The airway to heaven (Pulmonary Critical Care Medicine)
Name at least 1 of the 4 terrible T's of anterior mediastinal masses
1. Thyroid (substernal goiter)
2. Thymic Neoplasm/Thymoma
3. Teratoma
4. "Terrible" lymphoma
Reference:
First Aid 2020 - Respiratory Section
This antimicrobial agent, which provides prophylaxis against Pneumocystis jirovecii pneumonia, should be initiated in all HIV patients when the CD4 count falls below 200 cells/µL.
What is trimethoprim-sulfamethoxazole (TMP-SMX / Bactrim)?
Pneumocystis pneumonia (PCP), a diffuse interstitial pneumonia caused by Yeast-like fungus (originally classified as protozoan). Most infections are asymptomatic. Immunosuppression (eg, AIDS) predisposes to disease. Diffuse, bilateral ground-glass opacities on chest imaging, with pneumatoceles (cystic lung).
Diagnosed by bronchoalveolar lavage or lung biopsy. Disc-shaped yeast seen on methenamine silver stain of lung tissue or with fluorescent antibody.
Treatment/prophylaxis: TMP-SMX, pentamidine, dapsone (prophylaxis as single agent, or treatment in combination with TMP), atovaquone. Start prophylaxis when CD4+ count drops to < 200 cells/mm3 in HIV patients.
Reference:
First Aid - Microbiology section
Teaching points:
1. Bactrim also covers toxoplasma (if CD4 <100).
2. Other lab tests that may suggest PCP
2a. Positive 1,3-ß-D-glucan/Fungitell assay
2b. ↑ PCP PCR
2c. ↑ Lactate dehydrogenase (LDH)
Patient who has underlying type II diabetes, presents to the ED with confusion. These are the following lab values:
1. Glucose >600mg/dL
2. Bicarb >18 mEq//L
3. Normal anion gap
4. Negative or small serum ketones
5. Serum osmolality >320 mOsm/kg
6. Normal pH
Name the diagnosis
"What is HHS (hyperosmolar hyperglycemic state) and fluid resuscitation?"
This patient has clinical features of diabetic Hyperosmolar Hyperglycemic State (HHS) is a life-threatening diabetic emergency, characterized by marked hyperglycemia (sometimes with blood glucose levels ≥600 mg/dL), hyperosmolality ≥320 mOsm/kg, and absence of significant ketoacidosis. In patients with HHS like DKA, there is significant hyperosmolar diuresis that results in significant volume depletion. Starting insulin therapy before appropriate fluid resuscitation (especially in a hypotensive patient) may shift remaining glucose (with water following solutes via osmosis) may result in catastrophic hemodynamic changes resulting in worsening intravascular volume depletion. Thus initial management requires initial treatment with aggressive intravenous fluid resuscitation before insulin therapy is initiated.
Reference:
First Aid - Endocrinology section
Teaching points:
1. Fluid resuscitation first due to hyperosmolar diuresis
2. Replace electrolytes if with derangements
3. Treat with insulin
What is the preferred first-line treatment for acute gout flares in patients with end stage kidney disease (ESKD)?
What are glucocorticoids (oral, intravenous, or intra-articular)?
In patients with end-stage kidney disease or severe renal impairment (eGFR 30 mL/min), glucocorticoids are preferred over colchicine for acute gout flares. Colchicine is renally cleared and has a narrow therapeutic window, with significant risk of life-threatening toxicity including neuromuscular toxicity, rhabdomyolysis, and myelosuppression in patients with severe kidney disease. The FDA recommends reducing colchicine to a single 0.6 mg dose for gout flares in dialysis patients, with treatment courses no more than once every two weeks. Short courses of glucocorticoids (e.g., prednisone 30 mg daily for 3-5 days) provide effective anti-inflammatory treatment with a better safety profile in this population.
Name at least 1 of the 3 types of Ischemic Stroke.
1. Thrombotic (ruptured atherosclerotic plaque) - most commonly MCA
2. Embolic (embolus from another part of the body) - examples: atrial fibrillation, carotid artery stenosis, DVT with patent foramen ovale, infective endocarditis
3. Hypoxic - due to hypoperfusion or hypoxemia. Common during cardiovascular surgeries, tends to affect watershed areas
Treatment: tPA (if within 3-4.5 hr of onset) and no hemorrhage/risk of hemorrhage and/or thrombectomy (if large artery occlusion). Reduce risk with medical therapy (e.g. aspirin, clopidogrel); control BP, blood glucose, lipids, smoking cessation, treat conditions that ↑ risk (atrial fibrillation, carotid artery stenosis, PFO, etc)
Reference:
First Aid- Neurology
The American Heart Association recommends maintaining blood pressure below 185/110 mm Hg before initiating reperfusion therapy and maintaining this blood pressure below 180/105 mm Hg after treatment.
2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association - **NEWEST UPDATE**. If presence of salvageable tissue (penumbra) - the guidelines provide support for extended window thrombolysis for select patients with stroke of unknown onset or 4.5–9 hours from onset using advanced imaging criteria (eg, diffusion weighted imaging-fluid attenuated recovery or perfusion-based mismatch).
This type of hypersensitivity reaction, mediated by IgE antibodies and mast cells, is responsible for the immediate bronchoconstriction and airway inflammation seen in allergic asthma.
What is Type I hypersensitivity?
Allergic asthma is characterized by a Type I (immediate) hypersensitivity reaction. This involves allergen-specific IgE antibodies bound to mast cells, which become activated upon allergen reexposure, leading to degranulation and release of inflammatory mediators including histamine, leukotrienes, and prostaglandins. This IgE-mediated mechanism triggers both the early asthmatic response (within 30 minutes) and contributes to the late-phase response (3-12 hours later), ultimately resulting in eosinophilic inflammation, bronchospasm, and airway hyperresponsiveness.
Reference for Type 1 Hypersensitivity:
First Aid - Respiratory section
IM Resident Clinical Teaching points:
1. Asthma is an obstructive lung disease with reversible bronchoconstriction.
2. The postbronchodilator cutoff for asthma in adults is an increase in FEV₁ of ≥12% AND ≥200 mL from baseline. Both criteria must be met for a positive bronchodilator response.
3. Per GINA Guidelines: ICS-Formoterol is first line and preferred therapy for both reliever (rescue) or maintenance-and-reliever therapy (MART). - Landmark trial: Sygma trial
4. As a Type 1 Hypersensitivity reaction, inhaled corticosteroids are first-line therapy because they target multiple inflammatory pathways that reduces eosinophils (via apoptosis), inhibits mast cell/T-lymphocyte/macrophage/neutrophil inflammatory/cytokine production that contributes to long-term lung damage, decreases airway hyperresponsiveness/structural remodeling
What are causes for false positive results on Venereal Disease Research Laboratory (VDRL)?
Name at least one cause, (First Aid lists five; >9 common causes).
VDRL detects nonspecific antibody that reacts with beef cardiolipin. Quantitative, inexpensive, and widely available test for syphilis (sensitive but not specific).
False-Positive results on VDRL with:
1. Pregnancy
2. Recent Viral infection (eg, EBV, hepatitis, HIV, Rheumatic fever)
3. Drugs (eg, chlorpromazine, procainamide)
4. Rheumatic fever (rare)
5. Lupus and leprosy
Other false-positives:
6. Rheumatoid arthritis
7. Anti-phospholipid syndrome (evaluation for cardiolipin ab is one of the diagnostic tests)
8. Really old age (65+)
9. Liver disease
List 3 electrolyte abnormalities seen in refeeding syndrome.
"What is hypophosphatemia, hypokalemia, and hypomagnesemia?"
These electrolyte disturbances are caused by insulin. When glucose is supplied during nutritional therapy in severely malnourished patients, insulin levels increase, triggering an intracellular shift of phosphate, potassium, and magnesium from the blood. This hormonal response decreases serum concentrations of these critical electrolytes, leading to hypophosphatemia and the clinical manifestations of refeeding syndrome including edema, cardiac failure (tachycardia), and respiratory failure (tachypnea).
Insulin drives phosphate, potassium, and magnesium intracellularly from the blood, leading to severe electrolyte depletion, edema, and potential cardiac and respiratory failure—a process that can be prevented by cautious initial caloric provision (starting at lower rates) and careful electrolyte monitoring during the first 4 to 7 days of nutritional therapy.
Reference:
First Aid - Endocrinology
Teaching points:
1. Complications of refeeding may include cardiac complications - edema, arrhythmias, rhabdomyolysis, seizures
What is a rare complication of untreated rheumatoid arthritis characterized by the triad of neutropenia, splenomegaly, and severe joint destruction?
What is Felty Syndrome?
Felty syndrome represents a rare but serious extra-articular manifestation of rheumatoid arthritis, occurring in less than 1% of RA patients. The syndrome is classically defined by the triad of rheumatoid arthritis, neutropenia, and splenomegaly, first described by Augustus Roi Felty in 1924.
The main clinical concern is recurrent bacterial infections due to severe neutropenia, which can lead to increased mortality. Patients typically present with severe destructive arthritis contrasting with moderate or absent joint inflammation, along with a high frequency of extra-articular manifestations including rheumatoid nodules, vasculitis, and leg ulcers. The prognosis is generally poor, with sepsis being a predominant cause of death.
Reference:
First Aid talks about Felty Syndrome under Musculoskeletal, Skin, and connective tissue
This transient postictal phenomenon—characterized by flaccid or spastic weakness lasting minutes to hours after a focal or generalized seizure. What am I?
"What is Todd's paralysis (or Todd's paresis)?"
Todd's paralysis represents a negative neurologic symptom that helps lateralize the seizure focus to the contralateral hemisphere in over 90% of cases. The clinical presentation is often heterogenous (weakness can be flaccid, spastic or even normal tone! with variable reflexes: increased, decreased, or normal). This variability occurs due to temporal cortical dysfunction and not a fixed upper motor neuron/lower motor neuron lesion.
The weakness lateralizes to the left hemisphere (contralateral to the deficit) with high reliability—Todd's paralysis occurs contralateral to the epileptogenic hemisphere in 93% of cases.
Duration: 30 minutes - 36 hours (mean 15 hours). Though rare cases lasting upwards of 3 months have been reported.
Risk Factors: Older age, prior stroke, underlying structural brain lesions, status epilepticus
Critical differential diagnosis: Distinguishing Todd's paralysis from acute stroke can be challenging. When postictal deficits persist beyond 1 hour, consider 30-minute EEG—if the 2HELPS2B score is >1, extended continuous EEG monitoring is warranted to exclude nonconvulsive status epilepticus, which occurs in 23% of cases with prolonged postictal deficits.
Negative symptoms (loss of function) in Todd's Paralysis includes: Weakness or paralysis (most common—present in all cases), Sensory loss (rare—only 7% of cases), Aphasia (36% of cases, always associated with underlying lesions), Gaze palsy (29% of cases).
These negative symptoms reflect temporary loss of parenchymal function following seizure-induced neuronal exhaustion or excessive inhibition, not structural damage to upper or lower motor neurons.
Positive symptoms (abnormal function) would suggest ongoing seizure activity rather than Todd's paralysis: Rhythmic jerking or twitching, Abnormal posturing, Myoclonus.
STEP2CK Concept.
Name at least two causes of this bronchiectasis defined by irreversible airway dilation, productive cough, and recurrent respiratory infections.
Acceptable answers:
A. Cystic fibrosis, Post-infectious, Allergic Bronchopulmonary Aspergillosis (ABPA), immunodeficiency/CVID, Aspiration, Nontuberculous mycobacteria (NTM) infection
B. Idiopathic
C. Primary ciliary dyskinesia (Kartagener syndrome is a subset)
D. COPD
E. Connective tissue disease/Rheumatoid arthritis
Reference: First Aid - Respiratory Section
ABIM/IM Clinical Teaching Pearls:
1. Treat underlying cause (e.g. infection - abx)
2. Mainstay therapy for bronchiectasis is airway clearance. Antitussives is counterproductive to this. (2025 European Respiratory Society - Strong Recommendation; First Line Therapy recommended by ATS)
3. Huff coughing (slow complete inhalation, 5-second breath hold, mouth shape in "O" (fogging mirror), forceful exhalation producing a huff sound)
4. Chest Physiotherapy/Handheld devices
5. Handheld positive expiratory pressure devices (flutter valve, acapella, etc)
6. Inhaled nebulized bronchodilators to prevent spasms, nebulized hypertonic saline to loosen secretions
7. Pulmonary Rehab
8. Long-term macrolide therapy for patients with ≥3 exacerbations per year, the ERS issues a strong recommendation for long-term macrolide treatment. (Azithromycin 250 mg qd or 500 mg qMWF)
This syndrome is characterized by paradoxical worsening of clinical symptoms due to restoration of pathogen-specific immune responses after initiating antiretroviral therapy in HIV-infected patients.
"What is Immune Reconstitution Inflammatory Syndrome (IRIS)."
IRIS manifests in two distinct patterns: paradoxical IRIS (worsening of a known, treated infection) and unmasking IRIS (new presentation of a previously subclinical infection). The most common triggering pathogens include mycobacteria (tuberculosis and M. avium complex), fungi (Cryptococcus neoformans and Pneumocystis jirovecii), and viruses (cytomegalovirus, herpes simplex, varicella-zoster).
Risk factors include CD4 count <50-100 cells/mm³, high HIV viral load, high pathogen burden, and short interval (<30 days) between treatment of opportunistic infection and ART initiation. [2-3][6] The overall incidence is approximately 16% in HIV patients starting ART, with most cases being self-limited. [1] Mortality is generally low (4.5%) except for cryptococcal meningitis-associated IRIS (20.8% mortality).
Management involves continuing ART without interruption in most cases, optimizing treatment for the underlying infection, and considering adjunctive corticosteroids for severe manifestations.
Name at least 2 causes of "Syndrome of Inappropriate antidiuretic hormone secretion" (SIADH)
1. Ectopic ADH (small cell lung cancer) - 24% of cases
2. CNS disorders/head trauma - 9% of cases
3. Pulmonary disease (e.g. Pneumonia, COPD exacerbation) -11% of cases
4. Drugs (SSRI, carbamazepine, cyclophosphamide, haloperidol, chlorpropamide) - 18% of cases
5. NSAIDs (enhances AVP)
6. Opiates, MDMA (Ecstasy), Platinum-compounds, vincristine (stimulates AVP release)
7. Pain-related, exercise-relate
8. Idiopathic
(First Aid lists the first 4.)
Which bowel-related diseases are most associated with spondyloarthritis? (Name 2)
1. Crohn's disease
2. Ulcerative colitis
Ankylosing spondylitis is a chronic inflammatory disease primarily affecting the sacroiliac joints and spine, characterized by inflammatory back pain, progressive spinal stiffness, and potential ankylosis. It represents the radiographic subset of axial spondyloarthritis, distinguished by definite structural damage visible on pelvic radiographs.
Axial (Latin "axis") - central axis of body, specifically spine/sacroiliac joints
Spondylo (Greek "spondylos") - vertebra/spine
Arthritis (Greek "arthron") - inflammation of the joints
Axial spondyloarthritis has somewhat replaced the older term ankylosing spondylitis to better capture early disease stages before ankylosis (fusion) occurs, reflecting the understanding that inflammation precedes structural damage and that early detection through MRI allows for earlier diagnosis and treatment.
Reference: First Aid - Musculoskeletal, skin, connective tissue
This classic encephalitic disease has two pathognomonic clinical features of hydrophobia and aerophobia and carries significant morbidity and mortality with an average survival from clinical onset to death being approximately 5-7 days without intensive care support.
Name the encephalitic disease
"What is rabies?"
Hydrophobia & Aerophobia - pharyngeal/laryngeal spasms triggered by attempts to swallow water (and sometimes even the sight, sound, perception of water) = hydrophobia, and air drafts respectively = aerophobia?
Progression of disease: fever, malaise → agitation, photophobia, hydrophobia, hypersalivation → paralysis, coma → death.
Reference:
First Aid - Microbiology/Virology
Furious rabies is the encephalitic form of rabies, accounting for approximately 80% of human cases, characterized by hyperactivity, fluctuating consciousness, and episodes of agitation alternating with lucidity. The hallmark features are hydrophobia and aerophobia—pathognomonic phobic pharyngeal/laryngeal spasms triggered by attempts to swallow water (and sometimes even the sight, sound, perception of water), and air drafts respectively.
The pathophysiology of both hydrophobia and aerophobia involves destruction of inhibitory neurons in the brainstem, resulting in exaggerated respiratory tract reflexes while higher brain centers remain relatively intact and consciousness is preserved. This selective neuronal damage creates hypersensitive inspiratory motor responses to stimuli that would normally be tolerated. These phobic spasms, combined with hypersalivation, autonomic dysfunction, and periods of terror and excitation, distinguish furious rabies from the paralytic form, which presents with ascending flaccid paralysis without these characteristic spasms.
No proven curative therapy exists for furious rabies once clinical symptoms develop; management is primarily palliative, focused on alleviating suffering through liberal use of sedatives, analgesics, and supportive care. Rabies is nearly always fatal after symptom onset, with survival extremely rare and typically occurring only in patients who received pre-exposure or early post-exposure prophylaxis.
What pleural fluid characteristics would suggest an empyema? (At least 3 features, need if low v. high, don't need the actual numerical value)
What is
1. LOW pH (<7.20)
2. LOW pleural glucose (< 60 mg/dL)
3. HIGH pleural LDH > 3x upper normal limit for serum (usually >1000)
4. Pleural fluid purulence/pus (pathognomonic)
ATS - Parapneumonic Effusions & Empyema 10/23/2025
Stages of parapneumonic effusions (secondary to pneumonia, bacterial or viral) or lung abscess. Empyema = pus in pleural space.
Stage 1: Exudative stage - rapid accumulation of pleural fluid due to increased pulmonary interstitial fluid, increased pulmonary capillary permeability. Negative bacterial studies. Pleural fluid glucose > 60 mg/dL, pH > 7.20, lactic dehydrogenase (LDH) < 3x upper limit of normal limit of serum.
Stage 2: Fibropurulent: Positive bacterial studies. Glucose <60 mg/dL, pH <7.20, pleural fluid LDH >3x upper limit of normal serum. Loculations.
Stage 3: Pleural peel - peel forms over visceral pleura preventing lung expansion. Pleural space must be eradicated if pleural infection is to be eradicated - requires decortication typically via video-assisted thoracotomy (VATS) vs open thoracotomy.
The pleural fluid in this stage is characterized by positive bacterial studies, a glucose level below 60 mg/dl, a pH below 7.20, and a pleural fluid LDH more than three times the upper normal limit for serum. In this stage, the pleural fluid becomes infected and progressively loculated. The pleural fluid needs to be drained in this stage and drainage becomes progressively difficult as more loculations form.
Treatment:
- Therapeutic thoracentesis with tube thoracostomy/drainage
- Intrapleural Fibrinolytics: TPA + DNase (Established by MIST2 trial - NEJM 2011) combination of TPA + DNase improved fluid drainage in patients with pleural infection and reduced frequency of surgical referral and the duration of the hospital stay. Treatment with DNase alone or t-PA alone was ineffective.
MIST-3 RCT completed 2021 with results published ~2023
MIST-4 trial ending 9/2029
Individuals who get infective endocarditis from this particular bacterium species should consider getting a colonoscopy as recommended by the American Heart Association.
What is Streptococcus bovis (now Streptococcus gallolyticus)?
Streptococcus bovis, now reclassified as Streptococcus gallolyticus (specifically S. gallolyticus subspecies gallolyticus, formerly S. bovis biotype I), has a well-established association with colorectal cancer and adenomas.
Among patients with S. bovis bacteremia who undergo colonoscopy, the median percentage with colorectal neoplasia is 60%, with 25-80% having concomitant colorectal tumors. The association is particularly strong with S. gallolyticus subspecies gallolyticus, which carries a 7-fold increased risk of colorectal cancer compared to other S. bovis biotypes.
The risk is even higher in patients with infective endocarditis caused by S. gallolyticus, where colorectal neoplasia is found in approximately 53-64% of cases. Importantly, most patients have no gastrointestinal symptoms at presentation, making the bacteremia a marker for occult malignancy. Current guidelines from the American Heart Association recommend that all patients with S. gallolyticus bacteremia or endocarditis undergo colonoscopy to evaluate for colorectal malignancy or premalignant lesions.
Reference:
First Aid - Cardiovascular section
AHA 9/15/2015
Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Scientific Statement for Healthcare Professionals From the American Heart Association
This common cause of hypothyroidism is associated with an increased risk of non-Hodgkin Lymphoma
What is Hashimoto's thyroiditis (chronic lymphocytic thyroiditis)?
Most common cause of hypothyroidism in iodine-sufficient regions; an autoimmune disorder with antithyroid peroxidase (antimicrosomal) and antithyroglobulin antibodies. Associated with HLA-DR3, HLA-DR5, ↑ risk of non-Hodgkin lymphoma (typically of B-cell origin).
May be hyperthyroid early in course due to thyrotoxicosis during follicular rupture.
Histology: Hürthle cells , lymphoid aggregates with germinal centers.
Findings: moderately enlarged, nontender thyroid.
Reference:
First Aid- Endocrinology
Teaching Points:
Hashimoto's thyroiditis is an autoimmune disorder characterized by lymphocytic infiltration of the thyroid gland, leading to gradual destruction and hypothyroidism. Positive thyroid Peroxidase Antibiotics (TPOAb) is the most clinically useful marker with sensitivity ~64% and specificity of ~89% with higher titers correlating with greater likelihood of disease.
The chronic antigenic stimulation and lymphocytic infiltration create a microenvironment that predisposes to lymphomagenesis
Primary thyroid lymphoma (PTL) is rare (<5% of thyroid malignancies), but patients with Hashimoto's have a 40–80 fold increased risk compared to the general population
Clinical pearl: A rapidly enlarging thyroid mass in a patient with known Hashimoto's thyroiditis should raise suspicion for thyroid lymphoma, especially if accompanied by compressive symptoms (dysphagia, dyspnea, hoarseness)
Histologic types:
MALT lymphoma – indolent, often localized
Diffuse large B-cell lymphoma (DLBCL) – more aggressive, may arise de novo or transform from MALT
Diagnosis requires tissue biopsy (FNA may be insufficient; core or excisional biopsy often needed)
What is the first-line treatment for this life-threatening complication of systemic sclerosis characterized by malignant hypertension and acute kidney injury?
What are ACE inhibitors?
Scleroderma renal crisis is characterized by acute onset of severe hypertension (often malignant), acute kidney injury, and frequently thrombotic microangiopathy in patients with systemic sclerosis. It occurs in 2-15% of SSc patients, typically within the first 3-5 years of disease, particularly in those with diffuse cutaneous disease.
Key risk factors include diffuse cutaneous SSc, rapid skin thickening, recent corticosteroid use (especially >15 mg/day prednisone), anti-RNA polymerase III antibodies (present in one-third of SRC cases), new anemia, pericardial effusion, and tendon friction rubs. Approximately 10% of cases present as normotensive renal crisis, which carries a particularly poor prognosis.
Reference: First Aid - Musculoskeletal, Skin, and connective tissues (lists ACE inhibitors as treatment for scleroderma renal crisis)
This clinical syndrome is characterized by dementia, visual hallucinations, cognitive fluctuations, and REM sleep behavior disorder. It is also characterized by neuroleptic sensitivity. What am I?
"What is Dementia with Lewy Body?"
Severe neuroleptic sensitivity that occurs in approximately 50% of patients with dementia with Lewy bodies. This potentially life-threatening reaction manifests as acute worsening of extrapyramidal symptoms, altered consciousness, autonomic instability, and features resembling neuroleptic malignant syndrome.
Cholinesterase inhibitors (rivastigmine, donepezil) are first-line treatment for hallucinations and other neuropsychiatric symptoms in dementia with Lewy bodies and should be optimized before considering antipsychotics.
Typical and atypical antipsychotics should be used with extreme caution in dementia with Lewy bodies due to insufficient evidence of efficacy and substantial risk of adverse effects, including increased mortality. When antipsychotics are absolutely necessary for severe psychosis, quetiapine appears to have the fewest side-effects, though evidence for efficacy remains limited. Clozapine has demonstrated efficacy but requires regular blood monitoring for agranulocytosis.
Dementia with Lewy Bodies (DLB) differs from Alzheimer's disease in cognitive profile and clinical features. DLB presents with prominent attentional, executive, and visuospatial deficits, whereas Alzheimer's disease typically begins with episodic memory impairment. Visual hallucinations (well-formed, featuring people, children, or animals), fluctuating cognition, and parkinsonism are core features of DLB that help distinguish it from Alzheimer's disease.
DLB can be distinguished from other Atypical Parkinsonian Syndromes (multiple system atrophy, progressive supranuclear palsy, and corticobasal degeneration) with several features: improved levodopa responsiveness, absence of severe early autonomic failure seen in MSA, falls & vertical gaze palsy seen in progressive supranuclear palsy, asymmetric limb apraxia seen in corticobasal degeneration, and the presence of visual hallucinations & cognitive fluctuations.
Reference:
First Aid - Neurology
Name at least 2 out of the 4 diagnostic criteria of acute respiratory distress syndrome? (include specific numerical values if needed)
Berlin Criteria for ARDS
(also present in First Aid - Respiratory section in an adapted form)
The Berlin criteria for ARDS (2012) require four components: acute onset within 7 days, bilateral opacities on chest imaging, respiratory failure not fully explained by cardiac failure/fluid overload, and hypoxemia with PaO₂/FiO₂ ≤300 mm Hg on PEEP ≥5 cm H₂O.
The Four Berlin Criteria:
Timing: Acute onset within 1 week of a known clinical insult or new/worsening respiratory symptoms
Chest imaging: Bilateral opacities on chest radiograph or CT not fully explained by effusions, lobar/lung collapse, or nodules
Origin of edema: Respiratory failure not fully explained by cardiac failure or fluid overload; objective assessment (e.g., echocardiography) needed to exclude hydrostatic edema if no ARDS risk factor is present
Oxygenation: PaO₂/FiO₂ ratio measured on PEEP or CPAP ≥5 cm H₂O
Teaching points:
1. P/F ratio severity: Mild (200-300 mmHg), Moderate 100-200), Severe (≤ 100)
2. Low tidal volume ventilation decreases mortality across all severity (4-8 mL/kg ideal body weight). ARMA study studied 6 mL/kg and found a 22% relative reduction in mortality in patients w/ 6 mL/kg than those with 12 mL/kg).
3. Maintain plateau pressures
4. Prone positioning in moderate-severe ARDS
5. Neuromuscular blocking agents (ACURASYS trial 2010, SUCRA meta-analysis 2025) - in moderate severe ARDS. Not recommended in all patients.
6. Corticosteroids - dexamethasone may increase ventilator-free days (DEXA-ARDS)
7. VV-ECMO
Name at least 3 antibiotic drug classes that can be used to treat Pseudomonas.
CAMPFIRE drugs (First Aid Acronym)
1. Carbapenems (Meropenem, Imipenem-cislastin, Doripenem can; Ertapenem CANNOT)
2. Aminoglycosides (Tobramycin, Amikacin, Gentamicin, Plazomicin can; Streptomycin/Neomycin CANNOT)
3. Monobactams (Aztreonam can)
4. Polymyxins (Colistin/Polymyxin E, Polymyxin B can; last line agents)
5. Fluoroquinolones - (Ciprofloxacin, Levofloxacin can; Moxifloxacin has poor pseudomonas activity)
6. Specific ThIRd & fouth-generation cephalosporins (Actually, certain 3rd, 4th, and even 5th generations can. Ceftazidime - 3rd, Ceftazidime-avibactam - 3th, Cefepime 4th, Ceftaroline-tazobactam -5th all can). Ceftriaxone & Cefotaxime are both 3rd generation cephalosporins without Pseudomonas activity.
7. Extended-spectrum penicillins (Piperacillin-tazobactam, Ticarcillin-clavulanate can)
Reference:
First Aid - CAMPFIRE Mnemonic
IDSA - Antibiotic activity
Name the 4 P's of treatment for thyroid storm.
Treat with the 4 P’s:
1. β-blockers (eg, Propranolol)
2. Propylthiouracil
3. Corticosteroids (eg, Prednisolone)
4. Potassium iodide (Lugol iodine). Iodide load → ↓ T4 synthesis via Wolff-Chaikoff effect (excess iodine temporarily turns off thyroid peroxidase leading to ↓ T3/T4 production (protective autoregulatory effect) .
Thyroid storm is an uncommon but serious complication that occurs when hyperthyroidism is incompletely treated/untreated and then significantly worsens in the setting of acute stress such as infection, trauma, surgery. Presents with agitation, delirium, fever, diarrhea, coma, and tachyarrhythmia (cause of death). May see ↑ LFTs.
Reference: First Aid - Endocrine
Teaching:
1. Patients with a Burch-Wartofsky score higher than 45 should be managed in an intensive care setting by a multidisciplinary team.
2. Beta blockers reduce T4 → T3 conversion (at high doses)
3. Propylthiouracil (PTU) blocks thyroid synthesis + blocks T4 → T3 conversion.
4. Methimazole only blocks thyroid synthesis
5. Lugol's Iodinne blocks thyroid synthesis (Wolff-Chaikoff effect) + hormone release
6. Hydrocortisone decreases T4 to T3 conversion + adrenal support (in event of adrenal crisis)
7. Plasmapheresis/plasma exchange for refractory cases +/- emergent thyroidectomy
8. Anti-thyroid drugs must be administered 1 hour before iodine to prevent iodine from being used as substrate for new thyroid hormone synthesis (e.g. from iodinated contrast during CT w/ contrast scan)
This neuromuscular junction disorder characterized by autoantibiotics to postsynaptic ACh receptors is most associated with this disease. (name disease, and name the association)
What is myasthenia gravis and thymoma?
Myasthenia gravis (MG) is an autoimmune neuromuscular junction disorder characterized by autoantibodies against postsynaptic acetylcholine receptors (AChR), and it has a well-established association with thymic abnormalities:
Thymoma is present in 10–15% of MG patients
Thymic hyperplasia is found in 60–70% of patients with early-onset MG
Conversely, 30–50% of patients with thymoma develop MG
AChE inhibitor administration reverses symptoms (pyridostigme is treatment)
Teaching Points:
Pathophysiology: Anti-AChR antibodies cause complement-mediated destruction of the postsynaptic membrane, reduce AChR numbers, and block acetylcholine binding → impaired neuromuscular transmission → fatigable weakness
Clinical presentation: Fluctuating weakness that worsens with activity; hallmark features include ptosis, diplopia, bulbar symptoms (dysarthria, dysphagia), and proximal limb weakness, ice pack test (>2 mm improvement in eyelid elevation after applying ice as cold increases acetylcholine availability at the NMJ)
Thymus connection: The thymus is thought to be the site of autoimmunization; thymic epithelial cells express AChR-like proteins that may trigger the autoimmune response
Clinical pearl: All patients with newly diagnosed MG should undergo CT or MRI of the chest to evaluate for thymoma
Thymectomy is recommended for:
All patients with thymoma
Non-thymomatous MG patients aged 18–65 with generalized disease (based on the MGTX trial showing improved outcomes)
Other antibodies: ~10–15% of MG patients are "seronegative" for AChR antibodies but may have anti-MuSK or anti-LRP4 antibodies
Monitor for bradycardia with pyridostigmine.
This classic fundoscopic finding, along with headache and vision changes in an obese woman of childbearing age, should prompt evaluation for idiopathic intracranial hypertension.
What is papilledema?
Also called pseudotumor cerebri. ↑ ICP with no obvious findings on imaging.
Risk factors include female sex, Tetracyclines, Obesity, vitamin A excess, Danazol (female TOAD). Associated with cerebral venous sinus stenosis.
Findings: headache, tinnitus, diplopia (usually from CN VI palsy), no change in mental status. Impaired optic nerve axoplasmic flow → papilledema. Visual field testing shows enlarged blind spot and peripheral constriction. Lumbar puncture reveals ↑ opening pressure and provides temporary headache relief.
Treatment: weight loss, acetazolamide, invasive procedures for refractory cases (eg, CSF shunt placement, optic nerve sheath fenestration surgery for visual loss).
Reference: First Aid - Neurology
Teaching Points
Modified Dandy Criteria require:
1. signs/symptoms of elevated ICP
2. papilledema
3. CSF opening pressure ≥25 cm H₂O (measured in lateral decubitus position) with normal CSF composition
4. normal neuroimaging excluding structural lesions and cerebral venous thrombosis.
Vision-Threatening Complications
Permanent visual loss occurs in up to 25% of patients from chronic papilledema leading to optic atrophy.
Two mechanisms of retinal damage exist:
1. Peripheral vision loss: Progressive retinal nerve fiber layer atrophy causes peripheral scotomata without affecting acuity
2. Central vision loss: Grade 4 papilledema with macular edema/exudate causes persistent acuity reduction
High-risk features for visual loss: male sex, Black ethnicity, morbid obesity, fulminant onset, anemia, uncontrolled hypertension, visual field defects at presentation, and absence of headache.
Medical Management:
Weight loss is crucial for all patients—even 6% reduction can resolve papilledema, though 15-24% may be needed for disease remission.
Acetazolamide 500 mg extended-release 2-4 times daily is first-line pharmacotherapy (safe in pregnancy). Escalate dose gradually to minimize paresthesias and nausea.
Topiramate offers dual benefits: carbonic anhydrase inhibition plus weight loss and migraine control.
GLP-1 receptor agonists are emerging as game-changers, showing 81% reduction in papilledema and 64% reduction in acetazolamide use at 1 year.