TEST BANK FOR Robbins Basic Pathology (Robbins Pathology) 10th Edition by Vinay Kumar & Abul K. Abbas , ISBN: 9780323353175 |Chapters 1-24| Guide A+
Test Bank for Robbins Basic Pathology 10th Edition by Vinay Kumar, Abul K. Abba & Jon C. Aster 9780323353175 Chapter 1-24 | Complete Guide A+
Test Bank for Robbins Basic Pathology 10th Edition by Vinay Kumar, Abul K. Abba & Jon C. Aster 9780323353175 Chapter 1-24 | Complete Guide A+
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Cerebrovascular Diseases
Hypoxia and Ischemia
Brain may be derived from oxygen by two general mechanisms:
1. Functional Hypoxia caused by: Deficiency of oxygen.
- Low partial pressure of oxygen (Example: being at high altitude place)
- Impaired oxygen-carrying capacity (Example: severe anemia & CO poisoning)
- Toxins that interfere with oxygen use (Example: cyanide poisoning)
2. Ischemia can be transient or permanent, caused by: Inadequate blood supply.
- Tissue hypoperfusion
- Hypotension
- Vascular obstruction
a. Global Cerebral Ischemia
§ In setting of severe systemic Hypotension (systolic pressure fall below 50 mmHg as in cardiac
arrest and shock) à Widespread Ischemic-hypoxic injury
§ When injury is Mild à only a Transient post-ischemic confused state + eventual complete
recovery
§ Neurons are more susceptible to Hypoxic injury than are glial cells à Pyramidal cells of the
Hippocampus and Neocortex, Purkinjee cells of the Cerebellum (most susceptible neurons)
§ In severe Global cerebral ischemia à widespread Neuronal death occurs
§ Patients who survive à remain Neurologically severely impaired + persistent Vegetative
state
§ Other patients might have irreversible injury à Brain death = all voluntary & reflex activities
+ brain stem function + respiratory drive is absent à patients are maintained on Mechanical
ventilation = brain gradually undergoes Autolysis so-called “Respirator brain”
§ Morphology:
i. Brian is swollen + Wide gyri + Narrowed sulci
ii. At cut surface à poor demarcation between Gray matter and White matter
§ Histology:
i. Early changes (occurring 12 to 24 hours after the injury) signs and symptoms:
ü Acute neuronal cell change (Red neurons)
ü Micro vacuolation
ü Cytoplasmic Eosinophilia
ü Nuclear Pyknosis
ü Karyorrhexis
ü Changes in Astrocytes and Oligodendroglia
, ü Reaction to tissue damage begins with infiltration of Neutrophils
ii. Subacute changes (occurring at 24 hours to 2 weeks after injury) signs and symptoms:
ü Necrosis of tissue
ü Influx of macrophage
ü Vascular proliferation
ü Reactive gliosis
iii. Repair (after 2 weeks):
ü Removal of necrotic tissue and gliosis
b. Focal Cerebral Ischemia
§ Watershed (border zone) Infarcts:
ü Occurs in regions of the brain & spinal cord that lie at most distal portions of Arterial
territories.
ü Seen after Hypotensive episodes.
ü Regions at great risk: border zone between Anterior and Middle Cerebral Artery
distribution à damage to this region = produces a Wedge-shaped band of necrosis
over the cerebral convexity (few centimeters lateral to Interhemispheric fissure)
§ Cerebral arterial occlusion à leads first to Focal Ischemia à then to Infarction in the
distribution of compromised Vessels.
§ Size, location, and shape of Infract and extent of tissue damage may be modified by
Collateral blood flow à through the Circle of Willis (or Cortical-Leptomeningeal
Anastomoses) which can limit damage in some regions.
§ There is collateral blood flow to structures, such as Thalamus, Basal ganglia, and deep White
matter, which are supplied by deep penetrating vessels.
§ Embolic Infractions:
o Caused by: Thrombosis and Atherosclerosis
o Cardiac Mural Thrombi à source of emboli, caused by:
ü Myocardial dysfunction
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