Task N 4 — Answers

1. Valvular Venous Structure and Its Role in the Pathogenesis of Post-Thrombotic Disease

• Reversal of the normal pressure gradient (venous hypertension)
• Blood refluxes from deep to superficial veins via incompetent perforators
• Sustained elevated venous pressure in the distal limb → the hallmark of chronic venous insufficiency / post-thrombotic syndrome (PTS)

2. Clinical Appearance of Thrombosis of the Inferior Vena Cava

• Bilateral lower limb edema — massive, symmetric, extending from feet to groin
• Bilateral leg pain and heaviness
• Cyanosis of both lower limbs (in severe cases)
• Dilated superficial collateral veins over the abdomen and flanks (serving as bypass channels)
• If the renal veins are involved at the level of the thrombus: bilateral flank pain, hematuria, and signs of renal impairment
• If hepatic veins or suprarenal IVC involved: features of Budd-Chiari syndrome (hepatomegaly, ascites, jaundice)

3. Diagnosis of Post-Thrombotic Disease — Its Risk Factors

• History of prior DVT (confirmed by Duplex Doppler or venography)
• Chronic limb symptoms: aching, heaviness, swelling (worse with standing/walking, relieved by elevation)
• Skin changes: brownish hyperpigmentation (hemosiderin deposition), lipodermatosclerosis, venous eczema
• Venous ulceration (typically at the medial malleolus/inner ankle)
• Duplex ultrasonography: demonstrates valvular incompetence, reflux, and residual thrombus/recanalization
• Venous pressure measurements: elevated ambulatory venous pressure confirms hemodynamic incompetence

• Extensive (proximal) DVT — iliofemoral segment most important
• Recurrent ipsilateral DVT
• Inadequate anticoagulation during acute DVT
• Obesity
• Older age
• Varicose veins or pre-existing venous insufficiency
• Female sex
• Persistent thrombus at 1 month (failure of early recanalization)

4. Complications of Deep Veins of Thrombosis

• Pulmonary embolism (PE) — the most feared complication; thrombus from femoral/popliteal veins breaks off, passes through the right heart, and occludes pulmonary arteries; massive PE causes cardiopulmonary arrest and death — Gray's Anatomy for Students
• Phlegmasia cerulea dolens — massive iliofemoral DVT with limb-threatening venous gangrene
• Phlegmasia alba dolens — extensive DVT causing arterial spasm; pale, cool leg

• Post-thrombotic syndrome (PTS) — valvular destruction → chronic venous hypertension → edema, skin changes, ulceration
• Venous ulcers — particularly at the medial malleolus ("gaiter area")
• Chronic venous insufficiency
• Recurrent DVT — damaged venous wall and stasis predispose to re-thrombosis

5. Patient with Trophic Ulcer at Inner Ankle of the Shin — Varicose Veins Secondary to Post-Thrombotic Disease: Examination and Treatment

• Previous DVT episode (confirm with records)
• Duration of ulcer, prior ulcers, previous treatments
• Symptoms of venous insufficiency (swelling, heaviness, aching)

• Location: inner (medial) ankle — classic for venous ulceration
• Ulcer characteristics: size, depth, edges, floor, exudate, signs of infection
• Surrounding skin: pigmentation, lipodermatosclerosis, eczema
• Limb: varicose veins, edema, calf tenderness
• Perforating vein incompetence (Trendelenburg test, cough impulse)

• Duplex Doppler ultrasound — gold standard; maps venous incompetence, identifies patent vs. occluded segments, perforator incompetence
• ABPI (Ankle-Brachial Pressure Index) — mandatory before compression therapy; must exclude arterial disease (ABPI < 0.8 contraindicates high-compression)
• Ascending venography or CT venography — if surgical reconstruction is planned
• Wound swab — if infection suspected
• Biopsy — if ulcer fails to heal or malignant transformation suspected

• Graduated compression therapy — multilayer bandaging or high-compression stockings (30–40 mmHg); cornerstone of venous ulcer management; reduces venous hypertension
• Leg elevation — reduces edema and promotes healing
• Wound care — debridement, appropriate dressings (non-adherent, moisture-retentive)
• Exercise — calf muscle pump activation (walking, ankle exercises)
• Treat infection — systemic antibiotics if cellulitis present

• Subfascial endoscopic perforator surgery (SEPS) — division of incompetent perforating veins
• Varicose vein surgery — stripping or endovenous ablation (laser/radiofrequency) of refluxing superficial veins
• Valvular reconstruction or venous bypass — in selected patients with deep venous reflux
• Skin grafting — for large, refractory ulcers once wound bed is clean

• PTS-related ulcers are chronic and recurrent; long-term compression is essential to prevent recurrence even after healing.

Task N 4 — Questions 4 & 5: Cardiospasm (Esophageal Achalasia)

Question 4: Cardiospasm (Esophageal Achalasia) — Classification, Etiology, Pathogenesis, Clinical Presentation

Terminology

Classification

Etiology

• The myenteric plexus infiltrate consists predominantly of cytotoxic T cells (resting and activated)
• Antibodies against myenteric neurons are detectable in patient sera, especially in those with specific HLA alleles
• The triggering antigen is suspected to be chronic/latent HSV-1 (Herpes Simplex Virus type 1) infection — HSV-1 DNA has been found in LES tissue, but disease development requires both viral exposure and genetic predisposition

• Chagas disease — Trypanosoma cruzi infection destroys the myenteric plexus (endemic in South America)
• Malignancy — carcinoma of the gastroesophageal junction or distal esophagus can mimic achalasia
• Paraneoplastic (lung cancer, lymphoma)
• Amyloidosis, sarcoidosis, infiltrative diseases

Pathogenesis

1. Loss of inhibitory neurons (nitrergic/VIP-ergic) — these neurons mediate:
   • Deglutitive inhibition (LES relaxation during swallowing)
   • Sequential propagation of peristalsis
   • Their destruction explains both key abnormalities: impaired LES relaxation and aperistalsis
   • Achalasia shows absent NO synthase and markedly reduced VIP-staining neurons at the gastroesophageal junction
2. Loss of excitatory neurons (cholinergic) — contributes to aperistalsis
3. Degree of ganglion cell loss parallels disease duration — progression: EGJ outflow obstruction → Type II → Type I → end-stage achalasia
4. Result: the LES remains tonically contracted, the esophagus fails to empty, and food accumulates → esophageal dilatation — Sleisenger and Fordtran's

Clinical Presentation

• Dysphagia — universal; both solids and liquids (distinguishes from mechanical obstruction which starts with solids only); gradual onset, often present for years before diagnosis; fluctuates then plateaus
• Regurgitation — undigested food, often from hours or days earlier; nonbilious, nonacid, mixed with copious saliva (patients often do not recognize the mucoid regurgitant as saliva); worsens with recumbency
• Chest pain — in ~2/3 of patients early in disease; crushing/squeezing character, thought to be from esophageal spasm; may spontaneously resolve over time; less responsive to achalasia treatment than dysphagia
• Weight loss — from reduced oral intake
• Halitosis — from retained, fermenting food
• Hiccups
• Aspiration pneumonia — in up to 10% of advanced cases; bronchopulmonary complications may be the presenting complaint
• Heartburn — paradoxically common, but caused by bacterial fermentation of retained esophageal contents (not true GERD)
• Rare: stridor/airway compromise from massive esophageal dilatation compressing the membranous trachea

Question 5: Patient with Significant Salivation Not Associated with Food Intake — What Examination Should Be Done?

Investigations to Perform:

• First-line investigation
• Shows: retained food/secretions in a dilated esophagus, tight/puckered LES that resists passage of the scope ("pop" on entry), excludes malignancy at the cardia (pseudoachalasia)
• Mandatory to rule out carcinoma

• Classic finding: "bird's beak" appearance — smooth, tapered narrowing at the LES with proximal dilatation
• Shows esophageal dilatation, absent peristalsis, and degree of stasis
• Detects epiphrenic diverticula, sigmoid esophagus in end-stage disease

• Defines the subtype (Type I, II, or III)
• Shows: elevated LES resting pressure, incomplete/failed LES relaxation (elevated integrated relaxation pressure, IRP), aperistalsis in the esophageal body
• Essential for confirming the diagnosis and planning treatment

• Measures esophageal emptying at 1 and 5 minutes
• Useful for baseline and post-treatment assessment

• Evaluates for submucosal or extrinsic tumor at the GEJ
• Particularly important in older patients with rapid weight loss or short symptom duration

Patient Details

• Name: Kuzmich N.I. (female)
• Age: 61 years | Height: 157 cm | Weight: 98 kg | BMI: 40 (obese)
• ICQ (IKU): 0
• Norm system: Clement

What the Test Does

Key Results Table

Interpretation

1. Obstructive Pattern

• FVC (ФЖЕЛ): 60% of predicted — reduced
• FEV1 (ОФВ1): 61% of predicted — reduced
• Tiffeneau index (FEV1/FVC): 73% — below the normal threshold of 70–75%, borderline obstructive
• FEF50% and FEF75% severely reduced (48% and 40%) — indicates obstruction in small and medium airways
• The flow-volume curve shape is consistent with obstruction

2. Bronchodilator Test: NEGATIVE (Проба отрицательная)

• FEV1 did not improve by ≥12% and ≥200 mL after bronchodilator — the diagnostic threshold for a positive (reversible) response
• The bar chart confirms: ΔОФВ1, ΔПОС, ΔСОС all fall in the "insufficient" (недост.) zone
• This means the obstruction is fixed/irreversible — more consistent with COPD than asthma

3. Hyperventilation

• Minute ventilation (МОД): 207% of predicted (14.1 L/min vs. normal ~6.8 L/min) — significantly elevated
• Tidal volume (ДО) also mildly elevated
• Respiratory rate: 25 breaths/min — tachypnea
• This indicates the patient is working hard to breathe, compensating for poor airway function

4. Air Trapping / Restriction

• Low FVC alongside low FEV1 may also suggest a mixed obstructive-restrictive pattern, possibly contributed to by her severe obesity (BMI 40)

Overall Clinical Summary

This 61-year-old obese woman has moderate fixed airway obstruction with small airway involvement and a negative bronchodilator response. The pattern is most consistent with COPD (chronic obstructive pulmonary disease). Her obesity likely contributes to reduced lung volumes. The negative bronchodilation test argues against asthma as the primary diagnosis. She has significant respiratory effort (tachypnea, elevated minute ventilation), suggesting symptomatic breathlessness at rest or on minimal exertion.