1-50 Flashcards
Pleuritic chest pain
She denies fever, vomiting, abdominal pain, wheezing, and trauma. She reports shortness of breath, but mainly because her chest hurts when she takes a deep breath. workup to include an electrocardiogram, laboratory tests including a troponin, and chest radiograph. Patient is pulmonary embolism rule-out criteria (PERC) negative. Her studies are all within normal limits. examination is unremarkable except for left-sided chest wall tenderness.
Conditions that may cause pleuritic chest pain include
pulmonary embolism, pericarditis, pneumonia, myocardial infarction, pleural effusion, and pneumothorax. There is no specific diagnostic tool to diagnose pleurisy other than ruling out more serious conditions. Other causes of pleurisy can be industrial exposures such as asbestos or some medications, as well as rheumatological diseases, such as lupus or rheumatoid arthritis.
drugs are the recommended initial therapy of pleuritic chest pain.
Nonsteroidal anti-inflammatory drugs ; studies on their use have been limited to indomethacin. Therefore, the recommended treatment for pleuritic pain is indomethacin.
when should you give Azithromycin in the context of pleuritic chest pain
only be indicated if pneumonia or bacterial bronchitis is suspected.
when should you give Colchicine in the context of pleuritic chest pain
Colchicine (B) is the recommended therapy for familial Mediterranean fever, a genetic condition that causes pleuritic chest pain.
hallmarks of elapid (cobra, coral snake, mamba, and krait) envenomation
Blurred vision, paresthesia, ptosis, and general or respiratory paralysis (A)
the hallmark of brown recluse spider envenomation. This venom contains multiple cytotoxic components. The brown recluse bite is typically painless or associated with a mild stinging sensation, followed by blistering and ulceration over the next 8–12 hours. Over the next 1–3 days, the bite site typically increases in diameter and ulcerates further, sometimes becoming necrotic.
Dermatonecrosis
Severe pain that may be migratory and muscular rigidity (E) is common in
black widow spider envenomation, typically characterized by a sharp pinprick followed by a small puncture wound or wheal associated with a halo. The venom causes presynaptic calcium modulation and subsequent neurotransmitter release, subsequently causing exocytosis of dopamine, acetylcholine, glutamate, GABA, and norepinephrine. This results in pain (which may migrate proximally) and muscle cramping and rigidity that can be mistaken for an acute abdomen.
Most North American venomous snakes can be classified as either
crotalids or elapids.
Snakes
Viperidae
Depression between eyes
Significant local reaction → systemic toxicity
Compartment syndrome
Thrombocytopenia
Antivenom
Snakes
Elapidae
Red on yellow kill a fellow, red on black venom lack
Minimal local reaction → neurotoxicity
Respiratory paralysis
Due to scarcity of antivenom in US, give for symptomatic eastern coral snake bites, otherwise supportive treatment
A 65-year-old woman presents with back pain. She states that she slipped and fell on her back 2 days ago and reports shooting pains down both of her legs. The pain has been significant and worsening over the last 2 days. She is also experiencing increasing weakness in her legs and requires assistance to get into the room today. She has a history of diabetes mellitus, hypertension, and chronic back pain. Vital signs are within normal limits. On examination, the patient has diminished deep tendon reflexes. There is diminished sensation in the bilateral lower extremities and a palpable bladder.
Cauda equina syndrome
Etiologies Cauda equina syndrome
most commonly herniated discs, bone fragments, hematomas, epidural abscesses, tumors, or vascular insufficiency. A history of a recent spinal procedure, trauma, anticoagulation, intravenous drug use, and malignancy are all important risk factors.
Clinical features Cauda equina syndrome
; Acute onset of lower back pain with weakness and numbness ; include saddle anesthesia, motor and sensory deficits in the lower extremities, sciatica, decreased lower extremity reflexes, decreased anal sphincter tone, and bowel or bladder dysfunction. Urinary retention is the most consistent finding with a sensitivity of 90%.
Patients with a suspicious history and physical concerning for cauda equina syndrome require
emergency MRI. Treatment is surgical, and an emergent consultation with a spine surgeon is required.
If this patient had bacterial meningitis,
his cerebrospinal fluid results would show greater than 1,000–2,000 white blood cells/microliter, a high protein greater than 250 mg/dL, and low glucose at less than 45 g/dL.
West Nile Virus
Mosquitos
Summer and fall
Flulike Sx, URI Sx, rash
Complication: meningoencephalitis
uncomplicated candidal vaginitis
complaining of vaginal itching and irritation. She also complains of vaginal discharge.
Risk factors: diabetes, HIV, recent antibiotic use, steroid use, pregnancy, immunosuppression
Sx: vulvar pruritus, dysuria, dyspareunia
PE: white, cottage cheese-like discharge
Labs: normal pH < 4.5, wet prep: budding yeast, pseudohyphae, hyphae
Most commonly caused by Candida albicans
Tx: topical azoles, oral fluconazole
either bacterial vaginosis or Trichomonas vaginitis, not candidal vaginitis.
A positive amine odor with KOH preparation (B)
Visualizing mobile trichomonads on microscopic examination (C) is consistent with a diagnosis of Trichomonas vaginitis.
Migraine Headache
risk factors
treatments
symptoms
While migraines are no longer felt to be secondary to vasodilation, sumatriptan, which promotes vasoconstriction through vasoactive peptides, have proven benefit in randomized controlled trials. Sumatriptan is often given subcutaneously at a dose of 6 mg, but can be given orally or intranasally.
Migraine Headache
Risk factors: female sex, family history
Gradual onset, unilateral > bilateral, throbbing, pulsating headache
Without aura: most common, nausea or vomiting, photophobia, phonophobia
Aura: scotoma, flashing lights, sounds
Diagnosis is made clinically
Treatment
Abortive Rx: triptans, DHE, antiemetics, NSAIDs
Prophylaxis: TCAs, beta-blockers, anticonvulsants (valproic acid, topiramate), CCBs
Triptans, DHE: contraindicated in HTN or CV disease
Migraines themselves do not require neuroimaging, however, imaging should be considered when they are associated with other red flags such as
sudden onset of pain or new onset of headaches after 50 years of age
triptans should generally be avoided in conditions where
vasoconstriction could be harmful, including patients with histories of uncontrolled hypertension, ischemic stroke, coronary artery disease, and vasospastic angina. It is also generally avoided in pregnancy, though can be used as second-line therapy.
Aortic Dissection
risk factors
symptoms
diagnosis
treatment
which medications exactly>
Aortic Dissection
Risk factors: advancing age, male sex, HTN, Marfan syndrome
Sx: acute onset of “ripping” or “tearing” chest pain or back pain
PE: asymmetric pulses or SBP difference of > 20 mmHg
CXR: widened mediastinum
Dx: CT angiography or transesophageal echocardiogram (TEE)
Treatment: reduce BP and HR (beta-blockers), pain control, emergency surgery (Type A dissection)
Short-acting intravenous beta-blockers such as esmolol are ideal for this indication and form the cornerstone of initial aortic dissection management. Afterload reducing agents such as sodium nitroprusside or nicardipine can then be added to achieve further blood pressure control with a systolic blood pressure target < 120 mm Hg by 30 min. Labetalol, which has both alpha- and beta-blocking activity, can be used for this purpose as monotherapy.
Type A: involves ascending aorta
Type B: involves only descending aorta
Asymmetric pulses in the upper extremity will occur only if which artery is involved in an aortic dissection?
Subclavian artery.
The initial management for aortic dissection, regardless of type, is
blood pressure control. Because propagation depends on the degree of hypertension and the intensity of left ventricular ejection force, therapy must be aimed at both lowering blood pressure and slowing the rate of pressure rise (dP/dT).
is a compensatory mechanism in response to a drop in body temperature. It is a common complication associated with targeted temperature management and can inhibit induction of hypothermia.
Shivering
how to stop or prevent Shivering
Nonpharmacologic interventions, such as focal warming of the face, hands, and feet, as well as inhaled heat or humidified air can be used in conjunction with anti-shivering medications.
First-line pharmacotherapies that should be given to prevent shivering include acetaminophen, magnesium sulfate, and buspirone, a 5-hydroxytryptamine (5-HT) agonist that lowers the shivering threshold with only minimal sedative effects.
is an alpha-2 receptor agonist that provides anxiolysis and moderate sedation. It is considered a second-line treatment and can be combined with opioids if buspirone fails to control shivering.
Dexmedetomidine q
Benzodiazepines such as midazolam (C) have been associated with
prolonged mechanical ventilation
What effect can hypothermia have on the heart rate?
Bradycardia
initial steps in the management of postextraction bleeding
infiltration of lidocaine with epinephrine and biting on gauze for 30 minutes
initial management typically involves holding direct pressure on the site of bleeding. Local anesthetic (e.g., lidocaine or bupivacaine) with epinephrine can be administered to help with pain control if the patient cannot tolerate direct pressure on the wound site and can often stop the bleeding due to the vasoconstrictive effects of epinephrine.
This patient did not respond to the initial steps in the management of postextraction bleeding, and the most appropriate next intervention is to
pack the socket with an absorbable dressing and suture it in place.
Prothrombin complex concentrate (A) would be indicated to reverse the patient’s anticoagulation with warfarin only if
all other interventions have proven unsuccessful.
What is the therapeutic range for the INR in a patient with a mechanical heart valve?
2.5–3.5 therapeutic range for which patients?
What laboratory abnormalities should be expected in jaundice secondary to pyloric stenosis?
Hypokalemic, hypochloremic metabolic alkalosis.
Physiologic jaundice is typically seen within
two to three days of birth, and manifestation in a 10-day-old neonate, is not consistent with a diagnosis of physiologic jaundice.
Physiologic jaundice (D) results from
physiologic hemolysis of fetal hemoglobin following birth, leading to the accumulation of unconjugated bilirubin in the blood.
Breast milk jaundice is seen in breastfeeding neonates with which age? and the reason of this condition?
1 week of age and older. It is thought to be due to the presence of glucuronyl transferase inhibiting substances in breast milk, resulting in the buildup of unconjugated bilirubin in the blood and thus jaundice.
what happens to the childeren with Breast milk jaundice? and their appearing?
Neonates with breast milk jaundice are well appearing and gain weight appropriately.
what would you see in the lab in childeren with Breast milk jaundice
Laboratory workup will show elevated unconjugated bilirubin.
Increased conjugated bilirubin or other metabolic abnormalities should prompt a search for an alternative diagnosis, as these laboratory findings are not consistent with breast milk jaundice.
treatment for Breast milk jaundice? would you need phototherapy?
observation, though severe hyperbilirubinemia may require phototherapy. Hyperbilirubinemia associated with breast milk jaundice is not typically associated with the development of kernicterus.
charac breastfeeding failure jaundice? etiology? treatment? symptoms kind? stop breastfeeding?
seen in exclusively breastfed infants.
It results from inadequate milk production in a breastfeeding mom or difficulty breastfeeding an infant, leading to nutritional deficiency, weight loss, and dehydration in the infant.
Babies with breastfeeding failure jaundice are typically underweight and appear dehydrated.
Continuation of breastfeeding should be encouraged if possible. Lactation counseling and formula supplementation are the treatments of choice.
Where is the neurovascular bundle for each rib located?
Inferior to the rib.
flail chest: PE? etio? treatment?
History of chest wall blunt trauma
PE will show the pathognomonic paradoxical inward movement of the broken chest wall segment during inspiration and outward movement during expiration
Most commonly caused by three or more adjacent ribs fractured at two different points
Treatment is supportive care, avoid chest wrapping, intubation if necessary
Early intubation with positive pressure ventilation reduces mortality compared to delaying until respiratory failure ensues.
Indications for early ventilatory support (name 6)
shock, severe head injury, comorbid pulmonary disease, eight or more rib fractures, age >65 years, associated injuries, or arterial partial pressure of oxygen <80 mm Hg despite supplemental oxygen.
lyme disease stages?
what is most likely the cause of the rash in this patient? A 24-year-old man presents to the ED after a syncopal episode. He is an avid hiker. He had a rash a few weeks prior that has since cleared. Vital signs are a BP of 100/74 mm Hg, HR of 50 bpm, RR of 18/min, and T of 99.1°F.
Lyme disease
when does Acute disseminated Lyme disease occur?
approximately 4 weeks after initial infection and can include meningoencephalitis, Bell palsy (which may be bilateral), or carditis which often manifests with variable atrioventricular (AV) block.
which cardiac manifestation is associated with lyme disease and how does it resolve?
This AV blockade may be high-grade and require temporary transcutaneous or transvenous pacing, but it nearly universally resolves gradually with IV antibiotics and has a favorable prognosis with no need for permanent pacemaker placement.
when does late lyme disease occur? manifestiatons?
Late Lyme disease develops greater than 1 year after initial infection and includes chronic arthritis with or without chronic subtle encephalopathy. Only 50% of patients remember a tick bite, so diagnosis may be difficult.
how to diagnose lyme disease?
Erythema migrans is diagnostic, but not all patients present with this finding. Initial screening involves enzyme-linked immunosorbent assay (ELISA) testing with Western blot and PCR to confirm the diagnosis. If the diagnosis is suspected, empiric treatment should be administered.
what is the treatment for lyme disease?
Treatment for early Lyme disease and mild acute disseminated Lyme disease is doxycycline for 3–4 weeks. In pregnant women or children under the age of 8 years who require > 21 days of treatment, amoxicillin should be substituted. Patients with neurologic or cardiac manifestations should be admitted and treated with IV ceftriaxone.
summarize stages lyme disease?
Presentation
Stage 1: erythema migrans (pathognomonic), viral-like syndrome (fever, fatigue, malaise, myalgia, headache)
Stage 2: myocarditis, bilateral Bell palsy
Stage 3: chronic arthritis, chronic encephalopathy
history lyme disease?
History of being in the woods, hiking, or camping
PE will show slightly raised red lesion with central clearing, erythema migrans (bull’s-eye) rash
Bilateral facial nerve palsy is virtually pathognomonic for Lyme disease
