Management Sequence

• Initial: MONA (Morphine, Oxygen if Sat <90%, Nitroglycerin, Aspirin). Add Clopidogrel and Heparin.
• Definitive: Percutaneous Coronary Intervention (PCI) within 90 minutes. If PCI is unavailable within 120 minutes, administer Thrombolytics (Tenecteplase/Alteplase) within 30 minutes.

Diagnostic & Treatment Markers

• Diagnosis: Elevated Brain Natriuretic Peptide (BNP or NT-proBNP) indicates ventricular stretch. Echocardiography is the gold standard to assess Ejection Fraction.
• Chronic Management: ACE Inhibitors (or ARBs), Beta-blockers (Carvedilol, Metoprolol succinate, Bisoprolol), Spironolactone, and SGLT2 inhibitors (Dapagliflozin) improve mortality.

Diagnostic Algorithm

• Assess pre-test probability using the Wells Score (signs of DVT, alternative diagnosis less likely, HR>100, immobilization, prior DVT/PE, hemoptysis, malignancy).
• If Wells score is LOW (<4): Check D-dimer. If D-dimer is negative, PE is ruled out.
• If Wells score is HIGH (>4) or D-dimer is positive: Proceed directly to CT Pulmonary Angiography (CTPA) (Gold standard imaging).

Diagnostic Modalities

• Sputum AFB Smear: Ziehl-Neelsen stain. Rapid but lacks sensitivity.
• GeneXpert MTB/RIF:Investigation of Choice. Nucleic acid amplification test. Rapidly detects both MTB complex DNA and Rifampicin resistance within 2 hours.
• Liquid Culture (MGIT): Gold standard for definitive diagnosis and full drug susceptibility testing, but takes weeks.

Pathology & Management

• Degeneration of dopaminergic neurons in the Substantia Nigra pars compacta (basal ganglia).
• Presence of intracellular eosinophilic inclusions called Lewy Bodies (alpha-synuclein).
• Treatment: Levodopa + Carbidopa (gold standard). Dopamine agonists (Pramipexole, Ropinirole) preferred in younger patients to delay L-dopa motor complications.

Management of Complications

• Ascites: Sodium restriction, Spironolactone + Furosemide. Large volume paracentesis if tense.
• Hepatic Encephalopathy: Due to buildup of Ammonia (not cleared by liver). Triggers: constipation, GI bleed, infection, hypokalemia. Rx: Lactulose (acidifies gut to trap NH4+) and Rifaximin (kills ammonia-producing gut bacteria).
• Esophageal Varices: Primary prophylaxis with non-selective beta-blockers (Propranolol, Nadolol) or endoscopic band ligation.

Diagnosis & Management

• Caused by a Growth Hormone (GH) secreting pituitary macroadenoma occurring AFTER epiphyseal plate closure. (Before closure = Gigantism).
• Screening Test: Serum IGF-1 (Insulin-like Growth Factor 1). GH levels fluctuate too much, but IGF-1 (from liver) is stable.
• Confirmatory Test: Oral Glucose Tolerance Test (OGTT). Normal response is GH suppression; in Acromegaly, GH remains high (failure to suppress).
• Treatment: Transsphenoidal surgical resection. Medical Rx: Octreotide (Somatostatin analog).

Pathophysiology & Complications

• Defined as GFR < 60 mL/min for > 3 months or structural damage.
• Anemia: Due to loss of Erythropoietin (EPO) production by peritubular interstitial cells. Normocytic normochromic.
• Bone Mineral Bone Disease (Renal Osteodystrophy): Failing kidneys cannot excrete Phosphate (Hyperphosphatemia) and cannot activate Vitamin D. This leads to Hypocalcemia. Low calcium triggers severe Secondary Hyperparathyroidism, which strips calcium from bones, causing osteitis fibrosa cystica.

Hyperkalemia (>5.0 mEq/L)

• Causes: CKD, ACE-I/ARBs, Spironolactone, DKA, tumor lysis syndrome, massive muscle crush injury.
• ECG Changes: Tall peaked T waves (earliest), prolonged PR, widened QRS, sine wave pattern -> V-Fib/Asystole.

Key Differentiating Features

• ALL (Children): Most common childhood cancer. Bone pain, hepatosplenomegaly, lymphadenopathy. Smear shows Lymphoblasts (TdT positive).
• AML (Adults ~60 yrs): Rapid onset fatigue, bleeding, infections. Smear shows Myeloblasts with Auer Rods (MPO positive). APML subtype (t15;17) responds to ATRA.
• CML (Adults ~45-60 yrs): Massive splenomegaly, huge leukocytosis with full spectrum of granulocytes (shift to left). Characterized by the Philadelphia Chromosome t(9;22) BCR-ABL. Rx: Imatinib.
• CLL (Elderly >65 yrs): Asymptomatic, found incidentally. Smear shows mature lymphocytes and fragile Smudge Cells.

CD4 Count Thresholds & Prophylaxis

• < 200 cells/mm³:Pneumocystis jirovecii pneumonia (PCP). Fungal pneumonia. Treat and prophylax with TMP-SMX (Cotrimoxazole).
• < 100 cells/mm³:Toxoplasma gondii (Ring-enhancing brain lesions, prophylax with TMP-SMX). Cryptococcus neoformans (Meningitis).
• < 50 cells/mm³:Mycobacterium avium complex (MAC) (Prophylax with Azithromycin). CMV Retinitis (pizza pie appearance on fundus).

Pathology & Management

• Most common site: Ampulla of the fallopian tube. Isthmus is the most common site of early rupture.
• Medical Rx:Methotrexate (IM) for hemodynamically stable, unruptured mass < 3.5 cm, no fetal cardiac activity, Beta-hCG < 5,000 mIU/mL.
• Surgical Rx: Laparoscopic Salpingostomy (preserves tube) or Salpingectomy (removes tube).

Types based on Cervical Os

• Os CLOSED: Threatened (viable fetus), Missed (dead fetus, no bleeding/pain), Complete (all products expelled, bleeding stops).
• Os OPEN: Inevitable (bleeding/cramps, no tissue passed yet), Incomplete (partial tissue passed, ongoing severe bleeding).

Complete vs Partial Mole

• Complete Mole: 46,XX (all paternal chromosomes). Empty egg fertilized by sperm. No fetal parts. Massively elevated Beta-hCG. Higher risk of malignancy (Choriocarcinoma).
• Partial Mole: Triploid (69,XXY). Egg fertilized by 2 sperm. Fetal parts present. Lower hCG.

Pathology & Management

• Exaggerated response to high Beta-hCG levels (common in twins/molar pregnancy).
• Treatment: IV hydration, antiemetics (Ondansetron, Promethazine, Doxylamine-Pyridoxine).

Chorionicity (Determined by cleavage timing of Zygote)

• Days 1-3: Dichorionic Diamniotic (DCDA). Lambda/Twin Peak Sign. Safest.
• Days 4-8: Monochorionic Diamniotic (MCDA). T-Sign. Risk of TTTS.
• Days 8-13: Monochorionic Monoamniotic (MCMA). High risk of cord entanglement.
• > 13 Days: Conjoined twins.

Classic Teratogens

• Warfarin: Chondrodysplasia punctata (stippled bone epiphyses), nasal hypoplasia. (Switch to LMWH/Heparin which does not cross placenta).
• ACE Inhibitors: Fetal renal agenesis, oligohydramnios, skull hypoplasia.
• Lithium: Ebstein’s anomaly (tricuspid valve displacement).
• Isotretinoin: Extremely teratogenic (craniofacial, cardiac, CNS defects). Strict contraception required.

Pathology & Monitoring

• Occurs when Rh-negative mother is sensitized to Rh-positive fetal RBCs, producing IgG anti-D antibodies that cross the placenta and destroy fetal RBCs in subsequent pregnancies.
• Monitor fetal anemia non-invasively using MCA-PSV (Middle Cerebral Artery Peak Systolic Velocity) via Doppler. High velocity = severe anemia.

Definitions & Management

• Gestational HTN: BP > 140/90 after 20 weeks. NO proteinuria.
• Preeclampsia: HTN + Proteinuria (>300mg/24h) OR end-organ damage (headache, high LFTs, low platelets).
• Eclampsia: Preeclampsia + Generalized tonic-clonic seizures.
• Severe Features: BP > 160/110, headache, visual changes, RUQ pain. Indicates urgent delivery regardless of gestational age.

Pathology & Screening (DIPSI Guidelines India)

• Caused by increased insulin resistance mediated by placental hormones (Human Placental Lactogen).
• DIPSI Single Step Test: Give 75g oral glucose irrespective of last meal. Measure plasma glucose at 2 hours. If ≥ 140 mg/dL = GDM.

Pathology & Management

• Physiological anemia of pregnancy: Plasma volume expands (50%) more than RBC mass (20-30%), causing hemodilution. True anemia is Hb < 11 g/dL (1st/3rd trimester) or < 10.5 g/dL (2nd trimester).
• Iron Deficiency (IDA): Most common cause. Microcytic hypochromic. Low Ferritin. Rx: Oral iron.

Risk & Management

• Mitral Stenosis is the most common rheumatic heart disease in pregnancy. Tachycardia of pregnancy shortens diastole, decreasing ventricular filling and causing pulmonary edema.
• Highest Risk Period: 28-32 weeks (maximum blood volume) and Immediately Postpartum (auto-transfusion from contracted uterus causes sudden fluid overload).
• Vaginal delivery is preferred over C-section. Use epidural analgesia. Cut the second stage short using forceps/vacuum (prophylactic instrumental delivery) to prevent maternal pushing.

Diagnosis of Rupture of Membranes

• Pooling: Fluid in posterior fornix on sterile speculum exam.
• Nitrazine Test: Turns blue (amniotic fluid is alkaline pH 7.1-7.3; normal vagina is acidic).
• Ferning Test: Amniotic fluid dries on a slide forming a microscopic fern-like crystallization pattern (due to NaCl).

Stages of Labor

• 1st Stage: Onset of true labor pain to full cervical dilatation (10cm). Divided into Latent phase (up to 4-6cm) and Active phase (rapid dilatation).
• 2nd Stage: Full dilatation to expulsion of the fetus.
• 3rd Stage: Expulsion of the fetus to delivery of the placenta.
• 4th Stage: 1-2 hours postpartum observation for hemorrhage.

The 4 T’s of PPH Etiology

• Tone (70%): Uterine Atony (boggy uterus). Risk factors: Macrosomia, polyhydramnios, twins, prolonged labor. Rx: Uterine massage, IV Oxytocin.
• Trauma (20%): Vaginal/cervical lacerations. Bleeding despite a firmly contracted uterus. Rx: Suture tear.
• Tissue (10%): Retained placental fragments. Rx: Manual removal of placenta.
• Thrombin (<1%): Coagulopathy (DIC, Hemophilia). Rx: Blood products.

Rotterdam Criteria (Requires 2 of 3)

• 1. Oligo/Anovulation.
• 2. Clinical or biochemical signs of Hyperandrogenism (hirsutism, high free testosterone).
• 3. Polycystic ovaries on ultrasound (≥ 20 follicles or volume ≥ 10cc).

Pathology: High LH/FSH ratio (>2:1). Hyperinsulinemia drives ovarian theca cells to overproduce androgens.

Systematic Evaluation

• Male Factor (30%): First step is ALWAYS a Semen Analysis. Must evaluate 2 samples taken weeks apart.
• Ovulatory Factor (30%): Best confirmed by checking Day 21 Serum Progesterone (>3 ng/mL confirms ovulation occurred).
• Tubal Factor (30%): Evaluated via Hysterosalpingography (HSG) to check for tubal blockages (common after PID/Tuberculosis).

Pathophysiology

• Ovarian follicle depletion leads to loss of Estrogen. Lack of negative feedback causes a massive rise in FSH (>40 IU/L) and LH.
• The main estrogen in postmenopausal women is Estrone (E1), produced by peripheral conversion of adrenal androgens in adipose tissue.

Organisms & Complications

• Most common organisms: Chlamydia trachomatis and Neisseria gonorrhoeae.
• Long-term complications: Ectopic pregnancy (due to tubal scarring), Tubal factor Infertility, and Chronic pelvic pain.
• Tubo-ovarian Abscess (TOA): Severe complication presenting with a palpable adnexal mass. Rupture requires emergency surgery.

Pathology & Screening

• Almost 100% caused by Human Papillomavirus (HPV). High-risk oncogenic strains: HPV 16 and 18. They produce viral proteins E6 (inhibits p53) and E7 (inhibits Rb).
• Most common histology: Squamous cell carcinoma (occurs at the squamocolumnar junction / Transformation Zone).
• Screening: Pap smear. Cells show Koilocytes (wrinkled nuclei with perinuclear halos).

High-Yield Tumor Markers

• Epithelial Tumors (Serous/Mucinous Cystadenocarcinoma): Most common malignant. Marker: CA-125 (used to monitor response to therapy, not for primary screening). Often presents with ascites.
• Dysgerminoma: Most common malignant germ cell tumor in young girls. Marker: LDH and hCG. Highly radiosensitive.
• Yolk Sac Tumor (Endodermal Sinus Tumor): Young girls. Marker: AFP. Histology: Schiller-Duval bodies (glomerulus-like structures).
• Choriocarcinoma: Marker: Beta-hCG.
• Granulosa Cell Tumor (Sex Cord-Stromal): Secretes Estrogen (causes precocious puberty in kids, postmenopausal bleeding in adults). Marker: Inhibin. Histology: Call-Exner bodies.

Urinary Incontinence Differentiation

• Stress Incontinence: Leakage with coughing/sneezing/laughing due to weak pelvic floor muscles (pudendal nerve injury during birth) or urethral hypermobility. Rx: Kegel exercises, Mid-urethral sling (TVT/TOT).
• Urge Incontinence: Sudden intense urge to void followed by leakage. Caused by Detrusor Overactivity. Rx: Anticholinergics (Oxybutynin, Tolterodine) or Mirabegron.
• Overflow Incontinence: Continuous dribbling from an overdistended bladder. Rare in women unless severe prolapse kinks the urethra or neurologic bladder. Rx: Intermittent catheterization.

Types & Systemic Associations

• Senile Cataract: Most common. Cortical (cuneiform) or Nuclear (sclerotic – causes index myopia, “second sight” where presbyopes can read without glasses again).
• Diabetic Cataract: “Snowflake” appearance. Caused by accumulation of Sorbitol via the Aldose Reductase pathway.
• Complicated Cataract: Secondary to Uveitis/Retinitis Pigmentosa. Classic “Bread-crumb” or “Polychromatic luster” at the posterior pole.

Pathology & Stages

• Non-Proliferative (NPDR): Microaneurysms (earliest sign), Dot-and-blot hemorrhages, Hard exudates (lipid deposits), Cotton wool spots (nerve fiber layer infarctions).
• Proliferative (PDR): Hallmark is Neovascularization (new, fragile blood vessels at the disc or elsewhere) due to VEGF release from ischemic retina.

Pathophysiology & Types

• Separation of the Neurosensory Retina from the Retinal Pigment Epithelium (RPE).
• Rhegmatogenous RD: Most common. Caused by a full-thickness retinal tear allowing fluid to accumulate under the retina. Associated with myopia and lattice degeneration.
• Tractional RD: Fibrovascular bands pull the retina off (seen in advanced Diabetic Retinopathy or sickle cell).
• Exudative RD: Fluid accumulation without a tear (seen in malignant melanoma or choroiditis). Shifting fluid is a hallmark.

Types & Management

• Dry AMD (Non-exudative): 90% of cases. Slow progression. Deposition of yellowish extracellular material (Drusen) between RPE and Bruch’s membrane. Rx: Antioxidant vitamins.
• Wet AMD (Exudative): 10% of cases, but severe rapid vision loss. Choroidal Neovascularization (CNVM) leaks blood/fluid.

Clinical Differentiation

• Viral (Adenovirus): Watery discharge, preauricular lymphadenopathy, highly contagious (Epidemic Keratoconjunctivitis).
• Bacterial: Purulent (pus) discharge, eyes glued shut in the morning. (Neisseria gonorrhea causes hyperacute purulent conjunctivitis).
• Allergic (Vernal): Extreme itching, “Cobblestone” papillae on upper tarsal conjunctiva, Horner-Trantas dots.

Anterior Uveitis (Iridocyclitis) Pathology

• Inflammation of Iris and Ciliary body.
• Signs: Ciliary congestion (circumcorneal flush), Aqueous Cells & Flare (protein), Keratic Precipitates (KPs) on the corneal endothelium.
• Complications: Posterior synechiae (iris adheres to lens, causing a Festooned/irregular pupil), Secondary Glaucoma.
• Treatment: Topical Steroids + Cycloplegics (Atropine/Homatropine) to relieve ciliary spasm pain and break synechiae.

Concomitant vs. Paralytic

• Concomitant (Non-Paralytic): Angle of deviation is the SAME in all directions of gaze. Common in children. Full extraocular movements. No diplopia (brain suppresses the image to prevent double vision, leading to Amblyopia/lazy eye).
• Paralytic: Caused by nerve palsy (CN III, IV, or VI). Angle of deviation is MAXIMUM in the direction of the paralyzed muscle action. Presents with Diplopia and compensatory head tilt.

Genetics & Pathology

• Most common primary intraocular malignancy of childhood.
• Mutation in the Rb1 tumor suppressor gene on Chromosome 13q14. Requires “two hits”.
• Presentation: Leukocoria (white pupillary reflex / amaurotic cat’s eye) is the most common sign.
• Histology: Characteristic Flexner-Wintersteiner rosettes (cells surrounding a central empty lumen).

Principles & Corrections

• Myopia (Short-sightedness): Eyeball is too long. Light focuses IN FRONT of retina. Correction: Concave (-) spherical lens.
• Hypermetropia (Long-sightedness): Eyeball is too short. Light focuses BEHIND retina. Correction: Convex (+) spherical lens.
• Astigmatism: Unequal curvature of the cornea. Correction: Cylindrical lens.
• Presbyopia: Age-related loss of accommodation (hardening of the lens) starting around age 40. Correction: Convex lenses for near vision (reading glasses).

Differential Diagnosis

• Meniere’s Disease (Endolymphatic Hydrops): Triad: Vertigo (episodes of hours), Tinnitus, SNHL. Path: Increased endolymph pressure. Rx: Low salt diet, Diuretics, Betahistine.
• BPPV (Benign Paroxysmal Positional Vertigo): Sudden vertigo lasting seconds to <1 min provoked strictly by head movement (rolling in bed). NO hearing loss. Due to otoliths in posterior semicircular canal. Diagnose: Dix-Hallpike maneuver. Treat: Epley maneuver.
• Vestibular Neuritis: Sudden severe continuous vertigo lasting days following a viral URTI. NO hearing loss.

Pathology & Audiometry

• Abnormal spongy bone growth fixing the stapes footplate to the oval window.
• Causes Conductive Hearing Loss (CHL).
• Schwartze Sign: Flamingo pink blush seen through the TM (active phase).
• Pure Tone Audiometry (PTA):Carhart’s Notch (dip in Bone Conduction at 2000 Hz).
• Treatment:Stapedotomy with prosthesis insertion.

Pathology & Presentation

• Benign tumor of Schwann cells of the vestibular nerve (CN VIII). Located in the Cerebellopontine (CP) Angle.
• Bilateral Acoustic Neuromas are pathognomonic for Neurofibromatosis Type 2 (NF2).
• Earliest symptom: Unilateral progressive sensorineural hearing loss (high frequency) and tinnitus.
• As it grows in the CP angle, it compresses CN V (loss of corneal reflex) and CN VII (facial palsy).
• Investigation of choice: Gadolinium-enhanced MRI.

Pathways of Spread

• Acute Mastoiditis: Most common complication. Post-auricular swelling, pinna pushed down and out, “ironing out” of retroauricular fold.
• Brain Abscess: Most common intracranial complication (usually Temporal lobe or Cerebellum).
• Lateral Sinus Thrombosis: “Picket-fence” spiking fever (hectic fever), positive Griesinger’s sign (edema over mastoid due to emissary vein thrombosis), Tobey-Ayer test positive.

Pathology & Management

• Organism: Fungi of Mucorales order (Mucor, Rhizopus). Broad, non-septate hyphae branching at 90 degrees.
• Mechanism: Highly angioinvasive, causing thrombosis and necrosis of tissues. Thrives in acidic, high-glucose environments.

Anterior vs. Posterior Bleeds

• Anterior Epistaxis: Most common (especially children/trauma). Bleeding from Little’s Area (Kiesselbach’s Plexus) on the anterior septum. Plexus formed by: Sphenopalatine, Greater palatine, Superior labial, and Anterior ethmoidal arteries. Pinching nose stops it.
• Posterior Epistaxis: Common in elderly/hypertensives. Bleeding from Woodruff’s Plexus (lateral wall). Blood flows down the throat. Requires posterior nasal packing.

Characteristics

• Highly vascular, locally aggressive but histologically benign tumor.
• Occurs almost exclusively in Adolescent Males (testosterone dependent).
• Originates from the sphenopalatine foramen.
• Investigation: CECT or MRI. Shows Holman-Miller sign (anterior bowing of posterior maxillary wall).

Pathology & Presentation

• Strongly associated with Epstein-Barr Virus (EBV) and Chinese/Southeast Asian descent.
• Arises most commonly from the Fossa of Rosenmuller.
• Trotter’s Triad (Classic Presentation):
  1. Unilateral conductive hearing loss (Eustachian tube blockage).
  2. Ipsilateral temporoparietal neuralgia (CN V involvement).
  3. Ipsilateral palatal paralysis (CN X).
• Most common presentation is actually a painless cervical lymph node metastasis.
• Treatment: Highly radiosensitive (Radiotherapy is treatment of choice).

Peritonsillar Abscess (Quinsy)

• Collection of pus in the peritonsillar space (between tonsil capsule and superior constrictor muscle).
• Trismus (difficulty opening mouth) is due to spasm of the medial pterygoid muscle.
• Management: I&D (Incision and Drainage) at the point of maximum bulge, IV antibiotics (Penicillin/Clindamycin). Interval tonsillectomy done 6 weeks later.

Pathology

• Most common benign tumor of the larynx in children.
• Caused by HPV types 6 and 11 (transmitted vertically during birth).
• Presents with progressive hoarseness, stridor, and respiratory distress.
• Multiple warty lesions on vocal cords. Tends to recur frequently.
• Treatment: Microlaryngoscopy with CO2 laser or microdebrider excision. (Avoid tracheostomy as it seeds the virus lower down).

Glottic vs. Supraglottic

• Glottic Cancer (True Vocal Cords): Most common. Presents early with Hoarseness. Excellent prognosis because true vocal cords have NO lymphatic drainage (very late nodal metastasis).
• Supraglottic Cancer: Presents late with vague throat pain, dysphagia, or a neck mass. Rich lymphatic supply, hence early bilateral lymph node metastasis. Worse prognosis.
• Risk factors: Smoking and Alcohol (synergistic). Histology: Squamous Cell Carcinoma.

Timeline of Death

• Algor Mortis (Cooling): Body cools to ambient temperature. Formula for Time Since Death uses rectal temperature.
• Livor Mortis (Post-mortem Lividity): Pooling of blood in dependent areas. Starts 1-3 hrs, fixed by 6-8 hours. Fixing differentiates it from a bruise (pressing a fixed lividity does not blanch).
  
  Color Changes: Normal is bluish-purple. Cherry Red = CO poisoning. Brick Red = Cyanide. Brown = Nitrates/Phosphorus.
• Rigor Mortis (Stiffening): Due to depletion of ATP. Follows Nysten’s Law (starts small muscles of face/eye, moves downward). Starts 1-2 hrs, peaks at 12 hrs, passes off by 36 hrs.

Wound Ballistics

• Entry Wound: Usually smaller than the bullet (skin stretches). Edges are inverted. Features an Abrasion Collar / Dirt Ring.
• Exit Wound: Usually larger. Edges are everted. NO abrasion collar, NO tattooing/blackening.
• Range of Fire (Contact/Close): Presence of Blackening (unburnt powder) and Tattooing/Peppering (embedded burnt powder grains) indicates a close-range shot. Muzzle imprint indicates contact shot.

Burn Assessment

• Rule of Nines (Adults): Head 9%, Arms 9% each, Anterior trunk 18%, Posterior trunk 18%, Legs 18% each, Perineum 1%.
• Ante-mortem vs Post-mortem Burns: Ante-mortem burns show a Line of Redness / Vesicles containing protein-rich fluid (chloride) and soot in the trachea. Post-mortem burns have hard, dry blisters with air, no soot in trachea.
• Pugilistic Attitude: Boxer’s posture in severe burns. This is due to heat-induced coagulation and shrinking of muscle proteins (flexors are bulkier than extensors). It is NOT related to rigor mortis or fighting before death.

Examination and Evidence

• Consent for examination of a rape victim must be obtained from the victim (if >18). If <18, from parents/guardian. (Note: Under POCSO, reporting is mandatory).
• Seminal Fluid Markers:Acid Phosphatase (screening test), Florence test (Choline), Barberio’s test (Spermine). Definitive proof is the presence of spermatozoa under microscopy.
• Presence of smegma under the foreskin of the accused indicates that penile intromission did not happen recently (smegma is rubbed off during intercourse).

Classic Toxidromes

• Lead (Plumbism): Burtonian line (blue line on gums), Extensor motor palsy (Wrist drop/Foot drop), Basophilic stippling, Colicky abdominal pain. Rx: EDTA, BAL, Penicillamine.
• Arsenic: Odor of garlic, severe cholera-like diarrhea, Raindrop pigmentation, Mees’ lines on nails, Aldrich-Mees lines. Hyperkeratosis of palms/soles. Enters hair roots. Rx: BAL (Dimercaprol).
• Mercury (Hydrargyrism): Minamata disease. Tremors (Danse Macabre), Erethism (Mad Hatter syndrome – severe behavioral changes, shyness), Acrodynia (Pink disease in children).

Classic Intoxications

• Datura (Anticholinergic): “Dry as a bone, red as a beet, blind as a bat, hot as a hare, mad as a hatter.” Contains atropine/scopolamine. Often used for railway robberies (causes amnesia). Rx: Physostigmine.
• Strychnos Nux Vomica (Strychnine): Inhibits Glycine (inhibitory neurotransmitter) in the spinal cord. Causes severe convulsions and Opisthotonos (backward arching) while fully conscious. Risus sardonicus. (Mimics Tetanus).
• Aconite (Monkshood): “Sweet poison.” Tingling and numbness of lips/tongue, followed by fatal cardiac arrhythmias. Hippus (alternate dilation/constriction of pupils).

Legal Concepts & Sections

• Res Ipsa Loquitur: “The thing speaks for itself.” Example: Surgeon leaves a sponge in the abdomen. The patient does not need to prove negligence; the burden of proof shifts to the doctor.
• Novus Actus Interviens: A new intervening act that breaks the chain of causation. (e.g., A attacks B, B goes to hospital, hospital gives wrong blood type and B dies. A is not charged with murder).
• IPC 320: Defines Grievous Hurt (emasculation, permanent loss of sight/hearing, bone fracture, any hurt endangering life or causing >20 days of severe pain).
• IPC 304-A: Causing death by negligence (applicable to medical negligence resulting in patient death).

Types of Necrosis

• Coagulative: Cell outlines preserved (ghost cells). Seen in ischemia/infarcts in all solid organs EXCEPT the brain.
• Liquefactive: Tissues dissolve into liquid viscous mass. Seen in Brain infarcts and Bacterial Abscesses (due to neutrophil enzymes).
• Caseous: “Cheese-like” friable appearance. Characteristic of Tuberculosis and systemic fungi.
• Fat Necrosis: Chalky-white deposits due to saponification. Seen in Acute Pancreatitis and Breast trauma.

Pathology & Cytokines

• Characterized by collections of Epithelioid Macrophages (modified macrophages) and Multinucleated Giant Cells.
• Formation: Th1 cells secrete IFN-gamma, activating macrophages. Macrophages secrete TNF-alpha to maintain the granuloma structure.

Tumor Suppressors (Require “Two Hits”)

• p53: “Guardian of the genome.” Halts cell cycle at G1/S. Mutation causes Li-Fraumeni syndrome (sarcomas, breast, leukemia, adrenal gland tumors).
• Rb: Binds/inhibits E2F. Mutation causes Retinoblastoma and Osteosarcoma.
• APC: Inhibits beta-catenin. Mutation causes Familial Adenomatous Polyposis (FAP) – 100% risk of colon cancer.

Key Differentiating Markers

• ALL (Children): TdT positive. CD10+. May present with mediastinal mass (T-cell) or bone pain. Good prognosis.
• AML (Adults 15-39): Myeloperoxidase (MPO) positive. Shows Auer Rods (can trigger DIC). APML subtype (t(15;17)) treated with ATRA.
• CML (Adults 40-59): Massive splenomegaly. Basophilia. Philadelphia chromosome t(9;22) BCR-ABL. Treated with Tyrosine Kinase Inhibitors (Imatinib).
• CLL (Elderly >60): Most common adult leukemia. Characteristic Smudge Cells on peripheral smear.

Hodgkin Lymphoma (HL)

• Hallmark: Reed-Sternberg Cells (CD15+, CD30+).
• Spread is localized and contiguous. Excellent prognosis.
• Nodular Sclerosis: Most common subtype. Affects young females, characterized by mediastinal masses and broad bands of collagen on biopsy.

Location & Associations

• Small Cell Carcinoma (Oat Cell): Central location. Undifferentiated Kulchitsky cells (neuroendocrine). Secretes ACTH (Cushing) or ADH (SIADH). Antibodies against presynaptic Ca2+ channels (Lambert-Eaton Syndrome). Inoperable; treat with chemo.
• Squamous Cell Carcinoma: Central location. Histology: Keratin pearls, intercellular bridges. Produces PTHrP causing Hypercalcemia.
• Adenocarcinoma: Peripheral location. Most common lung cancer in non-smokers and females. Glandular pattern, mucin positive. Activating mutations in EGFR, ALK, KRAS.

Pathological Hallmarks

• Cirrhosis: Defining feature is bridging fibrosis (collagen laid down by Hepatic Stellate / Ito cells in the Space of Disse) + Regenerative hepatocyte nodules.
• Alcoholic Hepatitis: Swollen, necrotic hepatocytes containing Mallory-Denk bodies (eosinophilic inclusions composed of cytokeratin intermediate filaments).
• Hepatocellular Carcinoma (HCC): Associated with HBV/HCV, Aflatoxin B1 (aspergillus on peanuts), and Hemochromatosis. Tumor marker: Alpha-fetoprotein (AFP).

Benign vs. Malignant

• Intraductal Papilloma: Most common cause of bloody or serous nipple discharge. Benign tumor within lactiferous ducts.
• Invasive Ductal Carcinoma: Most common malignant breast cancer. Rock-hard mass. Histology shows duct-like structures in a dense, fibrous desmoplastic stroma.
• Invasive Lobular Carcinoma: Histology shows Single-file cells (Indian file pattern) due to a genetic loss of E-cadherin. High rate of bilaterality.

Adult vs. Pediatric

• Adult – Glioblastoma Multiforme (GBM): Most common malignant primary brain tumor. Rapidly crosses corpus callosum (“Butterfly glioma”). Histology: Pseudopalisading pleomorphic tumor cells bordering central areas of necrosis and hemorrhage. GFAP positive.
• Adult – Meningioma: Most common benign. Extra-axial (arises from arachnoid cells). Often has a dural tail. Histology: Whorled pattern, Psammoma bodies.
• Child – Medulloblastoma: Malignant cerebellar tumor (vermis). Histology: Homer-Wright rosettes, small blue cells. Causes “Drop metastasis” to the spinal cord.

Microbiology Features

• Obligate aerobe. Cell wall is incredibly rich in Mycolic acid (retains carbolfuchsin stain, making it Acid-Fast).
• Culture medium: Löwenstein-Jensen (LJ) agar (takes 4-6 weeks to grow).
• Virulence factor: Cord factor (creates a “serpentine cord” appearance in vitro; in vivo, it inhibits macrophage maturation and induces granuloma formation).

Gram-Positive Spore-Forming Anaerobes

• C. tetani: Toxin (Tetanospasmin) cleaves SNARE proteins, blocking release of inhibitory neurotransmitters (GABA and Glycine) from Renshaw cells in the spinal cord. Causes Spastic paralysis (lockjaw, risus sardonicus, opisthotonos).
• C. botulinum: Toxin cleaves SNARE proteins to block the release of excitatory Acetylcholine at the neuromuscular junction. Causes Flaccid descending paralysis. Found in improperly canned food or honey (infant botulism).
• C. perfringens: Causes Gas gangrene (via Alpha toxin/lecithinase which cleaves cell membranes).
• C. difficile: Causes pseudomembranous colitis secondary to antibiotic use (Clindamycin/Ampicillin). Toxin A (watery diarrhea) and Toxin B (cytotoxin).

MacConkey Agar Differentiation

• Lactose Fermenters (Pink colonies): E. coli, Klebsiella, Enterobacter. (Note: E. coli also displays a metallic green sheen on Eosin Methylene Blue (EMB) agar).
• Non-Lactose Fermenters (Colorless colonies): Salmonella (produces H2S/black colonies on TSI agar), Shigella (no H2S), Proteus, Pseudomonas.

Clinical Stages

• Primary: Painless chancre (localized).
• Secondary (Disseminated): Maculopapular rash (classically includes palms and soles), Condylomata lata (smooth, moist, highly infectious lesions on genitals), patchy alopecia.
• Tertiary: Gummas (destructive granulomas), Aortitis (tree-bark appearance of ascending aorta), Neurosyphilis (Tabes dorsalis, Argyll Robertson pupil – accommodates but doesn’t react to light).

Interpreting the Markers

• HBsAg (Surface Antigen): Indicates active infection (acute or chronic). If present > 6 months = Chronic carrier.
• Anti-HBs (Surface Antibody): Indicates immunity (either recovered from infection or vaccinated).
• HBeAg: Indicates high viral replication and high infectivity.
• Anti-HBc IgG (Core Antibody): Indicates past or chronic infection. (Note: This is NOT present if immunity is strictly from the vaccine).

CD4 Count Thresholds & Prophylaxis

• < 200:Pneumocystis jirovecii pneumonia (PCP). Bilateral ground glass opacities. Prophylaxis/Rx: TMP-SMX.
• < 100:Toxoplasma gondii (Ring-enhancing brain lesions on MRI, Rx: Pyrimethamine/Sulfadiazine), Cryptococcus neoformans (Meningitis, India ink shows thick capsules).
• < 50:Mycobacterium avium complex (MAC) (Prophylaxis: Azithromycin), CMV Retinitis (“pizza pie” retinopathy, cotton wool spots, Rx: Ganciclovir).

Key Characteristics

• HSV-1 & HSV-2: Latent in trigeminal (1) and sacral (2) ganglia. Tzanck smear shows multinucleated giant cells with intranuclear inclusions (Cowdry A bodies).
• VZV (HHV-3): Chickenpox (lesions in multiple stages: macule, papule, vesicle, crust) and Shingles (painful, dermatomal distribution).
• EBV (HHV-4): Infectious Mononucleosis. Pharyngitis, hepatosplenomegaly, generalized lymphadenopathy. Peripheral smear shows atypical lymphocytes (Downey cells), which are actually reactive cytotoxic T-cells reacting against infected B-cells. Positive Monospot test (heterophile antibodies).

Morphology on Biopsy

• Candida albicans: Pseudohyphae and budding yeast at 20°C. Forms Germ tubes at 37°C. Causes oral thrush, vulvovaginitis, diaper rash, and candidemia in IV drug users.
• Aspergillus fumigatus: Septate hyphae branching at 45-degree acute angles (V-shaped). Causes allergic bronchopulmonary aspergillosis (ABPA) in asthmatics, or aspergilloma (fungus ball) in pre-existing TB cavities.
• Mucor/Rhizopus: Broad, non-septate (ribbon-like) hyphae branching at 90-degree right angles. Causes aggressive, rapidly fatal rhinocerebral mucormycosis, classically in patients with Diabetic Ketoacidosis (DKA) or neutropenia.

Species Differentiation

• P. falciparum: Most severe. Irregular fever spikes, cerebral malaria, blackwater fever. Peripheral smear shows multiple small rings per RBC and characteristic banana/crescent-shaped gametocytes.
• P. vivax / P. ovale: 48-hour fever cycle. Forms Hypnozoites (dormant stage in the liver) causing relapses months to years later.

Key Parasites & Presentations

• Giardia lamblia: Campers drinking unfiltered mountain stream water. Foul-smelling, fatty diarrhea (steatorrhea). Trophozoite looks like a “falling leaf” or an “old man face” with 2 nuclei. Rx: Metronidazole.
• Entamoeba histolytica: Bloody diarrhea (dysentery). Flask-shaped ulcers in the colon mucosa. Trophozoite identified by engulfed RBCs in the cytoplasm. Causes amebic liver abscess (“anchovy paste” aspirate).
• Cryptosporidium: Severe, unrelenting watery diarrhea in immunocompromised (HIV) patients. Identified by acid-fast cysts in stool.

Mnemonic: ACID

• Type I (Anaphylactic/Allergic): IgE mediated. Mast cell and basophil degranulation (histamine release). Fast. (e.g., Asthma, Bee sting, Urticaria, Anaphylaxis).
• Type II (Cytotoxic): IgG/IgM autoantibodies directed against fixed antigens on cells/tissues, leading to complement activation or phagocytosis. (e.g., Goodpasture syndrome, Rheumatic fever, Autoimmune Hemolytic Anemia).
• Type III (Immune Complex): Free circulating Antigen-Antibody complexes deposit in tissues, activating complement and attracting neutrophils. (e.g., SLE, PSGN, Serum sickness, Arthus reaction).
• Type IV (Delayed):T-cell mediated (NO antibodies involved). Takes 48-72 hours to develop. Macrophages are recruited. (e.g., TB PPD skin test, Contact dermatitis/Poison ivy, Multiple Sclerosis, Graft-vs-host disease).

Classification & Contraindications

• Non-selective (Beta 1 & 2): Propranolol, Timolol, Nadolol. Contraindicated in asthmatics/COPD (B2 blockade causes severe bronchospasm) and variant (Prinzmetal) angina.
• Cardioselective (Beta 1 only): Mnemonic “A to M” (Atenolol, Metoprolol, Esmolol, Bisoprolol). Safer for patients with lung disease.
• Combined Alpha 1 & Beta blockers: Labetalol, Carvedilol. Excellent for hypertensive emergencies and heart failure mortality reduction.

Pathology & Stepwise Management

• Mechanism: Irreversible inhibition of Acetylcholinesterase (AChE), leading to massive acetylcholine buildup at both muscarinic (DUMBELS symptoms) and nicotinic (muscle weakness/fasciculations) receptors.
• Treatment Step 1:Atropine (Antimuscarinic). This crosses the BBB and reverses life-threatening bronchoconstriction, secretions, and bradycardia. Does NOT fix muscle paralysis.
• Treatment Step 2:Pralidoxime (PAM). This is a cholinesterase regenerator. It works on nicotinic muscle receptors to reverse respiratory muscle paralysis. Must be given before “aging” (permanent chemical binding) of the enzyme complex occurs.

ACE Inhibitors (The “-prils”)

• Block conversion of Angiotensin I to II (decreasing vasoconstriction and aldosterone). Also prevent the breakdown of Bradykinin.
• First-line for Hypertension in patients with Diabetes or Proteinuria (preferentially dilates efferent arteriole, reducing intraglomerular pressure and delaying diabetic nephropathy).
• Side Effects: Dry cough (due to bradykinin accumulation in lungs), life-threatening Angioedema, Hyperkalemia. Teratogenic (strictly avoid in pregnancy).

Site of Action & Electrolyte Effects

• Loop Diuretics (Furosemide, Torsemide): Inhibit Na-K-2Cl cotransporter in Thick Ascending Limb of Henle. Most potent. Causes massive diuresis. Loses Calcium (Hypercalciuria), K+, and Mg2+. Causes Ototoxicity (especially if pushed fast IV) and Sulfa allergy.
• Thiazides (Hydrochlorothiazide, Chlorthalidone): Inhibit Na-Cl cotransporter in Early Distal Tubule. Causes Calcium Retention (Hypercalcemia). Highly useful in patients with osteoporosis or recurrent calcium oxalate kidney stones. Side effects: HyperGLUC (HyperGlycemia, Lipidemia, Uricemia, Calcemia).
• K-Sparing (Spironolactone): Aldosterone receptor antagonist in collecting duct. Saves K+ (causes hyperkalemia). Side effect: Gynecomastia and anti-androgen effects.

Class III (Potassium Channel Blockers)

• Amiodarone is the most efficacious and broad-spectrum anti-arrhythmic (has Class I, II, III, and IV properties).
• Because it is highly lipophilic and contains iodine, it has a massive volume of distribution, a very long half-life (weeks), and widespread tissue toxicities.

First-Line Drugs & Specific Side Effects

• Phenytoin: Blocks Na+ channels. Side effects: Gingival hyperplasia, Hirsutism, Fetal Hydantoin Syndrome (cleft palate), megaloblastic anemia (decreases folate), Osteopenia. Exhibits zero-order kinetics at therapeutic doses.
• Valproic Acid: Broadest spectrum (first line for generalized tonic-clonic and myoclonic). Hepatotoxic, highly teratogenic (Neural Tube Defects like spina bifida due to folate inhibition).
• Carbamazepine: First line for focal seizures and Trigeminal Neuralgia. Causes agranulocytosis, aplastic anemia, and SIADH (hyponatremia). Induces its own metabolism (CYP450 auto-induction).
• Ethosuximide: First line for Absence Seizures ONLY. Mechanism: Blocks T-type Ca2+ channels in the thalamus. (Mnemonic: EFG – Ethosuximide, Fatigue, GI distress).

High-Yield Pharmacology

• Aspirin: Irreversible COX-1 & COX-2 inhibitor. Causes GI ulcers and tinnitus/hyperventilation (respiratory alkalosis followed by metabolic acidosis) in overdose. Avoid in children with viral illnesses as it causes Reye’s Syndrome (rapid, fatal acute encephalopathy and hepatic microvesicular steatosis).
• Acute Gout: NSAIDs (Indomethacin/Naproxen) are 1st line. Colchicine is 2nd line (mechanism: binds intracellular tubulin, inhibiting microtubule polymerization and preventing neutrophil chemotaxis into the joint).
• Chronic Gout: Allopurinol (Xanthine oxidase inhibitor) reduces uric acid production. Probenecid increases renal excretion. Never start Allopurinol during an acute gouty attack as it will rapidly mobilize tissue stores and worsen the flare!

The RIPES Regimen Side Effects

• Rifampin: Red-orange discoloration of bodily fluids (urine, tears, sweat – warn the patient). Extremely potent CYP450 inducer (decreases efficacy of Oral Contraceptive Pills and warfarin).
• Isoniazid (INH): Hepatotoxic. Causes peripheral neuropathy due to increased excretion of Vitamin B6 (must co-administer with Pyridoxine). Can cause Drug-induced lupus (Anti-histone antibodies).
• Pyrazinamide: Hyperuricemia (can trigger gout attacks), severe hepatotoxicity.
• Ethambutol: Optic neuritis (Red-green color blindness, decreased visual acuity). Mnemonic: E = Eyes. Not hepatotoxic.
• Streptomycin: Aminoglycoside. Causes permanent Ototoxicity and Nephrotoxicity.

Penicillins & Cephalosporins

• Mechanism: Bind to Penicillin-Binding Proteins (PBPs), effectively blocking the transpeptidation (cross-linking) of peptidoglycan in the bacterial cell wall. They are bactericidal.
• Methicillin-Resistant S. aureus (MRSA): MRSA is resistant to all penicillins and cephalosporins because it genetically mutates its binding site (altered PBP-2a via the mecA gene). Drug of choice is Vancomycin (which binds the D-ala-D-ala tail directly, bypassing the PBP).

Mnemonic: “Buy AT 30, CCEL at 50”

• 30S Subunit Inhibitors: Aminoglycosides (Gentamicin – bactericidal, requires O2 for uptake, ototoxic/nephrotoxic), Tetracyclines (Doxycycline – bacteriostatic).
• 50S Subunit Inhibitors: Chloramphenicol, Clindamycin (high risk of C. diff pseudomembranous colitis), Erythromycin/Azithromycin (Macrolides), Linezolid.

Key Classes for Type 2 Diabetes

• Metformin (Biguanide): First line universally. Decreases hepatic gluconeogenesis and increases peripheral insulin sensitivity. Does NOT cause hypoglycemia. Side effect: GI upset, Vitamin B12 deficiency, and Lactic acidosis (strictly contraindicated in renal failure or before giving IV contrast).
• Sulfonylureas (Glipizide, Glyburide): Stimulate insulin release by closing K+ channels in pancreatic beta cells. Major risk of severe Hypoglycemia and weight gain.
• SGLT2 Inhibitors (-gliflozins): Block glucose reabsorption in the proximal convoluted tubule, causing glucosuria. Causes weight loss and reduces heart failure mortality. Side effects: UTIs, vaginal candidiasis, and euglycemic DKA.
• GLP-1 Agonists (-tides): Exenatide, Liraglutide. Delay gastric emptying, increase satiety (massive weight loss), and increase glucose-dependent insulin release. Given SC. High risk of pancreatitis.

Phases of Clinical Trials

• Phase 1: Healthy volunteers (<100). Checks Safety and maximum tolerable dose.
• Phase 2: Small patient group. Checks Efficacy.
• Phase 3: Large multi-center RCT. Compares to current Gold Standard treatment. Drug gets approval here.
• Phase 4: Post-marketing surveillance. Detects rare, long-term adverse effects.

National TB Elimination Programme (NTEP)

• Goal: Eliminate TB in India by 2025 (SDG goal is 2030).
• Diagnosis:CBNAAT (GeneXpert MTB/RIF) or Truenat are now preferred upfront tests because they detect TB and Rifampicin resistance simultaneously in 2 hours.
• Nikshay Poshan Yojana: Financial support of ₹500/month to all notified TB patients for nutrition.

Cold Chain Temperatures

• Standard temperature for most vaccines at PHC: +2°C to +8°C (in ILR – Ice Lined Refrigerator).
• Oral Polio Vaccine (OPV) is the most heat-sensitive and is stored at the bottom of the ILR. At regional/state levels, OPV is stored at -20°C in Deep Freezers.
• Freeze-sensitive vaccines: DPT, Hep B, TT. (Never freeze these. Shake Test is used to check if DPT/Pentavalent was accidentally frozen).

Clinical Markers & Toxicity

• Lead inhibits enzymes in heme synthesis (ALA dehydratase and Ferrochelatase).
• Causes Microcytic Hypochromic Anemia with Basophilic Stippling of RBCs.
• Burtonian Line: Blue-black line on the gingival margin (lead sulfide deposit).
• Coprolalial/Neurological: Wrist drop/foot drop (motor neuropathy in adults), Encephalopathy and low IQ in children (pica behavior).

Principles of Chlorination

• Chlorine Demand: Amount of chlorine required to destroy bacteria and oxidize organic matter in water.
• Free Residual Chlorine: The active chlorine (Hypochlorous acid, HOCl) left OVER after the demand is met. Must be 0.5 mg/L for 1 hour contact time to ensure water is safe to drink.
• Break-point Chlorination: The point at which all ammonia is oxidized and free residual chlorine begins to appear proportionally to the dose added.

Types and Lifespan (Govt Supply)

• CuT 380A: Most effective copper IUD. Lifespan is 10 years. Acts by causing sterile inflammation and copper ions acting as spermicides.
• CuT 375: Lifespan is 5 years.
• Levonorgestrel IUS (Mirena): Releases progesterone locally. Lifespan is 5-7 years. Excellent for treating heavy menstrual bleeding (menorrhagia).

WHO Categories & Actions

• Category I: Touching/feeding animals, licks on INTACT skin. Action: Wash with soap and water. No vaccine needed.
• Category II: Minor scratches/abrasions without bleeding, licks on broken skin. Action: Wash wound + Vaccine.
• Category III: Transdermal bites/scratches drawing blood, wild animal bites. Action: Wash wound + Vaccine + Rabies Immunoglobulin (RIG) infiltrated exactly into and around the wound.

Acute Flaccid Paralysis (AFP) Surveillance

• Any child <15 years with acute onset of flaccid (floppy) paralysis must be reported.
• Stool Sample Rule: Must collect two stool samples 24-48 hours apart, within 14 days of paralysis onset, transported in a cold chain to detect wild poliovirus.
• India was declared Polio-free in 2014. The last case was in 2011 (Howrah, West Bengal).

NP-NCD Screening Guidelines

• National Programme for Prevention & Control of NCDs.
• Population-based screening starts at 30 years of age.
• Screens for: Hypertension, Diabetes, and common cancers (Oral, Breast, Cervical).

Dosing Schedule

• 1st Dose: Given at 9 months with MR vaccine. Dose = 100,000 IU (1 ml).
• Subsequent Doses: Given every 6 months up to 5 years of age. Dose = 200,000 IU (2 ml).
• Total doses given = 9. Total amount = 17,00,000 IU.

The 6x6x6 Strategy

• 6 Beneficiaries, 6 Interventions, 6 Institutional mechanisms.
• Prophylactic Doses (Iron & Folic Acid – IFA):
• Children (6-59 months): 20 mg elemental Iron + 100 mcg FA (Bi-weekly syrup).
• Children (5-9 years): 45 mg Iron + 400 mcg FA (Weekly Pink tablet).
• Adolescents (10-19 years): 60 mg Iron + 500 mcg FA (Weekly Blue tablet).
• Pregnant/Lactating Women:60 mg Iron + 500 mcg FA (Daily Red tablet starting from 4th month for 180 days, and 180 days postpartum).

Salt Iodization

• Potassium Iodate is used in India (more stable in tropical climates than iodide).
• Standard requirement: 30 ppm at production level, and at least 15 ppm at the consumer level.

Diagnostic Markers

• Days 1-5:NS1 Antigen test is positive. Virus is circulating in blood.
• After Day 5: IgM MAC-ELISA becomes positive.
• Severe Dengue (DHF/DSS): Characterized by massive capillary leak. Look for rising Hematocrit (>20% increase) alongside rapidly falling platelet counts.

Key Legislations

• Factories Act (1948): Defines a factory as 10+ workers with power, or 20+ without power. Mandates crèches if >30 women employed. Safety officer required if >1000 workers. Maximum working hours: 48 hrs/week, 9 hrs/day.
• ESI Act (Employees’ State Insurance): Covers workers earning wages up to ₹21,000/month. Employer contributes 3.25%, Employee 0.75%. Provides sickness, maternity, disablement, and medical benefits.

ABCDE Approach

• Airway: Secure airway with cervical spine restriction. (Gurgling = suction, then intubate if needed).
• Breathing: Assess chest for tension pneumothorax, massive hemothorax, flail chest.
• Circulation: Assess pulses, control hemorrhage (direct pressure), establish 2 large-bore IVs.

Burn Assessment (Rule of Nines)

• Adults: Head 9%, Arms 9% each, Anterior Trunk 18%, Posterior Trunk 18%, Legs 18% each, Perineum 1%.