patho exam 3

Unit 5 Chapter 44: Brain Injuries and Cerebrovascular Disease

  • Types of Brain Injuries     - Primary Injury: Occurs immediately at the onset of the initial insult.     - Secondary Injury: Refers to damage or physiological changes that occur subsequent to the primary injury.         - Ischemia and Hypoxia: Result in reduced ATP production and mitochondrial failure.         - Blood Pressure Influences: Hypotension predisposes the brain to ischemia, while Hypertension (HTN) leads to vascular damage and brain edema.         - Carbon Dioxide (CO2CO_2) Levels: Increased CO2CO_2 results in vasodilation, while decreased CO2CO_2 results in vasoconstriction.

  • Ischemia and Hypoxia     - Ischemia: Delivery of oxygenated blood is too low to meet the metabolic demands of brain tissue. This can function as both a primary and secondary injury mechanism.     - Hypoxia: A deficiency of oxygen reaching the tissues, often the result of ischemia or hypoxemia (low blood oxygenation).

  • Intracranial Pressure (ICP)     - Normal Range: 0−15 mmHg0-15\,mmHg.     - Monro-Kellie Hypothesis: States that the cranium is a fixed-volume compartment containing brain tissue, blood, and CSF; an increase in one component must be compensated by a decrease in one or both of the other two.     - Etiology of Elevation:         - Vasogenic Edema: Increased capillary pressure; severe HTN may occur surrounding tumors.         - Cytotoxic Edema: Ischemic tissue swells due to cellular energy failure.         - Obstruction/Excessive Production: Related to Cerebrospinal Fluid (CSF).     - Complications: Brain herniation and brain compression.     - Clinical Manifestations (Early): Headache, nausea/vomiting (n/vn/v), restlessness, drowsiness, and blurry vision (papilledema).     - Clinical Manifestations (Late): Decreased Level of Consciousness (LOC), sluggish pupil response, dilated pupils, and altered respiratory patterns.     - Cushing’s Reflex: A late sign of high ICP involving widened pulse pressure, bradycardia, and irregular respirations.

  • Level of Consciousness (LOC)     - Change in LOC is the earliest sign of increased ICP.     - Manifestations include being drowsy, restless, or confused.

  • Glasgow Coma Scale (GCS)     - A standardized tool for assessing LOC in Traumatic Brain Injury (TBI).     - Evaluates three categories: Eye opening, verbal utterances, and motor reactions.     - Scores: Best score is 1515; worst score is 33.

  • Cranial Nerve (CN) Reflexes     - CN 3 (Oculomotor): Controls motor response to light; dysfunction leads to a dilated pupil.     - Oculovestibular Reflex: Used primarily to identify brain death.         - CN 8 (Vestibulocochlear): Transmits auditory info and inner ear vestibular info, interacting with CN 3 and 4 to control eye movements during head rotation.         - Dolls Eye Test: If the brainstem is intact, eyes turn in the opposite direction of head rotation. If absent, eyes stay midline and do not turn.         - Cold Calorics: Ice cold water is irrigated into a comatose patient’s ear. If brain function is present, the eyes will follow the irrigated ear; if absent, eyes remain forward.     - Corneal Reflex: Testing the blink response (CN 5) with a Q-tip to the cornea. An absent response indicates impaired brain function.

  • Traumatic Brain Injury (TBI) Severity and Classification     - Severity Scores (GCS):         - Mild: 13−1513-15         - Moderate: 9−129-12         - Severe: 88 or below.     - Primary Injury Types:         - Focal (Coup): Localized to the site of impact.         - Polar (Coup Contracoup): Acceleration-deceleration injury affecting opposite poles of the brain.         - Diffuse: Widespread injury involving stretching and shearing of axonal white matter (e.g., Shaken Baby Syndrome).

  • Basilar Skull Fracture     - Evaluation is mandatory for head injury patients with clear fluid draining from the ears or nose.     - CSF Identification: High glucose content; separates into layers forming a "halo" sign on dressings.     - Physical Signs: Black eyes (raccoon sign) and bruising under the ear (Battle sign).     - Risk: High risk of Central Nervous System (CNS) infection.

  • Intracranial Hematomas     - General Patho: Hemorrhage increases ICP. Diagnosis via CT, MRI, or CT Angiogram.     - Subdural Hematoma:         - Collection of blood between the dura and arachnoid membrane; involves shearing of bridging veins.         - Acute: Symptoms appear within 2424 hours.         - Subacute: ICP increases 2−102-10 days later.         - Chronic: Prone to rebleeding.     - Epidural Hematoma:         - Typically involves a fractured temporal bone disrupting the middle meningeal artery.         - Blood collects between the dura and the skull; involves arterial injury with rapid symptom onset.         - Lucid Interval: Patient loses consciousness upon impact, awakens and is Alert and Oriented (A×3A \times 3), then rapidly declines in LOC.

  • Ischemic Stroke     - Patho: Sudden occlusion of a cerebral artery.     - Clinical Manifestations: Contralateral hemiplegia, hemisensory loss, and visual field blindness.     - Risk Factors: Age >65> 65, being male, African American, smoking, HTN, Atrial Fibrillation (Afib), previous stroke, Diabetes Mellitus (DM), hyperlipidemia, and family history.

  • Transient Ischemic Attack (TIA)     - Patho: Transient symptoms that resolve completely within 2424 hours without evidence of a permanent infarct.     - Significance: Serves as a major risk factor for subsequent strokes.

  • Hemorrhagic Stroke     - Patho: Hemorrhage within brain parenchyma (basal ganglia or thalamus), usually secondary to severe chronic HTN.     - Clinical Manifestations: Signs of increased ICP and brain herniation.

  • Stroke Sequelae     - Motor/Sensory: Deficits occur contralateral to the side of the stroke.         - Right-sided Stroke: Blindness in the left visual field; disturbances in visual-spatial relations.     - Language Deficits (Aphasia): Usually involves the dominant (Left) hemisphere.         - Broca Aphasia: Verbal motor/expressive deficit; poor articulation.         - Wernicke Aphasia: Secondary/acoustic/receptive deficit; impaired comprehension (speech is fluent but nonsensical).

  • Cerebral Aneurysm and Arteriovenous Malformation (AVM)     - Aneurysm: Congenital defect in the medial layer of the arterial wall leading to dilation/ballooning. Common in the Circle of Willis at bifurcations. Rupture causes subarachnoid hemorrhage (severe headache, photophobia, stiff neck).     - AVM: Capillary system fails to develop, shunting blood directly into the venous system under high pressure, leading to rupture, seizures, and neurological dysfunction.

Unit 5 Chapter 45: Neurological Disorders

  • Seizures     - Patho: Excess cortical electrical discharges; neurons are hyperactive/hypersensitive (epileptogenic focus).     - Generalized Seizures (Whole Brain):         - Absence: Staring spells in children.         - Myoclonic: Sudden jerks.         - Atonic: Drop attacks.         - Tonic-Clonic: "Hulk phase" followed by jerking.     - Status Epilepticus: Continuous seizures without recovery; risks include oxygen lack, dysrhythmias, and lactic acid build-up.     - Partial Seizures (One Hemisphere):         - Simple: No change in LOC.         - Complex: Starts with consciousness, then leads to altered LOC.

  • Parkinson’s Disease     - Patho: Degeneration of dopaminergic neurons in the substantia nigra; presence of Lewy body plaques.     - Clinical Manifestations: Pill rolling, shuffled gait, drooling, akinesia, bradykinesia, infrequent blinking, tremors, muscle rigidity.

  • Bell’s Palsy and Trigeminal Neuralgia     - Bell’s Palsy: Idiopathic neuropathy of CN 7; nerve is demyelinated leading to unilateral facial paralysis and decreased lacrimation. Rapid onset within 24−4824-48 hours.     - Trigeminal Neuralgia: Pain in CN 5 caused by nerve demyelination or compressed vessels. Presents as sharp electrical pains with periods of remission.

Unit 6 Chapter 46: Hearing, Balance, and Vision

  • Hearing Impairment     - Conductive Hearing Loss: Sounds cannot reach the cochlea due to dysfunction in the external or middle ear (cerumen impaction, foreign bodies).     - Otosclerosis: Resorption of bone followed by spongy bone formation in the middle ear. Family history; common in middle-aged Caucasian women. Tinnitus is common.     - Sensorineural Hearing Loss: Disturbance in inner ear (cochlea) or CN 8; often irreversible.     - Ototoxicity: Caused by medications like Aminoglycoside antibiotics, Salicylates, Quinine, Furosemide, and Cytotoxic antineoplastic drugs.

  • Trauma and Age-Related Hearing     - Noise Trauma: Repeated exposure above 85 dB85\,dB. Includes Temporary Threshold Shift (sensitivity returns) and Permanent Threshold Shift (irreversible).     - Presbycusis: Hearing loss in elderly (>65> 65). Includes Sensory (hair cell atrophy), Neural (neuron loss), Metabolic (cochlea wall atrophy), and Mechanical types.

  • Meniere’s Disease     - Patho: Accumulation of endolymph in the labyrinth; distention and rupture of the scala media.     - Clinical Manifestations: Triad of fluctuating hearing loss, tinnitus, and Vertigo (classic sign). Nystagmus (CN 6 involvement) occurs during acute attacks.

  • Vision Disorders     - Myopia: Elongated eye; nearsighted; focus is in front of the retina.     - Hyperopia: Shortening of eye; farsighted; focus is behind the retina.     - Presbyopia: Loss of accommodation; inability to see close objects in middle age.     - Astigmatism: Irregular curvature of the lens; distorted image.     - Strabismus: Ocular misalignment (cross-eyedness). Risk factors include low birth weight and cigarette smoking during pregnancy.     - Amblyopia: Altered visual development despite normal pathways; most common cause of vision loss.     - Cataracts: Opacity (cloudy lens) causing gradual, painless visual loss.

  • Retinal and Glaucoma Disorders     - Retinal Detachment: Sudden appearance of floaters and flashes; "curtain being pulled over eye."     - Diabetic Retinopathy: Tissue