STEP 2 Flashcards
RESTLESS LEG SYNDROME
Uncomfortable urge to move legs with:
Unpleasant sensations in the legs
Onset with inactivity or at night
Relief with movement (eg, walking, stretching)
Risk factors &
associated conditions
RISK FACTORS
Iron deficiency
Uremia
Pregnancy
Diabetes mellitus (especially with neuropathy)
Multiple sclerosis, Parkinson’s disease
Drugs: antidepressants, antipsychotics, antiemetics
NON PHARMACOLOGIC THERAPY
Limit caffeine & alcohol
Regular, moderate exercise
Warm &/or cold soaks or compresses
Medications
MEDICATIONS
Supplemental iron (if serum ferritin <75 ng/mL)
Mild intermittent symptoms: carbidopa-levodopa as needed
Frequent/daily symptoms: α2δ calcium channel ligand (eg, gabapentin, pregabalin)
Dopamine agonists (eg, pramipexole, ropinirole) not preferred
MERALGIA PARESTHETICA
Etiology
Lateral femoral cutaneous nerve entrapment or injury due to:
Compression (eg, tight clothing, obesity, pregnancy)
Iatrogenic injury (eg, total hip arthroplasty)
Clinical features
Paresthesia & ↓ sensation at lateral thigh
Normal motor & reflex examination
Management
Avoidance of tight garments, weight loss
Nonopioid analgesics (eg, NSAIDs)
Anticonvulsants (eg, gabapentin), nerve block, or surgical release for refractory cases
conjunctivitis treatment
Bacterial conjunctivitis
Erythromycin ointment
Polymyxin-trimethoprim drops
Azithromycin drops
Preferred agent in contact lens wearers: fluoroquinolone drops
Viral conjunctivitis
Warm or cold compresses
± Antihistamine/decongestant drops
Allergic conjunctivitis
Over-the-counter antihistamine/decongestant drops for intermittent symptoms
Mast cell stabilizer/antihistamine drops for frequent episodes
A 58-year-old woman comes to the office due to recent-onset tremor, palpitations, weight loss, and fatigue. She has no other medical conditions and takes no medications or over-the-counter supplements. The patient’s mother had hypothyroidism and osteoporosis. Blood pressure is 144/80 mm Hg, pulse is 110/min, and respirations are 18/min. On examination, there is diffuse, nontender enlargement of the thyroid gland. Ocular examination shows bilateral proptosis, lid lag, and periorbital puffiness. The patient has diplopia and ocular discomfort on extremes of lateral gaze. Laboratory tests show a suppressed TSH and elevated thyroid hormone levels. Which of the following treatment options is most likely to worsen this patient’s eye disease?
radioactive IODINE
Complications of Graves disease treatment
Adverse effects
Antithyroid drugs
(thionamides)
Agranulocytosis
Methimazole: 1st-trimester teratogen, cholestasis
Propylthiouracil: hepatic failure, ANCA-associated vasculitis
Radioiodine ablation
Permanent hypothyroidism
Worsening of ophthalmopathy
Possible radiation adverse effects
Surgery
Permanent hypothyroidism
Risk for recurrent laryngeal nerve damage
Risk for hypoparathyroidism
Chronic lymphocytic leukemia
Clinical features
Lymphadenopathy (cervical, supraclavicular, axillary)
Hepatosplenomegaly
Mild thrombocytopenia & anemia
Often asymptomatic
Diagnosis
Severe lymphocytosis & smudge cells
Flow cytometry
Lymph node & bone marrow biopsy not generally needed
Prognosis
Median survival 10 years
Worse prognosis with:
Multiple chain lymphadenopathy
Hepatosplenomegaly
Anemia & thrombocytopenia
Complications
Infection
Autoimmune hemolytic anemia
Secondary malignancies (eg, Richter syndrome)
Clinical features of pulmonary hypertension
Classification
Pulmonary arterial hypertension (WHO group 1)
Due to left heart disease (group 2)
Due to chronic lung disease or hypoxemia (eg, COPD, OSA) (group 3)
Due to chronic thromboembolic disease (group 4)
Due to other causes (eg, sarcoidosis) (group 5)
Symptoms
↓ Cardiac output: exertional syncope/presyncope, fatigue, weakness
↑ PA pressure: chest tightness, hemoptysis (rare)
RV demand ischemia: exertional angina/tightness
Venous congestion: abdominal distension (bowel edema), early satiety
Signs
Precordial heave due to RV hypertrophy
Loud P2, right-sided S3 &/or S4
Holosystolic murmur of tricuspid regurgitation
JVD, ascites, peripheral edema, hepatomegaly
Diffuse alveolar hemorrhage
causes
Pulmonary capillaritis: ANCA vasculitis, SLE, antiphospholipid antibodies
Bland hemorrhage: mitral stenosis, anticoagulation
Alveolar damage: viral pneumonitis, ARDS, drug-induced (eg, cocaine, amiodarone)
Clinical presentation & diagnosis of Diffuse alveolar hemorrhage
Dyspnea, hypoxemia, hemoptysis (absent in ~50%) & blood loss anemia
CXR or CT: diffuse ground-glass opacities
Bronchoscopy: progressive blood on serial lavage
Management of Diffuse alveolar hemorrhage
Treat underlying (eg, rheumatologic, infectious) cause
Supportive care: oxygen, mechanical ventilation; avoid anticoagulation
Glucocorticoid-induced myopathy
Prominent atrophy
Lower extremities most affected
Colon cancer screening
Patients at average risk
Start at age 45:
Colonoscopy every 10 years
gFOBT or FIT every year
FIT-DNA every 1-3 years
CT colonography every 5 years
Flexible sigmoidoscopy every 5 years (or every 10 years with annual FIT)
Patients with FDR with CRC or high-risk adenomatous polyp*
Colonoscopy at age 40 (or 10 years prior to the age of diagnosis in FDR, whichever comes first)
Repeat every 5 years (every 10 years if FDR diagnosed at age >60)
Patients with ulcerative colitis
Start screening 8-10 years after diagnosis
Colonoscopy every 1-3 years
*Adenomatous polyp ≥10 mm, high-grade dysplasia, villous elements (for example).
Initial workup of suspected cognitive impairment
Cognitive testing
MMSE (score <24/30 suggestive of MCI/dementia)
Montreal Cognitive Assessment (score <26/30)
Mini-Cog (abnormal 3-word recall &/or clock-drawing test)
Laboratory testing
Routine: CBC, vitamin B12, TSH, CMP
Selective (specific risk factors): folate, syphilis, vitamin D level
Atypical (early onset): CSF
Imaging
Routine: CT scan or MRI of the brain
Atypical: EEG
CBC = complete blood count; CMP = complete metabolic panel; CSF = cerebrospinal fluid; EEG = electroencephalogram; MCI = mild cognitive impairment; MMSE = Mini-Mental State Examination.
Polymyalgia rheumatica
Clinical features
Rapid-onset pain & stiffness in shoulders & hips ± neck involvement
Fatigue, weight loss, low-grade fever
~10% associated with GCA (eg, headache, jaw claudication, visual symptoms)
Diagnostic testing
Elevated acute-phase markers (eg, ESR, CRP)
Temporal artery biopsy if symptoms of GCA
Treatment
Very rapid response to oral glucocorticoids
Clinical features of androgen abuse
Types of androgens
Exogenous (eg, testosterone replacement therapy)
Synthetic (eg, stanozolol, nandrolone)
Androgen precursors (eg, DHEA)
Side effects/clinical presentation
Reproductive
Men: decreased testicular function & sperm production, gynecomastia
Women: acne, hirsutism, voice deepening, menstrual irregularities
Cardiovascular: left ventricular hypertrophy, possible ↓ HDL & ↑ LDL
Psychiatric: aggressive behavior (men), mood disturbances
Hematologic: polycythemia, possible hypercoagulability
Optic neuritis
Epidemiology
Primarily in young women
Associated with multiple sclerosis
Immune-mediated demyelination
Manifestations
Acute, peaks at 2 weeks
Monocular vision loss
Eye pain with movement
“Washed-out” color vision
Afferent pupillary defect
Diagnosis
MRI of the orbits & brain
Treatment
Intravenous corticosteroids
35% of cases recur
causes of secretory diarrhea
Secretory diarrhea occurs due to toxins (eg, produced by Vibrio cholerae), hormones (eg, produced by VIPomas), congenital disorders of ion transport (eg, cystic fibrosis), or bile acids (in postsurgical patients). It is caused by secretion of electrolytes and water into the intestine, resulting in a low SOG (<50 mOsm/kg). The diarrhea is typically large in volume and persists while fasting and at night.
Comorbidities that encourage atrial fibrillation
Advanced age
Systemic hypertension
Mitral valve dysfunction
Left ventricular failure
Coronary artery disease & related factors (eg, DM, smoking)
Obesity & obstructive sleep apnea
Chronic hypoxic lung disease (eg, COPD)
Triggers of increased automaticity
Hyperthyroidism
Excessive alcohol use
Increased sympathetic tone
Acute illness (eg, sepsis, PE, MI)
Cardiac surgery
Sympathomimetic drugs (eg, cocaine)
Antipsychotic extrapyramidal effects
Acute dystonia
Sudden, sustained contraction of the neck, mouth, tongue & eye muscles
Benztropine
Diphenhydramine
Akathisia
Subjective restlessness, inability to sit still
Beta blocker (propranolol)
Benzodiazepine (lorazepam)
Benztropine
Parkinsonism
Gradual-onset tremor, rigidity & bradykinesia
Benztropine
Amantadine
Tardive dyskinesia
Gradual onset after prolonged therapy (>6 months): dyskinesia of the mouth, face, trunk & extremities
Valbenazine
Deutetrabenazine
A 55-year-old woman comes to the office with a one-week history of pain in multiple joints. She has achy pain and stiffness in both wrists and multiple metacarpophalangeal and proximal interphalangeal joints in both hands. The patient’s symptoms are worst in the morning and partially improve over 10-15 minutes of normal activity. There is no associated fever, chills, rash, or weight loss. She works in a day care center and does not use tobacco, alcohol, or illicit drugs. Vital signs are normal. On examination, there is mild swelling with no redness or tenderness of the involved joints. Laboratory studies show normal blood counts and serum chemistries. Erythrocyte sedimentation rate is 12 mm/hr. Which of the following is the most likely diagnosis in this patient?
A.Acute rheumatic fever
B.Fibromyalgia
C.Polymyalgia rheumatica
D.Rheumatoid arthritis
E.Systemic lupus erythematosus
F.Viral arthritis
Viral arthritis - parvo virus B19
Signs & symptoms
Most patients are asymptomatic or have flulike symptoms
Erythema infectiosum (fifth disease): Fever, nausea & “slapped cheek” rash (more common in children)
Acute, symmetric arthralgia/arthritis: Hands, wrists, knees & feet (resembles RA)
Transient pure red cell aplasia; aplastic crisis in patients with underlying hematologic disease (eg, sickle cell)
Diagnosis
Acute infection
B19 IgM antibodies in immunocompetent patients
NAAT for B19 DNA in immunocompromised patients
Previous infection: B19 IgG antibodies (documents immunity)
Reactivation of previous infection: NAAT for B19 DNA
Stiff person syndrome
an autoimmune condition, can present with rigidity, but it primarily involves the axial muscles, and patients usually have severe gait disturbances due to stiffness. In addition, the most classic feature is severe, painful muscle spasms that are precipitated by loud noises and usually result in falling. It is much more common in women; patients also typically have comorbid type 1 diabetes mellitus.
A 28-year-old man is brought to the emergency department after being found confused in his garage. Blood pressure is 110/64 mm Hg, pulse is 48/min, and respirations are 22/min. Oxygen saturation is 92% on room air. The patient is lethargic and diaphoretic. The pupils are constricted bilaterally, and significant drooling is noted. Lung auscultation reveals diffuse wheezing and scattered rhonchi. Which of the following is the best next step in management of this patient?
A.Atropine
B.Buprenorphine
C.Epinephrine
D.Hemodialysis
E.Naloxone
Common exposures
Pesticide: farmer/field worker, pediatric ingestion, suicide attempt
Nerve agent: multiple patients presenting with similar symptoms
Manifestations
Muscarinic:
Diarrhea/diaphoresis
Urination
Miosis
Bronchospasms, bronchorrhea, bradycardia
Emesis
Lacrimation
Salivation
Nicotinic: muscle weakness, paralysis, fasciculations
Management
Remove patient’s clothes, irrigate skin
Atropine reverses muscarinic symptoms
Pralidoxime reverses nicotinic and muscarinic symptoms (administer after atropine)
cerebellar gait Causes and Associated signs
Description
Ataxic: Staggering, wide-based
Associated signs
Dysdiadochokinesia, dysmetria, nystagmus, Romberg sign
Causes
Cerebellar degeneration
Stroke
Drug/alcohol intoxication
Vitamin B12 deficiency
Clinical features & management of tricyclic antidepressant overdose
Clinical presentation
CNS
Mental status changes (eg, drowsiness, delirium, coma)
Seizures, respiratory depression
Cardiovascular
Sinus tachycardia, hypotension
Prolonged PR/QRS/QT intervals
Arrhythmias (eg, ventricular tachycardia, fibrillation)
Anticholinergic
Dry mouth, blurred vision, dilated pupils
Urinary retention, flushing, hyperthermia
Management
Supportive care & therapy
Supplemental oxygen, intubation
Intravenous fluids
Activated charcoal for patients within 2 hours of ingestion (unless ileus present)
Intravenous sodium bicarbonate for QRS interval widening or ventricular arrhythmia
Revised Cardiac Risk Index (RCRI)
(cardiovascular risk of noncardiac surgery)
6 risk predictors
High-risk surgery (eg, vascular, intrathoracic)
Ischemic heart disease
History of congestive heart failure
History of cerebrovascular disease (stroke or TIA)
Diabetes mellitus treated with insulin
Preoperative creatinine >2 mg/dL
Risk of cardiac death,
nonfatal cardiac arrest,
or nonfatal MI
0-1 factor: low risk*
≥2 factors: elevated risk
A 29-year-old registered nurse comes to the office due to sleep difficulties since receiving a promotion several weeks ago. The patient finds the new job and its many responsibilities interesting but stressful. Her sleep schedule changed when she took the new position; previously, she worked from 4:00 PM to 12:00 AM and had no sleep difficulties. Now she works from 7:00 AM to 4:00 PM. On a typical night, the patient stays up until 1:00 AM and cannot fall asleep until 2:00 AM. She then awakens by alarm at 6:00 AM to get to work on time and feels exhausted all day at work with pronounced sleepiness during required meetings. On weekends, she normally falls asleep at 2:00 AM but feels less tired because she is able to sleep in until 11:00 AM. The patient is concerned that her sleep difficulties are interfering with her job performance. She has had sleep disturbances in the past with jobs or schooling that required early start times. She does not use tobacco or alcohol. Which of the following is the most likely cause of the patient’s sleep difficulties?
A.Advanced sleep-wake phase disorder
B.Delayed sleep-wake phase disorder
C.Melatonin deficiency
D.Poor sleep hygiene
E.Shift work disorder
This patient has a life-long history of sleep difficulties that occur when she is required to wake up early. She also has a natural, pronounced “night owl” tendency to fall asleep and wake up late. This is most consistent with delayed sleep phase disorder, a type of circadian rhythm disorder most commonly seen in adolescents and young adults.
When patients with delayed sleep phase disorder fall asleep and wake up according to their internal circadian rhythm, they have normal sleep quality and duration and no bothersome symptoms (as in this patient who did well with shift work that allowed her late sleep and wake times). However, the disorder is typically unmasked when patients attempt to conform to a different schedule requiring early wake times, leading to bothersome symptoms such as daytime drowsiness, malaise, and gastrointestinal issues.
Diagnosis can be established with a sleep log with or without actigraphy (recording sleep patterns using a wearable device). Management includes bright light therapy in the morning and slowly advancing sleep and wake times.
(Choice A) Advanced sleep-wake phase disorder is also a circadian rhythm abnormality; however, it manifests with markedly early (rather than delayed) sleep and wake times (eg, drowsiness starting in early evening, waking several hours before dawn).
Disease-modifying antirheumatic drugs
Agent
Mechanism
Adverse effects
Methotrexate
Folate antimetabolite
Hepatotoxicity
Stomatitis
Cytopenias
Leflunomide
Pyrimidine synthesis inhibitor
Hepatotoxicity
Cytopenias
Hydroxychloroquine
TNF & IL-1 suppressor
Retinopathy
Sulfasalazine
TNF & IL-1 suppressor
Hepatotoxicity
Stomatitis
Hemolytic anemia
TNF inhibitors
(eg, adalimumab, certolizumab,
etanercept, golimumab, infliximab)
Infection
Demyelination
Congestive heart failure
Malignancy
Lifestyle interventions for hypertension
Modification
Recommended plan
Approximate Decrease in systolic BP (mm Hg)
DASH diet
-Diet high in fruits & vegetables & low in saturated & total fats
-11
Weight loss
Reduction of BMI to <25 kg/m2
6 per 10-kg loss
Aerobic exercise
30 minutes/day for 5+ days/week
7
Dietary sodium
<1.5-2.3 g/day (response varies)
5-8
Alcohol limitation
≤2 drinks/day in men, ≤1 drink/day in women
5
Migraine therapies
Abortives
Preventives
Abortives
Triptans (eg, sumatriptan)
NSAIDs (eg, naproxen)
Acetaminophen
Antiemetics (eg, metoclopramide, prochlorperazine)
Ergotamines (eg, dihydroergotamine)
Preventives
Topiramate
Divalproex sodium
Tricyclic antidepressants
Beta blockers (eg, propranolol)
Spinal cord compression
Causes
Mechanical (eg, disc herniation, spinal stenosis)
Malignancy (eg, lung, breast, prostate cancers)
Infection (eg, epidural abscess)
Symptoms
Gradually worsening, severe back pain
Pain worse in recumbent position/at night
Physical examination
Early signs
Symmetric extremity weakness
↓ Deep tendon reflexes
Late signs
↓ Rectal tone
↑ Deep tendon reflexes, bilateral Babinski reflex
Paralysis
Management
Emergency MRI of the spine
Emergency surgical ± radiation oncology consultation
Intravenous glucocorticoids (eg, malignancy) or antibiotics (eg, infection)
A 29-year-old man comes to the emergency department with a 5-day history of diarrhea and abdominal pain. The diarrhea occurs 5 or 6 times a day; it was initially watery but has become bloody. The patient describes the pain as colicky and severe, with associated nausea and decreased appetite but no vomiting. Medical history is insignificant, with no prior episodes of similar symptoms and no recent hospitalizations or illnesses. The patient works as a digital marketing specialist and has not traveled outside the United States. Temperature is 36.6 C (97.9 F), blood pressure is 123/82 mm Hg, and pulse is 102/min. The patient has prominent periumbilical and right lower quadrant tenderness but no guarding or rebound. Rectal examination shows brown stool mixed with blood. Which of the following is the most likely etiology in this patient?
A.Clostridioides difficile
B.Clostridium perfringens
C.Escherichia coli
D.Listeria monocytogenes
E.Rotavirus
Bloody diarrhea is most often caused by infectious gastroenteritis due to bacterial pathogens, specifically Shiga toxin–producing Escherichia coli (STEC), Shigella, or Campylobacter; other organisms that often cause watery stools (eg, Salmonella) can occasionally cause bloody stools. Of the given answer choices, STEC is the most likely diagnosis.
STEC transmission typically occurs via consumption of contaminated beef products, although outbreaks can occur in association with other foods such as fruits, leafy vegetables, and milk products. Isolated cases without a clear source are also common. The presentation classically involves inflammatory diarrhea with abdominal pain and stools that are initially watery but later contain blood. This patient’s lack of fever is typical of infection with STEC; although a minority of patients with STEC gastroenteritis may have low-grade fever, the presence of a temperature >38.5 C (101.3 F) suggests an alternate diagnosis.
The diagnosis can be confirmed with multiplex nucleic acid amplification testing or assay for Shiga toxin in stool; stool culture should always be obtained for strain identification and outbreak tracing. Treatment is generally supportive (eg, aggressive fluid administration), and antibiotics should be avoided due to the increased risk for hemolytic uremic syndrome.
A 46-year-old man comes to the office due to bilateral ankle and facial swelling, especially prominent in the periorbital area. He has no shortness of breath, fever, or changes in urine color. The patient does not use tobacco, alcohol, or illicit drugs. He has no significant medical history and takes no medications. His temperature is 37.1 C (99 F), blood pressure is 130/70 mm Hg, pulse is 78/min, and respirations are 14/min. Examination shows bilateral 1+ pitting ankle edema. Auscultation shows clear lungs, normal heart sounds, and no murmurs. Dipstick urinalysis is positive for protein. A 24-hour urine collection shows proteinuria of 4.6 g/day. Laboratory results are as follows:
Total serum calcium 7.5 mg/dL
Albumin 2.2 g/dL
Phosphorus 3.5 mg/dL
Magnesium 2.2 mg/dL
Creatinine 0.8 mg/dL
Which of the following is the most likely cause of this patient’s low serum calcium level?
A.Decreased 1-alpha-hydroxylation of 25-OH vitamin D
B.Decreased 25-hydroxylation of vitamin D
C.Decreased levels of parathyroid hormone
D.Decreased serum albumin
E.Normal levels of parathyroid hormone with impaired action at target organs.
Assessing the clinical significance of hypocalcemia detected in a common serum metabolic panel requires correction for the serum albumin concentration. The serum calcium concentration decreases by 0.8 mg/dL for every 1 g/dL decrease in serum albumin; the corrected calcium level can be calculated using the following formula:
Corrected calcium = (measured total calcium) + 0.8 × (4.0 g/dL − serum albumin in g/dL)
This patient with nephrotic syndrome (heavy proteinuria, hypoalbuminemia, edema) has a corrected calcium of 8.94 mg/dL ([7.5 mg/dL] + 0.8 × [4 g/dL − 2.2 g/dL]). The hypocalcemia is most likely due to hypoalbuminemia (from nephrotic-range proteinuria) and is not clinically significant. Direct measurement of ionized calcium is performed in many clinical laboratories, but it requires special handling and may not be readily available.
A 50-year-old man comes to the emergency department due to sudden-onset severe, colicky pain in the right flank. The patient had a similar episode 3 years ago; it resolved a few days later after he passed “gravel” in his urine. He has no other medical conditions and no history of urinary infections. The patient usually eats precooked food from a local store and has a soda with each meal. Vital signs are stable. He is given intravenous fluids and pain medication. Laboratory results are as follows:
Hemoglobin 14.5 g/dL
Leukocytes 13,000/mm3; no bands
Platelets 300,000/mm3
Blood urea nitrogen 16 mg/dL
Creatinine 0.8 mg/dL
CT scan of the abdomen without contrast reveals renal calculi. Urinalysis shows moderate levels of blood and calcium oxalate crystals. Which of the following dietary changes is most likely to decrease this patient’s risk for recurrence of similar symptoms?
A.Decreased calcium
B.Decreased potassium
C.Decreased sodium
D.High animal protein
E.High oxalate
Dietary interventions
All calcium stones:
↑ Fluid (produce >2 L/day urine) - ↑ Urine flow, ↓ solute concentration
↓ Sodium (<2,300 mg/day) - ↑ Renal calcium reabsorption
↑ Citrate (fruits & vegetables) - Binds urinary calcium to inhibit stone formation
↑ Potassium - ↑ Urinary citrate excretion
↓ Animal protein - ↓ Urinary calcium excretion
Calcium oxalate stones:
Adequate calcium intake (1,200 mg/day) - ↓ Oxalate absorption in GI tract
↓ Oxalate (spinach) - ↓ Urinary oxalate excretion
Pharmacologic
interventions
Thiazide diuretics - ↑ Renal calcium reabsorption
Potassium citrate - ↑ Urinary citrate concentration
A 36-year-old woman comes to the office after a month of almost daily, bandlike headaches, dizziness, and fatigue. She has experienced irritability, inability to concentrate, and poor sleep of the same duration. Prior to the onset, she had an accident at work; a box fell on her head, and she lost consciousness briefly. The patient was taken to an emergency department and all tests were normal, so she was discharged. She has had no nightmares or flashbacks of the event. She has no known medical problems. She drinks 1-2 glasses of wine every evening but does not use tobacco or illicit drugs. The patient is afebrile. Blood pressure is 125/85 mm Hg and pulse is 76/min. Cardiopulmonary and abdominal examinations are unremarkable. She appears anxious but her neurologic evaluation including attention and memory is normal. Which of the following is the most likely diagnosis?
A.Acute stress disorder
B.Delayed subdural hematoma
C.Factitious disorder
D.Korsakoff syndrome
E.Postconcussive syndrome
F.Post-traumatic stress disorder
G.Somatic symptom disorder
This patient is showing signs of postconcussive syndrome following a mild traumatic brain injury (TBI). TBI of any severity can lead to (a few hours or days later) postconcussive syndrome, which is clinically described by the following constellation of symptoms: headache, confusion, amnesia, difficulty concentrating or with multitasking, vertigo, mood alteration, sleep disturbance, and anxiety. Typically, these symptoms resolve with symptomatic treatment within a few weeks to months following TBI; however, some patients may have persistent symptoms lasting >6 months.
(Choice A) Acute stress disorder develops following exposure to threatened death, serious injury, or sexual violation and is characterized by intrusive memories, nightmares, flashbacks, avoidance, and arousal symptoms (eg, hypervigilance, insomnia, irritability, poor concentration). Symptoms last 3 days to 1 month. Although acute stress disorder symptoms overlap with those of TBI, the type of trauma, prominent physical symptoms, and lack of nightmares or flashbacks in this patient make TBI more likely.
hepatic hydrothorax,
Patients with cirrhosis and portal hypertension frequently have abdominal ascites and peripheral edema due to low albumin levels and abnormal extracellular fluid volume regulation. A small number of these patients may also develop hepatic hydrothorax, a pleural effusion not due to underlying cardiac or pulmonary abnormalities.
Hepatic hydrothorax generally results in transudative pleural effusions and is thought to occur due to small defects in the diaphragm. These defects permit peritoneal fluid to pass into the pleural space, which occurs much more commonly on the right side due to the less muscular hemidiaphragm. Patients have dyspnea, cough, pleuritic chest pain, and hypoxemia. Diagnosis involves documentation of the effusion (eg, chest x-ray) and testing to exclude other causes (eg, thoracentesis, echocardiogram).
Treatment involves salt restriction and diuretic administration. Therapeutic thoracentesis could be attempted in patients with prominent symptoms. Chest tube placement should be avoided as it can result in large-volume protein, fluid, and electrolyte losses as well as other severe complications (eg, renal failure). The definitive option for treatment is liver transplantation, although this may not be appropriate for all patients depending on other factors.
pancreatitis
Didanosine, glucocorticoids, alcohol, valproate, azathioprine, diuretics (eg, furosemide, HCTZ)
Modifiable risk factors for TIA & ischemic stroke
Risk factor
Estimated attributable risk
Hypertension 4×
Smoking 2.5×
Diabetes mellitus 2×
Hypercholesterolemia ≤2×
Alcohol intake
Variable/inconsistent effect
Sedentary lifestyle, obesity
Small effect
Diagnosis of brain death
Clinical criteria
Known cause (eg, TBI, stroke)
Evidence (eg, clinical, neuroimaging) of devastating CNS event
Exclusion of confounding conditions (eg, electrolyte abnormality, intoxication, paralytics)
Core temperature >36 C (96.8 F), SBP >100 mm Hg
Clinical examination
Coma
Absent brainstem reflexes:
Pupillary
Corneal
Oculocephalic, oculovestibular
Jaw jerk
Cough
Gag
Absent brain-originating* motor responses (including decerebrate & decorticate posturing)
Apnea test: no respiratory response to PaCO2 >60 mm Hg
Treatment of ankylosing spondylitis
Nonpharmacologic measures
Exercise (postural exercises, ROM/stretching exercises)
Physical therapy
Initial treatment
NSAIDs (eg, ibuprofen, naproxen)
COX-2 inhibitors (eg, celecoxib)
Treatment failure/disease progression
TNF-α inhibitors (eg, etanercept, infliximab)
Anti–IL-17 antibodies (eg, secukinumab)
A 23-year-old man is brought to the emergency department by ambulance due to a seizure. According to a witness, the patient fell on the sidewalk while leaving a pub and had rhythmic movements of the extremities for about 2 minutes. He has no history of seizures. In the emergency department, the patient is lethargic and confused but follows simple commands. Temperature is 37.3 C (99.1 F), blood pressure is 122/70 mm Hg, and pulse is 97/min. The pupils are equal and reactive to light. He moves all extremities, and deep tendon reflexes are symmetric. Complete blood count, serum electrolytes, and ECG are normal. A urine toxicology screen is ordered. What is the most appropriate next step in management of this patient?
A.CT scan of the head with contrast
B.CT scan of the head without contrast
C.Electroencephalography
D.Intravenous phenytoin infusion
E.Lumbar puncture
First-time seizure in adults
Etiology
Metabolic (eg, hypoglycemia, electrolyte disorders)
Toxic (eg, substance use/withdrawal, medications)
Acute brain injury (eg, hemorrhage, meningoencephalitis, stroke)
Structural (eg, temporal sclerosis, dysplasia, tumor)
Idiopathic/unknown (eg, juvenile myoclonic epilepsy)
Evaluation
Laboratory: glucose, complete blood count, electrolytes, renal function, liver function, ± urine drug screen
Neuroimaging: CT scan (for acute injury; faster) or MRI (for smaller lesions; more time-consuming)
± Lumbar puncture (for fever or nuchal rigidity)
EEG
Indication to start antiepileptic medications
Abnormal EEG or neuroimaging
Nocturnal seizure
Focal neurologic examination
