
• Beta-blocker (at least 1 year, longer if EF reduced)
• ACE-I/ARB lifelong if EF <40% or hypertension/diabetes
• Cardiac rehabilitation
• Risk factor control: smoking cessation, BP <130/80, LDL <55 mg/dL, HbA1c <7%, weight, exercise

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