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重庆医科大学:《儿科学》课程教学资源(PPT课件)Tuberculous Meningitis

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EPIDEMIOLOGY TBM Tuberculous Meningitis (TBM) The younger the children, the more readily to develop TBM. 60% in Children aged 1-3 years Death rate:15-30%
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Tuberculous Meningitis CHCUMS CHCU DIVISION OF INFECTIOUS DISEASEAND GASTROENTEROLOGY November 24th. 2004

1 Tuberculous Meningitis CHCUMS DIVISION OF INFECTIOUS DISEASE AND GASTROENTEROLOGY November 24th, 2004

EPIDEMIOLOGY-TBM Tuberculous Meningitis (TBM The younger the children, the more 'eadily to develop TBM. o 60%in Children aged 1-3 years ◆ Death rate:15-30%

2 EPIDEMIOLOGY - TBM Tuberculous Meningitis (TBM) ◆ The younger the children, the more readily to develop TBM. ◆ 60% in Children aged 1-3 years ◆ Death rate: 15-30%

TBM (Tuberculous meningitis) TBM is the most serious complication of tuberculosis in children and is usually fatal without treatment o tBM always be a part of systemic disseminated tuberculosis TBM often occurs within 1 vear of initial infection, especially in the first 2 to 6 months of infection

3 TBM (Tuberculous meningitis) ◆ TBM is the most serious complication of tuberculosis in children and is usually fatal without treatment. ◆ TBM always be a part of systemic disseminated tuberculosis. ◆ TBM often occurs within 1 year of initial infection, especially in the first 2 to 6 months of infection

PATHOPHYSIOLOGY Primary Bacteremia Com plex Brain Tuberculous B one Bacilli ☆ Lung Kidne Miliary TB Meningitis)(Subarachnoid Space Trauma/Diseases measles, pertussi Tuberculomas Brain or Spinal Cord Aerenchyma R 4

4 Tuberculous Bacilli Primary Complex Bacteremia Rich Foci Subarachnoid Space Brain or Spinal Cord Perenchyma Tuberculomas Meningitis PATHOPHYSIOLOGY Trauma/Diseases measles, pertussis Miliary TB

PATHOLOGICAL EFFECTS Meninges Diffuse Hyperemia ◆ Edema Inflammatory Exudates Conformation of Tubercles

5 PATHOLOGICAL EFFECTS Meninges ◆ Diffuse Hyperemia ◆ Edema ◆ Inflammatory Exudates ◆ Conformation of Tubercles

PATHOLOGICAL EFFECTS Subarachnoid Space a large amount of thick gelatinous exudates concentrate to the pavimentum cerebri, optic chiasma, bridge of varolius bulbus rhachidicus and sylvian fissure Basal meningitis accounts for the frequent dysfunction of cranial nerves III VI and vil

6 PATHOLOGICAL EFFECTS Subarachnoid Space ◆A large amount of thick gelatinous exudates concentrate to the pavimentum cerebri, optic chiasma, bridge of varolius, bulbus rhachidicus and Sylvian fissure. ◆ Basal meningitis accounts for the frequent dysfunction of cranial nerves III, VI, and VII

PATHOLOGICAL EFFECTS Cerebral Parenchyma Tuberculous meningoencephalitis swelling and hyperemia of the parenchyma contribute to the intracranial hypertension, the en ischemia of parenchyma occur, finally lead to the foci of encephalomalacia and necrosis Hemiplegia may be present because of this change o Meninges, spinal, and spinal nerve root also involvement. The later al ways leads to paraplegina

7 PATHOLOGICAL EFFECTS Cerebral Parenchyma Tuberculous meningoencephalitis ◆ swelling and hyperemia of the parenchyma contribute to the intracranial hypertension, then ischemia of parenchyma occur, finally lead to the foci of encephalomalacia and necrosis. Hemiplegia may be present because of this change. ◆ Meninges, spinal, and spinal nerve root also involvement. The later always leads to paraplegina

PATHOLOGICAL EFFECTS Cerebral vessels The bacteria invade the adventitia directly in the early stage and initiate the process of acute vasculitis Progressive destruction of adventitia disruption of elastic fibers, and finally intimal destruction(endarteritis). lead to the obliterative vasculitis, which may facilitate the ischemia, encephalomalacia and necrosis of parenchyma

8 PATHOLOGICAL EFFECTS Cerebral Vessels ◆The bacteria invade the adventitia directly in the early stage and initiate the process of acute vasculitis. ◆Progressive destruction of adventitia, disruption of elastic fibers, and finally intimal destruction (endoarteritis), lead to the obliterative vasculitis, which may facilitate the ischemia, encephalomalacia and necrosis of parenchyma

Circulation Arachnoid Granulation of csF Dural Sinus (Venous Bloood) Choroid plexus Sub arachnoid Lateral ventricle Space Interventricular foramen Choroid Plexus the 3rd ventricle (Site of CSF Production Cerebral aqueduct 4th ventricle Lateral Ventricle 2 Lateral foramina Fourth Ventricle 1 Medial foramen ye Spinal cord Subarachnoid space Papilledema Arachnoid granulations Sub Arachnoid Space Sub Arachnoid (Spinal Canal) Dural sinus S pace Venous drainage Optic Foramen Pituitary Gland

9 Circulation of CSF Choroid plexus Lateral ventricle Interventricular foramen the 3rd ventricle Cerebral aqueduct 4th ventricle 2 Lateral foramina 1 Medial foramen Subarachnoid space Arachnoid granulations Dural sinus Venous drainage

PATHOLOGICAL EFFECTS Hydrocephalus Hyperemia of choroids overproduction of CSF Inflammatory adherence of defective absorption Meninge of csf CSf flow is obstructed on the route Communicating before the cerebral aqueduct and the hydrocephalus 4th ventricle Noncommunicating hydrocephalus 10

10 PATHOLOGICAL EFFECTS Hydrocephalus Hyperemia of choroids overproduction of CSF Inflammatory adherence of Meninge defective absorption of CSF Communicating hydrocephalus CSF flow is obstructed on the route before the cerebral aqueduct and the 4th ventricle Noncommunicating hydrocephalus

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