N Topics Study 1st Revision 2nd Revision 1 Congenital heart disease 2 Coronary Artery disease 3 Hypertension 4 Acute Rheumatic fever 5 Infective Endocarclitis 6 Syncope 7 Heart failure 8 Cardiogenic shock 9 Peptic ulcer TOPICS AND PROGRESS TRACKING PLAN 1

Congenital Heart DiseaseCongenital Heart Disease ""CHD"CHD" Congenital Heart Disease "CHD" 2 0.8% of the population is born with CHD. 40% resolve spontaneously (mainly small VSDs). 56–98% survive into adulthood with current surgical techniques. 4.Etiology Structural defect in the heart and great vessels present at, birth In adults: VSD & ASD (~20%), followed by PDA and pulmonary valve stenosis. Most common CHD overall = Bicuspid aortic valve + VSD. Most common cyanotic CHD = Fallot's Tetralogy.NB Causes Fallot's Tetralogy ⭐ (most common) Fallot's Trilogy Less common. Eisenmenger 's Syndrome Pulmonary Stenosis. Aortic Stenosis. VSD, ASD, PDA. Coarctation of the Aorta. Dextrocardia. 2.Epidemiology 3.Common defects Diseases Cyanotic Ayanotic 5.Classification Congenital heart block, ASD No specific association PDA, Pulmonary stenosis No specific association VSD Coarctation of aorta Septal defects Genetic abnormalities Irradiation Maternal rubella Premature infants Down's syndrome Turner's syndrome Maternal alcohol abuse 1.Definition:

Digital clubbing Chronic hypoxia Renal dysfunction Sclerotic glomeruli → ↑Creatinine + Proteinuria + Hyperuricemia Gallstones ↑ RBC breakdown → ↑ Calcium bilirubinate stones Hypertrophic osteoarthropathy Thickened periosteum + Scoliosis Cerebrovascular events Embolic/Hemorrhagic + Brain abscess + Cognitive problems Arrythmias Post-surgical scars or pressure/volume loads NB Type Definition Cause Central Arterial saturation <85% or >5g reduced Hb Right-to-left shunting / Reduced pulmonary flow Peripheral Bluish discoloration of extremities Vasoconstriction / Polycythemia / Poor cardiac output Differential Lower limbs only PDA with reversed shunt Cyanosis types: 6-When to Suspect CHD ?! 1.Age < 5 years 2.Hypertension in a child 3.Positive prenatal history 4.Associated congenital anomalies 5.Cyanosis since birth 6.Negative history of rheumatic fever 7.Thrill over the base (AS/PS) or left parasternal (VSD). Explanations 7-Clinical presentation Other Clinical Manifestations: Signs Note that: Most important complication is Infective endocarditis

Chronic stable angina = initial presentation in ~50% of CAD patients. ACS (Acute Coronary Syndrome) = acute imbalance of myocardial O2 supply/demand. 4 2. Risk Factors Type Definition Key Marker STEMI MI with ST elevation or new LBBB Enzyme rise NSTEMI MI without ST elevation Enzyme rise Unstable Angina New/worsening ischemia symptoms, ST depression/T inversion Normal biomarkers Age Gender (male) Family history Hypertension Smoking Type 2 DM Obesity Dyslipidemia (↑LDL-C) Lifestyle Non- Modifiable ACS subtypes: CAD is the Most common cause of death in developed world.NBNB Coronary artery diseaseCoronary artery disease CADCAD Coronary artery disease CAD 1.Definition Persons with atherosclerosis may be asymptomatic, present with angina, or develop ACS. Modifiable

5 4. Management of Stable Angina: Type Key Marker Typical angina All 3 characteristics present Atypical angina 2 of 3 characteristics Non-anginal pain 1 or none Character: heaviness / compressing / burning / squeezing / crushing / gripping Location: retrosternal or left-sided → radiates to shoulder, arm, jaw, epigastrium Trigger: exertion or emotion Relief: rest or nitrates Classification: Never: Localized Stitching or throbbing < 30 seconds Patient education Lifestyle modification Risk factor modification Prevention of cardiovascular events → Antiplatelets, lipid-lowering agents, ACE inhibitors (Clopidogrel if aspirin intolerance) Antianginal medications → Beta blockers, CCBs, Nitrates Myocardial Revascularization → PCI or CABGNB 3- Anginal Pain — Clinical Features

3- Clinical Considerations: Visit duration: Brief (<30 min), avoid early morning/late afternoon. Position: Semi-supine; rise slowly (avoid orthostatic hypotension). Anesthesia: No intravascular injection;max 2carpules with VC Monitoring: BP + pulse oximetry as needed 4- If surgery needed: Anticoagulated patient: determine INR on the day of treatmen Antiplatelet patient: local hemostatic measures. 6 5. Dental Management in IHD Antiplatelet/Anticoagulant Management: 1- General Timing Rules: Safety period: 6 months before any oral surgical procedure post-MI. Within 6 months + urgent treatment needed (extraction/RCT) → hospital setting only 2- Medications: Nitrates Patient brings them; preventive dose before LA; use if chest pain develops Very anxious patients Premedication: Diazepam 5-10mg night before + 1-2h before Warfarin Check INR day of treatment; keep <3.5; local hemostasis if surgery Aspirin/Clopidogrel - no stent, low risk Stop 7-10 days before surgery Aspirin/Clopidogrel - WITH stent Do NOT stop: ≥1 month (bare metal) / ≥12 months (drug-eluting) Drug interactions NSAIDs, Penicillin, Tetracycline, Metronidazole, and anticoagulantsNB

7 Avoid diathermy — if must use → bipolar preferred ICD programmed OFF before surgery → ON after Patient brings manufacturer ID card No electrical cords over patient's chest Unshielded pacemakers → cover with lead apron Know malfunction symptoms: dizziness / breathing difficulty / chest pain / pulse change → refer to cardiologist Monitor BP and pain throughout the intervention. Anticoagulants: stop heparin 6-12 hours before → resume 6 hours after bleeding stops. Anesthesia: minimal amount + epinephrine 1:100,000 or 1:200,000. If stroke symptoms appear → oxygen immediately + refer to hospital. 7.Stroke Patient — Dental Management: 6.Cardiac Pacemakers — Dental Management: 5- Local Hemostatic Measures: Bone wax, sutures, gelatin, oxidized cellulose, collagen, platelet-rich plasma, thrombin, fibrin sealants, electric/laser scalpel, tranexamic acid Anesthesia Caution: ⚠ Max 3 ml of 2% Lignocaine + 1:80,000 adrenaline

Primary (Essential) No identifiable cause Most common type Related to cardiovascular risk factors Secondary Renal: Renovascular, Glomerulonephritis, Chronic nephritis Endocrine: Hyperaldosteronism, Pheochromocytoma, Hypo/Hyperthyroidism, Cushing Vascular: Coarctation of aorta Pregnancy Drugs: Contraceptive pills, Corticosteroids, Sympathomimetics, NSAIDs Diet: Licorice, Tyramine-rich food, Salty food Arterial hypertension in adults = persistent elevation of: Diastolic BP > 90 mmHg OR Systolic BP > 140 mmHg On at least two subsequent visits 2. Classification of BP Levels: Category Systolic Diastolic Optimal <120 and <80 Normal 120-129 and/or 80-84 High normal 130-139 and/or 85-89 Grade 1 HTN 140-159 and/or 90-99 Grade 2 HTN 160-179 and/or 100-109 Grade 3 HTN ≥180 and/or ≥110 Isolated systolic HTN ≥140 and <90 3. Etiology:NBNB 8 HypertensionHypertensionHypertension 1. Definition:

Usually asymptomatic,or presents with complications: Heart failure (Dyspnea) Stroke (weakness of one side) Encephalopathy (loss of consciousness) Angina (chest pain). High normal / Prehypertension Systolic 120–139 / Diastolic 80–89 Isolated systolic HTN Systolic > 140, Diastolic normal — common in elderly due to ↑ arterial stiffness Isolated diastolic HTN Rare White coat HTN BP > 140/90 in office only, ambulatory reading < 135/85 Masked HTN Normal in office, elevated elsewhere — linked to alcohol/smoking Pseudohypertension Stiff calcified vessels → falsely high reading — seen in elderly + long-standing DM 6. Clinical Picture 9 5. Causes of Systolic HTN: 8. Major Risk Factors:7. Target Organ Damage: Smoking Dyslipidemia Diabetes Mellitus Age > 60 Male / Postmenopausal female Family history of CVD (Men <55 / Women <65) 4. Subtypes of Primary HTN: Atherosclerosis → ↓ arterial compliance Thyrotoxicosis Complete heart block → ↓ HR → ↑ stroke volume → ↑ systolic BP Aortic incompetence Heart → LVH / Angina / MI / Heart failure Brain → Stroke / TIA Kidney → Nephropathy Peripheral arteries → Peripheral arterial disease Eyes → Retinopathy Ν.Β.: Systolic blood pressure depends on COP (stroke volume x heart rate). Diastolic component depends on P.R and blood viscosity.

Smoking & Alcohol Stop Diet ↓ Salt / ↑ Potassium / ↑ Calcium / ↑ Fresh vegetables & fruits / Low-fat dairy Weight Reduction Exercise walking 30–45 min most days + relaxation exercise 10 9. Management....Lifestyle Modification 10. Management of Rapid Severe HTN 11. Dental Management in hypertension⭐ General Considerations: Take medical history + vital signs (BP + HR) at every dental visit Acute high BP may be physiologic response to pain/anxiety Hypertensive crisis symptoms: headache / vision changes / SOB / chest pain → immediate referral Watch for orthostatic hypotension — rise slowly after treatment BP (mmHg) Elective Care Emergency Care < 160/100 No modification No modification > 160/100 Repeat measurement → if confirmed, no elective + refer to physician Repeat → if confirmed systolic 160–180 + dental pain contributing → treat with BP monitoring every 10–15 min > 180/110 Defer elective treatment Consult physician before proceedingNB

11 Treatment Considerations Well-controlled HTN = no risk in dental practice Patient takes medication as usual on day of treatment Brief morning appointments preferred Anxious patients → Diazepam 5–10mg night before + 1–2h before appointment Emergency only → analgesics + antibiotics; NSAIDs max 5 days only (cause salt & water retention → ↑ BP) Vasoconstrictor limit → max 0.04 mg adrenaline BP monitoring during complex procedures (implants, periodontal surgery, long sessions) Hypertensive crisis → postpone treatment + send to hospital immediately Side Effects of Antihypertensive Drugs: Most drugs cause dry mouth & taste changes Calcium channel blockers → Gingival enlargement ⭐ ACE inhibitors → Dry cough & Angioedema Diuretics → Orthostatic hypotension Drug Interactions: NSAIDs + most antihypertensives →↓ antihypertensive effect ⚠ NSAIDs → cause salt & water retention →↑BP avoid long-term use (> 5 days) CCBs + Benzodiazepines → ↑ sedation CCBs + Erythromycin/Clarithromycin → ↑ hypotension (avoid) Beta-blockers + Local anesthetics → ↓ amide metabolism Losartan + Fluconazole/Rifampin → altered drug levels via CYP450NB

Acute Rhumatic FeverAcute Rhumatic Fever ARFARF Acute Rhumatic Fever ARF 12 Polyarthritis(75%) Carditis (40-50%) Chorea Subcutaneous nodules Erythema marginatum Cause = GAS pharyngeal infection Skin infections (impetigo) → NOT proven to cause ARF Arthralgia Fever ≥ 102°F Elevated acute-phase reactants (↑ CRP, ↑ ESR, leukocytosis) Prolonged PR interval on ECG 4.Pathophysiology 1.Definition: ARF = autoimmune response to Group A Beta-hemolytic Streptococcus (GAS) infection, occurring 2-3 weeks after pharyngeal infection. 💡 "Licks the joints & bites the heart" 2. Predisposing Factors Family history of rheumatic fever Low socioeconomic status (poverty, poor hygiene) Age 5–15 years 3. Etiology GAS pharyngeal infection → autoimmune response via molecular mimicry Similarities between streptococcal M protein and myosin → rheumatic carditis NOT due to direct infection or toxin production 5.Clinical Manifestations MinorMajor

1. Polyarthritis (75%) Large joints (knee, ankle, wrist, elbow). Migratory & asymmetrical. Red, hot, tender, swollen, leaves no damage. Responds to salicylates & NSAIDs within 3 days 2. Carditis (40-50%) Pan carditis (endo + myo + pericarditis). New/changed murmur, Cardiac enlargement, Heart failure, Arrhythmia, Subclinical carditis detected by echo. 3. Chorea — Sydenham's Jerky uncoordinated movements (hands, feet, tongue, face). Disappears during sleep. Strong association with carditis. Resolves within 6 months. Can be stand-alone criterion 4. Subcutaneous nodules Rare (<2%) but highly specific . Round, firm, painless. Extensor surfaces. Strongly associated with carditis. 5. Erythema marginatum Pink circular rash on trunk and proximal extremities (never face) Not itchy / Transient (< 1 day) . Not affected by anti-inflammatory drugs 13 7. Diagnosis — Jones vs WHO Criteria Jones Criteria (1992) WHO Criteria (2001) First episode 2 major OR 1 major + 2 minor + GAS evidence Same as Jones Chorea / Indolent carditis No GAS evidence needed No GAS evidence needed Recurrent RHD 1 major OR several minor + GAS evidence no RHD: Same as Jones WITH RHD:2 minor only + GAS evidence 6. Clinical Picture — Major Manifestations

General: Absolute bed rest. Eradication of GAS infection: Oral Penicillin V / Amoxicillin / Erythromycin × 10 days. OR single IM injection of Benzathine Penicillin. Then → long-term antibiotic prophylaxis. Arthritis: Salicylates 100 mg/kg/day × 3–5 days → then 75 mg/kg/day × 4–8 weeks. Carditis: Heart failure → conventional measures Severe carditis → Prednisone 2 mg/kg/day × 2–6 weeks (tapering. Chorea: Self-limited (resolves within 6 months) Mild → rest + calm environment Severe → Valproic acid or Carbamazepine 14 8. Investigation: Anti-streptolysin O (ASO titre) — repeat in 10–14 days if not confirmatory Throat swab (before antibiotics) ESR / CRP / CBC ECG / Chest X-ray Echocardiography 9. Treatment: Evidence of GAS infection: Hallmarks of GAS sore throat: strawbarry tongue, petechia on palat, tender lymph nodes. Positive throat culture / rapid antigen test ↑ ASO titre / anti-DNase B / antihyaluronidase Recent scarlet fever

15 Penicillin V Children ≤27kg: 250mg 2-3x daily / Adults: 500mg 2-3x daily 10 days Amoxicillin 50 mg/kg once daily (max 1g) 10 days Benzathine Penicillin G ≤27kg: 600,000 U / >27kg: 1,200,000 U — single IM dose once Cephalexin/ Cefadroxil Variable 10 days Clindamycin 20 mg/kg/day ÷ 3 doses (max 1.8g) 10 days Azithromycin 12 mg/kg once daily (max 500mg) 5 days Clarithromycin 15 mg/kg/day ÷ twice per day (max 250mg) 10 days 9. Primary Prevention: Treatment of GAS pharyngitis to prevent ARF: If allergic to Penicillin: 10. Secondary Prevention:Penicillin G benzathine1.2 million units IM every 4 weeksPenicillin V potassium250 mg orally / Twice per daySulfadiazine12 mg/kg once daily (max 500mg)Macrolide(if allergic)15 mg/kg/day ÷ twice per day (max 250mg) 11. Duration of Prophylaxis: ARF + carditis + residual heart disease 10 years or until age 40 (whichever longer) ARF + carditis + no residual disease 10 years or until age 21 (whichever longer) ARF without carditis 5 years or until age 21 (whichever longer)

Infective EndocarditisInfective Endocarditis IEIE Infective Endocarditis IE Staphylococcus aureus (most common overall) Skin infection / IV cannula / IV drug users Streptococcus viridans Mouth — dental disease or procedure ⭐ Other streptococci (mutans, oralis, milleri) Bowel or urinary tract Gram-positive organisms > 80% of all cases Candida Most common fungal cause 16 2. Pathophysiology Native valve endocarditis Prosthetic valve endocarditis (early <1 year / late >1 year) IE in IV drug users Nosocomial IE Primary event = bacterial adherence to damaged endocardium. Excoriation of endothelium → coagulation → vegetation 1.Definition: Infection of the endocardial surface of the heart, most commonly involving mitral and aortic valves. The characteristic lesion = vegetation (platelets + fibrin + microorganisms + inflammatory cells) Categories 3. Etiology 4. Investigation Blood cultures. Transthoracic echocardiography (TTE) — sensitivity 60–70% Transesophageal echocardiography (TOE) — ~ 75–95% ⭐ ESR / CRP / CBC / microscopic haematuria Cerebral angiography / MRI — for mycotic aneurysms PCR

Major Criteria: Positive blood cultures (typical organisms from 2 separate cultures) Imaging positive (echo showing vegetation/abscess/perforation) Minor Criteria: Predisposing heart condition or IV drug use Fever > 38°C Vascular phenomena (emboli, Janeway's lesions) Immunological phenomena (Osler's nodes, Roth's spots, glomerulonephritis) Microbiological evidence 17 5.Clinical Features Fever LOW grade, Most common sign. Heart murmurs Found in up to 50% / worsening of old murmur in 20% Myo-skeletal symptoms Arthralgia, myalgia, back pain Splinter haemorrhages Linear petechiae in mid-nailbed Osler's nodes Tender raised nodules on finger/toe pads Janeway's lesions Non-tender haemorrhages on palms & soles Conjunctival haemorrhage - Roth's spots Haemorrhagic spots with central white area in retina Systemic embolism Brain/spleen/kidneys (left-sided IE) / Lungs (right-sided IE) Heart failure From valve destruction or chordal rupture 6- Diagnosis — Modified Duke Criteria

Prophylaxis NOT required for High-Risk Conditions Native valve disease (AS / MS / MVP). All other forms of CHD. Routine anaesthetic injections through non-infected tissue. Dental radiographs. Placement/adjustment of orthodontic/prosthodontic appliances. Shedding of deciduous teeth Bleeding from trauma to lips or oral mucosa. 18 Definite IE 2 major OR 1 major + 3 minor OR 5 minor OR pathological criteria Possible IE 1 major + 1 minor OR 3 minor Rejected IE Firm alternate diagnosis / symptoms resolve ≤4 days of antibiotics Ampicillin + Cloxacillin or Oxacillin + Gentamicin 12g/day IV ÷ 4-6 doses 12g/day IV ÷ 4-6 doses 3mg/kg/day IV or IM If penicillin-allergic: Vancomycin + Gentamicin 30-60mg/kg/day IV ÷ 2-3 doses 3mg/kg/day IV or IM 7- Empirical Antibiotic Treatment for IE Acquired native valves OR late prosthetic valves (≥12 months post-surgery): Early prosthetic valve (<12 months) OR nosocomial IE: Vancomycin + Gentamicin + Rifampin 30mg/kg/day IV ÷ 2 doses 3mg/kg/day 900-1200mg IV or oral ÷ 2-3 doses 8. Dental Management — Prophylaxis Prosthetic cardiac valve. Previous infective endocarditis. Unrepaired cyanotic CHD (including palliative shunts). Repaired CHD with prosthetic material within first 6 months. Repaired CHD with residual defects at prosthetic site. Cardiac transplant with valvulopathy.

Prevention Measures (High & Intermediate Risk Patients): Strict dental & cutaneous hygiene Dental follow-up twice yearly (high-risk) / yearly (others) No self-medication with antibiotics Discourage piercing and tattooing Disinfection of wounds Curative antibiotics for any bacterial infection focus Situation Agent Adults Children Oral Amoxicillin 2g 50 mg/kg Unable oral Ampicillin OR Cefazolin/Ceftriaxone 2g / 1g IM/IV 50 mg/kg Allergic — Oral Clindamycin OR Azithromycin 600mg / 500mg 20 / 15 mg/kg Allergic — Unable oral Cefazolin/Ceftriaxone OR Clindamycin 1g / 600mg IM/IV 50 / 20 mg/kg 19 Prophylaxis required ONLY before: Manipulation of gingival tissue Periapical region of teeth Perforation of oral mucosa Antibiotic Regimen: (Single dose 30–60 minutes before procedure) Prevention Measures (High & Intermediate Risk Patients):

Cardic Syncope Obstruction to blood flow → AS or HOCM (Exertional syncope). Arrhythmias → Adams-Stokes, severe. bradycardia/tachycardia (Syncope at rest) ↓ Venous return → hemorrhage / burns / peripheral vasodilatation. Ball & valve embolus / Left atrial myxoma (Positional syncope). Vasomotor Syncope Vasovagal attack → excessive vagal stimulation → ↓ HR + ↓ BP → pale + sweating. Carotid sinus syndrome → hypersensitive carotid sinus → vagal stimulation. orthostatic Syncope Autonomic neoropathy ex.diabetic or uremic. Huge Varicose Veins. HypoVelemin ex. Haemorrhage or dehydration. Muscles of lower limb weakness. Cerebral Syncope Cerebral embolism or Hyperventilation —> cerebral vasoconstriction. Hypoxia Syncope Marked hypoxia e.g. Fallot's tetralogy. other Cough syncope → ↑ intrathoracic pressure → ↓ venous return Micturition syncope → sudden relief of bladder pressure → reflex vasodilation. Autonomic epilepsy.20 2. Causes 1.Definition: Transient loss of consciousness due to transient global cerebral hypoperfusion, characterized by: Rapid onset, Short duration, spontaneous complete recovery. SSyncopeyncopeSyncope

Pregnancy / Pills Rheumatic activity Infective endocarditis Negative inotropic drugs Discontinuation of digitalis Arrhythmia Anaemia Thyrotoxicosis Infection IV fluids Heart FailureHeart Failure HFHF Heart Failure HF 21 Ejection fraction (by echo). Heart failure with reduced EF < 40-5 —> Systolic Hf. Heart failure with preserved EF > 40-50 —> diastolic Hf. Anatomical (clinical) left Hf in palmonary vein with fluid retention & pulmamry edema. Right HF in systemie vein with fluid retention & periphreal edem. congestive Hf start in left then refers to right. output low cardic output HF. High Cardic output HF: Due to anaemia / thyrotoxicosis / sepsis / AV shunts. onset & duration chronic HF —> slow. acute Hf —> fast. 2. Classification 1.Definition: Complex clinical syndrome resulting from any structural or functional impairment of ventricular filling or ejection of blood → heart fails to pump sufficient cardiac output to meet body's metabolic needs. Hypertension Cardiomyopathies Infectious diseases Alcohol 3. Etiology Coronary artery disease Valvular heart disease Congenital heart disease Tobacco & cocaine (↑ CAD risk) 4.Precipitating Factors

Failure of the heart as a pump → inadequate cardiac output → evidence of reduced peripheral perfusion: Clinical signs: Cool & clammy skin Weak distal pulses Altered mental status Urine output < 30 mL/hour Hemodynamic criteria: Systolic BP < 90 mmHg for ≥ 30 minutes PCWP > 15 mmHg Other causes: Mechanical complications of MI → acute mitral regurgitation / VSD / free wall rupture Right ventricular MI End-stage cardiomyopathies Acute myocarditis Severe arrhythmias Post-traumatic 22 2. Common causes: Most common cause = Acute MI (pump failure). 1.Definition: CCardiogenic shockardiogenic shockCardiogenic shock

An ulcer in the duodenum, stomach, lower esophagus, or jejunum (after gastrojejunostomy) exposed to acid-peptic juices, with a defect/erosion extending through the muscularis mucosa into the submucosa or deeper. 23 2. Etiology: 1.Definition: Peptic ulcerPeptic ulcerPeptic ulcer H. pylori spiral-shaped, gram-negative, urease-producing organism; lives under the mucus layer near gastric epithelial cells; transmitted faeco-oral or oral-oral (saliva) NSAIDs inhibit COX-1 → ↓ prostaglandins → ↓ mucosal barrier (↓mucus, ↓bicarbonate, ↓blood flow) → erosion/ulceration. COX-2 inhibitors spare the GI mucosa Smoking ↓ healing, ↑ recurrence Other factors reflux (esophageal ulcers), gastrinoma (Zollinger-Ellison), more common in men, familial tendency (especially DU), more common with blood group O 3- Symptoms: Epigastric pain: DU: worse when hungry & at night; relieved by food/antacids/vomiting GU: occurs 0.5–1 hr after meals; relieved by fasting/antacids/vomiting Nausea. Vomiting. GI bleeding. Appetite change. Heartburn. Episodic pain. 4- D.D: Pancreatitis Cholecystitis GERD / gastric cancer Inferior wall MI/ischemia 5. Complications: Hemorrhage → hematemesis, melena, anemia Fibrosis/obstruction Perforation (more common in DU) Penetration

Lifestyle avoid NSAIDs (or use COX-2 selective), stop smoking Medical Antacids H2 blockers (4–6 wks): Ranitidine,Famotidine Proton pump inhibitors: Omeprazole, Pantoprazole, Lansoprazole. H. pylori Eradication: First-line: 4 PPI + Clarithromycin + (Metronidazole or Tinidazole) + Amoxicillin. Quadruple therapy: 4 PPI bd + Bismuth (subsalicylate/subcitrate) + Metronidazole + Tetracycline. 7. Dental Care in Peptic Ulcer: Check platelet count before surgical procedures. Avoid aspirin-containing analgesics; selective analgesic use preferred. Minimize stress — shorter appointments Avoid steroids (worsen acid production). Avoid tetracycline/erythromycin in patients on aluminium/calcium/magnesium antacids. Sialogogues may be needed for anticholinergic-associated xerostomia. Bismuth subsalicylate (used for H. pylori) can harmlessly turn the tongue black. Long-term NSAID use for dental pain can itself cause ulcers — heals once stopped. 24 6. Treatment: