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"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."

 


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.



• 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.

 

 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)


(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.

 


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. 


Common features and patterns:
  • Color:
  1. Red or erythematous: Common in inflammatory or allergic reactions.
  2. Purple or purpuric: May suggest vascular or hematologic issues, such as small blood vessel inflammation (vasculitis).
  3. White or hypopigmented: Seen in fungal infections or depigmentation disorders.
  4. Brown or hyperpigmented: May occur in chronic skin conditions or post-inflammatory hyperpigmentation.
  • Texture:
  1. Flat (macular): Rash appears as flat, discolored spots.
  2. Raised (papular or nodular): Bumps that may be small or large.
  3. Scaly or flaky: Seen in psoriasis or fungal infections.
  4. Smooth or shiny: Can occur in viral rashes or early dermatitis.
  • Moisture:
  1. Dry and cracked: Common in eczema or chronic irritation.
  2. Moist or oozing: May suggest infection, blistering, or acute contact dermatitis.
  • Distribution:
  1. Symmetrical: Seen in systemic causes like eczema, psoriasis, or drug reactions.
  2. Localized: Often indicates contact dermatitis or insect bites.
  3. Peripheral patterns: Rashes that concentrate around the edges of the palms can be seen in certain fungal infections.
  • Associated Symptoms:
  1. Itching: Common in eczema, scabies, or allergic reactions.
  2. Pain or burning: Suggests irritation, infection, or vascular issues.
  3. Blisters: Seen in contact dermatitis, hand-foot-and-mouth disease, or bullous skin conditions.
  4. Peeling or desquamation: Seen after infections (e.g., scarlet fever) or in conditions like Kawasaki disease.
  • Causes & Features:
  1. Contact Dermatitis: Red, itchy patches, sometimes with vesicles or blisters.
  2. Atopic Dermatitis: Chronic, itchy, scaly rash; may worsen with exposure to irritants.
  3. Psoriasis: Thick, scaly, silvery patches, often with well-defined edges.
  4. Hand-Foot-and-Mouth Disease: Small, red spots or blisters on palms, soles, and sometimes around the mouth.
  5. Fungal Infections (Tinea Manuum): Asymmetric scaling and redness, often with peeling.
  6. Scabies: Small, red papules with linear burrows, typically between fingers.
  7. Drug Reactions: Diffuse rash that can affect the palms, often accompanied by systemic symptoms.

 

  1. Involuntary, rhythmic, shaking movement of part of the body
  2. Occur when muscles repeatedly contract and relax.
  3. Classification:

  • Physiologic (Normal)
  • Abnormal (Pathologic)
  • Essential (Hereditary disorder)
  • Cerebellar (Damage to cerebellum)
  • Secondary (medication, or substance use, etc.)
  • Psychogenic (Psychologic factors)


 

Blood pressure–lowering therapy and treatment targets should be individualized in patients with frailty, a high risk of falls, very limited life expectancy, or symptomatic postural hypotension.

Therapies with strong evidence for delaying chronic kidney disease (CKD) progression include renin–angiotensin system inhibitors (RASi) and sodium–glucose cotransporter 2 inhibitors (SGLT2i). In patients with CKD and heart failure, SGLT2i provide benefits regardless of albuminuria status.

A modest initial decline in estimated glomerular filtration rate (eGFR) is expected following the initiation of hemodynamically active agents such as RASi and SGLT2i. However, a reduction in eGFR of ≥30% from baseline exceeds anticipated variability and should prompt further evaluation.

CKD is not a contraindication to invasive management strategies in patients with acute or unstable cardiac conditions. Similarly, imaging studies are not absolutely contraindicated in patients with CKD; the decision should be based on a careful assessment of individual risks and benefits.


  • A substance is more radiopaque if it contains atoms of high atomic number (AN) such as calcium, iodine, barium, or lead.
  • Bone, which contains calcium (AN 20), is more radiopaque than soft tissue, which is made up mostly of carbon (AN 6), hydrogen (AN 1), and oxygen (AN 8). 
  • Iodine (AN 53) is the key constituent of radiocontrast material and lead (AN 82) is an effective barrier to x-rays.


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