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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Palm Rashes

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.

 

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Tremor

TREMOR

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)

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Chronic Kidney Disease (CKD)

 

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.

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Radio-opaque shadows on ABDOMINAL X-RAY

• 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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What Do You See

The eye is a highly complex organ composed of various tissues and structures that function together to enable vision. Ocular disorders can range from benign, self-limiting conditions to malignant, potentially metastatic tumors. A wide array of factors can contribute to eye diseases, leading to a spectrum of signs and symptoms. These symptoms may be as mild as minor irritation or discomfort, or as severe as blurred vision or complete blindness. One example of an ocular disorder is strabismus, a condition characterized by misalignment of the eyes. In strabismus, one eye typically fixates on an object of interest while the other deviates inward (esotropia), outward (exotropia), downward (hypotropia), or upward (hypertropia).

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Management of DM in Patients With CKD

Monitor blood pressure, serum creatinine, and serum potassium levels within 2 to 4 weeks after initiating or increasing the dose of an angiotensin-converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB). ACEi or ARB therapy should generally be continued unless serum creatinine increases by more than 30% within 4 weeks of initiation or dose escalation.

According to FDA recommendations, metformin should not be used in men with a serum creatinine level ≥ 1.5 mg/dL or in women with a level ≥ 1.4 mg/dL, or in individuals over 80 years of age with decreased creatinine clearance. However, treatment with metformin is recommended in patients with type 2 diabetes (T2D), chronic kidney disease (CKD), and an estimated glomerular filtration rate (eGFR) ≥ 30 mL/min/1.73 m².

ADA/KDIGO Consensus Statements:

All patients with type 1 or type 2 diabetes and CKD should be managed using a comprehensive, individualized care plan developed collaboratively between healthcare professionals and the patient. This plan should focus on optimizing nutrition, physical activity, smoking cessation, and weight management. Evidence-based pharmacologic therapies should be implemented to preserve organ function, alongside additional treatments aimed at achieving intermediate targets for glycemic control, blood pressure, and lipid management.

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Non-ST Elevation Acute Coronary Syndrome (NSTE-ACS)

Myocardial Infarction (MI)

Myocardial infarction is classified into five types based on the underlying etiology and clinical circumstances:

• Type 1 MI: Spontaneous myocardial infarction resulting from ischemia due to a primary coronary event, such as plaque rupture, erosion, fissuring, or coronary artery dissection.

• Type 2 MI: Myocardial ischemia secondary to an imbalance between oxygen supply and demand. This may occur in the setting of increased demand (e.g., severe hypertension) or decreased supply (e.g., coronary artery spasm, embolism, arrhythmias, or hypotension).

• Type 3 MI: Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia and presumed new ECG changes or ventricular fibrillation before biomarkers can be obtained.

• Type 4a MI: Myocardial infarction associated with percutaneous coronary intervention (PCI), defined by an elevation in cardiac troponin (cTn) values >5 times the 99th percentile upper reference limit (URL), along with evidence of ischemia.

• Type 4b MI: Myocardial infarction associated with documented stent thrombosis.

• Type 5 MI: Myocardial infarction occurring in the context of coronary artery bypass grafting (CABG), with cTn elevation >10 times the 99th percentile URL and supporting clinical or imaging findings.

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Infarct Location and Clinical Implications

• Right Ventricular (RV) Infarction: Most commonly results from obstruction of the right coronary artery or a dominant left circumflex artery. It is characterized by elevated right ventricular filling pressures, which may be accompanied by severe tricuspid regurgitation and reduced cardiac output. RV infarction can significantly impair hemodynamics.

• Inferoposterior Infarction: Often leads to some degree of RV dysfunction in approximately 50% of cases and hemodynamic compromise in about 10–15%. In patients with inferoposterior infarction, elevated jugular venous pressure in conjunction with hypotension or shock should prompt consideration of RV involvement. RV infarction in the setting of left ventricular infarction markedly increases mortality risk.

• Anterior Infarction: These infarcts are typically larger and are associated with worse outcomes compared to inferoposterior infarctions. They usually result from obstruction of the left coronary artery, particularly the left anterior descending artery. In contrast, inferoposterior infarctions are commonly due to right coronary artery or dominant left circumflex artery occlusion.

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Acute Cholangitis

Cholangitis

Cholangitis was first defined in 1877 by Jean-Martin Charcot, who described the pathognomonic triad of fever, right upper quadrant pain, and jaundice. Today, cholangitis is defined as the presence of increased hepatic intraductal pressure along with concurrent infection of the obstructed bile ducts.

Chole: Derived from the Greek word “cholē,” meaning bile.
Angio: Comes from the Greek “angeion,” meaning vessel.
Cholangitis: Refers to a bacterial infection of the biliary tree.

The pathogens most commonly identified as causative agents of acute ascending cholangitis are gram-negative and anaerobic organisms. The most common pathogens include Escherichia coli, Klebsiella, Enterobacter, Pseudomonas, and Citrobacter.

Iatrogenic introduction of bacteria often occurs following endoscopic retrograde cholangiopancreatography (ERCP) in individuals with biliary obstruction.

• Charcot's Triad: The classical triad (fever, right upper quadrant pain, and jaundice) has high specificity (95.9%) but low sensitivity (26.4%).

• Tokyo Guidelines (2018): The sensitivity of the Tokyo guidelines is 100%, with a specificity of 87.4%.

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