Block 5 Case 5

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Carpal Tunnel: Tinel's sign: Tap over a nerve to illicit tingling, "pins and needles" in the distribution of the nerve.
Heberden's nodes: Nodes at DIP joints (most distal), sign of osteoarthritis.
Bouchard's nodes: Nodes at PIP joints (middle), sign of osteoarthritis.
Carpal Tunnel: pathophysiology: Compression of median nerve between carpal ligament and other structures in the tunnel.
Due to: Synovitis, factures, tumors, congenital abnormalities, and overuse.
Carpal Tunnel: treatment: NSAIDS + split for 2-6 weeks

Surgery if that fails.
Ulner nerve compression sites: Cubital tunnel syndrome at elbow.

Canal of Guyon at the wrist.
Phalen maneuver: Acute wrist flexion mantained for 30-60s duplicates carpal tunnel symptoms.
Extent of anterior, middle, posterior mediastinum.: Anterior: Posterior sternum to anterior pericardium.
Middle: anterior pericardium to the spine.
Posterior: Paravertebral sulci and associated structures.
Cause of anterior mediastinal mass:: Thymoma
Thyroid masses
Teratoma (germ cell tumor)
T-cell lymphoma (or other lymphoma)
Thyroid masses in thorax: features: 5% thyroid in thorax malignant.
Symptoms related to upper airway or esophageal compression (cough, wheezing, stridor, dyspnea, dysphagia)

Classic finding on CT is tyroid continuity from cervical area to mediastinum.
Teratoma: features: Germ cell tumors that vary from benign to highly malignant.

3rd most common AMT in adults, 2nd most common in children.

Asymptomatic or cough/dyspnea/chest pain.
T-cell lymphoma: features: 45% of AMT in children, 2nd most common in adults.
50-70% Hodgkin, 15-25% non-Hodgkin.
Causes airway compression, great vessel compression, esophageal compression and pleural effusions.
Constitutional symptoms, chest pain, cough, dyspnea.
Must perform biopsy to diagnose.
Cause of middle mediastinal mass:: Thoracic Aortic Aneurysm
Hematomas
Adenopathy
Mediastinal cysts

Others:
Neoplasm
Diaphagramatic hernias
Systemic granuloma
Cause of posterior mediastinal mass:: Neurogenic tumors (90%):
Benign nerve sheath tumors (neurilemoma, schwannoma, neurofibroma)
Maignant nerve sheath tumors (malignant neurofibromas, malignant schwannomas, neurogenic fibrosarcomas).
Neuroblastomas
Thymoma: epidemiology: Most common neoplasm of anterior mediastinum.
50% of anterior mediastinal masses.
Thymoma: pathophysiology: Unknown, but p27 plays an important roll along with other cell cycle regulators.
Thymoma: Paraneoplasic conditions... incidence in thymoma patients.: Myasthenia gravis (30-50%)
Pure red cell aplasia (5-15%)
Hypogammaglobulinemia (10%)
Thymoma: clinical manifestations: 40-50% asymptomatic

Otherwise, cough, chest pain, dyspnea, fever, wheezing, fatigue, weight loss, night sweats, anorexia.
Thymoma: diagnosis: Must be confirmed by mediastinoscopy or limited thoracotomy to get large tissue sample. Fine needle biopsy INSUFFICENT to distinguish between lymphoma and thymomas.
Thymoma: staging and 5 yr survival rate: Masaoka Staging system:
1. Complete encapsulation, no capsular invasion (96-100%)
2. Invasion into fatty tissue/pleura or capsule invasion (86-95%)
3. Invasion into neighboring organs (56-69%)
4a. Pleural or pericardial dissemination (11-50%)
4b. Lymphogenous or hematogenous mets (???%)
Thymoma: pathologic classification: WHO Histologic Classification
A. spindle cell, medullary
AB. Mixed
B1. Lymphocyte rich, Lymphocytic, cortical, organoid
B2. Cortical
B3. Epithelial, atypical, squamoid, well differentiated thymic carcinoma
Thymoma: treatment: Surgical excision treatment of choice.

Radiation therapy, chemotherapy if invasive, surgery not possible, or as adjuvant therapy.
A-Fib: characteristics: Disorganized atrial activity w/o discrete P waves. Rate 350-600bpm. Ventricular response is highly irregular due to AV node refractory period.
A-Fib: causes: Normal: stress, surgery, exercise, caffeine, medications etc.

Heart/Lung disease: hypoxia, hCHF, COPD, MI, rheumatic heart disease, etc.
A-Fib: treatment: Look for underlying cause, fix it.

Slow ventricular rate: beta blockers (atenolol/metoprolol), calcium channel blockers (verapamil, diltiazem) to prolong AV refactory period.

Convert to sinus: antiarrhythmics, direct current cardioversion.

Reduce risk of embolization with warfarin, aspirin.

Pacemaker if drugs ineffective.
Digoxin: class, uses, MOA, adverse effects: cardiac glycoside
CHF, A-fib/flutter
Inhibits Na/K pump, increases intracellular Na, inhibiting the Na/Ca exchange pump, leading to higher Ca = stronger contraction, slower AV conduction.
Narrow therapeutic index, drug interactions (NSAIDS, verapmail etc)
Metoprolol: class, uses, MOA, adverse effects: betablocker, antiadrenergic
MI, arrhythmias, CHF, cardiomyopathy, aortic dissection
Beta1 blocker decreases cAMP = lower calcium. Decreases conduction rate, slowing HR.
At high dose blocks Beta2s causing broncospasm.
Verapamil: class, uses, MOA, adverse effects: Ca-channel blocker, antiarrhythmic
HTN, ventricular arrhythmia, SVT
Blocks L-type calcium channels, inhibiting Ca influx and decreasing HR, contractility.
Heart block, bradycardia, edema, CHF... can increases serum digitalis levels.
Quinidine: class, uses, MOA, adverse effects: antiarrhythmic, antiprotazoal
SV arrhythmias (Afib,flutter,SVT). Malaria.
Causes Na, K channel blockade leading to prolonged repolarization. Anticholinergic and alpha-adrenergic blocker.
Increased QT interval. !Cholenergic = increased AV conduction.
Codeine: class, Uses, MOA, adverse effects: opiod
analgesia, antitussive
Weak antagonist to mu receptors blocking nocioceptive neurotransmission. Supresses cough reflex.
Dependence, overdose, constipation, N&V, respiratory depression at high doses.
CHF: drug treatment, mortality reducers: ACE inhibitors (decrease afterload/preload)
B-blockers (decrease afterload/preload)
Spironolactone (decrease preload)
CHF: drug treatment, symptomatic management: Na/H2O restriction: (decrease preload)
Diuretics: (decrease preload)
Digoxin: (increased contractility)
Organic nitrates: (Decreased preload)
Dobutamine (incrased contractility, decrased afterload)
Milrinone (increasec contractility, decreased pre/afterload)
Causes of acute CHF: Acute MI
Volume overlaod
Severe ischemia
myocarditis
mitral stenosis
valvular regurg/dysfunction
exacerbation of chronic CHF.
Causes of low voltage EKG: Obesity
Hypothyroidism
Pericardial fluid
COPD
Cardiomyopathy
Improper lead location
Treshold of low voltage EKG: Limb leads < 5mmm
V leads < 10mm
Transudate vs Exudate Exudate if...: Light's criteria-- meets 1:
Fluid protein:serum protein ratio > .5
Fluid LDH:serum LHD > .6
Fluid LDH > 2/3 upper limit of serum LDH (200).
5 basic causes of pleural effusion: Increased hydrostatic, decreased oncotic pressure.
Abnormal capillary permeability.
Decreased lymphatic clearance.
Infection in pleural space
Bleeding into pleural space.
CHF and pleural effusion: features: CHF causes 90% of all transudative pleural effusion.
Treat CHF and effusions go away 75% of time.
Top 7 causes of pleural effusion:: CHF
Pneumonia
Cancer
PE
Viral disease
CABG
Cirrhosis w/ascites
Indications for thoracostomy and predictors: Chest tube. MUST be performed to drain rapid recurring effusion. Predictors:

Loculated pleural fluid
Fluid pH < 7.20
Fluid glucose < 60mg/dL
Postive gram stain/culture
Presence of gross pus.
7 criteria for a good screening test: Morbidity/mortality of disease significant
High risk population exists
Effective early interventions
Sensitive/specific
Test has minimal risk
Further diagnostic workup relatively safe.
Acceptable to target population.
Pleural fluid: Hct: >50% Hemothorax
1-50% trauma, malignancy, infarct
<1% no clinical significance
Pleural fluid: protein: Exudate usually > 3g/dL
Transudate usually < 3g/dL
Pleural fluid: normal glucose: 70-100 mg/dL normal
Pleural fluid: white count and differential: Transudates: WBC < 1000/mm3
Exudates: WBC > 1000/mm3

WBC > 10,000/mm3 indicates empyema and parapneumonic effusion.

PMNs: acute cause
Mononuclear: chronic cause
PCIS: full name and sister conditions: Postcardiac Injury Syndrome
Dressler's syndrome (DS)
Postcommissurotomy Syndrome (PCS)
Postpericardiotomy syndrome (PPS)
PCIS: clinical manifestations: Pleuritic chest pain, dyspnea.
Pericardial friction rub, low fever.
ESR, leukocytosis, AHA titers, Antimyocardial antibodies.
Abnormal CXR showing pericardial or pleural effusion.
PCIS: differential: Diagnosis of exclusion. Eliminate:

Acute coronary syndrome
HF
PE
pneumonia
PCIS: diagnosis: Fever+chest pain > 1week post MI or cardiac operation: PCIS (Dressler's or PPS)

Fever w/o pericarditis or pleuritis + atypical lymphocytosis > 1week post MI or cardiac operation = postperfusion syndrome. Confirm with increased CMV titer.
PCIS: pathophysiology: Autoimmune reaction.
Myocardial injury --> release of cardiac antigens --> production of !cardiac antibodies --> formation and deposition of immunecomplex in pericardium, lungs, pleura --> inflammation, clinical manifestations.
PCIS: treatment: NSAIDS
Corticosteroids (if NSAIDS fail)
Colchicine (may prevent recurrent PCIS)
Surgery (pericardiocentesis + window placement)
Edrophonium: class, trade name, uses, MOA, adverse effects: cholinesterase inhibitor
tensilon
MG, edrophonium test
Competes with acetylcholine for binding site on acetylcholinesterase (AChE) reducing degredation of Ach.
Rapid onset (30-45s), short duration (5-10min)
Nause, diarrhea, salivation, rarely syncope and bradycardia.
Tensilon test: 2mg edrophonium IV every 60 seconds until 10mg given.

Watch for improvement in muscle weakness. Sensitivity 80-90%.

MG: improvement -- less receptors but more time
LE: no improvement -- less ACh, time irrelevant
Thymus: general: Site where immature lymphocytes develop into T lymphs.

Only lobulated lymphatic organ. 2 lobes.
Thymus: histology: Thin capsule with trabeculae.
Cortex: dark, packed with dividing T lymphs, site of positive selection (kill unsensitive T cells).
Medulla: fewer lymphs, stains lighter. Has Hassall's corpuscles, collections of epithelial cells that produce thymic hormones. Medulla is site of negative selection (kill self-sensitive T cells).
Concept of central tolerance: Exposure of T and B lymphs during maturation phase to self-antigens... those that react undergo apoptosis.
Mechanisms of peripheral tolerance: Anergy: inactivation in absence of co-stimulatory molecule (B7 for Tcells).
Activation induced celldeath/deletion: Fas-Fas ligand system, which induces apoptosis in repeatedly activated T-cells that, as a result, express Fas.
Mechanisms of autoimmune disease: Costimulatory/activation problems:
Breakdown of Tcell anergy
B cells no longer need helper Ts
Failure of Fas-Fas ligand system

Others:
Molecular mimicry
Release of sequestered antigens
Immune complex deposition
Ankylosing spondylitis... marker: HLA-B27
Hallmark of cardiac tamponade: Pulsus paradoxus:

10mmHg drop in systolic BP with inspiration. Due to SVC dilation-->increased return-->right heart filling-->left heart compression-->decreased CO
Cardiac tamponade: treatments: NSAIDS
Corticosteroids
Pericardiocentesis
Pericardial window
Pericardiectomy if chronic.

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