Chapter 35_2 flashcards
(21 cards)
Epilepsy: Pathophysiology (Epileptogenesis)
The transformation of a normal neuronal region into a chronically hyperexcitable area. It involves an imbalance of excitatory and inhibitory impulses, leading to high-frequency, synchronized firing of neurons.
Seizure Types: Focal vs. Generalized
Focal Onset: Arises from one cerebral hemisphere; symptoms relate to that area and the person may remain aware. Generalized Onset: Involves both cerebral hemispheres from the start; typically involves loss of consciousness and tonic-clonic muscle movements.
Seizure First Aid: Key Safety Measures
The main goal is to protect the patient from injury. Move objects away, do not restrain the person, and do not put anything in their mouth. Afterward, place the person on their left side to prevent aspiration.
Status Epilepticus: Definition & Treatment
A medical emergency defined as a seizure lasting longer than 5 minutes, or multiple seizures within 5 minutes without returning to normal consciousness. First-line treatment is an IV benzodiazepine (e.g., lorazepam, diazepam).
Tension-Type Headache (TTH): Characteristics
The most common primary headache. Described as bilateral, “band-like” pressure of mild-to-moderate intensity. Not worsened by physical activity.
Migraine Headache: Pathophysiology & Stages
A neurovascular headache likely involving trigeminal nerve activation and inflammation of cranial blood vessels. Stages: Prodrome (neural hyperexcitability), Aura (cortical spreading depression), Pain, and Postdrome.
Migraine Headache: Classic Symptoms & Treatment
Symptoms: Severe, throbbing, often unilateral headache accompanied by nausea, vomiting, photophobia (light sensitivity), and phonophobia (sound sensitivity). Treatment: Acute attacks are treated with triptans (serotonin agonists) or NSAIDs. Preventive therapy may include beta-blockers or CGRP antagonists.
Cluster Headache: Characteristics
A type of Trigeminal Autonomic Cephalgia (TAC) that causes excruciating, unilateral, orbital, or temporal pain. Accompanied by same-sided autonomic symptoms like eye tearing/redness, rhinorrhea, and sweating.
Parkinson’s Disease: Core Pathophysiology
A progressive loss of dopamine-producing cells in the substantia nigra (a part of the basal ganglia). The resulting dopamine deficiency leads to an imbalance with acetylcholine, causing movement disorders.
Parkinson’s Disease: Classic Motor Symptoms (TRAP)
T: Tremor at rest (often a “pill-rolling” tremor). R: Rigidity (cogwheel stiffness). A: Akinesia or Bradykinesia (slowness or absence of movement). P: Postural instability (imbalance, shuffling gait).
Parkinson’s Disease: Treatment
The cornerstone of treatment is dopamine replacement therapy using Levodopa (a precursor to dopamine) combined with Carbidopa (which prevents peripheral breakdown of levodopa).
Amyotrophic Lateral Sclerosis (ALS): Pathophysiology
Also known as Lou Gehrig’s disease, it is a progressive neurodegenerative disorder that destroys both upper and lower motor neurons, leading to muscle weakness, atrophy, and eventual paralysis.
ALS: Clinical Manifestations
Key feature is painless muscle weakness while sensory and cognitive functions remain intact. The disease is fatal, typically from respiratory failure due to paralysis of the diaphragm muscle.
Multiple Sclerosis (MS): Pathophysiology
An autoimmune, demyelinating disorder where the body’s own T-cells attack the myelin sheath of motor and sensory neurons in the CNS. This disrupts nerve impulse conduction and leads to the formation of scar tissue (plaques).
MS: Clinical Manifestations
Characterized by a course of remissions and exacerbations. Common symptoms include weakness, numbness, tingling, balance problems, blurred vision (optic neuritis is often an early sign), and profound fatigue.
MS: Diagnosis & Treatment
Diagnosis: Requires evidence of demyelinating lesions separated in space and time, confirmed by MRI scans. The McDonald criteria are used for diagnosis. Treatment: Immunomodulating agents (e.g., interferon, monoclonal antibodies) are used to reduce inflammatory attacks and slow disease progression.
Huntington’s Disease (HD): Pathophysiology
An autosomal-dominant genetic disorder caused by a mutation on chromosome 4. This leads to an abnormal huntingtin protein that causes progressive neurodegeneration, particularly in the basal ganglia.
Huntington’s Disease (HD): Clinical Manifestations
The three main domains of symptoms are: 1. Involuntary motor movements (chorea and athetosis). 2. Emotional and behavioral changes (depression, irritability). 3. Cognitive decline (dementia).
Guillain-Barré Syndrome (GBS): Pathophysiology
An acute, post-infectious peripheral neuropathy where an autoimmune response attacks the myelin of peripheral nerves. It typically causes a rapidly ascending paralysis, starting in the lower limbs.
Myasthenia Gravis (MG): Pathophysiology
An autoimmune disease caused by autoantibodies that attack and destroy acetylcholine (ACh) receptors at the neuromuscular junction, which prevents proper muscle contraction.
Myasthenia Gravis (MG): Cardinal Feature & Treatment
The cardinal feature is true muscle fatigue (not just tiredness) that worsens with repetitive motion and improves with rest. Ptosis (drooping eyelids) is often an early sign. Treatment: Acetylcholinesterase inhibitors (e.g., pyridostigmine) to increase the amount of ACh available at the synapse.
