Palliative care focuses on relieving suffering and improving quality of life for patients with serious illnesses, not curing disease (A) or prolonging life at all costs (B).

Morphine is the WHO-recommended first-line strong opioid for moderate to severe cancer pain.

The WHO analgesic ladder has three steps: non-opioids, weak opioids, and strong opioids.

Total pain includes physical, psychological, social, and spiritual dimensions.

Low-dose morphine reduces the sensation of breathlessness in terminal dyspnea.

Hospice care provides comfort-focused care for patients with terminal illness and limited life expectancy.

Alzheimer’s disease accounts for 60–70% of dementia cases.

The 5 I’s of Geriatric Giants are: Immobility, Instability, Incontinence, Intellectual impairment, and Iatrogenesis.

Polypharmacy is commonly defined as using 5 or more medications simultaneously.

The Geriatric Depression Scale (GDS) is specifically designed for elderly depression screening.

Vertebral compression fractures are the most common osteoporotic fractures, followed by hip and wrist.

Delirium has acute onset with fluctuating consciousness and attention impairment.

ASA has 6 classes: I (healthy), II (mild systemic disease), III (severe systemic disease), IV (life-threatening), V (moribund), and VI (brain-dead organ donor).

ASA II = mild systemic disease, ASA III = severe systemic disease, ASA IV = life-threatening disease.

PT/INR monitors warfarin’s anticoagulant effect and bleeding risk.

≥4 METs (climbing one flight of stairs) indicates adequate functional capacity. <4 METs suggests poor capacity and higher perioperative risk.

Beta-blockers should be continued to prevent rebound tachycardia and hypertension.

Mallampati score assesses oropharyngeal structures to predict difficult intubation.

Normal hemoglobin in adult males is 13–17 g/dL (females: 12–16 g/dL).

Iron deficiency causes microcytic (small MCV) and hypochromic (pale) RBCs due to impaired hemoglobin synthesis.

Serum ferritin is the most specific marker for iron stores.

Vitamin B12 and folate deficiency impair DNA synthesis, causing megaloblastic changes.

Pernicious anemia is an autoimmune condition destroying parietal cells, leading to intrinsic factor deficiency and B12 malabsorption.

Subacute combined degeneration (posterior and lateral column involvement) is unique to B12 deficiency.

Codocytes are target cells seen in thalassemia, liver disease, and hemoglobinopathies.

In HbS, valine replaces glutamic acid at position 6 of the beta-globin chain.

Direct Coombs test detects antibodies on RBC surface, positive in autoimmune hemolytic anemia.

In anemia of chronic disease, iron is trapped in stores (normal/high ferritin) but unavailable (low serum iron).

Aplastic anemia shows pancytopenia (low RBCs, WBCs, platelets) with hypocellular/empty bone marrow.

Hereditary spherocytosis is the most common inherited hemolytic anemia in Northern Europeans.

Leukopenia is WBC <4,000/μL (or <4 × 10⁹/L).

Neutropenia is ANC <1,500/μL.

Clozapine (antipsychotic) is notorious for agranulocytosis, requiring regular WBC monitoring.

Febrile neutropenia is a medical emergency requiring immediate empirical broad-spectrum antibiotics due to infection risk.

Neutrophils are the primary defense against bacteria.

G-CSF (Granulocyte Colony-Stimulating Factor) stimulates bone marrow to produce neutrophils.

Philadelphia chromosome [t(9;22)] producing BCR-ABL fusion is the hallmark of CML (>95% cases).

ALL accounts for 75–80% of childhood leukemias.

Auer rods are crystallized granules seen in myeloblasts, pathognomonic for AML.

Smudge cells (fragile lymphocytes that rupture during smear preparation) are characteristic of CLL.

Reed-Sternberg cells (“owl-eye” binucleated giant cells) are pathognomonic for Hodgkin lymphoma.

Burkitt lymphoma (especially endemic African type) is strongly associated with EBV.

Burkitt lymphoma shows rapid cell turnover with tingible body macrophages creating a “starry sky” pattern.

Hyperkalemia in TLS can cause fatal cardiac arrhythmias.

Allopurinol inhibits xanthine oxidase, preventing uric acid formation.

TLS occurs with rapid cell death in highly proliferative tumors like acute leukemias and Burkitt lymphoma.

Leukocytosis is WBC >11,000/μL (varies slightly by lab).

Malaria is the most common cause of splenomegaly worldwide due to its high prevalence in endemic regions.

Massive splenomegaly occurs in CML (A), myelofibrosis (B), and kala-azar (D).

Painful (tender) lymph nodes suggest acute inflammation/infection with rapid node expansion.

Infectious mononucleosis (EBV) causes generalized lymphadenopathy with atypical lymphocytes (Downey cells).

Virchow’s node is an enlarged left supraclavicular lymph node, often indicating abdominal malignancy (especially gastric cancer) via thoracic duct spread.

Hemophilia A is Factor VIII deficiency.

Hemophilia affects the intrinsic pathway (factors VIII, IX), prolonging aPTT.

VWD is caused by deficiency or dysfunction of von Willebrand factor, which carries Factor VIII and aids platelet adhesion.

Platelet disorders (quantitative or qualitative) cause prolonged bleeding time with normal PT/aPTT.

DIC shows consumption of clotting factors and platelets: prolonged PT, aPTT, low fibrinogen, elevated D-dimer, and thrombocytopenia.

Vitamin K-dependent factors are II, VII, IX, X (and proteins C, S).

Von Willebrand disease affects 1% of the population, making it the most common inherited bleeding disorder.

Vitamin K reverses warfarin by restoring synthesis of vitamin K-dependent factors.

Monoarthritis = 1 joint; oligoarthritis = 2–4 joints; polyarthritis = ≥5 joints.

Prolonged morning stiffness (>1 hour) suggests inflammatory arthritis (e.g., RA).

Osteoarthritis shows bony enlargement (osteophytes), crepitus, and lack of inflammation.

OA commonly affects DIP joints (Heberden’s nodes).

Methotrexate is the anchor DMARD for RA due to efficacy and safety profile.

Folic acid supplementation reduces methotrexate side effects (stomatitis, cytopenias) by counteracting folate antagonism.

Infliximab is a TNF-alpha inhibitor.

Colchicine, NSAIDs, or corticosteroids treat acute gout.

Urate-lowering therapy (allopurinol/febuxostat) is started 2–4 weeks after acute attack resolves with prophylactic colchicine to prevent flares.

Gout shows negatively birefringent, needle-shaped monosodium urate crystals (yellow under parallel light).

Acetaminophen and topical NSAIDs are first-line for OA pain.

Periarticular osteopenia is seen in RA, not OA.

Pseudogout is caused by CPPD crystal deposition.

Reactive arthritis develops 1–4 weeks after GI or GU infection.

Dual-energy X-ray absorptiometry (DEXA) measures bone mineral density and is the gold standard.

T-score ≤-2.5 = osteoporosis.

Bisphosphonates (alendronate, risedronate) are first-line anti-resorptive agents.

Proximal myopathy causes weakness in hip/shoulder girdle muscles, affecting climbing and rising.

Anti-Mi-2 antibodies are highly specific for dermatomyositis.

Gottron’s papules (violaceous papules over knuckles) are pathognomonic for dermatomyositis.

Herpes simplex virus causes acantholysis, producing multinucleated giant cells (Tzanck cells) on smear.

Koplik spots are bluish-white spots on buccal mucosa opposite molars, appearing before the measles rash.

Coxsackievirus A16 (and Enterovirus 71) causes hand, foot, and mouth disease with vesicles at these sites.

Chickenpox vesicles are superficial, clear, and surrounded by erythema, resembling dew drops on rose petals.

Hutchinson’s sign (vesicles on nose tip) indicates nasociliary nerve involvement, predicting ocular complications in herpes zoster ophthalmicus.

VZV remains dormant in dorsal root ganglia after primary chickenpox and reactivates as herpes zoster (shingles) along a dermatome.

Ramsay Hunt syndrome is herpes zoster oticus affecting the facial nerve (CN VII), causing facial palsy, ear pain, and vesicles in external auditory canal.

HPV 6 and 11 are low-risk types causing 90% of genital warts.

Koilocytes are squamous cells with perinuclear halo and nuclear atypia, pathognomonic of HPV infection.

HPV 1, 2, and 4 cause plantar warts (verruca plantaris) on soles.

Molluscum contagiosum virus belongs to the Poxviridae family.

Henderson-Patterson bodies are large eosinophilic intracytoplasmic inclusion bodies pathognomonic of molluscum contagiosum.

Molluscum contagiosum presents as dome-shaped, pearly/waxy, umbilicated papules with central dell.

Oral hairy leukoplakia presents as white, corrugated, non-scrapable plaques on lateral tongue margins, caused by EBV in immunocompromised patients.

Human herpesvirus 8 (HHV-8), also called Kaposi sarcoma-associated herpesvirus (KSHV), causes Kaposi sarcoma.

CD4 count < 200 cells/μL defines AIDS and indicates high risk for opportunistic infections like Pneumocystis pneumonia. < 500 shows immune decline. < 50 increases risk of CMV/MAC.

Staphylococcus aureus is the most common cause of impetigo (both bullous and non-bullous types), followed by Group A Streptococcus.

Non-bullous impetigo presents with honey-colored/golden crusts over erythematous base, typically around nose and mouth.

Erysipelas involves superficial dermis and lymphatics, presenting with sharply demarcated, raised, erythematous borders (“peau d’orange”).

Exfoliative toxins (ETA and ETB) from S. aureus phage group II cleave desmoglein-1, causing superficial epidermolysis in SSSS.

Group A Streptococcus (S. pyogenes) and S. aureus are the most common causes of cellulitis.

Mycobacterium leprae, an obligate intracellular acid-fast bacillus, causes leprosy (Hansen’s disease).

Borderline leprosy (BB, BT, BL) is the most common type worldwide, as most patients fall on the spectrum between tuberculoid and lepromatous poles.

Leonine facies (lion-like face) due to diffuse skin infiltration and loss of eyebrows/eyelashes is characteristic of lepromatous leprosy.

Ulnar nerve is the most commonly affected nerve in leprosy, followed by lateral popliteal, posterior tibial, and facial nerves.

Ridley-Jopling classification (TT, BT, BB, BL, LL) is based on the immunological spectrum from strong cell-mediated immunity (TT) to absent (LL).

WHO MDT for multibacillary leprosy (≥6 lesions or smear positive) is for 12 months with rifampicin, clofazimine, and dapsone.

Treponema pallidum subspecies pallidum causes venereal syphilis.

Chancre is a painless, indurated ulcer with clean base at the site of inoculation in primary syphilis.

Secondary syphilis causes symmetric, maculopapular, non-pruritic rash involving palms and soles – this distribution is highly characteristic.

Condyloma lata are moist, flat, wart-like lesions in warm, moist areas (anogenital region) seen in secondary syphilis, highly infectious.

VDRL and RPR are non-treponemal (reagin) tests detecting antibodies to cardiolipin; used for screening and monitoring treatment.

Trichophyton rubrum is the most common dermatophyte worldwide causing tinea corporis, cruris, pedis, and unguium.

KOH (10-20%) dissolves keratin, making fungal hyphae and spores visible under microscopy.

Malassezia furfur (lipophilic yeast, formerly Pityrosporum) causes pityriasis versicolor.

Pityriasis versicolor shows short hyphae (spaghetti) and round yeast cells (meatballs) on KOH mount.

Malassezia produces azelaic acid which inhibits tyrosinase, blocking melanin synthesis, causing hypopigmentation.

Tinea capitis affects the scalp and hair.

Tinea pedis (athlete’s foot) affects feet, common in athletes due to sweaty footwear.

Tinea corporis (ringworm) shows annular lesions with active, scaly, raised borders and central clearing due to centrifugal spread of fungus.

Trichophyton tonsurans is the most common cause of tinea capitis in children (in most countries).

Microsporum species (M. audouinii, M. canis) produce pteridine pigments that fluoresce bright green under Wood’s lamp.

Candida albicans causes oral thrush (pseudomembranous candidiasis) – white, curd-like patches that can be scraped off.

Candida causes erythematous patches with satellite pustules/papules beyond the main lesion border, especially in skin folds.

Candida shows budding yeast cells with pseudohyphae (elongated yeast cells attached end-to-end) on KOH mount.

Acne vulgaris involves the pilosebaceous unit (hair follicle + sebaceous gland).

Comedone (open = blackhead, closed = whitehead) is the primary non-inflammatory lesion of acne due to keratin and sebum plugging the follicle.

Cutibacterium acnes (formerly Propionibacterium acnes) colonizes pilosebaceous follicles and triggers inflammation in acne.

Topical retinoids (tretinoin, adapalene) are first-line for comedonal acne as they normalize follicular keratinization.

Oral isotretinoin is indicated for severe nodulocystic acne, acne resistant to other treatments, or acne causing scarring.

Pemphigus vulgaris has IgG antibodies against desmoglein 3 (and often desmoglein 1), causing suprabasal acantholysis.

Pemphigus vulgaris causes suprabasal acantholysis (split just above basal layer) due to loss of desmosomal adhesion.

Nikolsky sign (lateral pressure on normal skin causes epidermal separation) is positive in pemphigus due to intraepidermal acantholysis.

DIF in pemphigus shows intercellular/chicken-wire/fishnet pattern of IgG and C3 deposition between keratinocytes.

Bullous pemphigoid typically affects elderly individuals (>60 years) with tense blisters on erythematous base.

Bullous pemphigoid causes tense, intact blisters because the split is subepidermal (thicker roof).

Bullous pemphigoid has IgG antibodies against hemidesmosomal proteins BP180 (type XVII collagen) and BP230 (dystonin).

Pruritus (itch) is the cardinal symptom of eczema – “the itch that rashes.” Scratching leads to lichenification.

In infants, atopic dermatitis typically affects face (cheeks), scalp, and extensor surfaces.

Dennie-Morgan folds are extra skin folds beneath the lower eyelids, a minor criterion for atopic dermatitis.

Allergic contact dermatitis is a Type IV (delayed-type) hypersensitivity reaction mediated by T cells.

Pompholyx presents with intensely pruritic, deep-seated vesicles on palms, soles, and lateral fingers (like tapioca pearls).

Psoriasis shows parakeratosis (retained nuclei in stratum corneum), acanthosis, Munro microabscesses (neutrophils in stratum corneum), and elongated rete ridges.

Auspitz sign is pinpoint bleeding when psoriatic scales are removed, due to dilated capillaries in dermal papillae close to thin, parakeratotic epidermis.

Koebner phenomenon (isomorphic response – new lesions at sites of trauma) occurs in psoriasis, lichen planus, vitiligo, and warts.

Nail pitting (small punctate depressions) is most commonly seen in psoriasis due to parakeratotic foci in the nail matrix.

Plaque psoriasis (psoriasis vulgaris) accounts for ~80-90% of cases, presenting with well-demarcated, erythematous plaques with silvery scales on extensor surfaces.

The 6 Ps are Purple, Polygonal, Planar (flat-topped), Pruritic, Papules, and Plaques.

Wickham striae are fine white lines/network on the surface of lichen planus papules due to focal hypergranulosis.

Lichen planus is a T cell-mediated (Type IV) immune reaction causing interface dermatitis with damage to basal keratinocytes.

Buccal mucosa is the most commonly affected site in oral lichen planus, showing white reticular (lacy/Wickham-like) pattern.

Seborrheic dermatitis affects sebum-rich areas: scalp, nasolabial folds, eyebrows, external ears, and central chest.

Seborrheic dermatitis is associated with Malassezia yeasts (M. globosa, M. restricta), though the exact pathogenic role is debated.

Cradle cap is infantile seborrheic dermatitis presenting as greasy, yellowish scales on the scalp in the first few months of life.

Erythema nodosum presents as painful, red, subcutaneous nodules on the anterior shins (most common site).

Erythema nodosum is septal panniculitis (inflammation of subcutaneous fat).

Streptococcal pharyngitis is the most common identifiable cause of erythema nodosum worldwide.

Erythema nodosum lesions resolve in 3-6 weeks with bruise-like color changes (contusiform) and may leave temporary hyperpigmentation, but never ulcerate or scar.

Since streptococcal infection is the most common cause, throat swab for culture and ASO titer are important initial investigations.

Erythema nodosum is 3-6 times more common in females, typically in young adults (20-40 years).

Parents or caregivers spend the most time with the child and can provide accurate details about symptoms, feeding, and developmental milestones.

Newborns have smaller lungs and higher metabolic demands, requiring 40–60 breaths/min.

The anterior fontanelle closes between 12–18 months.

Axillary temperature is safest and most practical in neonates.

Head circumference is measured until 2 years because brain growth is most rapid during this period.

Social smile is a response to human faces and appears around 6 weeks (2 months).

Independent walking typically occurs by 12 months.

Pincer grasp (thumb and index finger opposition) develops at 9 months.

Two-word phrases (“mama go”) appear by 18 months.

By 3 months, an infant can hold the head steady when upright.

Iron deficiency anemia is the most prevalent nutritional deficiency globally, especially in children aged 6 months to 3 years due to rapid growth.

Physiological anemia occurs at 2–3 months due to decreased erythropoietin production as oxygen delivery improves postnatally.

Newborns have hemoglobin levels of 14–20 g/dL due to fetal erythropoiesis.

Breast milk contains low iron, though it is highly bioavailable.

WHO defines anemia in children 6–59 months as Hb <11 g/dL.

CBC provides hemoglobin, hematocrit, RBC indices, and WBC/platelet counts–essential for initial evaluation.

Microcytic (low MCV) and hypochromic (low MCH) anemia occurs in iron deficiency and thalassemia.

Hemolytic anemia causes increased RBC destruction, prompting the bone marrow to release more reticulocytes (compensatory response).

Ferritin is the storage form of iron; serum ferritin correlates with total body iron stores.

Target cells (codocytes) appear in thalassemia due to excess membrane relative to hemoglobin content.

Oral iron (ferrous sulfate, 3–6 mg/kg/day) is first-line treatment.

Iron therapy continues for 1–3 months after Hb normalizes to replenish iron stores.

B12 deficiency often results from malabsorption; parenteral cyanocobalamin bypasses the GI tract.

Exchange transfusion removes antibody-coated RBCs and bilirubin in severe hemolytic disease (e.g., Rh incompatibility).

Sickle cell disease causes chronic hemolysis, increasing folate demand for RBC production.

Conjunctival pallor is the most reliable sign of anemia in children as it is less affected by skin pigmentation.

Koilonychia results from chronic iron deficiency causing abnormal nail matrix formation.

Iron deficiency causes epithelial changes including angular stomatitis (mouth corner cracks) and glossitis (smooth, red tongue).

Thalassemia major causes extramedullary hematopoiesis, leading to bone marrow expansion in the skull (“chipmunk facies”).

Hemolytic anemia causes RBC destruction, releasing bilirubin (jaundice) and causing hepatosplenomegaly from reticuloendothelial hyperactivity.

Thalassemia major requires two defective genes (one from each parent).

Each unit of blood contains iron that accumulates since the body has no excretion mechanism, causing hemosiderosis affecting heart, liver, and endocrine organs.

Deferoxamine binds excess iron for urinary excretion.

Hematopoietic stem cell transplant from a matched donor can cure thalassemia by replacing defective marrow.

Since thalassemia is autosomal recessive, siblings and extended family may be carriers.

Normal WBC count is 4,000–11,000/μL; below 4,000/μL is leukopenia.

Viral infections (measles, influenza, HIV) commonly cause transient leukopenia through bone marrow suppression.

Chemotherapy agents suppress bone marrow, causing leukopenia, anemia, and thrombocytopenia.

Neutrophils are the first-line defense against bacteria.

Cyclic neutropenia is characterized by neutrophil count oscillations every 21 days due to a mutation in the ELANE gene.

ALL accounts for approximately 25–30% of all childhood cancers and 75–80% of childhood leukemias.

ALL peaks between 2–5 years of age.

Leukemia causes bone marrow failure: anemia (pallor, fatigue), thrombocytopenia (bleeding, petechiae), and neutropenia (fever, infections).

Leukemic blast cells proliferate in bone marrow, causing expansion and periosteal stretching, leading to bone pain.

Bone marrow aspiration showing >20% blasts confirms acute leukemia.

The spleen becomes palpable below the left costal margin when it enlarges 1.5–2 times its normal size.

Thalassemia major causes massive splenomegaly due to extramedullary hematopoiesis and RBC sequestration.

Infectious mononucleosis (EBV infection) causes the classic triad of fever, pharyngitis, and lymphadenopathy with splenomegaly.

Hypersplenism results in excessive sequestration and destruction of all blood cell lines, causing pancytopenia (anemia, leukopenia, thrombocytopenia).

The spleen enlarges diagonally across the abdomen toward the right iliac fossa (following its embryological axis).

Petechiae are pinpoint hemorrhages <2 mm.

Petechiae result from blood leaking out of vessels into tissue (extravasation).

Purpura are intermediate-sized hemorrhages (2–10 mm) between petechiae (<2 mm) and ecchymoses (>10 mm).

Ecchymosis is a large area of hemorrhage (>10 mm) into skin or mucous membranes–commonly called a bruise.

Non-blanching petechiae or purpura with fever is a red flag for meningococcemia (Neisseria meningitidis sepsis), a life-threatening emergency.

Hemophilia A results from Factor VIII deficiency.

Hemophilia A and B are X-linked recessive disorders, affecting males while females are carriers.

PTT measures intrinsic pathway factors (VIII, IX, XI, XII).

Vitamin K is required for factors II, VII, IX, X synthesis.

Genu varum (outward bowing of knees) is normal until 2 years due to intrauterine positioning.

Genu valgum (knees angled inward) is normal between 2–7 years, peaking at 3–4 years.

Flat feet are normal in toddlers due to fat pad in the arch and ligamentous laxity.

In-toeing causes vary by age: metatarsus adductus (infants), internal tibial torsion (toddlers), and femoral anteversion (3–8 years).

Ortolani (relocation) and Barlow (dislocation) maneuvers detect hip instability in newborns.

Oligoarticular JIA (affecting ≤4 joints) accounts for 50% of JIA cases, typically affecting large joints in young girls.

ANA-positive oligoarticular JIA carries the highest risk of chronic anterior uveitis, which is often asymptomatic.

NSAIDs (naproxen, ibuprofen) are first-line for symptom relief in JIA.

Systemic JIA presents with daily (quotidian) high-spiking fever, salmon-pink macular rash that appears with fever and fades when afebrile, plus arthritis and hepatosplenomegaly.

MAS is a life-threatening hyperinflammatory syndrome occurring in systemic JIA, characterized by pancytopenia, hepatosplenomegaly, coagulopathy, and hyperferritinemia.

Vitamin D deficiency causes defective mineralization of growth plates (rickets in children) and bone matrix (osteomalacia in adults).

Alkaline phosphatase (ALP) rises early as osteoblasts attempt to mineralize bone.

Rachitic rosary is the visible and palpable enlargement of costochondral junctions due to defective mineralization, resembling rosary beads.

Harrison’s sulcus is a horizontal groove along the lower chest wall at the diaphragm attachment, caused by softened ribs being pulled inward during respiration.

Nutritional rickets requires vitamin D (cholecalciferol or ergocalciferol) plus calcium to restore bone mineralization.

Duchenne muscular dystrophy (DMD) affects 1 in 3,500 males, making it the most common and severe form.

DMD results from mutations in the dystrophin gene on the X chromosome, leading to absent dystrophin protein in muscle cells.

Gowers’ sign indicates proximal muscle weakness: the child uses hands to “walk up” the thighs when rising from the floor due to weak hip and thigh muscles.

Calf muscles appear enlarged but are actually weak because muscle fibers are replaced by fat and connective tissue–hence “pseudo” (false) hypertrophy.

CK is released from damaged muscle cells.

Nylon is the most commonly used non-absorbable suture for skin closure due to its high tensile strength, minimal tissue reaction, and easy removal.

Surgical scrubbing proceeds from the cleanest area (fingertips) to the least clean (elbows) to prevent contamination of already scrubbed areas.

Blade 15 is small and curved, ideal for precise, delicate skin incisions such as in hand surgery or excision of small lesions.

Tissue forceps (toothed or non-toothed) are designed to grasp and hold tissues during dissection.

Simple interrupted sutures allow precise alignment of wound edges with minimal scarring, essential for cosmetic areas like the face.

Carbon dioxide is preferred because it is highly soluble in blood, rapidly absorbed, non-combustible, and does not support combustion.

12–15 mmHg provides adequate visualization and working space without compromising venous return or causing respiratory compromise.

Minimally invasive surgery causes less tissue trauma, leading to reduced pain, faster recovery, and shorter hospitalization.

The Veress needle is a spring-loaded needle designed to safely pierce the abdominal wall and insufflate CO₂ to create pneumoperitoneum.

Gas embolism occurs when CO₂ enters the bloodstream through an open vessel, a complication unique to insufflation-based procedures.

Informed consent requires explaining the procedure, risks, benefits, and alternatives.

In most countries, 18 years is the age of majority, allowing independent consent.

In emergencies where delay would endanger life and the patient cannot consent, implied consent applies under the doctrine of necessity.

Valid consent requires mental competence to understand information and voluntarily agree.

A living will (advance directive) documents a patient’s wishes regarding future medical treatment, including refusal of life-sustaining measures.

Primary intention healing involves clean, approximated wound edges healing with minimal scarring.

The proliferative phase (days 3–21) involves fibroblast activity and collagen deposition to strengthen the wound.

Healed wounds reach approximately 80% of original tensile strength by 3 months but never achieve 100%.

Keloids extend beyond the original wound margins due to excessive collagen production.

Myofibroblasts contain actin filaments that contract to pull wound edges together.

Staphylococcus aureus is the most common cause of surgical site infections, especially in clean wounds, due to skin colonization.

Clean-contaminated wounds involve controlled entry into colonized tracts (GI, GU, respiratory) without significant spillage.

Antibiotics should be given within 60 minutes of incision to ensure adequate tissue levels during the procedure.

Clostridium perfringens produces alpha toxin causing rapid tissue destruction with gas production in anaerobic conditions.

Severe pain disproportionate to skin findings is the classic early sign of necrotizing fasciitis due to nerve involvement.

Early mobilization improves venous return and prevents stasis, reducing DVT and pulmonary embolism risk.

Day 1 fever is typically from atelectasis (collapsed lung segments) due to shallow breathing after anesthesia.

Anesthesia and opioid analgesics inhibit bladder detrusor muscle contraction and relax the sphincter, causing retention.

Serosanguinous (“salmon-colored”) discharge indicates fascia separation and impending evisceration.

Hand hygiene and sterile technique are the cornerstones of infection prevention.

Adults require approximately 30–35 mL/kg/day, translating to 2500–3000 mL for average adults.

Vomiting causes loss of gastric H⁺ and K⁺, leading to hypokalemia and metabolic alkalosis.

Crystalloids (NS or RL) are first-line for volume expansion due to availability and effectiveness.

The Parkland formula (4 mL × kg × %TBSA burn) uses Ringer’s lactate, which is isotonic and contains lactate for buffering.

When feeding resumes after starvation, insulin release shifts potassium, phosphate, and magnesium intracellularly, causing dangerous hypophosphatemia and hypokalemia.

TPN bypasses the GI tract and is reserved for patients unable to use enteral nutrition for extended periods.

RA typically affects small joints of hands (MCP, PIP) and feet first, sparing DIP joints.

Swan-neck deformity (PIP hyperextension, DIP flexion) results from synovitis and tendon imbalance in RA.

Surgery in RA aims to relieve pain, restore function, and improve quality of life – it does not cure the disease.

Synovectomy removes diseased synovium to decrease inflammation and slow joint destruction.

RA causes ligamentous laxity at C1-C2, leading to atlantoaxial subluxation with risk of cord compression.

The spine is the most common site of skeletal TB (Pott’s disease), typically affecting the thoracolumbar region.

TB causes vertebral body destruction with anterior wedging leading to kyphotic “gibbus” deformity.

Pott’s triad includes back pain, kyphosis (gibbus), and neurological deficit (paraplegia).

MRI detects early soft tissue involvement, marrow edema, and cold abscesses before bony changes appear on X-ray.

ATT is the mainstay of treatment for skeletal TB, with surgery reserved for complications like abscess, instability, or neurological deficit.

Staphylococcus aureus is the most common cause across all ages.

The knee is the most commonly affected joint in septic arthritis due to its superficial location and vascularity.

Septic arthritis shows turbid fluid with WBC > 50,000/mm³ (often > 100,000), predominantly neutrophils, and low glucose.

Septic arthritis requires both drainage (aspiration or surgical) to remove pus and IV antibiotics to eradicate infection.

Bacterial enzymes and inflammation rapidly destroy articular cartilage, leading to permanent joint damage within days.

Scoliosis is lateral (sideways) spinal curvature > 10° on X-ray.

Idiopathic adolescent scoliosis (unknown cause, occurring in teens) accounts for approximately 80% of cases.

Adams forward bend test reveals rib hump (rotational deformity) indicating structural scoliosis.

Cobb’s angle measures the degree of spinal curvature between the most tilted vertebrae above and below the curve.

Spinal fusion corrects the abnormal curve and uses rods/screws to maintain correction and prevent progression.

Hematogenous osteomyelitis occurs when bacteria travel through blood to bone, especially in children with good blood supply to metaphysis.

The femur, especially the distal metaphysis, is most commonly affected due to its rich blood supply and slow blood flow in metaphyseal sinusoids.

Sequestrum (dead bone) surrounded by involucrum (new periosteal bone) is pathognomonic of chronic osteomyelitis.

MRI detects bone marrow edema and soft tissue changes within days, before X-ray changes appear (which take 10–14 days).

Acute osteomyelitis requires prolonged IV antibiotics (4–6 weeks) due to limited bone penetration and slow bacterial clearance.

Poliovirus destroys anterior horn cells in the spinal cord, causing flaccid paralysis.

LMN destruction causes flaccid, areflexic paralysis with muscle atrophy.

Lower limb muscles, especially quadriceps and hip flexors, are most commonly and severely affected.

Multiple procedures may be needed: tendon transfers redistribute motor power, arthrodesis stabilizes joints, and osteotomies correct deformities.

Surgery improves function by stabilizing joints, transferring tendons, and correcting deformities – it cannot regenerate nerves.

X-rays use ionizing radiation to create images.

Non-contrast CT is the first-line imaging in acute stroke to rapidly rule out hemorrhage before thrombolysis.

MRI provides excellent soft tissue contrast, ideal for muscles, ligaments, tendons, and cartilage.

Free air rises to the highest point – under the diaphragm on erect CXR or along the lateral abdominal wall on left lateral decubitus.

Ultrasound is first-line in children due to no radiation exposure and good sensitivity.

Barium swallow examines esophageal morphology and motility as the patient swallows contrast.

Non-contrast CT KUB is the gold standard – highly sensitive for stones of all types and identifies alternative diagnoses.

Iodinated contrast can cause contrast-induced nephropathy in patients with renal impairment.

Doppler ultrasound uses frequency shift of sound waves to assess blood flow direction and velocity in real-time.

Mammography is the standard screening tool for breast cancer due to its ability to detect microcalcifications and early lesions.

Erect films show air-fluid levels as air rises above fluid in dilated obstructed loops.

String sign represents narrowed terminal ileum from strictures in Crohn’s disease.

HRCT uses thin slices (1–2 mm) to provide detailed lung parenchymal images, ideal for interstitial lung diseases like fibrosis.

CTPA is the gold standard for diagnosing PE, directly visualizing clots in pulmonary arteries.

Low-dose opioids like morphine are first-line for refractory dyspnea in palliative care, as they reduce the sensation of breathlessness by acting on central respiratory centers and decreasing anxiety.

Anticholinergic agents like glycopyrrolate or hyoscine reduce secretion production and are first-line for death rattle.

Haloperidol is a potent D2 antagonist effective for chemical/metabolic causes of nausea in palliative care when 5-HT3 antagonists fail.

When a patient lacks capacity and has no advance directive, a legally appointed surrogate (healthcare proxy) or next of kin makes decisions based on substituted judgment or best interests.

Gabapentin or pregabalin are first-line adjuvants for neuropathic pain, acting on calcium channels to reduce neuronal excitability.

A competent patient has the right to refuse or withdraw any treatment, including mechanical ventilation.

In inoperable malignant bowel obstruction, medical management with octreotide (reduces secretions), dexamethasone (reduces edema and inflammation), and antiemetics provides symptom relief.

Normal pressure hydrocephalus (NPH) presents with the classic triad of dementia, urinary incontinence, and gait apraxia (“wet, wacky, and wobbly”), with ventriculomegaly out of proportion to atrophy on imaging.

Delirium is characterized by acute onset, fluctuating course, inattention, and often visual hallucinations, commonly precipitated by surgery, infection, or medications in elderly patients.

IADLs include complex activities required for independent living: managing finances, shopping, using transportation, cooking, housekeeping, medication management, and using telephone.

Benzodiazepines like lorazepam significantly increase fall risk in elderly due to sedation, impaired coordination, and cognitive effects.

Getting lost in familiar areas indicates significant visuospatial and memory impairment that directly impacts driving safety and warrants driving cessation.

Levofloxacin is renally excreted and requires dose reduction when CrCl <50 mL/min.

In advanced dementia with feeding difficulties, careful hand feeding respects patient dignity and provides comfort.

A patient with good functional capacity (≥4 METs, equivalent to climbing two flights of stairs) can generally proceed to intermediate-risk surgery without additional cardiac testing, per ACC/AHA guidelines.

Patients with high thromboembolic risk (CHA₂DS₂-VASc ≥5) should receive bridging anticoagulation with LMWH when warfarin is held for surgery.

Metformin should be held before and for 48 hours after IV contrast in patients with eGFR <60 to prevent contrast-induced nephropathy leading to metformin-associated lactic acidosis.

Severe symptomatic aortic stenosis significantly increases perioperative mortality in non-cardiac surgery.

Recent VTE (within 3 months is highest risk, but within 12 months still elevated) combined with major surgery requires aggressive dual prophylaxis: pharmacological (LMWH) plus mechanical (compression devices).

Quantitative V/Q scan helps calculate predicted postoperative FEV1 (ppoFEV1) by determining the functional contribution of lung segments to be resected.

In emergency surgery, the urgency takes precedence.

Serum ferritin <15 ng/mL is highly specific for iron deficiency, reflecting depleted iron stores.

Anemia of chronic kidney disease is primarily due to decreased erythropoietin production by failing kidneys.

Vitamin B12 deficiency causes subacute combined degeneration of the spinal cord, affecting posterior columns (proprioception, vibration sense) and lateral corticospinal tracts.

G6PD deficiency causes episodic hemolysis triggered by oxidative stress from infections or drugs (sulfonamides, primaquine, fava beans).

Anemia of chronic disease (inflammation) shows normocytic or mildly microcytic anemia with normal or elevated ferritin (acute phase reactant) and low TIBC.

Elevated HbA2 (>3.5%) is diagnostic of beta-thalassemia trait, resulting from reduced beta-globin synthesis with compensatory increase in delta chains (HbA2 = α2δ2).

Multiple myeloma presents with CRAB criteria (hyperCalcemia, Renal insufficiency, Anemia, Bone lesions), M-spike on SPEP, and Bence Jones proteins (free light chains) in urine.

Febrile neutropenia (ANC <500/μL with fever ≥38.3°C or sustained ≥38°C) is a medical emergency requiring immediate broad-spectrum IV antibiotics (e.g., cefepime, piperacillin-tazobactam) after cultures but before results.

Clozapine-induced agranulocytosis (ANC <500) mandates immediate and permanent discontinuation due to risk of life-threatening infection.

Severe congenital neutropenia presents with recurrent bacterial infections from infancy due to maturation arrest of myeloid precursors.

Methotrexate-induced neutropenia is often related to folate depletion and is usually reversible.

CLL is characterized by mature lymphocytosis with CD5+/CD19+/CD23+ immunophenotype and smudge cells (fragile lymphocytes crushed during smear preparation).

Classic Hodgkin lymphoma has Reed-Sternberg cells that are characteristically CD15+ and CD30+ (Ki-1).

Tumor lysis syndrome (TLS) occurs after chemotherapy for rapidly proliferating tumors, causing release of intracellular contents: hyperuricemia, hyperkalemia, hyperphosphatemia, and secondary hypocalcemia, leading to acute kidney injury.

Allopurinol (xanthine oxidase inhibitor) prevents uric acid formation, while rasburicase (urate oxidase) breaks down existing uric acid.

Warm autoimmune hemolytic anemia (IgG-mediated, Coombs positive) is commonly associated with CLL.

Hyperleukocytosis with neurological symptoms suggests leukostasis, a medical emergency.

Chronic myeloid leukemia (CML) presents with marked leukocytosis showing full myeloid maturation spectrum (left shift to blasts), basophilia, and the Philadelphia chromosome t(9;22) creating BCR-ABL1 fusion. t(15;17) (A) is APL. t(8;14) (C) is Burkitt lymphoma. t(14;18) (D) is follicular lymphoma.

Hairy cell leukemia presents with pancytopenia (notably monocytopenia), massive splenomegaly, dry tap on aspiration (due to reticulin fibrosis), and TRAP-positive hairy cells.

Infectious mononucleosis caused by EBV presents with lymphadenopathy, pharyngitis, fever, and positive heterophile antibody test (Monospot).

Follicular lymphoma is characterized by t(14;18) translocation causing BCL-2 overexpression, which inhibits apoptosis.

Trauma causes stress leukocytosis through cortisol and catecholamine release, leading to demargination of neutrophils from vessel walls and release from marrow reserves.

Von Willebrand disease (vWD) is the most common inherited bleeding disorder, presenting with mucocutaneous bleeding, prolonged bleeding time, and reduced ristocetin cofactor activity (reflecting vWF function). aPTT may be normal or mildly prolonged.

Hemophilia A (Factor VIII deficiency) presents with deep tissue bleeding (hemarthrosis, muscle hematomas), prolonged aPTT that corrects with mixing (indicating factor deficiency, not inhibitor), and normal PT.

Life-threatening bleeding with supratherapeutic INR requires immediate reversal with 4-factor PCC (provides concentrated factors II, VII, IX, X) plus IV vitamin K (for sustained effect).

Antiphospholipid syndrome with thrombosis requires lifelong anticoagulation with warfarin (INR 2-3).

HIT type II presents 5-10 days after heparin exposure with >50% platelet drop and paradoxical thrombosis.

Immune thrombocytopenic purpura (ITP) is a diagnosis of exclusion with isolated thrombocytopenia and large platelets.

DIC shows consumption of platelets and clotting factors (prolonged PT/aPTT, low fibrinogen), elevated D-dimer (fibrinolysis), and schistocytes (microangiopathic hemolysis).

RA characteristically involves MCPs and PIPs symmetrically with synovitis while sparing DIPs.

Ankylosing spondylitis (AS) presents with inflammatory back pain (morning stiffness improving with exercise), sacroiliitis, and extra-articular features including anterior uveitis.

Psoriatic arthritis presents with dactylitis (sausage digits from entire finger inflammation), DIP involvement (unlike RA), nail changes (pitting, onycholysis), and asymmetric oligoarthritis in association with psoriasis.

Osteoarthritis is a degenerative process involving cartilage breakdown, subchondral bone changes, and osteophyte formation–not primarily inflammatory.

Gout presents with acute monoarthritis (classically podagra–first MTP), triggered by alcohol, with negatively birefringent needle-shaped monosodium urate crystals under polarized microscopy.

Methotrexate is first-line DMARD for RA, proven to slow radiographic progression and improve outcomes.

Folic acid supplementation (1 mg daily, not on methotrexate day) reduces methotrexate side effects including mucositis, GI upset, and cytopenias without diminishing anti-inflammatory efficacy.

Allopurinol (xanthine oxidase inhibitor) is first-line urate-lowering therapy for patients with recurrent gout, tophi, or uric acid nephrolithiasis.

For axial spondyloarthritis failing NSAIDs, TNF inhibitors (adalimumab, etanercept, infliximab) are recommended.

TNF-alpha is crucial for granuloma formation and TB containment.

Topical NSAIDs provide effective pain relief for knee OA with minimal systemic absorption, avoiding GI risks–ideal for patients with peptic ulcer history.

Intra-articular corticosteroid injection provides significant short-term pain relief in OA, especially when effusion is present.

Pseudogout (calcium pyrophosphate deposition disease) presents similarly to gout but with positively birefringent rhomboid crystals.

Reactive arthritis (formerly Reiter’s syndrome) is a seronegative spondyloarthropathy triggered by GI or GU infection, presenting with the classic triad of arthritis, urethritis, and conjunctivitis.

For psoriatic arthritis failing conventional DMARDs, TNF inhibitors (adalimumab, etanercept) or IL-17 inhibitors are recommended.

T-score ≤-2.5 defines osteoporosis.

Atypical femoral fractures are a rare complication of long-term bisphosphonate use (>5 years), presenting with prodromal thigh pain and lateral cortical thickening/beaking on X-ray before complete fracture.

IV bisphosphonates (zoledronic acid yearly, or ibandronate quarterly) bypass the esophagus, avoiding GI intolerance.

Glucocorticoids cause osteoporosis primarily by decreasing bone formation (osteoblast and osteocyte apoptosis) and increasing bone resorption.

Bisphosphonates (including zoledronic acid) are contraindicated in severe CKD (eGFR <35) due to risk of accumulation and worsening renal function.

Proximal muscle weakness without sensory involvement and with preserved reflexes suggests myopathy.

Statin-induced myopathy presents with proximal weakness and elevated CK.

Hypothyroidism causes myopathy with proximal weakness, cramps, myalgias, and characteristic delayed relaxation of reflexes (“hung-up” reflexes).

Rhabdomyolysis causes myoglobinuria (positive dipstick for blood without RBCs–myoglobin cross-reacts).

Dermatomyositis presents with proximal myopathy plus characteristic skin findings: heliotrope (purple) rash on eyelids and Gottron’s papules (erythematous plaques over knuckles/extensor surfaces).

Dermatomyositis (especially in adults >40 years) is strongly associated with underlying malignancy (ovarian, lung, GI, breast, lymphoma).

Steroid myopathy causes proximal weakness without CK elevation, occurring with prolonged high-dose corticosteroid use.

Interstitial lung disease (ILD), particularly nonspecific interstitial pneumonia (NSIP) pattern, is a significant complication of inflammatory myopathies, especially dermatomyositis with anti-MDA5 or anti-Jo-1 antibodies.

Anti-Jo-1 and other antisynthetase antibodies define antisynthetase syndrome, characterized by inflammatory myopathy, interstitial lung disease, arthritis, mechanic’s hands (hyperkeratotic cracking on fingers), fever, and Raynaud’s phenomenon.

High-dose corticosteroids (prednisone 1 mg/kg/day) are first-line for inflammatory myopathies.

Opioid rotation is indicated when dose escalation causes toxicity (sedation) without adequate analgesia–suggesting incomplete cross-tolerance or metabolite accumulation.