Cervical Artery Dissection (CAD)

Occurs as a result of the interplay among risk factors, minor trauma, anatomic &

congenital abnormalities, & genetic predisposition.

Diagnosis can be challenging both clinically & radiologically.

In those with acute ischemic stroke attributable to CAD, acute treatment

strategies such as thrombolysis & mechanical thrombectomy are reasonable in

otherwise eligible patients.

AHA suggest that the antithrombotic therapy choice be individualized &

continued for at least 3 to 6 months.

Risk of recurrent dissection is low, & preventive measures may be considered

early after the diagnosis & continued in high-risk patients. 

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Perioperative Antithrombotic Management:

The recommended pre-operative workup for patients taking anticoagulants involves

 stratifying both thromboembolic & bleeding risk, determining appropriate timing for

 medication interruption, & deciding whether bridging therapy is needed. The

 specific approach depends on the type of anticoagulant, renal function, and

 procedure-related bleeding risk.

• Direct Oral Anticoagulants (DOACs)

1. For apixaban, rivaroxaban, and Edoxaban, the American College of Chest Physicians recommends stopping these agents 1-2 days before low-to-moderate bleeding risk procedures and 2 days before high bleeding risk procedures.

• For dabigatran, interruption timing depends on renal function. 

1. With normal renal function (CrCl ≥50 mL/min), stop 1-2 days before low-risk procedures and 2 days before high-risk procedures. 
2. With impaired renal function (CrCl <50 mL/min), extend interruption to 3-4 days before high-risk procedures due to predominantly renal clearance.

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Urinary Tract Infections (UTI)

• Women have a lifetime risk of 53% of experiencing UTI. 
• Men prior to age 50, have lifetime risk is 14%.
• Risk of experiencing a UTI increase with age in both sexes.

Classification:

• Uncomplicated UTI

Infection confined to the bladder in afebrile women or men.

• Complicated UTI: 

Infection beyond the bladder in women or men. 

• Pyelonephritis 
• Febrile or bacteremic UTI 
• Catheter-associated (CAUTI)
• Prostatitis.

Catheter- Associated UTI (CA-UTI)

• CAUTIs are one of the most common healthcare-associated infection (HAI).
• 75% of UTIs developed in hospitals are associated with a urinary catheter.
• 15-25% of hospitalized pts receive urinary catheters during their hospital stay.
• CAUTIs are associated with increased morbidity, mortality, healthcare costs & LOS.
• They are preventable.

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Invasive Fungal Infection (IFI

 

Invasive fungal infections are severe infections in which fungal pathogens invade normally sterile body sites. They predominantly affect immunocompromised patients, including those with neutropenia, hematologic malignancies, solid organ or stem cell transplants, and prolonged corticosteroid or broad-spectrum antibiotic use.

Common Pathogens

• Candida species (most frequent cause of bloodstream infections)
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• Aspergillus species (primarily pulmonary infections)
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• Cryptococcus species (commonly CNS involvement)
• 
  
• Emerging molds and rare fungi in high-risk populations

Risk Factors

• Immunosuppression (neutropenia, chemotherapy, transplant)
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• Indwelling catheters or prosthetic devices
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• Prolonged ICU stay and broad-spectrum antibiotic exposure

Clinical Presentation

• Symptoms vary by site of infection and may include fever, organ dysfunction, respiratory distress, or neurological deficits

Diagnosis

• Culture and microscopy from sterile sites
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• Antigen/antibody testing (e.g., β-D-glucan, galactomannan, cryptococcal antigen)
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• Imaging studies (CT, MRI) for organ involvement
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• Histopathology when feasible

Management Principles

• Early initiation of targeted antifungal therapy
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• Source control, including removal of infected catheters or drainage of abscesses
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• Selection of therapy guided by species identification and antifungal susceptibility
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• Multidisciplinary approach with infectious diseases consultation

Prognosis

• Dependent on timely diagnosis, host immunity, and pathogen virulence
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• Delays in treatment significantly increase morbidity and mortality

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Ulcerative Colitis

 

The diagnosis of UC is best made with endoscopy and mucosal biopsy for

 histopathology. Laboratory studies are helpful to exclude other diagnoses and assess

 the patient's nutritional status, but serologic markers can assist in the diagnosis of

 inflammatory bowel disease. Radiographic imaging has an important role in the

 workup of patients with suspected inflammatory bowel disease and in the

 differentiation of UC from Crohn disease by demonstrating fistulae or the presence of

 small bowel disease seen only in Crohn disease.

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Orbital Cellulitis

Peri-orbital and orbital cellulitis are distinct clinical diseases, though have overlapping clinical features and therefore can be difficult to differentiate

• Orbital cellulitis: Infection within the orbit, (ie post-septal, the structures posterior to the orbital septum); Surgical emergency with major complications including loss of vision, abscess formation, venous sinus thrombosis and extension to intracranial infection with subdural empyema, and meningitis; & the majority (>80%) of cases relate to local sinus disease.
• Peri-orbital cellulitis: Infection of the eye lids and surrounding skin not involving the orbit (ie pre-septal, the structures anterior to the orbital septum)
• The globe is not involved in either infection.

The causative organisms, commonly bacterial but can also be polymicrobial, often including aerobic and anaerobic bacteria and even fungal or mycobacteria. The most common bacterial organisms causing orbital cellulitis are Staphylococcus aureus and Streptococci species. Rare cases of orbital cellulitis caused by non-spore-forming anaerobes Aeromonas hydrophila, Pseudomonas aeruginosa, and Eikenella corrodens have also been reported. 

 

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MSSA and MRSA

Methicillin-Sensitive Staphylococcus aureus (MSSA) and Methicillin-Resistant Staphylococcus aureus (MRSA). 

MSSA arrived quietly, without unnecessary drama. Predictable and courteous, he followed the usual clinical trajectory of fever, positive blood cultures, appropriate management, and steady improvement. The team appreciated his transparency; he respected the rules of engagement and left promptly once his source was addressed. There were no consult wars, no prolonged discussions but just a clean resolution and a satisfied discharge summary.

MRSA, however, was a different story altogether. He entered the bloodstream with confidence and defiance, fully aware of his reputation. The moment his name appeared on the microbiology report, the atmosphere changed. The primary team sighed, pharmacy frowned, and infection control started whispering about isolation protocols. MRSA thrived on attention and turning every simple bacteremia into a multidisciplinary production involving ID, nursing, infection prevention, and sometimes even hospital administration. He lingered longer than anyone wanted, testing the limits of patience, policy, and resource allocation. With coordinated teamwork, careful management, and more meetings than anyone cared to count, MRSA was finally cleared from the bloodstream.

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MRSA-PCR

Picture MRSA-PCR as the hospital’s ultimate crime-fighting superhero team, but instead of capes and laser eyes, it wields test tubes and genetic scanners. MRSA the notorious “bad boy” of bacteria, likes to sneak into hospitals, pick fights with antibiotics, and then hide in plain sight like a germy ninja. Old-school tests stumble around like detectives in a black-and-white movie, muttering “the culture will be ready in a few days,” while MRSA laughs and throws confetti in the background.

😷⚕️⭐️But PCR? Oh no, PCR doesn’t waste time. It storms in like a caffeinated detective on double espresso, grabs a swab, and yells: “Aha! There’s the MRSA DNA, hiding in your nose like it pays rent!” In just hours, the mystery is solved, the bacteria is busted, and the lab gets to feel like it just solved the medical equivalent of a bank heist. Fast, flashy, and way more reliable than waiting around for Petri dishes to gossip, MRSA-PCR is basically the hospital’s drama-filled reality show where the germs always get exposed.

 

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Drug Induced Hyponatremia

 

Think of sodium as the ultimate event planner in your body, the one who keeps everything orderly, balanced, and running on time. Sodium knows how to keep water in the right places: not too little, not too much, just the perfect hydration vibe. It’s like that one responsible friend who prevents the party from getting out of control.

Now, here’s where the drama starts: certain medications like thiazide diuretics, SSRIs, carbamazepine, and their buddies decide they know better. Instead of appreciating sodium’s years of experience, they“reassign” it, often flushing it away or silencing its role in water regulation. It’s like firing the competent manager and hiring an overenthusiastic intern.

With sodium out of the picture, water seizes the opportunity. It floods the party like uninvited guests crashing a wedding buffet pouring into cells, especially in the brain. At first, the brain cells are polite, trying to squeeze in a little extra water. But soon they swell like overfilled balloons, and the nervous system throws a fit: headaches, confusion, unsteady gait, seizures and in severe cases, a medical emergency that’s about as fun as a power outage during surgery.

The irony? This whole watery rebellion isn’t caused by an exotic tropical disease or some rare genetic mutation it’s often the very “helpful” medications prescribed to make life better. That’s drug-induced hyponatremia: when well-meaning pills accidentally kick sodium out of its leadership role, and water runs the show like a toddler hyped on sugar.

So, the moral of the story? Respect sodium, it may be small, but it’s mighty. And always keep an eye on those meds, because sometimes the cure sneaks in with a side hustle as the troublemaker.

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Mitral valve regurgitation

 Mitral valve regurgitation is the heart’s version of a plot twist — just when you think everything’s flowing forward, boom, blood decides to moonwalk back into the left atrium. Picture the mitral valve as a pair of elegant French doors between the left atrium and ventricle: they’re supposed to swing shut with precision and class. But in MR, one or both of those doors get a little loose, floppy, or just plain defiant — thanks to degenerative disease, ischemic insults, or the occasional rheumatic meddler still hanging around like it’s the 1940s. The result? Blood backflows during systole, the atrium gets flooded like a poorly planned basement, and the ventricle starts pumping harder than a med student during exam week just to keep up. Clinically, it’s a delicious mix of holosystolic murmurs, volume overload, atrial fibrillation auditions, and left ventricular eccentric hypertrophy trying to make it all work. And let’s not forget the symptoms — fatigue, dyspnea, and that glorious pulmonary congestion that says, “I’m leaking but fabulous.” Diagnosis by echocardiography turns into a cardiac detective story, and treatment spans the spectrum from medical finesse to surgical drama, complete with valve repair or replacement. So while MR might sound like just another leaky valve, in the world of internal medicine and cardiology, it’s a charismatic troublemaker — dramatic, unpredictable, and never boring.

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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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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

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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