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2015 - Year 3 Summative > Pathology > Flashcards

Pathology Flashcards

0
Q

Disc prolapse reason

A

Degeneration of annulus fibrosus -> nucleus pulposus forced out

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1
Q

Why is spinal cord injury serious (pathological changes)

A

1) neuron regeneration impossible 2) primary injury will lead to secondary injury due to hemorrhage, oedema and accumulation of necrotic cells ——— 1) Neuronal and glial cell death (1º & 2º) 2) Axontomy and intrinsic changes of injured neurons 3) Demyelination 4) Glial Scars 5) Inhibit molecules 6) Poor blood supply

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2
Q

Occlusion of PICA

A

Lateral medullary syndrome (Wallenberg syndrome) 1) Spinal trigeminal nucleus -> ipsilateral facial analgesia and thermoanesthesia 2) Spinothalamic tract -> contralateral analgesia and thermoanesthesia below neck 3) nucleus ambiguus -> dysphagia, hoarseness of voice; ipsilateral paralysis of palatal and laryngeal muscles 4) sympathetic nerve -> Horner’s syndrome

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3
Q

Wallenberg syndrome

A

PICA occlusion: Lateral medullary syndrome (Wallenberg syndrome) 1) Spinal trigeminal nucleus -> ipsilateral facial analgesia and thermoanesthesia 2) Spinothalamic tract -> contralateral analgesia and thermoanesthesia below neck 3) nucleus ambiguus -> dysphagia, hoarseness of voice; ipsilateral paralysis of palatal and laryngeal muscles 4) sympathetic nerve -> Horner’s syndrome

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4
Q

Occlusion of vertebral artery or ASA

A

Medial medullary syndrome 1) medial lemniscus -> contralateral impaired sensation of position and movement and tactile discrimination 2) corticospinal tract -> contralateral hemiparesis 3) CN XII -> ipsilateral tongue paralysis; deviation to ipsilateral side when protrude

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5
Q

Reticular formation lesion

A

Loss of life function -> death Interrupt ARAS -> sleep and coma

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6
Q

Brown-séquard syndrome

A

Hemisection of spinal cord 1) ipsilateral loss of discriminative touch and proprioceptive sense below lesion (DC/ML pathway) 2) contralateral analgesia and thermoanesthesia below lesion (spinothalamic pathway) 3) loss of all sensation at the lesion level 4) ipsilateral UMN sign below lesion (corticospinal tract) 5) ipsilateral LMN sign at lesion level

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7
Q

Pathological manifestation of cerebellar dysfunctions

A

1) Ataxia and unsteady gait 2) Error in movement range and force (intention tremor, past-pointing, dysmetria) 3) Error in movement rate and regularity (dyssynergia, dysdiadochokinesia) 4) nystagmus (normally purkinje cells exert inhibitory influence to VOR neural network) 5) Delay in initiating responses 6) hypotonus

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8
Q

Horner’s syndrome

A

Lesion of spinal cord above T1 -> sympathetic ganglion damage PAM Ptosis Anhidrosis Miosis

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9
Q

definition of raises ICP

A

Elevation of mean CSF pressure above 15mmHg when measured in lateral decubitus position

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10
Q

Raised ICP signs

A

Headache (meningeal stretching) Vomiting (brainstem distortion) Cushing’s reflex (irregular respiration, bradycardia, hypertension) Unilateral mydriasis (CN III lesion) —- Infant: separation of sutures Long term: skull bone erosion, brain atrophy

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11
Q

Brain herniation types

A

1) Subfalcine/ supra callosal 2) transtentorial/ uncal 3) reverse tentorial 4) cerebellar tonsil herniation (coning) 5) transcalvarial/ fungus

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12
Q

Raised ICP effect consideration

A

1) Age 2) stage of spatial compensation 3) rate of development 4) pressure gradient

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13
Q

Transtentorial herniation effects

A

1) compress ipsilateral CN III -> mydriasis, ophalmplegia (downward outward) 2) optic nerve and retinal vein compression -> papilloedema 2) compress aqueduct of sylvius -> hydrocephalus 3) compress vital structure - midbrain and pontine infarction and haemorrhage (loss of consciousness, bradycardia, respiration changes, hypertension) 4) contralateral cerebral peduncle pushed against tentorium -> ipsilateral hemiplegia (false localising sign) 5) compress posterior cerebral artery -> ipsilateral occipital cortex infarction -> cortical blindness

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14
Q

Tonsillar herniation effects

A

Displacement of cerebellar tonsils through foramen magnum: - compression and distortion of medulla -> apnoea

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15
Q

Hydrocephalus definition

A

CSF increase in ventricles and/or subarachnoid space

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16
Q

Brain swelling causes

A

1) cerebral oedema (vasogenic, cytotoxic, hydrocephalic) 2) congestive brain swelling due to vasodilation alone (in hypoxia, hypercapnia, loss of vasomotor tone)

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17
Q

UNN vs LMN lesion

A

Location: CNS vs CNS/PNS Structure: cortex/corticospinal tract/ corticobulbar tract vs alpha motor neurons/ motor fibres in cranial or spinal nerves Distribution: groups of muscles vs segmental muscle fibres Spastic paralysis vs flaccid paralysis Hyperreflexia vs hyporeflexia Mild disuse muscle atrophy vs pronounced muscle atrophy Babinski sign vs none

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18
Q

Common sites of metastatic intracranial tumour

A

~25% Lung, breast, kidney and malignant melanoma Metastatic choriocarcinoma common in Chinese female

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19
Q

Primary intracranial carcinoma classified by origin

A
  1. Neuroectodermal tumours a. Glial cells (gliomas) - astrocytoma - ependymoma - oligodendroglioma - etc b. Neurons and primitive cells - neuroblastoma - medulloblastoma 2. Other structure tumours E.g. Meningioma, schwannoma, pituitary adenoma, carniopharngioma, haemangioblastomas
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20
Q

Supratentorial intracranial tumours

A

CEREBRAL LOBE AND DEEP HEMISPHERE - astrocytoma - glioblastoma - meningioma - metastatic tumours SELLA TURCICA - pituitary adenoma - carniopharyngioma

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21
Q

Intracranial tumours in ventricular system

A

Ependymoma Choroid plexus papilloma

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22
Q

Sites of cerebral astrocytoma, glioblastoma and oligodendroglioma

A

Commonly in frontal and temporal lobe; uncommon in occipital lobe

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23
Q

Biological malignancy of intracranial tumours

A

1) while histologically well differentiated, neuroectodermal tumours are rarely encapsulated and diffusely infiltrate tissues 2) may be in inoperable sites e.g medulla, pons, midbrain or deep hemisphere 3) may become histologically malignant with years, esp astrocytoma to glioblastomas multiforme

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24
Q

Spread of poorly differentiated neuroectodermal tumours

A

Spread within brain and spinal cord, by direct infiltration or CSF spread Rarely metastasise outside CNS

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25
Q

Most common site for adult intracranial tumour

A

Supratentorial in the cerebral lobes (70%)

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26
Q

Common CNS tumour and site in children

A

70% infratentorial Posterior fossa in midline, usually: - Cerebellum (astrocytoma, medulloblastoma) - brainstem (astrocytoma, ependymoma)

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27
Q

Astrocytoma histological types

A

Protoplasmic Pilocytic Gemistocytic Fibrillary

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28
Q

Astrocytoma grading

A

1 to 4 Grade 2: Nuclear pleomorphism (astrocytoma grade 2) Grade 3: mitotic activity (anaplastic astrocytoma) Grade 4: necrosis, endothelial hyperplasia (glioblastoma multiforme)

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29
Q

Astrocytoma gross appearance

A

Diffuse infiltration thus no clear border Cerebral astrocytoma: diffuse enlargement of region Cerebellar astrocytoma: cystic with proteinaceous fluid

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30
Q

Glioblastoma multiforme histology

A
  • Variable histology - pseudo palisade - central necrosis zone surrounded by degenerate tumour with extensive cytoplasmic pleomorphism - endothelial hyperplasia
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31
Q

Oligodendroglioma gross and histo

A

Grossly well differentiated with little necrosis Histo: box like cells with clear halo Well marked cell border Calcification common

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32
Q

Ependymoma gross and histo

A

Gross: mass protruding into ventricles, encapsulated Histo: - rosette (cuboidal tumour cells around central lumen) - pseudo rosette (pink Fibrillary halo around vessels) - spindle cells - blepharoplasts

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33
Q

Medulloblastoma histo

A

Good radiotherapy response Histo: - small cells - densely stained ovoid nuclei - little cytoplasm - rosette formation with Central Fibrillary extension

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34
Q

Meningioma Gross and histo

A

Well circumscribed and lobulated Histo: - cellular whorls - psammoma bodies Site: parasagittal, fall cerebri, base of skull, inner surface of calvaria

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35
Q

Schwannoma sites

A

Most commonly cranial nerve roots: - Vestibulocochlear nerve - Trigeminal nerve Can be in spinal nerve root or peripheral nerve

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36
Q

Schwannoma histo

A

Antoni type A & B (Read)

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37
Q

Xerostomia definition and cause

A

Def: USF reduce by 50% Cause: 1) water or electrolyte loss 2) damage to salivary gland 3）interference with neural transmission

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38
Q

Rhinitis classifications

A

Allergic rhinitis Infectious rhinitis Occupational rhinitis Drug induced rhinitis

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39
Q

Sinusitis radiological finding

A

X Ray: -air fluid level -sinus opacification

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40
Q

Sinusitis complication

A

Extension of infection to: Orbital cellulitis Orbital abscess Cavernous sinus thrombosis

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41
Q

Sinusitis pathogenesis

A

Anatomical or functional obstruction of normal mucociliary clearance of sinuses -> Fluid accumulation in sinus or ostemeatal complex -> Infection

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42
Q

Otitis media pathogensis

A

Ear canal skin inflammation Swelling blocking rapid cell turnover More dead skin produced, which allow germ breed Pus filled ear canal Tympanic membrane bulge outwards, leading to pain, fever, hearing loss (AOM) Tympanic membrane bursts and perforation, discharge of pus (active CSOM) Perforation persists, discharge stops (inactive CSOM)

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43
Q

Otitis media complications

A

TM rupture with pus discharge Mastoid abscess if pus moves in Facial nerve palsy or CN VI Brain abscess

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44
Q

Otitis media pathogens

A

Viral or bacteria (S pneumoniae, HI)

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45
Q

Tonsillitis pathogen

A

Bacterial: s pyogenes, Staphylococci, S pneumoniae, HI Viral: rhinovirus, adenovirus, EBV Others: diphtheria, syphilis, TB, candida

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46
Q

Clinical features of tonsillitis

A

Fever Sore throat Odynophagia Otalgia Trismus Red swollen tonsils Throat redness Swollen uvula Gary furry tongue Whitish spots ALWAYS BILATERAL

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47
Q

Sialoadenitis pathogensis

A

1) ascending duct infection related to dehydration and debilitation e.g. Old age –> thicker more mucous salvia that stuck in ducts –> infection OR 2) secondary to ductal obstruction e.g. Stones (submandibular duct most likely)

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48
Q

Sialoadenitis pathogen

A

Viral: Mumps Coxsackievirus HIV Echovirus Bacterial: Staphylococcus TB Syphilis No infectious: Sjogren’s

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49
Q

Acute epiglottitis presentation

A

Children 2-4 yo Fever Severe sore throat Stridor Dysphonia Drooling Laryngoscopy: cherry red epiglottis XR neck: thumb sign Blood culture: HIB

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50
Q

HI microbiology

A

Gram negative Beta lacamase producing Coccibacilli Factor V and X for growth Type a to f, b most invasive

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51
Q

Epiglottitis management

A

Airway protection Antibiotic (amoxiclav) Rifampicin prophylaxis HIB vaccination

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52
Q

Quinsy presentation

A

Adolescents and young adults Low grade fever Severe sore throat Stridor (if bilateral) Dysphagia Medial deviation of tonsils

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53
Q

Epiglottitis pathogen

A

HiB

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54
Q

Quinsy pathogen

A

GAS (strep pyogenes) Mixed oropharyngeal organisms: anaerobes, viridans streptococcus

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55
Q

GAS microbiology

A

Beta hemolytic Lancefield group A Bacitracin sensitive

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56
Q

Strep pneumoniae microbiology

A

Alpha hemolytic Optochin sensitive Bile soluble

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57
Q

Croup (laryngotracheobronchitis) presentation

A

Young children of 3 months to 3 yo Fever Barking cough Tripod position Hoarseness Stridor XR neck: subglottic swelling - hourglass or steeple sign Nasopharyngeal aspirated (NPA) - viral antigens

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58
Q

Quinsy management

A

Airway protection Antibiotic Abscess drainage

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59
Q

Croup pathogen

A

Viral mainly: Parainfluenza Influenza Respiratory syncytial Adenovirus Rhinovirus Mycoplasma

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60
Q

Croup management

A

Airway protection Racemic adrenaline +- steroid

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61
Q

Deep oropharyngeal fascial space infections

A

1) submandibular and sublingual space (Ludwig’s agina) 2) lateral pharyngeal space 3) retropharyngeal space

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62
Q

Ludwig’s angina presentation

A

Board like floor swelling High fever Systemic toxicity Dysphagia Often with dental root abscess

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63
Q

Ludwig’s angina management

A

Airway protection Antibiotic Soft tissue decompression Dental assessment

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64
Q

Lateral pharyngeal space infection presentation

A

Fever Sore throat Dysphagia Neck stiffness Jaw angle swelling Great pain and trismus (if ant) Great dyspnea (if post) CT/MRI to see extension Blood culture Pus culture

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65
Q

Lateral pharyngeal space infection complications

A

Jugular venous thrombophlebitis Carotid artery erosion

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66
Q

Lateral pharyngeal space infection management

A

Airway protection Antibiotic Surgical drainage (if abscess) Treat primary infective focus

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67
Q

Prothrombin time

A

Extrinsic and common pathway -> I, II, V VII X

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68
Q

APTT

A

Activated partial thromboplastin time Intrinsic and common pathway -> all factors except VII and XIII

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69
Q

Thrombin time

A

Fibrinogen deficiency or dysfunction Thrombin inhibition e.g by heparin

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70
Q

Bleeding disorder lab tests

A

PT APTT TT fibrinogen level Platelet tests -> platelet count, platelet function test by aggregometry, skin bleeding time

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71
Q

Platelet disorder presentation and classes

A

All present with mucocutaneous bleeding Autoimmune thrombocytopenia Alloimmune thrombocytopenia -neonatal allo TP -post transfusion purpura -platelet refactoriness Inherited -Bernard-soulier syndrome -grey platelet syndrome -storage pool disease -glanzmann’s thrombasthenia DIC dilutional (eg after massive transfusion)

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72
Q

Haemophilia A gene linkage

A

Long arm of X chromosome -> x linked Maternal side 1/3 are due to spontaneous mutation

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73
Q

Haemophilia A and B problem

A

Haemarthrosis -> recurrent bleeding in major joints leading to progressive joint deformity Inhibitor to infused factor concentrate -> replacement therapy less effective High cost of treatment Transfusion transmitted infection (esp viral HIV HBV HCV) Carrier female detection

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74
Q

VWD genetic

A

Short arm of chromosome 12

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75
Q

VWD lab test

A

Increased APTT Increased bleeding time VWF antigen assay Ristocetin assay Collagen binding assay Factor VIII assay

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76
Q

Other hereditary coagulation disorder

A

Deficiency of VII XII X fibrinogen Autosomal recessive

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77
Q

Vit K deficiency causes

A

Obstructive jaundice Malabsorption Post oral broad spectrum antibiotics that killed intestinal flora

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78
Q

Haemorrhagic disease of newborn

A

Immature liver that cannot perform K dependent post translation gamma carboxylate on of glutamic acid on II VII IX X C S sterile gut with no intestinal flora for K production Low vit K in breast milk

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79
Q

INR

A

International normalised ratio INR = (PT/ mean normal PT)^ ISI ISI is international sensitivity index Used for monitoring oral anticoagulant so no vitamin K antagonism occur

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80
Q

Vitamin antagonism

A

Result of oral anticoagulant usage Competitive inhibitor of vitamin K epoxide reductase needed for recycling vitamin k during gamma carboxylation

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81
Q

Liver disease and bleeding aetiology

A

Reduced hepatic synthesis of clotting factors and inhibitors (except VIII and VWF) Reduced vit K absorption due to cholestasis -> further decrease clotting factor production Failure of reticuloendothelial cells to clear activated products and intermediates of coagulation and fibrinolysis -> interfere with platelet function and fibrin formation Portal hypertension -> hypersplenism -> platelet sequestration Acquired dysfibrinogenaemia -> abnormal fibrinogen synthesis

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82
Q

Liver induced coagulation disease treatment

A

Parenteral vit K replacement Clotting factor replacement via FFP

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83
Q

Uraemia and bleeding tendency aetiology

A

Defect in platelet function (inhibition by nitric oxide) Low haematocrit -> Platelet-vessel wall interaction

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84
Q

How to treat uraemia bleeding tendency

A

Increase haematocrit by red cell transfusion erythropoietin therapy Peritoneal or haemodialysis DDA VP administration Cryoprecipitate transfusion

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85
Q

DIC pathogenesis

A

Entry of tissue thromboplastin into blood stream Direct activation of coagulation Severe endothelial injury Direct activation of platelet Thrombin activation which convert fibrinogen to fibrin, activating secondary fibrinolysis Widespread coagulation —> intravascular fibrin formation —> micro thrombotic occlusion of small vessels —> tissue ischaemia and multi organ dysfunction Widespread coagulation and fibrinolysis depletes clotting factors, platelets and coagulation inhibitors —> severe bleeding

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86
Q

Causes of DIC

A

Infection (septicaemia and viral infection) Trauma (serious tissue injury, fat embolism, extensive burns) Cancers (acute promyelochtic leukemia, metastatic carcinoma) Obstetric condition (septic abortion, amniotic fluid embolism, abruptio placentiae) Immunological (haemolytic blood transfusion reaction eg ABO incompat; organ transplant rejection)

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87
Q

DIC diagnosis

A

Underlying related condition Increase PT APTT TT Reduced fibrinogen level, low antithrombin Thrombocytopenia Increase fibrin degradation product namely D-dimers from secondary fibrinolysis Microangiopathic change in blood film as RBC damaged when passing through clots

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88
Q

DIC. Management

A

Platelet transfusion FFP to replenish clotting factors Anticoagulants (to overt thromboembolism or extensive fibrin deposition) Antithrombin concentrate *** treat precipitating trigger first!!

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89
Q

IPEX

A

Autoimmune disease X linked single gene deletion Immune dysfunction Polyendocrinopathy Enteropathy X linked Deletion in foxp3 transcription regulator -> loss of Treg cells (Cd4 Cd25 foxp3)

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90
Q

Autoimmune aetiology

A

Lack of Treg cells (IPEX) Release of sequestrated antigens (sympathetic ophthalmia, vasectomy) Induction of MHC II antigen on non-APC (interferon gamma on thyroid epithelial cells) Cross reaction between microbial antigen and similar autoantigen (rheumatic heart disease)

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91
Q

Autoimmune disease factors

A

Genetic Hormonal Environmental (infective, drug)

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92
Q

Genetic factors in autoimmune

A

Demonstrates familial clustering and higher concordance rate in identical twins No clear mandelian traits Multiple genes involve with low penetrance Genetic heterogeneity MHC gene esp associated -> HLA-DR4 and rheumatoid arthritis; HLA-DR3/4 and IDDM

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93
Q

Hormonal factors in autoimmune

A

Sex preponderance in many SLE female:male = 9:1 (admin of male sex hormone and female castration helps with SLE in mice)

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94
Q

Infective factor and autoimmune

A

IDDM and rubella or enterovirus infection

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95
Q

Drug induced autoimmune

A

SLE - hydrallazine, penicillamine Hemolytic anaemia - methyldopa

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96
Q

Environment factor and autoimmune

A

Drug, infection SLE -> Sun exposure

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97
Q

Neutrophilia causes

A

1) infection (bacterial fungal) 2) Acute inflammation 3) tissue damage/ infarction 4) MPN 5) drugs eg corticosteroids

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98
Q

Neutropenia causes

A

Infection (neonate) Leukemia, metastases Aplastic anaemia Drugs Myelofibrosis Cyclical

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99
Q

Lymphopenia causes

A

HIV AIDS Drugs eg corticosteroid

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100
Q

Lymphocytosis causes

A

Children: Viral infection (CMV), sometimes bacterial (pertussis) Adolescent: Viral (EBV) Adult: Chronic lymphocytic leukemia, acute stress

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101
Q

Eosinophilia causes

A

Allergy Parasitic infection Drug hypersensitivity Autoimmune Neoplasm

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102
Q

Basophilia causes

A

Chronic myelogenous leukemia (CML) Acute leukemia

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103
Q

Monocytosis

A

Chronic infection eg TB chronic inflammation Neoplasm: CML, other MPN MDS

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104
Q

Crude Haematological findings in AML ALL CML CLL and MDS

A

AML -> presence of blast cells; auer rods ALL -> blast cells CML -> basophilia, mature and immature CLL -> abnormal mature looking lymphoid cells MDS -> funny looking white and red cells; abnormal nucleus shape

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105
Q

Functional white cells disorders

A

Lazy leukocyte syndrome -> defect in chemotaxis Opsonin deficient -> defect in phagocytosis Chronic granulomatous disease, myeloperoxidase deficiency -> defect in killing or digestion

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106
Q

WBC disease investigations

A

1) PBS, CBC 2) Bone marrow - BMA or - touch imprints - trephine biopsy 3) cytochemistry staining - non specific esterase (AML) - myeloperoxidase (AML) - PAS (ALL) 4) flow cytometry 5) lymph node / other tissue biopsy 6) cytogenetic karyotypin 7) FISH 8) PCR

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107
Q

Both quality and quantity abnormality WBC disorder

A

B cell - X linked agammaglobulinaemia - severe combined immunodeficiency T cells - DiGeorge syndrome - MHC class II deficiency

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108
Q

Multiple myeloma (presentation, diagnosis)

A

Plasma cell neoplasm Present as: Anaemia Bone pain Recurrent infection Renal failure PBS-> rouleaux formation; no abnormal white cells Bone marrow-> plasma cells 30% and clinal Urine/ serum -> monoclonal protein

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109
Q

BMA usage in WBC disorder diagnosis

A

Assessment of BM cellularity and differential counts Identification of abnormal cells Stain with Wright-Giemsa stain

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110
Q

BM trephine biopsy usage in WBC disorder diagnosis

A

Assess BM cellularity Identification of abnormal cells Assess architecture and topographic relationship of cells in BM staging of lymphoma

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111
Q

Cytogenetic karyotyping limitations

A

There might be no metaphase cells

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112
Q

What is a blood cancer

A

Malignancy arising from haematopoietic system or lymphpoietic system

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113
Q

Lymphoma definition

A

Clonal malignancy of lymphoid system (ie from lineage B cells T cells NK cells)

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114
Q

Aetiology of lymphoma

A

Increase with age Related to viral infection - EBV, HIV HTLV human T cell lymphoproliferative virus

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115
Q

Lymphoma manifestation

A

1) enlargement of nodal (lymph node) or extranodal tissues 2) A symptoms -> asymptomatic 3) B symptoms -> systemic, eg Fever, night sweats, loss of body weight

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116
Q

Lymphoma classifications

A

Hodgkin lymphoma B cell lymphoma T cell lymphoma NK cell lymphoma

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117
Q

Lymphoma metastasis

A

Via lymphatics (Hodgkin) Hematogenous spread in other types of lymphoma Local infiltration to different organs

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118
Q

B cell lymphoma treatment

A

1) R-CHOP chemotherapy + targeted therapy Rituximab anti CD20 cyclophosphamide, hydroxydaunorubicin, vincristine [Oncovin], prednisone (Purine analogue containing regimen for low grade; mab for maintenance treatment) 2) HSCT autologous HSCT for relapses lymphoma (Source from peripheral blood, BM) If there is BM involvement, then allogenic HSCT

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119
Q

Hodgkin lymphoma treatment

A

1) chemotherapy with/wo radiotherapy 2) Mab against CD30 for relapse 3) autologous HSCT for relapse

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120
Q

NK lymphoma treatment

A

1) chemotherapy, esp L-asparaginase containing regimen 2) otherwise similar to B cell

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121
Q

T cell lymphoma treatment

A

Similar to B cell lymphoma 1) early use of autologous HSCT may be useful

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122
Q

Hodgkin lymphoma nature

A

Less common in Chinese Good prognosis; most patients curable

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123
Q

NK cell lymphoma nature

A

Found mainly in Asians (ninja!) Nose affected as main site EBV related Highly aggressive with poor prognosis

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124
Q

T cell lymphoma nature

A

Uncommon Variable prognosis Related to HTLV-1 (Japan and TW)

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125
Q

Lymphoma prognosis

A

1) International prognostic index -tumour stage - serum LDH - extranodal sites - age -performance 2) Histology types -lineage - high/low grade 3) chemotherapy intensity

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126
Q

AML clinical features

A

-adults -myelosuppresion -> anaemia and thrombocytopenia -leucocytosis with >20% blasts in BM and blood -associated with toxic exposure, toxic drugs and antecedent myelodysplastic syndrome - Auer rods

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127
Q

AML treatment

A

Induction of remission Consolidation of remission with high doses of chemotherapy Maintenance of remission usually not given HSCT for relapse or high risk cases All trans retinoids acid and arsenic trioxide for acute promyelocytic leukemia

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128
Q

ALL clinical features

A

-mainly adults, sometimes children - leucocytosis -myelosuppresion -> anaemia and thrombocytopenia -enlargement of lymph nodes, liver and spleen as lymphoblastic cells return to origin - CNS involvement -not obviously associated with toxic exposure B cell origin?

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129
Q

ALL treatment

A

Induction of remission Consolidation chemotherapy Maintenance treatment for 2 years CNS prophylaxis HCST transplant in relapse or high risk

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130
Q

CML clinical features

A

-adults; incidence increase with age -leucocytosis with mature and immature cells, basophilia -enlarged liver and spleen -associated with irradiation exposure eg atomic bomb -triphasic if untreated: 1) chronic 3-4y 2) acceleration <6m 3) blastic crisis 1-2 months -Philadelphia gene - BCR-ABL 9-22 translocation (cytogenetic karyotyping or FISH or PCR)

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131
Q

CML treatment

A

Chemotherapy ineffective Targeted therapy with tyrosine kinase inhibitors (eg imatinib dasatinib bosutinib I’m da boss) Hydroxyurea for symptomatic treatment HSCT for blastic transformation patient or not responding to TKI

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132
Q

CLL clinical features

A

-elderly, never in childhood -uncommon in Chinese -late stage myelosuppresion -> anaemia and thrombocytopenia -lymph node enlargement, late stage liver and spleen enlargement -leucocytosis with mature cells -associated with toxic exposure, toxic drugs and antecedent myelodysplastic syndrome

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133
Q

CLL treatment

A

No early stage treatment Chemotherapy with Purine analogue (oral alkylation agent not preferred in <50

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134
Q

MDS clinical features

A

Pancytopenia Hyper cellular BM Myelodysplastic blood cells in blood or BM BM abnormal karyotyping Increased blasts Progress to AML Associated with previous chemotherapy irradiation or toxic exposure

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135
Q

MDS classes

A

Refractory cytopenia with unilineage dysplasia Refractory cytopenia with multilineage dysplasia Refractory anaemia with ringed sideroblasts Refractory anaemia with excess blasts MDS with 5q- Childhood MDS

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136
Q

MDS diagnosis

A

PBS CBC -> pancytopenia BMA -> hypercellularity Cytogenetic -> monosomy 5 or 7, deletion of long arm of 5 or 7 5q- 7q-

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137
Q

MDS management

A

1) risk stratification 2) supportive, transfusion for most - erythropoietin for anaemia - iron chelation for chronic transfusion 3) allogeneic HSCT in younger patients for RAMD RAEB 4) lenalidomide for 5q- syndrome 5) demethylating agents (eg azacytidine decitabine)

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138
Q

MDS prognosis

A

Incurable except in young patients after HSCT May transform to AML, especially in RAEB

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139
Q

MPN features

A

Clonal disease of pluripotent HSC 1) increased circulating cells of all haematopoietic lineages 2) hypercellularity in BM 3) absence of muelodysplastic features Pre-leukemia

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140
Q

MPN common subtypes

A

CML -> myeloid Polycythaemia Vera -> erythroid Primary myelofibrosis -> fibrous tissue Essential thrombocythaemia -> megakaryocytic

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141
Q

MPN genetic mutations

A

CML -> BCR-ABL1 PV -> JAK2 MF -> 50% JAK2; 40% CALR ET -> 50% JAK2; 40% CALR CALR = calreticulin gene

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142
Q

PV features

A

MPN *) pruritus 1) high Hb -> facial plethora 2) leucocytosis thrombocytosis 3) splenomegaly 4) suppressed serum erythropoietin diagnosis by exclusion JAK2 mutation

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143
Q

PV treatment

A

Venesection -> replace venesected blood with normal saline Cytoreduction with hydroxyurea Avoid secondary leukemia inducing agents eg alkylating agents or radioactive phosphorus Thrombosis prophylaxis eg aspirin

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144
Q

Primary myelofibrosis features

A
  • Hepatosplenomegaly; Extramedullary hematopoiesis, which is non functional Leuco-erythroblastic picture with tear drop RBC JAK2, CALR mutation Diffuse fibrosis of BM -> megakaryocytic proliferation Terminally present with hepatic fibrosus -> variceal bleeding and portal hypertension CELLULAR PHASE (prefibrotic) -anaemia -leucocytosis -thrombocytosis FIBROTIC PHASE -pancytopenia
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145
Q

Primary myelofibrosis management

A

1) supportive 2) early splenectomy helps to decrease blood transfusion requirement 3) alligeneic HSCT in younger patient 4) JAK2 inhibitor for high risk 5) Cytoreduction with hydroxyurea 6) avoid secondary leukemia inducing agents eg alkylating agents or radioactive phosphorus

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146
Q

ET features

A

Sustained thrombocytosis (must exclude chronic inflammatory disorder, infection, neoplasm) JAK2 CALR mutation

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147
Q

ET treatment

A

Treatment not required in young patient Prophylactic anti thrombotic agents eg aspirin esp in elderly Cytoreduction with hydroxyurea Anagrelide to reduce platelet count Avoid leukarmogenic agents eg alkylating agents or radioactive phosphorus

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148
Q

MDS/MPN feature

A

Increased circulating cells Hypercellularity of BM Myelodysplastic features of blood cells

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149
Q

MDS/MPN classification

A

Chronic myelomonocytic leukemia (CMML) atypical chronic myeloid leukemia (aCML)

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150
Q

CMML features

A

Elderly Monocytic lineage proliferation High monocyte count No Philadelphia chromosome

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152
Q

Cortical lesion of S1

A

Contralateral loss of discriminative touch and position sense; thermoception and nociception relatively unaffected

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153
Q

Lesion of association somatosensory cortex

A

Tactile agnosia - inability to recognise object despite sensation Constructional apraxia - deficit in ability to relate extra personal space Neglect syndrome (contralateral) Spatial orientation difficulty eg map reading, driving

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154
Q

MDS/MPN management

A

Supportive in elderly patients Allogeneic HSCT in children Tyrosine kinase inhibitor for some CMML

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155
Q

Thalamic pain syndrome

A

Lesions in the Ventral Posterior nuclei of thalamus (VPM, VPL) Analgesia followed by paraesthesia and hyperalgesia or even severe spontaneous pain; associated with exaggerated affective response

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156
Q

Lesion of M1

A

Interferes with motor proficiency and manual dexterity Independent control of fingers may be lost (corticospinal tract)

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157
Q

Lesion of PMA

A

Paresis or weakness of axial and proximal muscles (medial descending system) Interfere with choreography of complex movement (complex movement possible but slow execution) Severely affects visually guided movement

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158
Q

Lesion of SMA

A

Interferes with goal-directed behaviours that require planning and execution of complex motor sequence e.g. circumventing a transparent screen deficit in bimanual coordination

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159
Q

Unilateral UMN lesion of corticobulbar tract

A

No symptoms for CN III IV V VI upper face (VII) IX X XI Contralateral symptoms for lower face VII (e.g. lower face paralysis, sagging mouth corner obicularis oris) and XII (tongue deviate to contralateral side of lesion)

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160
Q

Unilateral LMN lesion of corticobulbar tract

A

Ipsilateral LMN symptoms for cranial nuclei III-XIII except VIII

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161
Q

Unilateral supranuclear facial paralysis

A

UMN lesion of corticobulbar tract Contralateral lower face paralysis (sagging mouth corner - orbicularis oris)

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162
Q

Unilateral peripheral facial paralysis

A

LMN lesion of corticobulbar tract Ipsilateral upper and lower face paralysis (incomplete closure of eyelid - obicularis oculi; sagging mouth corner - orbicularis oris)

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163
Q

Lentico-striate artery occlusion

A

Leads to capsular infarction/ haemorrhage -> internal capsule function affected UMN paralysis of contralateral limbs and lower face

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164
Q

Causes of UMN lesion

A

Lentico-striate artery occlusion -> capsular infarction MCA infarction Pontine infarction Corona radiata tumour etc.

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165
Q

UMN vs LMN lesions

A

CNS vs CNS/PNS Involve cortex, corticospinal or corticobulbar tract vs alpha motor neuron, motor fibres of cranial or spinal nerves Distribute to groups of muscles vs segmental muscles Spastic paralysis (antigravity muscle, clasp-knife rigidity) vs flaccid paralysis Hyperreflexia vs hyporeflexia Mild disuse atrophy of muscle vs pronounced atrophy Babinski’s sign vs no Babinski’s sign

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166
Q

Lesion above red nucleus (midbrain)

A

Decorticate posturing: Rubrospinal cord intact, therefore UL flexion (elbow and wrist flexed) - wrist flexed - leg extended - plantar flexion

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167
Q

Lesion between red nucleus and vestibular nucleus

A

Decerebrate posturing/rigidity Unopposed pontine reticular nucleus and vestibular nuclrus -> extensor activities –> UL extension (extension of elbow, pronation) - wrist flexed - leg extended - plantar flexion

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168
Q

Visual field defect in optic nerve lesion

A

Monocular amaurosis (ipsilateral) e.g. in optic neuritis

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169
Q

Visual field defect in optic chiasma lesion

A

Bitemporal hemianopia e.g. pituitary macroadenoma

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170
Q

Visual field defect in optic tract lesion

A

Homonymous hemianopia (contralateral side of visual field busted in both eyes) e.g. craniopharyngioma

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171
Q

Visual field defect in optic radiation lesion

A

Temporal: homonymous upper quadrantic hemianopia Parietal: homonymous lower quadrantic hemianopia

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172
Q

Visual field defect in visual cortex lesion

A

Dense homonymous hemianopia with macular sparing

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173
Q

Prefrontal cortex lesion

A
  • primitive reflex(grasp, snout, suck, rooting) - high distractibility - lack of foresight/insight - inability to switch tasks - lack of ambition/ responsibility - lack of social propriety and self-monitoring
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174
Q

Limbic lesion

A
  • Amnesia - Flat emotion/ affect - Akinetic mutism
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175
Q

Types of aphasia

A

Expressive (Broca’s) non-fluent Receptive (Wernicke’s) fluent Global

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176
Q

Mental retardation defintion

A

2 SDs less than mean intelligence; never had a normal IQ

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177
Q

Dementia definition

A

loss of previously acquired intelligence

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178
Q

Causes of dementia

A

1) Primary neurodegenerative dementia - alzheimer’s - Lewy bodies 2) Vascular dementia - infarct ——–uncommon— 3) Infective dementia - e.g. syphilis, AIDS, CJD 4) Intracranial pathology - tumour - hydrocephalus - subdural hematoma 5) Chronic alcoholism etc.

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179
Q

Vascular dementia

A

History of stroke Abrupt decline Focal neurological signs Management: Stroke prevention

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180
Q

Spinal cord injury repair strategy

A

1) Neuronal and glial cell death (1º & 2º) - reduce cell death with methylprednisolone - block death receptor activation to reduce 2º injury - Stem cell transplant to replace neurons 2) Axontomy and intrinsic changes of injured neurons - Enhance regeneration by modifying intrinsic environment e.g. increase cAMP, inhibit PKC 3) Demyelination - Oligodendrocyte or Schwann cell transplant 4) Glial Scars 5) Inhibit molecules 6) Poor blood supply - reduce glial scar and inhibit molecules by enzymes, antibodies

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181
Q

Ectopic Thyroid Tissue

A

may be found anywhere along the path of descent of the thyroid gland. It is commonly found in the base of the tongue or with the lateral cervical lymph nodes.

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182
Q

Thyroglossal duct cyst

A

found anywhere along the path of descent of the thyroid gland, but always in the midline of the neck Sometimes connected to the outside by a canal, a thyroglossal fistula

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183
Q

Ectopic parathyroid tissue

A

persist along the path of migration (may be as low as aortic arch) Can be visualised by Parathyroid scintigraphy dual phase planar imaging

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184
Q

Parathyroid scintigraphy dual phase planar imaging

A

Patients are injected with tracer (Tc99m, Technetium -99m) and imaged at 5 min and images repeated at 2h. This radiotracer is taken up by the thyroid gland, but cleared from the thyroid with a half-life of 30 min. It is usually retained by abnormal parathyroid tissue

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185
Q

Recurrent laryngeal nerve injury

A

(normally supplies all laryngeal muscles except cricothyroid; especially important as it innervates superior cricoarytenoid muscle, the only abductor of vocal cords) Unilateral: Hoarseness, dysphagia, partial (abductor) paralysis of the vocal cord Bilateral: Bilateral (abductor) paralysis of vocal cord, airway obstruction, which may leads to death

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186
Q

Pituitary adenoma classification

A

1) By size: Macroadenoma 1cm+; microadenoma 1cm - 2) - Functional (hormone overproduction with clinical manifestation) or - silent (hormone overproduction without clinical manifestation) or - hormone negative

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187
Q

Pituitary adenoma histology

A

Monotonous pinkish secretory cells - uniform polygonal cells in sheets/cord Rare mitosis, little pleomorphism Increased vascularity

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188
Q

GH hypersecretion causes

A

PRIMARY: 1) pituitary adenoma (acidophil cell tumour) SECONDARY: 1) Hypothalamic tumour releasing GHRH 2) Ectopic GH or GHRH from lung cancer or pancreatic cancer

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189
Q

GH hypersecretion pathology

A

Gigantism in children; Acromegaly in adults Symptoms: 1) outgrowth of all organs, bones, joints and soft tissues (excessive height in gigantism; skeletal overgrowth with large nose feet hands on acromegaly) 2) hyperglycaemia (osmotic diuresis?)

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190
Q

GH deficiency causes

A

PRIMARY: 1) idiopathic in childhood 2) Pituitary tumours e.g. Silent or hormone negative pituitary adenoma; carniopharyngioma

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191
Q

GH deficiency pathology

A

Pituitary dwarfism in children Symptoms: 1) delayed physical maturation 2) short stature 3) reduced skeleton and muscular mass - affected walking jumping and standing 4) sparse hair growth and frontal recession

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192
Q

GH secretion tests

A

1) Blood test for GH or IGF-1 - difficult as t1/2 is short 2a) Functional test - stimulation test - insulin tolerance test - arginine infusion test 2b) functional test - suppression test - glucose tolerance test

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193
Q

GH deficiency functional test

A

Arginine infusion test and insulin resistance test Arginine and insulin normally reduces plasma glucose, thus increasing GH secretion -> if GH not increased, GH hyposecretion

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194
Q

GH over secretion functional test

A

Suppression test (glucose tolerance test) Increased glucose normally lead to reduction of GH secretion If GH level not decreased, then GH hypersecretion

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195
Q

Hyper prolactinemia causes

A

PRIMARY: 1) prolactinoma (a pituitary adenoma) SECONDARY: 1) pregnancy 2) psychiatric medications

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196
Q

Hyper-prolactinemia symptoms

A

Men: loss of libido, impotency, low sperm count, gynaecomastia Women: menstrual disturbances (amenorrhea), galactorrhea, loss of libido, infertility

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197
Q

ACTH hypersecretion causes and pathology

A

Cause: pituitary adenoma Pathology: Cushing’s disease (secondary hypercortisolaemia) - ACTH and Cortisol increased - symptoms: Cushing’s syndrome

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198
Q

Cushing’s disease definition

A

Hypercortisolaemia (Cushing’s syndrome) caused by increased ACTH production due to pituitary adenoma

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199
Q

ACTH hyposecretion causes and pathology

A

Causes: inefficient pituitary production; or use of exogenous steroids Pathology: secondary hypocortisolism (secondary adrenal insufficiency) - reduced ACTH and cortisol - Nausea, vomiting - fatigue, weakness, hypotension - hyperpigmentation and hyperkalemia NOT SEEN

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200
Q

TSH hypersecretion causes and pathology

A

Cause: pituitary adenoma Pathology: secondary hyperthyroidism - increase TSH and TH

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201
Q

TSH hyposecretion pathology

A

Secondary hypothyroidism - decrease TSH and decrease TH

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202
Q

LH and FSH hyposecretion

A

Hypogonadotropic hypogonadism female: - breast atrophy - vaginal dryness - reduced libido Male: - reduced libido - impotency

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203
Q

Panhypopituitarism

A

Where all pituitary hormones are insufficient GH, Prolactin, FLAT

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204
Q

Causes of hypopituitarism (especially Panhypopituitarism)

A

1) post surgery or radiation 2) trauma 3) infection/ inflammation 4) pituitary tumour (silent/ hormone negative) 5) Sheehan syndrome

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205
Q

Sheehan’s syndrome

A

Aka postpartum hypopituitarism - caused by ischaemia necrosis of pituitary gland due to blood loss during or after childbirth

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206
Q

ADH deficiency due to hypopituitarism

A
  • Neurogenic diabetes insipidus (polyuria, polydipsia) - hypernatremia
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207
Q

Diabetes insipidus classes

A

1) Neurogenic DI (decreased ADH release due to hypopituitarism) 2) nephrogenic DI (inability of kidney to respond to ADH) 3) Dipsogenic (defect in hypothalamic thirst mechanism) 4) Gestational (placenta produce vasopressinase that cleaves ADH)

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208
Q

Pancreatic islet cell tumours classifications

A

A. FUNCTIONAL: 1) insulinoma (beta cells) 2) gastrinoma (G cells) 3) glucagonoma (alpha cells) 4) VIP-oma (VIP cells) B. NON-FUNCTIONAL

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209
Q

Insulinoma pathology

A

Hypoglycaemia Triad: 1) recurrent hypoglycaemic attack 2) CNS symptoms (confusion, loss of consciousness) 3) Attack promptly relieved by glucose administration

210
Q

Gastrinoma pathology

A

Excess gastrin over stimulated H+ production by gastric parietal cells: Severe peptic ulcer - Zollinger-Ellison Syndrome

211
Q

Glucagonoma pathology

A

Secondary diabetes with hyperglycaemia

212
Q

VIP-oma pathology

A

Increased digestive motility -> watery diarrhoea

213
Q

Pancreatic islet cell tumour histology

A

In ribbons and anastomosing trabeculae Richly vascularised Round nuclei with fine chromatin Eosinophilic cytoplasm

214
Q

Adrenal insufficiency types

A

PRIMARY (both aldosterone and cortisol deficient) 1) acute primary (Waterhouse-friderichsen syndrome) 2) chronic primary (addison’s disease) SECONDARY (only cortisol deficient) 1) reduced ACTH secretion due to hypopituitarism

215
Q

Waterhouse-Friderichsen Syndrome

A

Acute primary adrenal insufficiency Due to overwhelming bacterial infection -> hypotension and shock -> DIC -> adrenocortical insuffiency -> massive adrenal haemorrhage - reduce cortisol and aldosterone

216
Q

Causes of Addison’s disease

A

Autoimmune adrenalitia, amyloidosis TB, infections Metastasis

217
Q

How to distinguish primary and secondary hypoadrenalism

A

Primary vs secondary Reduction in cortisol and aldosterone vs reduction in cortisol ACTH increase vs ACTH decrease Hyperpigmentation vs none Hyperkalemia vs none

218
Q

Addison’s disease pathology

A
  • reduce cortisol and aldosterone - Nausea, vomiting - fatigue, weakness, hypotension (due to hyponatremic volume contraction) - hyperpigmentation - hyperkalemia
219
Q

Hyperpigmentation in primary adrenal insufficiency

A

Reduced cortisol leads to negative feedback increase in pituitary ACTH secretion, which will lead to concomitant MSH secretion as ACTH is the precursor

220
Q

Hyperadrenalism presentation

A

1) Primary hyperaldosteronism (Conn’s syndrome) 2) primary hypercortisolaemia (Adrenal Cushing’s syndrome) 3) Primary androgen hypersecretion (Androgenital syndrome or virilism)

221
Q

Hyperadrenalism causes

A

Congenital Adrenal Hyperplasia Cortical adenoma

222
Q

Hyperaldosteronism causes

A

PRIMARY (hyperadrenalism) 1) adrenal hyperplasia 2) cortical adenoma —- SECONDARY (renal perception of low intravascular volume -> overreaction of renin-angiotensin system) 1) renal artery stenosis 2) CHF 3) chronic renal failure 4) cirrhosis

223
Q

Primary hyperaldosteronism features

A

Conn’s: HypoK, HyperNa, alkalosis, ↑ plasma & urinary aldosterone - muscle weakness (due to hypokalemia) - tetany (metabolic alkalosis, hypokalemia) - hypertension (hypernatremia) - decrease plasma renin

224
Q

Primary vs secondary hyperaldosteronism

A

Low plasma renin VS High plasma renin

225
Q

Cushing’s syndrome causes

A

1) iatrogenic/ exogenous glucocorticoid 2) Cushing’s disease (secondary to pituitary ACTH hypersecretion from adenoma) 3) ectopic ACTH (from SCLC or pancreatic cancer) 4) Adrenal adenoma, carcinoma or hyperplasia (PRIMARY) 5) hypothalamic CRH hypersecretion

226
Q

Cushing’s syndrome presentation

A

1) CVS - hypertension (hypernatremia, water retention) - left ventricular hypertrophy - capillary weakness 2) GI - peptic ulcer 3) U - sodium and water retention - hypokalemia - hypercalciuria -> ureteric calculus - polyuria sometimes 4) G - increased androgen with clitoral hypertrophy, virilism, hirsutism, and amenorrhea 5) MSS - muscle weakness (hypokalemia) - osteoporosis - decrease bone mass -> fractured - thin limbs 6) Skin - truncal obesity - buffalo hump - moon face - abdominal striae 7) CNS - irritability 8) Immune - poor wound healing - immunosuppresion 9) endocrine - hyperglycemia - diabetic

227
Q

Pheochromocytoma presentation

A

Adult adrenal medullary tumour - pressure (hypertension) - pain (headache) - perspiration - palpitation, tachycardia - pallor - tremor, sense of apprehension Complication: –> MI due to vasoconstriction Increase urine catecholamine and vanillylmandelic acid

228
Q

Pheochromocytoma 10% rule

A

10% extra-adrenal 10% bilateral 10% malignant 10% without hypertension

229
Q

Adrenal Neuroblastoma

A

Adrenal medullary neoplasm of children less than age of 3 Often metastasise Soft and lobulated (small blue round cells)

230
Q

Retropharyngeal space infection underlying causes and pathogen

A

(Oral flora): Odontitis Pharynx perforation Quinsy (Staph aureus): Cervical vertebral osteomyelitis

231
Q

Retropharyngeal space infection features

A

Fever Dysphagia Neck stiffness Sore throat

232
Q

Retropharyngeal space infection complications

A

Spread of infection -> mediastinitis

233
Q

Retropharyngeal space infection investigation

A

Neck XR: prevertebral soft tissue swelling CT to check involvement extent Blood and pus culture

234
Q

Retropharyngeal space infection management

A

Airway protection Antibiotic Surgical drainage

235
Q

Acute epiglottitis vs croup

A

Epi vs croup 2-4 yo VS 3 m - 3yo Toxic and unwell VS well looking Abrupt onset VS viral prodrome High fever VS moderate Fever More sever stridor vs less Minimal cough VS barking cough Dysphonia vs hoaseness Drooling and Dysphagia vs intact swallow

236
Q

Non infective URT obstruction

A

Foreign body aspirations Tumour Goitre Bilateral vocal cord palsy

237
Q

Nasal cavity pathologies

A

V: juvenile angiofibroma I: nasal polyps N: Nasal papilloma, squamous carcinoma, malignant melanoma, adenocarcinoma D: / I: TB, leprosy, Scleroma, aspergillosis, candidiasis C: cleft palate, choanal atresia or stenosis A: Wegener’s granulomatosis, lethal midline granuloma T: wood dust associated adenocarcinoma E: allergic nasal polyps

238
Q

Oral cavity and tongue pathologies

A

V I: aphthous ulcer N: squamous cell carcinoma D I C A: lichen planus T: ulcer E

239
Q

Salivary gland pathologies

A

V I: sialadenitis N: pleomorphic adenoma, warthin’s tumour, mucoepidermoid carcinoma, adenoid cyst, lymphoepithelioma-like- carcinoma D I: viral mumps C A: Sjögren’s syndrome T E

240
Q

Larynx pathologies

A

V I: vocal polyps (singer’s nodule) N: squamous papilloma, carcinoma in situ, invasive squamous cell carcinoma D I: viral (influenza, adenovirus, chicken pox) Acute laryngitis, acute epiglottitis, croup, TB C: laryngeal web A: laryngeal edema T E

241
Q

Aphthous ulcer

A

May be due to HSV infection

242
Q

Oral cavity squamous cell carcinoma (risk)

A

Commonest oral cavity neoplasm Risks: - smoking!! - alcohol abuse - HSV HPV infection - sunlight - poor dentition

243
Q

Sialadenitis complication

A

Mucocele - obstruction of minor salivary gland

244
Q

Salivary gland neoplasm

A

1) pleomorphic adenoma 2) Warthin’s tumour —MALIGNANT 3) mucoepidermoid carcinoma 4) adenoid cyst 5) lymphoepithelioma like carcinoma

245
Q

Sjögren’s syndrome

A

Autoimmune destruction of salivary glands; Lymphocyte, fibrous tissue in glands -> dry mouth -> tooth decay -> dry eye

246
Q

Pleomorphic adenoma

A

Most commonly in parotid gland (ensure facial nerve preservation in excision!) Pleomorphic histology 1) Epithelium forming small ducts and myoepithelial cells 2) Myxoid (shiny surface) or chondroid stroma

247
Q

Warthin’s tumour

A

Mostly in parotid gland, bilaterally Aka cystadenoma lymphomatosum papilliferum

248
Q

Mucoepidermoid carcinoma

A

Malignant salivary gland tumour Combination of glandular and squamous epithelium

249
Q

Adenoid cystic carcinoma

A

Common in submandibular and sublingual glands Locally invasive Mixture of glandular cells and myoepithelial cells

250
Q

Lymphoepithelioma-like- carcinoma

A

Salivary gland tumour Common in Chinese Resembles NPC and associated with EBV Metastasise to lungs and lymph nodes

251
Q

Vocal polyp

A

Chronic laryngitis due to mechanical injury to vocal folds eg voice misuse - squamous metaplasia - localised stromal edema - degeneration

252
Q

Laryngeal edema

A

Autoimmune or traumatic eg when patient is allergic to bee sting or medication Massive swelling of larynx -> obstruct inlet -> death due to respiratory distress

253
Q

Laryngeal squamous papilloma subtypes

A

JUVENILE - multiple - wide area - high recurrence ADULT - single - from vocal cord exclusively - rare recurrence

254
Q

Laryngeal carcinoma in situ

A

Occurs on true vocal cords

255
Q

Laryngeal invasive squamous cell carcinoma subtypes

A
  • history of chronic laryngitis - heavy smoking - hoarseness, pain - dysphagia - haemoptysis Supraglottic - metastatic to lymph nodes, lungs Glottic - commonest, beat prognosis - confined to larynx Subglottic - rare, worst prognosis - metastatic to lymph nodes, lungs
256
Q

Laryngeal web

A

Thin and translucent membrane between vocal folds near anterior commisure (congenital)

257
Q

NPC epidemiology

A

Common in southern Chinese Male more common than female Middle aged

258
Q

NPC aetiology

A

1) Genetics - combination of HLA A2 and BW 46 (not found in western populations) 2) Diet - dimethylnitrosamines in salted fish and phorbol ester in plant and oil are mutagenic compounds 3) EBV - IgA component of Viral Capsid Antigen for EBV found in patient serology; may due to proliferators effect on epithelial cells

259
Q

NPC location (and metastases)

A

Fossa of Rosenmuller of nasopharynx - clinically obscure area therefore will be clinically silent until widespread metastases occur Local spread to parapharyngeal space -> base of skull -> cranium via foramina Distal spread -> usually by lymphatics to H&N lymph nodes - may be hemat spread to organs

260
Q

NPC clinical presentation

A

1) deafness and tinnitus - blockage of Eustachian tube 2) Bleeding - postnasal drip bleeding 3) headache and facial pains - trigeminal nerve compression - test for corneal reflex - temporal headache 4) neck nodes - upper jugular group at posterior triangle apex - contralateral most common; sometimes bilateral

261
Q

NPC histology subtypes

A

Squamous cell carcinoma (-> squamous cells) Nonkeratinising carcinoma (-> transitional cells) Undifferentiated carcinoma

262
Q

Most common histological subtype of NPC

A

Undifferentiated carcinoma (95%)

263
Q

Undifferentiated carcinoma (NPC) character

A

Sheets of polygonal cells or spindle cells Prominent lymphoid infiltrate (only reactive)

264
Q

NPC treatment and complication

A

Radiotherapy (best for undifferentiated carcinoma, SCC least) with adjuvant chemotherapy Routine follow up - High recurrence in first 2 year and after 10 years Use of plasma EBV tests to determine relapse COMPLICATION: - sarcomas after radiotherapy

265
Q

Common extranodal lymphoma

A

1) GI lymphoma 2) malignant nasal lymphoma

266
Q

Malignant nasal lymphoma

A
  • second most frequent extranodal lymphoma in Chinese - T cell lymphoma mostly - associated with EBV - polymorphic reticulosis - early biopsy may be mistaken for benign lesion
267
Q

Epithelial nasal neoplasms

A

BENIGN 1) squamous papilloma 2) transitional papilloma MALIGNANT 1) squamous cell carcinoma 2) malignant melanoma 3) Adenocarcinoma (from mucosal glands; associated with wood dust)

268
Q

Juvenile angiofibroma

A

Young boys nasal vascular lesion; develop around puberty and regress afterwards 1) nasal obstruction 2) epistaxis - due to malformation of nasal erectile tissue

269
Q

Nasal polyps

A

Covered by respiratory epithelium with goblet cell hyperplasia Inflammation, allergy cystic fibrosis

270
Q

Scleroma

A

Chronic bacterial infection (in form of granulomatous disease) beginning in the nose and extend progressively to nasopharynx, orophaynx and larynx

271
Q

Wegener’s granulomatosis

A

Autoimmune nasal pathology - necrotising giant cell granulomas (histiocytes, multinucleated giant cells) - will spread to trachea and lungs - death in a year from renal failure due to: 1) renal arteritis 2) necrotising glomerulitis

272
Q

Lethal midline granulomas

A

Non inflammatory destructive lesion of URT - Wegener’s granulomatosis - conventional malignant lymphoma - polymorphic reticulosis

273
Q

Polymorphic reticulosis

A

TYPICAL OF NASAL MALIGNANT LYMPHOMA Small number of lymphoma cell presented intermixed with reactive cells (plasma, immuneblast, histiocytes, neutrophil, eosinophil), forming a polymorphic mixture

274
Q

Cerebral edema comparison

A

Vasogenic vs cytotoxic vs hydrocephalic 1) due to increased capillary permeability and filtration pressure VS disturbed cellular osmoregulation from metabolic derangement VS increased CSF accumulation 2) white matter VS Gray and White matter VS periventricular white 3) Edema formed by plasma filtrate with plasma protein VS intercellular Na and water VS CSF 4) ECF increased vs Decreased vs increased

275
Q

Stroke definition

A

A clinical term for rapid onset of focal cerebral dysfunction of presumed vascular origin, of more than 24 hours with structural brain damage

276
Q

transient ischaemic attack definition

A

A fully reversible neurological deficit, lasting less than 24 hours with no structural brain damage

277
Q

Stroke subtype epidemiology

A

HK: Ischaemic stroke (70%) common than haemorrhagic stroke (30%) Western: Ischaemic stroke (85%) vs haemorrhagic stroke (15%)

278
Q

Brain infarction causes

A

1) atherosclerosis or lipohyalinosis causing occlusion 2) Emboli 3) Hypotension eg boundary zone infarct 4) vasculitis eg TB/ HI meningitis 5) vascular complication of raised ICP 6) vasospasm in subarachnoid haemorrhage 7) venous occlusion

279
Q

Morphology change in cerebral infarct

A

Pale vs haemorrhagic PALE - swollen and softened - cracking and liquefaction in 5 days - resorption with replacement by fluid filled cavity in weeks Ischaemic necrosis in 6 hours Macrophage in 6-12h In a week heavy macrophage infiltration with astrocytic proliferation

280
Q

Common source of atherosclerotic artery

A

Intracranial artery or extracranial artery like vertebral artery or **internal carotid artery at carotid bifurcation

281
Q

Vascular occlusion site epidemiology

A

Caucasian: more extracranial African, Asian: more intracranial

282
Q

Common source of emboli leading to stroke

A

Atheroma plaque in carotid bifurcation Mural thrombi in the heart (chronic rheumatic heart disease)

283
Q

Small vessel disease

A

Lipohyalinosis of deep penetrating arteries leading to thalamus, basal ganglia and pons - hyalinization - fibrinoid degeneration - lipid deposition - foamy macrophage accumulation Severe in hypertension Lead to lacunar infarct

284
Q

Lacunar infarct

A

Small infarct that lie deep in cerebral cortex or brainstem, usually due to small vessel disease or lipohyalinosis Significant neurological deficit

285
Q

Cerebral infarct caused by vasculitis

A

Endarteritis obliterans in TB meningitis or haemophilia influenzae meningitis

286
Q

Boundary zone infarct most common site

A

Border between ACA and MCA

287
Q

Boundary zone infarct

A

Cause: diffuse intracranial atherosclerosis with drop in systemic blood pressure or congestive heart failure -> zone between 2 arterial beds becomes maximally deficient in blood supply and progressively ischaemia and necrosis May not have clear neurological signs

288
Q

Intracranial haemorrhage pathological types

A

1) Intracerebral 2) subarachnoid 3) Epidural and subdural

289
Q

Intracerebral haemorrhage common causes

A

1) blood vessel abnormality - hypertension with small vessel disease and microaneurysm - saccular aneurysm - angioma - congophilic angiopathy - arteritis 2) blood disorder - thrombocytopenia - coagulopathy - anti-coagulants 3) brain tissue abnormality - infarct, tumour 4) traumatic 5) drugs, alcohol 6) idiopathic

290
Q

Congophilic angiopathy

A

Amyloid deposition in pial and intracortical arterioles Incidence increase with age Cause lobar Intracerebral haemorrhage

291
Q

Thrombocytopenia intracranial haemorrhage site

A

Multifocal, lobar

292
Q

Angioma subtypes

A

Congenital malformation of vessels 1) arteriovenous malformation AVM (most aggressive) 2) venous angioma (most common) 3) capillary angioma 4) cavernous angioma

293
Q

Angioma clinical effect

A

Rupture with massive haemorrhage Mass effect Steal (adjacent tissue deprived of blood supply), leading to epilepsy and neurological deficit

294
Q

Subarachnoid haemorrhage causes

A

1) rupture of saccular aneurysm (65%) 2) rupture of AVM (5%) 3) idiopathic (20%)

295
Q

Location of berry aneurysm

A

Arterial bifurcations, 90% in anterior circulation: 1) middle cerebral artery’s first main branch in Sylvian fissure 2) anterior communicating artery’s origin from anterior cerebral artery 3) internal carotid artery’s terminal bifurcation and origin of posterior communicating artery

296
Q

Berry aneurysm prevalence

A

All ages post puberty

297
Q

Berry aneurysm co existing condition

A

Adult polycyclic kidneys Aorta coarctation

298
Q

Berry aneurysm size

A

Rupture: 5mm to 10mm Mass effect: > 3cm

299
Q

Berry aneurysm rupture

A

1) Spontaneous closure 2) rebleeding 3) cerebral ischaemia and infarction due to vasospasm of artery harbouring ruptured aneurysm 4) expanding haematoma 5) progressive hydrocephalus due to subarachnoid space occlusion by haematoma 6) epilepsy

300
Q

Reason for high morbidity and mortality of CNS infection

A

1) neurons don’t regenerate - permanent neurological dysfunction 2) little space in cranium -> mass effect prominent 3) meninges damage will lead to hydrocephalus

301
Q

Clinical signs of CNS infection

A

1) meningeal irritation 2) encephalopathic signs (seizures or altered consciousness) 3) raised ICP presentation 4) Focal neurological sign -> paralysis, anaesthesia, endocrine, focal epilepsy 5) primary or metastatic foci of infection: skin rashes, pneumonia, endocarditis l, sinusitis 6) systemic signs: Fever, leucocytosis

302
Q

Acute pyogenic meningitis pathology

A

1) pus is subarachnoid space, may infiltrate ventricles and choroid plexus, posterior spinal cord 2) petechia haemorrhages and focal infarction 3) small abscess in white matter 4) subarachnoid space filled with neutrophils then lymphocytes, plasma cells and macrophage

303
Q

Acute pyogenic meningitis complications

A

1) Organization of inflammatory exudate -> fibrosis, thickening of meninges and obliteration of subarachnoid space 2) hydrocephalus 3) cranial nerve palsy due to entrapment by fibrosis - CN 2 and 6 7 8 4) septic thrombosis of cerebral vessels may lead to cerebral infarction 5) if parenchyma involved by infection or infarction, then epilepsy, mental retardation and focal neurological sign

304
Q

Acute pyogenic meningitis pathogensis

A

1) asymptomatic colonisation of nasopharyngeal mucosa (usu via fimbriae) 2) bacteria pass mucosal barrier and enter blood stream via phagocytic vacuole 3) bacterial capsule evade phagocytosis and complement pathway 4) sustained high grade bacteraemia 5) bacteria attach to laminin receptor on brain microvascular endothelium 6) meningeal invasion -> breakdown of epithelial tight junction or cross BBB by endocytosis 7) uncontrolled replication of bacteria in subarachnoid space (defenceless due to low complement, antibody and WBC) 8) bacterial release endotoxins and components that activate endothelial and macrophage Toll like receptor -> release of pro inflammatory cytokines 9) inflammation of subarachnoid space, increased permeability of BBB and endothelium

305
Q

Acute pyogenic meningitis pathogen in age 0-8wks

A

E coli (K1) Streptococcus agalactiae Listeria monocytogenes (unpasteurised milk) Enterobacteriaceae eg salmonella

306
Q

Acute pyogenic meningitis pathogen in 3mon to 18 yo

A

HIB Neisseria meningitidis Streptococcus pneumoniae

307
Q

Acute pyogenic meningitis pathogen in 18yo to 50yo

A

Neisseria meningitidis Streptococcus pneumoniae

308
Q

Acute pyogenic meningitis pathogen in 50yo+

A

Neisseria meningitidis Streptococcus pneumoniae Aerobic gram neg (Klebsiella, Escherichia, salmonella)

309
Q

Acute pyogenic meningitis pathogen in immunocompromised

A

Neisseria meningitidis Streptococcus pneumoniae Aerobic gram neg (Klebsiella, Escherichia, salmonella) Listeria monocytogenes Pseudomonas aeruginosa

310
Q

Acute pyogenic meningitis pathogen in pig contact

A

Streptococcus suis

311
Q

Acute pyogenic meningitis pathogen in fresh water contamination

A

Nagleria fowleri Other amoeba

312
Q

Acute pyogenic meningitis pathogen in ingestion of raw mollusk

A

Angiostrongylus cantonensis (eosinophilia meningitis)

313
Q

Acute pyogenic meningitis pathogen in head trauma, post neurosurgery or intrathecal injection

A

Staphylococcus aureus Staphylococcus epidermidis Aerobic gram neg (Klebsiella, Escherichia, salmonella) Aspergillus

314
Q

Acute pyogenic meningitis pathogen post shunting

A

Staphylococcus aureus Staphylococcus epidermidis Aerobic gram neg (Klebsiella, Escherichia, salmonella) Proprionibacterium acne

315
Q

Management of Acute pyogenic meningitis

A

1) LP for CSF gram smear and culture and antigen detection, after exclusion of SOL by CT/MRI 2) empirical IV high dose antibiotic that crosses BBB eg penicillin G, ceftriaxone 3) adjunctive dexamethasone before/with first dose of antibiotics to decrease inflammatory complications in HIB or strep pneumoniae 4) elevation of head by 30 degrees and anticonvulsant for ICP symptoms relief 5) chemoprophylaxis with rifampicin before HIB or Neisseria meningitidis contact 6) active immunisation eg HIB vaccination, meningococcus/ pneumococcal vaccination

316
Q

Subacute or chronic meningitis common pathogen

A

1) mycobacterium tuberculosis 2) cryptococcus neoformans 3) Treponema pallidum (syphilis) 4) Lyme’s disease - ticks 5) nocardia 6) candida,

317
Q

TB meningitis pathology

A

1) granulomatous inflammation - granuloma - central caseous necrosis bordered by epithelioid histiocytes - Langhan’s giant cells with fibrosis in periphery 2) thick gelatinous exudate around granuloma

318
Q

TB meningitis complications

A

0) chronic inflammation causes intimal proliferation and luminal narrowing of cerebral arteries (endarteritis obliteran) -> superficial infarct 1) Organization of inflammatory exudate -> fibrosis, thickening of meninges and obliteration of subarachnoid space 2) hydrocephalus 3) cranial nerve palsy due to entrapment by fibrosis - CN 2 and 6 7 8 4) septic thrombosis of cerebral vessels may lead to cerebral infarction 5) if parenchyma involved by infection or infarction, then epilepsy, mental retardation and focal neurological sign

319
Q

TB meningitis Lab results

A

1) CSF lymphocytosis and monocytosis 2) CSF high protein low sugar 3) CSF and sputum LJ medium culture positive 4) CSF ZN stain positive 5) CSF TB PCR positive 6) CXR may reveal concomitant pulmonary TB

320
Q

TB meningitis treatment

A

PIER Pyrazinamise Isoniazid Ethambutol Rifampicin Steroid for reducing inflammatory complication

321
Q

Cryptococcal meningitis presentation and lab

A

Underlying immunodeficiency - malignant lymphoma, AIDS, post transplant - positive CSF Indian ink - CSF high protein low glucose - serum or CSF cryptococcal antigen - positive fungal culture

322
Q

Fungal meningitis pathology

A

Thickened opalescent meninges Contains mucoid exudate Small cysts Granuloma

323
Q

Cryptococcus treatment

A

Fluconazole Amphotericin B

324
Q

Brain abscess pathogenesis

A

A spread from contiguous suppurating focus, hematogenous spread from distant focus, direct inoculation for trauma 1) bacteria crosses BBB and enter brain parenchyma 2) acute inflammation -> early cerebritis, late cerebritis 3) early capsule formation with tissue necrosis and collagen fiber encapsulation 4) late capsule formation

325
Q

Brain abscess pathogen and site in immunocompromised

A

Multiple sites Toxoplasma gondii Aspergillosis Mucomycosis Nocardia

326
Q

Brain abscess pathogen and site in otitis media

A

Temporal or cerebellar Streptococcus viridans Bacteroides Peptostreptococcus

327
Q

Brain abscess pathogen and site in sphenoidal abscess

A

Frontal, temporal Streptococcus viridans Peptostreptococcus Bacteroides

328
Q

Brain abscess pathogen and site in dental root

A

Frontal Streptococcus viridans Peptostreptococcus Bacteroides

329
Q

Brain abscess pathogen and site in congenital heart disease or pulmonary suppurations

A

Multiple sites Viridans strep Peptostreptococcus Bacteroides Enterobacteriaceae

330
Q

Brain abscess pathogen and site in endocarditis

A

Multiple sites Staphylococcus aureus Streps

331
Q

Brain abscess pathogen and site in trauma

A

Related to wound Staphylococcus aureus Streps

332
Q

Intracerebral abscess pathology

A

1) acute inflammation with pus, tissue necrosis and neutrophilia (cerebritis) 2) capsule formation and collagen fibre encapsulation 3) gliosis 4) may cause cerebral herniation 5) epilepsy

333
Q

Intracerebral abscess management

A

1) contrast CT or MRI shows focal lesion with hypodense centre with perilesional ring 2) surgical aspiration yield pus for gram smear, aerobic culture 3) empirical high dose IV antibiotic that crosses BBB

334
Q

Meningeal irritation clinical sign

A

Neck stiffness Headache Photophobia Kernig’s sign (when hip and knee bent at 90 degree in supine patient, extension of knee is painful) Brudzinski’s sign (forced flexion of neck of supine patient will lead to flexion of hips)

335
Q

CSF finding in bacterial, virus and TB/fungal infection

A

Turbid vs clear or sl turbid vs clear or sl turbid Cell count >500 VS <500 Neutrophil vs lymphcyte vs lymphcyte Low glucose vs normal vs low High protein vs high vs high

336
Q

Pathogensis of viral CNS infection

A

1) direct invasion of CNS -cytoplasmic effect of virus replication in CNS 2) post infection syndrome - cross reacting immunological response to myelin -> dysmyelination of CNS

337
Q

Post infective encephalitis pathology and viral encephalitis pathology

A

Follow vaccination measles VZ, influenza - wide spread perivascular demyelination, with lymphocytic cuffing - astrocytic proliferation and perivascular gliosis at later stage —– Same + neurophagia by microglia

338
Q

CNS infection virus detection

A

1) cell line culture from CSF (good isolation rate in meningitis, poor in encephalitis esp post infection; enterovirus subtypes are often inculturable) 2) cell culture from other sites Eg throat swab (mumps, enterovirus) Stool (enterovirus) 3) serology - paired titre with raising - IgM antibody for EBV JE CMV - intrathecal antibody detection - enterovirus seri types got no common antigen 4) brain biopsy 5) PCR RT-PCR of CSF

339
Q

Common viral meningitis pathogen

A

1) enterovirus (echovirus, coxsackie A, B, EV71) 2) HSV 2 (recurrent genital herpes) —– 3) mumps 4) LCM 5) HIV

340
Q

Common viral encephalitis pathogen

A

1) HSV 1 2) Enterovirus (echovirus, EV71) 3) VZV —— 4) Japanese encephalitis 5) Febrile exanthems (measles, rubella) 6) rabies

341
Q

Viral myelitis pathogen

A

Enterovirus (polio, EV71) HSV 2 VZV Mumps Exanthems JE EBV CMV

342
Q

Enterovirus virology

A

Picornavirus RNA, single strand Non encapsulated Summer seasonality

343
Q

HSV meningitis

A

HSV type 2 (usu recurrent genital lesion) Self limiting (may not require acyclovir) Winter seasonality

344
Q

HSV encephalitis

A

HSV 1 (in neonate is type 2) Entry to CNS via - blood; - or spread along olfactory nerve from nasopharynx -> frontal lobe - reactivation from trigeminal ganglion -> pia mater Often affects temporal lobe or orbital surface of frontal lobe

345
Q

Why is serology or isolation of HSV from throat swab of little use in CNS infection

A

May be reactivation of latent virus unconnected with CNS Approximately 1% of population have HSV isolated from mouth

346
Q

Treatment of HSV encephalitis

A

Treatment with acyclovir upon clinical suspicion -> mortality is 70% if untreated

347
Q

Japanese encephalitis virology

A
  • arbovirus - common is South China or SE Asia but not HK (check travel history) - mostly asymptomatic - water birds and pigs as reservoir, mosquito as vector; no human to human infection - vaccine
348
Q

VZV CNS infection

A

Especially prominent in immunocompromised (reactivation in AIDS) - latent infection in dorsal root ganglion - skin lesion may precede (shingles) - skin lesion may absent (zoster sine herpete)

349
Q

Rabies virology

A

Rhabdovirus Zoonosis -> animal reservoir dogs and other mammals Animal saliva infectious when introduced on mucosal surface Human human transmission not known Replicates in striated muscles, enter nerve endings via acetylcholine receptor -> carried via axon to brain/ spinal cord -> replication in brain -> travels to salivary gland, skin, muscles via peripheral nerves Incubation in face bite is shorter due to shorter travel distance

350
Q

Rabid encephalitis diagnosis

A

Viral antigen via immunofluorescence Negri bodies

351
Q

Clinical presentation of rabies

A

Prodrome: itching at bite wound Furious rabies: hydrophobia, aerophobia, meningo-encephalitis Paralytic rabies: paralysis of bitten limb and spread

352
Q

Management and prevention of rabies

A

1) wound toilet; clean with soap and water with good debridment 2) assess rabies risk by observing animal and area —— Prevention: 1) control/ vaccination of dogs 2) passive immunisation - human rabies globulin - infiltrate wound and inject IM 3) active immunisation - 6 doses of killed vaccine

353
Q

Prion nature

A

Relatively resistant to heat, UV, ionising radiation, formalin Protease resistant protein Isoform of normal cell prion-related protein PrPc Accumulation leads to disease

354
Q

Spongiform encephalopathy nature

A

Accumulation of PrPsc in brain Loss of neuron -> spongiform vacuolation Lack of inflammatory or immune response Long incubation time -> rapidly progressive dementia -> loss of memory -> intellect loss -> personality change -> clumsiness

355
Q

Example of spongiform encephalopathy

A

Human: 1) Kuru (cannibalism) 2) Creutzfeldt-Jakob disease - classical sporadic - familial - new variant CJD (BSE in human) Sheep: Scrapie Cattle: Bovine SE (BSE)

356
Q

iatrogenic CJD

A

Implantation of contaminated graft (dura mater, cornea) Human GH Human pituitary gonadotropin Contaminated surgical equipment

357
Q

How to minimise CJD risk in surgery

A

Inform relevant department Use disposable equipments in contact with CSF blood or tissues Avoid aerosol generating procedures in high risk tissues eg high speed drill Special sterilisation (chlorine, NaOH, enzymatic detergents, autoclave)

358
Q

H&N Treatment’s side effecs

A

FORM AND FUNCTION 1) Form - H&N not covered - treatment will affect external appearance - psychosocial well being 2) Function

359
Q

Virchow’s node

A

Left supraclavicular node adenopathy; indicates infraclavicular lesion or infra diaphragmatic lesion from thoracic duct eg pelvic cancer or gastric cancer

360
Q

Radical neck dissection

A

Removal of neck lymphatic that harbours cancer metastasis - Level I to V nodes - sternocleidomastoid muscle - internal jugular vein - Accessary nerve - Cervical plexus

361
Q

Modified radical neck dissection

A

Removal of level I-V neck lymphatics - cervical plexus With preservation of one or more: - sternocleidomastoid muscle - internal jugular vein - accessory nerve

362
Q

Selective neck dissection

A

Removal of areas of lymphatics with highest chance of occult nodal metastasis, for those with no clinical evidence of nodal metastases but high chance of occult nodal metastases - supraomohyoid neck dissection (I, II, III for oral tongue cancer) - central compartment dissection (bilateral VI) for thyroid cancer

363
Q

Laryngectomy (physiological effects)

A

Complete removal of larynx - loss of speech - loss filter function of the nose - loss of humidification - ineffective cough

364
Q

Tetanus toxin biochemical effect

A

Cleaves synaptobrevin (V-SNARE)

365
Q

Botulinum toxin biochemical effects

A

B, D, F, G cleaves synaptobrevin (V-SNARE) C cleaves syntaxin (T-SNARE) A, E cleaves SNAP-25 (T-SNARE)

366
Q

Alpha-latrotoxin

A

Venom of female black widow spider Causes CA independent discharge of synaptic vesicles - Binds neurexin, bypass Ca dependent requirement for triggering vesicle fusion - Blinds CL1 and activate intracellular signal transduction cascade for Ca independent action

367
Q

Presynaptic congenital myasthenic syndrome

A

Decreased production or release of Ach Syndromes: - episodic apnea - weakness of eye muscles (diplopia) - weakness of throat and mouth muscles (dysphagia, cannot chew)

368
Q

Congenital mysasthenia graves with episodic apnea (CMG-EA)

A

Autosomal recessive (usually missense) - loss of function of choline acetyltransferase - defective ACH resynthesis and packaging Treatment: - Acetylcholine esterase inhibitors

369
Q

Lambert-Eaton myasthenic syndrome (LEMS)

A
  • Serum IgG against presynaptic voltage-gated calcium channels - P>Q>N - Reduced presynaptic voltage based calcium influx and calcium-dependent quantal exocytosis of Ach
370
Q

Porphyrias

A
  • Enzyme dificiency in heme synthesis - autosomal dominant - intermediates of heme excreted in urine (uro, copro) or faeces (copro, proto)
371
Q

what is the most prevalent porphyria

A

Acute intermittent porphyria

372
Q

Acute intermittent porphyria

A
  • most prevalent porphyria affecting liver - lack of porphobilinogen deaminase - accumulation of ALA and porphobilinogen I Symptoms: - sever abdominal pain - neurological dysfunction
373
Q

Congenital erythropoietic porphyria

A
  • prematurely destroys RBC - insufficient co-enzymes - excess uroporphyrinogen I produced - accumulation of uroporphyrin I, coproporphyrin I Symptoms: - port wine urine - red fluorescent teeth under UV - light sensitivity of skin
374
Q

Causes of cutaneous symptoms in porphyria

A

porphyrins under sunlight will produce Oxygen free radicals (those from less water soluble ones will attack organelle targets) -> inflammation

375
Q

Iron-overloading etiology

A

1) Over absorption - thalassemia, alcoholic cirrhosis 2) Defect in iron absorption - hereditary hemochromatosis

376
Q

Plasma transferrin and ferritin in pathology

A

High plasma iron: increased ferritin, decreased transferrin Low plasma iron: increased transferrin, decreased ferritin

377
Q

Chronic Iron toxicity biochemistry

A

The Fenton reaction is catalysed by ferric and ferrous irons: O2-*(superoxide) + H2O2 => O2 + OH- + OH* Which produces highly reactive hydroxyl radicals that damage polysaccharides, proteins, lipids, DNA

378
Q

Free radical damage caused by iron toxicity

A

Caused by hydroxyl radicals 1) Lipid peroxidation - lysosome, mitochondria, and microsome damage 2) Fibrosis - stimulate collagen synthesis (stimulate prolyl hydroxylase) - Fibrosis and lipid peroxidation tgt => liver cirrhosis 3) Ascorbic acid depletion - iron overload => excretion of oxalic acid - scurvy - reduce iron for erythropoiesis - osteoporosis

379
Q

Hereditary hemochromatosis pathology

A
  • Iron mainly stored as hemosiderin - large amount of iron in spleen, BM, liver, thyroid, pancreas, heart - accumulation takes many years -> symptoms not present until middle aged - increased ferritin, decreased transferrin, increased transferrin saturation Symptoms: - skin pigmentation - Hepatomegaly and cirrhosis - diabetes - hypogonadism (reduce libido) - arthritis, osteoporosis - diabetes - Heart failure
380
Q

Hereditary hemochromatosis genetics

A

2 possible HFE gene mutations on chromosome 6: 1) C282Y (cysteine to tyrosine) - mutant HFE protein does not bind Beta2-microglobulin, preventing its transport to cell surface - decreased affinity of transferrin receptor for transferrin => iron accumulation 2) H63D (histidine to aspartic acid) - prevent HFE protein from interacting with cell surface proteins that detect iron concentration => failed iron absorption regulation, thus accumulation

381
Q

Hereditary hemochrombtosis Management

A

1) Phlebotomy until all excess of iron is removed (monitor Hb level to prevent anaemia) 2) Stop phlebotomy when ferritin level normalised 3) continuous monitoring of ferritin level and periodic phlebotomy to prevent iron reaccumulation 4) Iron chelators (Removal of iron before irreversible pathologies improve prognosis)

382
Q

G6PD deficiency genetics

A
  • Defect in G6PD gene (Xq28) - X-linked - Heterogenous (No single mutation, large insertion or deletion) - Never complete absence of G6PD - Most common enzymopathy
383
Q

G6PD deficiency offending agents

A

Food: fava bean Drugs: primaquine, pamaquine (malaria), sulfamethoxazole, chloramphenicol, trimethoprim, aspirin, Vitamin K Chinese herbal medicine (especially breast feed!) Others: Mothballs

384
Q

Mechanism of oxidative damage in G6PD deficiency

A

With offending agent: 1) Cells have lowered reduced glutathione dur to lack of G6PD 2) Offending agent generates peroxides 3) Glutathione peroxidase cannot reduce peroxides due to absence of reduced glutathione 4) Oxidative attacks lead to homeless Without offending agent: 1) Cells have lowered reduced glutathione due to lack of G6PD 2) sulfhydryl groups of Hb cannot maintain in reduced form without G6PD 3) Hb crosslink to form Heinz body 4) RBC membrane more prone to oxidative stress -> haemolysis

385
Q

Motor Neuron Disease aetiology

A

1) Infective (poliomyelitis, HIV) 2) Toxic 3) Immunological (multifocal motor neuropathy) 4) Degenerative (sporadic e.g. ALS; or genetic e.g. familial ALS)

386
Q

Amylotrophic Lateral Sclerosis symptoms

A

Both UMN and LMN damage: UMN: - spastic paralysis - fasciculation (twitching) - clonus (shaking) LMN: - profound muscle atrophy - muscle weakness

387
Q

Spinal onset ALS presentation

A
  • more common (75%) - progressive weight loss - 6 months of progressive weakness of hand grip - loss of ambulation within 1 year - death from respiratory failure after 40 months - fasciculation of muscle in affected limbs - cramps and spasms
388
Q

Bulbar onset ALS presentation

A
  • less common (25%); usu elderly women - profound progressive weight loss - 9 months of progressive dysphonia and dysphagia - ambulation maintained to death - death from respiratory failure after 12 months - inappropriate laughing or crying - apnoea when lying flat
389
Q

DDx for spinal onset ALS

A
  • Spinal muscular atrophy - spondylotic myelopathy - conductive block neuropathy
390
Q

DDx for bulbar onset ALS

A
  • Myasthenia Gravis - progressive supranuclear palsy
391
Q

ALS cytopathology

A

**Deposition of neurofilament - Bunina bodies in motor neurone - “skeins” in anterior horn cells (rare glial inclusions) - Hyaline bodies in anterior horn cells - Dystrophic neurites in anterior horn **AXONAL SWELLING **increased anterograde and decreased retrograde axonal transport **decreased mitochondrial transport

392
Q

Genetic deposition of ALS

A

1) SOD1 dismutase mutation (AD) 2) Dynactin gene point mutation (AD)

393
Q

SOD1 in familial ALS

A

-> impaired dismutase activity; Gain of toxic function 1) Aberrant redox chemistry; change in conformation of SOD1 dismutase that allow channel to accept larger molecules 2) Protein instability and SOD1 aggregation

394
Q

Neurodegenerative disease by common

A

1st Alzheimer’s disease 2nd Parkinson’s disease

395
Q

Parkinson’s disease epidemiology

A

1) Increase with age 2) men more common than women

396
Q

Cardinal features of parkinsonism

A

6 1) Resting tremor (pill-rolling) 2) Bradykinesia/ Akinesia 3) Cogwheel rigidity 4) Flexed posture of neck, trunk, limb 5) Loss of postural reflexes 6) Freezing phenomenon

397
Q

Lewy bodies

A
  • Intracellular eosinophilic masses made up of alpha-synuclein - pathologic landmark of PD, but not specific
398
Q

Parkinson’s pathology

A

1) Dopamine depletion in SN and nigrostriatal pathway to caudate and putamen -> increased inhibition of thalamus and reduced excitatory input to motor cortex 2) Depigmentation (loss of neuromelanin) in SNpc and LC (neuromelanin is derived from oxidised dopamine) 3) Presence of Lewy bodies, and increased glial cells in SNpc and LC 4) Loss of monoaminergic neurons in SNpc and LC leading to decreased monoamine level at site and nerve terminals

399
Q

Parkinson’s disease genetic mutation

A

PARK1 -> alpha-synuclein mutation (AD) PARK2 -> parkin (ubiquitin ligase) mutation (AR)

400
Q

PARK1 mutation

A

Parkinson’s disease alpha-synuclein mutation (AD) Alpha-synuclein aggregate to large fibrillar forms, and form Lewy body with ubiquitin Alpha-synuclein and Abeta peptides, also form calcium channels at plasma surface -> calcium overload -> mitochondrial dysfunction -> cell death

401
Q

PARK2 mutation

A

Parkinson’s disease Parkin (E3 ubiquitin ligase) mutation (AR) Inactivation -> accumulation of parkin substrate in neutrons -> selective toxicity to DA neurons

402
Q

Classification of AD

A

1) Age on onset - early: 65yo 2) Family history - familial - sporadic

403
Q

AD Risk factors

A

1) Age (increase) 2) Down’s syndrome 3) severe head injury 4) Family history of dementia (esp early onset)

404
Q

Pathological hallmark of AD

A

1) Amyloid plague -> amyloid proteins and other associated proteins 2) Neurofibrillary tangles -> abnormal microtubules associated with protein tau 3) Macroscopically wide spread cortical atrophy (deepening of sulcus)

405
Q

Diagnostic criteria of AD

A

1) Deficits in 2 or more areas of cognition 2) MMSE score <24, with neuropsychological test evaluation 3) progressive worsening of cognitive function

406
Q

Cognitive deficits in AD

A

1) Memory - impaired anterograde episodic memory - delayed recall of stories - Sparring working memory - Poor word list learning (12 words memorise after 3 readings) 2) Attention and execution - poor concentration - selective attention - problem with complex tasks - Wisconsin card sorting test (ability to display flexibility in changing schedules) 3) Language and knowledge - impaired semantics - word definition poor - word finding poor - later phonological and syntactic deficits 4) Visuospatial and perceptual abilities - impaired drawing esp 3D - Conceptual apraxia

407
Q

neuropsychological features of AD

A
  • Apathy - Anxiety - agitation and destructive behaviour later - Depression - Delusions in late stage - Theft of items or paranoia - phantom lodger
408
Q

Early onset AD common genetic mutation

A

50% of early onset AD APP gene PSEN1 gene PSEN2 gene (ApoE4 allele increases AD risk and reduce onset age) (MAPT gene in tau hypothesis)

409
Q

AD pathogenesis hypotheses

A

1) Amyloid hypothesis - amyloid precursor protein (APP gene) is broken down by secretases - a non-soluble fragment of APP, Aβ-42, accumulates and deposit outside cell - Aβ-42 helps other protein fragments (e.g. apoE) to gather into plagues - plagues cause neuronal death - PSEN1 and PSEN2 gene -> gamma secretase subunits 2) Tau hypothesis (less favourable) - microtubule associated protein tau (MAPT gene) is associated with microtubule responsible for axonal transport - accumulation of phosphate on tau causes “Paired Helical Filaments) and form neurofibrillary tangles - impaired axonal transport cause neuronal death

410
Q

Apolipoprotein E and AD

A

Risk factor for AD - for transport of plasma lipids within tissues - mechanism is associated with Aβ clearance and neuronal repair ApoE2 allele - protective for AD, risk for cardiovascular disease ApoE3 allele - normal ApoE4 allele - risk allele for AD (increase risk and earlier onset age)

411
Q

Pathologic Haemoglobin tetramers in thalassemias

A

HbH (β4) - 3 gene deletion α thal Hb Bart (γ4) - 4 gene deletion α thal HbF (α2γ2) - β thal major Inviable tetramer (α4) - precipitate immediately - β thal major

412
Q

α thalassemia genetic haplotypes

A

(- -) α-thal-1 (i.e. α0-thal) means both α-globin genes deleted in the chromosome (α -) α-thal-2 (i.e. α+-thal) means only one α-globin gene deleted in the chromosome

413
Q

α thalassemia genotypes and phenotypes

A

(αα/αα) = normal (αα/α-) = silent carrier (clinically and haematologically silent) (αα/- -) cis OR (α-/α-) trans = α thalassemia trait or α thalassemia minor -> considered carrier (α-/- -) = HbH disease (- -/- -) = Hydrops fetalis: could not survive and die shortly after birth due to lethal haemolytic anaemia from Hb Bart precipitation

414
Q

α thalassemia descriptive classifications

A

α thalassemia major: sever and transfusion dependent α thalassemia intermediate: between major and minor α thalassemia minor (asymptomatic carrier state, trait) silent carrier: clinically and haematologically silent

415
Q

α thalassemia molecular epidmiology

A

cis 2-gene deletion more common in Asians. Most common single gene disorder in the world

416
Q

De novo mutation leading to α-thal

A

Unequal crossover of chromosome 16 during meiosis 1) Two homologous sister chromatids of chromosome 16 align side by side and form chiasma 2) if misaligned, then the DNA crossover recombination may remove α-globin gene (gene deletion) from one of the chromosome

417
Q

β thalassemia genetic haplotypes

A

β0: mutation that produce little or no β chain β+: mutation that produce detectable β chain level β++: mild β chain production defect

418
Q

β thalassemia descriptive classes

A

β thalassemia major (Cooley’s anemia) - severe anaemia - require lifelong regular transfusion starting in infancy - severe iron overload - splenomegaly and bone disease common β thalassemia intermedia - mild to moderate anaemia, may be asymptomatic - relatively independent from transfusion - variable iron overload - splenomegaly and bone deformity common β thalassemia minor (trait) - mild or no anaemia - microcytosis - no splenomegaly no bone deformities

419
Q

Genetic basis of phenotypical diversity of β thal

A

Primary modifier - β-globin gene genotype (greater production of β globin -> better condition) Secondary modifier - α-globin gene genotype (less production of α globin -> alleviate imbalance and reduce α4 precipitation -> better condition) - α-hemoglobin stabilizing protein (AHSP) -> stabilise α-harmohlobin to reduce α4 precipitation -> better condition - γ gene (more γ chain -> functional HbF formation -> better condition) - BCL11A SNP (low BCL11A -> higher HbF formation -> better condition)

420
Q

β thal pathogenesis

A

Excess α globin chain which leads to: - inclusion bodies - ineffective erythropoiesis - anaemia which then cause: > Jaundice, gallstone, iron overload, bone deformity

421
Q

AHSP and β thal

A

α-hemoglobin stabilizing protein (AHSP) -> stabilise α-harmohlobin to reduce α4 precipitation -> better condition

422
Q

BCL11A SNP and β thal

A

BCL11A SNP (AA) -> low BCL11A -> higher HbF formation -> better condition BCL11A SNP (GG) -> high BCL11A -> lower HbF formation -> worse condition

423
Q

β thal genetic mutation (specific and general)

A

Codon 41/42 (frameshift) Intron 2-654 (single nucleotide change that create new splice site that cause extra exon) General ——- 1) splicing mutation (SNP that activate cryptic splice sites, or create new splice site thus extra exon, or destroy normal splice site thus exon skip) 2) Missense 3) Frameshift by insertion/deletion 4) Nonsense mutation -> premature terminated mRNA undergo nonsense-mediated decay

424
Q

X linked agammaglobulinaemia

A

Failure of B cell signal transduction (lack of Bruton’s tyrosine kinase) - Bruton’s syndrome - recurrent infection - no humeral response - few or no mature B cells

425
Q

Genes predisposition to DM type 1

A

1) mutated MHC gene on chromosome 6 leading to faulty positive and negative selection of T cells -> active autoreactive T cells in periphery that kills B cells 2) Proinsulin gene class I VNTR leads to under expression of thymic insulin -> faulty selection of T cells and Treg cells; class III VNTR is protective as it promotes thymic insulin expression 3) PTPN22 (specific phosphatase) 4) AIRE (autoimmune regulator for thymic epithelial cell self-antigen expression)

426
Q

DM type 1 aetiology

A
  • Immune-related (T cell autoimmune) - genetically predisposed - may need virus or environmental hit (diet, trauma) - loss of beta cell mass - presence of insulitis
427
Q

DMT1 virus mediated beta cell death

A

Viral Infected beta cells -> beta cell’s MHC class I display viral antigen -> activation of Tc cells for killing -> APC’s MHC II display viral antigen -> activate Th2 cell -> B cell activation to make beta cell auto antibody for killing

428
Q

DMT1 environmental stimuli mediated beta cell death

A

Damaged B cell release B cell autoantigen that is taken up by APC, processed and presented via MHC II -> Th1 cell activation -> release cytokines, and activate Tc cell -> killing

429
Q

Development and spreading of otitis media

A
  • Spread posteriorly to mastoid antrum - damage structures deep to the walls of tympanic cavity (e.g. internal carotid artery, IJV) - and then spread to middle or posterior cranial fossa by bone resorption, and then extend to brain!
430
Q

Rhinitis definition and spread

A

Inflammation of nasal mucosa Spread to: 1) Anterior cranial fossa 2) Middle ear via auditory tube 3) Paranasal sinus 4) Lacrimal apparatus and conjunctiva

431
Q

Nasal septal deviation

A

Caused by birth injury, congenital malformation or postnatal trauma -> severe may obstruct breathing and need surgery

432
Q

Nose fracture

A

If extends above, may affect roof and cribriform plate of ethmoid bone May tear meninges => CSF rhinorrhea

433
Q

Most likely infected paranasal sinus

A

Maxillary sinus, because the drainage site (hiatus semilunaris) of the maxillary sinus is located superior to the sinus floor Thus secretions more likely to be retained and easily infected

434
Q

Orbital floor fracture with herniation symptoms

A

Visual symptoms: Vertical diplopia Sensory symptoms: Cheek hypothesia

435
Q

Pharyngeal diverticulum (most likely site?)

A

Herniation of pharyngeal mucosa, at the region between thyropharyngeus and cricopharyngeus, the only region without constrictor overlapping

436
Q

Recurrent palatine tonsil infection

A

Shows an enlarged jugulodigastric lymph nodes -> if chronic then perform tonsillectomy

437
Q

Tonsillectomy

A

Used for chronic tonsillitis - safe if the fibrous capsule is respected - large vein between tonsil and soft palate may cause bleeding during operation - CN IX (lateral wall accompanies tonsillar artery) and internal carotid artery (lateral to tonsils) may be damaged (!!)

438
Q

Hyperparathyroidism causes

A

1) Primary (PTH secretion without known stimuli): - parathyroid Adenoma (80%) - parathyroid Hyperplasia (15%) - parathyroid Carcinoma (5%) - MEN I, IIa 2) Secondary (chronic ↓ Ca2+ stimulates PTH secretion): - chronic renal disease (decreased phosphate excretion, which results in hyperphosphataemia. The elevated serum phosphate levels depress ionized calcium levels) - Vitamin D deficiency - Calcium deficiency in diet - Malabsorption 3) Tertiary (develops after secondary hyperparathyroidism; The glands become autonomous and do not respond to the level of calcium in blood)

439
Q

Hyperparathyroidism diagnosis

A

fasting then blood test for plasma Ca2+ & PTH level. PTH high Ca high -> primary PTH high Ca low/normal -> secondary

440
Q

Primary Hyperparathyroidism clinical manifestation

A

1) Hypercalcaemia: Metastatic calcification in multiple sites e.g. stomach, lungs, myocardium, cardiac valves, blood vessels, skin, etc 2) Hypercalciuria - Urinary stones and associated infection 3) Gastrointestinal disturbances - pancreatitis, gallstones, constipation 4) hyperpolarization -> depression of CNS/PNS, muscular weakness, cardiac arrhythmias 5) Bone disease: - Osteopenia (Prominent osteoclasts erode bone matrix and resorption) - Osteitis fibrosa cystica - Fracture - Brown tumors of hyperparathyroidism (Aggregates of osteoclasts, reactive giant cells, and hemorrhagic debris occasionally form masses that may be mistaken for neoplasm)

441
Q

Secondary hyperparathyroidism clinical manifestation

A

Low and normal calcium level, therefore: 1) Bone disease: - Osteopenia (Prominent osteoclasts erode bone matrix and resorption) - Osteitis fibrosa cystica - Fracture - Brown tumors of hyperparathyroidism (Aggregates of osteoclasts, reactive giant cells, and hemorrhagic debris occasionally form masses that may be mistaken for neoplasm)

442
Q

Hypercalcemia causes

A

1) Primary Hyperparathyroidism - parathyroid Adenoma (80%) - parathyroid Hyperplasia (15%) - parathyroid Carcinoma (5%) - MEN I, IIa 2) malignancy (releases PTH-related protein) - PTHrP is an essential tissue factor - It can bind to PTH receptors and acts like PTH - produced in excess by some malignant tumors e.g. squamous cell carcinoma of lung and breast cancers

443
Q

Hypoparathyroidism causes

A

A. Surgical removal, or iatrogenic (damage to blood supply during thyroidectomy) B. Congenital absence, as in DiGeorge syndrome. C. Autoimmune parathyroiditis, ends up in primary (idiopathic) atrophy.

444
Q

Hypoparathyroidism clinical manifestation

A
  • hypocalcaemia - enhanced neuromuscularexcitability (tetany)
445
Q

Genetic changes in Parathyroid Adenoma

A
  1. Somatic mutation of MEN1 2. Relocation of cyclin D1 to near the PTH gene, leading to transcriptional activation Each of the above is found in about 20% of all sporadic parathyroid adenomas.
446
Q

Parathyroid hyperplasia pathology

A

The weights of the glands are increased. The hyperplastic gland shows decreased stromal fat

447
Q

Parathyroid adenoma pathology

A
  • Fat content virtually absent in adenoma - The presence of capsule or compressed gland strongly favors adenoma
448
Q

Parathyroid gland pathological examinations

A

1) Sestamibi scan (parathyroid scintigraphy dual phase planar imaging) using Tc99m 2) Intra-operative (frozen section) diagnosis -> Determine if the tissue is of parathyroid origin -> look at stromal fat content, capsule, and compressed gland to Determine the nature of the lesion (Definite diagnosis depends on the examination of at least 2 glands, preferably all 4 glands) 3) Radioguided Parathyroidectomy - hyperactive parathyroid tumor is made radioactive before surgery so probe can detect

449
Q

Pseudohypoparathyroidism

A

resistance to parathyroid hormone (PTH insensitivity in the target organs): - hypocalcaemia - elevated PTH levels - parathyroid gland hyperplasia - Type Ia, associated developmental bone defects (Albright hereditary osteodystrophy) Chromsome 20 GNAS1 mutation

450
Q

Adrenal gland Neoplasms

A

Cortical - cortical adenoma (adult) - cortical carcinoma (children, adult) Medullary - Pheochromocytoma (adult) - Neuroblastoma (children)

451
Q

Adrenal cortical neoplasm histology

A

1) Arranged in packets 2) vascularized background 3) Central regular nuclei & pale to clear cytoplasm 4) Monotonous cells

452
Q

Pheochromocytoma histology

A

Grossly - Pale gray or brown - Cystic change - Haemorrhage Histo: - Finely granular basophilic or amphophilic cytoplasm (dirty blue) - Zellballen, trabecular or solid pattern - Polygonal or spindle cells in rich vascular network

453
Q

Thyroid neoplastic or hyperplastic diseases

A

1) Thyroid hyperplasia - Diffuse nontoxic (simple) goiter - Multinodular goitre 2) Thyroid adenoma (more than 90% of neoplasm) - Follicular adenoma 3) Thyroid carcinoma - Papillary carcinoma (>85%) - Follicular carcinoma - Medullary carcinoma - Anaplastic carcinoma

454
Q

Diffuse nontoxic (simple) goiter pathology

A

Involves entire thyroid gland Two stages i) Hyperplastic stage (enlarged follicles filled with colloid) ii) Colloid involution -> long standing ones may convert to multi nodular goitre

455
Q

Simple goitre causes

A

Thyroid hyperplastic - Endemic due to compensatory increase in TSH (e.g. Poor nutrition, lack of iodine in diet)

456
Q

Multinodular goitre pathology and symptoms

A

long-standing simple goiter convert into multi nodular goiter Symptoms: - Toxic or non-toxic - Most patients are euthyroid or with subclinical hyperthyroidism

457
Q

Multinodular goitre histology

A

Thyroid hyperplastic : Nodular hyperplasia with variably sized colloid-filled follicles

458
Q

Thyroid Follicular adenoma histology

A
  • forms fibrous capsule (benign) - Hurtle cell change
459
Q

Major histological subtypes of thyroid carcinoma

A

1) Papillary carcinoma (>85%) 2) Follicular carcinoma (5% - 15%) 3) Anaplastic carcinoma 4) Medullary carcinoma

460
Q

Thyroid Papillary carcinoma pathology (prognosis, risk and symptoms)

A

EXCELLENT PROGNOSIS; 25-50 yo Risk factor: ionizing radiation exposure Symptoms: - asymptomatic thyroid nodules - mass in cervical lymph nodes - hoarseness, dysphagia, cough, dyspnoea

461
Q

Thyroid Papillary carcinoma histology

A
  • Orphan annie eye Nuclear inclusions - Nuclear grooves - Papillary structure - Psammoma bodies - multinucleated giant cells - over-lapping ground-glass nucleus
462
Q

Thyroid Follicular carcinoma epidemiology

A

40-60 yo; Female: male= 3:1

463
Q

Thyroid Follicular carcinoma histology

A

SAME AS FOLLICULAR ADENOMA - encapsulated - Hurtle cell change - Malignancy defined by **Vascular invasion and **capsular invasion

464
Q

Thyroid Follicular carcinoma spread

A

Prone to haematogenous metastasis (bone, liver, lungs)

465
Q

Thyroid Anaplastic carcinoma patho and histo

A

65 yo, Mortality rate approaching 100% Preceding or concurrent well-differentiated thyroid carcinoma Histologically: markedly pleormorphic cells/spindle cells/squamoid cells

466
Q

Thyroid Medullary carcinoma

A

Derived from parafollicular C cells -> secrete calcitonin 70% sporadic and remaining as MEN syndrome (MEN 2a and 2b)

467
Q

Management of thyroid carcinoma

A

1) Surgical (thyroidectomy) 2) Hormone replacement 3) Radiotherapy for ablation 4) Serum thyroglobulin level for monitoring relapse

468
Q

Hypothyroidism causes

A

PRIMARY: 1) due to thyroid gland insufficiency: - congenital absence of thyroid tissue - autoimmune destruction of thyroid tissue (e.g. Hashimoto’s thyroiditis, Fibrous atrophy of thyroid) - surgical removal of thyroid tissue - radio ablation of thyroid by radioactive iodine - tumour (Thyroid Follicular adenoma) 2) due to Impaired thyroid hormone synthesis: - iodine deficiency - Goitrogens (cabbage) - congenital enzymatic defects - drug mediated inhibition SECONDARY: - Insufficient secretion of TRH or TSH (e.g. hypothalamic tumour or pituitary non-functional macroadenoma, Sheehan’s, etc.)

469
Q

Primary or secondary hypothyroidism difference

A

Primary: Low free T4 and elevated TSH (feedback), may present with goitre Secondary: Low TSH leading to low free T4, no goitre

470
Q

Symptoms of hypothyroidism

A

1) Cretinism in Infant: delayed/incomplete physical and mental development -> IRREVERSIBLE mental retardation and dwarfism 2) Youth: impaired physical growth 3) Adult onset: ** myxedema - decreased basal metabolic rate, cold intolerance, lack of energy and tiredness (decrease Na/K ATPase) - Anorexic, weight gain - bradycardia, decrease in cardiac output - slowing of mental function and motor activity (decreased catecholaimine response and Na/K ATPase) - goiter (in primary due to TSH increase) - dry skin (reduced sebaceous gland activity) - constipation (⇩GI tract motility & secretion) - menorrhagia, amenorrhea

471
Q

Myxedema

A

Characteristic of hypothyroidism -> due to deposition of glycosaminoglycan Mechanism: accumulation of mucopolysaccharides, hyaluronic acid and chondroitin sulphate (highly hydrophilic molecules) that retain fluid in the subcutaneous area - Facial puffiness and periorbital swelling - Peri-orbital haemorrhage is due to increased fragility of swollen dermal tissues

472
Q

How does hypothyroidism induce goiter?

A

In primary hypothyroidism, thyroid hormone production decreases this results in increased TSH release (less negative feedback) TSH acts on thyroid, stimulating follicular cell proliferation and increasing colloid production (hypertrophy)

473
Q

Hashimoto’s thyroiditis clinical picture

A

Middle-aged women - Diffusely enlarged thyroid -> Progressive thyroid enlargement - (early phase of hyperthyroidism) -> euthyroid -> hypothyroid COMPLICATIONS: - Tracheal compression, especially when thyroid is retrosternal - Malignant lymphoma (diffuse large B cell lymphoma)

474
Q

Hashimoto’s thyroiditis - Pathogenesis

A

Cell mediated autoimmune reaction against the thyroid cells - parenchymal destruction Thyroid enlargement is a result of lymphoid infiltration and TSH-stimulated proliferation TSH is elevated due to ineffective production of thyroid hormones (Hurthle cell change) in thyroiditis

475
Q

Hashimoto’s thyroiditis - test

A

1) Thyroid function tests (TSH, T3, T4) 2) Antithyroid antibodies assay i) anti-thyroglobulin ii) anti-thyroid (microsomal) peroxidase antibodies

476
Q

Antithyroid antibodies test

A

antibodies usually measured clinically as a confirmatory test for autoimmune thyroiditis (Grave’s, Hashimoto’s, and fibrous atrophy of thyroid) i) anti-thyroglobulin ii) anti-thyroid (microsomal) peroxidase antibodies

477
Q

Hashimoto’s thyroiditis - Treatment

A
  • Observe and wait (early period) - Replacement thyroid hormone - Surgery, to relieve pressure effects (especially for retrosternal goiter), or for cosmetic reasons
478
Q

Hurthle cells

A

Enlarged thyroid follicular cells - eosinophilic, full of mitochondria, but with ineffective hormone production - e.g. in Hashimoto’s thyroiditis, and Thyroid Follicular adenoma

479
Q

Lymphocytic thyroiditis

A

Variant of Hashimoto’s thyroiditis

480
Q

Fibrous atrophy of thyroid pathology

A

autoimmune thryoiditis AKA idiopathic myxedema: - progressive shrinking of the thyroid gland - loss of epithelium and follicles; oxyphilic and squamous metaplasia of follicular cells - dense infiltration by sensitized lymphocytes and plasma cells - Chronic inflammation - final replacement of the gland by keloid tissue-like fibrous tissue (when 90% gland destroyed -> hypothyroidism) - increased TSH, but with no hyperplastic effect - inability to respond to TSH suggests that blocking antibodies exist in this disease which compete with TSH for its receptors

481
Q

Fibrous atrophy of thyroid pathogenesis

A

Antibodies directed against thyroglobulin and microsomal antibodies, detectable years before the onset of hormonal failure, and cell-mediated immune mechanisms contribute to the pathogenesis

482
Q

Non-autoimmune thyroiditis

A

1) Granulomatous thyroiditis - TB, fungal infections - subacute granulomatous (De Quervain’s) thyroiditis 2) Drug induced thyroiditis 3) Radiation thyroiditis

483
Q

De Quervain’s thyroiditis

A

aka subacute granulomatous thyroiditis Follows a viral URT infection Pain and tenderness, enlarged thyroid Self limiting

484
Q

Riedel’s thyroiditis

A

Invasive fibrous thyroiditis -> IDIOPATHIC - May be mistaken clinically for malignancy because: Hard and adherent to surrounding soft tissues; and Fibrosis may compress the trachea or esophagus - May remain stable over many years, or it may progress slowly and produce hypothyroidism - May be associated with multifocal fibrosis (IgG4-related disease) - May overlap with autoimmune thyroiditis

485
Q

Autoimmune thyroid disorders

A
  1. Graves’ disease (diffuse toxic goiter, autoimmune hyperthyroidism) 2. Hashimoto’s thyroiditis 3. Fibrous atrophy of thyroid (idiopathic myxoedema)
486
Q

Thyrotoxicosis causes

A

1) Grave’s disease 2) Toxic Adenoma 3) Toxic Multinodular Goiter 4) TSH-Secreting Pituitary Adenoma

487
Q

Hyperthyroidism symptoms

A
  • exophthalmos - increase in basal metabolic rate, heat intolerance, sweating, warm and moist skin - Tachycardia - weight loss, very hungry - tremour - diarrhoea - nervousness
488
Q

Graves’ disease cause and clinical picture

A

an autoimmune disorder characterized by a variable combination of hyperthyroidism, goitre, ophthalmopathy (exophthlamos) and dermopathy (**Pretibial myxoedema), DIFFUSE INVOLVEMENT OF thyroid - production of autoantibodies that bind to and activate the TSH receptor, promoting TH secretion and growth of the thyroid gland Autoantibodies: - thyrotropin receptor antibodies (TRA), - thyroid stimulating immunoglobins (TSI), and - thyroid growth stimulating immunoglobins

489
Q

Grave’s disease risk factors

A

smoking, high dietary iodine intake, stress and infections.

490
Q

exophthalmos pathogenesis

A

Eye lid retraction and protrusion of eye balls (in Grave’s Disease) - T cells and autoantibodies reactive to the extraocular eye muscles and retro-orbital tissues => inflammation and swelling (tissue deposit) of the extraocular muscles and orbital fat, eyelid retraction, periorbitaledema =>swelling of soft tissues within the confines of the orbits precipitated by fibroblast growth and inflammatory cell infiltration.

491
Q

Exophthalmos complication

A
  • Keratoconjunctivitis => blindness - Compression of optic nerve => blindness
492
Q

Dermopathy in Grave’s

A

Pretibial myxedema: - Localized non-pitting edema of skin - Hyaluronic acid accumulates in dermis and subcutis

493
Q

half-life of TSH?

A

1-2 hours

494
Q

Genetic factors of Grave’s

A

HLA-DR3 HLA-B8 (25% concordance in identical twins)

495
Q

Grave’s disease recurrence test

A

Positive thyrotropin receptor antibody at end of treatment predicts disease recurrence

496
Q

Toxic Adenoma

A

solitary, autonomously functioning thyroid neoplasm (uncontrolled growth of abnormal tissue or tumor) that synthesizes and secretes excessive amounts of TH -> hyperthyroidism

497
Q

Toxic Multinodular Goiter

A
  • composed of multiple autonomously functioning thyroid nodules that synthesize and secrete excessive TH (Like Grave’s, but NODULAR FOCI) - common in old people -> hyperthyroidism; goiter with multiple palpable thyroid nodules
498
Q

Thyrotoxicosis suscipion clinical tests

A

1) TSH immunoassay (all primary are TSH suppressed; increased in secondary from TSH secreting pituitary adenoma) 2) Thyroid function test (test serum T3 T4) to check underlying cause: 3) screening for autoantibodies 4) radioactive iodine uptake assay 5) thyroid ultrasonography

499
Q

Genetic defect in MENs

A

MEN1: MEN1 encoding MENIN MEN2a, 2b: RET gene

500
Q

MEN characteristics

A

A group of genetically inherited diseases resulting in proliferative lesions (hyperplasia, adenomas, and carcinomas) of multiple endocrine organs - Younger age of onset - Multiple organs - Agressive and recur

501
Q

MEN pathology

A

MEN1: - pituitary tumour, frequently prolactinoma - parathyroid hyperplasia/adenoma - pancreas endocrine tumour MEN2a: - Parathyroid hyperplasia - Pheochromocytoma - Medullary thyroid carcinoma MEN2b: - Pheochromocytoma - Medullary thyroid carcinoma - Neuromas or ganglioneuromas of the skin, oral mucosa, eyes, respiratory tract, and gastrointestinal tract

502
Q

Wermer Syndrome

A

aka MEN1

503
Q

MEN2 management

A

Prophylactic thyroidectomy is generally recommended

504
Q

Depression classes

A

Minor depression disorder - less severe symptoms - short duration Major depression disorder - severe symptoms that interfere with function - more than 2 weeks Dysthymic disorder - less severe symptoms - more than 2 years

505
Q

Depression causes

A

Monoamine hypothesis - caused by dysfunction or deficiency of monoamine neurotransmitters (decreased synaptic availability) Neurotrophic hypothesis - caused by dropped Brain Derived Neurotrophic Factor BDNF, leading to impaired growth of neurons -> loss of hippocampal volume

506
Q

Problems with depression cause hypothesis

A

Monoamine - monoamine level improve immediately with drug, but depression not immediately cured - removal of monoamine precursor does not cause depression Neurotrophic - BDNF knock out mice does not experience depression

507
Q

psychosis symptoms

A

1) Hallucination (5 senses perception without stimulation) 2) Delusion (believe in untrue things) 3) Confused and disturbed thoughts (rapid random constant speech, with abrupt stop and change in direction) 4) A lack of insight and self-awareness

508
Q

Causes of psychosis

A

1) Psychological problems - Schizophrenia - Bipolar disorder - severe depression or stress - lack of sleep 2) Medical condition - Stroke - Hyponatremia - CNS tumour - neurosyphilis - HIV encephalitis 3) alcohol or drugs - cocaine, ketamine, LSD

509
Q

Psychosis pathogenesis

A

Dopamine hypothesis - Excess dopamine interrupts the mesolimbic and mesocortical pathways responsible for memory, social behaviour, emotion, self awareness

510
Q

Grave’s Disease Gross and Histology

A

Gorss 1) Diffuse parenchymal goitre 2) Beefy red colour of thyroid gland Histo 1) Hyperplastic follicle (from cuboidal turned to low columnar or squamous) with papillary infolding 2) Scanty colloid content; patchy lymphocytoc infiltration 3) Increased vascularity

511
Q

Feedback and feed forward of cerebellum

A

FEEDBACK: correct ongoing movement when deviate from intended movement FEEDFORWARD: modify central programs so that subsequent movement fulfil goal with few errors

512
Q

Lingual nerve injury

A

Operation on molar teeth or mandible eg sublingual glands -> loss of general sensation to anterior 2/3 tongue -> loss of secretomotor and special taste to anterior 2/3 tongue IF distal to joining of chorda tympani

513
Q

Pterion fracture

A

Anterior branch of middle meningeal artery, may produce haematoma and cause death due to raises ICP

514
Q

Mechanism of brain trauma damage

A

Primary damage: sudden acceleration or deceleration, focal impact Secondary: alteration of cerebral blood flow and ICP

515
Q

Traumatic head injury radiology considerations

A

1) plain skull X-Ray -> USELESS low diagnostic value since can only visualise skull fractures ——– Not all patient need neuroimaging, so only perform following if proper identification 2) conventional CT + more available than MRI + relatively cheaper than MRI + short time + great for bone and acute subarachnoid and parenchymal hemorrhage - still costly - image quality problems due to metal objects - miss small amt of blood - CT comes late after intracranial damage - radiation 3) MRI + greater sensitivity in chronic settings eg after surgery + better than CT for detecting axonal damage, subtle changes + better for brainstem, basal ganglia and thalamus - more costly and inaccessible

516
Q

Criteria that need imaging after head trauma

A

Based on New Orleans Criteria or Camadian Head CT rules: *) low Glasgow Coma Scale 1) vomiting and headache (not for children) 2) amnesia esp longer and severe 3) ethanol or drug intoxication 4) Age greater than 60 or 65 5) maybe Coagulopathy/ anticoagulant use 6) sign of basal skull fracture

517
Q

New Orleans criteria

A

Glasgow coma score of 15/15 CT After TBI: 1) headache 2) vomit 3) age greater than 60 4) drug or alcohol intoxication 5) persistent anterograde amnesia 6) visible trauma above clavicle 7) seizure

518
Q

Canadian Head CT Rule

A

1) GCS <15 2) 65 yo 3) vomit X 2 4) signs of basal skull fracture 5) suspected open or depressed skull fracture 6) amnesia 7) dangerous impact mechanism eg fall from more than 5 stairs, ejected from motor vehicles, struck by vehicle

519
Q

Glasgow coma scale categories

A

Eye opening Verbal ability Motor ability

520
Q

Basal skull fracture signs

A
  • Racoon eyes - Battle’s sign - Hemotympanum - CSF otorrhea or rhinorrhea
521
Q

Bell’s palsy

A
  • incomplete eye closure (obicularis oculi) -> exposure keratitis and ectropion - incomplete mouth closure (obicularis oris), sagging mouth corner, dribbling saliva - alteration of anterior 2/3 tongue taste (chorda tympani) - hyperacusis (stapedius)
522
Q

Trigeminal neuralgia

A

Intensive pain in facial area due to vascular compression upon trigeminal nerve root -> suicidal disease

2015 - Year 3 Summative (3 decks)

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