INDEX 1. Angina Pectoris 2. Myocardial Infarction 3. Congestive Heart Failure 4. Hypertensive 5. Rheumatic Fever 6. Infective Endocarditis 7. Resp - Asthma 8. COPD 9. Endocrine – Diabetes 10. Corticosteroid Theraphy 11. Liver – Hepatitis 12. Chirrosis 13. Anemia Overview &Classification 14 Macro : Vit B12, Folate 15. Micro : IDA 16. Normo : Aplastic 17. Vascular- Hereditary Haemorrhagic Telangiectasia 18. Platelet – Itp 19. Coagulation : Haemophilia A, Haemophilia B, Vwb 20. Haemolytic – Sickling, Thalassemia (211-215) 21. Steroid (149-152) 22. Endocrine- Thyroid

Please note that this is a brief summary of Medical problems in Dentistry lectures discussed. based from the book Crispian Scully, Medical Problems in Dentistry 6th edition. Kindly refer the book for further details.

Episodes of chest pain caused by myocardial ischaemia secondary to CAD Severity and prognosis : degree of coronary artery narrowing Causes : Artherosclerotic plaque > rupture > platelet activation, adhesion and : thrombosis aggregationimpeding coronary artery blood flow : arterial spasm : pain only on exertion and relieved in a few minutes by rest and sublingual GTN : angina at rest or sudden onset with rapid increase in severity : clinical features of angina but normal coronary arteries on angiogram : pain on lying down : caused by coronary artery spasm

Types      Stable angina Unstable angina (acute coronary syndrome) Cardiac syndrome X (microvascular angina) Decubitus angina Vasospastic (prinzmetal) angina

Clinical features    Chest pain described as a pressure sensation. Fullness or squeezing in the mid-portion of thorax Radiation of chest pain into jaw/teeth, shoulder, arm, back Occasionally associated dyspnoea (shortness of breath), epigastric discomfort or sweating

General management  Investigations : resting ECG – ST segment depression with flat/inverted T wave : myocardial perfusion scan (ischaemic myocardium) : coronary angiography (assess coronary blood flow) Identify and correct the risk factor : diabetes, cigarette smoking, hypercholestrol, physical inactivity, obesity Medication : Acute angina -oxygen -GTN (sublingual/ in buccal sulcus) -reducing anxiety -CCB, K-channel activator -long-acting nitrates (isosorbide mononitrate) -beta-adrenergic blocking drugs (atenolol) -Ca antagonist (amlodipine)

 

Frequent angina

Percutaneous transluminal coronary angioplasty (PTCA) : open up coronary blood flow, inserting ballon-tipped catheter

Coronary artery bypass grafts (CABG) : bridge the obstruction in the coronary blood vessels

Dental aspects      Pre-operative GTN Oral sedation (sometimes) Dental care with minimal anxiety, oxygen saturation and blood pressure and pulse monitoring Emergency care : stop tmt, GTN sublingual+oxygen, kept sitting upright Adverse effects : CCB - gingival swelling nicorandil . - lichenoid lesion - ulcer

Complete occlusion of one or more coronary arteries CLINICAL FEATURES 1) Chest pain (pressure sensation, fullness or squeezing in mid portion of thorax) not relieved by rest or with sublingual nitrates 2) Radiates into jaw/teeth, shoulder, arm or back 3) Dyspnea 4) Epigastric discomfort with or without nausea and vomiting 5) Diaphoresis 6) Syncope or near-syncope without other cause 7) Impairment of cognitive function without other cause 8) Sudden attack or due to stress or exercise 9) Dressler syndrome (post-myocardial infarction syndrome and post-cardiotomy pericarditis)

Killip class I II III IV

Defining features

Mortality rate (%) No clinical sign of heart failure 6 Rales or crackles in the lung, an S3 gallop and elevated 17 jugular venous pressure Frank acute pulmonary oedema 38 Cardiogenic shock or hypotension and evidence of 81 peripheral vasoconstriction (oliguria, cyanosis or sweating)

GENERAL MANAGEMENT Diagnosis Severe unremitting chest pain Collapse Changes in heart rate Arrythmias Hypotension Shock Electrocardiogram changes Rise in serum ‘cardiac’ enzymes Fever and leukocytosis

1) 2) 3) 4) 5) 6) 7) 8) 9)

Serum enzyme level changes after myocardial infarction Enzyme Abbreviation Number of days after MI that maximum rise seen Troponin T (troponin 1) TT 0.5-1.0 Creatine kinase MB CK-MB 1.5 Aspartate transaminase AST 2.0 Lactic dehydrogenase LDH 3.0 Myocardial infarction electrocardiogram tracings:-large Q -ST elevation -inverted T Immediate treatment of myocardial infarction:Chew Aspirin (300 mg). Clopidogrel Rest and reassure Opioid analgesia (diamorphine), IV- 2mg/min or 15 mg i.m plus cyclizine 50 mg. Oxygen or Nitrous oxide with at least 28% oxygen (face mask or intranasally) Streptokinase/ tissue plasminogen activator (t-PA), alteplase, reteplase, or tenecteplase Insulin Glyceryl trinitrate Cardiopulmonary resuscitation (tx. of complications)

Non-ST-Segment Elevation MI (NSTEMI) No evidence from ECG or serum enzyme levels of myocardial damage (acute coronary syndromes) Glycoprotein IIb / IIIa inhibitors are given

DENTAL ASPECTS Within 6 months of MI- major surgery can cause re-infarction Simple emergency dental tx. under LA may be given More than 6 months and under 12 months of MI – elective simple dental care can be carried out More than 12 months of MI- elective dental care can be carried out Stop dental procedures if there is chest pain, dyspnoea, HR of 40 beats/min or more, arrhythmias, or BP > 20 mmHg Elective surgery under GA should be postponed for at least 3 months Patients with AICDs – do not need antibiotics to prevent endocarditis Lower dose of vasoconstrictors

AUTOMATIC IMPLANTABLE CARDIAC DEFIBRILLATOR (AICD) INTERFERENCE WITH MEDICAL/DENTAL PROCEDURES Safe procedures Interference can be reduced if safety measures are taken Trancutaneous electrical nerve stimulation (TENS) Ultrasound for dx. or therapeutic purposes (transducer head 25 cm from defibrillator) Interference with AICD is likely MRI External defibrillation Diathermy, electrocautery, lithotripsy, radiation therapy

Dx. RG, CT scans. Dental drills,ultrasonic scalers or endo. instruments, and dental RG. Fluoroscopy



Structural or functional impairment of the pumping action of the heart, leading to blood output insufficient to meet body demands. LEFT-SIDED -Ischaemic heart disease -Aortic valve disease -Mitral valve disease Hypertension RIGHT-SIDED -Chronic obstructive pulmonary disease -Pulmonary embolism BIVENTRICULAR -Ischaemic heart disease -Aortic valve disease -Mitral valve disease -Hypertension -Cardiomyopathies -Hyperthyroidism -Chronic anaemias -Arrhythmias -Rapid and irregular pulse (if atrial fibrillation is present) -extreme cases: patients are cyanotic, polycythaemic, dyspnoeic at rest and oedematous with pulmonary oedema and distension of the neck veins (raised jugular venous pressure). -Arrhythmias and sudden death may result.


-damming of blood back from the left ventricle to the pulmonary circulation with pulmonary hypertension, pulmonary oedema, dyspnoea, respiration less efficient, and cyanosis. -Coughing CLINICAL FEATURES -sputum is frothy and, pink with blood (severe cases) -advanced stage: inadequate cerebral oxygenation leading to symptoms such as loss of concentration, restlessness and irritability or, in older people, disorientation.

-causes congestion of the main venous systems -affects primarily the liver, gastrointestinal tract, kidneys and subcutaneous tissues -peripheral (dependent) oedema, fatigue and hepatomegaly due to passive congestion, causing abdominal discomfort -severe cardiac failure: raised portal venous pressure, ascites

STAGES OF HEART FAILURE (American College of Cardiology/American Heart Association) A High risk of failure in the future but no structural heart disorder B Structural heart disorder but no symptoms C Previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment D Advanced disease requiring hospital-based support, heart transplant or palliative care DIAGNOSIS -clinically -chest radiography (cardiomegaly) - echocardiography - ECG -biochemistry GENERAL MANAGEMENT 1. treating the symptoms and signs -reducing the heart workload and correcting precipitating factors such as hypertension, anaemia, valvular disease and thyrotoxicosis. (rest, stress reduction, control of hypertension, weight loss, stopping smoking, and salt restriction) 2. First-line therapies: (delaying progression of failure, reducing mortality, improve myocardial contractility, tissue and organ perfusion and oxygenation) -Angiotensin-converting enzyme inhibitors -angiotensin II receptor blockers 3. Vasodilators people who fail to respond to ACEi. 4. Diuretics : increase sodium and water excretion. 5. Beta-blockers (patients with systolic heart failure due to left ventricular systolic dysfunction after stabilization with ACEi and diuretics.) 6. Recombinant BNP (nesiritide) -patients with acute heart failure who have dyspnoea at rest. 7. Antagonists of vasopressin receptor (tolvaptan and conivaptan) and aldosterone receptor (spironolactone and eplerenone) 8. Phosphodiesterase inhibitors (enoximone or milrinone) -support cardiac function. 9. Digoxin -atrial fibrillation. 10. Supplemental oxygen 11. Surgery (heart transplantation) -severe cardiac failure. DENTAL MANAGEMENT: 1. Elective dental treatment should be delayed until the condition has been stabilized medically ( poorly controlled or uncontrolled cardiac failure) 2. Emergency dental care should be conservative, principally with analgesics and antibiotics. 3. Appointments should be short and in the late morning (Endogenous adrenaline levels peak during the morning hours and cardiac complications are most likely in the early morning.)

4. The dental chair should be kept in a partially reclining or erect position. (left-sided heart failure may severely worsen dyspnoea if placed supine) 5. Effective analgesia (Pain and anxiety may precipitate arrhythmias, angina or heart failure): Lidocaine or prilocaine can be used but bupivacaine should be avoided as it is cardiotoxic. 6. An aspirating syringe should be used to give the LA. 7. Adrenaline/epinephrinecontaining LA should not be given in large doses to patients taking beta-blockers. (may induce hypertension) 8. Gingival retraction cords containing adrenaline/epinephrine should be avoided. 9. Cardiac monitoring is and supplemental oxygen should be readily available. 10. Conscious sedation can usually safely be used. (GA is contraindicated in cardiac failure until it is under control. Care should be taken after GA since there is a predisposition to venous thrombosis and pulmonary embolism.)

DRUGS COMPLICATING DENTAL TREATMENT DRUGS ACE inhibitors (ACEi) Digitalis COMPLICATIONS Coughing Erythema multiforme, angioedema, burning mouth ECG changes (e.g. ST-segment depression during dental extractions) Vomiting Orthostatic hypotension Can aggravate cardiac failure Increases the risk of renal damage from ACEi May induce digitalis toxicity by impairing its gut flora metabolism May induce digitalis toxicity by impairing its gut flora metabolism Hyponatraemia

Diuretics Itraconazole NSAIDs other than aspirin Erythromycin Tetracycline


  Persistent raise of BP (blood pressure)- factor: Cardiac output & peripheral resistance. Factor involved: - Baroreceptors: alter HR (heart rate) & force of contraction - Renin-Angiotensin system - reduced BP result in increase of vasoconstrictor: Angiotensin II - also release of adrenocotical Aldosterone - result in: increase in Na retention & K secretion. - Endothelin-I - most potent vasoconstrictor - released from vascular endothelium - regulate vascular tone BP - lowest(night) & highest(morning)  increase with anxiety & age  measurement: sphygmomanometer, measured in relaxed & fully at rest  Normal: 120/80 mmHg  Pre-hypertensive: >120/80 – 139/89 mmHg  Hypertensive: 140/90 or more 90% - cause unknown - ‘essential’/’idiopathic’/’primary’ 1-2% - identified cause o - ‘secondary’

 

CLINICAL FEATURES - usually asymptomatic.

GENERAL MANAGEMENT - avoid/ control anxiety/fear - Tx reduce risk of stroke, heart failure & renal failure - Lifestyle risk factors modify HTN: raise BP: obesity, salt intake, alcohol, smoking, physical activity in excess, stress/anxiety Reduce BP: relaxation, high fibre intake, omega 3 fatty acids, fruits&vegetables, vit K ANTIHYPERTENSIVE DRUGS Goal: use the minimum dose of drugs commensurate the with achieving the desired BP (<140/90), with minimal adverse effects. Urgently indicated: >200/110 mmHg - lower level if there are vascular complications, diabetes or end organ damage

Antihypertensive agents Alpha-adrenergic blockers Angiotensin-converting enzyme (ACE) inhibitor Angiotensin II receptor blocker (ARBs) B-blocker Ca-channel blocker Diuretics Symphatolitics Vasodilators DENTAL ASPECTS

Examples Doxazosin, prazosin Captopril, enalapril, ramipril Candesartan, losartan Atenolol, propanolol Amlodipine, nifedipine, verapamil, diltiazem Thiazides, furosemide, spironolactone Clonidine, methyldopa Hydralzine, minoxidil

- pre-operative reassurance & sedatives (e.g:temazepam) is helpful. - late morning Tx (endogenous/epinephrine peak during early morning hours) - short, minimal stressful dental appointments - avoid anxiety & pain - raise the patient slowly from the supine position: avoid postural hypotension & loss of consiousness - use aspirating syringe: avoid LA injected into bloodstream as containing vasoconstrictor) - do not give excessive epinephrine/adrenaline-containing LA (high dose) to pts taking Bblocker (not more than 4 cartridges): may cause HTN & cardiovascular complications. - gingival retraction - continue taking anti-HTN drugs during GA because may cause ‘rebound hypertension’ if GA has stopped. - IV Barbiturates may be dangerous to patients with anti-HTN therapy, however halothane, enfluane & isoflurane may cause hypotension. - GA is C/I by cardiac failure, coronary or cerebral artery insufficiency or renal insufficiency - Sysytemic corticosteroids may raise BP - NSAIDs can reduce efficacy of anti-HTN agents. - No recognized oral manifestation of HTN. Facial palsy- malignant HTN. - Anti-HTN drugs SOMETIMES cause side effects: Xerostomia (E.G: Clonidine) Salivary Gland Swelling Or Pain Lichenoid Reactions Erythema Multiforme Angioedema Gingival Swelling Sore Mouth Parasthesiae

Inflammatory disease developed after infection of Streptococcus pyogenes, such as streptococcal pharyngitis. Antibody cross-reactivity. Inflammation in the heart, joints, skin or central nervous system FEATURES Fever Painful and tender joints — most often the ankles, knees, elbows or wrists; less often the shoulders, hips, hands and feet Pain in one joint that migrates to another joint Red, hot or swollen joints Small, painless nodules beneath the skin Chest pain Palpitations Fatigue Shortness of breath Painless rash with a ragged edge (erythema marginatum) Outbursts of unusual behavior, crying or inappropriate laughing EARLY SYMPTOMS Sore throat without cold symptoms, such as a runny nose Tender, swollen lymph glands (nodes) Rash Difficulty swallowing saliva Thick or bloody discharge from the nose COMPLICATIONS Damage to heart valve Endocarditis Heart failure Arrhythmias Pericarditis Sydenham’s Chorea - rapid, uncoordinated jerking movements affecting the face, hands and feet. TREATMENTS -Anti-inflammatory medications : aspirin or corticosteroids. -Antibiotic (usually penicillin) or a single intramuscular penicillin injection. -Prevention of recurrent attack – Regular administration of antibiotics. - Steroids are reserved for cases where there is evidence of involvement of heart. -Surgery – repair/replace heart valves in patients with severely damaged valves.

DENTAL CONSIDERATIONS -Preventive antibiotics, before any procedure that involves gum bleeding e.g. scaling, extraction, injections. .


GENERAL ASPECT 1. Rare 2. predominantly affecting damaged heart valve 3. natural heart valves sometimes damaged by disease that affected by I.E. Main groups affected by Infective Endocarditis Aetiology Approximate % of all cases of I.E. No obvious cardiac valve disease 40 Chronic rheumatic heart disease 30 Congenital heart disease 10 Prosthetic heart disease 10 I.V. drug abuse 10 Patients at highest risk from I.E 1. Prosthetic valves 2. Previous I.E 3. Complex cyanotic congenital heart disease e.g. tetralogy of Fallot, TGA, Gerbode defect 4. Surgically constructed systemic-pulmonary shunts or conduits 5. Mitral valve prolapsed with regurgitation or thickened leaflets FACTORS DEVELOPMENT OF I.E. 1. Susceptible surface (damaged endocardium) 2. High bacterial loads in the circulation 3. Oral viridans streptococci from plaque enter bloodstream during chewing, oral hygiene, tooth extractions 4. Dental extractions ( 1 in 3000) 5. Intravascular access device ( hickman lines/uldall catherers) 6. Intravenous drug abuse

CLINICAL FEATURES -highly variable -often with an insidious onset -fever -new or changing heart murmur -pallor (anemia) / light pigmentation (café au lait) of skin - joints pain -hepatospenomegaly -increasing disability (changing cardiac murmurs,infection,embolic damage of many organs) -loss of peripheral pulse to sudden death from stroke (release of emboli) -haematuria, cerebrovascular occlusion, petechiae / purpura of skin & mucous membrane, splinter haemorrhage under the fingernails -roth spots -vasculitis, arthritis, retinal and renal damge -osler’s nodes GENERAL MANAGEMENT 1.ECG 2.Echocardiography 3.blood culture – 3 samples of blood should be taken aseptically, at half hourly intervals for +ve culture 4. 30% fatal without tx, pt should be admitted to hospital for IV antibiotic theraphy (benzylpenicillin & gentamicin / vancomycin (staph. Endocarditis) 5. prosthetic valve endocarditis, early removal of the infected valve & insertion of a sterile replacement. (severe cases) DENTAL ASPECTS Intensive preventive oral health care Need for antibiotic prophylaxis for high risk from I.E. were doubted

bronchial hyper-reactivity bronhospasm ( smooth muscle constrict ) mucosal edema hypersecretion mucus

Reversible airway obstruction

TYPES 1.extrinsic : allergen, drug ( NSAID, antibiotic ), food, dust 2.intrinsic : mast cell instability, hyper-responsive *drug trigger asthma : NSAID, B-blocker, ACEI CLINICAL FEATURES: Dyspnea Cough Expiratory Wheeziness+ Labored Expiration

SEVERITY & TYPICAL THERAPHY Mild (duration hours)  beta Agonist moderate ( duration days) beta Agonist + steroid severe ( duration persistent) beta Agonist+steroid+theophyl line

INVESTIGATION Chest Rg, spirometry, skin test, blood exam ( eosinophilia/ IgE)

MEDICAL MANAGEMENT ( WITH POSSIBLE COMPLICATIONS) 1.beta agonist (dry mouth) 2.corticosteroid (adrenal crisis, oral pharyngeal thrush, angina bullosa haemorrhagica) 3.leukotriene receptor antagonist (impaired liver metabolism, bleeding, prolonged INR) 4.omalizumab/ anti IgE 5.antimuscarinic bronchodilator/ ipratropium (dry mouth) 6. Methylxanthine / theophyline (enhanced by epinephrine, erythromycin) 7.mast cell stabilizer 8. 5 lipoxygenase inhibitor

DENTAL MANAGMENT -bring medication -avoid LA solution containing vasoconstrictor (may react with sulfite as preservative) -epinephirine contraindicated with theophylline and beta agonist  arrhythmia -analgesia (nitrous oxide &oxygen) : safe -sedative better avoided, ex: benzodiazepine  resp failure - GA best avoided: complicated by hypoxia and hypercapnia -preferred anaesthetics: halothane/enflurane -avoid drug precipitate asthma attack (aspirin. NSAID, ..) -gastro-oesophageal reflux cause tooth erosion, and periodontal inflammation is common . .

-chronic obstructive pulmonary disease. -irreversible disease -chronic bronchitis + emphysema. CLINICAL FEATURES 7. Breathlessness and wheeze 8. Cough and sputum 9. Low O2 high CO2 Chronic Bronchitis Excess production of mucus, and persistent cough with sputum daily more than 3 month in over more than 2 years. -Blue bloaters- fail maintain by adequate ventilation, hypoxic. Chronic Copious and mucoid Common Raised Low low Emphysema Dilatation of airspaces distal to terminal bronchiole with destruction of alveoli, reducing alveolar surface area for respiratory exchange. -pink puffers- maintain normal blood gasses by hyperventilation. Pink due to vasodilation. Minimal Minimal Uncommon Normal Low low

Clinical appearance

Cough Sputum Infections P CO2 P O2 Forced Expiratory volume

INVESTIGATION -chest radiography, arterial blood gases, spirometry, lung f(x) test. GENERAL MANAGEMENT -lifestyle change and medication -non drug therapy : stop smoking, exercise, loss weight,vaccination -drug therapy : ipratropium (bronchodilator), salbutamol (B2 agonist), corticosteroid, antibiotic. -advanced emphysema: treat with surgery. DENTAL MANAGEMENT Treat in upright position. Appointment in mid morning or early afternoon. May be difficult to use rubber dam LA preferred but AVOID palatal injection and bilateral mandibular. Diazepam and midazolam should not use as they are respirator depressant. Cessation of smoking AT LEAST 1 WEEK preoperatively. Ipratropium can cause dry mouth Pt. low risk: can receive all treatment with minor modification Pt. moderate risk: medical consultation to see level control before dental treatment Pt. high risk: medical consultation essential before any dental treatment.



GENERAL ASPECTS:        Absolute/relative lack of insulin (low ouptut insulin/peripheral resistance Results : hyperglycecmia, glucosuria, polyuria, polydipsia Fat & Protein stores are metabolized weight loss, ketone bodies(typeI) Chronic hyperglycemia causes microvascular complications, artherosclerosis Risk factors: family history, overweight, inactivity, age, race, genetics Type I is more common in Caucasians and Europeans Type II is more common in Africans, Asians, Hispanics

Type I (IDDM/juvenil-onset) – organ-specific autoimmune disease or may have viral aetiology. Latent Autoimmune Diabetes in Adult is a slow presentation of type I DM Type II (NIDDM/maturity-onset) – 80-90% of DM. over age 40, overweight, insulin resistant Gestational Diabetes – insulin-resistant state exposing future risk of type II

CLINICAL FEATURES:        Lethargy – most common symptoms Hyperglycemia, polyuria, polydipsia are prominent Weight loss Ketone bodiesacidosishyperventilationketonuria, acetone breath Immune deficiencies Type I –children and young adults, excessive thirst & urination, weight loss, blurred vision, extreme fatigue. –Insulin is required daily Type II –overweight, symptoms develop gradually (same with type I) & slow healing –managed by diet and oral hypoglycemic drugs

ACUTE COMPLICATIONS OF DM    Can lead to hypoglycemic coma (main) Less common : excess insulin@hypoglycemic drugs, missed meal, unaccustomed exercise, alcohol Treat first : hypoglycemic with glucose. If not, brain damage can result. o Never give insulin (severe brain damage/kill hypoglycemic pt) o If pt is conscious, give solution glucose/gel orally @ 10g sugar o If comatose, give 10-20mL of 20-50% sterile dextrose IV @ glucagon 1mg IM (if vein can’t be found) o On arousal, give glucose orally, in form of longer-acting carbs (breads, biscuits) Hyperglycemic coma-slow onset, deepening drowsiness, dehydration, acidosis, ketosis (type I)  IV insulin & rehydration

CHRONIC COMPLICATIONS OF DM    Smoking increase risk Phagocytic defets leads to immune defect & liability to infections Associations type I DM with autoimmune disorders (Addison’s disease) -occasionally


Renal Ocular Neuropathies


Atherosclerosis leading to IHD, cerebrovascular disease & peripheral gangrene Cardiorespiratory arrest Risk of Myocardial Infarction is tripled Renal damage & failure Retinopathy Cataracts Peripheral polyneuropathies Mononeuropathies Autonomic neuropathy (postural hypotension) Candidosis Staphylococcal infections Systemic mycoses(rarely)

GENERAL MANAGEMENT  Blood Glucose Level Test Fasting Plasma Glucose (after fated 8h) Random Blood Glucose (anytime) Plasma Glucose taken 2h after a person has consumed 75g of glucose in Oral Glucose Tolerance Test (OGTT) Long-term glucose control HbA1c (3months)

Confirm DM >7.0mmol/L ≥11.1mmol/L >11.1mmol/L

Excludes DM <6mmol/L ≤8mmol/L <11.1mmol/L


PRE-DIABETES  Impaired glucose tolerance (IGT) – 7.8-11.0mmol/L  Impaired fasting glucose (IFG) -6.1-6.9 mmol/L  Likely to develop type II DM PREVENTION:  Weight reduction  Diet-eat more starches TREATMENT:    Reduction of hyperglycemia Prevent hypoglycemia Maintain normal BGL   Reduce other CVS risk factor Control is assessed by BGL, HbA1c

Type I tx :  SC insulin administration Origin Analogue Examples Lispro Aspart Glulisine Soluble insulin Actrapid Humulin I Insulatard Glargine Detemir Hypurin bovine lente Hypurin bovine Protamine Zn Effect starts in (min) 15 Effect lasts (h) 4-6

Type Rapid-acting

Short-acting Intermediate Long-acting

human Human isophane Analogue Bovine Insulin Zn suspension Bovine Protamine Zn insulin

30-60 60-120 120

6-8 10-14 24

Type II tx:    Controlled eating, physical activity Hypoglycemic drug might be needed Intensive control of BGL & BP lower the risk of chronic complications

Drug group Biguanides Glitazones (thiazolidinedi ones) Incretins Incretin mimetics Intestinal αglucosidase inhibitors Meglinitides Sulfanylureas

Administration Oral Oral

Oral hypoglycemic drugs Examples Mode of action Metformin Decrease tissue insulin resistance Pioglitazone Overcome insulin resistance Rasiglitazone Saxagliptin Exenatide Liiaglutide Acarbose Miglitol Nateglinide Gliclazide Stimulating insulin secretion Stimulating insulin secretion w/out producing weight gain Delay breakdown of oligosaccharides to glucose Stimulate insulin release Stimulate insulin release

Oral Injected Oral

Oral Oral

EMERGING TREATMENTS   Combine kidney & pancreas transplantationrenal failure in type I (no longer require insulin after 1 year) Islet cell transplantation

DENTAL ASPECTS :            . Predispose to infections, severe periodontal disease, oral candidosis, angular stomatits Insulin-treated : circumoral parasthesia, swelling of salivary glands (neuropathy), dry mouth Administrating oral glucose just before the appointment Check pt’s BGL before surgical procedures, oral glucose is given if it’s too low Single extractions under LA is carried out within 2h of breakfast & morning insulin injection Multiple extractions – in hospital refer table 6.14 -operation on the early morning, BGLK is monitored 2-4h intervals Drugs- sugar-free, avoid steroids (can increase BGL), tetracyclines, ciprofloxacin. Acetaminophen/paracetamol/codeine are analgesics of choice LA & conscious sedatives are safe to be used Supine pt should be slowly raised upright DM pt controlled by diet alone – LA & GA can be given w/out special precautions -routine prophylactic antibiotics only in situation where it would be needed Dm pt controlled by diet & hypoglycemic drugs-safe under LA, GA. .

o Corticosteroid may suppress HPA axis ( hypothalamic-pituitary –adrenal axis) and the adrenals may become unable to produce a steroid response to stress, acute adrenal insufficiency can result, with rapidly developing hypotension, collapse and possibly death.

DOSAGE o Suppression of HPA axis- if exogenous steroid is prolonged and exceed physiological level ( over 7.5 mg/day of prednilosone) o Adrenocorticol function may be suppressed if : -pt is currently on daily systemic corticosteroid at doses above 5 mg prednilose -corticosteroid have been taken regularly during the previous 30 days - corticosteroid have been taken for more than 1 mont during the past year.

MANAGEMENT o Steroid supplement should be given before stressful procedures : dentoalveolar and maxillofacial surgery may result in stress. - The blood pressure maust be carefully watched, and steroid supplementation given immediately if the blood pressure starts to fall. o Minor operations under LA : - Oral steroid in the morning - Oral steroid 2-4 h pre and post-operatively ( 25-50 mg hydrocortisone or 20 mg prednilose or 4mg dexamethasone) - Intra venous 25-50 mg hydrocortisone immediately before operation

o Major operations: - Give at least 25-50 mg hydrocortisone sodium succinate intramuscularly or intravenously and then 6- hoursly for a further 24-72 hours. o Topical corticosteroid - Unlikely to have any systemic effects but predispose to oral candidosis.

MANAGEMENT OF CORTICOSTEROID No contraindication such as hypertension, diabetes or latent tuberculosis The smallest effective steroid dose should be given, best in the morning on alternate days Systemic corticosteroid cause the greatest risk of adrenalcorticol suppression, so topical steroid should be used in preference, provided that the desired therapeutic effect is achievable.



The patient must be given a warning card and told of danger of withdrawal, and side ffects. There should never be abrupt withdrawal of the steroid. The dose should be raised if there is illness, infection, trauma or operation. Weight, chest readiography, bone mineral density, blood pressure and blood glucose baseline measures should be taken and these parameters monitored. Ranitidine and calcitriol or didronel are often given.


HEPATITIS A VIRUS General Aspects Clinical Features Hepatitis A virus Mainly by faecal-oral (contaminated water and food) Can also by sexually, person-person contact & bodu fluids Incubation period : 2-6 weeks Fatigue, nausea, vomitting Abdominal pain, loss of appetite, low-grade fever Jaundice, and itching Diagnosis: Test serum antibodies ---> virus (HAAb) Vaccine: Available (especially for travellers) Combined vaccine ---> [HAV&HBV] also available Unlikely for them seeking treatment during acute phase Appears to be no risk of transmission

General Management Dental Aspects

HEPATITIS B VIRUS General Aspects Clinical Features Hepatitis B virus Cause lifelong infection, liver (cirrhosis, cancer, failure) Mainly by parental, sexually, perinatally Incubation period : 2-6 months Anorexia, malaise,pruritus, and nausea Jaundice (pale stools & dark urine) Muscle pains, arthralgia, rashes, and fever Complications: 1) Carrier state 2) Chronic infection 3) Cirrhosis 4) Liver cancer 5) Polyarteritis nodosa 6) Death Diagnosis: Serum enzyme estimations (AST & ALT) Electron microscopy: 1) Dane particle (intact HBV) 2) Core = Inner [DNA+core antigens (HBcAg)] + outer [surface antigen (HBsAg)] 3) Smaller spherical forms and tubular forms (excess HBsAg)

General Management

HBsAg develops 20-100 days after esposure (detectable in serum for 1-120 days) Serum becomes -ve for HBsAg (6 weeks) Anti-HBc + anti-HBs = recovery & immunity to hepatitis HBeAg = Ongoing viral activity + ability to infect others Anti-HBe = Inactive state of virus + less risk of trans. High carbohydrate diet & avoiding hepatotoxins (acute hepatitis B) Chronic HBV infection, treated w/interferon-alpha 2b If failed, use Lamivudine Minimized by giving HBIG & vaccine within 12h after birth (from HBV mothers) Post-vaccination test for (completed 1-2 mths after 3rd vacc. dose) : 1) Immunocompromised pts 2) One who get the vaccine from the buttock 3) Infants to HBV mothers 4) Health care workers who deals with blood 5) Sex partners dia have chronic HBV infection Pt w/normal platelet counts, PT and INR can undergo intervention Saliva may contain HBV, and may be a source for non-parental transmission HBV can transmitted by human bites Needlestick injuries (main danger)

Dental Aspects

HEPATITIS C VIRUS General Aspects Hepatitis C virus Cause of liver disease Responsible for sporadis viral hepatitis Persons at risk: 1) Received blood from positive donor 2)Injected illegal drugs 3) Received blood transfusion / solid organ transplant before 1992 4) Received a blood product for clotting disorders, long-term renal dialysis 5) Have evidence of liver disease

Clinical Features

Incubation period : 60-150 days Abnormal liver function tests Chronic liver disease, liver cancer Assoc. with: 1) Sicca syndrome 2) Lichen planus 3) Lymphoma 4) Cryoglobulinaemia 15% of HCV pts, co-infected with HGV (w/SEN also common) Diagnosis: Detection of HCV RNA and anti-HCV antibody in the blood Chronic HCV: Treated w/ribavirin + interferon-alpha / pegylated interferon No vaccine against HCV HCV found in saliva, human bite, and needlestick injuries HCV Post-Exposure Management Status of the source, and exposed person should be determined Immune globulin and anti-viral agents are not recommended Health Care Personnel Exposed to HCV Follow up HCV testing should be performed Should not perform exposure-prone procedures May assoc. with: 1) Sicca syndrome 2) n-Hodgkin lymphoma 3) Lichen planus *chronic hepatitis C & sicca syndrome = assoc.w/HLADQB1*02

General Management

Dental Aspects

HEPATITIS D VIRUS General Aspects Clinical Features General Management Hepatitis D virus (delta agent) An incomplete virus carried in HBV, and only replicate w/HBsAg Spread parentally by hypodermic needles Incubation period: Unknown May coincide w/HBV or superinfact pts w/chronic hepatitis B Biphasic pattern w/double rises in liver enzymes & blirubin HDV antigen = recent infection Delta antigen = Chronic hepatitis / recovery

Dental Aspects

Vaccination against HBV, indirectly against HDV Drug treatment w/interferon-alpha is effective Pt w/normal platelet counts, PT and INR can undergo intervention Saliva may contain HBV, and may be a source for non-parental transmission HBV can transmitted by human bites Needlestick injuries (main danger)


Hepatitis E virus Mainly via faecal-oral route Causes a disease = HAV Pregnant women has a high mortality Not known to be trans. during dentistry Hepatitis G virus May co-infect HCV/HBV pts Produces clinical hepatitis Appears to respond to interferon-alpha Not known to be transmitted during dentistry


Hepatitis G virus May co-infect HCV/HBV pts Produces clinical hepatitis Appears to respond to interferon-alpha Not known to be transmitted during dentistry

ALCOHOL HEPATITIS General Aspects Clinical Features

Alcohol hepatitis Blocking the metabolism of protein, fats, and carbohydrates--->fatty change Liver fibrosis Liver cirrhosis N-alcoholic steatohepatitis (NASH), may be caused by obesity/ diabetes/ protein mal./ coronary artery disease/ CCS treatment

DRUG-INDUCED HEPATITIS General Drug-induced hepatitis Aspects Halothane, some NSAIDs, some herbs, nutritional supplements, paracetamol/acetaminophen (overdose) Dental Aspirin ingestion ---> Reye syndrome Aspects (liver damage w/encephalopathy, abnormal fat accumulations, and severe rise in intracranial pressure)

First stage: 1) Persistent vomitting 2) Severe tiredness 3) Belligerence 4) Nausea 5) Energy loss Second stage: 1) Personality changes 2) Bizarre mental 3) Physical behaviour 4) Lethargy 5) Coma and convulsions Antimicrobials: 1) Liver damage 2) Hepatotoxicity Halothane: 1) Hepatitis 2) More common when Anaes. given repeatedly at intervals of <3 months (mid age women & obese) 3) Causes pyrexia, (may appear) malaise, anorexia, and jaundice

AUTOIMMUNE HEPATITIS General Autoimmune hepatitis: Aspects 1) Autoimmune liver disease 2) Autoimmune chronic active hepatitis Assoc. with: 1) Autoantibodies 2) Complement allele C4AQO 3) HLA halotypes B8, B14, DR3, DR4, and Dw3 4) Progress to cirrhosis Multisystem manifestations Arthralgia Acne Amenorrhoea Haemolytic anaemia Nephritis Pulmonary fibrosis Thyroiditis Ulcerative colitis Responsive to immunosuppressants

Clinical Features

General Management

CIRRHOSIS Pathogenesis (due to): 1) Portal hypertension (elevation of sinusoidal portal vein pressure more than 10 mmHg) 2) Liver cell dysfunction (fatigue, fever, jaundice, loss of muscle mass and subcutaneous fat) -biopsy is the gold standard -3 types: 1) Compensated cirrhosis -fatigue(most common sign) -usually asymptomatic -spider nevi, palmar erythema, nail changes (if chronic) 2)decompensated cirrhosis -Jaundice -bleeding esophageal varices -ascites -hepatic encelopathy 3)Hepatocellular carcinoma (HCC) Significance of liver cirrhosis to dentist 1)increased incidence of infection 2)decreased wound healing 3)increase bleeding 4)may precipitate hepatic encelopathy 5)defective teeth and caries *risk to dentist -increased infection of HBV or HCV if the patient have them

DEFINITION  Hb level below normal o Up to puberty : <11.0 g/dl o Adult female : <11.5 g/dl o Adult male :<13.5 g/dl Not a disease in itself,definition of many other disease.

CAUSE   TYPE  Microcytic o Most common o Mostly due to iron deficiency,thallasemia ad chronic disease. o MCV <78 fl Macrocytic o Occur due to ; - Chronic hemolysis - Pregnancy - Malignancy - Drugs (methotrexate,azathioprine,cytosine,hydroxycarbamide) - Liver disease - Myoxoedema - Aplastic anemia o MCV >99 fl Normocytic o Occur due to chronic disease ; - Leukemia - Chronic inflammatory disease - Liver disorder - Renal failure - Infections - Malignancy - Sickle cell disease #1- chronic blood loss,consequent iron deficiency #2 – folate and vitB12 deficiency

CLINICAL FEATURES  Early stage or slow onset : o Symptomless

Late stage (oxygen carrying capacity of blood decrease) : o Cardiac signs & symptoms ; - Tiredness - Dyspnea - Palpitation - Tachycardia - Flow murmurs - Cardiac failure o Pallor of oral mucosa or conjunctiva / palmar creases (*can be misleading) o May worsen symptom of pre existing coronary/peripheral/CVD

GENERAL MANAGEMET   Key - establishment and treatment of underlying cause Investigations o Full Blood Count (FBC) o Blood film o Erythrocyte Sedimentation Rate (ESR) or Plasma Viscosity (PV) o Hg electrophoresis o Haemanitics (serum Vit B12,folate,ferritin) o Endoscopy o Bone marrow biopsy Deficiency state – corrected with FA or Vit B12 supplements Rapid onset – blood transfusion (Hg <7 g/dl) End stage Renal Failure or cytotoxic therapy – administration of erythropoietin

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DENTAL ASPECTS       If possible,should be corrected pre-operatively ( raise Hg level by transfusion) LA – satisfactory for pain control Conscious or deeper sedation – only if supplemental O2 available (*may lead to hypoxia) Nitrus Oxide – contraindicated in Vit B12 deficiency GA – need full oxygenation Emergency o Young and fit patient : whole blood transfusion o Older patient : packed RBC + diuretics Hg estimation – unreliable 12 hours post-transfusion or after acute blood loss Oral lesions o Ulcers o Glossitis o Angular stomatitis

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MACROCYTIC ANAEMIA MCV > 99 fl Pernicious anaemia is one of the megaloblastic anaemia form. *typically affect women in middle age or more and sometime it's seen with other autoimmune disease. ( hypothyroidism) Usually cause by vitamin B12 or folate deficiency *both function in: amino acid synthesize n breakdown, and to synthesize DNA /RNA (for making new cells) Also cause by liver disease, myxoedema or sometimes aplastic anaemia.





14. VITAMIN B12 (cobalamin) DEFICIENCY (Macrocytic anaemia)
source and absorption of vit B12 :

CAUSE OF DEFICIENCY :     defect in intrinsic factor [IF] due to pernicious anaemia or gastrectomy. ileal disease or resection congenital ileal absorption defect a vegan diet or drugs nitrous oxide – interfere with vitB12 metabolism n neurologic function if administration continue for 12 hours or more.

EFFECT OF DEFICIENCY :     accumulation of homocysteine and methylmalonic acid. Gastro intestinal symptom and risk of stomach cancer Defective DNA synthesis Ultimately is Macrocytic (megaloblastic) anaemia – pernicious anaemia - depressed production of all blood cell and many other cell.

CLINICAL FEATURES :  Vit b12 deficiency develop slowly since liver stores last up to 3 years.  usual symptom and sign of anaemia.  Neurological symptoms : - paraesthesiae in extremities (in 10%) - early sign include loss of toe positional sense and diminish perception of vibration of tuning fork. These changes are reversible with treatment.  Neurological damage can precede anaemia/macrocytosis and lead to subacute combined degeneration of spinal cord and ultimately, paraplegia  Premature graying of hair. GENERAL MANAGEMENT :  Diagnosis of pernicious anaemia is by - clinical finding - decrease serum B12 level - autoantibodies against gastric parietal cell and IF  impairment of B12 absorption can be measured by 'schilling test' : Box 8.10 Schilling test for vitB12 deficiency 1. radiolabelled vitB12 given orally (small dose) 2. unlabelled vit B12 given i.m 2h later (large dose) 3. collect urine over 24h ( or whole-body counting) - normal : excrete > 15% of radiolabelled B12 in 24hrs - deficient : excrete <15 % 4. repeat with added Intrinsic factor - pernicious anaemia : B12 excretion increase to normal - ileal disease : B12 excretion remains low  measurement raised serum level of methylmalonic acid and homocysteine appear to be more specific and sensitive for detecting deficiency. Though renal and other disorder may confuse interpretation. Pernicious anaemia is treated for life with i.m hydroxycobalamin 1mg,5 times at 3 days interval to replete liver stores and then at 3 months interval.

DENTAL ASPECT :       LA – satisfactory Conscious sedation – can be given only if Hb level is moderately depressed Supplemental oxygen – can be given Nitrous oxide – contraindicated GA – postponed until low Hb has been remedied. at early vitB12 deficiency with normal Hb level : - anaemia or macrocytosis may be absent - may be associated with neurological disorders. - sore, burning tongue, alternatively red sore patches may form. [range from pin head red spot to circular areas resemble erythroplasia, they'll resolve with treatment of anaemia] candidosis can be aggravated angular stomatitis may be uncommon aphthous stomatitis occasionally the presenting features if ulceration start in middle age or more, should consider pernicious anaemia. .

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14. FOLATE (FOLIC ACID) DEFICIENCY (Macrocytic anaemia)
causes of deficiency :  mostly is due to dietary deficiency.

Sources and absorption :  no body stores

CLINICAL FEATURES :   similar effect as VitB12 deficiency. Folate deficiency in : - Adult ;cause anaemia and predispose to raised homocysteine levels. [IHD] - Pregnancy; predispose to neural tube defect or cleft lip-palate in fetus. Folic acid prophylaxis is recommended.

GENERAL MANAGEMENT :     Red cell folate levels are low – clear evidence of folate deficiency. May remain normal for a time until older erythrocytes are replaced. Serum folate assay are less reliable Serum B12 normal, schilling test show normal. Once cause has been found – treatment with folic acid [5mg daily orally] rapidly restore. Given for at least 4 months.

DENTAL ASPECT :       . LA , conscious sedation and GA apply as for pernicious anaemia. No contraindicated for nitrous oxide. At early deficiency with normal Hb level : - Soreness of tongue without depapillation or color change. Atrophic glossitis – best known effect of severe anaemia. Angular stomatitis – well known sign, but effect minority only. Aphthous stomatitis – sometimes associated . if remedied can bring about a cure.

15. IRON DEFICIENCY ANAEMIA (microcytic anaemia)
1. GENERAL APECTS & EPIDEMIOLOGY -haem( iron salts)from animal: myoglobin &haemoglobin (dietary iron: meat) -non haem from plants : wholegrain, cereal, green vegetables

• In plant foods where it present as non-haem iron, it is less easily absorbed compared to

which in animal tissues. • There are some foods that can inhibit the absorption of iron in human body :-

Fibres Phytates Oxalates Phosphates Tannin

• Some foods absorption of iron in intestinal :-

Foods rich in vitamin C (Citrus fruits,green peppers,etc.)—> mainly non-haem Citric acid Sugars Amino acids Alcohol Meat Poultry Fish

• Storage of iron in our body :-

Bone marrow as hemosiderin Liver Spleen Muscle tissue as myoglobin (oxygen storage)

• Function of iron in our body :- Synthesis of haem, respiratory cytochromes, and myeloperoxidase - Vital roles in various metabolic process • Common causes of IDA in :-

Developed country ( Nutritional deficiency, Chronic blood loss ) Developing country ( Malaria, Chronic blood loss ) Women in child bearing age ( Excessive chronic menstrual or GIT blood loss ) Neonates ( Constant milk diet ) Older children ( High demands )

2. CLINICAL FEATURES •Achlorhydria ( Absence of HCL in gastric secre-tion •Blood loss •Dietary ignorance •Malapsorption •Old age •Poor iron intake •Poverty •Beeturia* •Koilonychia* •Impaired exercise activi-ty* 3. GENERAL MANAGEMENT
• Iron deficiency is the main cause of microcytic anaemia and to detect it, there are several

test can be done :- Falling serum ferritin levels ( most sensitive ) —> C/I : Inflammation - Erythrocyte size ( microcytosis & low MCV ) - Fall in haemoglobin and hypochromic RBCs - Bone marrow iron stores are depleted

• Treatment :- Iron salts 1. Ferrous sulphate 200mg x twice daily 2. Ferrous gluconate 250mg x once daily if ferrous sulphate intolerable - Oral Iron ( 3 months after Hb at normal level ) -

Paraentral ( intramuscular ) – orally avoided due to inflammatory bowel diseases

• Local anesthesia is satisfactory for pain control and conscious sedation also can be given if

there are full oxygenation • Several oral problem related to iron deficiency :- Atropic glossitis - soreness of the tongue with depapillation or colour changes ( -

Paterson-Brown-Kelly syndrome of glossitis + dysphagia + hypochromic ) Candidosis ( Aggravated or Precipitated or Presenting feature ) Angular stomatitis Aphtous-like ulceration Staining of the teeth ( use sodium iron edetate to prevent ) .


  Pancytopenia (with a non-functioning bone marrow) Rare disease Causing – Leukopenia, thrombocytopenia and refractory anaemia

Cause of aplastic anaemia. Genetic Immunological Drug Fanconi anaemia Dyskeratosis congenita Autoimmune Graft-versushost disease NSAIDs Antithyroids Allopurinol Phenylbutazone Chloramphenicol Sulfonamides Gold Penicillamine Anticonvulsants Cytotoxic agent

Chemicals Benzene Toluene Heavy metal Gluesniffing

Viruses Hepatitis


CLINICAL FEATURES -Susceptibility to infection and bleeding -Purpura is often first manifestation GENERAL MANAGEMENT  Removal of the cause  Isolation and antibiotics to control infection  Bone marrow transplantation  Androgenic (anabolic) steroid  Blood transfusion ( may cause iron overload or infection) The prognosis is poor and 50% of patient die within 6 month, usually from haemorrhage or infection. DENTAL ASPECT (TREATMENT MODIFICATION) Anaemia Haemorrhagic tendencies Susceptibility to infection Effect of corticosteroid therapy Hepatitis B and other other viral infection

LA is satisfactory Conscious sedation and GA should be avoided .

- Rare autosomal dominant disorder with bone marrow failure - Absent radii - Predispose to malignant disease included oral cancer Pure red cell aplasia - Rare disease (congenital or acquired) - Associated with a thymoma and chronic mucocutaneous candidosis - Pt need regular blood transfusion (risk from hepatitis and HIV) Anemia caused by bone marrow infiltration Abnormal cell (metastases, leukemias,myeloma or myelofibrosis), causes normocytic anaemia and often leucopenia or thrombocytopenia with leukoerythroblastic peripheral blood. Extramedullary haemopoiesis.


Anaemia associated with systemic disease . Chronic inflammation Neoplasm Leukemia Liver disease Uraemia HIV infection Endocrinopathies .

  Share common bleeding symptoms. Ex: epistaxis, bleeding after surgery/ wound More common causes include: a) 1 tablet of aspirin which impairs platelet function for almost one week b) Warfarin (most common anti-coagulant) : interfere with clotting factor production, via vitamin K blockage & Von Willebrand disease (MOST common inherited bleeding disorder)

CLINICAL FEATURES      Signs of Purpura in the skin Underlying disease : a) anemia b) lymphadenopathy in leukemia NOT associated with abnormal bleeding tendency : Angina Bullosa Haemorrhagica (purpura localized to mouth) Joint deformities from hemarthroses Characteristics of haemophilia

GENERAL MANAGEMENT    MOST IMPORTANT : history of previous haemorrhagic episodes Physical examination : o Deep haemorrhage into muscles, joints or skins – suggests a clotting defect o Bleeding from and into mucosae – suggests purpura Laboratory test include : o Full blood count, film, platelet count o Prothrombin time(PT), and International Normalized Ratio(INR) o Activated Partial Thromboplastin Time (APTT) o Thrombin Time (TT)

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o Serum for blood grouping and cross-matching ASPIRIN should be avoided at least 7 days before assessing platelet function Recombinant factors are preferred MORE THAN Blood transufusion(may leade to transmission of blood-borne viruses and other infections)



   Rarely cause serious bleeding any bleeding into mucous membrane OR skin starts immediately after trauma stops within 24-48 hours



  Autosomal Dominant (AD) characterize by telangiectasia on the skin and mucosa May be associated with IgA deficiency / Von Willebrand disease(rarely)

CLINICAL FEATURES  Telangiectasia on : 1) Skin 2) Any part of oral 3) Nasal 4) GI 5) Urogenital mucosa  Leads to : 1) Bleeding 2) Iron-def anemia 3) Cardiac failure (rarely) GENERAL MANAGEMENT  Cryosurgery  Argon laser treatment DENTAL ASPECT  May be in any part of the mouth. May be conspicuous on the lips  Brain abscess / infections (rarely)  No need for antibacterial prophylaxis  AVOID Regional LA . may cause deep bleeding  Can be given conscious sedation  If GA, avoid nasal intubation & close post-operative observation is advisable.

Telangiectasias (also known as spider veins) [1] are small dilated blood vessels near the surface of the skin or mucous membranes, measuring between 0.5 and 1 millimeter in diameter

Causes: Lack of platelet due to failed platelet production ; ● rare congenital disorders ● megakaryocyte depression ● general bone marrow failure ● excessive platelet destruction

Box 8.1 Main coagulation defects          Anticoagulants & thrombolytic agents Chronic renal failure Deficiencies of factors XII and XIII and others Disseminated intravascular coagulation Dysproteinaemias (esp multiple myeloma) Haemophilia Liver diseases Lupus erythematosus Von Willebrand disease

- Abnormal platelet function : Glanzmann disease & dysproteinamias. - Abnormal platelet distribution : Splenomegaly & transfusion of stored blood.

Common causes : Thrombocytopenia CHARACTERISTICS : -Autoimmune -lead to purpura & prolonged bleeding. CLINICAL FEATURES : -petechiae -echymoses -postop. Hemorrhage

GENERAL MANAGEMENT : -full blood picture -platelet counts -corticosteroids/ other Igsuppressive -splenectomy ( sometimes).

DENTAL ASPECTS OF PLATELET DISORDERS: 1. Hemorrhage : - 30 x10 9/L  regional LA block injection - 50 x10 9/L  haemorrhage after dentoalveolar surgery - 75 x10 9/ L  major surgery - Conscious sedation *Note:- not to damage veins!* - GA given in hosp by expert * Avoid risk of submucous bleeding into airway * 2. Platelet infusion :


Risk of isoimmunization Infection of blood-borne agents Graft vs host disease (rare)

3. Splenectomy : - Antimic. Prophy not recommended bfore invasive dental procedure ( as systemic infection post-splenectomy involving oral streptococci is rare )

4. NSAID : - Aspirin can affect platelet irreversibly for ~1 week. - Others can affect platelet reversibly for only about 48h. . .

 Due to : - Genetic defects of clotting factors or, - Anti-coagulant therapy or, - Other disease (liver/kidney disease)

 Congenital coagulation defects

General aspects :  X-linked disorders  Deficiency in blood clotting factor VIII  Affects approximately 1:5000 males Clinical aspects:  Excessive bleeding ( trauma/spontaneously)  Stop immediately after injury  Intractable oozing  Dangerous because of acute blood loss or bleeding into tissues  Severity correlates with the level of factor VIII : coagulant activity and degree of trauma  Bleeding into tissues :  Into cranium, Can be fatal  Haematoma in the neck  Prolonged bleeding after dental extraction  Abdominal haemorrhage  Haemathroses/joint bleeding  Spontaneous gingival bleeding



General management :  Adequate Factor VIII or IX replacement during episodes of bleeding  Synthetic vasopressin (DDAVP) acts to increase factors VIII levels and used in mild hemophilia  ‘gene therapy’ and ‘gene-delivery systems’  potential cure for hemophilia in the future  Adequate replacement of factor VIII to ensure haemostasis if bleeding is starts or expected  Desmopressin and antifibrinolytics (eg: tranexamic acid) for mild hemophilia  Porcine factor VIII or recombinant factor VIII to replace missing clotting factors  Regular prophylactic replacement of factor VIII is used when possible.


Dental aspect :  Teeth erupt and exfoliate without problems  Non-invasive procedures are safe under antifibrinolytic cover (except in severe hemophiliacs)  Many of coagulation defects present a hazard to surgery and LA injections  Persistent bleeding for days or weeks following LA injection or surgery  May be life-threatening  LA regional blocks, lingual infiltrations or injections into floor of the mouth must not be used in the absence of factor VIII  risk of hemorrhage hazarding the airway  regional blocks can be used if factor VIII replacement therapy is given (maintained factor VIII to 30%)  Caries must be minimized/avoided  Preservation of teeth from the early age is essential.(fluoride application/regular dental inspection/sugar restriction)  Prevention of periodontal disease is imperative.  Bleeding tendency may be aggravated by NSAIDs and other factors (liver damage, HIV, thrombocytopenia, other drugs)  IM drugs injections must be avoided (unless replacement therapy is given)  large hematoma may be formed  Bleeding must be avoided during procedures (eg : soft tissues trauma )  Periodontal surgery needs LA and VIII replacement to 50-75%  No problem for orthodontic treatments ; just avoid the sharp edges of appliances(trauma to the soft tissues)  Extractions and dentoalveolar surgery :  Shold be carefully planned.

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Factor VIII replacement therapy of 50-75% is required Panoramic radiograph is needed  to assess any unsuspected lesions and whether further extractions might prevent future trouble Minimize risks of post-operative bleeding. Minimal trauma Suturing is desirable (but minimal; vicryl is preferred, avoid catgut)  stabilize the flap and prevent post-operative disturbances of wound Use non-traumatic needle Flap should not be opened in lingual tissues of lower molar region  hemorrhage endanger the airwayuse buccal approach Watch for hematoma post-operatively  manifest by swelling, dysphagia or hoarseness. Post-operative infection, give oral penicillin V 250mg or amoxicillin 500 mg four times daily for full course of 7 days to reduce the risk of secondary hemorrhage. Antibiotic prophylaxis may be given for pt with prosthetic joints.

Christmas disease ; X factor deficiency General and clinical aspects :  Clinically identical to hemophilia A  1/10 as common as hemophilia A (except in some Asians) General management :  Replacement therapy with synthetic factor IX (20 units of factor IX per kg body weight is given IV 1 hour pre-opratively.) Clinical management :  Same as hemophilia A except the usage of factor IX and not using desmopressin.



General aspects:  Pseudohaemophilia  Due to deficiency of von Willebrand factor (vWF)  Most common inherited bleeding disorder

vWF acts as a carrier for factor VIII and protecting it from proteolytic degradation. Deficiency leads to low factor VIII in the blood


Clinical features:  Bleeding  Similar to plt dysfxn  May resemble hemophilia,if severe.  Common pattern  bleeding from/purpura of mucous membranes and skin.  Gingival hemorrhage is common than in hemophilia  Excessive hemorrhage after dental treatment and surgery.  Excessive menstrual bleeding in female  Hemathroses is rare.  Severity varies from patient to patient, time to time.  Severity does not correlate with factor VII General management:  Pre-operatively, treatment to reduce the risk of hemorrhage is needed.  Administration of factor VIII concentrate  Synthetic vasopressin (DDAVP) Dental aspects:  Desmopression (DDAVP) IV or SC injection or nasal spray  for type 1 vWD and type 2A contraindicated in type 2B (because it stimulates release of dysfxnal vWF; need clotting factor replacement) and type 3 ( need clotting factor replacement)  In all types, aspirin and NSAIDs should be avoided  Infiltration and intraligamentary LA should be used.  Conscious sedation can be given but care should be taken not to damage vein.  Intubation is a possible hazard  risk of submucosal bleeding in airway.



Common in Ashkenazi Jews Factor IX deficiency Autosomal disorders (homozygosity/compound heterozygosity) Patient cannot activate thrombin-activatable fibrinolytic inhibitor TAFI  results in rapid fibrinolysis  bleeding tendency. Fresh frozen plasma/factor IX is required.

Factor XII is important for bradykinin and stimulation of fibrinolysis. Patients rarely show sign of hemorrhage.

Factor XIII is the pro-enzyme of plasma transglutaminase  activated by thrombin on the presence of calcium catalyse the cross-linking of fibrin monomers. Leads to neonatal umbilical cord bleeding, intracranial hemorrhage and soft tissue hematomas. Delayed bleeding.


Rare Raised plasma fibrinogen levels in coronary artery disease,diabetes,HTN,periphery artery disease, hyperlipoproteinemia,hypertriglyceridaemia,pregnancy,menopause,hyperchole strolaemia, smoking and oral contraceptives usage

Far more prevalent than congenital Less severe (except in anticoagulant therapy or liver disease) Causes:  Anticoagulant therapy  Liver disease  Vit K deficiency/malabsorption  Disseminated intravascular coagulation  Fibrinolytic states  Amyloidosis  Autoimmune disease Some pts have clinical bleeding tendency ; no defect detectable. .


General aspects May result from: 1) inherited abnormalities of haemoglobin formation 2) erythrocyte structure or function [spherocytosis; glucose-6-phosphate dehydrogenase (G6PD) deficiency] 3) damage to erythrocytes (autoimmune, drug-induced or infective). 4) Worldwide, malaria is the most common cause. Clinical features 1) Accelerated erythrocyte destruction  bilirubin overproduction, sometimes jaundice. 2) The spleen may enlarge, the increased red cell turnover raises:

a. reticulocyte count b. plasma lactate dehydrogenase (LDH) c. bilirubin d. uric acid levels This raises the demand for folic acid and may in turn cause macrocytic changes. General management 1) The cause should be treated if possible. 2) Folic acid may be required 3) Blood transfusion (possibility of iron overload.)

Dental aspects 1) Local anaesthesia is the safest method of pain control. 2) Conscious sedation, supplemental O2 if necessary. 3) Haemolytic anaemias C/I to GA - sickle cell disease is the most important cause of difficulties in dental management. HAEMOGLOBINOPATHIES Main fetus’ haemoglobin: (HbF) In infancy: replaced with adult haemoglobin (HbA) and small amount HbA2. These haemoglobins differ in their peptide chain composition 1) Haemoglobinopathies are genetically determined 2) Qualitative defects in the production of haemoglobin  ‘variant haemoglobins’. 3) Quantitative defects in the production of globins  thalassaemias. 4) Haemoglobinopathies are seen mostly in non-Caucasians Haemoglobinopathies result in: 1) significant morbidity and mortality, to no significant clinical effect 2) May have combinations of more than one haemoglobinopathy. 3) Short stature, abnormal skeletal development and jaundice often found 4) Signs and symptoms of anaemia. Diagnosis: 1) History, examination and laboratory investigations. Family history is important. 2) Full blood picture and red cell indices 3) Electrophoresis (4 ml of EDTA-anticoagulated blood) 4) Assay of variant haemoglobins. Special tests: Sickledex THE SICKLING DISORDERS (sickle cell) General aspects 1) Amino acid substitution in the Hb globin chain  changes in haemoglobin (HbS) a. gross distortions in the shape of erythrocytes b. impaired deformability c. membrane damage d. The erythrocytes cause vascular occlusions in microcirculation.

2) Integrins on the erythrocyte surface bind to vascular endothelial adhesion molecules (upregulated by tumour necrosis factor (TNF) and other pro-inflammatory cytokines), thus obstruction is more common during infections. 3) Homozygous, usually a serious disease with widespread complications. 4) Apparent about the third month of life. 5) Sickle cell trait (HbSA is present) is heterozygous and is frequently asymptomatic, may have renal complications causing haematuria or splenic infarcts, may be associated with another haemoglobinopathy. Clinical features 1) Painful crises, usually due to infarction Infarcts form mainly in the spleen (with eventual auto-splenectomy), bones and joints, brain, kidneys, lungs, retinae and skin. 2) Haematological crises are caused by parvovirus infection and can be haemolytic, aplastic or sequestration. 3) Chronic anaemia – with a haemoglobin level as low as 5–9 g/dl. 4) Chronic hyperbilirubinaemia predisposes to bile pigment gallstones. 5) Infections: results from splenic infarction and dysfunction. The main cause of death particularly by pneumococci, meningococci, Haemophilus and salmonellae. Most patients are kept on prophylactic phenoxymethyl penicillin. 6) Sequestration syndromes – these include sequestration of sickle cells in: a. the lungs impeding gas exchange (chest syndrome) b. the spleen (septicaemia may result) c. the liver, or ‘girdle syndrome’ may be associated with bowel dilatation. d. Morbidity and early mortality rates are high in sickle cell disease. e. Most eventually succumb to cardiac failure, renal failure, overwhelming infection or stroke. General management 1) Many already carry warning cards. 2) Haemoglobin level: below 9 g/dl. 3) Stained blood film: target cells, reticulocytosis of 5–25%, sometimes sickled erythrocytes 4) Haemoglobin electrophoresis: mainly HbS, up to 15% HbF, no HbA. 5) In sickle cell trait, haematological findings: normal. Electrophoresis shows 40% HbS and up to 60% HbA. 6) Tests relying on the low solubility of HbS (Sickledex) or by reducing agent (such as 10% sodium metabisulfite or dithionite). 7) Need regular blood pictures, a comprehensive care programme, folic acid regularly and sometimes blood transfusions. 8) Many patients remain with moderate degrees of anaemias. Transfusions should usually be minimised, especially because of the risk of hepatitis virus and HIV infection. 9) Infections and thromboses are the main causes of death. 10) Prevent trauma, infection, hypoxia, acidosis or dehydration, all of which can precipitate a crisis. Infections must be treated early. 11) Painful crises should be treated promptly with analgesics: diamorphine or pethidine, and hydration. 12) Patients with sickle cell anaemia are treated with hydroxycarbamide (hydroxyurea).

Dental aspects 1) Should be investigated if GA is to be given, if Hg <11g/dl  hazard 2) If GA is necessary, full oxygenation must be maintained. 3) LA is the preferred mode of pain control, avoid prilocaine 4) Aspirin is best avoided: paracetamol and codeine are effective alternatives. 5) Conscious sedation with relative analgesia can be used safely. 6) At least 30% O2 is needed. 7) Benzodiazepines are best avoided. 8) Elective surgery should be carried out in hospital and during a phase when haemolysis is minimal. 9) Anaemia should be corrected before GA and the haemoglobin brought up to at least 10 g/dl. Exchange transfusion is occasionally required for major surgery. It carries the risk of red cell alloimmunization in up to 20%. 10) Prophylactic antimicrobials (penicillin V or clindamycin) 11) Drugs that can cause respiratory depression, should not be given. 12) Acidosis and hypotension must also be avoided. 13) Orofacial manifestations: a. Painful infarcts in the jaws (which may be mistaken for toothache) b. Osteomyelitis c. Pulpal symptoms d. Pulpal necrosis e. Lesions suggestive of bone infarction (dense radioopacities) may be seen in the jaws and/or skull. f. Hypercementosis g. Bone marrow hyperplasia  enlarged haemopoietic maxilla with excessive overjet, and overbite. h. Skeletal but not dental maturation is delayed. i. The skull is thickened but osteoporotic with a hair-on-end pattern to the trabeculae. j. The diploë are thickened, especially in the parietal regions,  tower skull appearance. k. Enamel hypomineralization and calcified pulp canals may be seen. l. The lamina dura is distinct and dense m. Permanent teeth may be hypomineralized, THE THALASSAEMIAS 1) autosomally dominant: either alpha- or beta-globin chains are synthesized at a low rate, thereby lessening the production of haemoglobin A. 2) excessive erythrocyte fragility and haemolysis. 3) Hypochromic microcytic anaemia. Alpha-thalassaemias 1) There are four main subtypes, of varying degrees of severity. 2) In alpha-thalassaemia major, the condition is lethal in utero or infancy. Beta-thalassaemias (Mediterranean anaemia) General aspects 1) Beta-thalassaemias result from the depressed production of beta chains. 2) In the homozygous form they can be life-threatening.

3) A relative increase in delta and gamma chains is associated with raised levels of haemoglobin A2 and F. Homozygous beta-thalassaemia (Cooley anaemia; thalassaemia major) is characterized by: a. failure to thrive b. increasingly severe anaemia c. hepatosplenomegaly d. skeletal abnormalities. 4) Heterozygotes for beta-thalassaemia may be asymptomatic.

Clinical features 1. Homozygotes for thalassaemia: a. chronic anaemia b. marrow hyperplasia c. skeletal deformities d. splenomegaly e. cirrhosis f. gallstones g. iron overload. h. There is no pubertal growth spurt. i. Susceptible to folate deficiency and infection j. Overloaded with iron (haemosiderosis) - high gut absorption and from repeated transfusions. i. The iron damages the heart (cardiac haemosiderosis) causing cardiomyopathy and arrhythmias, which often result in death in early adult life. 2. Heterozygous beta-thalassaemia (thalassaemia minor or thalassaemia trait): common and usually asymptomatic, except for mild hypochromic anaemia. a. may be aggravated by pregnancy or intercurrent illness. General management 1. Great increase in HbF and some increase in HbA2. 2. The main treatment: blood transfusions, folic acid supplements and iron-chelating agents (desferrioxamine, deferasirox or deferiprone) and ascorbic acid. 3. Hydroxycarbamide is used: side-effects can be a significant disadvantage. 4. Splenectomy if there is hypersplenism. Dental aspects Hepatitis B or C, or HIV carriage, may be a complication in repeatedly transfused patients. surgical procedures with prophylactic antimicrobials. Local anaesthesia is safe. Conscious sedation: oxygen levels not less than 30%. Orofacial manifestations: 1) expansion of the diploë of the skull: hair-on-end appearance, frequently conspicuous on lateral skull radiographs. 2) Enlargement of the maxilla (chipmunk facies); 3) spacing of the teeth and forward drift of the maxillary incisors 4) Alveolar bone rarefaction: chicken-wire appearance on radiography. 5) Pneumatization of the sinuses may be delayed.

6) Less common oral complications: a. painful swelling of the parotids b. xerostomia c. sore or burning tongue Sickle cell trait with another haemoglobinopathy 1) sickle cell trait + haemoglobinopathy (eg. thalassaemia, both sickle cell haemoglobin S and C (SC disease)) 2) not as ill as those with isolated sickle cell disease. 3) about the same level of risk from GA as are those with sickle cell disease. 4) should be managed in the same way as those with sickle trait alone. . .

Essential part of the body’s response to stresses – trauma, infection, GA, operation 1) To suppress inflammation 2) To suppress graft rejection 3) To replace missing hormone (Addison d.) [cortisol is the major glucocorticoid in human] Corticosteroids have –ve feedback control on hypothalamic activity and ACTH production – > suppress HPA axis, no steroid production in response to stress –> cause acute adrenal insufficiency ( adrenal crisis) –> rapidly developing hypotension –> collapse –> possibly death CLINICAL FEATURES Table 6.18 Complication of systemic corticosteroid therapy Cardiovascular Cerebrovascular accident Hypertension MI Dermatological Acne Bruising Hirsutism Striae Peptic ulcer Increased susceptibility to infection Neoplasm long-term

Gastrointestinal Immunosuppressive


Cataract Mood changes Psychosis Fat redistribution(moon face and buffalo hump) Growth retardation HPA suppression DM Loss of sodium and potassium Muscle weakness Osteoporosis Weight gain


GENERAL MANAGEMENT 1. Give steroids on alternate days 2. Given drugs prophylactically to minimize the effects as below : a) No C/I – HTN, DM, latent TB b) Smallest effective steroid dose, best in morning, alternate days c) Preference on topical streroid rather than systemic steroid (greatest risk of adrenocortical suppression) d) Give the pt. a warning card and told of the dangers of withdrawal and side-effects e) Weight, chest xray, bone mineral density, BP, blood glucose baseline measure should be taken and monitored f) Ranitidine and calcitriol are often given

DENTAL ASPECTS 1) Steroid supplementation before stressful procedures – dentoalveolar or maxillofacial surgery 2) BP must be carefully monitored during surgery and recovery 3) For minor operations under LA – usual oral steroids in the morning + 2 - 4h pre and post operatively / give IV immediately before operation 4) For major operations – give IM / IV (with pre medication)+ 6 hourly for 24-72h

Sedatives and GA  a hazard, extremely important to avoid hypoxia, hypotension, haemorrhage Avoid aspirin and NSAIDs  increase risk of peptic ulcer

Osteoporosis  danger of fractures when handling pt. Require special management  DM, HTN, poor wound healing or infection ( careful aseptic surgery, prophylactic antimicrobials are indicated) Topical corticosteroids (in mouth)  predispose to oral candidosis Systemic corticosteroid  herpes simplex, chicken pox, varicella-zoster (immunization within 3 days of exposure) Long term profound immunosuppression  hairy leukoplakia, Kaposi sarcoma, lymphoma, lip cancer, oral keratosis

Table 6.19 Suggested management of pt. with history of systemic corticosteroid therapy

No steroids for previous 12months

Steroids taken during previous 12 months

Steroids currently taken

Cons dentistry/ No cover required dentoalveolar surgery (eg. Single extraction under LA)

Give usual oral steroids dose in morning/ IV hydrocortisone pre operatively

Double oral steroid dose in morning/ IV hydrocortisone preoperatively. Cont. normal steroid medication post operatively

Intermediate surgery (eg. Multiple extraction, under GA)

Consider cover if large doses of steroid were given. Test ACTH stimulation

Give usual oral steroids dose in morning/ IV hydrocortisone pre operatively and IM 6hourly for 24h

Double oral steroid dose in morning + IV hydrocortisone preoperatively + IM 6 hourly for 24h. Cont normal medication

Maxillofacial surgery/ trauma

Consider cover if large doses of steroid were given. Test ACTH stimulation

Give usual oral steroids dose in morning + IV hydrocortisone pre operatively + IM 6hourly for 72h

Double oral steroid dose in morning+ IV hydrocortisone preoperatively + IM 6-hourly for 72h. Cont normal medication

*all hydrocortisone dosage given are 25-50mg* . .

Under influence of thyroid stimulating hormone (TSH/thyrotropin) from pituitary gland. TSH regulated by thyrotropin releasing hormone (TRH) from hypothalamus.

THYROID HORMONE Stored as iodide-rich ‘thyroid colloid’: 1. Thyroxine (T4: tetraiodothyronine)  Half- life 1 week, converted to 2. Triiodothyronine (T3)- active form  Half life 1 day Feed back to hypothalamus and pituitary to regulate TSH release. Act on metabolism by regulating protein synthesis via effects on: o Gene transcription o mRNA stabilization have profound effect on: o sensitivity of tissue to catecholamines o mitochondrial oxidative activity o synthesis and degradation of proteins o differentiation of muscle fibres o capillary growth o levels of antioxidant compounds



THYROID FUNCTION TESTS include serum level of T3 and T4 Free T3 and free T4 provide better assessment as 95% thyroid hormone bound to plasma proteins : thyroid- binding globulin (TBG) and thyroid- binding pre- albumin (TBPA) TSH also can be test by: o Thyroid antibody test o Ultrasound o Radio-iodine uptake using 131I or 123I TEST HYPERTHYROIDISM HYPOTHYROIDISM T4 serum level T3 serum level Free thyroxine index T3 resin uptake Serum TSH Depessed in pituitary hypofunction Not done Not suppressed Not done by administration of T3 Long acting thyroid Thyroglobulin stimulator autoantibodies


TRH test (release of TSH by TRH) Radio-iodine uptake Thyroid autoantibodies

LINGUAL THYROID Thyroid normally develops as a downgrowth from foramen caecum at the junction of posterior third with anterior two- third of the tongue Ectopic thyroid remain in the tract may see as lump in the midline btw foramen caecum and epiglottis; but also found in: o Oropharynx o Infra-hyoid region o Larynx o Oesophagus o Heart o Mediastinum Seen mainly in female Often symptomatic but may cause o Dysphagia




o Airways obstructions o Haemorrhage o Hypothyroidism( 1/3 of cases) Occasionally malignant Not be suspected until lump in the tongue biopsied or excised and examined histologically Diagnosis confirmed by: o iodine -123 or -131 o technetium -99 uptake in the tongue o biopsy o CT scanning without contrast o MRI Treatment depends on size of the lingual thyroid but thyroxine may be needed o If does not regress, can be ablated;  best by surgery  if patient unfit by iodine -131 if normal functioning thyroid tissue found in the neck

GOITRE enlarged thyroid gland seen in Graves disease or thyroiditis cause is medullary carcinoma of thyroid, can be part of multiple endocrine adenomatosis syndrome (MEA II and MEA III) thyroid function tested to determine normal (euthyroid), hyperactive (hyperthyroid), or hypoactive (hypothyroid) most does not require surgery but indicated if : o danger of airway obstructions (cough, voice changes, dyspnea, tracheal deviation, dysphagia) o cosmetic reason dental management influenced by o abnormal thyroid function o underlying cause of the goiter o complications such as respiratory obstruction


THYROID NODULES Can be benign or malignant Examined by: o radio-iodine thyroid scans o Ultrasound- guided needle biopsy o Thyroid function test

HOT NODULE >take up radio-iodine >unlikely malignant >usually adenoma

COLD NODULE >fails to take up radio-iodine >may be malignant >usually papillary, follicular, or medullary cell carcinoma  Needle biopsy indicated

HYPERTHYROIDISM General aspects Associated with diffuse goiter due to autoimmune disease (Graves disease, primary hyperthyroidism) when thyroid- stimulating autoantibodies against thyroid TSH receptor (TRAbs) and thyroid microsomal antibodies (TMAbs) Hyperfunctioning (toxic) multi nodular goiter or nodule due to one or more thyroid adenoma produce excess thyroxine 90% swelling are benign Rarely,thyroiditis, thyroid hormone overdosage or ectopic thyroid tissue cause goiter


Clinical features Exophthalamus, eyelid lag and retraction Mimics effect of epinephrine, causes : o Anorexia o Vomiting o Diarrhea o Weight loss Cardiac disturbances in older patients include : o Tachycardia o Arrhythmias (atrial fibrillation) o Cardiac failure Amenorrhea Gynaecomastia Increase apetite Irritability No hair loss No voice changes Psychosis Warm moist skin Myasthenia gravis

o o o o

Anxiety Tremor Sweating Heat intolerance



General management Diagnosis confirmed by raised serum level of T3 and T4 Circulating TMAbs and TRAbs found in patients with Graves disease Scan or radioactive iodine uptake can differentiate causes of hyperthyroidism either subacute thyroiditis (low uptake) or Graves disease (high uptake) Treated with 1. Beta-blocker a. Rapid control of many signs and symptoms by moderating sympathetic overactivity b. BUT sudden stop may precipitate thyroid crisis within 4h 2. Carbimazole a. Usual antithyroid drug b. Can suppress bone marrow c. Cause rashes 3. Iodine -131 a. Effective b. Can result hypothyroidism c. No risk of neoplastic change 4. Surgery a. Effective b. May lead to hypothyroidism in 30% c. Hypoparathyroidism and recurrent laryngeal nerve palsy may indicated Untreated patients may precipitated thyroid (thyrotoxic) crisis o characterized by anxiety, tremor, dyspnea which can go to ventricular fibrillation o Medical assistance require use of :  Potassium iodide and prophylthiouracil  Propanolol  Chlorpromazine


Dental aspects LA main means of pain controls: o Any risk from epinephrine exacerbating sympathetic overactivity only theoretical o Prilocaine with felypressin not known to be safer than lidocaine Conscious sedation frequently desirable to control excessive anxiety Benzodiazepines may potentiate antithyroid drugs; therefore nitrous oxide(more controllable) is safer Avoid: o Providone- iodine and similar compound o Carbimazole  Cause agranulocytosis  cause oral / oropharyngeal ulceration o MAIN POINT IS: If GA IS REQUIRED!


HYPOTHYROIDISM General aspects: -- primary >due to thyroid dz -- secondary >hypothalamic/pituitary destruction --common cause: thyroid loss fr surgery/destruction by irradiation --other causes:: autoimmune dz (Hashimoto dz) associate w autoantibodies to thyroglobulin and thyroid microsomes :: drugs (carbimazole,lithium,radio-iodine) :: iodine defeciency (rare)

Clinical features: --weight gain -- constipation --lassitude --dry skin --myxoedema --loss of hair --IHD --bradychardia --serrous effusion --anemia

--neurological changes --cold intolerance --decrease appetite --decrease sweating -- hoarsness --menorrhagia --psychosis --slow reaction --angina --periorbital edema

General management: --low serum T4 and T3 --high TSH level in primary hypothyroidism --low TSH level in secondary hypothyroidism >>symptomatic patient manage with daily oral thyroxine sodium >>tx is started slowly Dental aspects: sedative (diazepam/midazolam),opiods,analgesic may precipitate myxoedema coma --associated problems include:hypoadrenocorticotism,anemia,hypotension,diminsih cardiac output,bradychardia --occasional association:hypopituitarism,sjogren syndrome (autoimmune) avoid povine iodine

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