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Staatsexamen (Subject) / BAG Fragen (Lesson)
- Achilles tendon rupture Etiology - Indirect trauma from physical activities (e.g., tennis, basketball)- Rarely, direct trauma or longstanding paratenonitis (possibly with tendinosis) Risk factors:- Pre-existing degenerative conditions (including polyarthritis)- ↓ Physical conditioning (poor physical condition)- Medication: Glucocorticoids, immunosuppressants Clinical features:- Popping or snapping sound/sensation when the injury occurs - Sudden, severe pain in the Achilles tendon- Difficulty mobilizing: loss of plantar flexion power on the affected side The patient may retain enough strength for mild plantar flexion because of other intact muscle groups (peroneal muscles, flexor hallucis tendons, or posterior tibilais tendon) in the foot and leg- Deformity: calf swelling (i.e., hematoma) and/or palpable interruption of the affected Achille's tendon- Thompson test: squeezing the calf (i.e., gastrocnemius muscle) of the patient, in prone position with legs extended→ Normal: results in passive plantar flexion→ Rupture: absent passive plantar flexion Diagnostics: Mainly a clinical diagnosis- Ultrasound (best initial test)- X-ray: mainly to rule out suspected bone fractures- MRI (confirmatory test): only imaging modality that can distinguish between a partial and complete rupture Treatment:- Conservative therapy: Rest, analgesia, serial casting; Rehabilitation- Surgical therapy: Open or percutaneous tendon repair; Casting; Rehabilitation
- Keloid - Skin lesions caused by high fibroblast proliferation and collagen production as excessive tissue response to typically small skin injuries- Grows beyond the boundaries of the original lesion- Does not regress spontaneously- Recurs after resection Etiology: imbalance in wound healing processes due to local factors and genetics Clinical features:- Scar tissue of varying consistency (soft or hard) that may be brownish-red in color- Pruritus- Pain Localization: earlobes, face (especially cheeks), upper extremities, chest, and neck Diagnosis: based on clinical appearance of lesion and patient history of trauma or surgery Treatment: - First-line treatment: intralesional steroid injection → decreases scar thickening, and, if present, relieves pain and pruritus- Surgery: Cryotherapy; Laser treatment; Surgical excision
- Selective mutism Selective mutism is a relatively uncommon disorder in which children do not speak in situations when speech is expected. It may coexist with social anxiety disorder and/or result in school refusal. Age of onset: generally occurs by 5 years of age, although usually not diagnosed until the child starts school Diagnostic criteria (DSM-5):- Duration: at least 1 month- Child consistently fails to speak in specific situations- Interferes with normal life (e.g., social interactions, school)- Not attributable to language difficulties or other disorders Treatment: SSRIs (fluoxetine) and cognitive behavioral therapy
- Achalasia Etiology:- Primary achalasia (most common): cause is unknown- Secondary achalasia (pseudoachalasia): The presentation and manometric findings of a mechanical cause of obstruction (e.g., a malignancy) that mimics achalasia.→ Stomach cancer→ Esophageal cancer→ Chagas disease→ Amyloidosis→ Neurofibromatosis type I→ Sarcoidosis Clinical features:- Dysphagia to solids and liquids- Regurgitation- Retrosternal pain and cramps- Weight loss Diagnostics - In general, all patients with suspected achalasia should initially undergo upper endoscopy and/or barium esophagram.- Esophageal manometry is indicated to establish the diagnosis (confirmatory test of choice), irrespective of the initial imaging findings.- If manometry is inconclusive and a barium esophagram was not obtained initially, esophagram can also play a confirmatory role.- Endoscopy should be performed to rule out pseudoachalasia because the presentation and manometric findings of a mechanical cause of obstruction (e.g., a malignancy) may mimic achalasia. If a low surgical risk:- Pneumatic dilatio- LES myotomy (Heller myotomy) If a high surgical risk:- Botulinum toxin injection in the LES- If other measures are unsuccessful: nifedipine or calcium channel blockers Complications:- Pulmonary complications (e.g., pneumonia, abscess, asthma) caused by aspiration- Megaesophagus- Increased risk of esophageal cancer
- Barrett esophagus Pathophysiology:- Reflux esophagitis → stomach acid damages squamous epithelium → squamous epithelium becomes replaced by columnar epithelium and goblet cells (intestinal metaplasia, Barrett's metaplasia) - The physiological transformation zone ("Z-line") between squamous and columnar epithelium is shifted upwards Pathology:- Short-segment Barrett's esophagus (< 3 cm of columnar epithelium between Z-line and GEJ)- Long-segment Barrett's esophagus (> 3 cm of columnar epithelium between Z-line and GEJ) → higher cancer risk! Complications: precancerous condition for adenocarcinoma (see esophageal cancer) Management and surveillance:- Medical treatment with PPIs- Endoscopy with four-quadrant biopsies at every 2 cm of the suspicious area (salmon colored mucosa)→ If no dysplasia: repeat endoscopy every 3-5 years→ If indefinite for dysplasia: repeat endoscopy with biopsies after 3-6 months of optimized PPI therapy→ If low-grade dysplasia: Endoscopic therapy of mucosal irregularitiesAlternatively: surveillance every 12 months with biopsies every 1 cm→ If high-grade dysplasia: endoscopic therapy of mucosal irregularities
- Ranula Retention cyst arising in the sublingual gland Epidemiology:- ♂ ≈ ♀- Most common between 10-30 years of age- Rare (∼ 3% of salivary cysts) Clinical features:- Translucent blue swelling below the tongue- Can cause problems swallowing and speaking Treatment:- Extirpation of the ranula, including the sublingual gland- Marsupialization
- Stimmlippen Beidseitig:- Stimmlippenknötchen Einseitig:- Vorne: Stimmlippenpolyp- Hinten: Kontaktgranulom
- Erythema nodosum Etiology:- Idiopathic (most common)- Infection (e.g. streptococcal pharyngitis, histoplasmosis, coccidioidomycosis, TB, leprosy)- Autoimmune diseases (e.g. sarcoidosis, Crohn's disease, ulcerative colitis, Behcet's syndrome)- Drugs (oral contraceptives, sulfonamides, iodide)- Pregnancy- Malignancy
- Salicylate poisoning Clinical features:- Early symptoms: tinnitus, nausea, vomiting, tachypnea, hyperpnea- Severe toxicity: hyperthermia, agitation, delirium, seizures, noncardiogenic pulmonary edema Diagnosis- ABG analysis: mixed: respiratory alkalosis; increased anion gap metabolic acidosis- Serum salicylate levels: Levels > 40 mg/dL indicate salicylate toxicity.- Renal function tests and electrolyte levels: ↑ BUN and creatinine and/or hypokalemia Treatment:- Stabilization of vitals: Oxygenation; IV fluids; IV glucose boluses; correction of hypokalemia- Oral/orogastric activated charcoal: indicated if time since ingestion is < 3 hoursActivated charcoal absorbs gastrointestinal salicylate and prevents further toxicity.- IV sodium bicarbonate- Hemodialysis: Indicated in patients with severe acidosis, very high levels of serum salicylate, cerebral/pulmonary edema, or renal failure
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