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AMC MCQ exam Prep by Dr Jayse

AMC MCQ exam Prep by Dr Jayse

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📈 Analytical overview of Telegram channel AMC MCQ exam Prep by Dr Jayse

Channel AMC MCQ exam Prep by Dr Jayse (@amcmcqprep) in the English language segment is an active participant. Currently, the community unites 10 404 subscribers, ranking 2 631 in the Medicine category and 315 in the Singapore region.

📊 Audience metrics and dynamics

Since its creation on невідомо, the project has demonstrated rapid growth, gathering an audience of 10 404 subscribers.

According to the latest data from 02 September, 2026, the channel demonstrates stable activity. Although there has been a change in the number of participants by -26 over the last 30 days and by -2 over the last 24 hours, overall reach remains high.

  • Verification status: Not verified
  • Engagement rate (ER): The average audience engagement rate is 7.37%. Within the first 24 hours after publication, content typically collects 2.15% reactions from the total number of subscribers.
  • Post reach: On average, each post receives 767 views. Within the first day, a publication typically gains 224 views.
  • Reactions and interaction: The audience actively supports content: the average number of reactions per post is 1.
  • Thematic interests: Content is focused on key topics such as statin, patient, mcq, symptom, examination.

📝 Description and content policy

The author describes the resource as a platform for expressing subjective opinions:
Contact Dr Jayse @jayse89

Thanks to the high frequency of updates (latest data received on 03 September, 2026), the channel maintains relevance and a high level of publication reach. Analytics show that the audience actively interacts with content, making it an important point of influence in the Medicine category.

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MCQ ‼️ A 24-year-old patient with severe acute asthma has persistent bronchospasm despite repeated nebulized albuterol/ipratropium and IV corticosteroids. Which is the most appropriate next therapy? A. Magnesium oxide 400 mg PO B. Magnesium sulfate 2 g IV over 20 minutes C. Magnesium sulfate 2 g IV push over 1 minute D. Calcium gluconate 1 g IV over 10 minutes E. Observe

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Internal branch → sensory above vocal cords Loss of laryngeal sensation → aspiration risk ⸻ Thyroid & ENT Surgical Anatomy Superior thyroid artery → close to external branch of superior laryngeal nerve Inferior thyroid artery → relationship with recurrent laryngeal nerve Thyroidectomy complication + hoarseness → RLN injury Thyroidectomy + inability to produce high-pitched sounds → external SLN injury ⸻ Ludwig Angina ⭐⭐⭐ Bilateral submandibular/sublingual infection → Ludwig angina Dental infection → floor-of-mouth cellulitis → Ludwig angina “Woody” induration of floor of mouth → Ludwig angina Tongue elevation → Ludwig angina Airway compromise → major danger Usually odontogenic → mandibular molar infection ⸻ Parotitis Painful parotid swelling + fever → parotitis Purulent drainage from Stensen duct → bacterial parotitis Stensen duct opens opposite upper second molar → parotid gland Dehydrated hospitalized patient → bacterial parotitis risk Mumps → bilateral parotitis + fever ⸻ Facial Nerve ⭐⭐⭐ CN VII → facial expression Bell palsy → LMN facial nerve palsy Entire ipsilateral face affected → Bell palsy Cannot wrinkle forehead + cannot close eye + drooping mouth → LMN CN VII lesion Forehead spared → UMN lesion/stroke Bell palsy treatment → corticosteroids ± antivirals depending on presentation Ramsay Hunt syndrome → vesicles in ear + ipsilateral facial paralysis Ramsay Hunt → VZV reactivation ⸻ Bell Palsy vs Stroke ⭐⭐⭐ Bell palsy: Forehead + eye closure + lower face all affected UMN stroke: Forehead relatively spared + contralateral lower facial weakness ⸻ Ramsay Hunt Syndrome Facial paralysis + painful vesicles around ear → Ramsay Hunt Varicella-zoster virus → Ramsay Hunt Geniculate ganglion involvement → Ramsay Hunt Can cause hearing loss/tinnitus/vertigo → Ramsay Hunt ⸻ Parotid Tumors Most common benign salivary gland tumor → pleomorphic adenoma Painless slow-growing parotid mass → pleomorphic adenoma Facial nerve weakness + parotid mass → malignant salivary gland tumor Facial nerve involvement in parotid mass → concerning for malignancy 🔥 20 Ultra-HY ENT Buzzwords Bulging TM → Acute otitis media Pain with tragal movement → Otitis externa Foul-smelling otorrhea + white keratin → Cholesteatoma 4-kHz notch → Noise-induced hearing loss Carhart notch → Otosclerosis Weber → affected ear → Conductive hearing loss Weber → unaffected ear → Sensorineural hearing loss Vertigo + tinnitus + fluctuating hearing loss → Ménière disease Positional vertigo + positive Dix-Hallpike → BPPV Unilateral SNHL → Vestibular schwannoma Bilateral vestibular schwannomas → NF2 Aspirin + asthma + nasal polyps → AERD Hot potato voice + uvular deviation → Peritonsillar abscess Drooling + tripod + thumbprint → Epiglottitis Barking cough + steeple sign → Croup Foul unilateral nasal discharge in child → Foreign body Hoarseness after thyroidectomy → Recurrent laryngeal nerve injury Cannot produce high-pitched sounds → External superior laryngeal nerve injury Woody floor of mouth + dental infection → Ludwig angina Facial paralysis + ear vesicles → Ramsay Hunt syndrome #usmleprep #USMLEStep2CK #usmlestep1 #ent
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Nasal obstruction + facial pressure + nasal discharge → chronic sinusitis Nasal polyps → chronic rhinosinusitis association ⸻ Nasal Polyps ⭐ Pale, translucent, boggy nasal masses → nasal polyps Usually painless → nasal polyps Bilateral nasal obstruction → nasal polyps Associated with asthma → nasal polyps Aspirin sensitivity + asthma + nasal polyps → AERD/Samter triad Nasal polyps + cystic fibrosis → classic association Treatment → intranasal corticosteroids ⸻ AERD / Samter Triad ⭐⭐⭐ Asthma + nasal polyps + aspirin/NSAID sensitivity → AERD NSAID ingestion → bronchospasm → AERD COX-1 inhibition → ↓ prostaglandins + ↑ leukotrienes Avoid nonselective NSAIDs → AERD ⸻ Adenoid Hypertrophy Child + chronic nasal obstruction → adenoid hypertrophy Mouth breathing → adenoid hypertrophy “Adenoid facies” → chronic adenoid hypertrophy Hyponasal speech → adenoid hypertrophy Snoring/OSA in child → adenoid/tonsillar hypertrophy Eustachian tube dysfunction/recurrent otitis media → enlarged adenoids ⸻ Tonsillitis / Peritonsillar Abscess ⭐⭐⭐ Fever + sore throat + tonsillar exudates → tonsillitis Group A strep → Streptococcus pyogenes Palatal petechiae → GAS pharyngitis Tender anterior cervical lymphadenopathy → GAS Cough + rhinorrhea → viral rather than GAS Peritonsillar abscess “Hot potato” muffled voice → peritonsillar abscess Unilateral tonsillar swelling → peritonsillar abscess Uvula deviates AWAY from affected side → peritonsillar abscess ⭐ Trismus → peritonsillar abscess Drooling → peritonsillar abscess Treatment → drainage + antibiotics ⸻ Retropharyngeal Abscess ⭐ Young child + fever + neck stiffness → retropharyngeal abscess Drooling + dysphagia → retropharyngeal abscess Neck swelling/stiffness → retropharyngeal abscess Recent URI → possible precipitating infection Posterior pharyngeal bulging → retropharyngeal abscess Can cause airway obstruction → emergency ⸻ Epiglottitis ⭐⭐⭐ Child + high fever + drooling + respiratory distress → epiglottitis Tripod position → epiglottitis Muffled voice → epiglottitis Stridor → epiglottitis “Thumbprint sign” on lateral neck X-ray → epiglottitis Do NOT aggressively examine the throat → risk of airway obstruction Airway first → epiglottitis Historically Hib → classic USMLE association Unvaccinated child → think Hib ⸻ Croup ⭐⭐⭐ Barking cough → croup Seal-like barking cough → croup Inspiratory stridor → croup Steeple sign → croup Usually viral → parainfluenza Usually age 6 months–3 years → croup Treatment: dexamethasone → croup Moderate/severe disease → nebulized epinephrine Croup vs Epiglottitis Barking cough → Croup Drooling + tripod + toxic appearance → Epiglottitis ⸻ Foreign Body Sudden unilateral foul-smelling nasal discharge in child → nasal foreign body Unilateral purulent rhinorrhea → nasal foreign body Sudden coughing/choking episode → airway foreign body Unilateral decreased breath sounds → bronchial foreign body Most common site of aspiration → right main bronchus ⸻ Laryngeal Cancer ⭐ Persistent hoarseness >2–3 weeks → evaluate for laryngeal malignancy Smoking + hoarseness → laryngeal squamous cell carcinoma Alcohol + smoking → increased risk Supraglottic tumor → dysphagia/odynophagia Glottic tumor → early hoarseness Persistent unilateral otalgia with normal ear exam → referred pain from head/neck malignancy ⸻ Vocal Cord Paralysis Hoarseness after thyroid surgery → recurrent laryngeal nerve injury Unilateral recurrent laryngeal nerve damage → hoarseness Bilateral recurrent laryngeal nerve injury → airway obstruction/stridor Left recurrent laryngeal nerve travels under aortic arch → thoracic lesions can cause hoarseness Left vocal cord paralysis + mediastinal mass → recurrent laryngeal nerve compression ⸻ Recurrent Laryngeal Nerve Motor innervation of most intrinsic laryngeal muscles → recurrent laryngeal nerve Exception = cricothyroid → external branch of superior laryngeal nerve RLN injury → hoarseness Bilateral RLN injury → airway compromise ⸻ Superior Laryngeal Nerve External branch → motor to cricothyroid Cricothyroid → tenses vocal cords External SLN injury → weak/high-pitched voice
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Sensorineural hearing loss → presbycusis Bilateral symmetric → presbycusis ⸻ Noise-Induced Hearing Loss Chronic loud-noise exposure → SNHL 4-kHz notch on audiogram → noise-induced hearing loss ⭐ Concert worker / factory worker / firearm exposure → noise-induced SNHL Usually bilateral → occupational noise exposure ⸻ Vestibular Schwannoma ⭐⭐⭐ Unilateral sensorineural hearing loss → vestibular schwannoma Unilateral tinnitus → vestibular schwannoma Balance problems + unilateral hearing loss → vestibular schwannoma CN VIII tumor → vestibular schwannoma Cerebellopontine angle mass → vestibular schwannoma Bilateral vestibular schwannomas → NF2 NF2 + bilateral CN VIII tumors → classic association MRI with gadolinium → diagnostic imaging ⸻ Ménière Disease ⭐⭐⭐ Episodic vertigo + hearing loss + tinnitus → Ménière disease Fluctuating sensorineural hearing loss → Ménière Aural fullness → Ménière Endolymphatic hydrops → underlying mechanism Low-frequency hearing loss initially → Ménière Episodes last minutes to hours → Ménière No focal neurologic deficits → supports peripheral vertigo Buzzword triad: Vertigo + tinnitus + fluctuating hearing loss ⸻ BPPV ⭐⭐⭐ Brief episodes of vertigo triggered by head movement → BPPV Rolling over in bed → vertigo → BPPV Looking up → vertigo → BPPV Positive Dix-Hallpike → BPPV Nystagmus with positional testing → BPPV Most commonly posterior semicircular canal → BPPV No hearing loss → BPPV Treatment → Epley/canalith repositioning maneuver Key distinction: BPPV = positional + seconds + NO hearing loss ⸻ Vestibular Neuronitis Acute prolonged vertigo after viral illness → vestibular neuritis Vertigo lasting days → vestibular neuritis No hearing loss → vestibular neuritis No tinnitus → vestibular neuritis Peripheral vestibular disorder → vestibular neuritis Labyrinthitis Vertigo + hearing loss after viral infection → labyrinthitis Vestibular neuritis + hearing loss → think labyrinthitis ⸻ Central vs Peripheral Vertigo Peripheral Severe vertigo → peripheral Nausea/vomiting → peripheral Unidirectional horizontal nystagmus → peripheral Nystagmus suppressed by visual fixation → peripheral Hearing symptoms may occur → peripheral Central Vertical nystagmus → central Direction-changing nystagmus → central Neurologic deficits → central Severe gait ataxia → central Nystagmus not suppressed by visual fixation → central Cerebellar stroke → central vertigo ⸻ Eustachian Tube Dysfunction Ear fullness after URI/flight → eustachian tube dysfunction Retracted TM → eustachian tube dysfunction Barotrauma during airplane descent → eustachian tube dysfunction Difficulty equalizing pressure → eustachian tube dysfunction ⸻ Epistaxis ⭐ Most common site of anterior epistaxis → Kiesselbach plexus Children + nose picking → anterior epistaxis Visible bleeding vessel on anterior septum → Kiesselbach Most common overall epistaxis → anterior Posterior epistaxis → older adults, hypertension/atherosclerosis Posterior bleeding → sphenopalatine artery Blood flowing into posterior pharynx → posterior epistaxis Posterior epistaxis often requires packing/ENT intervention Management First step → sit forward + pinch soft nose Topical vasoconstrictor → oxymetazoline Persistent visible anterior bleeding → cautery Uncontrolled posterior bleeding → posterior packing + ENT ⸻ Nasal Fracture Most common facial fracture → nasal fracture Nasal trauma + deformity → nasal fracture Septal hematoma → emergency Fluctuant swelling of nasal septum → septal hematoma Untreated septal hematoma → cartilage necrosis → saddle-nose deformity Septal hematoma requires drainage → urgent ENT management ⸻ Sinusitis ⭐ Acute bacterial rhinosinusitis Symptoms >10 days without improvement → bacterial sinusitis Severe fever + purulent nasal discharge ≥3 days → bacterial sinusitis “Double worsening” → bacterial sinusitis Initial viral URI improves then worsens → bacterial sinusitis Common organisms → S. pneumoniae, H. influenzae First-line treatment when antibiotics indicated → amoxicillin-clavulanate Chronic sinusitis Symptoms ≥12 weeks → chronic rhinosinusitis
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👂 Whole ENT amc Buzzwords in one post 🔥 Otitis Media Acute otitis media (AOM) → bulging, erythematous tympanic membrane + middle-ear effusion Ear pain + fever + recent URI → AOM Pneumatic otoscopy: decreased TM mobility → middle-ear effusion Most common organism in children → Streptococcus pneumoniae Other AOM organisms → H. influenzae, Moraxella catarrhalis AOM after viral URI → bacterial superinfection Antibiotic first-line → amoxicillin Amoxicillin recently used / conjunctivitis → amoxicillin-clavulanate → β-lactamase-producing H influenzae AOM + otorrhea through tympanostomy tube → topical fluoroquinolone ear drops Otitis media with effusion “Glue ear” → otitis media with effusion Fluid behind TM without acute inflammation → OME Conductive hearing loss after URI → OME Usually no fever or significant ear pain → OME Persistent unilateral middle-ear effusion in adult → evaluate for nasopharyngeal mass Children + recurrent OME + speech delay → hearing evaluation ± tympanostomy tubes ⸻ Otitis Externa “Swimmer’s ear” → acute otitis externa Pain with tragal manipulation → otitis externa Pain when pulling pinna → otitis externa Ear canal edema + erythema → otitis externa Most common organism → Pseudomonas aeruginosa Treatment → topical antibiotic ear drops Tympanic membrane perforation/tube present → use non-ototoxic fluoroquinolone drops Avoid aminoglycoside-containing drops if TM perforation → risk of ototoxicity Malignant otitis externa Older patient + diabetes + severe otalgia → malignant otitis externa Severe pain out of proportion → malignant otitis externa Granulation tissue in external auditory canal → malignant otitis externa Cranial nerve palsy → advanced malignant otitis externa Typical organism → Pseudomonas Treatment → systemic antipseudomonal antibiotics ⸻ Tympanic Membrane Dull, bulging TM → AOM Retracted TM → eustachian tube dysfunction Air-fluid level/bubbles behind TM → middle-ear effusion Perforated TM + purulent drainage → otitis media with perforation Central TM perforation → usually chronic otitis media Attic/marginal perforation + foul-smelling discharge → cholesteatoma ⸻ Cholesteatoma ⭐ Painless chronic otorrhea → cholesteatoma Foul-smelling ear discharge → cholesteatoma White keratin debris behind TM → cholesteatoma Retraction pocket containing keratin → cholesteatoma Conductive hearing loss + chronic ear disease → cholesteatoma Erosion of ossicles → cholesteatoma Can erode bone → cholesteatoma Treatment → surgical removal Classic clue: Foul-smelling otorrhea + conductive hearing loss + white mass ⸻ Hearing Loss Conductive External/middle ear problem → conductive hearing loss Otosclerosis → conductive hearing loss Cerumen impaction → conductive hearing loss Otitis media → conductive hearing loss Tympanic membrane perforation → conductive hearing loss Ossicular damage → conductive hearing loss Sensorineural Cochlea/CN VIII problem → sensorineural hearing loss Presbycusis → bilateral high-frequency sensorineural hearing loss Noise exposure → high-frequency SNHL Ototoxic drugs → SNHL Vestibular schwannoma → unilateral SNHL ⸻ Rinne & Weber ⭐⭐⭐ Rinne Normal → air conduction > bone conduction Conductive hearing loss → bone conduction > air conduction Sensorineural hearing loss → air conduction > bone conduction Weber Conductive hearing loss → sound lateralizes to affected ear Sensorineural hearing loss → sound lateralizes to unaffected ear Easy rule: Conductive → Weber goes toward the bad ear Sensorineural → Weber goes toward the good ear ⸻ Otosclerosis ⭐⭐⭐ Young/middle-aged adult + progressive hearing loss → otosclerosis Usually conductive hearing loss → otosclerosis Stapes fixation → otosclerosis Normal TM + progressive conductive hearing loss → otosclerosis Pregnancy may worsen symptoms → otosclerosis Carhart notch at 2 kHz → otosclerosis Treatment → hearing aid or stapedectomy/stapedotomy ⸻ Presbycusis Elderly patient + gradual bilateral hearing loss → presbycusis High-frequency hearing loss → presbycusis Difficulty understanding speech, especially in noisy environments → presbycusis
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Autosomal dominant usually Mucocutaneous bleeding Epistaxis Menorrhagia Easy bruising ↓ platelet adhesion May cause ↑ PTT because vWF stabilizes factor VIII Treatment → desmopressin Buzzword: “Mucosal bleeding + normal platelets + desmopressin” ⸻ Bernard-Soulier Syndrome Defective GpIb Cannot bind vWF Giant platelets Thrombocytopenia ↑ bleeding time Remember: Bernard-Soulier = GpIb ⸻ Glanzmann Thrombasthenia Defective GpIIb/IIIa Cannot bind fibrinogen Impaired platelet aggregation Normal platelet count ↑ bleeding time Remember: Glanzmann = GpIIb/IIIa ⸻ ⚡ Ultra-High-Yield “Instant Diagnosis” Lines Auer rods → AML Auer rods + DIC → APL t(9;22) → CML Smudge cells → CLL Reed-Sternberg → Hodgkin t(14;18) → Follicular lymphoma t(8;14) → Burkitt t(11;14) → Mantle cell CRAB → Multiple myeloma IgM + hyperviscosity → Waldenström Spherocytes → hereditary spherocytosis / warm AIHA Heinz bodies + bite cells → G6PD Sickle cells → sickle cell disease Schistocytes + thrombocytopenia → TTP/HUS/DIC Bloody diarrhea + AKI → HUS Neurologic symptoms + MAHA → TTP ↑ PT + ↑ PTT + ↓ fibrinogen → DIC Hemarthrosis + ↑ PTT → Hemophilia Mucosal bleeding + vWF problem → vWD GpIb → Bernard-Soulier GpIIb/IIIa → Glanzmann Pancytopenia + hypocellular marrow → aplastic anemia Microcytosis + low ferritin → iron deficiency Microcytosis + high RBC count → thalassemia Low iron + low TIBC + high ferritin → anemia of chronic disease
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Acute Myeloid Leukemia — AML Auer rods Myeloperoxidase positive Myeloblasts Older adults t(15;17) → acute promyelocytic leukemia PML-RARA Severe DIC Treatment → ATRA APL is a hematologic emergency Buzzword: “Auer rods + DIC → APL → ATRA” ⸻ ALL Most common leukemia in children TdT positive B-cell or T-cell lineage Bone pain Fever Hepatosplenomegaly CNS involvement t(12;21) → favorable B-ALL t(9;22) → worse prognosis T-ALL Adolescent male Mediastinal mass Thymic origin Buzzword: “Child + lymphoblasts + TdT” ⸻ CML t(9;22) Philadelphia chromosome BCR-ABL Constitutively active tyrosine kinase Very high WBC Basophilia Splenomegaly Low leukocyte alkaline phosphatase Treatment → imatinib Buzzword: “Massive leukocytosis + basophilia + splenomegaly → CML” ⸻ CLL Most common leukemia in older adults Smudge cells CD5+ CD23+ B-cell malignancy Hypogammaglobulinemia Recurrent infections Autoimmune hemolytic anemia Can transform into aggressive lymphoma → Richter transformation Buzzword: “Older adult + lymphocytosis + smudge cells” ⸻ 🧫 Lymphomas Hodgkin Lymphoma Reed-Sternberg cells CD15+ CD30+ Painless lymphadenopathy B symptoms Fever Night sweats Weight loss Alcohol-induced lymph node pain Contiguous spread Often cervical lymph nodes Buzzword: “Reed-Sternberg + CD15/CD30” ⸻ Non-Hodgkin Lymphoma Usually noncontiguous spread Extranodal involvement common Multiple subtypes Can involve GI tract, skin, CNS, bone marrow ⸻ Follicular Lymphoma t(14;18) BCL2 overexpression Indolent Painless lymphadenopathy “Back-to-back” follicles Buzzword: “t(14;18) → BCL2 → follicular lymphoma” ⸻ Burkitt Lymphoma Extremely rapid growth t(8;14) MYC activation “Starry-sky” appearance African endemic → jaw mass Sporadic → abdominal mass Tumor lysis syndrome risk Buzzword: “Fast-growing + starry sky + t(8;14)” ⸻ Mantle Cell Lymphoma t(11;14) Cyclin D1 ↑ CD5+ Older adults GI involvement Multiple lymphomatous polyposis Buzzword: “CD5+ lymphoma + cyclin D1 + t(11;14)” ⸻ Multiple Myeloma Older adult CRAB Calcium ↑ Renal dysfunction Anemia Bone lesions Lytic bone lesions “Punched-out” lesions Monoclonal IgG Rouleaux formation M-spike Bence Jones proteins β2-microglobulin → prognosis Bone marrow → plasma cells Recurrent infections Buzzword: “CRAB + punched-out lesions + M-spike” ⸻ MGUS Monoclonal protein ❤ g/dL Bone marrow plasma cells <10% No CRAB features Precursor to multiple myeloma ⸻ Waldenström Macroglobulinemia IgM Lymphoplasmacytic lymphoma Hyperviscosity Headache Blurred vision Neurologic symptoms No lytic bone lesions No hypercalcemia typically Buzzword: “IgM + hyperviscosity + no lytic lesions” ⸻ 🩸 Platelet Disorders ITP Isolated thrombocytopenia Petechiae/purpura Normal PT/PTT Large/young platelets Autoimmune destruction Children → often after viral infection Adults → chronic Associated with HIV/SLE Treatment → steroids ± IVIG Buzzword: “Isolated low platelets + normal PT/PTT” ⸻ TTP Think MAHA + thrombocytopenia + neurologic/renal findings Thrombocytopenia Renal dysfunction Anemia/MAHA Fever Neurologic symptoms Schistocytes ↓ ADAMTS13 Usually normal PT/PTT Treatment → plasma exchange immediately Buzzword: “Schistocytes + thrombocytopenia + neurologic symptoms → TTP” ⸻ HUS MAHA Thrombocytopenia Acute kidney injury Often follows bloody diarrhea Shiga toxin → EHEC Children Normal PT/PTT Treatment usually supportive Buzzword: “Bloody diarrhea → AKI + thrombocytopenia + schistocytes” ⸻ DIC Consumption of clotting factors + platelets Bleeding and thrombosis ↑ PT ↑ PTT ↑ D-dimer ↓ fibrinogen ↓ platelets Schistocytes Causes: Sepsis Trauma Obstetric complications Malignancy APL Buzzword: “Bleeding + prolonged PT/PTT + low fibrinogen + high D-dimer” ⸻ Hemophilia A Factor VIII deficiency X-linked recessive Hemarthroses Deep tissue bleeding ↑ PTT Normal PT Normal bleeding time Treatment → factor VIII Desmopressin can help mild disease Buzzword: “Male + hemarthroses + isolated ↑ PTT” ⸻ Hemophilia B Factor IX deficiency X-linked Clinically similar to hemophilia A Christmas disease ⸻ von Willebrand Disease Most common inherited bleeding disorder
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🩸 Whole HY Hematology in one post 🔥✅ Iron Deficiency Anemia Microcytic, hypochromic anemia ↓ Ferritin = most specific clue ↓ Serum iron ↑ TIBC ↑ RDW Pica → especially ice (pagophagia) Koilonychia → spoon-shaped nails Chronic blood loss → think GI bleeding Premenopausal woman → menstrual blood loss Most common cause in adult men/postmenopausal women → GI blood loss until proven otherwise ⸻ Anemia of Chronic Disease Usually normocytic, sometimes microcytic ↓ Serum iron ↓ TIBC ↑/normal ferritin ↑ Hepcidin Chronic infection, inflammation, malignancy Iron trapped inside macrophages Think: “Iron is there, but unavailable.” ⸻ Thalassemia Severe microcytosis out of proportion to anemia ↑ RBC count despite anemia Normal/↑ ferritin Target cells Basophilic stippling may occur β-thalassemia major: severe anemia beginning in infancy “Chipmunk facies” “Crew-cut” skull Hepatosplenomegaly Transfusion dependence β-thalassemia minor: mild anemia, often asymptomatic Hb electrophoresis: ↑ HbA₂ → β-thalassemia trait α-thalassemia → HbH / Hb Bart’s ⸻ 🧬 Hemolytic Anemias General Hemolysis Think: ↑ LDH + ↑ indirect bilirubin + ↓ haptoglobin + ↑ reticulocytes Jaundice Splenomegaly Dark urine may occur Extravascular hemolysis Spleen/macrophages ↑ indirect bilirubin Splenomegaly Spherocytes Intravascular hemolysis RBC destruction inside blood vessels Hemoglobinuria ↓↓↓ haptoglobin Hemosiderinuria ↑ LDH ⸻ Hereditary Spherocytosis Spherocytes ↑ MCHC Extravascular hemolysis Splenomegaly Autosomal dominant Defect in RBC membrane proteins Ankyrin/spectrin/band 3 Positive family history Eosin-5-maleimide binding ↓ Splenectomy → definitive treatment in severe disease Pigment gallstones Buzzword: “Spherocytes + increased MCHC + family history” ⸻ G6PD Deficiency Episodic hemolysis Oxidative stress triggers: Sulfonamides Dapsone Primaquine Nitrofurantoin Fava beans Infection Heinz bodies Bite cells X-linked recessive African/Mediterranean ancestry can be a clue G6PD protects RBCs by generating NADPH ↓ glutathione → oxidative damage Buzzword: “Fava beans/drug + hemolysis + bite cells/Heinz bodies” ⸻ Sickle Cell Disease HbS β-globin mutation: Glu → Val Autosomal recessive Vaso-occlusive crises Severe pain Acute chest syndrome Dactylitis Autosplenectomy Increased risk of encapsulated bacteria Salmonella osteomyelitis Pigment gallstones Aplastic crisis → Parvovirus B19 Howell-Jolly bodies Hydroxyurea → ↑ HbF Pain crisis → hydration + analgesia Acute chest → oxygen + antibiotics + analgesia ± transfusion Classic triggers Dehydration Infection Hypoxia Acidosis Buzzword: “Pain + autosplenectomy + Howell-Jolly bodies” ⸻ Sickle Cell Trait Usually asymptomatic Hematuria Renal papillary necrosis Splenic infarction at high altitude Usually does not cause severe vaso-occlusive disease ⸻ Pyruvate Kinase Deficiency ↓ ATP production Hemolytic anemia Echinocytes/burr cells ↑ 2,3-BPG Autosomal recessive Splenomegaly Chronic hemolysis Buzzword: “Hemolysis + echinocytes + ↑ 2,3-BPG” ⸻ Autoimmune Hemolytic Anemia Warm AIHA IgG Extravascular hemolysis Spherocytes Positive direct Coombs Associated with: SLE CLL Methyldopa Treatment → glucocorticoids Buzzword: “IgG + 37°C + spherocytes” Cold AIHA IgM Complement-mediated Agglutination Associated with: Mycoplasma pneumoniae EBV Symptoms worse with cold Treat underlying disease ± rituximab Buzzword: “Cold exposure + IgM + RBC agglutination” ⸻ PNH — Paroxysmal Nocturnal Hemoglobinuria Intravascular hemolysis Hemoglobinuria Thrombosis Abdominal pain Pancytopenia PIGA mutation Defective GPI anchor ↓ CD55 and CD59 Complement-mediated RBC destruction Treatment → eculizumab/ravulizumab Buzzword: “Hemolysis + thrombosis in unusual sites + pancytopenia” ⸻ 🩸 Bone Marrow Disorders Aplastic Anemia Pancytopenia Hypocellular bone marrow Few/no hematopoietic cells No splenomegaly Causes: Benzene Radiation Drugs Viral infections Autoimmune Parvovirus B19 usually causes pure red cell aplasia, not classic aplastic anemia Treatment → stem-cell transplant in appropriate young patients Buzzword: “Pancytopenia + empty/hypocellular marrow” ⸻
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Triceps → elbow extension Musculocutaneous → anterior arm Radial → posterior arm/forearm Median → most anterior forearm Ulnar → most intrinsic hand muscles FDS → PIP flexion FDP → DIP flexion PAD/DAB → ulnar nerve Gluteus maximus → hip extension Gluteus medius → hip abduction Superior gluteal nerve → Trendelenburg Quadriceps → knee extension → femoral nerve Hamstrings → knee flexion → sciatic nerve Anterior leg → dorsiflexion → deep fibular Lateral leg → eversion → superficial fibular Posterior leg → plantarflexion → tibial
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If left side of pelvis drops → right gluteus medius/minimus weakness → right superior gluteal nerve lesion. Gluteus minimus Hip abduction + medial rotation Superior gluteal nerve. TENSOR FASCIAE LATAE Hip abduction + medial rotation Tightens iliotibial tract Nerve → superior gluteal nerve. HIP FLEXORS Iliopsoas Main hip flexor Psoas major + iliacus Nerve → femoral nerve + direct branches of lumbar plexus Sartorius Flexes hip Abducts hip Laterally rotates hip Flexes knee Nerve → femoral nerve. Mnemonic: Tailor’s muscle → sartorius. THIGH — ANTERIOR COMPARTMENT Main nerve → Femoral nerve Quadriceps Rectus femoris Knee extension Hip flexion Vastus lateralis Knee extension Vastus medialis Knee extension Helps stabilize patella. Vastus intermedius Knee extension All: → Femoral nerve → L2–L4. THIGH — MEDIAL COMPARTMENT Main action → hip adduction Main nerve → Obturator nerve Adductor longus → adduction Adductor brevis → adduction Adductor magnus Adduction Hamstring portion → hip extension Gracilis Hip adduction Knee flexion Medial rotation of leg Obturator nerve. THIGH — POSTERIOR COMPARTMENT Main nerve → Sciatic nerve Hamstrings Semitendinosus Hip extension Knee flexion Medial rotation Semimembranosus Hip extension Knee flexion Medial rotation Biceps femoris Hip extension Knee flexion Lateral rotation Nerve Semitendinosus → tibial division of sciatic Semimembranosus → tibial division Biceps femoris long head → tibial division Biceps femoris short head → common fibular division LEG — ANTERIOR COMPARTMENT Main nerve → Deep fibular nerve Main action → dorsiflexion Tibialis anterior Dorsiflexion Inversion Deep fibular nerve Extensor hallucis longus Extension of great toe Dorsiflexion Extensor digitorum longus Extension of toes Dorsiflexion Deep fibular nerve injury → foot drop LEG — LATERAL COMPARTMENT Main nerve → Superficial fibular nerve Main action → eversion Fibularis longus → eversion Fibularis brevis → eversion Superficial fibular nerve injury → weak eversion. LEG — POSTERIOR COMPARTMENT Main nerve → Tibial nerve Main action → plantarflexion Gastrocnemius Plantarflexion Knee flexion Soleus Plantarflexion Important postural muscle. Plantaris Weak plantarflexion + knee flexion. Tibialis posterior Plantarflexion Inversion ACHILLES TENDON Gastrocnemius + soleus → Achilles tendon. Achilles reflex: → S1–S2 → tibial nerve. Achilles rupture → difficulty plantarflexing. FOOT INVERSION vs EVERSION Inversion Tibialis anterior + Tibialis posterior Eversion Fibularis longus + Fibularis brevis Easy memory: TA + TP = inversion FL + FB = eversion NECK MUSCLES Sternocleidomastoid Unilateral → rotates face to opposite side Lateral flexion to same side Bilateral → neck flexion Nerve → CN XI Sensory/proprioceptive contribution → C2–C3. CN XI injury → difficulty turning head against resistance → shoulder droop due to trapezius weakness. TRAPEZIUS Elevates scapula → upper fibers Retracts scapula → middle fibers Depresses scapula → lower fibers Upward rotation → upper + lower fibers Nerve → CN XI Clinical CN XI injury → difficulty shrugging shoulder. SERRATUS ANTERIOR Protracts scapula Upward rotation of scapula Keeps scapula against thoracic wall Nerve → long thoracic nerve Roots → C5–C7 Injury → winged scapula Classic cause: axillary lymph node surgery / trauma RHOMBOIDS Scapular retraction Downward rotation Nerve → dorsal scapular nerve Root → C5. DIAPHRAGM Main muscle of inspiration Nerve → phrenic nerve Roots → C3–C5 Mnemonic: C3, 4, 5 keep the diaphragm alive. Phrenic nerve injury → ipsilateral diaphragmatic paralysis. EXTRAOCULAR MUSCLES LR6 SO4, 3 all the rest Lateral rectus → CN VI Superior oblique → CN IV All others → CN III Superior rectus → elevation + medial rotation + adduction Inferior rectus → depression + lateral rotation + adduction Superior oblique → depression + medial rotation + abduction Inferior oblique → elevation + lateral rotation + abduction. 20 MUSCLE FACTS TO MEMORIZE FOR USMLE Supraspinatus → initiates abduction Deltoid → abducts 15–90° Axillary nerve → surgical neck of humerus Biceps → supination
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💪 HIGH-YIELD MUSCLES TESTED IN EVERY MEDICAL EXAMS 💯🔥 ROTATOR CUFF-> SITS Supraspinatus Action → initiates abduction (0–15°) Nerve → Suprascapular nerve Root → C5–C6 Injury → difficulty initiating shoulder abduction Most commonly injured rotator cuff tendon. Infraspinatus Action → external/lateral rotation Nerve → Suprascapular nerve Root → C5–C6 Teres minor Action → external rotation Nerve → Axillary nerve Root → C5–C6 Subscapularis Action → internal/medial rotation Nerve → Upper and lower subscapular nerves Root → C5–C7 Classic question Cannot initiate abduction → supraspinatus/suprascapular nerve. Cannot abduct arm from 15–90° → deltoid/axillary nerve. DELTOID Action → abduction 15–90° Nerve → Axillary nerve Roots → C5–C6 Axillary nerve injury → loss of shoulder abduction Associated fracture → surgical neck of humerus Sensory loss → regimental badge area Sequence of abduction 0–15° → supraspinatus 15–90° → deltoid 90° → trapezius + serratus anterior BICEPS BRACHII Action → elbow flexion Strongest action → forearm supination Nerve → Musculocutaneous nerve Roots → C5–C6 Long head → originates from supraglenoid tubercle Short head → originates from coracoid process Clinical Musculocutaneous nerve injury → weak elbow flexion + weak supination → sensory loss over lateral forearm. BRACHIALIS Main action → elbow flexion Nerve → Musculocutaneous nerve Root → C5–C6 It is the primary flexor of the elbow regardless of forearm position. TRICEPS ⭐⭐⭐ Action → elbow extension Nerve → Radial nerve Roots → C6–C8 Long head → originates from infraglenoid tubercle. Classic Radial nerve lesion → weak elbow/wrist/finger extension. CORACOBRACHIALIS Action → shoulder flexion + adduction Nerve → Musculocutaneous nerve Root → C5–C7 Musculocutaneous nerve pierces coracobrachialis. FOREARM — ANTERIOR COMPARTMENT Superficial muscles Pronator teres Action → pronation Nerve → Median nerve Roots → C6–C7 Flexor carpi radialis Action → wrist flexion + abduction Nerve → median nerve Palmaris longus Action → wrist flexion Nerve → median nerve Frequently absent. Useful clinically for tendon grafting. Flexor carpi ulnaris Action → wrist flexion + adduction Nerve → ulnar nerve Roots → C8–T1 ANTERIOR FOREARM Flexor digitorum profundus Flexes DIP joints Lateral half → median nerve / anterior interosseous nerve Medial half → ulnar nerve Classic USMLE Cannot flex DIP of index/middle finger → anterior interosseous nerve lesion. Cannot flex DIP of ring/little finger → ulnar nerve lesion. Flexor digitorum superficialis Flexes PIP joints Nerve → median nerve. Remember: FDS → PIP FDP → DIP Flexor pollicis longus Flexes thumb IP joint Nerve → anterior interosseous nerve Pronator quadratus Main pronator Nerve → anterior interosseous nerve POSTERIOR FOREARM Main nerve → Radial nerve / posterior interosseous nerve Extensor carpi radialis longus Wrist extension + abduction Extensor carpi radialis brevis Wrist extension + abduction Extensor carpi ulnaris Wrist extension + adduction Extensor digitorum Extends fingers. Extensor pollicis longus Extends thumb. Extensor pollicis brevis Extends thumb. HAND — THENAR MUSCLES LOAF Lateral 3½ digits → median nerve Lumbricals 1 & 2 Median nerve Flex MCP Extend IP joints. Lumbricals 3 & 4 Ulnar nerve. Thenar muscles Abductor pollicis brevis → median Flexor pollicis brevis → median Opponens pollicis → median Classic Thenar atrophy + loss of thumb opposition → median nerve lesion. HAND — HYPOTHENAR Abductor digiti minimi → ulnar Flexor digiti minimi → ulnar Opponens digiti minimi → ulnar Most intrinsic hand muscles → Ulnar nerve Mnemonic: PAD/DAB PAD → Palmar interossei ADduct DAB → Dorsal interossei ABduct Both → ulnar nerve GLUTEAL MUSCLES Gluteus maximus Action → hip extension Also lateral rotation Nerve → inferior gluteal nerve Roots → L5–S2 Clinical Difficulty climbing stairs/rising from chair → gluteus maximus weakness. Gluteus medius Action → hip abduction Stabilizes pelvis during walking Nerve → superior gluteal nerve Roots → L4–S1 Trendelenburg sign Patient stands on right leg.
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Oral montelukast Explanation The immediate bronchodilator for an acute asthma exacerbation is inhaled salbutamol, preferably via a pressurised metered-dose inhaler with spacer when appropriate. The Australian Asthma Handbook recommends repeated inhaled salbutamol during the first hour according to severity AMC sequence: ipratropium. Acute asthma → SABA first → assess severity → O₂ if hypoxaemic + steroids ±
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No treatment is required Explanation: Paroxysmal coughing followed by post-tussive vomiting strongly suggests pertussis. In a clinically stable child without hypoxaemia, oxygen is not the primary treatment. Appropriate antibiotics—typically a macrolide—reduce infectivity and transmission, particularly when given early. AMC Clue Coughing fits → whoop/post-tussive vomiting → think PERTUSSIS. A mother notices a painless abdominal mass while bathing her 3-year-old child. Examination demonstrates a firm, irregular abdominal mass that extends across the midline. What is the most likely diagnosis? A. Neuroblastoma B. Wilms tumour C. Pancreatic pseudocyst D. Intussusception E. Mesenteric cyst Explanation: An abdominal mass is the most common presentation of neuroblastoma, and the disease predominantly occurs in young children Important differentiation Neuroblastoma → irregular abdominal mass → may cross the midline → often adrenal/sympathetic origin Wilms tumour → renal mass → classically painless abdominal/flank mass in a young child. A patient has a suspected Candida infection, but the appearance is atypical and the diagnosis is uncertain. What is the most appropriate investigation to confirm the diagnosis? A. No investigation B. HbA1c only C. Swab/specimen for microscopy and/or culture D. Skin biopsy routinely E. HPV PCR Explanation : A specimen for microscopy/culture can help when candidiasis is atypical, recurrent, refractory, or diagnostically uncertain. Important AMC point: if the original picture showed classic uncomplicated candidiasis, a routine swab may not be required because many Candida presentations are diagnosed clinically. Therefore, I would need the original Q89 clinical picture/stem to confirm that “Swab” is definitely the intended answer. A 58-year-old postmenopausal woman presents with an abnormal whitish vulvovaginal lesion with well-defined margins. She has been using menopausal hormone therapy. Examination confirms a persistent focal lesion. What is the most appropriate next step? A. Vaginal swab B. Biopsy of the lesion C. Reassurance only D. Increase the dose of HRT E. Empirical antifungal therapy Explanation A persistent or suspicious vulval lesion in a postmenopausal woman requires further evaluation, and biopsy is appropriate when malignancy, lichen sclerosus, lichen planus or another significant dermatosis needs to be excluded. A simple swab is more appropriate when the main concern is infection or discharge rather than an abnormal focal lesion. Queensland Health specifically flags abnormal vulval lesions in postmenopausal women for specialist assessment. AMC clue: Postmenopausal + abnormal focal vulval lesion → think biopsy, not reassurance. A 29-year-old woman who is 9 weeks pregnant presents with mild vaginal spotting. She has systemic lupus erythematosus and has previously experienced two miscarriages. She has also recently developed a lupus-type rash. Which underlying condition should be particularly suspected as the cause of her recurrent pregnancy losses? A. Chromosomal abnormality B. Cervical insufficiency C. Antiphospholipid syndrome D. Gestational diabetes E. Placenta praevia Explanation In a woman with SLE and recurrent pregnancy loss, antiphospholipid syndrome (APS) is an important diagnosis to consider. APS is associated with pregnancy morbidity including recurrent miscarriage and fetal loss. The rash suggests underlying SLE activity, but the important clue explaining the recurrent pregnancy loss is possible APS associated with SLE. RANZCOG specifically includes recurrent miscarriage and antiphospholipid syndrome among important pregnancy-related immunological conditions. AMC clue: SLE + recurrent miscarriages → think APS A 25-year-old patient with known asthma presents with acute wheeze, cough, chest tightness and increased work of breathing. An acute asthma exacerbation is diagnosed. What is the most appropriate immediate treatment? A. Oral antibiotics B. IV aminophylline C. Inhaled salbutamol via pMDI and spacer D. Long-acting beta₂ agonist alone E.
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Oral corticosteroids Explanation: The combination of chronic dry cough + postnasal drip + nasal/coryzal symptoms + normal chest X-ray strongly suggests upper airway cough syndrome (UACS), previously called postnasal drip syndrome. An intranasal corticosteroid, such as fluticasone, is appropriate first-line treatment because it reduces inflammation in the nasal and upper airway mucosa. It can be combined, when appropriate, with: Saline nasal irrigation A non-sedating antihistamine, particularly when allergic rhinitis is present. AMC Exam Pearl: Chronic cough + postnasal drip/nasal symptoms + normal CXR → Upper airway cough syndrome → intranasal corticosteroid. A 58-year-old postmenopausal woman reports a persistent burning sensation affecting her tongue and oral cavity for several months. Examination of the mouth shows normal-appearing oral mucosa with no ulcers or visible lesions. She also reports a dry mouth and altered taste. Investigations for nutritional deficiency, diabetes, thyroid disease, candidiasis, and Sjögren syndrome are unremarkable. What is the most likely diagnosis? A. Oral candidiasis B. Geographic tongue C. Burning mouth syndrome D. Oral lichen planus E. Aphthous ulceration Explanation : Burning mouth syndrome is characterized by chronic burning oral pain despite a clinically normal oral mucosa. It is particularly common in postmenopausal women and may be associated with xerostomia and altered taste. It is a diagnosis of exclusion , so secondary causes should first be ruled out, including: Oral candidiasis Iron, vitamin B12 and folate deficiency Diabetes mellitus Hypothyroidism Sjögren syndrome/xerostomia Medication effects, including some ACE inhibitors Denture-related trauma/contact allergy Geographic tongue Management Reassurance + explanation → remove/treat reversible causes → CBT Other options may include topical or low-dose clonazepam and treatment directed at neuropathic pain. AMC Key Burning mouth + normal oral examination + postmenopausal woman = Burning mouth syndrome. A 69-year-old man presents with a slowly enlarging, well-demarcated erythematous scaly plaque on a chronically sun-exposed area of his skin. The lesion has persisted for several months and does not heal. What is the most likely diagnosis? A. Basal cell carcinoma B. Actinic keratosis C. Bowen disease D. Keratoacanthoma E. Malignant melanoma Explanation: Bowen disease is squamous cell carcinoma in situ, meaning malignant keratinocytes are confined to the epidermis and have not invaded the dermis. It classically presents as a persistent erythematous, scaly or crusted plaque. Cancer Council Australia categorises Bowen disease as SCC in situ AMC clue: Persistent red scaly plaque → Bowen disease → SCC in situ. A sexually active young adult presents with multiple soft, painless, papillomatous/cauliflower-like lesions around the genital region. What is the most likely diagnosis? A. Genital herpes B. Molluscum contagiosum C. Primary syphilis D. Anogenital warts E. Lichen sclerosus Explanation: Anogenital warts are caused by human papillomavirus (HPV) and are usually diagnosed clinically from their characteristic appearance. Routine HPV PCR testing is not used to diagnose genital warts. AMC clue: Painless cauliflower/papillomatous genital lesion → HPV wart. A 25-year-old patient develops multiple symmetrical target-shaped lesions over the hands and extensor surfaces following a recent herpes simplex infection. The patient is otherwise well and has no significant mucosal involvement. What is the most appropriate initial management? A. IV immunoglobulin B. Oral prednisolone routinely C. Broad-spectrum antibiotics D. Supportive symptomatic treatment E. Emergency surgical debridement A child is brought to the GP with recurrent paroxysms of severe coughing followed by vomiting. Between coughing episodes, the child appears well. Oxygen saturation and other vital signs are normal. What is the most appropriate management? A. Supplemental oxygen alone B. Commence appropriate antibiotic therapy C. Oral corticosteroids D. Salbutamol inhaler E.
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Exam sequence: Suspected PAD → ABPI first → if ABPI unreliable in diabetes/CKD → TBI/toe pressure → Duplex Doppler for anatomical assessment → CTA/MRA if planning intervention. A 28-year-old Rh-negative pregnant woman has not attended antenatal follow-up since 22 weeks of gestation and therefore missed her routine anti-D prophylaxis. She now presents at 33 weeks and ultrasound demonstrates polyhydramnios. What is the most likely underlying cause? A. Rh alloimmunisation (Rh isoimmunisation) B. Parvovirus B19 infection C. Oesophageal atresia D. Gestational diabetes mellitus E. Fetal renal abnormality Explanation The major clue is that the mother is Rh-negative and missed routine anti-D prophylaxis. Maternal sensitisation to Rh-positive fetal red blood cells can lead to production of anti-D antibodies, which cross the placenta and cause fetal haemolysis. Pathway: Rh alloimmunisation → fetal haemolysis → severe fetal anaemia → high-output cardiac failure → hydrops fetalis → may be associated with polyhydramnios. AMC Key Point Rh-negative mother + missed anti-D + fetal anaemia/hydrops ± polyhydramnios → think Rh alloimmunisation. A 68-year-old man presents with a rapidly enlarging skin lesion on a sun-exposed area. The lesion developed over the past 6 weeks and is a dome-shaped nodule with a central crater filled with keratin. There are no features of systemic illness. What is the most likely diagnosis? A. Basal cell carcinoma B. Squamous cell carcinoma C. Keratoacanthoma D. Melanoma E. Seborrhoeic keratosis Explanation : Keratoacanthoma typically presents as a rapidly growing, dome-shaped lesion with a characteristic central keratin-filled crater. It usually enlarges over several weeks, which is much faster than many other common skin cancers. Rapid growth over 4–8 weeks Dome-shaped nodule Central keratin plug/crater Clinically resembles SCC Management → complete excision / treat as SCC, rather than observation Memory clue: “Rapid growth + central keratin crater = Keratoacanthoma. ” During an antenatal ultrasound, a pregnant woman is found to have a 4.5 cm ovarian/adnexal cyst containing multiple internal echoes with a relatively thick wall. She also reports a maternal history of breast cancer. What is the most appropriate next step? A. Reassess the cyst at the morphology ultrasound B. Measure serum CA-125 C. Immediate surgical removal D. CT abdomen and pelvis Explanation: For a relatively small adnexal cyst detected during pregnancy, the next step is generally ultrasound follow-up to reassess its size and morphology, rather than immediately relying on a tumour marker. Australian referral guidance also uses repeat ultrasound surveillance for smaller ovarian cysts when appropriate AMC pearl: Adnexal cyst in pregnancy + clinically stable → ultrasound surveillance first. Suspicious morphology/persistent or enlarging mass → specialist review. An otherwise healthy patient is found to have an isolated elevation in serum bilirubin on blood tests performed after a period of fasting. The patient is completely asymptomatic, and the remainder of the liver profile is normal. What is the most appropriate next step? A. No further investigation is required B. Abdominal ultrasound C. Hepatitis serology D. MRCP E. CT abdomen Explanation: This presentation is typical of Gilbert syndrome, a common benign condition caused by reduced activity of the bilirubin-conjugating enzyme UGT1A1. It produces a mild, intermittent unconjugated hyperbilirubinaemia, particularly during: Fasting Illness Stress Dehydration Strenuous exercise AMC Exam Pearl: Asymptomatic + isolated unconjugated bilirubin ↑ + fasting/illness trigger + normal other LFTs → Gilbert syndrome → reassurance. A man presents with a persistent dry cough associated with postnasal drip and coryzal/nasal symptoms. His chest X-ray is normal. What is the most appropriate initial treatment? A. Intranasal fluticasone spray B. Oral antibiotics C. Salbutamol inhaler D. Proton-pump inhibitor E.
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Endometriosis commonly presents with chronic or cyclical pelvic pain, dysmenorrhoea, deep dyspareunia, dyschezia, and possible subfertility. Examination may reveal pelvic/adnexal tenderness, uterosacral nodularity, or a fixed retroverted uterus, but it can also be normal. Why not PID? Acute PID usually presents over days to weeks with lower abdominal pain, cervical motion tenderness, fever, abnormal/purulent vaginal discharge, and STI-related features. The long-standing symptoms without acute infective features make endometriosis more likely. A doctor is on holiday at a beach resort with his brother-in-law, who has chronic pain following a motor vehicle accident one year ago. He regularly takes temazepam or oxycodone but has lost his prescription and does not have enough medication to last for the remainder of the trip. He asks the doctor to prescribe the medication for him. What is the most appropriate course of action? A. Recommend meloxicam as an alternative analgesic B. Arrange for him to be assessed by a local GP C. Advise him to contact his usual prescribing doctor D. Prescribe a short supply of his usual medication Explanation: The doctor should not prescribe oxycodone to a family member. Australian Medical Board guidance advises doctors to avoid treating family members except in emergencies and specifically states they must not prescribe Schedule 8 medicines to family members. Oxycodone is a Schedule 8 controlled medicine. AMC Exam Point Family/friend + controlled drug + non-emergency → do NOT prescribe → arrange independent medical assessment. Answer: B — Arrange appointment with a local GP. This situation is not an emergency. The brother-in-law has chronic pain and needs a proper, independent clinical assessment, medication-history review, and appropriate documentation. Therefore, arranging an appointment with a local GP is the safest and most professionally appropriate option. A woman is found to have a 3 cm painless cystic swelling at the posterior vaginal fourchette, consistent with a Bartholin gland cyst. What is the most appropriate management? A. Marsupialisation B. Oral antibiotics C. Incision and drainage alone D. Complete gland excision Explanation: A Bartholin cyst results from obstruction of the Bartholin duct, typically producing a swelling near the posterior vaginal introitus (4 or 8 o’clock position). Marsupialisation creates a permanent drainage opening and is commonly used for symptomatic or recurrent cysts. AMC nuance : If the cyst is genuinely small, painless and completely asymptomatic, observation is generally appropriate rather than intervention. The recall appears to be testing marsupialisation as definitive treatment for a Bartholin cyst. Exam pearl : Painful + fluctuant → think Bartholin abscess. New Bartholin mass in a woman >40 years → biopsy/excision to exclude malignancy. A 62-year-old man with a long history of diabetes mellitus presents with pain in his right toes. On examination, the right foot is cool and the dorsalis pedis pulse is weak. Peripheral arterial disease is suspected. What is the most appropriate next investigation? A. Ankle–brachial pressure index (ABPI) B. Arterial duplex Doppler ultrasound C. CT angiography of the lower limb D. MR angiography E. Digital subtraction angiography Explanation The combination of toe pain + reduced peripheral pulse + diabetes suggests peripheral arterial disease (PAD). In general practice, ABPI is the initial diagnostic test for suspected PAD. Duplex Doppler is mainly used when more anatomical information about the site and severity of arterial stenosis is required Important AMC Exam Point In patients with diabetes or chronic kidney disease, arterial calcification can make ankle arteries poorly compressible and the ABPI may be falsely normal or falsely elevated. In this situation, toe pressure / toe–brachial index (TBI) is particularly useful because toe arteries are less affected by medial calcification. Queensland Health includes both ABI and TBI in lower-limb vascular assessment pathways.
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#aug2026 AUGUST DAY 3 A 73-year-old woman presents with burning pain over the right mandibular region. The pain is not precipitated by chewing, but eating causes significant discomfort. Examination of the right buccal mucosa and palate shows unilateral erythematous erosive plaques. What is the most appropriate management? A. Famciclovir B. Antibiotics C. Fluconazole or clotrimazole D. Mouthwash HERPES ZOSTER (SHINGLES) - AUSTRALIAN GUIDELINES Early diagnosis and treatment within 72 hours reduces acute symptoms and risk of complications (e.g., PHN) OVERVIEW CLINICAL FEATURES TYPICAL RASH • Reactivation of latent Varicella zoster virus (VZV) in sensory ganglia. • Presents with unilateral, painful, vesicular rash in a dermatomal distribution. / Prodrome: burning pain, tingling, or itching in a dermatomal area / Unilateral vesicular rash on erythematous base / Severe neuropathic pain / Possible complications: • Common in older adults and immunocompromised patients. post-herpetic neuralgia (PHN), ophthalmic involvement, encephalitis (rare) Thoracic dermatome Ophthalmic (V1) involvement INVESTIGATIONS (IF UNCERTAIN DIAGNOSIS OR COMPLICATIONS SUSPECTED) TREATMENT 1ST LINE THERAPY 2ND LINE / ALTERNATIVE THERAPY • PCR for VZV DNA - most sensitive test (vesicle fluid, swab, or blood) • Antiviral therapy - start as early as possible (within 72 h • Tzanck smear - multinucleated giant cells of rash onset) & • Use if contraindicated, intolerant, or severe/immunocompromised (consider IV therapy) (less specific) • Acyclovir • Valaciclovir (alternative dosing) 800 mg 5 times daily PO for 7 days 1 g 2 times daily PO for 7 days• Serology - rarely needed (not useful in acute setting) • Valaciclovir • Famciclovir (alternative dosing) 1 750 mg 2 times daily PO for 7 days• Full blood count, U&E - if severe illness 1 g 3 times daily PO for 7 days or immunocompromised • Famciclovir • Ophthalmology review - if eye involvement 500 mg 3 times daily PO for 7 days s u s p e c t e d Severe disease / unable to take PO Acyclovir IV 10 mg/kg 8 hourly for 7-10 days (adjust for renal function) ADJUNCTIVE MANAGEMENT All above are first-line options per Australian guidelines (RACGP, Therapeutic Guidelines, eTG) for immunocompetent adults. Consult infectious diseases or hospital team for immunocompromised or disseminated zoster. Analgesia: Paracetamol or NSAIDs ‡ opioids for severe pain Neuropathic pain (e.g., PHN): Amitriptyline, Pregabalin, or Gabapentin Topical care: Keep lesions clean and dry, calamine lotion for comfort Eye involvement: Urgent ophthalmology referral + antiviral therapy SPECIAL CONSIDERATIONS • • Immunocompromised patients - more severe disease, consider IV acyclovir i • Pregnancy - antivirals can be used if needed (acyclovir preferred) & • Renal impairment - adjust dose of antivirals • Start treatment within 72 hours for best outcome, but may still benefit if started later in severe cases COMPLICATIONS • Post-herpetic neuralgia (most common) • Ophthalmic zoster → keratitis, uveitis, vision loss • Ramsay Hunt syndrome (facial palsy, ear pain) • Disseminated zoster (immunocompromised) • Bacterial superinfection PREVENTION • Recombinant zoster vaccine (Shingrix®) - recommended for: Adults ≥ 50 years Immunocompromised adults ≥ 18 years • 2 doses (0 and 2-6 months apart) • Reduces risk of shingles and PHN KEY POINTS • Start antivirals ASAP (within 72 h) • Pain control is essential • Vaccination prevents herpes zoster References: RACGP - Herpes zoster (Shingles) Management, Therapeutic Guidelines (eTG) - Antiviral, Australian Immunisation Handbook A 32-year-old woman presents with a long-standing history of chronic pelvic pain and deep dyspareunia. On pelvic examination, there is bilateral adnexal tenderness, but no adnexal mass is palpable. She has no fever or purulent vaginal discharge. What is the most likely diagnosis? A. Pelvic inflammatory disease B. Endometriosis C. Ovarian torsion D. Ectopic pregnancy E. Ruptured ovarian cyst Explanation The key clue is the chronic nature of the pelvic pain associated with deep dyspareunia.
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#aug2026 as above
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