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- NEETMDS- courses
NEET MDS Lessons
Periodontology

Pathophysiology

  • Enzyme defect: Glucose-6-phosphate dehydrogenase deficiency
  • Result: Impaired NADPH production → reduced glutathione → oxidative damage
  • Inheritance: X-linked recessive (affects males predominantly)

Key Clinical Features

  • Heinz bodies: Characteristic finding (precipitated denatured hemoglobin)
  • Hemolytic episodes: Triggered by oxidative stress
  • Chronic hemolysis: Usually absent between episodes
  • Neonatal jaundice: May be severe

Important Clinical Points

  • Estrogen does NOT induce hemolysis (unlike other conditions)
  • Favism: Hemolysis after eating fava beans
  • Drug-induced: Most common trigger for hemolytic crisis

Oxidative Stressors to Avoid

Medications

  • Antimalarials: Primaquine, chloroquine
  • Antibiotics: Sulfonamides, nitrofurantoin, chloramphenicol
  • Analgesics: Aspirin (high doses), phenazopyridine
  • Others: Methylene blue, naphthalene (mothballs)

Infections

  • Bacterial infections
  • Viral hepatitis
  • Pneumonia
  • Typhoid fever

Other Triggers

  • Fava beans (favism)
  • Diabetic ketoacidosis
  • Severe illness/stress

🔁 Pulse Patterns

Pulse Type Condition
Slow rising pulse Aortic stenosis (AS)
Pulsus alternans CHF
Pulsus bigeminus Digoxin therapy
Pulsus paradoxus Tamponade, pericarditis, asthma
Water hammer pulse Aortic regurgitation
Pulsus bisferiens Best felt in radial artery

🔊 Heart Sounds

  • Loud S1: Short PR interval, tachycardia, mitral stenosis
  • Fourth Heart Sound (S4): Heard during ventricular filling
  • Opening snap: High-pitched, diastolic sound

  • Junctional Epithelium: Attached to enamel via hemidesmosomes; to connective tissue via external basal lamina.
  • Corneocyte Formation: Keratinohyalin granules disappear, forming filaggrin.
  • Langerhans Cells: Suprabasal level; antigen-presenting with Birbeck granules.
  • Keratinization: Oral epithelium is 0.2 – 0.3 mm thick; may be keratinized or parakeratinized.

🧬 Blood Disorders

  • Polycythemia vera: Common cause of Budd – Chiari
  • PNH: Rare cause of Budd – Chiari
  • Thalassemia & Hemolytic anemia: Lead to unconjugated hyperbilirubinemia
  • Anemia: Can cause high-output heart failure
  • Hemophilia A: Deficiency of Factor VIII
  • ITP vs TTP: ITP = isolated thrombocytopenia; TTP = microangiopathy

Condition Key Insight
Autoimmune Hemolysis Spherocytes; seen in CLL, SLE
Cold AIHA Donath – Landsteiner antibodies
Hereditary Spherocytosis ↑ Osmotic fragility; Parvovirus risk
PNH Stem cell disorder; thrombosis risk
Sickle Cell Disease Hb defect: Glu → Val substitution
Commonest presentation Bone pain (vaso-occlusive crisis)
Sickle Trait Protection against malaria
Radiologic sign Crew haircut, Gandy gamma bodies
Chronic cases Splenomegaly often absent

  • 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

Calculus Composition

  • Brushite: More common in mandibular anterior
  • Magnesium whitlockite: More common in posterior
  • Ca:P ratio: Higher subgingivally
  • Mineralization: 50% in 2 days, 60 – 90% in 12 days

Microbiology

  • First colonizers: S. salivarius and S. mitis
  • Red complex: P. gingivalis, T. denticola, T. forsythia (cause BOP)
  • Growth enhancement: P. gingivalis grows better with succinate (C. ochracea) and protoheme (C. rectus)

Pellicle Structure

  • Basal layer: Thin, difficult to remove
  • Globular layer: 1 μm thick, easier to detach

Bacterial Recognition

  • Gram positive: Activate TLR2 → IL – 8
  • Gram negative: Activate TLR4 → TNF – α

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