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Pathology Review-Term3

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medical school pathology lectures. Year end review of Term3. Endocrine & CNS. Note: Video of this lecture is on on youtube.

medical school pathology lectures. Year end review of Term3. Endocrine & CNS. Note: Video of this lecture is on on youtube.

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  • 1. As is our Pathology, so is our Practice. -- Sir William Osler, M.D. (Father of Modern Medicine & Founding professor of John Hopkins, developed first residency program for physicians.) Pathology: The science of medicine !
  • 2. CPC31: Week Overview 2013 Term 3 CPC 1 Title: Endocrine 1/1 Thyroid System: Endocrine Aim: To educate students in Clinical, pathology & population study of patients with Endocrine disorders (using example of thyroid disorder). Learning Outcomes: 1. Demonstrate an ability to take a focused History & Students will be able carry out a focused clinical examination of patients to with neck swelling and systemic symptoms 2. Describe the Pathophysiology of common endocrine disorders. 3. Describe the pathophysiology of thyroid disorders. 4. Outline the basic sciences relating to hypothalamic/pituitary/thyroid axis; thyroid function testing; role of anti thyroid antibodies in differentiating thyroid disease 5. Outline first line treatment of thyroid disorders.
  • 3. Head injury, infections, Inflammations & Tumours Central Diabetes Insipidus, Hypogonadism Adenoma, Ischemia (Sheehans), Diabetes insipidus, Atrophy / hyperfunction Hyper/Hypo parathyroidism Graves, Hashimoto, MNG, Cancer. Hypothal: Tertiary Pituitary: Secondary Gland: Primary Cushings, Addisons, Pheochromocytoma Adenoma, carcinoma Tumours, Cysts, DIABETES Adenoma, carcinoma Tumours, Cysts, Atrophy, Dysfunction Tumours, Cysts, Atrophy, Dysfunction
  • 4. Hyper – Thyroidism - Hypo • Hyper-Metabolic… • Hypo-Metabolic…
  • 5. Nontoxic-Multi Nodular Goitre. A: conspicuous neck mass. B: Coronal section showing numerous irregular nodules, some with hemorrhage. C: Microscopy: variation in the size of the follicles. Note: TSH, T3,T4  Normal (Euthyroid)
  • 6. Carcinoma of Thyroid Type (%) age spread Prognosis Papillary 60-70 young adults 20-40 (<45y) Lymphatic, to local nodes Follicular 20-25 Young-middle 4050 (>45) Blood stream, Good with radioespecially to bone iodine therapy. Papillary Carcinoma: Psammoma Body Excellent
  • 7. SIADH: Sy of Inappropriate ADH secretion SIADH • • • • • Too Much ADH Water Intoxication Low Serum Sodium Low Serum Osmolality High Urine Osmolality Diabetes Insipitus • • • • • Too Little ADH Dehydration High Serum Sodium High Serum Osmolality Low Urine Osmolality
  • 8. Adrenal Glands: • Cortex (glands) – Glomerulosa - Mineralocorticoids – Fasciculata - Glucocorticoids – Reticularis – Gonadal hormones • Medulla (Neural) – Chromaffin cells & sympathetic nerve endings - Noradrenaline  Adrenaline (epinephrine) • Pathology: common. – – – – – Pheochromocytoma – medulla  hypertension. Addison‟s disease* Cushing‟s syndrome* & Disease*. Conn‟s syndrome*. Congenital adrenal hyperplasia(21-hydroxylase deficiency) Precocious puberty Excess Androgens
  • 9. Pheochromocytoma: • • • • • • Tumor of medullary Chromaffin cells. Increased catecholamines Secondary hypertension. Young age. May be familial (MEN syndrome). Increased Urinary VMA
  • 10. Waterhouse-Friderichsen Sy • • • • • • Acute hemorrhagic necrosis (apoplexy). Shock/Septicemia Lack of aldosterone Salt & water loss K Hypovolemic shock Hypoglycemia. K The adrenals from a child dying of meningococcal septicaemia are destroyed by haemorrhage.
  • 11. Addison’s Disease: • • • • • • • • Chronic adrenal insufficiency. anorexia, weight loss, vomiting Weakness, lethargy, hypotension skin pigmentation hyponatraemia with hyperkalaemia chronic dehydration, sexual dysfunction. Low plasma cortisol. ACTH high (primary) or low (sec) • Autoimmune 70%, • Infections (TB, fungal), tumours,
  • 12. Type I MEN MEN - Gene - RET Type II
  • 13. Education is what remains after we have forgotten all the facts taught in the class! --
  • 14. CPC32: Week Overview 2013 Term 3 CPC 2 Endocrine 2 - Diabetes System: Endocrine Aim: To educate students in: Clinical, Pathology & population study of patients with Diabetes Mellitus Learning 1. Demonstrate an ability to carry out a focused History & Outcomes clinical examination of patients with diabetes. Students will be 2. Describe the pathophysiology of Diabetes Mellitus able to Types 1 + 2 and their complications. 3. Outline the Basic sciences relating to endocrine function. 4. Explain the abnormalities of Blood supply common in diabetic patients including - ischaemia, infarction & necrosis. 5. Outline the epidemiology and aetiology of Diabetes Mellitus in Australia and world wide. 6. Outline first-line management and demonstrate an understanding of the process of care of a diabetic patient.
  • 15. Most likely .. What type of DM ? II NIDDM II GDM I IDDM Sec IDDM Sec IDDM I LADA Sec IDDM I IDDM LADA MODY 1. 56 year male obese 2. 30 year female following pregnancy 3. 8 year old boy, poor growth, DKA. 4. 24 year female Cushing‟s sy 5. 68 Year male following Ca. pancreas. 6. 32 male, DM, BMI 18, Anti-GAD +ve. 7. 34 year male, extensive tuberculosis. 8. 12 year old female following viral fever 9. 41y DM2, BMI 17.1, HbA1c 14.1, DKA 10.15y male, BMI 16.2, recurrent infect.
  • 16. DM Questions • • • • • • • Definition? types common? Diagnosis? Primary & Sec? Congenital? Gestational? Monogenic? MODY, LADA, drugs? List functions of Insulin? Antagonists? Etiology & Pathogenesis of Type 1 & 2. Stages of DM & their pathological basis? Obesity & Insulin resistance * – FFAs, PKC, Adipkines, PPARγ – Inflammation & Insulin resistance. • Mechanism of β cell destruction type 1, 2. • Islet Amyloid PolyPeptide (IAPP)?
  • 17. DM Questions • MODY & LADA – pathogenesis, subtypes. • Pathogenesis of Complications: – – – – – – Mechanism: AGEs, Activate of PKC, & Polyols. Infections – common & pathogenesis. Foot ulcer, Retinopathy (prol & non-prol), Neuropathy? Central, peripheral, autonomic… Difference Angiopathy Micro & Macro? MI, Stroke. Diabetic Nephropathy – albuminuria, KW lesion, Papillary Necrosis, Pyelonephritis, CRF. – Hypertension, Cataract, • Metabolic: Diabetic Coma, DKA, HONK **
  • 18. Insulin Anabolic Steroid GLUT4 * only these tissues….!
  • 19. Obesity & Insulin resistance. Peripheral Res. Diabetes is a state of inflammation
  • 20. GIP : glucose-dependent insulinotropic polypeptide (GIP) GLP-1: glucagon-like peptide-1 (GLP-1) DPP 4: enzyme dipeptidyl peptidase-4 (DPP-4) – breaks down GIP & GLP-1
  • 21. Insulin Resistance: JCU Research…!
  • 22. Diabetes Classification: (not a single disease) – Type I – IDDM / Juvenile – 5-10%. – Type II – NIDDM /Adult onset – 90-95%. – MODY – 5% Maturity Onset Diabetes of Youth • Genetic, sub types MODY 1–6 (3 & 2 common), – LADA – Latent Autoimmune Diabetes in Adults (LADA) – Gestational Diabetes Mellitus. – Other. (neonatal diabetes, – Insulin gene defects) Endocrinopathy, Downs Sy. – Excess hyperglycemic stimulus (drugs & disease). • Cushings, Phaeochromocytoma, acromegaly, Steroid therapy. – Beta cell destruction: • Pancreatitis/tumors/Hemochromatosis – Bronze diabetes. • Infectious – congenital rubella, CMV, TB,
  • 23. Pathogenesis of Type I DM Insulin deficiency ß cell Destruction Antibodies: Islet cell Ab - ICA Insulin Auto Ab - IAA Glut. Acid Decarb - GAD65 Autoimmune Insulitis Ab to ß cells/insulin Environment Viral infe..? Genetic HLA-DR3/4 Secondary DM Inflammation, Tumor, Infection Trauma Pancreatitis
  • 24. Type-1 clinical course
  • 25. ? β cell dysfunction Relative Insulin Def. Type II Pathogenesis IDDM Β cell Exhaustion
  • 26. Progression of Type II Years ..
  • 27. Type-I Insulitis: Lymphocytic infiltrate within islets. Type-II Islet Hyalinization: Central hyaline deposits replacing dead beta cells (only in late stage…!)
  • 28. DM: Complications:
  • 29. DM Microangiopathy – pathogenesis Normal     Glucose Glycosylation BM damage leak „AGE‟ deposition PATHOGENESIS OF DM COMPLICATIONS: 1. Chronic Hyperglycemia. 2. Glycosylation of BV B. membrane 3. Leakage of proteins, excess BM matrix. 4. Narrow, Diabetic thick, fragile, Leaky BV + Inflam. 5. Leakage of LDL, protein, angiogenesis. • Ischemia • Proteinuria (kidney) • Micro Aneurysms (retina) • Atherosclerosis.
  • 30. “A man must be big enough to admit his mistakes, smart enough to profit from them, and strong enough to correct them!” --John C. Maxwell
  • 31. CPC33: Week over veiw 2013 Term 3 CPC 3 Title: Neurology 1 – Head injury, Stroke. System: CNS-Neurology Aim: To educate students in: Clinical, Pathology & population study of patients with Head Injury, including non traumatic brain injury & stroke. Learning 1. Demonstrate an ability to take a focused history & perform a relevant Outcomes: and focused clinical examination of patients with loss of Students will be consciousness/alteration in neurological function able to 2. Describe the Pathophysiology of cerebrovascular accidents. 3. State the Pathophysiology of hypertension (review). 4. Recall the components of Basic sciences relating to function of the brain. 5. Define the Epidemiology and Pathology of cerebrovascular disease (stroke). 6. Describe the Epidemiology of neurological diseases in Australia and world wide. 7. Define the first line management of patients with impaired Glasgow Coma Scores 8. Demonstrate an understanding of the complications of intra-cerebral events
  • 32. Learning Objectives: • CNS: Functional Anatomy, Physiology & Blood supply – Revision • Stroke: Definition, types, etiology, clinical features, complications. • Brain Ischemia: TIA, Embolic, Hemorrhagic & Ischemic. • Healing in brain tissue – liquifactive necrosis, gliosis. • • • • Head Injury: types, pathophysiology, clinical & complications. Concussion, Contusion, Laceration. Hemorrhage: Epidural, Subdural, Subarachnoid, intra cerebral. Brain herniation – types & clinical features. Subfalcine, uncal, tonsillar. • Hypertension: Pathophysiology, diagnosis & Complications *Self Study • Hypertension & CNS damage, Hypertensive encephalopathy. • Epilepsy: Overview, types, pathophysiology, Clinical *Self Study
  • 33. Anatomy – Stroke.
  • 34. Berry Aneurysm Incidence Pathogenesis
  • 35. CNS - Blood supply MCA - Common site of Hem
  • 36. Blunt Head Injury: • Primary Injury: – Coup & Contra-Coup – Focal damage-concussion, contusion, – Diffuse axonal injury. • Secondary Injury: – – – – Concussion Epidural/subdural Hematoma Oedema Infection • Post Traumatic Complications: – Epilepsy – Dementia – Coma. Contre Coup
  • 37. Epidural - Hematoma - Subdural Old age, fall, delayed symptoms Arachnoid Pia fixed to brain Sub arachnoid Hptn, Atherosclerosis
  • 38. Subarachnoid Hem: alone is not trauma..! Think of: • Hypertension, • Berry aneurysm, • Atherosclerosis.
  • 39. Hypertensive Intracerebral Hem: Sites 1. Putamen-Claustrum 2. Cerebral white matter 3. Thalamus 4. Pons 5. Cerebellum 55% - MCA deep br. 15 10 10 10 Aetiology: Atherosclerosis – most common. Hypertension, smoking, diabetes. Heart disease – Atrial fibrillation Other: Trauma – fat embolism Tumor, Infection Caissons disease – Bends *Pacific.
  • 40. MCA stroke.
  • 41. Left (Dominant) Hemisphere Stroke: Clinical • • • • • • • Aphasia Right hemiparesis Right-sided sensory loss Right visual field defect Poor right conjugate gaze Dysarthria Difficulty reading, writing, or calculating Diagnosis: Recent cerebral infarction in left MCA distribution. Left cerebral hemisphere shows swelling with compression of the lateral ventricle mainly in the frontal area, due to recent infarct in the Middle Cerebral Artery (MCA) distribution. The brain in the MCA area shows discoloration of the cortex and also blurring between the cortex and white matter.
  • 42. ACA stroke. • Paralysis of contralateral foot and leg • Sensory loss over toes, foot and leg • Impairment of gait and stance • Abulia (slowness and prolonged delays to perform acts) • Flat affect, lack of spontaneity, slowness, distractibility • Cognitive impairment, such as perseveration and amnesia • Urinary incontinence Wikipedia: GNU Free Documentation license
  • 43. PCA stroke. Peripheral (cortical) • Homonymous hemianopia • Memory deficits • Perseveration (repeat response) • Several visual deficits (cortical blindness, lack of depth perception, hallucinations) Central (penetrating) • Thalamus - contralateral sensory loss, spontaneous pain, mild hemi • Cerebral peduncle - CN III palsy with contralateral hemiplegia • Brain stem - CN palsies, nystagmus, pupillary abnormalities Wikipedia: GNU Free Documentation license
  • 44. Infarct Pathogenesis: Hours 1-day 3-day 1 wk. >4wk • • • • • • • • • hypoxia/anoxia. Na/K pump block. Calcium influx. Red neuron, vacuolation. Cell death, karyorrhexis. Inflam- neutrophils, hem. Lympho, Macrophages. Liquefaction  cavity Peripheral Gliosis (astrocytes)
  • 45. CNS AV Malformations: • Many types: – – – – AV Malformation * Cavernous angioma Telangiectasia Venous angioma • Cause of Seizure disorders & hemorrhage. • Most common congenital vascular malformation. • Typically located in the outer cerebral cortex underlying white matter.
  • 46. Hypertension Stroke: Hemorrhagic stroke (new) & Lacunar infarct (old)
  • 47. Central Pontine Hem – Herniation, IC pressure
  • 48. Our greatest glory is not in never falling, but in rising every time we fall. -- Confucius
  • 49. CPC34: Week over view 2013 Term 3 CPC Title: Neurology 2 4 System: Neurology Aim: To educate students in: Clinical, Pathology & population study of patients with dementia Learning 1. Demonstrate an ability to take a relevant and focused history and Outcomes: carry out a relevant clinical examination of patients with dementia. (Students will be 2. Carry out a competent physical examination of neurological system. able to) 3. Describe the Pathophysiology & Pathology of common causes of dementia (Alzheimer’s Disease, multi infarct dementia) 4. Recognsise rare neurological causes of dementia (Huntington’s disease, CJD, HIV). 5. Outline the basic sciences relating to structure and function of the brain. 6. Describe the difference between age associated memory impairment, mild cognitive impairment and Alzheimer’s disease 7. Outline the epidemiology of Alzheimer’s disease and other causes of dementia in Australia. 8. Explain the first line management of common causes of dementia 9. Outline ethical dilemmas in caring for patients with dementia
  • 50. Broca‟s area - Cingulate and Parahippocampal gyri. Hippocampus: where short-term memories are converted to longterm memories Thalamus: receives sensory and limbic information and sends to cerebral cortex (cognition) Limbic system: controls emotions and instinctive behavior (includes the hippocampus and parts of the cortex)
  • 51. CNS Degenerations: Classification • Neuronal Degenerations. – Primary Degenerations: • Global – Alzheimer, Lewy body, Fronto-temporal • Selective/System – Parkinsons, Huntingtons, MND – Secondary Degenerations: • Toxic, metabolic(storage), infections, nutritional. • Alcohol & B12 def. • Myelin Degenerations: – Demyelinating Disorders - Multiple sclerosis – Dysmylinating disorders – Leukodystrophies. 51
  • 52. Alzheimers Disease: Morphology Gross • Cortical Atrophy Microscopy • Intraneuronal Neurofibrillary tangles • Interstitial amyloid Neuritic plaques • Loss of neurons with gliosis. 52
  • 53. Pick‟s Disease: • Severe, 40-65y, Rare. • knife blade atrophy of Frontal & temporal lobe Progressive aphasia / language dysfunction • Behaviour & personality change. • Preserved memory. • Micro: Neurons with round intracytoplasmic Pick‟s bodies (tau protein) 53
  • 54. Diffuse Lewy body Dementia: DLD • 10-15% of Parkinsons with dementia within a year of motor symptoms. • impaired memory of recent events, confusion, language problems. (Alzheimer) • Dementia + visual Hallucinations. • Lewy body (α-synuclein) in many part of cortex & substantia nigra (global) • Atrophy of cortex like AD. • Rapidly progressive – early 54 death. cortical Lewy bodies (αsynuclein) special stain.
  • 55. Parkinson‟s: • "shaking palsy" • Parkinsonism: Clinical sy. – Drugs: dopamine antagonists – Toxins: MPTP(heroin), – Diseases: Multiple system atrophy, Post encephalitic. • Parkinson‟s disease – Primary atrophy of substantia nigra. Dopaminergic nerves with α-synuclein - Lewy body. • Clinical features: – Adults (45-60y), tremor, bradykinesia & rigidity – Diminished facial expressions, stooped posture, – Slow voluntary movements, festinating gait, & fine rolling resting tremors. Dementia in some cases. – When dementia arises within 1 year of the onset of motor symptoms, it is referred to Lewy body dementia (LBD).
  • 56. Pathology of Parkinson‟s disease: • Gross: Loss of pigment in substantia nigra. • Neuronal loss, degeneration, • Loss of neurons replaced by gliosis (microglia) • Loss of neuromelanin. • Neuronal degeneration • Reactive gliosis. • Lewy bodies (αsynuclein) in neurons. 56 Parkinson Normal L
  • 57. Huntington‟s • Dementia, depression, choreiform movement (Jerking dementia) • 5th decade. Autosomal dom. • Huntington gene on 4p – Huntingtin. • Excess CAG tandem repeats = severity.   Atrophy of caudate & putamen (striatum) Compensatory hydrocephalus of lateral ventricles*. 57
  • 58. Metabolic CNS Disorders: Alcohol • Vit. B1 (thiamine) def. • In Chronic alcoholics, malabsorption syndromes. • Wernicke encephalopathy ataxia, confusion, double vision… • Korsakoff psychosis: memory loss with confabulations. Hallucinations. • Cortical atrophy. • Central pontine myelinolysis. • Atrophy of vermis of the cerebellum. 58
  • 59. Wernicke's encephalopathy: Recurrent petechial hemorrhages in the hypothalamus, mamillary bodies with atrophy. Central pontine myelinolysis. 59
  • 60. Vitamin Def & Neuropathy: • B1 Wernicke-Korsakoff syndrome • B2 Peripheral neuropathy, ataxia,dementia • B6 Convulsions in infants • B12 - SCDC. • C Scurvy • E Weakness, sensory loss, ataxia, nystagmus 60
  • 61. Multiple Sclerosis: • Common 1:1000, adults, females 2:1, HLA DR2, <50y. • Autoimmune (Gen+Env+AI) • Episodes of Limb Weakness, paraesthesia. • Relapsing & remitting. • Progressive  death in years. • Multiple soft pink plaques of demyelination- periventricular. • Inflammation, perivascular T lymphocytes & plasma cells. • CSF - oligoclonal IgG. • Reactive gliosis. 61
  • 62. Multiple Sclerosis: Demyelinated plaques Microscopy showed loss of myelination with many lipid  macrophages around BV. 62
  • 63. • • • • • • ALS: Amyotrophic Lateral Sclerosis Also known as Lou Gehrig's disease, is the most common type of Motor Neurone Disease (MND). Genetic: Mutations in SOD1 gene on Chromosome 21. Progressive neuron loss. Middle age, men, sporadic common, Familial 10% Muscle weakness, fasciculations, Degeneration of lateral and ventral spasticity, Sensation normal. corticospinal tracts (myelin stain). Degeneration of LMN tracts in the MND subtypes: lateral portion of the spinal cord • Amyotrophic Lateral Sclerosis* ("lateral sclerosis"). and of UMN • Progressive muscle atrophy (LMN) Betz cells in the motor cortex. • Primary lateral sclerosis (UMN) • Progressive bulbar palsy 63
  • 64. Dementia Cases: Disease Huntington‟s 49y woman, chronic cognitive difficulty, irritability, depression, poor movememnts, no significant memory loss, muscle rigidity, wide gait, choriform movements of trunk & limbs. (Father & many of relatives had involuntary movements.) 74y man, mild cognitive decline, slow gait, depression, resting tremors, visual hallucinations, episodes of “absent” “confused” MMSE 27/30, ACE-R score 78/100. Rigid muscles, Parkinson‟s with Dementia 75y man, rapid decline in cognitive function with fluctuations, MMSE 22/30. Ten point clock face drawing test - 0. Day time sleepiness. Apathy, visual and auditory hallucinations. Diffuse Lewy body Dementia 64
  • 65. Dementia Cases: Fronto-Temporal / Pick‟s 56y man, progressive speech difficulty 2y. Slow to respond, paucity of words. Lack of judgement, disorganized, aggression, impulsive. Good memory. Left hand weakness, progressive motor weakness. MMSE 27/30. FH of dementia. 58y man, mild cognitive impairment, weakness of distal limbs, loss of muscle mass, fasciculations, rigidity. Babinski sign +ve. Recurrent respiratory infections. 59y professional foot ball player. Progressive dementia & tremor. 67y man, previously healthy, 3m h/o rapid dementia, weakness of hands & fingers, insomnia, irritability, inability to find his way home. visual hallucinations and tremor, speech 65 difficulty, admitted with Gen. seizure. Amyotropic Lateral Sclerosis Dementia pugillistica. CJD – Mad Cow Disease
  • 66. Alzheimers Pathogenesis: YouTube The only real mistake is the one, from which we learn nothing! JOHN POWELL:
  • 67. CPC35: Week over view 2013 Term 3 Title: Neurology 3 CPC 5 System: Neurological Aim: To train students in : History taking + clinical examination of post ictal/acutely unwell patient; pathology of brain tumours; pathology of meningitis; pathology of epilepsy; process of care + population health especially rural and remote Learning 1. Demonstrate an ability to take a relevant and focused History Outcomes & clinical carry out a relevant examination of patients after a Students will witnessed seizure be able to 2. Describe the Pathophysiology of primary and secondary brain tumours; meningitis; epilepsy 3. Recall the relevant basic sciences including normal anatomy and blood supply of the brain 4. Recall the differential diagnoses for a patient with a first fit 5. Describe first line management in a patient with a first fit or altered level of consciousness.
  • 68. Scenario: Meningitis Fever, Headache, neck stiff, Brudzinski sign, Kernig sign, CSF… Scenario: Brain Tumor Crescendo Chronic Morning headache*, Seizures, localizing signs Scenario: Epilepsy: Negative signs, chronic/recurrent, family / past history.
  • 69. CNS Infections - Overview • • • • • Meningitis – commonest. Meningo-encephalitis – combined. Infections of Dura – Pachymeningitis – rare. Arachnoid – Leptomeningitis – common. Bacterial, Viral, fungal, TB, (Chem, Ca, drugs) Lepto - Meningitis Cerebrum - normal Subdural Abscess - Sinusitis Encephalitis
  • 70. Septic Meningitis: common causes Age Neonates Causes Escherichia coli, group B streptococci. N. meningitidis, S. pneumoniae, TB Children / Adolescents S. pneumoniae, Listeria monocytogenes, TB, crypto, Adults      Asymptomatic carriers  nasal spread  blood  CNS. Headache, photophobia, irritability, clouding of consciousness & neck stiffness. Limited to lepto-meninges - Acute, inflam, pus. Both cranial and spinal. Cloudy, high protein, low sugar, neutrophils, + Bacteria.
  • 71. Septic Meningitis-Microscopy
  • 72. Septic Meningitis-Spinal fluid Normal Septic Contraindications for CSF examination: • Increased intracranial pressure. • CNS infarctions (A), Hydrocephalus (B) abscess (C) or edema(D). Gram +ve Diplococci+Neutrophils
  • 73. Viral Meningitis: Perivascular cuffs of lymphocytes and Microglial nodules • • • • • Acute, Self limiting, Less severe than bacterial. Clear CSF, sugar normal, lymphocytes, protein. Cerebral edema, perivascular lymphocyte cuffing. Reactive microglial nodules. Arbovirus*, Herpes, Varicella Zoster, CMV, Polio, Rabies.
  • 74. CSF-Examination Cells Protein Glucose 0-4 lympho 0.1-0.4(n) 2.7-4.0 (n) Clear colorless > Poly High Low Turbid Viral > Lymph High normal Clear TB > lymph High Low Opalescent (cob-web) Norm Septic Appearance
  • 75. The 10-10-10 rule… Think about effect of your decision in…. 10 – 10 – 10 minutes months years "I wasn't living my life. My life was living me. I realised I made many of my decisions without thinking their consequences… “I realised all I really had to do to reclaim my life was to Start making decisions by considering their consequences in the immediate present, near term and distant future.. i.e . In ten minutes, in ten months and in ten years”. -- The 10-10-10 rule, Suzy Welch.
  • 76. Most common CNS Tumors: Adults (Glioblastoma) children
  • 77. Meningioma Capsulated, spindle cells in whorls and psammoma bodies (common type).
  • 78. Astrocytomas • Adults: – Commonest 80%, Cerebral. – Low Gr: Solid, Fibrillary. – High Gr: glioblastoma multiforme Varigated, Hemorrhagic - Malignant,. • Children: – Cystic, Low grade*, Pilocytic – Infratentorial (Cerebellum),
  • 79. Astrocytomas - Glioma • Adults: – Commonest 80%, Cerebral. – Low Gr: Solid, Fibrillary glioma – High Gr: glioblastoma multiforme Varigated, Hemorrhagic - Malignant,. • Children: – Cystic, Low grade*, Pilocytic – Infratentorial (Cerebellum), mutations of the metabolic enzyme Isocitrate DeHydrogenase (IDH1 and IDH2) are common in lower-grade astrocytomas. As a result, immunostaining for the mutated form of IDH1 has become an important diagnostic tool for low grade gliomas.
  • 80. Glioma/GBM: • • • • • Commonest Low  high grade. cerebral supratentorial. Chromosome 10 (80%) Most GBMs have lost one entire copy of C – 10 • Microscopy: • Pleomorphic astrocytes, Necrosis, palisading. Necrosis
  • 81. Common CNS Herniations: • Subfalcine: common, Headache contralateral leg weakness. • Transtentorial: occulomotor (CN III) paresis (ipsilateral dilated pupil, abnormal EOM's), contralateral hemiparesion. • Tonsillar: Obtundation.
  • 82. Why pupils dilate? Sympathetic / parasympathetic Balance. “Sympathetic system shows sympathy to your dress!”
  • 83. One of the first duties of the physician is to educate the masses not to take medicine! -- Sir William Osler (1849 - 1919), Aphorisms from his Bedside Teachings (1961) p. 105
  • 84. CPC36: Week over view 2013 Term 3 CPC 6 Title: Infections & PUO System: Infectious disease Aim: Develop understanding pathology & clinical diagnosis of patient with pyrexia of unknown origin Learning Outcomes: 1. Demonstrate competency in taking a focused History Students will be able taking & clinical examination of patients with pyrexia to 2. Demonstrate relevant focused physical examination of all systems relevant to a patient with PUO 3. Demonstrate competency in formulating the differential diagnoses of patients with PUO 4. Outline the Management of PUO 5. Outline the Basic sciences applicable to PUO including – Infection & Immunity. 6. Describe the pathology of arboviruses including transmission of disease. (Tropical diseases)
  • 85. Viral Infections • • • • • • Infectious Mono. • CMV • HIV • Hepatitis B • Herpes • Viral exanthema• mumps etc. • • Ross River Fever • Dengue • Australian Encephalitis. Bacterial TB Leptospirosis Brucellosis Q Fever Relapsing fever Nocardiosis Typhoid Tropical Infections • • • • Ross River Fever Dengue, Leptospirosis Malaria, Q fever, Melioidosis.
  • 86. Major Arboviruses: • Alphaviruses – Ross River Virus (RRV) – epidemic arthritis – Barmah Forest Fever – Equine Encephalitis – many types. • Flaviviruses – – – – Dengue – Hemorrhagic fever. Murray Valley Encephalitis – meningitis like. Japanese encephalitis Yellow fever • Bunyaviruses – LaCrosse encephalitis – Reo viruses – Colorado tick fever The major arboviruses of concern in Australia are: • • • • • Dengue Ross River Virus Barmah Forest Virus Japanese Encephalitis Murray Valley Encephalitis Ref: UQ.edu.au
  • 87. Ross River Fever - Symptoms: • Fever • Rash • Arthritis • Fatigue • Headache • Lymphnode enlargement.
  • 88. Warning Signs for Dengue Shock Four Criteria for DHF: • Fever • Hemorrhagic manifestations • Excessive capillary permeability • 100,000/mm3 platelets Initial Warning Signals: • Disappearance of fever • Drop in platelets • Increase in hematocrit Alarm Signals: • Severe abdominal pain • Prolonged vomiting • Fever to hypothermia • Change in level of consciousness When Patients Develop DSS: • 3 to 6 days after onset of symptoms
  • 89. Melioidosis A: Cutaneous melioidosis B: lung abscesses on Chest X-Ray C: corresponding CT Scan Intracellular gram-neg Burkholderia pseudomallei, Saprophyte in Soil. Northern Australia -"hyperendemic" seasonal peaks in the wet seasons. Inhalation / inoculation / soil or water. D: Skin in a fatal disseminated melioidosis. E: splenic abscesses abdominal CT F: Aspirated pus- Prostatic abscess G: Abscesses on a CT scan.
  • 90. Leptospirosis spirochete: • Severe jaundice, fever, hemorrhage with renal involvement - Weil‟s disease. • Leptospira icterohemorrhagica.. • Zoonotic: Pri. hosts - mammals, birds, reptiles, Contact with water, food, soil containing urine of infected animals. • No spread from person to person. • NQ - Banana & dairy farmers. • Biphasic: Flu like first phase followed in a week by Hemorrhage meninges, liver, renal failure - Weil‟s disease. Icterohemorhagic fever Jaundice + Hemorrhage
  • 91. Q Fever • • • • • “Q - ? In an abattoir in Brisbane. Coxiella burnetii, highly infectious Cattle, sheep,goat and other live stock. Biphasic:Acute & Chronic phase. Acute: Fever, headache, fatigue, muscle & joint pains, pneumonia. • Most recover - life long immunity but some become chronic fatigue, hepatitis, endocarditis, pneumonia - serious. • Meningitis/encephalitis: in both acute and chronic form in 1% patients. • Vaccine – pre vaccine testing is important.
  • 92. Chronic Fatigue Syndrome: (CFS) Infections in CFS: • Herpes, entero vir. • EBV, RRV • Q fever, Lyme & mycoplasma. Immunity in CFS. • Reduced lymphocytes. • Decreased immunoglobulins. • Altered immune response to virus.
  • 93. We can change our lives. We can do, have, and be exactly what we wish. - - Anthony Robbins
  • 94. CPC37: Week over view 2013 Term 3 Title: Multiple Co-morbidities CPC 7 System: Musculoskeletal, Neurological , CVS, Endocrine Aim: Educate students in clinical and pathological processes in patients with bone abnormalities. Learning 1. Demonstrate competency in History taking skills & focused Outcomes: clinical examination of patients who have sustained trauma Students will be 2. Describe the pathophysiology of fractures, osteoporosis, able to to bone tumours (primary and secondary) 3. Describe the risk factors of osteoporosis. 4. Describe the Healing in bone and other tissues following trauma 5. Describe the Basic sciences specific to tissue injury and repair 6. Outline the clinical approach to patient with multiple comorbidities and polypharmacy
  • 95. Fracture Healing: >8 Weeks 1 day 6 Wk (Hard) 1-3 Wk (Soft) 95
  • 96. Paget‟s Disease • Unknown etiology: • Excess osteolytic followed by osteoblastic stage and finally exhaustion of cellular activity (osteosclerotic stage) • Common (10%), Adult, One or all bones. Mild to severe types. • Pain, sclerosis, deformity, fracture, nerve compression, deafness. • Gross: thick, deformed, mosaic bone. • Micro: mosaic lamellae, sclerosis, increased osteoclasts & blasts. • Osteosarcoma - late age complication. 96
  • 97. Vit-D deficiency: • Rickets (Children), Osteomalacia (adults). • Defective mineralization, more osteoid (protein). • Bowing of legs, Lumbar lordosis, rachitic rosary, Harrison groove, Pigeon breast, Frontal bossing. 97
  • 98. Benign - Malignant Bone Disorders
  • 99. Osteosarcoma: • • • • • • 10-20y, (secondary in aged) Knee* & shoulder* painful Metaphysis of long bones. Tumor of osteoblasts. Rb gene mutations. osteoid forming (fine lacy microscopic osteoid) microscopic calcification, no lamellae. 99
  • 100. Skeletal Muscle: Atrophic fibres ATPase stain Normal Re-innervation group atrophy (nerve) • Normal: Checkerboard mix of type 1 & 2 fibers. “One Slow Fat Red Ox” • • • • Atrophy – neuronal, ischemic, inflammatory. Myositis (inflam), Muscular Dystrophy (dis-org.) Myopathy (non inflam) Toxic / Cong. Tumours: Rhabdomyoma, Rhabdomyosarcoma. 10
  • 101. Muscular Dystrophy: • Inherited, defective muscle structure. Dystrophin - Xp21. • Hypertrophy / Atrophy, degeneration  fat & fibrosis (pseudohypertrophy) • Common X linked 2 types: – Duchenne MD – common, early 5y, severe, death by 20y. – Becker MD -rare, late, less severe. • Normal at birth, starts with pelvic & limb weakness  heart failure.
  • 102. Dec 2011: Remember the Challenge….! 4th Year Students at JCU School of Medicine set new record.…!!! 100% Pass & Class Average over 70%
  • 103. Wish you all Success, Health, & Happiness in life. Need help for exams? You can still contact me..