NEET MDS Lessons
Periodontology
🧬 Risk Factors
- Increased homocysteine levels
- Raised lipoprotein(a)
- Nephrotic syndrome increases CAD risk
- Unsaturated fatty acid intake: Protective
- Best probability predictor in elderly: LDL/HDL ratio
⚕️ Diagnosis & Presentation
| Condition | Diagnostic Best Practice |
|---|---|
| Angina pectoris | History |
| Stable angina | Cardiac markers unchanged |
| Acute MI | Tall T wave (earliest ECG sign) |
| MI ≥12 hrs post-onset | Test of choice: Cardiac troponin |
| Prinzmetal’s angina | First-line agent: Nitrates |
| Intraoperative MI | Transesophageal echocardiography |
| Best biomarker of MI | Troponin T |
| WHO MI criteria | Echo not part of official criteria |
🧪 Enzymes & Drugs
- Enzyme ↑ at 4 – 6 hrs, ↓ in 3 – 4 days: CPK
- Stress ECHO agent: Dobutamine
- Intervention of choice: Streptokinase + Heparin
- Thrombolytics window: Within 12 hrs of MI
🚨 Prognosis & Complications
- Day 1: Maximum MI mortality
- Post-MI valvular lesion: Mitral regurgitation
- Best predictor of morbidity: LVEF
- Fatal thrombolysis complication: Intracranial hemorrhage
- LAD artery nicknamed: Widow’s artery
Blood Components
- Leukocyte-depleted RBCs: Reduces febrile reactions and CMV transmission
- Platelets: For thrombocytopenia or platelet dysfunction
- Fresh Frozen Plasma (FFP): Contains all coagulation factors
- Cryoprecipitate: High concentration of fibrinogen, Factor VIII, vWF
- Albumin: Volume expansion, hypoalbuminemia
Transfusion Reactions
Most Common: Febrile Non-Hemolytic Transfusion Reaction (FNHTR)
- Incidence: Most frequent transfusion reaction
- Mechanism: Recipient antibodies against donor leukocytes/cytokines
- Presentation: Fever, chills, rigors during or after transfusion
- Management: Stop transfusion, antipyretics, rule out hemolysis
- Prevention: Leukocyte-depleted blood products
Other Important Reactions
- Acute hemolytic: ABO incompatibility (most dangerous)
- Allergic: Urticaria, anaphylaxis (plasma protein sensitivity)
- TRALI: Transfusion-related acute lung injury
- TACO: Transfusion-associated circulatory overload
Pre-transfusion Testing
- ABO/Rh typing
- Antibody screening
- Crossmatching
- Direct antiglobulin test (DAT)
- Steroids, Thiazides, Niacin, Phenytoin
- Protease inhibitors, Alpha IF, Clozapine, Beta agonists
🧠 Endocrine-Related DM
- Cushing’s, Acromegaly, Pheochromocytoma
- Thyroid disorders, Glucagonoma, Somatostatinoma
- (Note: Hypoglycemia in Addison's disease)
💓 Cardiovascular & Renal
- ↑GFR → Earliest sign of diabetic nephropathy
- Microalbuminuria → Most reliable marker
- ACEIs → Nephroprotective, but contraindicated in CRF (hyperkalemia)
👁️🗨️ Complications
- Wet gangrene, Blindness, Amputation (2nd most common after trauma)
💊 Special Drug Mention
- Telmisartan → Only ARB acting on PPAR-γ → preferred in DM
🧪 GERD & Barrett’s Esophagus
| Feature | Insight |
|---|---|
| Diagnosis | Intestinal metaplasia |
| Sequelae | Stricture, adenocarcinoma |
| Risk classification | Premalignant |
| Cancer association | Esophageal adenocarcinoma |
🧫 Peptic Ulcer
- Commonest site: Duodenal bulb (1st part)
- Most frequent complication: Hemorrhage
- Best residual H. pylori test: Urea breath test
- Treatment for Zollinger – Ellison syndrome: PPI
ANUG (Acute Necrotizing Ulcerative Gingivitis)
- Signs: Punched – out crater depressions of interdental papilla
- Symptoms: Metallic foul taste, pasty saliva
- Treatment: 3 visits (2nd visit: 1 – 2 days after 1st; 3rd visit: 5 days after 2nd)
NUG/NUP
- No pocket formation (destroys junctional epithelium)
Primary Herpetic Gingivostomatitis
- Cellular change: Ballooning degeneration → Tzanck cells
- Treatment:
- Within 3 days: Acyclovir 15 mg/kg × 5 times × 7 days
- After 3 days: Supportive care with NSAIDs
Leukemic Gingivitis
- Most common in acute monocytic leukemia
Lead Intoxication
- Steel gray linear pigmentation (Burton's line)
Wilson's disease is an autosomal recessive disorder of copper metabolism caused by mutations in the ATP7B gene, resulting in impaired biliary copper excretion and toxic copper accumulation in tissues.
Pathophysiology
- Basic defect: Decreased biliary copper excretion due to defective ATP7B protein
- Mechanism: Impaired incorporation of copper into ceruloplasmin and reduced copper transport into bile
- Result: Copper accumulation in liver, brain, cornea, and other organs
Clinical Manifestations
Hepatic (Most common initial presentation)
- Acute hepatitis
- Chronic hepatitis
- Cirrhosis
- Fulminant hepatic failure
Neurological
- Movement disorders (tremor, dystonia, chorea)
- Psychiatric symptoms (depression, psychosis, behavioral changes)
- Dysarthria and dysphagia
- Cognitive impairment
Ophthalmologic
- Kayser-Fleischer rings (pathognomonic copper deposits in Descemet's membrane)
- Sunflower cataracts
Other Features
- Renal tubular acidosis
- Hemolytic anemia
- Arthritis
- Cardiomyopathy (rare)
Diagnostic Workup
- Serum ceruloplasmin: Usually decreased (<20 mg/dL)
- 24-hour urine copper: Elevated (>100 μg/24h)
- Hepatic copper content: Gold standard (>250 μg/g dry weight)
- Ophthalmologic examination: Slit-lamp for Kayser-Fleischer rings
- Genetic testing: ATP7B gene mutations
- Brain MRI: "Face of giant panda" sign in severe cases
Treatment
Chelation Therapy
- D-penicillamine: First-line, may worsen neurological symptoms initially
- Trientine: Alternative chelator, better tolerated neurologically
- Tetrathiomolybdate: For neurological presentations
Zinc Therapy
- Zinc acetate/sulfate: Blocks copper absorption, maintenance therapy
- Preferred for asymptomatic patients and maintenance
Diagnosis Criteria
- FBS ≥ 126 mg/dL
- HbA1C > 6.5%
- eAG based on HbA1C
- Oral GTT 2-hr post-load: 140–199 mg/dL → Impaired Glucose Tolerance
- HbA1C 5.7–6.4% → Pre-diabetic range