Definition: What are the four criteria for medical decisional capacity?

• Consistent choice
• Understanding risks/benefits
• Understanding personal significance
• Reasoning through options

Principle: Is decisional capacity global or decision-specific?

• Decision-specific; capacity must be assessed for each decision

Legal distinction: Who determines a patient's global competence?

• Courts determine competence; physicians assess decision-specific capacity

When is discussing the case with a durable power of attorney (son) appropriate?

• If patient lacks decision-making capacity, then defer decision to durable POA

When is petitioning the court to appoint a guardian appropriate for a patient with incapacity?

• Only if permanently incapacitated AND no surrogate decision maker (eg, no durable POA or next of kin)

When is proceeding with recommended surgical treatment despite patient refusal justified?

• Not justified here; proceeding would violate autonomy. First assess capacity; if lacks capacity, involve durable POA rather than proceed

When is using cast immobilization to honor a refusal appropriate for this open tibial fracture?

• Premature; if patient has capacity, abide by her refusal; if lacks capacity, decision goes to durable POA

Practical: How should a clinician assess the 90-year-old patient's decisional capacity for refusing surgery?

• Discuss fracture care preferences and evaluate the four capacity criteria

Answer includes image:

Decisional capacity assessment: who must assess it?

• Physician must assess patient's decisional capacity

Decisional capacity timing: when must assessment occur?

• For each specific care decision

Decisional capacity and demographics: when should assessment be done relative to age or cognitive status?

• Regardless of patient age or cognitive ability, assess capacity

Decisional capacity: concise rule combining actor, timing, and scope

• Physician assesses decisional capacity for each specific care decision, regardless of patient age or cognitive ability

Anchor: Initial step for asymptomatic elevated blood pressure (140/100) in 21-year-old

Repeat blood pressure measurements: confirm with in-office and/or at-home serial readings over weeks to months before diagnosing hypertension.

Anchor: Why no additional diagnostic studies now for isolated elevated BP in asymptomatic patient

One isolated elevated reading does not diagnose hypertension; confirmation with repeat measurements required before further testing.

Anchor: Primary determinants of blood pressure (3 systems)

• Renin-angiotensin-aldosterone system
• Sympathetic nervous system
• Plasma blood volume

Anchor: Risk factors contributing to primary (essential) hypertension

• Advancing age
• Obesity / sedentary lifestyle
• Smoking, high-sodium diet, excess alcohol, insufficient sleep, genetics

Anchor: When to measure serum aldosterone:renin ratio (hyperaldosteronism workup)

Use when secondary hypertension suspected with hypokalemia or metabolic alkalosis suggesting excess aldosterone.

Anchor: Why aldosterone:renin ratio is unlikely in this patient

Patient has normal serum electrolytes (no hypokalemia) making hyperaldosteronism unlikely.

Anchor: When to evaluate renal artery stenosis (renal Doppler/arteriography)

Suspect when resistant hypertension requiring multiple agents or abdominal bruit; more common from atherosclerosis (older) or fibromuscular dysplasia (younger).

Anchor: Why renal artery imaging is inappropriate now for this patient

No resistant hypertension, no abdominal bruit, and patient is young without features pointing to renal artery stenosis.

Anchor: Role of renal CT scan in hypertension evaluation

Not routine; may show atrophic kidneys with renal artery stenosis or used for pyelonephritis/abscess when fever, flank pain, dysuria present.

Anchor: Next steps if hypertension is confirmed

Evaluate for end-organ damage and discuss lifestyle modification and antihypertensive therapy with primary care.

Anchor: Educational point: long-term risks of untreated hypertension

• Heart failure
• Ischemic/hemorrhagic stroke
• Chronic kidney disease

Anchor: Image: slide with highlighted text (supplemental)

Supplementary image: Use image only as illustration of exam explanation.

Primary hypertension: key risk factors (group 1)?

• Advancing age
• Obesity
• Sedentary lifestyle

Primary hypertension: key risk factors (group 2)?

• Tobacco smoking
• Excessive alcohol consumption

Primary hypertension: major long-term complications if untreated?

• Heart failure
• Ischemic and hemorrhagic stroke
• Chronic kidney disease

Primary hypertension: does a single elevated BP reading establish diagnosis?

• No. One isolated elevated BP in an asymptomatic patient does not indicate hypertension

Primary hypertension: acceptable methods to confirm elevated BP before diagnosis?

• Both in-office and at-home measurements
• Or serial in-office measurements over weeks–months

Primary hypertension: recommended timing for serial in-office BP measurements to confirm diagnosis?

• Over a period of weeks to months

Clinical decision: 18-year-old post-blunt chest trauma with left pleural effusion, tachycardia, tachypnea, rising O2 needs — most appropriate immediate management?

• Tube thoracostomy

Pathophysiology: What causes traumatic hemothorax?

• Blood in pleural space from pulmonary, bronchial, or intercostal vessel injury (eg, rib fractures)

Presentation: Key clinical features of hemothorax?

• Chest pain, shortness of breath, dullness to percussion, decreased breath sounds on affected side

Definition: When is hemothorax classified as massive?

• Initial chest-tube output >1000–1500 mL or >200 mL/hr for ≥4 hr

Management decision: Purpose of initial tube thoracostomy in traumatic hemothorax?

• Promote lung expansion; exclude ongoing hemorrhage; prevent residual pneumothorax, empyema, fibrothorax, fistula

When is video-assisted thoracoscopy (VATS) or thoracotomy indicated in hemothorax?

• If massive hemothorax (see criteria) or ongoing high-volume drainage after chest tube

Ultrasonography role in blunt chest trauma with effusion: when is it appropriate?

• Useful for initial detection of pleural fluid and to guide thoracentesis, but unnecessary if CXR already shows effusion and urgent tube needed

CT chest role in traumatic hemothorax: when is CT appropriate?

• Characterizes injuries further (eg, vascular, parenchymal) but defer if patient needs immediate chest-tube intervention

Thoracentesis in traumatic pleural effusion: when is thoracentesis appropriate?

• Diagnostic/therapeutic for small, stable effusions or ultrasound-guided sampling; not for initial management of suspected traumatic hemothorax with respiratory compromise

Comparison: Tube thoracostomy vs thoracentesis in traumatic hemothorax — main distinguishing indication?

• Tube thoracostomy: active/large hemothorax or respiratory compromise
• Thoracentesis: small, stable effusion for diagnosis/relief

Indicators of massive hemothorax (visual aid in answer)

• Massive hemothorax criteria:
• Initial chest-tube output >1000–1500 mL
• Drainage >200 mL/hr for ≥4 hr

What is hemothorax?

• Blood accumulating within the pleural space

What are chest x-ray and CT features of hemothorax?

• CXR: fluid along diaphragm with blunted costophrenic angle
• CT: hyperdense material between visceral and parietal pleura

Which clinical signs mandate immediate tube thoracostomy for hemothorax?

• Tachycardia, tachypnea, increasing O2 requirements

Why is tube thoracostomy preferred over thoracentesis for large/rapid hemothorax?

• Removes large blood volume + can be left in place to trend/monitor ongoing bleeding

When would thoracentesis be appropriate for pleural blood?

• Diagnostic use for small/stable pleural effusion; not therapeutic for rapidly accumulating hemothorax

What is the primary therapeutic goal of tube thoracostomy in hemothorax?

• Evacuate blood, prevent retained hemothorax, allow monitoring of bleeding

Name complications of hemothorax (grouped into ≤3 items).

• Infectious: empyema, superimposed infection
• Pulmonary: atelectasis, fibrothorax
• Hemorrhagic: hemorrhagic shock

Imaging features of hemothorax (illustration)

• CXR: blunted costophrenic angle; CT: hyperdense pleural material

Preoperative splenectomy: which vaccines are recommended?

• Streptococcus pneumoniae
• Haemophilus influenzae type b
• Neisseria meningitidis

Splenectomy: primary splenic immune functions?

• Mechanical filtration of opsonized pathogens in sinusoids
• Phagocytosis by splenic macrophages
• Houses immunoglobulin-producing B lymphocytes

Asplenia: which organisms cause increased severe infection risk?

• Encapsulated bacteria:
• Streptococcus pneumoniae
• Haemophilus influenzae
• Neisseria meningitidis

Splenectomy patients: is antibiotic prophylaxis indicated and which agents?

• May require antibiotic prophylaxis
• Typical agents: penicillin or amoxicillin

Why is vaccinating for S. pneumoniae, H. influenzae, and N. meningitidis before splenectomy correct?

• Spleen clears encapsulated organisms; vaccinate against the major encapsulated pathogens to reduce post-splenectomy sepsis risk

Why is answer choice A (only N. meningitidis) incorrect for preoperative splenectomy vaccination?

• Choice A vaccinates only N. meningitidis; incomplete because S. pneumoniae and H. influenzae also require vaccination

Why is answer choice B (only H. influenzae) incorrect for preoperative splenectomy vaccination?

• Choice B vaccinates only H. influenzae; incomplete because S. pneumoniae and N. meningitidis also require vaccination

Why is answer choice C (H. influenzae + N. meningitidis) incorrect for preoperative splenectomy vaccination?

• Choice C omits S. pneumoniae; vaccination must include S. pneumoniae, H. influenzae, and N. meningitidis

Why is answer choice D (only S. pneumoniae) incorrect for preoperative splenectomy vaccination?

• Choice D vaccinates only S. pneumoniae; incomplete because H. influenzae and N. meningitidis also require vaccination

Why is answer choice E (S. pneumoniae + N. meningitidis) incorrect for preoperative splenectomy vaccination?

• Choice E omits H. influenzae; vaccination must include all three encapsulated organisms

Why is answer choice F (S. pneumoniae + H. influenzae) incorrect for preoperative splenectomy vaccination?

• Choice F omits N. meningitidis; vaccination must include S. pneumoniae, H. influenzae, and N. meningitidis

Acute pancreatitis: classic presentation and key symptoms

• Severe epigastric abdominal pain that radiates to the back
• Nausea and vomiting

Acute pancreatitis: common etiologies

• Gallstones
• Alcohol use
• Trauma
• Hypertriglyceridemia
• Hypercalcemia

Traumatic epigastric blow: diagnostic relevance

Direct blunt trauma to the epigastrium can cause acute pancreatitis

Acute pancreatitis: major complications

• Necrosis
• Hemorrhage
• Abscess
• Pseudocyst

Acute pancreatitis: typical laboratory findings

Elevated serum amylase and elevated serum lipase

Acute pancreatitis: initial supportive management

• IV fluids (normal saline or lactated Ringer)
• Bowel rest
• Pain control

When is surgical intervention indicated in acute pancreatitis?

Surgery if complications develop (eg, necrosis with infection, hemorrhage, persistent pseudocyst requiring intervention)

Esophageal rupture: presentation and causes

• Severe retrosternal pain
• Signs of sepsis (fever, tachycardia, hypotension)
• Causes: trauma, endoscopic instrumentation, violent retching

Gastric ulcer: symptoms and complications

• Pain worsens with food
• Complications: perforation, stricture, upper GI bleeding (melena or hematochezia)
• Endoscopy: mucosal discontinuity/erythema

Gastroenteritis: typical features and etiology

• Nausea, vomiting, diarrhea
• Mild generalized abdominal discomfort
• Typically infectious (viral or bacterial); not trauma-related

Hepatitis: causes and distinguishing features

• Causes: viral, autoimmune, alcohol, medications
• Features: hyperbilirubinemia with jaundice; typically chronic and not caused by blunt trauma

Distinguish acute pancreatitis vs gastroenteritis (key differentiators)

• Pancreatitis: severe focal epigastric pain, nausea/vomiting, often elevated amylase/lipase
• Gastroenteritis: mild generalized pain with diarrhea, infectious, not trauma-related

Why pancreatitis is the correct diagnosis in a teen with epigastric pain after a kick

Focal severe epigastric pain after epigastric trauma with nausea/vomiting matches acute pancreatitis; trauma is a recognized cause

What is 'postpartum endometritis' (anchor: diagnosis)?

Acute infection of the uterine endometrium after delivery, typically polymicrobial involving aerobes and anaerobes from the genital tract.

Pathophysiology of postpartum endometritis (anchor: pathophysiology)?

Genital-tract microbes enter the uterine cavity during labor/delivery causing polymicrobial infection of the endometrium.

Key clinical features of postpartum endometritis (anchor: clinical features)?

• Fever
• Uterine fundus tenderness
• Mucopurulent or foul-smelling lochia
• Leukocytosis

Risk factors for postpartum endometritis (anchor: risk factors)?

• Cesarean delivery
• Prolonged rupture of membranes or prolonged labor
• Bacterial vaginosis
• Group B Streptococcus colonization
• Manual removal of placenta

Immediate management of suspected postpartum endometritis (anchor: management)?

Start broad-spectrum IV antibiotics promptly; recommended regimen example: clindamycin plus gentamicin.

Why is antibiotic therapy correct as the next step in this postpartum patient (anchor: answer-choice logic)?

Clinical picture (fever, uterine tenderness, foul lochia, leukocytosis) indicates endometritis requiring immediate broad-spectrum antibiotics.

Why is CT abdomen/pelvis not the best next step for suspected endometritis (anchor: answer-choice logic)?

CT can identify intra-abdominal sources but does not confirm endometritis; it is not routinely used to diagnose endometritis.

When is CT abdomen/pelvis useful after postpartum fever (anchor: diagnostics)?

To identify intra-abdominal causes such as surgical-site abscess, retained products of conception, appendicitis, or colitis.

Why is culture of the lochia not the most appropriate next step (anchor: answer-choice logic)?

Culture is not the immediate management step; treating suspected infection with antibiotics is prioritized.

Why are endometrial biopsy and transvaginal ultrasound not the immediate next steps (anchor: answer-choice logic)?

They are not first-line tests to manage suspected postpartum endometritis; immediate empiric antibiotics take priority.

Example presentation anchor: 36 hours postpartum with fever and foul-smelling lochia—most likely diagnosis?

Postpartum endometritis given timing, uterine tenderness, foul lochia, fever, and leukocytosis after cesarean delivery.

Supplementary: slide illustrating key points about postpartum infection (anchor: visual aid)?

See slide for summarized features and management:

Smoking cessation and pulmonary function in a 37-year-old long-term smoker

• Smoking cessation slows the accelerated age-related decline in pulmonary function and prevents further accelerated worsening

Pathophysiology of normal aging lungs

• Loss of parenchymal scaffolding → dilation of air spaces (senile emphysema)
• ↑ alveolar dead space

Effect of smoking on age-related pulmonary decline

• Smoking increases the rate of age-related decline in pulmonary function

Diagnosis of chronic obstructive pulmonary disease (COPD)

• COPD is diagnosed by spirometry

Medical management for obstructive lung disease in long-term smokers

• Inhaled antimuscarinics
• Short and long-acting β-agonists
• Inhaled corticosteroids

Oxygen therapy criteria in chronic lung disease

• Resting or ambulatory O2 saturation < 88% → candidate for oxygen therapy

Lung cancer risk after smoking cessation (relation to choices B and D)

• Former smokers retain an increased lung cancer risk vs never-smokers, but risk decreases compared with continued smoking

Why 'pulmonary function will not decrease further' is incorrect (choice C)

• Age-related pulmonary decline normally continues from ~age 25; cessation slows but does not stop decline

Smoking and risk of myocardial infarction versus cerebral infarction (relation to choice E)

• Smoking increases risk of both myocardial and cerebral infarction via atherosclerotic buildup in coronary and intracranial arteries

Illustration: highlighted teaching points about smoking and lung aging

• Key points: senile emphysema, ↑ dead space, smoking accelerates decline, cessation prevents worsening

What is the diagnosis: multiple small (3–5 mm), bright red, slightly raised dome-shaped papules on trunk in a 38-year-old?

Cherry angiomas - Common benign vascular lesions - Appear after age 30

What are the typical clinical locations of cherry angiomas?

• Scalp
• Trunk
• Extremities

What is the histologic appearance of a cherry angioma?

Congested, dilated capillaries and venules within the superficial dermis

What diagnostic study is most appropriate to confirm cherry angiomas?

None — no diagnostic studies required; diagnosis is clinical

When is excisional biopsy appropriate for cherry angiomas?

Not required for diagnosis; biopsy/excision only if cosmetic concern or irritation

How should physicians manage patients who develop cherry angiomas?

Provide reassurance; offer removal only if desired for cosmetics/irritation

Gastroenteritis: typical features and relation to blunt abdominal trauma?

Nausea, vomiting, diarrhea, mild generalized abdominal discomfort; usually infectious (viral/bacterial); not associated with abdominal trauma

When is acute pancreatitis likely and what lab findings support it?

Severe epigastric pain radiating to back with nausea/vomiting; can follow direct epigastric trauma; labs show ↑ serum amylase and lipase

Hepatitis: common causes and typical presentation features?

Caused by viral infection, autoimmune disease, alcohol, or medications; often with hyperbilirubinemia/jaundice; typically chronic, not usually from blunt trauma

Visual: example appearance of cherry angiomas (illustration)

Small red dome-shaped papules on trunk consistent with cherry angiomas

Diagnosis: Chronic bacterial prostatitis — key presenting features in this case?

• Painful ejaculation, sometimes dark/foul ejaculate
• Chronic pelvic or low back pain (weeks–months)
• **Mildly tender, minimally enlarged prostate on DRE

Risk factors: What sexual history findings increase suspicion for chronic bacterial prostatitis?

• Multiple sexual partners
• Inconsistent condom use / unprotected anal sex
• Concomitant STIs

Diagnostic test: What is the two-glass test for prostatitis?

• Urine sample before prostatic massage then urine sample after prostatic massage used for microscopy/culture

Diagnostic criterion: How is prostate localization established using post-massage cultures?

A ≥10-fold increase in bacterial concentration after prostatic massage localizes infection to the prostate

Treatment: First-line therapy for chronic bacterial prostatitis?

• Fluoroquinolone antibiotics (prolonged courses; recurrences common)

Prognosis modifiers: Factors affecting cure rates for chronic bacterial prostatitis?

• Higher cure in antibiotic-naive patients
• Lower cure with prostatic calculi

Choice rationale: When is CT pelvis useful instead of two-glass test for prostate-related disease?

• CT pelvis: evaluate prostate cancer metastasis or prostatic abscess (abscess usually has systemic symptoms: fever, chills, malaise)

Choice rationale: When is abdominal ultrasonography appropriate vs prostatitis testing?

• Abdominal US: evaluate pyelonephritis or kidney stones (flank pain, fever, nausea) — not for uncomplicated prostatitis

Choice rationale: When is placement of urinary catheter for culture appropriate?

• Urinary catheter cultures: when patient cannot void or to evaluate suspected bacterial cystitis from obstruction; not for localizing prostate infection

Diagnostic aid: Example of two-glass test visual aid

Illustration of pre- and post-prostatic massage urine collection for microscopy and culture

Chronic bacterial prostatitis: core presenting symptoms?

• Recurrent UTI symptoms
• Pelvic/lower abdominal pain
• Dysuria or painful ejaculation

Chronic bacterial prostatitis: additional possible features?

• Obstructive urinary symptoms
• Sexual dysfunction

Risk factors for chronic bacterial prostatitis?

• Multiple sexual partners
• Unprotected anal sex
• Concomitant STIs

Diagnostic test that establishes chronic bacterial prostatitis?

• Urine cultures before and after prostatic massage showing a ten-fold increase in bacterial concentration

First-line treatment for chronic bacterial prostatitis?

• Fluoroquinolone antibiotics

Prognosis after treatment for chronic bacterial prostatitis?

• Recurrences are common

When is transrectal prostate ultrasonography useful?

• To identify prostatic calculi or prostatic abscesses

Why transrectal prostate ultrasonography is not diagnostic for chronic bacterial prostatitis?

• Findings nonspecific and insufficient to establish diagnosis; lacks sensitivity without abscess/calculi

When would transrectal ultrasonography be the correct test in prostatitis-like illness?

• Suspected prostatic abscess or suspected prostatic calculi with systemic/abscess signs

Foul-smelling or dark ejaculate: suggests which diagnosis over cystitis?

• Suggests prostatic or seminal tract involvement; not consistent with isolated cystitis

Diagnosis: Key features supporting cardiogenic shock in a 76-year-old man

• Hypotension (BP 84/56 → 78/42)
• Pulmonary edema (diffuse crackles, respiratory distress, low O2 sat)
• Elevated JVD to angle of jaw
• Low EF (10%) after anterior MI

Pathophysiology: How cardiogenic shock causes hypotension and pulmonary edema

• Pump failure → reduced cardiac output → hypotension
• ↑Left-sided end‑diastolic pressure → pulmonary venous congestion → pulmonary edema

Management: First-line pharmacologic therapy for cardiogenic shock after MI

• Dobutamine (inotropic support) often first-line; may combine with vasopressor if needed

Drug: Dobutamine mechanism relevant to cardiogenic shock

• β1 agonist → ↑contractility, ↑HR, ↑cardiac output
• Modest α1 activity → modest ↑peripheral vascular tone to help MAP

Drug: Norepinephrine role in cardiogenic shock

• α‑agonist predominance → strong vasoconstriction to raise MAP
• Minimal inotropy; used alone or with dobutamine if vasoplegia or severe hypotension

Comparison: Dobutamine vs Norepinephrine in cardiogenic shock

• Dobutamine: primary inotrope (↑CO)
• Norepinephrine: primary vasopressor (↑MAP)
• Use dobutamine for pump failure; add norepinephrine if MAP remains low

Drug: Why vasopressin (ADH) is not first-line for cardiogenic shock

• V1 receptor → vasoconstriction ↑MAP
• No inotropy; causes reflex ↓HR and ↓cardiac output → worsens pump failure

Drug: Why isoproterenol is harmful after acute MI with cardiogenic shock

• Nonselective β agonist → ↑HR and contractility but ↓SVR → ↓coronary perfusion and ↑myocardial O2 demand → worsens ischemia

Drug: Why phenylephrine is not recommended as first-line in cardiogenic shock

• Pure α1 agonist → ↑afterload and peripheral resistance
• No inotropy; ↑afterload may reduce stroke volume and cardiac output in pump failure

Clinical decision: When to add a vasopressor to dobutamine in cardiogenic shock

• Add vasopressor (eg, norepinephrine) if mean arterial pressure remains low despite inotropic support

Visual aid: Dobutamine mechanism and effect on hemodynamics (image on answer)

• Dobutamine: β1 → ↑contractility and CO; modest α1 → mild ↑SVR

Cardiogenic shock: defining clinical presentation?

• Hypotension
• Evidence of end-organ damage
• Context: acute decompensated heart failure

Cardiogenic shock: first-line therapy?

• Inotropic support (first-line)
• Examples: dobutamine or dopamine

Dobutamine: role in cardiogenic shock?

• Inotropic agent recommended as a first-line option for cardiogenic shock

Dopamine: role in cardiogenic shock?

• Inotropic agent recommended as a first-line option for cardiogenic shock

Norepinephrine: role in cardiogenic shock?

• Vasopressor adjunct: may be used in conjunction with inotropic agents

Cardiogenic shock: summary slide (visual aid)?

Slide shows key points: hypotension, end-organ damage, first-line inotropes (dobutamine, dopamine), norepinephrine adjunct.

Upper-extremity deep venous thrombosis (UEDVT): key pathophysiology

• Thoracic outlet compression injures axillary/subclavian vein with repetitive use
• Repetitive vigorous upper-extremity activity predisposes to thrombosis

Upper-extremity DVT: typical clinical presentation

• Young healthy athlete after vigorous upper-body exercise
• Arm/shoulder/neck pain, unilateral swelling, bluish forearm/hand discoloration
• Dilated superficial collateral veins (Urschel sign)

Why is venous thrombosis the most likely cause of this patient's unilateral arm swelling?

• Presentation matches UEDVT: recent vigorous upper-body activity, unilateral edema, bluish discoloration, prominent superficial chest/shoulder veins

Diagnosis of upper-extremity DVT: preferred test and finding

• Doppler ultrasonography showing a noncompressible vessel with intravascular thrombus

Initial management of upper-extremity DVT

• Anticoagulation (initial therapy)

Arterial occlusion: when would this explain limb findings?

• Acute limb ischemia with severe pain, pallor, paresthesia, pulselessness, poikilothermia (not isolated swelling)

Compartment syndrome: pathophysiologic mechanism

• Compartment pressure ≈/> diastolic BP → impaired blood flow → ischemia of compartment and downstream structures

Hematoma: clinical clues making it the correct cause of limb swelling

• Focal, palpable collection after trauma or in anticoagulated patients; large hematoma would be evident on exam

Lymphedema: distinguishing features vs venous obstruction

• Causes: lymphatic obstruction/excision (eg, node dissection, lymphoma)
• Usually localized to a limb; no dilated superficial veins because venous drainage intact

UEDVT epidemiology and typical setting

• UEDVT is rare; often occurs in young healthy patients after vigorous upper-extremity activity and thoracic outlet anatomy abnormalities

Bacterial tracheitis: key presenting signs in a child

• Severe cough
• Inspiratory stridor
• High fever
• Intercostal/suprasternal retractions
• Generally clear lung sounds

Bacterial tracheitis: typical causative organisms

• Streptococcus pneumoniae
• Haemophilus influenzae
• Staphylococcus aureus

Bacterial tracheitis: characteristic chest x-ray finding

• Tracheal air column with irregular ('shaggy') borders; may have peribronchial cuffing

Bacterial tracheitis: first-line management

• IV antibiotics plus corticosteroids; admit for monitoring; intubate if respiratory failure

Why is croup (laryngotracheobronchitis) less likely in this child?

• No improvement after 2 doses of nebulized racemic epinephrine, making bacterial tracheitis more likely

When is epiglottitis the correct diagnosis instead of bacterial tracheitis?

• Acute severe throat pain, drooling, difficulty swallowing, muffled voice, trismus, visible swollen epiglottis

When is bronchiolitis the correct diagnosis instead of bacterial tracheitis?

• Infant/young child with runny nose, cough, tachypnea, wheezing, often due to RSV; usually low-grade fever

When is peritonsillar abscess the correct diagnosis instead of bacterial tracheitis?

• Sore throat, unilateral tonsillar swelling, trismus, drooling, fever, difficulty opening mouth

Bacterial tracheitis: diagnosis cues and role of imaging

• Diagnosis clinical: severe cough, high fever, stridor, clear lungs; chest x-ray may show 'shaggy' tracheal air column (see image)

Bacterial tracheitis: what is the definition?

Potentially serious bacterial upper respiratory infection of the trachea.

Bacterial tracheitis: common presenting respiratory signs/symptoms?

• Cough
• Increased work of breathing
• Stridor

Bacterial tracheitis: systemic symptom commonly present?

• Fever

Bacterial tracheitis: typical chest auscultation findings?

• Lungs generally clear on auscultation

Bacterial tracheitis: chest x-ray finding?

Tracheal air column with irregular borders on chest x-ray.

Bacterial tracheitis: first-line management components?

• Antibiotics
• Corticosteroids
• Often hospitalization

ar abscess unlikely: clinical statement

ar abscess unlikely.

Bacterial tracheitis: supportive image illustrating tracheal air column (useful but not required to answer)

Chest x-ray may show a tracheal air column with irregular borders.

ECMO decision for a 37-year-old woman with cystic fibrosis, recurrent pulmonary failure, and refusal of lung transplant: what is the appropriate assessment?

• ECMO is unlikely to change the patient's outcome

Patient competence in treatment decisions: what is the documented status for this patient?

• Mentally competent per psychologic testing during the past year

Scope of the patient's living will in this case:

• No cardiopulmonary resuscitation (no CPR) if cardiac arrest while hospitalized

Relevance of the patient's repeated refusal of lung transplant to decision-making:

• Patient repeatedly refused consideration for lung transplant

Current respiratory support status of the patient in the ICU:

• Heavily sedated, intubated, and mechanically ventilated

Why does the living will not automatically prohibit ECMO in this patient?

• Living will specifies no CPR only; it does not state refusal of ECMO

When should family members initiate medical treatment plans for a hospitalized patient?

• When the patient lacks decision-making capacity; not when patient is documented competent

Gastroenteritis: typical features described in the text

• Nausea, vomiting, diarrhea, mild generalized abdominal discomfort; typically infectious and self-limiting

Acute pancreatitis: characteristic clinical presentation

• Severe epigastric pain radiating to the back with nausea and emesis

Acute pancreatitis: diagnostic laboratory findings

• Increased serum amylase and lipase activity

Acute pancreatitis: possible relation to trauma per the text

• Can occur after direct abdominal trauma to the epigastric region

Hepatitis: typical features and causes mentioned

• Causes: viral, autoimmune, alcohol, medications; feature: hyperbilirubinemia with jaundice; typically chronic

Chronic transplant nephropathy: key pathophysiologic mechanism?

• CD4+ T cell response to donor peptides (eg, MHC) → cytokines → humoral (type II) + cellular (type IV) injury → vascular arteriosclerosis, smooth muscle proliferation → parenchymal fibrosis and atrophy

Chronic transplant nephropathy: typical clinical manifestations?

• Progressive transplant dysfunction over months–years → fatigue, anorexia, edema; rising BUN/creatinine and anemia as in this patient (BUN 50 mg/dL, Cr 5.3 mg/dL, Hb 8 g/dL)

Chronic transplant nephropathy: diagnostic evaluation?

• Serum/urine tests, kidney ultrasonography, biopsy showing arteriosclerosis, fibrosis, atrophy

Chronic transplant rejection: response to standard immunosuppression?

• Not adequately prevented by immunosuppressive therapy; leads to organ failure and may require dialysis or repeat transplant

Acute cellular rejection of a renal allograft: immune mediator and timing?

• CD8+ T lymphocytes recognizing donor class I MHC on graft cells; occurs within 6–12 months posttransplant and responds to increased immunosuppression

Gastroenteritis: typical features that distinguish it from transplant failure?

• Nausea, vomiting, diarrhea, mild generalized abdominal discomfort; usually viral or bacterial and self-limited, not linked to progressive renal dysfunction

Examples of chronic rejection in other transplanted organs

• Liver: vanishing bile duct syndrome
• Lung: bronchiolitis obliterans
• Heart: accelerated atherosclerosis

Chronic transplant nephropathy: illustrative biopsy/ultrasound as supplement

Image: chronic transplant changes (arteriosclerosis, fibrosis, atrophy) shown for illustration

Viral hepatitis: key lab pattern suggesting acute viral hepatitis in this case

• Markedly ↑ AST/ALT (AST 1095, ALT 1300 U/L)
• Hyperbilirubinemia (total 11 mg/dL, direct 2.2 mg/dL)
• Normal leukocyte count (5800/mm3)

Viral hepatitis: common causes of acute hepatitis listed

• Viral infections
• Alcohol, medications
• Autoimmune disease, ischemic injury

Viral hepatitis: common presenting symptoms

• Fatigue, nausea, vomiting
• Right upper quadrant pain, jaundice, pruritus, abdominal distension

Viral hepatitis: initial serologic tests mentioned

• Anti-hepatitis A IgM and IgG
• Anti-hepatitis C IgM and IgG
• Multiple anti-HBV antibodies and antigens

Viral hepatitis: initial management approach

• Supportive care
• Treat complications (metabolic abnormalities, hepatic encephalopathy)
• Pursue specific therapy after identifying cause

Cholangitis: clinical features and typical labs that distinguish it from viral hepatitis

• Features: fever, jaundice, RUQ pain (Charcot triad)
• Labs: leukocytosis, ↑ALP, ↑GGT, ↑bilirubin; transaminase rise usually milder than hepatitis

Cholecystitis: presentation and typical lab expectations

• Presentation: RUQ pain, fever, leukocytosis; usually due to cystic duct obstruction (gallstone)
• Labs: bile duct usually patent → ALT/AST and bilirubin often not elevated unless concomitant cholangitis/choledocholithiasis

Choledochal cyst: typical age, symptoms, and usual lab findings

• Age: often <10 years but can present in adults
• Symptoms: abdominal pain, jaundice, palpable mass, nausea/vomiting
• Labs: usually normal liver enzymes (biliary duct often not obstructed)

Comparison: Why viral hepatitis fits this patient vs cholangitis or cholecystitis

• Viral hepatitis fits: marked ALT/AST rise + normal leukocytes
• Cholangitis expects: leukocytosis + cholestatic pattern (↑ALP/GGT)
• Cholecystitis expects: leukocytosis and localized gallbladder disease without major transaminase rise

Viral hepatitis: illustrative slide of teaching points (image on answer side)

Key tests and features summarized below.

• Marked ↑ AST/ALT; hyperbilirubinemia; normal WBC

Acute viral hepatitis: key clinical features?

• Fatigue
• Nausea/vomiting
• RUQ pain
• Jaundice
• Pruritus
• Abdominal distension

Acute viral hepatitis: characteristic lab pattern?

Large acute increases in ALT and AST

Viruses often implicated in acute viral hepatitis (group 1)?

• Hepatitis A virus (HAV)
• Hepatitis B virus (HBV)
• Hepatitis C virus (HCV)

Viruses often implicated in acute viral hepatitis (group 2)?

• Varicella zoster virus (VZV)
• Cytomegalovirus (CMV)
• Epstein-Barr virus (EBV)
• Herpes simplex virus 1/2 (HSV-1/2)

Acute viral hepatitis: initial management approach?

Supportive care; treat complications until specific antiviral chosen after virus ID

Complications to manage in acute viral hepatitis?

• Electrolyte abnormalities
• Hepatic encephalopathy

Pancreatic pseudocyst: patient population and frequency?

Occurs in about 10% of patients with chronic pancreatitis

Pancreatic pseudocyst: common presenting symptoms when symptomatic?

• Abdominal pain
• Early satiety
• Weight loss (from mass effect)

Acute pancreatitis: typical clinical presentation?

• Epigastric pain
• Nausea/vomiting
• Often with gallstones, alcohol, or trauma

Pancreatitis: most common nontraumatic causes?

• Gallstones
• Heavy alcohol use

Pancreatitis: diagnostic lab marker specificity?

Elevated lipase is a specific indicator of pancreatitis

Why acute viral hepatitis is more likely than pancreatitis in a patient with very large ALT/AST rise and no clear pancreatitis history?

Because acute viral hepatitis produces large acute ALT/AST increases; pancreatitis usually causes prominent abdominal pain and elevated lipase

When would pancreatitis be the correct diagnosis instead of acute viral hepatitis?

When patient has epigastric pain, nausea/vomiting, risk factors (gallstones, alcohol), and elevated lipase

When would pancreatic pseudocyst explain symptoms instead of acute viral hepatitis?

When chronic pancreatitis history plus mass symptoms (early satiety, weight loss, abdominal pain) suggest a pseudocyst

Clinical diagnosis: 9-year-old with 5-month intermittent right flank pain, absent left kidney on ultrasound, severe dilation of right renal pelvis. What is the clinical problem?

• Single functioning kidney with hydronephrosis

Pathophysiology: How does vesicoureteral reflux lead to kidney failure?

• Reflux → hydroureter/hydronephrosis → compression atrophy (reflux nephropathy) → progressive renal parenchymal loss

Key management: Most appropriate immediate intervention to prevent progression of renal failure from proximal ureteral obstruction in a single kidney?

• Insert percutaneous nephrostomy tube (temporary decompression)

Rationale: Why is percutaneous nephrostomy preferred here?

• Directly decompresses proximal obstruction/hydronephrosis to preserve renal parenchyma before definitive repair

When is a urinary catheter the correct immediate intervention for urinary obstruction?

• Bladder outlet obstruction (eg, urethral stricture/retention) with overflow incontinence or palpable suprapubic mass

Why is a urinary catheter NOT appropriate for this patient?

• Obstruction is proximal (ureteral), not bladder outlet; catheter won't decompress hydronephrosis

When is cystoscopy with bladder outlet dilatation appropriate for urinary obstruction?

• Distal bladder outlet obstruction amenable to endoscopic dilation (eg, urethral stricture, posterior urethral valves)

Why is cystoscopy with bladder outlet dilatation NOT appropriate for this patient?

• No bladder outlet obstruction signs; imaging shows proximal ureteral/renal pelvis dilation

When is intravenous furosemide indicated in renal/volume management?

• Acute hypervolemia (eg, pulmonary edema from heart failure) to increase diuresis

Why is intravenous furosemide inappropriate in obstruction-related hydronephrosis?

• Increasing urine production with outflow obstruction can worsen postrenal azotemia and hydronephrosis

When is IV 0.9% saline bolus indicated in acute management?

• Hypovolemia or distributive shock with signs of volume depletion (eg, hypotension, dry mucous membranes)

Why is IV 0.9% saline bolus inappropriate for this patient?

• No hypovolemia signs; extra intravascular volume may worsen hydronephrosis and renal injury

Congenital urinary tract anomalies associated with ureteral obstruction or reflux (examples relevant to single-kidney patients)

• Unilateral renal agenesis,
• Duplex collecting system,
• Ureteral stricture/stenosis

Clinical priority in patients with unilateral renal agenesis

• Preserve function of the solitary kidney (prevent obstruction/reflux injury)

Ultrasound finding anchor: Absent left kidney and severe right renal pelvic dilation implies what immediate risk?

• High risk of progressive renal parenchymal loss and kidney failure from obstruction

Supplement: Illustration of hydronephrosis in single kidney—useful for visualizing severe renal pelvis dilation

• See image for renal pelvic dilation:
• Image is illustrative only; diagnosis based on ultrasound and clinical features above

Percutaneous nephrostomy tube: primary clinical indication?

• Temporary drainage to prevent progression of kidney failure
• When definitive management of vesicoureteral reflux or ureteral obstruction is pending

Vesicoureteral reflux (VUR) or ureteral obstruction: role of percutaneous nephrostomy?

• Bridge therapy: provides temporary urinary diversion before definitive repair of VUR or relief of obstruction

Percutaneous nephrostomy tube: intended immediate benefit to renal function?

• Prevents progression of kidney failure by decompressing obstructed urinary tract

Anchor: Nonadherence in 21-year-old with type 2 diabetes; defining features?

• Age 21, type 2 diabetes, A1c 9%, admits not checking glucose to be 'like everyone else', on metformin + glipizide

Anchor: Best physician approach for young diabetic nonadherent due to social perception

• Organize multidisciplinary care + peer support group for young patients with diabetes

Anchor: Why multidisciplinary care + peer support is correct for social-perception nonadherence?

• Addresses emotional/social causes, connects patient with similar peers, improves disease perception and adherence

Anchor: When is contacting a patient's parent appropriate?

• Appropriate when patient lacks decision-making capacity; otherwise contacting parent breaches trust and HIPAA

Anchor: When is a mobile glucose app likely effective for nonadherence?

• Effective when barrier = difficulty/complexity of monitoring; not effective when barrier = social desire to fit in

Anchor: When is scare/threatening counseling (eg, 'you will be blind') appropriate?

• Scare tactics are inappropriate; education about complications should be empathetic and nonthreatening

Anchor: Use of humor with a patient admitting nonadherence due to social stigma

• Humor may damage rapport here; prefer empathetic, nonjudgmental, open-ended inquiry

Anchor: Clinical communication principle for nonadherence evaluation

• Use open-ended, curious, nonjudgmental questions to identify root cause before planning interventions

Anchor: Study-note rule: overriding refusals or contacting others

• Assess decision-making capacity before overriding refusals or notifying others

Anchor: Choice E — strengthen physician-patient relationship. Why is this option insufficient for treatment nonadherence?

Strengthening relationship is humanistic but does not address underlying nonadherence drivers; the patient needs multi‑front support to realize others share his experience.

Anchor: Treatment nonadherence. Common practical reasons (group A)?

• Financial strains
• Treatment side effects
• Poor health literacy causing misunderstanding

Anchor: Treatment nonadherence. Common psychosocial reasons (group B)?

• Social perception or judgment
• Mental/emotional strain from adjustment

Anchor: Approach to a nonadherent patient. What clinician attitude is recommended?

Use an open‑ended, curious, nonjudgmental approach to explore reasons for nonadherence.

Anchor: When is peer support indicated for a nonadherent patient?

When the patient needs reassurance that many others share his experience and multi‑front support beyond the clinician relationship.

Anchor: Use of image. What supplementary purpose can a highlighted slide image serve when teaching about nonadherence?

Illustrate emphasized teaching points; image as supplement only, not as sole source of the answer.

Diagnosis: Tingling in left ring and small fingers + medial forearm sensory loss in a 62-year-old with left arm dialysis fistula — most likely diagnosis?

• Ulnar nerve compression

Pathophysiology: How does an elbow arteriovenous fistula cause neuropathy?

• AV fistula at elbow → local compression/traction of ulnar nerve

Feature: Sensory distribution of ulnar nerve compression at the elbow?

• Numbness/paresthesia: ring and small fingers; medial hand; medial forearm to elbow

Feature: Motor findings expected with ulnar nerve compression at the wrist vs elbow?

• Wrist compression → hand weakness and intrinsic atrophy; Elbow compression → sensory ± weakness

Diagnostic test to confirm suspected ulnar nerve compression?

• Electrodiagnostic testing (nerve conduction/EMG)

Initial management for ulnar nerve compression related to dialysis fistula?

• Behavior modification and ergonomic measures

When is surgery indicated for ulnar nerve compression?

• Severe or refractory symptoms after conservative measures

Arteriovenous steal syndrome: when would this diagnosis fit in a dialysis patient?

• Ischemic distal limb signs: pallor, pain during dialysis, pain at rest; uncommon to localize only to ring/small fingers

Why is diabetic neuropathy unlikely to explain isolated ring/small finger and medial forearm sensory loss?

• Diabetic neuropathy causes symmetric distal polyneuropathy, not focal ulnar distribution

Why are central causes (eg, cerebral infarction) unlikely for isolated medial hand and forearm sensory loss?

• Cerebral infarction causes contralateral cortical or hemispheric deficits, not focal peripheral nerve distribution to ring/small fingers and medial forearm

Use of provided image: What clinical sign near a dialysis fistula suggests local hemodynamic device presence without inflammation?

• Palpable thrill at fistula site

Essential (pre-existing) hypertension in pregnancy: diagnostic blood pressure criteria and timing?

• Systolic > 140 mm Hg or diastolic > 90 mm Hg
• On ≥2 measurements ≥4 hours apart
• Before 20 weeks' gestation

Why is the 37-year-old patient in the vignette diagnosed with essential hypertension?

• BP 150/100 and 150/98 at 18 wk (before 20 wk) with trace urine protein → meets pre-existing HTN criteria; urine protein can be normal in essential HTN

Normal urine protein result significance in essential hypertension during pregnancy?

• Urine protein often normal in essential (pre-existing) hypertension

Gestational hypertension: when would this diagnosis apply?

• New hypertension after 20 weeks' gestation without proteinuria

Preeclampsia: defining feature that distinguishes it from essential hypertension?

• Hypertension with new proteinuria or end-organ dysfunction after 20 weeks' gestation

Superimposed preeclampsia on essential hypertension: when is this diagnosis correct?

• Patient has pre-existing hypertension before 20 wk and then develops new proteinuria or worsening HTN/end-organ signs

Transient hypertension in pregnancy: defining features?

• Temporary BP elevation without persistent hypertension and no proteinuria, typically resolves

Physiologic blood pressure change in early pregnancy relevant to diagnosis?

• BP decreases between 12 and 19 weeks' gestation, which can mask pre-existing HTN

Maternal and fetal risks associated with essential hypertension in pregnancy?

• Mother: superimposed preeclampsia, postpartum hemorrhage
• Fetus: fetal growth restriction, preterm birth, placental abruption

Initial management principles for essential hypertension in pregnancy?

• Oral antihypertensives and increased maternal-fetal monitoring

Slide image: visual highlight of teaching points (supplementary)

• Supplementary image:
• Image illustrates highlighted teaching points; question answers must be known without the image

Diagnosis: 42-year-old transplant patient with Ca2+ 11.7 mg/dL and PTH 425 pg/mL; chronic kidney failure history. What is the most likely diagnosis?

• Tertiary hyperparathyroidism

Pathophysiology: What causes tertiary hyperparathyroidism in chronic kidney disease?

• Long-term secondary hyperparathyroidism → parathyroid hyperplasia → autonomous PTH secretion → persistent hypercalcemia

Lab pattern: What combination of serum calcium and PTH occurs in tertiary hyperparathyroidism?

• Elevated serum Ca2+ with persistently elevated PTH

Treatment: Primary management for tertiary hyperparathyroidism?

• Surgical removal of one or more hyperplastic parathyroid glands

Why is hypervitaminosis D (excess vitamin D) an unlikely cause of this patient's labs?

• Hypervitaminosis D → hypercalcemia but causes suppressed PTH via negative feedback

When would hypervitaminosis A be the correct diagnosis instead of tertiary hyperparathyroidism?

• Excess vitamin A with symptoms: dry/itchy skin, hair loss, headaches, nausea/vomiting, fatigue, irritability, joint pain

Why is parathyroid adenoma (primary hyperparathyroidism) less likely in this patient with CKD history?

• CKD history more consistent with tertiary hyperparathyroidism from hyperplasia; text states parathyroid adenoma would present with decreased PTH concentrations

Why is thyrotoxicosis an unlikely explanation for this patient's hypercalcemia and PTH elevation?

• Thyrotoxicosis causes hyperthyroid symptoms (palpitations, tremor, weight loss) and involves thyroid hormones, not autonomous PTH secretion

Clinical features of hyperparathyroidism to recognize in patients:

• Fatigue; muscle weakness; bone pain; kidney stones

Distinguishing parathyroid hyperplasia vs adenoma in hyperparathyroidism context:

• Hyperplasia: multiple glands enlarged, occurs in long-term secondary → tertiary; Adenoma: single gland, primary disease

Define the procedure parathyroidectomy.

• Parathyroidectomy: operation to remove one or more hyperplastic parathyroid glands.

Meningococcal disease: key clinical presentation

• Fever
• Headache
• Nuchal rigidity
• Altered mental status
• Often preceded by upper respiratory prodrome

Neisseria meningitidis: important epidemiologic risk factor

• Communal living (eg, homeless shelters) increases risk of meningococcal disease

Definition of 'close contacts' for meningococcal prophylaxis

• Close contact = proximity within feet for >8 hours or direct exposure to oral secretions

Management anchor: appropriate prophylaxis strategy for hospital personnel exposed to N. meningitidis

• Chemoprophylaxis for close contacts only

Why prophylaxis for close contacts is correct for meningococcal exposure

• Chemoprophylaxis decreases spread; close contacts (prolonged proximity or oral secretions) are highest risk

Why prophylaxis for all ED personnel on arrival (Choice A) is incorrect

• Not necessary: personnel not in vicinity for prolonged time are low risk; avoid unnecessary antibiotics and resistance

Why prophylaxis for immunocompromised personnel only (Choice C) is incorrect

• Not inclusive: immunocompetent close contacts are also at risk and should receive prophylaxis

Why no prophylaxis for hospital personnel (Choice D) is incorrect

• Not appropriate: chemoprophylaxis has been shown to decrease transmission among close contacts

Preferred chemoprophylactic agents for meningococcal close contacts (set 1)

• Rifampin
• Ciprofloxacin

Preferred chemoprophylactic agent for meningococcal close contacts (set 2)

• Ceftriaxone

Diagnosis: What diagnosis is most consistent with acute onset severe dyspnea, hypoxemia (SpO2 88%), sinus tachycardia, 1+ bilateral leg edema, recent long-distance immobility (truck driving), and a chest x-ray shown?

• Acute pulmonary embolism (PE)

Pathophysiology: What ABG pattern is associated with acute pulmonary embolism?

• Acute respiratory alkalosis with hypoxemia and increased A–a gradient

Risk factors: Which immobility-related risk is highlighted for PE in this case?

• Prolonged sitting (long-distance truck driving)

Diagnostic test choice: What is the preferred imaging to confirm suspected acute pulmonary embolism?

• Spiral CT scan of the chest (CT pulmonary angiography)

D-dimer use: When is a serum D-dimer assay appropriate for suspected PE?

• When clinical suspicion is low but PE cannot be excluded

BNP use: When is serum BNP measurement indicated instead of primary PE testing?

• When concern is for congestive heart failure/cardiogenic pulmonary edema

Cardiac enzymes: When is measurement of cardiac enzymes the appropriate next step?

• When acute coronary syndrome is suspected (eg, ischemic ECG changes)

Chest tube: When is placement of a chest tube indicated in acute respiratory presentation?

• For large pneumothorax or sustained pleural fluid causing respiratory compromise, not for PE

Steroids: When is IV hydrocortisone appropriate in acute dyspnea?

• For severe bronchospasm/asthma or adrenal crisis, not for PE without those features

ECG/clinical features: What ECG and clinical findings are typical but nonspecific for PE?

• Sinus tachycardia and acute dyspnea; ECG often otherwise nonspecific

Imaging supplement: Show chest x-ray image associated with the case (illustration only).

- Chest x-ray provided as supportive image; chest x-ray alone does not confirm PE

Pulmonary embolism: typical presenting features?

• Acute chest pain
• Shortness of breath
• Hypoxemia

Pulmonary embolism: clinical risk factors that prompt rapid testing (group 1)?

• Immobility
• Recent surgery
• Trauma / long-bone fracture

Pulmonary embolism: additional clinical risk factors (group 2)?

• Obesity
• Malignancy
• Pregnancy or OCP use

Diagnostic test: preferred method to confirm pulmonary embolism?

• Spiral CT scan of the chest (CT pulmonary angiography)

D-dimer: limitation when Wells score indicates high pretest probability?

• Negative D-dimer may be false negative; CT angio required

Obstructive shock from massive pulmonary embolism: best immediate management principle?

• Remove obstruction: thrombectomy or thrombolysis

Hydrocortisone IV: when is it appropriate?

• COPD exacerbation causing SOB
• Hypotension refractory to fluids + vasopressors (suspect adrenal insufficiency)

Hydrocortisone IV: why not appropriate for this patient with suspected PE?

• Patient lacks adrenal insufficiency or fluid-refractory hypotension; PE causes obstructive shock not responsive to vasopressors alone

Chest tube placement: appropriate indications?

• Symptomatic pleural effusion
• Hemothorax
• Pneumothorax

Chest tube placement: why not appropriate for this patient?

• Patient chest x-ray lacks pleural effusion, hemothorax, pneumothorax

Educational rule: when to test rapidly for pulmonary embolism?

• Sudden SOB with risk factors (immobility, surgery, malignancy, pregnancy/OCP, trauma/fracture, thrombophilia) → rapid diagnostic testing

Clinical anchor: 82-year-old man with urinary retention (1700 mL turbid urine), hypotension unresponsive to fluids and norepinephrine, leukocytosis, hyponatremia, hyperkalemia, elevated BUN/Cr — what is the most likely endocrine contributor to persistent hypotension?

Adrenal insufficiency

Clinical anchor: Which laboratory pattern in this patient supports adrenal insufficiency as a contributor to shock?

• Hyponatremia
• Hyperkalemia (borderline)
• Elevated BUN/Cr

Clinical anchor: What is the most appropriate immediate therapy for suspected adrenal insufficiency causing refractory septic hypotension?

Intravenous hydrocortisone (glucocorticoid) supplementation

Clinical anchor: Why is hydrocortisone indicated for vasopressor-refractory septic shock?

Glucocorticoid supplementation restores adrenal hormones and improves vasopressor responsiveness in refractory septic hypotension

Clinical anchor: When would bladder irrigation with amphotericin B be appropriate instead of hydrocortisone?

Localized urogenital fungal infection requiring topical therapy; not for septic shock or hypotension

Clinical anchor: When is intravenous fluconazole appropriate in a septic patient?

Documented or strongly suspected systemic fungal infection sensitive to fluconazole; not for immediate reversal of hypotension

Clinical anchor: When is intravenous metronidazole appropriate in an infected patient with hypotension?

For infections by anaerobic bacteria (eg, intra-abdominal, pelvic) as antimicrobial therapy; not a vasopressor or shock reversal agent

Clinical anchor: When is immediate hemodialysis indicated for hypotension with elevated BUN/Cr?

Indications: refractory hyperkalemia, volume overload unresponsive to diuretics, or severe uremic complications; mild creatinine rise alone does not mandate emergent dialysis

Clinical anchor: What acute urologic finding in this case likely precipitated the sepsis?

Urinary retention with 1700 mL turbid urine indicating obstructive retention and likely infected bladder/UTI

Clinical anchor: How does limited vasopressor responsiveness relate to endocrine causes of shock in sepsis?

Limited vasopressor response is a hallmark of endocrine contributions (eg, adrenal insufficiency) to septic shock

Supplement: Slide illustrating key teaching (use as summary only)

See illustration:

Acute adrenal insufficiency: next immediate management for persistent hypotension after large-volume IV fluids and vasopressors?

IV glucocorticoids (eg, IV hydrocortisone)

Why is IV glucocorticoid therapy correct for acute adrenal insufficiency with refractory hypotension?

Restores cortisol effect when production or responsiveness is insufficient, reversing vasopressor-refractory hypotension

Pathophysiology of acute adrenal insufficiency mentioned in the text?

Insufficient adrenal hormone production or reduced responsiveness to adrenal hormones

Indications for immediate hemodialysis per the text (group 1 of examples)?

• Life-threatening acidosis (eg, pH <6.9)
• Severe electrolyte derangement (eg, K+ >6.5 mEq/L)

Indications for immediate hemodialysis per the text (group 2 of examples)?

• BUN >100 mg/dL with symptoms (pericarditis/encephalopathy)
• Dialyzable toxic ingestion (eg, aspirin)

Why is emergent hemodialysis NOT appropriate for this patient now?

Patient is producing urine and does not meet emergent dialysis criteria

How should hemodynamic instability be managed relative to dialysis initiation?

Address hemodynamics first or in parallel with dialysis to avoid circulatory collapse

When should you suspect acute adrenal insufficiency in a hypotensive patient?

When hypotension persists despite large-volume IV fluids and vasopressors

Which clinical action is emphasized as more appropriate than starting antibiotics for this patient's hypotension?

Treat suspected acute adrenal insufficiency with IV glucocorticoids rather than prioritizing empiric antibiotics