USMLE Mistake Deck 2 Flashcards
Systemic Sclerosis
Features:
- diffuse systemic sclerosis; including sclerodactyly (skin tightness and thickening, nonpurulent ulcers)
- pulmonary fibrosis (fine, inspiratory crackles)
- GERD (chest pain, weight loss) due to esophageal dysmotility.
Diffuse systemic sclerosis is commonly associated with antitopoisomerase I antibodies (anti-Scl-70), which can be found in up to 70% of individuals and indicates a poor prognosis.
Anticentromere antibody is the main parameter for limited systemic sclerosis, which may also show positive testing for anti-Scl-70.
Raynaud Phenomenon
Calcium channel blockers, in particular oral nifedipine, are the first-line pharmacotherapy for patients with primary RP because of their vasodilatory effect. Initial treatment should also include conservative measures, such as avoidance of triggers (e.g., cold, stress), smoking cessation, and discontinuation of vasoconstrictive drugs that may cause vasospasms (e.g., triptans).
Nailfold capillary microscopy can help distinguish primary RP from secondary disease. While primary RP is caused by idiopathic vasospasms of the digital arteries and arterioles and is not associated with vascular changes seen on nailfold capillary microscopy, patients with secondary RP typically have structural vascular changes caused by the underlying disease (e.g., systemic sclerosis), such as enlargement and/or loss of capillaries.
Opioid Medications in pts with impaired kideny fxn
Recommended: - fentanyl -Hydromorph -buponerphine Methadone
Medications to avoid:
- morphine
-codeine
Tramadol
- Morphine produces active metabolites that are renally secreted.
Several other metabolites (ex.
Cyanide Toxicity
etiologies: fires ( combustion of plastics) + mining + sodium nitroprusside
Pathophysiology: inhibit oxidative phosphorylation and forces anaerobic metabolic ( rapidly lethal if untreated)
Feature: HTN tachycardia, tachypne ( with circulatory collapse and death); Headache ( confusion, anxiety, seizure, coma), cherry red skin
Mngmt: Decontamination + Supportive care ( 100% care + IVF + Vasopressors); empiric treatment with hydroxocobalamin +/- sodium thiosulfate.
Decompression Sickness.
Decompression sickness
Pathophysiology: Abrupt decrease in ambient pressure causes formation of nitrogen gas bubbles with the body.
Risk factors:
Rapid ascent to the surface following a deep dive
Obesity ( nitrogen is fat soluble); male sex
Air travel soon after diving ( may further reduce ambient pressure).
Presentation:
Type I ( mild disease): MSK ( the bends), cutaneous and lymphatic; the elbow and shoulder joint pain is the most common pain. Cutaneous involvement is most pruitus and erythema. Lymphatic involvement may be lymphadenopathy and edema.
Type II ( severe): neurologic and pulmonary. Neurologic involvement may involve ataxia, dizziness, spinal cord involvement, weakness/paresthesia/loss of bladder control.
Treatmetn:
IV fluids and 100% oxygen
Hyperbaric oxygen as soon as possible
High Altitude Illness
Acetozolamide, dexamethasone, and nifedipine are used to treat high altitude illness.
Sx include encephalopathy and non-cardiogenic pulmonary edema.
High altitude Illness
Treatment:
supplemental oxygen
Acetozolamide for altered mental status, and dexamethasone for HACE
Descent to lower altitude
Organophosphate poisoning
Organophosphate Poisoning:
Exposure, farmer/field work, paediatric ingestion, suicie attempt
Manifestation: Muscuranic Diarrhea/ diaphoresis Urination Miosis Bronchospasm/bronchorrhea/bradycardia Emesis Lacrimation Salivation Nicotinic: muscle weakness, paralysis and fasiculation
Mngt:
Remove pts clothes, irrigate skin
Atropic reverse muscruanic symptoms; Pralidoxime reverses nicotinic and muscuranic symptoms ( administer after atropine)
Pt may present with bradycardia, mitosis and excessive secretion ( diaphoresis, ronchi and drooling) has evidence of cholinergic toxicity, likely due to accidental or intentional exposure to organophosphate pesticide. Organophosphates inhibit acetylcholinesterase leading to hyper stimulation of the muscuranic receptors ( leading to DUMBELS) and nicotnic ( muscle fascinations, weakness, and paralysis)
Management of Organophosphate toxicity include stabilization ( ABC), decontamination to prevent continued exposure, and reversal of cholinergic hyper stimulation. Atropine, a competitive ihibitor of acetylcholic at the muscuranic receptor, should be given immediately and leads to resolution of muscuranic symptoms ( e.x. bronchospasm). B/c Atropine does not act on the nicotinic receptors, pts with evidence of neuromuscular dysfunction should then receive pradiloxime, a cholinesterase reactivating agent that can relieve both the muscarinic and nicotinic effects.
TCA OD
-AMS, tachycardia, signs of anticholinergic toxicity ( e.x. mydriasis, urinary retention, and dry mucous membranes)
CNS: Mental status changes ( drowsiness, delirium, coma, seizures and respiratory depression)
CV: sinus tachycardia, hypotension, prolonged PR, QRS, QT intervals; Arrthymia ( ventricular tachycardia or ventricular fibrillatio)
Anticholinergic: Dry mouth, blurred vision, dilated pupils, urinary reteniosn, flushing, hypothermia
Supportive care: Supplemental oxygen, intubation, IVF, activated charcoal for pts with 2 hours of ingestion ( unless blues present) + IV sodium bicarbonate for QRS interval widening or ventricular arrhythmia.
Digoxin Toxicity:
N/V/Confusion and changes in color vision ( all objects may appear yellow)
Peritonsillar abscess
Peritonsillar abscess (PTA) is the most common deep neck infection in adolescents and young adults. The disease is caused by bacterial spread from an acute bacterial tonsillitis into the potential space between the tonsil and the pharyngeal muscles. It is usually a clinical diagnosis. Treatment in younger, less cooperative, patients consists of incision and drainage combined with IV antibiotics (e.g., ampicillin-sulbactam).
Features:
- fever, sore throat, dysphagia, change in her voice, difficulty opening her mouth (trismus), cervical lymphadenopathy, and a swollen, erythematous tonsil with a deviated uvula, which indicates a peritonsillar abscess.
Ttt: Incision/drainage + IV antibiotics
Otitis Externa
Most cases of otitis externa are caused by bacterial infection; Pseudomonas aeruginosa is the most common pathogen (∼ 40% of cases). Risk factors include increased moisture in the external auditory canal (e.g., from swimming) and/or injury to the overlying skin of the external auditory canal. Other causes of bacterial otitis externa include infection with Staphylococcus aureus, Escherichia coli, and Proteus mirabilis.
Mastoiditis
Mastoiditis is a severe complication of acute otitis media that usually manifests with persistent or recurrent symptoms of otitis media after initial improvement, profuse ear discharge, a tender and edematous mastoid, and anterolateral protrusion of the auricle. Otoscopy should always be performed first, as it is readily available and can help to evaluate the tympanic membrane for inflammatory signs. Mastoiditis should usually be confirmed via a CT scan of the temporal bone. Typical findings include opacification of the mastoid air cells, erosion of the air cell walls, and pus in the mastoid cavity seen as areas of enhancement. Treatment of mastoiditis consists of intravenous antibiotic treatment (e.g., with vancomycin) as well as tympanostomy and subsequent tympanostomy tube insertion in mild cases or mastoidectomy in more severe cases.
If patients present with characteristic symptoms that are highly suggestive of mastoiditis, imaging is not always necessary to confirm the diagnosis. As a CT scan is generally associated with considerable amounts of radiation, it should be used with caution, particularly in children. However, in severe or unresponsive illness, as well as in the case of clinical findings suggestive of complications (e.g., hearing loss, meningeal signs, focal neurological findings), a CT scan is essential to evaluate the temporal bone. In infants such as this patient, it is often difficult to rule out dangerous complications and a CT scan should be performed.
Epiglottitis
Cervical X ray of patients with this condition often shows an enlarged epiglottis and supraglottic narrowing, also known as a thumbprint sign. Various diseases manifest with inspiratory stridor as a main diagnostic feature, but only epiglottitis is notable for painful swallowing, neck extension, a muffled voice, and absence of cough.
Prinzmetal Angina
A combination of reversible ST elevations, normal troponin levels, and a cardiac angiography showing no more than 30% blockage of the coronary arteries makes vasospastic angina (Prinzmetal angina) the most likely cause of this patient’s chest pain.
Cholesterol Embolism
Cholesterol embolization syndrome is a known complication of cardiac catheterization, vascular interventions, and anticoagulant therapy. Cholesterol is released into the circulation, where it can travel to many organs, especially the kidneys (as they receive a large amount of the blood supply). This patient presents with the classic symptoms of livedo reticularis and acute kidney failure. Eosinophilia and eosinophiluria in the setting of cholesterol embolism are very suggestive findings. Kidney biopsy showing intravascular cholesterol deposits (spindle-shaped vacuoles) confirms the diagnosis.
