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Branchial Cleft Cysts
Cleft Lip and Palate
Ehlers-Danlos Syndrome
Epidermolysis Bullosa
Ichthyosis
Noonan Syndrome
Sturge-Weber Syndrome
Xeroderma Pigmentosum
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Traumatic Brain Injury

Pathophysiology

Disruption of brain function due to external mechanical force, involving:

  • Primary injury: occurs at the time of trauma; includescerebral contusions,diffuse axonal injury, andintracranial hemorrhages
  • Secondary injury: evolves over hours to days; includesexcitotoxicity → neuronal death andcerebral edema → increased intracranial pressure

These processes lead to neuronal damage, cerebral swelling, and compromised cerebral perfusion.

Clinical Presentation

  • Mild TBI (concussion): transient loss of consciousness, headache, dizziness
  • Moderate to severe TBI: prolonged loss of consciousness, focal neurological deficits, signs of increased intracranial pressure

Other features may include seizures, vomiting, altered mental status, and signs of skull fractures (e.g., CSF rhinorrhea).

Diagnosis

  • First-line imaging: non-contrast head CT scan to detect fractures, hemorrhages, edema
  • Glasgow Coma Scale: assess level of consciousness and injury severity

Additional workup may include MRI for diffuse axonal injury, laboratory tests, and intracranial pressure monitoring.

Management

  • Initial stabilization: ensure airway, breathing, circulation (ABCs), cervical spine immobilization if needed
  • Intracranial pressure management: elevate head of bed, osmotic agents (e.g., mannitol), sedation
  • Surgical intervention: evacuation of hematomas, decompressive craniectomy for refractory increased ICP

Preventing secondary injury involves maintaining adequate blood pressure, seizure prophylaxis, and temperature management.

Atrial Fibrillation

Pathophysiology

Uncoordinated atrial activation leads to ineffective atrial contraction and an irregularly irregular ventricular response. Key mechanisms include:

  • Multiple reentrant circuits → disorganized atrial depolarization
  • Ectopic foci in pulmonary veins → trigger and maintain AF episodes

Electrical and structural remodeling of the atria promote AF persistence ("AF begets AF").

Clinical Presentation

  • Palpitations: sensations of rapid or irregular heartbeat
  • Fatigue and dyspnea due to decreased cardiac output

Patients may also experience dizziness, chest discomfort, or be asymptomatic. AF increases the risk of thromboembolic events, such as stroke.

Diagnosis

  • Electrocardiogram (ECG): shows absent P waves and irregularly irregular rhythm
  • Echocardiography to assess atrial size and underlying heart disease

Additional tests include thyroid function tests and evaluation of stroke risk using the CHA2DS2-VASc score.

Management

  • Rate control: beta-blockers, calcium channel blockers, or digoxin to control ventricular rate
  • Anticoagulation to prevent thromboembolism based on CHA2DS2-VASc score

Rhythm control with antiarrhythmic drugs, electrical cardioversion, or catheter ablation may be considered in symptomatic patients or those with heart failure.

Amyloidosis

Pathophysiology

Extracellular deposition of misfolded proteins forming insoluble amyloid fibrils (β-pleated sheets) disrupts organ function. Main types include:

  • AL (Primary) Amyloidosis: Clonal plasma cells produce excess light chains → misfolding → amyloid fibrils.
  • AA (Secondary) Amyloidosis: Chronic inflammation → elevated serum amyloid A (SAA) → misfolding → amyloid fibrils.
  • ATTR Amyloidosis: Misfolded transthyretin (TTR) protein deposits; includes hereditary (mutations in TTR gene) and wild-type forms.

Other types include Aβ2M amyloidosis in long-term dialysis patients and localized amyloidosis (e.g., Alzheimer's disease).

Clinical Presentation

  • Renal involvement: Nephrotic-range proteinuria, hypoalbuminemia → edema, progressive renal failure.
  • Cardiac involvement: Restrictive cardiomyopathy, arrhythmias, heart failure.
  • Peripheral neuropathy: Sensory and motor deficits; autonomic dysfunction (orthostatic hypotension, GI symptoms).

Other features may include macroglossia, hepatomegaly, carpal tunnel syndrome, and easy bruising (e.g., periorbital purpura).

Diagnosis

  • First-line test: Tissue biopsy with Congo red staining showing apple-green birefringence under polarized light.
  • Serum and urine protein electrophoresis (SPEP/UPEP) with immunofixation to detect monoclonal proteins (in AL amyloidosis).

Assessment of organ involvement includes echocardiography (cardiac dysfunction), urinalysis (proteinuria), and nerve conduction studies (neuropathy).

Management

  • AL Amyloidosis: Chemotherapy (e.g., bortezomib-based regimens) to suppress plasma cell clone; possible autologous stem cell transplant.
  • AA Amyloidosis: Treat underlying inflammatory disease to reduce SAA production.
  • ATTR Amyloidosis: TTR stabilizers (e.g., tafamidis) to prevent TTR misfolding.

Supportive care for organ dysfunction includes diuretics for heart failure, ACE inhibitors for proteinuria, and medications for neuropathic pain.

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