Answer the following as per long abd short mentioned and according to university exam like pattern for bds oriented students 3rd year general medicine : 1. Describe the clinical features of Acute Myocardial infarction(AM) occurring in a 70 year old patient sitting on your dental chair. How will you manage such a patient immediately and in Hospital (10) Q 2. Describe the clinical features of Hyperthyroidism and Hypothyroidism. How will you diagnose them? Briefly outline the treatment of Hyperthyroidism. (10) Q3 Short notes (10X5.= 50 Marks) Tender Hepatomegaly Il. Acute Gastritis Bell's PalSnes IV. V. VI. VII. VIll. Scurvy Antitubercular Treatment Insulin Anaphylactic reaction Complication of Enteric fever 区KX Nephrotic Syndrore Herpes Zoster" 19X5

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Here are complete, exam-ready answers formatted for BDS 3rd Year General Medicine university pattern:

BDS 3rd Year General Medicine - University Examination Answers


Q1. Acute Myocardial Infarction (AMI) in a 70-Year-Old Patient on Dental Chair - Clinical Features and Management (10 Marks)

Introduction

Acute Myocardial Infarction (AMI) is defined as myocardial necrosis caused by prolonged ischemia, usually due to sudden occlusion of a coronary artery by a thrombus over an atherosclerotic plaque. In a 70-year-old patient on the dental chair, the risk is high due to pre-existing coronary artery disease, the stress of dental procedures (pain, anxiety, local anaesthetics with adrenaline), and the supine/semi-reclined position.

A. CLINICAL FEATURES

1. Symptoms

Chest Pain (Cardinal Feature)
  • Sudden onset, severe, crushing, squeezing, or constricting pain
  • Located in the centre of the chest (retrosternal), may radiate to:
    • Left arm (most common)
    • Jaw, neck, and teeth (of great dental relevance)
    • Left shoulder, epigastrium, back
  • Pain lasts >30 minutes (unlike angina which resolves in <15 min with rest or nitrates)
  • NOT relieved by sublingual nitrates
Important Note for Dental Surgeons: Pain referred to the jaw and teeth can mimic toothache; any elderly patient complaining of sudden jaw/tooth pain with no apparent dental cause must be evaluated for cardiac origin.
Atypical Presentation in the Elderly (70-year-old)
  • The elderly commonly present without chest pain (silent MI)
  • May present with:
    • Sudden breathlessness (dyspnoea)
    • Confusion, disorientation, or loss of consciousness
    • Profound weakness or fatigue
    • Nausea, vomiting, epigastric discomfort
    • Syncope or collapse
    • Sudden onset of heart failure

2. Associated Symptoms

  • Profuse sweating (diaphoresis) - cold, clammy skin
  • Nausea and vomiting
  • Severe anxiety, feeling of impending doom ("angor animi")
  • Palpitations (due to arrhythmias)
  • Breathlessness / dyspnoea

3. Signs on Examination

General:
  • Patient is pale, ashen, cold and clammy
  • Appears severely distressed and anxious
  • Breathless
Vital Signs:
  • Pulse: rapid and weak (tachycardia); may be irregular if arrhythmia present
  • Blood pressure: may fall (cardiogenic shock) or initially elevated
  • Temperature: mild fever may develop after 24-48 hours
  • Respiratory rate: increased
Cardiovascular:
  • Heart sounds may be faint
  • S3 gallop (indicates LV failure)
  • Soft systolic murmur (mitral regurgitation due to papillary muscle dysfunction)
  • Pericardial friction rub (in transmural MI, day 2-3)
Signs of LV Failure:
  • Fine basal crepitations in lungs
  • Raised JVP (if RV involved)
  • Central cyanosis in severe cases

B. IMMEDIATE MANAGEMENT IN THE DENTAL CHAIR

Act immediately - every minute counts ("Time is Muscle")

Step 1: Stop the Dental Procedure

  • Stop all dental work immediately
  • Remove instruments from the patient's mouth
  • Keep the patient calm and reassured

Step 2: Position

  • If conscious: Semi-reclined position (45 degrees) - do NOT lay flat (worsens breathlessness)
  • If unconscious: Lay flat and begin BLS (Basic Life Support)

Step 3: Call for Help - ACTIVATE EMERGENCY SERVICES

  • Call 108 / Emergency Medical Services immediately
  • Inform them of suspected cardiac emergency

Step 4: Oxygen

  • Administer high-flow oxygen 4-6 L/min by face mask
  • Maintain SpO2 >94%

Step 5: Aspirin (MONA Protocol - used in dental settings)

  • Aspirin 300 mg (chewed) - give immediately if not contraindicated
    • Chewing is important (faster absorption than swallowing)
    • Do not give if known aspirin allergy or active GI bleed

Step 6: Nitroglycerine (if available)

  • Sublingual Glyceryl Trinitrate (GTN) 0.4 mg - if BP >90 mmHg systolic
  • Repeat every 5 minutes x 3 doses if pain persists

Step 7: Monitor

  • Monitor pulse, BP, and consciousness continuously
  • Do NOT leave the patient alone

Step 8: Prepare for CPR

  • If patient loses consciousness and has no pulse, begin:
    • CPR: 30 chest compressions : 2 rescue breaths
    • Use AED (Automated External Defibrillator) if available
Remember MONA: Morphine - Oxygen - Nitrates - Aspirin

C. MANAGEMENT IN HOSPITAL

A. Initial Assessment

  • 12-Lead ECG - within 10 minutes of arrival
  • Blood tests: Serum Troponin I/T (gold standard), CK-MB, CBC, RFT, serum electrolytes, blood glucose, lipid profile
  • Chest X-ray
  • Echocardiography

ECG Changes in AMI:

StageECG Change
HyperacuteTall peaked T waves
Acute (STEMI)ST segment elevation (>1mm limb leads, >2mm chest leads)
Hours laterT wave inversion
Days laterPathological Q waves (permanent - "tombstone")

B. Reperfusion Therapy (Most Important)

1. Primary PCI (Percutaneous Coronary Intervention) - Gold Standard
  • Balloon angioplasty + stenting of occluded artery
  • Should be done within 90 minutes of first medical contact ("door to balloon time")
  • Superior to thrombolysis
2. Thrombolysis (if PCI not available within 120 min)
  • Streptokinase 1.5 million units IV over 60 min (older drug)
  • Alteplase (tPA) - more clot specific, preferred
  • Contraindicated in: recent surgery, active bleeding, stroke, uncontrolled hypertension

C. Medical Treatment

DrugDose & Purpose
Aspirin300 mg loading, then 75-100 mg daily (antiplatelet)
Clopidogrel/TicagrelorP2Y12 inhibitor - dual antiplatelet therapy
Heparin (LMWH)Anticoagulation - enoxaparin
NitratesIV nitroglycerin for pain and vasodilation
OxygenIf SpO2 <94%
Morphine2-4 mg IV for pain relief
Beta-blockersMetoprolol - reduce HR and O2 demand (if no bradycardia/hypotension)
ACE InhibitorsRamipril - reduce afterload, prevent remodelling
StatinsAtorvastatin 80 mg - plaque stabilization

D. Management of Complications

  • Arrhythmias: Lidocaine (VT/VF); atropine (bradycardia)
  • Cardiogenic shock: Dopamine/dobutamine; IABP (intra-aortic balloon pump)
  • Cardiac failure: Diuretics (frusemide IV)
  • VF: Immediate DC defibrillation

Q2. Hyperthyroidism and Hypothyroidism - Clinical Features, Diagnosis, and Treatment of Hyperthyroidism (10 Marks)

HYPERTHYROIDISM (THYROTOXICOSIS)

Definition: A clinical syndrome caused by an excess of circulating thyroid hormones (T3 and T4).
Common Causes:
  • Graves' disease (most common - autoimmune, TSI antibodies stimulate TSH receptor)
  • Toxic multinodular goitre
  • Toxic adenoma
  • Thyroiditis (subacute)
  • Excess iodine (Jod-Basedow effect)

A. CLINICAL FEATURES OF HYPERTHYROIDISM

Symptoms:
SystemFeatures
GeneralWeight loss despite increased appetite, heat intolerance, sweating, fatigue
CardiovascularPalpitations, tachycardia (even at rest), atrial fibrillation, hypertension
NeurologicalTremor of hands, anxiety, nervousness, irritability, emotional lability, insomnia
GIDiarrhoea, increased bowel frequency, vomiting
MenstrualOligomenorrhoea, amenorrhoea
MusculoskeletalProximal myopathy, weakness, osteoporosis
EyesExophthalmos/proptosis (specific to Graves'), lid lag, lid retraction, diplopia
SkinFine, smooth, moist skin; hair thinning, onycholysis (nail separation)
Signs:
  • Goitre (enlarged thyroid gland) - diffuse in Graves', nodular in MNG
  • Bruit over thyroid (in Graves')
  • Pretibial myxoedema (Graves' - skin thickening over shins)
  • Thyroid acropachy (Graves' - clubbing + soft tissue swelling)
  • Fine tremor on outstretched hands
  • Warm, moist skin
  • Tachycardia, hyperdynamic circulation
Graves' Disease Triad: Goitre + Exophthalmos + Pretibial myxoedema

HYPOTHYROIDISM

Definition: A clinical syndrome caused by insufficient production of thyroid hormones.
Common Causes:
  • Hashimoto's thyroiditis (autoimmune - most common in adults)
  • Iodine deficiency (most common worldwide)
  • Post-thyroidectomy / post-radioiodine
  • Drugs: amiodarone, lithium
  • Pituitary/hypothalamic disease (secondary/tertiary)
  • Congenital (Cretinism in neonates)

B. CLINICAL FEATURES OF HYPOTHYROIDISM

"SLOW" mnemonic:
SystemFeatures
GeneralWeight gain, cold intolerance, fatigue, lethargy, somnolence
Face/SkinPuffy face, periorbital oedema, non-pitting oedema (myxoedema), dry coarse skin, pallor, yellowish tinge (carotenaemia)
Hair/NailsDry coarse hair, loss of outer third of eyebrows (pathognomonic), brittle nails
CardiovascularBradycardia, cardiomegaly (myxoedema heart), pericardial effusion, hypertension, dyslipidaemia
NeurologicalSlow mentation, memory loss, depression, psychosis (myxoedema madness), cerebellar ataxia, carpal tunnel syndrome, delayed relaxation of deep tendon reflexes (most important sign)
GIConstipation, macroglossia
ReproductiveMenorrhagia, infertility, galactorrhoea
VoiceHoarse, deep voice (myxoedema voice)
MusculoskeletalMuscle cramps, proximal myopathy
Myxoedema Coma (Severe): Hypothermia, coma, bradycardia, hyponatraemia - medical emergency
Cretinism (Congenital Hypothyroidism):
  • Mental retardation, short stature, pot belly
  • Protruding tongue, umbilical hernia
  • Delayed milestones, deafness

C. DIAGNOSIS OF THYROID DISORDERS

InvestigationHyperthyroidismHypothyroidism
TSH (Thyroid Stimulating Hormone)Decreased / Suppressed (most sensitive)Elevated (earliest change)
Free T4 (FT4)ElevatedDecreased
Free T3 (FT3)ElevatedDecreased
TRAb/TSIPositive in Graves' disease-
Anti-TPO antibodiesMay be elevatedElevated in Hashimoto's
Radioactive Iodine Uptake (RAIU)Increased (diffuse in Graves', patchy in MNG)Decreased
Thyroid scan (Tc-99m)Diffuse increased uptake (Graves')Cold nodules
Ultrasound thyroidGoitre, vascularityHeterogeneous in Hashimoto's
CBCAnaemia possibleMacrocytic anaemia
LipidsNormal or low cholesterolElevated cholesterol/LDL
ECGTachycardia, AFBradycardia, low voltage, T wave flattening
Key Diagnostic Rule:
  • TSH is the single best screening test for thyroid dysfunction
  • Low TSH = Hyperthyroidism; High TSH = Hypothyroidism

D. TREATMENT OF HYPERTHYROIDISM

1. Anti-thyroid Drugs (Thionamides) - First Line

  • Carbimazole: Initial dose 10-20 mg every 12 hours; maintenance 5-10 mg/day
  • Methimazole: Active metabolite of carbimazole; once-daily dosing possible
  • Propylthiouracil (PTU): 100-200 mg every 6-8 hours; preferred in pregnancy (first trimester) and thyroid storm
  • Mechanism: Inhibit thyroid peroxidase (TPO), reducing oxidation and organification of iodide; PTU also inhibits peripheral conversion of T4 to T3
  • Course: 12-18 months for maximum remission (30-60%)
  • Titration regimen: Gradually reduce dose as euthyroidism achieved
  • Side effects: Agranulocytosis (monitor WBC if fever/sore throat), hepatotoxicity (PTU)

2. Beta-blockers (Symptomatic Relief)

  • Propranolol 40-80 mg 3-4 times daily
  • Reduces tachycardia, tremor, anxiety, sweating
  • Does not reduce thyroid hormone levels
  • Used until antithyroid drugs take effect (6-8 weeks)

3. Radioiodine Therapy (¹³¹I)

  • Oral dose of radioactive iodine
  • Destroys thyroid tissue permanently
  • Preferred in: Adults >45 years, relapse after antithyroid drugs, toxic nodular goitre
  • Contraindicated in: Pregnancy, breastfeeding, active Graves' ophthalmopathy
  • Eventually leads to hypothyroidism (requires lifelong thyroxine replacement)

4. Surgery (Thyroidectomy)

  • Total or near-total thyroidectomy
  • Indicated in: Large goitre with compressive symptoms, suspected malignancy, failed medical/radioiodine therapy, pregnant women in 2nd trimester who fail drugs
  • Must make patient euthyroid before surgery (with antithyroid drugs for 6-8 weeks + Lugol's iodine for 10 days pre-op)

5. Treatment of Graves' Ophthalmopathy

  • Mild: Lubricating eye drops, dark glasses
  • Moderate-severe: IV methylprednisolone pulses, teprotumumab (IGF-1R antibody)
  • Severe (optic nerve compression): Orbital decompression surgery

6. Thyroid Storm Management (Emergency)

  • PTU 600 mg orally, then 200-300 mg every 4 h
  • Propranolol IV
  • Lugol's iodine (after PTU) 1 hour later
  • Hydrocortisone 100 mg IV 8-hourly
  • IV fluids, paracetamol (not aspirin), ICU care

Q3. SHORT NOTES (10 x 5 = 50 Marks)


I. TENDER HEPATOMEGALY

Definition: Enlargement of the liver that is painful on palpation.
Causes:
  1. Infective:
    • Amoebic liver abscess (most common cause of painful hepatomegaly in India)
    • Pyogenic liver abscess
    • Acute viral hepatitis (A, B, E)
    • Infective mononucleosis
  2. Vascular:
    • Congestive cardiac failure (CCF) - acute - hepatic congestion stretches Glisson's capsule
    • Budd-Chiari syndrome
  3. Inflammatory:
    • Cholangitis
    • Acute alcoholic hepatitis
  4. Malignant:
    • Rapid hepatic metastases (capsule stretch)
    • Hepatocellular carcinoma
Clinical Features:
  • Right hypochondrial pain, sometimes referred to right shoulder
  • Liver enlarged, tender, smooth
  • In CCF: Hepatojugular reflux positive; pulsatile liver (TR)
  • In amoebic abscess: fever, leukocytosis, diarrhoea history
Investigation:
  • LFTs, Serum amylase, SGOT/SGPT
  • Ultrasound abdomen (abscess, vascular lesion)
  • CT scan, Liver biopsy if needed
  • Serology (amoebic abscess: indirect haemagglutination test)
Treatment:
  • Directed at the cause
  • Amoebic abscess: Metronidazole 800 mg TDS x 5-10 days
  • CCF: Diuretics, ACE inhibitors, treat primary cause

II. ACUTE GASTRITIS

Definition: Acute inflammation of the gastric mucosa.
Aetiology:
  1. NSAIDs / Aspirin (most common - inhibit prostaglandin synthesis, reduce mucosal defence)
  2. Alcohol
  3. H. pylori infection (acute phase)
  4. Stress - critically ill patients (ICU), burns (Curling's ulcer), brain injury (Cushing's ulcer)
  5. Corticosteroids
  6. Bile reflux
  7. Radiation
Pathology:
  • Erosions, petechial haemorrhages, mucosal oedema
  • Loss of surface epithelium
  • May progress to frank ulceration
Clinical Features:
  • Epigastric pain, burning, discomfort
  • Nausea, vomiting
  • Anorexia
  • Haematemesis or melaena (if bleeding erosion)
  • Often asymptomatic (especially NSAID-induced)
Diagnosis:
  • Upper GI endoscopy (OGD) - gold standard (erythema, erosions, haemorrhagic areas)
  • Biopsy for H. pylori (rapid urease test, histology)
  • H. pylori: Urea breath test, stool antigen test
Treatment:
  1. Stop the causative agent (NSAIDs, alcohol)
  2. Proton Pump Inhibitors (PPIs): Omeprazole 20-40 mg BD - reduce acid secretion (mainstay)
  3. H2 blockers: Ranitidine/Famotidine
  4. Antacids: Symptomatic relief
  5. Sucralfate / Misoprostol: Mucosal protection
  6. H. pylori eradication: Triple therapy - PPI + Amoxicillin + Clarithromycin x 14 days
  7. Stress ulcer prophylaxis in ICU: IV PPI or H2 blockers

III. BELL'S PALSY

Definition: Idiopathic unilateral lower motor neuron (LMN) facial nerve (VII nerve) palsy of acute onset.
Aetiology:
  • Reactivation of Herpes Simplex Virus (HSV-1) in geniculate ganglion is the most accepted cause
  • Results in oedema and entrapment of facial nerve in stylomastoid foramen
Clinical Features (ALL on the same side - ipsilateral):
  • Sudden onset weakness/paralysis of all muscles of one side of face
  • Inability to close eye (lagophthalmos) - corneal exposure risk
  • Loss of forehead wrinkling (differentiates from UMN palsy - in UMN, forehead spared)
  • Drooping of angle of mouth
  • Bell's phenomenon: on attempting to close eye, eyeball rolls up (white sclera visible)
  • Obliteration of nasolabial fold
  • Food/liquid trapping in cheek
  • Hyperacusis (if nerve to stapedius affected)
  • Loss of taste on anterior 2/3 of tongue (chorda tympani affected)
  • Decreased lacrimation (greater petrosal nerve affected)
Important for BDS: Dentists must be aware as dental procedures (mandibular block injection, parotid surgery) can injure facial nerve.
Investigations:
  • Clinical diagnosis
  • EMG/NCS: To assess nerve injury severity
  • MRI: Rule out central cause, acoustic neuroma
Treatment:
  1. Prednisolone 60 mg/day for 5 days, then taper over 10 days (must start within 72 hours) - reduces inflammation
  2. Acyclovir 400 mg 5 times daily x 10 days (antiviral - for HSV)
  3. Eye care: Artificial tear drops, eye pad at night, glasses during day (prevent corneal exposure)
  4. Physiotherapy, facial exercises
  5. Most cases resolve within 3-6 months (85% full recovery)

IV. SCURVY

Definition: Vitamin C (Ascorbic Acid) deficiency disease.
Mechanism: Vitamin C is essential for hydroxylation of proline and lysine in collagen synthesis. Deficiency leads to defective collagen, resulting in capillary fragility and impaired wound healing.
At-risk Groups: Elderly, alcoholics, infants on unsupplemented formula, malnourished
Clinical Features:
(Extremely important for BDS - oral manifestations)
SystemFeatures
Gums (Dental importance)Spongy, swollen, haemorrhagic gums; gums bleed easily on touch; gingival hypertrophy; loose teeth; pericoronitis
SkinPerifollicular haemorrhages (pathognomonic), corkscrew/swan-neck hairs, easy bruising, ecchymoses
MusculoskeletalBleeding into joints (haemarthrosis), subperiosteal haemorrhage, painful swollen legs (especially children)
Wound healingPoor wound healing
AnaemiaMicrocytic or normocytic anaemia
SystemicFatigue, irritability, weakness, low-grade fever
Radiological (children)Trummerfeld zone (zone of destruction), Pelkan spurs, Frankel line, Wimberger ring sign
Diagnosis:
  • Clinical (mainly)
  • Serum/leucocyte vitamin C levels (low)
  • X-ray (children): Ground glass appearance, cortical thinning
Treatment:
  • Vitamin C 500-1000 mg/day orally for 1 month; maintenance 75-90 mg/day
  • Dietary: Fresh fruits (amla, lemon, orange), green vegetables
  • Resolution of symptoms usually within days to weeks

V. ANTITUBERCULAR TREATMENT (ATT)

First Line Drugs:
DrugMechanismDaily DoseSide Effects
Isoniazid (H)Inhibits mycolic acid synthesis5 mg/kg (max 300 mg)Peripheral neuropathy (prevented by pyridoxine), hepatotoxicity, SLE-like syndrome
Rifampicin (R)Inhibits RNA polymerase10 mg/kg (max 600 mg)Hepatotoxicity, orange discolouration of urine/secretions, enzyme inducer (reduces efficacy of OCP, anticoagulants)
Pyrazinamide (Z)Disrupts mycobacterial membrane potential25 mg/kgHyperuricaemia, gout, hepatotoxicity, arthralgia
Ethambutol (E)Inhibits arabinosyl transferase15 mg/kgOptic neuritis (dose-dependent, regular eye checks needed), colour blindness
Streptomycin (S)Inhibits protein synthesis (30S)15 mg/kgOtotoxicity (vestibular/auditory), nephrotoxicity, avoid in pregnancy
Revised National TB Control Programme (RNTCP) / National TB Elimination Programme (NTEP) Regimen:
CategoryPatient TypeIntensive PhaseContinuation Phase
New casesNew PTB, EPTB2HRZE (2 months)4HR (4 months)
Previously treatedFailure, relapse2HRZES / 1HRZE5HRE
MDR-TBResistant to H + RIndividualised - bedaquiline, linezolid, clofazimine
Total Duration:
  • Pulmonary TB: 6 months (2 + 4)
  • TB meningitis, bone/joint TB, miliary TB: 9-12 months
  • All treatment under DOTS (Directly Observed Treatment Short course)
Important for Dentists: Rifampicin causes orange staining of saliva; reduces efficacy of benzodiazepines used in dentistry.

VI. INSULIN

Types of Insulin:
TypeOnsetPeakDurationExamples
Rapid-acting10-15 min1-2 h3-5 hLispro, Aspart, Glulisine
Short-acting (Regular)30-60 min2-4 h6-8 hRegular/Soluble insulin
Intermediate2-4 h4-10 h12-18 hNPH (Isophane)
Long-acting1-2 hPeakless20-24 hGlargine, Detemir
Ultra-long1-6 hPeakless>42 hDegludec
Mechanisms of Action:
  • Binds to insulin receptor (tyrosine kinase receptor)
  • Promotes glucose uptake in muscle and fat (GLUT-4)
  • Inhibits gluconeogenesis and glycogenolysis in liver
  • Promotes lipogenesis, inhibits lipolysis
  • Anabolic: promotes protein synthesis
Indications:
  • Type 1 Diabetes Mellitus (mandatory)
  • Type 2 DM: When oral drugs fail, during illness/surgery/pregnancy, DKA, HHS
  • Gestational diabetes mellitus (GDM)
  • Diabetic ketoacidosis (DKA) - IV regular insulin
  • Hyperkalaemia (drives K+ into cells)
Complications of Insulin Therapy:
  • Hypoglycaemia (most common and dangerous)
  • Lipodystrophy at injection sites
  • Weight gain
  • Oedema
  • Local allergic reactions
  • Insulin resistance
Dental Relevance:
  • Diabetics on insulin are at risk of hypoglycaemia during dental procedures
  • Never operate on a fasting diabetic on insulin
  • Have glucose (juice/sugar) ready in dental clinic

VII. ANAPHYLACTIC REACTION

Definition: A severe, life-threatening systemic hypersensitivity reaction (Type I - IgE mediated) to an antigen, involving multiple organ systems.
Common Triggers in Dental Practice:
  • Local anaesthetics (most common in dentistry - especially ester type)
  • Penicillin / antibiotics
  • NSAIDs (aspirin, ibuprofen)
  • Latex gloves
  • Contrast media
Pathophysiology:
  • Antigen binds to IgE on mast cells and basophils
  • Releases histamine, leukotrienes, prostaglandins, tryptase
  • Massive vasodilation, increased capillary permeability, bronchoconstriction
Clinical Features (ABCDE):
SystemFeatures
SkinUrticaria (hives), erythema, pruritus, angioedema, flushing
AirwayLaryngeal oedema (stridor), bronchoconstriction (wheeze), dyspnoea
CardiovascularHypotension (shock), tachycardia, arrhythmia, collapse
GINausea, vomiting, abdominal cramps, diarrhoea
CNSAnxiety, dizziness, confusion, unconsciousness
Signs: Hypotension, tachycardia, urticaria, angio-oedema, bronchospasm, cyanosis
IMMEDIATE MANAGEMENT:
  1. STOP the causative agent immediately
  2. Call for emergency help (108)
  3. Position: Lay patient flat with legs elevated (Trendelenburg); if breathing difficulty, sit up
  4. Adrenaline (Epinephrine) - FIRST AND MOST IMPORTANT DRUG:
    • 0.5 mg (0.5 mL of 1:1000) IM into outer thigh (vastus lateralis)
    • May repeat every 5-15 minutes
    • Mechanism: alpha-1 vasoconstriction (raises BP), beta-2 bronchodilation, prevents further mediator release
  5. Oxygen: High flow 10-15 L/min
  6. IV access + IV fluids: Normal saline 500-1000 mL rapid infusion
  7. Antihistamine: Chlorpheniramine 10 mg IM/slow IV
  8. Corticosteroids: Hydrocortisone 200 mg IV (prevents late-phase reaction)
  9. Bronchodilator: Salbutamol inhaler / nebulizer if bronchospasm persists
  10. If cardiac arrest: CPR + ALS
Note: Adrenaline is the drug of choice - do NOT delay for antihistamines or steroids.

VIII. COMPLICATIONS OF ENTERIC FEVER (TYPHOID)

Causative organism: Salmonella typhi (Gram-negative bacillus)
Common Complications (occur in 3rd-4th week):
A. Intestinal Complications:
  1. Intestinal Perforation - Most serious; Peyer's patches in terminal ileum perforate; presents with acute abdomen, guarding, peritonitis, free gas under diaphragm on X-ray
  2. Intestinal Haemorrhage - Due to sloughing of Peyer's patches; melaena/haematochezia
  3. Paralytic Ileus
B. Hepatic: 4. Typhoid hepatitis - jaundice, hepatomegaly 5. Hepatic abscess (rare)
C. Cardiac: 6. Myocarditis - ECG changes, arrhythmias, heart failure 7. Pericarditis
D. Neurological: 8. Typhoid encephalopathy - altered consciousness 9. Meningitis 10. Peripheral neuropathy
E. Haematological: 11. Disseminated Intravascular Coagulation (DIC)
F. Respiratory: 12. Bronchitis, lobar pneumonia (typhoid pneumonia)
G. Urological: 13. Typhoid nephritis, UTI
H. Other: 14. Relapse (in ~10% despite treatment) 15. Chronic carrier state (Salmonella persists in gallbladder) - especially women with gallstones
Treatment of typhoid: Ceftriaxone 2g/day IV x 10-14 days (drug of choice currently); Ciprofloxacin if sensitive; Azithromycin for uncomplicated cases.

IX. NEPHROTIC SYNDROME

Definition: A clinical syndrome characterised by the tetrad:
  1. Heavy proteinuria (>3.5 g/day in adults; >40 mg/m²/hr in children)
  2. Hypoalbuminaemia (<3.5 g/dL)
  3. Generalised oedema (anasarca)
  4. Hyperlipidaemia and lipiduria
Causes:
  • Primary (Idiopathic): Minimal Change Disease (MCD - most common in children), FSGS, Membranous nephropathy (most common in adults), Membranoproliferative GN
  • Secondary: Diabetes mellitus (diabetic nephropathy), SLE (lupus nephritis), Amyloidosis, Malaria, HIV, drugs (gold, penicillamine)
Pathophysiology:
  • Loss of negative charge on glomerular basement membrane (GBM) and/or structural damage
  • Allows proteins (mainly albumin) to pass into urine
  • Low albumin → low oncotic pressure → oedema
  • Liver compensates by increasing VLDL production → hyperlipidaemia
Clinical Features:
  • Oedema: Periorbital (early morning, most characteristic), dependent oedema, ascites, pleural effusion, scrotal/labial oedema
  • Frothy urine (lipiduria, proteinuria)
  • Pallor
  • Anorexia, fatigue
  • Possible hypertension (especially in secondary forms)
Complications:
  • Infections (bacterial - Streptococcus pneumoniae, peritonitis) - due to loss of immunoglobulins
  • Thromboembolism (renal vein thrombosis, DVT, PE) - loss of antithrombin III, protein C and S
  • Hyperlipidaemia → accelerated atherosclerosis
  • AKI
  • Protein malnutrition, vitamin D deficiency, anaemia
Investigations:
  • Urine: 24-hour protein, urine protein:creatinine ratio, lipid casts
  • Serum albumin (low), serum cholesterol (high), TG (high)
  • Serum creatinine and urea
  • Renal biopsy (gold standard for definitive diagnosis - except typical MCD in children)
  • Complement levels (C3, C4 - low in MPGN, SLE)
  • ANA, anti-dsDNA (SLE), HBsAg, HCV, blood glucose
Treatment:
  1. Specific: Based on histology - Steroids (MCD: prednisolone 60 mg/day - excellent response), cyclophosphamide, cyclosporine
  2. Salt restriction, fluid restriction if severe oedema
  3. Diuretics: Frusemide (loop diuretic)
  4. ACE inhibitors/ARBs: Reduce proteinuria (e.g., ramipril, losartan)
  5. Statins: Manage hyperlipidaemia
  6. Anticoagulation if thromboembolism
  7. Antibiotics/prophylaxis for infections (penicillin V in children)
  8. Dietary protein intake: 0.8-1 g/kg/day of high-quality protein

X. HERPES ZOSTER (SHINGLES)

Definition: Reactivation of latent Varicella-Zoster Virus (VZV - a herpes virus) from the dorsal root ganglion or cranial nerve ganglia, producing a painful vesicular eruption in a dermatomal distribution.
Pathogenesis: VZV remains dormant in dorsal root ganglia after primary varicella (chickenpox). Reactivation occurs due to declining cell-mediated immunity (old age, immunosuppression, stress, HIV, malignancy).
Clinical Features:
(A) Prodromal Stage (2-4 days before rash):
  • Burning, stabbing pain, hyperalgesia, itching along the dermatome
  • Malaise, fever, headache
  • No visible rash yet (often misdiagnosed)
(B) Eruptive Stage:
  • Unilateral, dermatomal distribution (does NOT cross midline)
  • Maculopapular rash → vesicles (clear fluid) → pustules → crusting
  • Thoracic dermatomes most common (T3-T11)
  • Intense pain (may persist as postherpetic neuralgia)
(C) Special Presentations (Dental/Medical Importance):
  • Herpes Zoster Ophthalmicus (V1 - ophthalmic branch of trigeminal): Vesicles on forehead, tip of nose (Hutchinson's sign), risk of corneal ulceration and blindness
  • Ramsay Hunt Syndrome (VII nerve - geniculate ganglion): Facial palsy + vesicles in external auditory canal/pinna + ipsilateral tinnitus, vertigo, deafness
  • Oral Herpes Zoster (V2/V3 - maxillary/mandibular branch): Unilateral vesicles and ulcers on oral mucosa, palate, gingiva; extreme dental pain - relevant to dentists as it can mimic pulpitis or periapical abscess
  • Zoster sine herpete: pain without rash
(D) Postherpetic Neuralgia:
  • Pain persisting >3 months after rash heals
  • Most common complication; seen in >50% patients above 60 years
  • Burning, lancinating, allodynia (light touch causes pain)
Investigations:
  • Mainly clinical diagnosis
  • Tzanck smear: Multinucleated giant cells (also seen in HSV)
  • PCR for VZV DNA (gold standard)
  • VZV-specific IgM (acute), IgG (past infection)
Treatment:
  1. Antiviral drugs (must start within 72 hours of rash onset):
    • Acyclovir 800 mg 5 times daily x 7-10 days (standard)
    • Valacyclovir 1 g TDS x 7 days (better oral bioavailability, preferred)
    • Famciclovir 500 mg TDS x 7 days
  2. Pain management:
    • Paracetamol, NSAIDs (mild)
    • Gabapentin / Pregabalin (neuropathic pain, postherpetic neuralgia)
    • Amitriptyline (tricyclic antidepressant - for postherpetic neuralgia)
    • Opioids (severe pain)
  3. Topical: Calamine lotion, antiviral cream
  4. Corticosteroids: Prednisolone may reduce acute pain and risk of postherpetic neuralgia (adjunct)
  5. Eye care: Topical acyclovir eye ointment, ophthalmology referral (Zoster ophthalmicus)
  6. Prevention: VZV vaccine (Shingrix - recombinant adjuvanted vaccine) - recommended for adults >50 years; 90% effective at preventing shingles

SUMMARY TABLE FOR QUICK REVISION

TopicKey Points to Remember
AMI in dental chairMONA; Aspirin 300 mg chewed; call 108; semi-reclined position; AED
HyperthyroidismGraves' triad; Low TSH; Carbimazole/Methimazole; Propranolol for symptoms
HypothyroidismDelayed DTR; High TSH; Thyroxine replacement
Tender hepatomegalyAmoebic abscess, CCF; U/S + serology
Acute gastritisNSAIDs, H. pylori; PPIs; Triple therapy
Bell's palsyLMN VII nerve; Steroids + Acyclovir within 72 hrs; Eye care
ScurvyVit C deficiency; Perifollicular haemorrhage; Spongy bleeding gums
ATTHRZE x 6 months; DOTS; watch for hepatotoxicity
InsulinTypes by duration; IM adrenaline; Hypoglycaemia risk in dental chair
AnaphylaxisAdrenaline 0.5 mg IM; Oxygen; IV fluids; Hydrocortisone
Typhoid complicationsIntestinal perforation; Myocarditis; DIC; Carrier state
Nephrotic syndrome4 features; Renal biopsy; Steroids (MCD); ACEi/ARB
Herpes zosterDermatomal; Ramsay Hunt; Oral zoster; Acyclovir within 72 hrs; Postherpetic neuralgia

All answers based on Harrison's Principles of Internal Medicine 22E, Goldman-Cecil Medicine, and standard BDS General Medicine curriculum. References: Harrison's, p.2150-2153 (AMI/ACS); Harrison's Thyroid section p.3079-3082 (Hyperthyroidism treatment); Washington Manual of Medical Therapeutics (Nephrotic Syndrome).
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