Clinical Decision Making

Sensitivity Vs Specificity

"Imagine you're running airport security, screening passengers (tests) to catch dangerous items (diseases). Now meet your two star agents: Sensitivity and Specificity.

Sensitivity is your overachiever. It’s all about catching every possible threat. If a test has high sensitivity, it correctly identifies most people with the disease—it rarely misses anyone. In other words, it’s great at picking up true positives. The downside? It might sometimes flag innocent travelers (false positives), just to be safe.

Specificity, on the other hand, is cool and precise. If a test has high specificity, it correctly clears people without the disease—it rarely calls someone sick if they’re actually healthy. That means fewer false alarms (false positives), but if it’s too strict, it might miss some real cases (false negatives).

In short:

High sensitivity = fewer false negatives.

High specificity = fewer false positives.

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Legionnaires’ disease

Legionella is a type of bacterium found naturally in freshwater environments, like lakes and streams. It can become a health concern when it grows and spreads in human-made water systems such as building premise plumbing and cooling towers (structures that contain water and a fan as part of centralized air-cooling systems for building or industrial processes). Legionella can continue to persist in the water system unless proper steps are taken to prevent the growth of bacteria.

Outbreaks of Legionnaires’ disease are often associated with large or complex potable water systems.

Urine antigen testing via immunochromatography is a widely available, quick diagnostic test with a > 85% sensitivity and > 99% specificity for Legionella pneumophila. However, the available assay only tests for L pneumophila serogroup 1

Antimicrobial therapy is dictated by the severity of the infection, underlying conditions or allergies, antimicrobial resistance, and medication availability. Some guidelines and studies suggest that macrolides may be superior to fluoroquinolones. Parenteral therapy is the preferred initial treatment modality; patients should be transitioned to oral therapies with clinical improvement.

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Trigeminal neuralgia (tic douloureux)

"Imagine your face has a super-sensitive alarm system—the trigeminal nerve. It’s supposed to quietly handle sensations like touch, warmth, or a gentle breeze. But with trigeminal neuralgia, that system goes haywire. Suddenly, even mild triggers like brushing your teeth, talking, or a light wind can set off intense, electric-shock-like pain. It’s like your nerve’s alarm is stuck on high alert, firing off pain signals when it shouldn’t.

The cause? Often, a blood vessel pressing on the nerve—or sometimes multiple sclerosis or other conditions—can irritate or damage the nerve’s protective covering.

Historically, trigeminal neuralgia was first described in the 17th century by physician Johannes Bausch. It was later more clearly defined in the 18th century by John Fothergill, who provided one of the earliest clinical descriptions, leading to the term “Fothergill’s disease.” The condition has long been recognized as one of the most severe forms of facial pain in medical literature."

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Key Takeaway Points in Medicine

 

As new medical residents, it's essential to build a strong foundation in both clinical reasoning and patient centered care. Prioritize thorough history-taking and physical exams, use evidence-based guidelines, and avoid unnecessary testing or treatment. Focus on communication, prevention, and safe prescribing practices, especially in complex or elderly patients. Embrace continuous learning, collaborate with your team, and remain aware of your limitations. These principles not only improve patient outcomes but also support your development into a thoughtful and effective physician.

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Prostate-Specific Antigen (PSA) Test

• Total PSA (tPSA):

o Measures overall PSA levels in the blood.

o Used as the primary screening test.

• Free PSA (fPSA): 

o Measures unbound PSA.

o Lower free PSA percentage suggests a higher cancer risk.

• PSA Density (PSAD): 

o Adjusts PSA levels based on prostate volume

o Helps differentiate BPH from cancer.

• PSA Velocity (PSAV): 

o Tracks PSA level changes over time.

o Rapid increase may indicate aggressive cancer.

• PSA Doubling Time (PSADT): 

o Measures how quickly PSA levels double.

o Faster doubling suggests more aggressive cancer.

• Pro-PSA & Prostate Health Index (PHI): 

o Includes p2PSA, total PSA, & free PSA

o To improve cancer detection & reduce unnecessary biopsies.

• 4Kscore Test: 

o Evaluates four PSA-related proteins along with clinical factors.

o To estimate the risk of high-grade cancer.

• PCA3 Test: 

o Urine-based genetic test detecting PCA3 mRNA.

o Highly specific to prostate cancer.

• IsoPSA Test: 

o Analyzes PSA structural changes to distinguish benign conditions from cancer.

 

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SIRS vs Sepsis

 Systemic Inflammatory Response Syndrome (SIRS)

1. Non-specific (infections vs non-infectious)
2. ≥2 of the following:
• Temp >38°C or <36°C
• HR >90 bpm
• RR >20 or PaCO₂ <32 mmHg
• WBC >12,000/mm³, <4,000/mm³, or >10% bands

Sepsis

1. Organ dysfunction due to dysregulated host response to infection.
2. SOFA score increases by ≥2.
3. qSOFA (≥2 indicates high risk):

• Altered mental status (GCS <15)
• RR ≥22/min
• SBP ≤100 mmHg

Severe Sepsis (Obsolete Term in Sepsis-3, 2016)

• Sepsis + tissue hypoperfusion/organ dysfunction.

Septic Shock

• Sepsis + circulatory failure

• Hypotension requiring vasopressors (MAP <65 mmHg).
• Lactate >2 mmol/L 

Management (Surviving Sepsis Campaign Guidelines)

• Early recognition & treatment (within 1 hour)
• IV fluids (30 mL/kg crystalloid in 1st 3 hours)
• Broad-spectrum antibiotics ASAP
• Vasopressors (norepinephrine) if MAP <65 mmHg
• Source control (drain abscesses, remove infected devices)
• Supportive care (oxygenation, ventilation, glycemic control, DVT/stress ulcer prophylaxis)

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Guillain–Barré syndrome (GBS)

(aka: Landry–Guillain–Barré–Strohl syndrome:

• Most common cause of acute flaccid paralysis
• Rapidly progressive ascending paralysis & areflexia
• Autonomic dysfunction, CSF albumin-cytologic dissociation.
• The sensory and motor systems may be equally affected. 
• The paralysis moves rapidly from lower to upper areas.

Differential diagnosis:

• Myasthenia gravis: Intermittent & worsened by exertion.
• Multiple Sclerosis: CNS demyelination, hyperreflexia, multiple lesions on MRI, oligoclonal bands in CSF.
• Botulism: Descending weakness fixed dilated pupils, food/wound toxin exposure & prominent cranial nerve dysfunction with normal sensation.
• Tick paralysis: Ascending paralysis but spares sensation.
• West Nile virus: Headache, fever, & asymmetric flaccid paralysis but spares sensation.
• Transverse myelitis: Pain, weakness, abnormal sensation, urinary dysfunction, sensory level, hyperreflexia, spinal cord lesion on MRI.
• CIDP: Chronic progression, relapses, requires long-term immunotherapy.
• Spinal Cord Compression: Hyperreflexia, sensory level, MRI shows mass or compression.

 

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Lower extremity edema

Lower extremity edema is a multifactorial clinical condition characterized by the abnormal accumulation of interstitial fluid within the subcutaneous tissues of the lower limbs. Clinically, it often presents as visible swelling, which may be either pitting or non-pitting, depending on the underlying etiology. The pathophysiology involves a complex interplay of mechanisms, including increased capillary hydrostatic pressure, decreased oncotic pressure, lymphatic obstruction, and increased capillary permeability. The differential diagnosis is broad, encompassing systemic causes such as congestive heart failure, chronic kidney disease, and hepatic dysfunction, as well as localized factors including venous insufficiency, lymphedema, and trauma. A thorough history and physical examination, complemented by appropriate diagnostic studies such as duplex ultrasonography and laboratory testing, are essential to identify the underlying cause and to inform appropriate management strategies. 

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