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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:
TABLE OFSyncope HF CONTENTS 01 02 03 04 05 CHD CAD HTN ARF IE 06 07 08 peptic ulcer1
1- Give short account on classification of CHD? Congenital Heart Disease (CHD) is classified into two main categories: Cyanotic: * Fallot's Tetralogy (most common). * Fallot's Trilogy. * Eisenmenger's Syndrome. Acyanotic: * Pulmonary Stenosis. * Aortic Stenosis. * VSD (Ventricular Septal Defect), ASD (Atrial Septal Defect), and PDA (Patent Ductus Arteriosus). *Coarctation of the Aorta. 2- Enumerate other clinical manifestations of (CHD)? Digital clubbing Renal dysfunction. Gallstones. Hypertrophic osteoarthropathy. Cerebrovascular events, like brain abscesses. Arrythmias. ﻛﺪا اﻟﻨﺒﻲ ع ﺻﻞ ﻗﻠﺒﻚ ف :)ﺑﻀﻤﻴﺮ واﺣﻔﻆ CHDرﻳﺘﻦ اﺳﺌﻠﺔ ﻓﻴﻪ ﻣﺠﺎش ﻟﻼﺣﺘﻴﺎط ﺑﺲ ﻛﺪا ﻗﺒﻞ 2
1- Dental management in patients with CAD (IHD): ﺟﺪا ﻣﻬﻢ 1. Timing & Scheduling Post-MI Safety: Wait 6 months for elective oral surgery; urgent care within this period requires a hospital setting. Appointments: Keep visits brief (<30 min) and avoid early morning or late afternoon slots. 2. Clinical Procedures Positioning: Use a semi-supine position and have the patient rise slowly to prevent orthostatic hypotension. Monitoring: Track blood pressure and pulse oximetry during the intervention. Anesthesia: Use a maximum of 2 carpules with a vasoconstrictor and ensure no intravascular injection. 3. Medication Management : ( ﺟﺪا ﻋﻠﻴﻪ ﺑﺘﺮﻛﺰ اﻟﺪﻛﺘﻮر ﻳﺘﻜﺘﺐ ﺟﺰء أﻫﻢ) Anxiety: Premedicate with Diazepam (5–10 mg) the night before and 1–2 hours before the visit if needed. Antiplatelets: Stop Aspirin/Clopidogrel 7–10 days before surgery for low-risk patients without stents. Stents: Do NOT stop antiplatelets if a bare-metal stent was placed ≥1 month ago or a drug-eluting stent ≥12 months ago. Anticoagulants: Ensure INR is <3.5 on the day of treatment for patients on Warfarin. 4. Emergency Protocol for Chest Pain Immediate Action: Stop treatment, provide 3 L/min Oxygen, and administer 0.4–0.8 mg sublingual nitrite. Follow-up: If pain persists after 5 minutes, give a second dose; if it continues for 15 minutes, transport the patient to a hospital. CAD 3
2- Enumerate risk factors of (CAD)? Non-modifiable Risk Factors: Age Gender (specifically male ) Family history Modifiable Risk Factors: Hypertension Smoking Type 2 Diabetes Mellitus (DM) Obesity Dyslipidemia (specifically increased LDL-C) Lifestyle 3- Dental management in cardiac pacemakers: Preparation & Documentation Identification: Patients must bring their manufacturer ID card. ICD Settings: Program the ICD OFF before surgery and ON immediately afterward. Equipment & Electrical Safety Cords: Do not place electrical cords over the patient's chest. Shielding: Cover unshielded pacemakers with a lead apron. Diathermy: Avoid use if possible; if necessary, bipolar is preferred. Clinical Procedures Anesthesia: Limit to a maximum of 3 ml of 2% Lignocaine with 1:80,000 adrenaline. Hemostasis: Use local measures such as bone wax, sutures, gelatin, collagen, thrombin, or tranexamic acid. Immediately refer to a cardiologist if the patient experiences: Dizziness, Breathing difficulty, Chest pain, or Changes in pulse. 4ﻫﺘﺤﻔﻆ ﻣﺘﻔﻜﺮش ﻣﺶ ازاي دا ﻛﻞ ﺗﺤﻔﻆ ﻻزم ف ﻛﻠﻬﺎ اﻻﺳﺌﻠﺔ :/واﺣﺪ ﻳﻮم
4- Dental management for stroke patients : Monitoring: Blood pressure and pain levels must be monitored throughout the entire intervention. Anesthesia: Use a minimal amount of local anesthesia combined with epinephrine at a concentration of 1:100,000 or 1:200,000. Anticoagulant Management: If the patient is on heparin, it should be stopped 6–12 hours before the procedure and can be resumed 6 hours after bleeding has stopped. Emergency Protocol: If symptoms of a stroke appear during treatment, immediately administer oxygen and refer the patient to a hospital.ﺧﺪ ﻣﻌﺪي واﻧﺖ ﺧﻤﺴﻪ ﺑﺮﻳﻚ ﻓﺎت اﻟﻠﻲ ع راﺟﻊ 5
1- Dental management in hypertensive patients: ﺟﺪااا ﻣﻬﻢ Pre-Treatment Evaluation: Record medical history, BP, and HR at every visit. BP <160/100 mmHg: proceed normally. BP >160/100 mmHg: postpone elective care and refer to physician. Emergency (160-180 mmHg): treat only if pain-related, with BP monitoring every 10-15 min. Signs of hypertensive crisis (headache, visual changes, SOB, chest pain) → immediate emergency referral Appointment Management Prefer short morning appointments. Reduce anxiety; Diazepam may be used if needed. Continue antihypertensive medications on the treatment day. During Treatment Limit adrenaline (vasoconstrictor) to 0.04 mg maximum. Monitor BP during long/complex procedures. Prevent orthostatic hypotension: advise patients to stand slowly. up Medication Considerations Limit NSAIDs to ≤5 days as they may increase BP and reduce antihypertensive effectiveness. 2- Enumerate target organ damage: Heart → Angina / MI / Heart failure Brain → Stroke / TIA Kidney → Nephropathy Peripheral arteries → Peripheral arterial disease Eyes → Retinopathy HTN 6
1- Give short account on clinical manifestations of (ARF) And diagnostic criteria according to Jones: ﻣﻬﻢ Major Manifestations Polyarthritis (75%): Migratory inflammation of large joints (e.g. knees, ankles) that leaves no permanent damage. Carditis (40-50%): Inflammation of all heart layers (pan- carditis), often presenting as a new murmur or heart failure. Sydenham’s Chorea: Jerky, uncoordinated movements of the limbs and face that disappear during sleep. Subcutaneous Nodules (<2%): Small, firm, painless bumps on extensor surfaces. Erythema Marginatum: A transient, pink, circular rash found on the trunk and limbs. Minor Manifestations Arthralgia (joint pain without swelling). Fever (≥ 102°F). Elevated acute-phase Diagnosis (Jones Criteria): A definitive diagnosis in first episode requires: two major manifestations one major + two minor manifestations, + evidence of a preceding Group A Streptococcal (GAS) infection. for recurrence diagnosis: Only one major or several minor manifestations. ARF 7
3- Discuss treatment of ARF: General Care: Absolute bed rest is required. GAS Eradication: A 10-day course of Penicillin V, Amoxicillin, or a single IM injection of Benzathine Penicillin to eliminate the initial infection. Symptom Management: Arthritis: High-dose Salicylates (100 mg/kg/day) for 3–5 days, then tapered. Carditis: Severe cases are treated with Prednisone (2 mg/kg/day); heart failure managed with conventional measures. Chorea: self limited but if sever treated with Valproic acid or Carbamazepine. 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 2- compare between / discuss Jones and WHO diagnostic criteria in ARF: 8
4- Discuss 1ry and 2ry prophylaxis of ARF ﻧﻔﺴﻨﺎ ﻧﺄﻣﻦ ﺑﺮﺿﻮ ﻻزم ﺗﺠﺪد ﺗﻔﻜﺮ اﻟﺪﻛﺘﻮر ﻟﺮﺑﻤﺎ ﺑﺲ ﻛﺪا ﻗﺒﻞ ﻣﺠﺎش: Primary Prevention: The goal is to prevent the initial onset of ARF by treating (GAS) pharyngitis through: Penicillin V: Orally for 10 days. Amoxicillin: Orally for 10 days. Benzathine Penicillin G: A single IM injection. Allergy Alternatives: Cephalexin, Clindamycin, Azithromycin, or Clarithromycin. Secondary Prevention: The goal is to prevent recurrent ARF episodes through long- term antibiotic prophylaxis through: Benzathine Penicillin G (1.2 million units IM every 4 weeks). Oral Alternatives: Penicillin V (250 mg twice daily), Sulfadiazine, or Macrolides if allergic. Duration of Prophylaxis: ARF without carditis: 5 years or until age 21 (whichever is longer). ARF with carditis (no residual disease): 10 years or until age 21 (whichever is longer). ARF with carditis and residual heart disease: 10 years or until age 40 (whichever is longer). 9
1- Diagnostic schemes according to the modified Duke criteria for diagnosis of infective endocarditis and what are the criteria of definite IE. ﺑﺎﻟﻨﺺ واﺗﻜﺮر ﺟﺪا ﻣﻬﻢ Major Manifestations Positive blood cultures (typical organisms from 2 separate cultures). Imaging positive (echocardiogram showing vegetation, abscess, or perforation). Minor Criteria Predisposing heart condition or IV drug use. Fever > 38°C. Vascular phenomena (such as emboli or Janeway's lesions). Immunological phenomena (such as Osler's nodes or Roth's spots). Diagnosis of definite IE: 2 major criteria Or 1 major + 3 minor or 5 minor criteria. IE2- what are the criteria of definite possible, and rejected IE ف ﻣﻨﻬﻢ وﺣﺪه وﻃﻠﺒﺖ ﻏﻴﺮت اﻟﺪﻛﺘﻮر ﻟﻮ ﻋﺸﺎن ﻋﺎرﻓﻴﻨﻬﻢ ﻧﻜﻮن ﻣﻬﻢ ﻓﺎت اﻟﻠﻲ اﻟﺴﺆال Diagnostic Classifications: Definite IE: 2 major or 1 major + 3 minor or 5 minor criteria. Possible IE: 1 major + 1 minor OR 3 minor criteria. Rejected IE: Firm alternate diagnosis, OR symptoms resolving in ≤4 days of starting antibiotics 10
3- Enumerate clinical features of IE: Fever Heart murmurs Myo-skeletal symptoms (including arthralgia, myalgia, and back pain) Splinter hemorrhages Osler's nodes Janeway's lesions Conjunctival hemorrhage Roth's spots Systemic embolism Heart failure 4- Cases for which prophylaxis is not required ﻗﺮﻳﺐ ﻣﻦ ﺟﻪ: Dental Procedures and Events: Routine local anaesthetic injections through non-infected tissue. Dental radiographs (X-rays). Placement or adjustment of orthodontic or prosthodontic appliances. Shedding of deciduous teeth. Cardiac Conditions: Native valve disease (such as Aortic Stenosis [AS], Mitral Stenosis [MS], or Mitral Valve Prolapse [MVP]). All other forms of Congenital Heart Disease (CHD) 11
5- The high-risk cardiac conditions where antibiotic prophylaxis is required before specific dental procedures include: Prosthetic cardiac valve. Previous infective endocarditis. Unrepaired cyanotic congenital heart disease (CHD), including palliative shunts. Repaired CHD with prosthetic material within the first 6 months of the procedure. Repaired CHD with residual defects remaining at the prosthetic site. 6- Antibiotic prophylaxis before dental procedures: Standard Oral Regimen Amoxicillin: 2 g for adults; 50 mg/kg for children. 2. Unable to Take Oral Medications Ampicillin: 2 g IM/IV for adults; 50 mg/kg for children. Cefazolin or Ceftriaxone: 1 g IM/IV for adults; 50 mg/kg for children. 3. Penicillin-Allergic (Oral) Clindamycin: 600 mg for adults; 20 mg/kg for children. Azithromycin: 500 mg for adults; 15 mg/kg for children. 4. Penicillin-Allergic & Unable to Take Oral Medications Cefazolin or Ceftriaxone: 1 g IM/IV for adults; 50 mg/kg for children. Clindamycin: 600 mg IM/IV for adults; 20 mg/kg for children. 12
1- Discuss classifications of Heart failure: 1.By Ejection Fraction (Echo): Systolic HF: Heart failure with reduced EF (< 40-5%). 2- Diastolic HF: Heart failure with preserved EF (> 40-50%). 2.Anatomical / Clinical: Left HF: Involves fluid retention and pulmonary edema in the pulmonary veins. Right HF: Involves fluid retention and peripheral edema in the systemic veins. Congestive HF: Begins in the left side and then refers to the right. 3.By Cardiac Output: Low Cardiac Output HF. High Cardiac Output HF: Caused by anemia, thyrotoxicosis, sepsis, or AV shunts. By Onset & Duration: Chronic HF: Slow onset. Acute HF: Fast onset. 2- Enumerate causes of HF: HF Hypertension Cardiomyopathies Infectious diseases Alcohol Coronary artery disease Valvular heart disease Congenital heart disease Tobacco & cocaine (↑ CAD risk) 3- Enumerate predisposing factors of HF: Arrhythmia Anaemia Thyrotoxicosis Infection IV fluids Pregnancy / Pills Rheumatic activity Infective endocarditis Negative inotropic drugs Discontinuation of digitalis 13
1- Discuss causes of syncope: 1.Cardiac: Exertional (obstruction): AS, HOCM At rest (arrhythmias): Adams-Stokes, brady/tachycardia Decreased venous return: Hemorrhage, burns, peripheral vasodilation Positional: Ball & valve embolus, left atrial myxoma 2.Vasomotor: Vasovagal attack, carotid sinus syndrome 3.Orthostatic: Autonomic neuropathy, huge varicose veins, hypovolemia (hemorrhage/dehydration), leg muscle weakness 4.Cerebral: Cerebral embolism, hyperventilation 5.Hypoxia: Marked hypoxia (e.g., Fallot's tetralogy) 6.Other: Cough, micturition, autonomic epilepsy. Syncope 14
1- Discuss treatment of peptic ulcer: 1.Lifestyle: Stop smoking and avoid traditional NSAIDs (switch to selective COX-2 inhibitors if analgesics are required). 2.Acid Suppression: Antacids. H2 Blockers (4–6 weeks): Ranitidine or Famotidine. Proton Pump Inhibitors (PPIs): Omeprazole, Pantoprazole, or Lansoprazole. 3.H. pylori Eradication: First-line: PPI + Clarithromycin + (Metronidazole or Tinidazole) + Amoxicillin. Quadruple therapy: PPI (twice daily) + Bismuth (subsalicylate/subcitrate) + Metronidazole + Tetracycline. 2- Enumerate Differential diagnosis of peptic ulces: Pancreatitis Cholecystitis GERD / gastric cancer Inferior wall MI/ischemia Peptic ulcer 15
ﻓﻤﻦ أﺧﻄﺄﻧﺎ وإن ﷲ ﻓﻤﻦ أﺻﺒﻨﺎ ان .اﻟﺸﻴﻄﺎن وﻣﻦ اﻧﻔﺴﻨﺎ أن أﺷﻬﺪ وﺑﺤﻤﺪك اﻟﻠﻬﻢ ﺳﺒﺤﺎﻧﻚ وأﺗﻮب أﺳﺘﻐﻔﺮك أﻧﺖ إﻻ إﻟﻪ ﻻ .إﻟﻴﻚ DECODE اﻟﺒﺎﻃﻨﺔ، ﻣﻦ اﻻﻧﺘﻬﺎء ﷲ ﺑﺤﻤﺪ ﺗﻢ .🤍اﻟﻐﻴﺐ ﺑﻈﻬﺮ دﻋﻮة ﻣﻦ ﺗﻨﺴﻮﻧﺎ ﻻ
Part 2 DERMATOLOGY 2
N Topics Study 1st Revision 2nd Revision 1 Skin anatomy 2 Skin lesions 3 Imptigo 4 Herpes virus 5 Scabies 6 Lichen planus TOPICS AND PROGRESS TRACKING PLAN 12
2 Layer Main Content Key Point Epidermis Keratinocytes, Melanocytes, Langerhans cells, Merkel cells 4 layers: Basale → Spinosum → Granulosum → Corneum Dermis Collagen, elastic fibers, blood vessels, glands, hair follicles Papillary (superficial) + Reticular (deep) Hypodermis Adipose tissue (subcutaneous fat) Energy reservoir + thermal insulation Keratinocytes Majority Form barrier, produce keratin Melanocytes ~3% Produce melanin Merkel cells ~4% Immune function (antigen recognition) Merkel cells <1% Tactile mechanoreceptors SSkin anatomykin anatomySkin anatomy 2- Skin layers 1.Definition: Largest body's organ, covers area of 1.5 to 2.0 m, accounts for about 15% of the total body weight. Consist of 3 layers: epidermis, dermis and hypodermis. Most of the skin is 1-2mm thick. Although eyelids (0.5mm) and (6mm) between the shoulder blades, variation is due to the thickness of the dermis. 3- Epidermal layers 4- Skin fuctions Prevent infection→ fungal, bacterial, and viral infections Maintain barinjury → againest infection, dehydration Repair injury → e.g.cancer, leg ulcers Provide circulation → prevent infarction, embolization, vasculitis Provide nutrition → prevent vitamin deficiency Regulate temperature → prevent hypothermia, hyperthermia Attract attention (appearance) → photoaging, vitiligo, alopecia 3
3 Macule Flat color/texture change < 1 cm Patch Same as macule ≥ 1 cm Papule Solid palpable elevation < 0.5 cm Nodule Solid, deeper/bigger > 0.5 cm Plaque Elevated flat-topped ≥ 2 cm Vesicle Fluid-filled, < 0.5 cm Bulla Fluid-filled, > 0.5 cm Pustule Like vesicle but pus-filled Skin LesionsSkin LesionsSkin Lesions A. Solid: B. Fluid: C. Special : Wheal Evanescent edema → classic of urticaria Comedo Keratin+sebum plug → classic of acne vulgaris Burrow S-shaped tunnel → classic of scabies 1. Primary: 2. Secondary: Scale Dry/greasy keratin masses Crust Dried serum/exudate Erosion Epidermis only → NO scar Ulcer Epidermis + dermis → scar Fissure Linear gap/slit Excoriation Scratch marks Lichenification Thickened skin from repeated rubbing4
Hyperkeratosis ↑ thickness of stratum corneum Spongiosis Intercellular oedema Acanthosis ↑ thickness of stratum spinosum Acantholysis Loss of adhesion between keratinocytes 3- Dermatopathology Terms: 5 4
5 Staphylococci Folliculitis, Furunculosis, Carbuncle, Impetigo (bullous), Ecthyma Streptococci Erysipelas, Cellulitis, Impetigo (non-bullous), Ecthyma ImptigoImptigoImptigo Organism: Type Non-bullous Ecthyma Bullous Impetigo Starts as pink macule →vesicle/pustule → crusted erosions like non- bullous impetigo Small vesicles → flaccid, transparent bullae Heals without scarring leaves a scar without scarring Notes Untreated: resolves in 2–4 weeks Develops into punched-out necrotic ulcer Mixed staphylococcal & streptococcal infection Particularly affects neonates Bacterial Skin Infections Definition & Epidemiology: Contagious, superficial, pyogenic infection of the skin Caused by staphylococci & streptococci Characterised by pustules and honey-coloured crusted erosions ("school sores") More common in children, mostly in summer Occurs on exposed parts: face, hands, neck, extremities Clinical Types: Impetigo of the scalp → complication of pediculosis capitis (acne necrotica miliaris). Acute glomerulonephritis → complication of group A beta- hemolytic streptococcal infection. Complications: Treatment: Control predisposing factors: insect bites, pediculosis, scabies Topical antibiotics: Fusidic acid, mupirocin, bactracin Systemic antibiotics: Flucloxacillin or erythromycin 6
6 Caused by Herpes virus hominis (HSV) HSV-1 → facial infection (skin & mucous membranes) HSV-2 → genital infection Modes: direct contact (saliva/sexual), droplet infection, infected secreti Incubation: 2–12 days Infection for the first time — mainly infants & young children Prodrome: fever & malaise, enlarged/tender lymph nodes, localized burning Vesicles show NO tendency to grouping Spontaneous healing in 1–2 weeks Viral InfectionsViral InfectionsViral Infections Main Viral Skin Diseases: Herpes Simplex & Herpes Zoster Classification of Human Herpes Virus (HHV): Herpes simplex, Herpes zoster, Wart, Molluscum contagiosum. Herpes Simplex: Etiology A) Primary Herpes Simplex: HHV-1 Skin & oral mucosa → Herpes labialis HHV-2 Genital area → Genital herpes HHV-3 Varicella zoster HHV-4 Epstein Barr Virus HHV-5 Cytomegalovirus HHV-6 Exanthem subitum HHV-7 Roseola HHV-8 Kaposi's sarcoma Clinical Varieties of Primary HSV: Herpetic gingivostomatitis Keratoconjunctivitis Herpes genitalis Neonatal herpes simplex Inoculation herpes simplex (herpetic whitlow) Eczema herpeticum (Kaposi's varicelliform eruption) 7
7 Occurs in previously infected persons Vesicles GROUPED on erythematous base (اﻟـ ﻋﻜﺲ Primary!) Regional LN not enlarged (ﺛﺎﻧﻮﻳﺔ ﻋﺪوى ﻟﻮ إﻻ) Prodrome: tingling, itching, burning Primary infection with varicella-zoster virus. Incubation period: 10–21 days (usually 2 weeks). Children under 10 years usually affected. One attack usually confers permanent immunity . Varicella = the primary infection. Herpes Zoster = reactivation of the same latent virus later in life. B) Recurrent Herpes Simplex: Triggering Factors (Recurrent HSV): Treatment of Herpes Simplex: Herpes Zoster: Minor trauma Immunodeficiency Ultraviolet radiation Menstruation Neural or dental surgery Emotional stress Upper respiratory tract infections Topical Systemic Drying lotions (5% aluminum acetate) Severe cases Antibiotics Acyclovir Acyclovir cream Valacyclovir & FamciclovirVaricella (Chicken Pox): Acute skin infection, characterized by an eruption of grouped vesicles following the distribution of a peripheral nerve (usually sensory). Etiology: Reactivation of the latent Varicella-Zoster virus Incubation period: 2–3 weeks Complications: Post-herpetic neuralgia Ocular complications 2ry bacterial infection & gangrene Encephalitis Facial palsy 8
8 Pain is usually the FIRST manifestation (before the rash!) Grouped vesicles on an erythematous base, following one dermatome Almost invariably UNILATERAL Most commonly affected: thoracic (commonest), cervical, trigeminal, lumbosacral dermatomes Recurrence is very rare (one attack gives permanent immunity) Topical treatment: same as herpes simplex Analgesics for pain Antibiotics for secondary bacterial infection Acyclovir & new anti-viral drugs Clinical Picture: Special Forms HSV vs HZTreatment: 1.Ophthalmic Zoster: Involves the ophthalmic division of the trigeminal nerve Ocular involvement: Uveitis & Keratitis 2.Ramsay-Hunt Syndrome: Due to involvement of the geniculate ganglion Vesicles on the external ear, facial palsy, and auditory symptoms (tinni vertigo) Herpes Simplex Herpes Zoster First symptom Burning/tingling then vesicles Pain, often before the rash Distribution Not restricted to a nerve Along one dermatome, unilateral Grouping Primary: no grouping / Recurrent: grouped Grouped Recurrence Common Very rare Scarring No Yes 9
9 Close contact with the patient Indirect (clothes/bed of patient) Contact with infected animals Sexual contact Severe itching, especially at NIGHT Burrows (skin-colored/grey curved ridges) = characteristic Papules, vesicles, pustules & scratch marks ScabiesScabiesScabies Definition & Etiology: Parasitic Infestations. Very common infectious disease caused by fertilized females of a mite called Sarcoptes scabiei. Associated with severe itching. Incubation period: 2–3 weeks. Mode of Infection: Clinical Picture: Clinical Varieties: Scabies in infants Scabies in the clean Scabies incognito Nodular scabies Animal scabies Norwegian scabies Scabies in Infants Atypical distribution: head, neck, palm, soles. 2ry bacterial infection is frequent. Frequent lack of burrow. Eczematous lesions are frequent. Nodular Scabies Inflammatory reddish-brown nodules، mostly on scrotum/penis. Post-scabietic nodules contains no mites or ova. Represent hypersensitivity reaction to dead mites Norwegian Scabies Infestation with large number of mites (2 million) usually in mental defect, in sever systemic disease as DM, and leukemia. 10
Secondary bacterial infection Eczematous changes Acarophobia 10 Treatment: 1.Prophylactic: early diagnosis + treatment + disinfection + treatment of other amily members & treatment of infected animals. 1.Topical: Permethrin 2.5–5% Crotamiton 10% Gamma benzene hexachloride 1% Benzyl benzoate 25% 2.Systemic: Ivermectin 250–400 μg/kg Antihistamines (for itching) Antibiotics (for 2ry bacterial infection) Intralesional steroid (post-scabetic nodules)Causes of Post-scabietic Pruritus: Irritation. Post-scabietic nodules/pruritus. Acarophobia. Complications: Diagnosis: Itching at night. Presence of burrows. Distribution of lesions. Contact cases . Demonstration of parasite under microscope. Differential Diagnosis: Papular urticaria, Prurigo, Eczema 11
Ordinary (classic) Standard violaceous polygonal papules Hypertrophic Extremely pruritic, thick plaque — mainly on shins Atrophic Thin, atrophic lesions Linear Lesions arranged in a line Annular Ring-shaped lesions Actinic On sun-exposed skin; violaceous-to-brown pigmented center, well-defined raised pale margin Follicular Keratotic plugs on the scalp → can cause cicatricial (scarring) alopecia 11 Genetic predisposition Immunological abnormalities Lichen PlanusLichen PlanusLichen Planus Definition: Chronic, intensely pruritic disease of the skin and mucous membranes, characterized by violaceous, flat-topped, shiny, polygonal papules. Etiology: Clinical Picture (Classical/Ordinary LP): Infections: Hepatitis C virus Drugs: e.g. antimalarials Violaceous, flat-topped, shiny, polygonal papules Affects flexures Mucous membranes affected in 30–70% of cases Itching is prominent (rubbing more than scratching) Deep post-inflammatory hyperpigmentatio Clinical Patterns of LP: 12
12 White reticular streaks on buccal mucosa White plaque on the tongue Ulcerative/erosive lesions Hyperpigmentation Lichen Planus of Nails Longitudinal ridging, grooving Pterygium formation Twenty-nail dystrophy LP of Mucous Membrane (Most Important): Types of Oral Lichen Planus: Reticular — the most common; interlacing white lines (Wickham's striae) on the cheek Erosive — the most painful type; requires more aggressive treatment Atrophic Plaque-like — can be confused with leukoplakia Papular Bullous Treatment: First-line (localized disease): Topical corticosteroids More extensive/resistant disease: Phototherapy → Oral retinoids → Immunosuppressant therapy (escalating ladder) Mnemonic: Like any chronic skin disease — start with the mildest option and escalate only if the case is resistant or widespread. 13
DERMATOLOGYWRITTEN 01 Skin 02 Imptigo 03 HHV 04 Scabies 05 Lichen planus 1
....ﺳﺮﻳﻊ ﺗﻨﻮﻳﻪ اﻟﻐﺎﻟﺐ ف اﻟﻔﺎﻳﻨﺎل ف اﻟﺮﻳﺘﻦ اﻟﺠﻠﺪﻳﺔ اﺳﺌﻠﺔ ﺑﻴﻜﻮن اﻟﺪﻛﺘﻮر ﻳﻌﻨﻲ ﻣﻔﺘﻮﺣﻪ اﺳﺌﻠﺔ ﺑﺘﻜﻮن اﻟﺘﻮﺑﻴﻚ ﻋﻦ ﺗﻌﺮﻓﻪ اﻟﻠﻲ اﻏﻠﺐ ﻓﻴﻬﺎ ﻣﻨﻚ ﻃﺎﻟﺐ وﺻﺒﺮ ﺣﻔﻆ وﻣﺤﺘﺎﺟﻪ ﻃﻮﻳﻠﺔ اﻻﺟﺎﺑﺎت ﻓﺸﻮﻳﻪ اﻻﺟﺎﺑﺔ وﻧﻘﺴﻢ ﺗﺜﺒﺖ ﻋﺸﺎن ﻛﺘﻴﺮ وﻣﺮاﺟﻌﺔ ﻻﻧﻪ ﻛﺎﻣﻠﺔ اﻟﺪرﺟﺔ ﺗﻀﻤﻦ ﻋﻠﺸﺎن ﻣﻨﻈﻤﺔ ﻟﻨﻘﺎط وﺗﻮﺗﺎل درﺟﺎت 8 و 7 ﻋﻠﻴﻪ ﺑﻴﻜﻮن اﻟﻮاﺣﺪ اﻟﺴﺆال ﺷﻴﺖ رﻳﺘﻦ + اﻟﻤﺎدة ﻓﺎﻳﻨﺎل درﺟﺔ ﻣﻦ 50٪ . اﻟﺸﻔﻮي ﺑﺎول اول وﻧﺤﻔﻆ ﻣﻨﺮاﻛﻤﺶ اﻧﻨﺎ ﺣﺎﺟﺔ اﻫﻢ ف ﻳﺜﺒﺖ ﻋﺸﺎن ﻓﺘﺮات ﻋﻠﻲ وﻧﺮاﺟﻌﻪ ﺗﻮﺑﻴﻚ ﻛﻞ .اﻻﻣﺘﺤﺎن ﻟﻴﻠﺔ وﻣﻨﻨﺴﺎش 2
1.Definition: contagious, superficial, pyogenic infection of the skin caused by staphylococci & streptococci 2.Clinical features: pustules and honey-coloured crusted erosions ("school sores") 3.Epidemiology: more common in children; occurs mostly in summer; affects exposed parts (face, hands, neck, extremities) 4.Clinical types: Non-bullous: pink macule → vesicle/pustule → crusted erosions; resolves in 2–4 weeks without scarring Ecthyma: develops into a punched-out necrotic ulcer; heals with scarring Bullous: small vesicles → flaccid transparent bullae; heals without scarring; mixed staph & strep infection; affects neonates 5.Complications: Impetigo of the scalp → complication of pediculosis capitis Acute glomerulonephritis → complication of group A beta-hemolytic streptococcal infection 6.Treatment: Control predisposing factors (insect bites, pediculosis, scabies) Topical antibiotics: fusidic acid, mupirocin, bactracin Systemic antibiotics: flucloxacillin or erythromycin 1- Enumerate skin functions? Skin 3 Prevent infection→ fungal, bacterial, and viral infections Maintain barinjury → againest infection, dehydration Repair injury → e.g.cancer, leg ulcers Provide circulation → prevent infarction, embolization, vasculitis Provide nutrition → prevent vitamin deficiency Regulate temperature → prevent hypothermia, hyperthermia Attract attention (appearance) → photoaging, vitiligo, alopecia Imptigo 1- Discuss Impetigo?
Non-Bullous Impetigo Bullous Impetigo Causative organism Staphylococci and/or streptococci streptococci only Onset Starts as a pink macule Starts as small vesicles Lesion evolution Macule → vesicle/pustule → crusted erosion Vesicles → flaccid, transparent bullae Characteristic appearance Honey-coloured crusted erosions ("school sores") Flaccid, transparent bullae Population affected More common in children generally Particularly affects neonates Healing Resolves in 2–4 weeks without scarring Heals without scarring 4 2- Compare Between Bullous and Non-Bullous Impetigo
1. Discuss Herpes Simplex: Herpes virus 1.Etiology: Herpes virus hominis (HSV); HSV-1 → facial infection; HSV-2 → genital infection 2.Modes of infection: direct contact (saliva/sexual), droplet, infected secretion 3.Incubation: 2–12 days 4.Primary HSV: First-time infection, mainly infants/young children Prodrome: fever, malaise, tender LN, localized burning No grouping of vesicles; heals spontaneously in 1–2 weeks Varieties: gingivostomatitis, keratoconjunctivitis, genitalis, herpetic whitlow, eczema herpeticum, neonatal HSV 5.Recurrent HSV: Previously infected persons Grouped vesicles on erythematous base → crust LN not enlarged (unless 2ry infection) Prodrome: tingling, itching, burning Triggers: trauma, immunodeficiency, UV, dental surgery, stress, menstruation, URTI 6.Types: herpes facialis, keratoconjunctivitis, genitalis 7.Treatment: Topical: drying lotions, antibiotics (2ry infection), acyclovir cream Systemic (severe only): acyclovir (drug of choice), valacyclovir/famciclovir 5 2. Triggering Factors of Recurrent Herpes Simplex? 1.Minor trauma 2.Immunodeficiency 3.Ultraviolet radiation 4.Neural or dental surgery 5.Emotional stress 6.Menstruation 7.Upper respiratory tract infections
6 3. Compare between primary and recurrent Herpes Simplex: Primary HSV Recurrent HSV Occurs in First-time infection (mainly infants/young children) Previously infected persons Vesicle grouping No tendency to grouping Grouped on erythematous base Regional LN Enlarged & tender Not enlarged (until 2ry infection) Prodrome Fever & malaise + localized burning Tingling, itching & burning only Healing Spontaneous, 1–2 weeks Crust formation Trigger (first exposure) Trauma, UV, dental surgery, stress, menstruation, immunodeficiency
1.Etiology: Varicella-Zoster virus — reactivation of the latent virus 2.Incidence: middle-aged & elderly most often affected; more frequent in immunocompromised persons 3.Incubation period: 2–3 weeks 4.Clinical picture: Pain usually the first manifestation of the disease Grouped vesicles on an erythematous base, distribution of a sensory nerve Vesicles become pustular, crust & heal in 2–4 weeks with scar Regional LN enlarged & tender Almost invariably unilateral, usually affects one dermatome Thoracic (commonest), cervical, trigeminal & lumbosacral dermatomes most commonly affected Recurrence very rare — one attack gives permanent immunity 5.Special forms: Ophthalmic zoster Ramsay-Hunt syndrome 6.Complications: post-herpetic neuralgia, ocular complications, 2ry bacterial infection & gangrene, encephalitis, facial palsy 7.Treatment: Topical: as for herpes simplex Systemic: analgesics for pain, antibiotics for 2ry infection, acyclovir & new antiviral drugs 4. Discuss Herpes Zoster: 7 1.Ophthalmic Zoster (H.Z. Ophthalmicus): H.Z. may affect any division of the trigeminal nerve, but the ophthalmic division is the most frequently involved Ocular involvement is most commonly in the form of uveitis & keratitis 2.Ramsay-Hunt Syndrome: Due to involvement of the geniculate ganglion Constitutes vesicles on the external ear, facial palsy & auditory symptoms as rhinitis, deafness & vertigo 5. Discuss Ophthalmic Zoster and Ramsay-Hunt Syndromer:
6. Virus Causing Herpes Zoster & Common Complications? 1.Causative virus: Varicella-Zoster virus (reactivation of the latent virus) 2.Complications: Post-herpetic neuralgia Ocular complications Secondary bacterial infection & gangrene Encephalitis Facial palsy 8 7. Diagnostic Criteria & Treatment of Chickenpox (Varicella)? 1.Diagnostic criteria (clinical picture): Polymorphic lesions: macules → vesicles → pustules → crusts (all stages present together) Centripetal distribution (mainly trunk, face & oral mucosa) Mild pruritus Low-grade fever, malaise & headache History of contact/incubation period 10–21 days 2.Treatment: Symptomatic Antipruritic lotions & antihistamines for itching Antibiotics for secondary bacterial infection
Herpes Simplex Varicella (Chickenpox) Herpes Zoster (Shingles) Virus HSV-1 / HSV-2 Varicella-Zoster virus (primary infection) Varicella-Zoster virus (reactivation) Occurs in First exposure (primary) or reactivation (recurrent) Children under 10 years, first exposure Middle-aged/elderly, immunocompromised Incubation 2–12 days Burning/tingling then vesicles 2–3 weeks First symptom Burning/tingling then vesicles Fever, malaise, headache (mild) Pain, often before the rash Lesion distribution Not nerve- restricted; primary = no grouping, recurrent = grouped Centripetal (trunk, face, oral mucosa), polymorphic Along one dermatome, unilateral Lymph nodes Enlarged in primary only Not a feature Enlarged & tender Recurrence Common (multiple triggers) Rare — permanent immunity Very rare — permanent immunity Scarring No No Yes 9 8. Compare between Herpes Simplex and Varicella- Zoster: .ﻣﻨﻬﻢ اﺗﻨﻴﻦ او ﺑﺒﻌﺾ اﻟﺘﻼﺗﻪ ﻣﻘﺎرﻧﺔ ﻋﻦ ﻳﺴﺄﻟﻚ ﻣﻤﻜﻦ
1.Definition: very common infectious disease caused by fertilized female mites (Sarcoptes scabiei); associated with severe itching 2.Incubation period: 2–3 weeks 3.Mode of infection: Close contact with patient, Indirect (clothes/bed of patient), Contact with infected animals, Sexual contact, 4.Clinical picture: Severe itching, especially at night Burrows (skin-colored/grey curved ridges) — characteristic Papules, vesicles, pustules & scratch marks 5.Clinical varieties: Scabies in infants Scabies in the clean Scabies incognito Nodular scabies Animal scabies Norwegian scabies 6.Complications: Secondary bacterial infection Eczematous changes Acarophobia 7.Diagnosis: itching at night, burrows, lesion distribution, contact cases in family, parasite demonstration under microscope 8.DD: papular urticaria, prurigo, eczema 9.Treatment: Prophylactic measures Topical: Permethrin, Crotamiton, Gamma benzene hexachloride, Benzyl benzoate Systemic: Ivermectin, antihistamines, antibiotics, intralesional steroid Scabies 10 1. Discuss Scabies:
1.Definition: chronic, intensely pruritic disease of skin & mucous membranes; violaceous, flat-topped, shiny, polygonal papules 2.Etiology: Genetic predisposition Immunological abnormalities Infections: Hepatitis C virus Drugs: e.g. antimalarials 3.Clinical picture (classical LP): Violaceous, flat-topped, shiny, polygonal papules Affects flexures Mucous membranes affected in 30–70% of cases Itching prominent (rubbing more than scratching) Deep post-inflammatory hyperpigmentation 4.Clinical patterns: Ordinary, Hypertrophic (thick plaque, shins), Atrophic, Linear, Annular, Actinic (sun-exposed skin), Follicular (scalp → cicatricial alopecia) Nail involvement: longitudinal ridging/grooving, pterygium formation, twenty-nail dystrophy Mucous membrane involvement: white reticular streaks (buccal mucosa), white plaque (tongue), ulcerative/erosive lesions, hyperpigmentation 5.Oral types: Reticular (most common), Erosive (most painful), Atrophic, Plaque-like, Papular, Bullous 6.Treatment: First-line (localized): topical corticosteroids Extensive/resistant: phototherapy, oral retinoids, immunosuppressant therapy Lichen Planus 11 1. Discuss Lichen Planus:
ﻓﻤﻦ أﺧﻄﺄﻧﺎ وإن ﷲ ﻓﻤﻦ أﺻﺒﻨﺎ ان .اﻟﺸﻴﻄﺎن وﻣﻦ اﻧﻔﺴﻨﺎ أن أﺷﻬﺪ وﺑﺤﻤﺪك اﻟﻠﻬﻢ ﺳﺒﺤﺎﻧﻚ وأﺗﻮب أﺳﺘﻐﻔﺮك أﻧﺖ إﻻ إﻟﻪ ﻻ .إﻟﻴﻚ DECODE اﻟﺠﻠﺪﻳﺔ، ﻣﻦ اﻻﻧﺘﻬﺎء ﷲ ﺑﺤﻤﺪ ﺗﻢ .🤍اﻟﻐﻴﺐ ﺑﻈﻬﺮ دﻋﻮة ﻣﻦ ﺗﻨﺴﻮﻧﺎ ﻻ
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