Pathophysiology weekly notes, Lecture notes of Pathophysiology

Download Pathophysiology weekly notes and more Lecture notes Pathophysiology in PDF only on Docsity!

NEUROLOGICAL

HEALTH PROBLEMS

Content Coverage

Definition – Self Study

Risk Factors Associated with Neurological Health Problems- Self Study

Increased intracranial Pressure (ICP) – Self Study

intracranial Hematomas- Self Study

Cerebrovascular Accident (CVA)/Stroke

Spinal Cord Injuries - Self Study

Encephalitis

Meningitis

Seizures

Guillain-Barre Syndrome

Myasthenia Gravis

Parkinson's Disease

Multiple Sclerosis (MS)

Amyotrophic Lateral Sclerosis (ALS)- Self Study

Pain

Alzheimer's Disease

Overview

1. Defined as an acute (sudden onset), rapidly progressing

inflammation of peripheral motor and sensory nerves

2. Characterized by:

a. Variable motor weakness and paralysis

b. Paralysis that ascends symmetrically from lower

extremities in most cases

c. With excellent care has a 96% complete recovery

3. Occurs most often between ages 30-50 years, equally

in both genders

4. Causes include unknown etiology:

-autoimmune attack

-common after viral infections

-Immunizations

-febrile illness

-injury, or surgery

Pathophysiology

1. A cell-mediated immune reaction is triggered by a viral illness or

immunization

2. Instead of normal antibody role of preventing invading organism

from causing harm, the antibody formed has a damaging effect on

peripheral nerve myelin; an IgM antimyelin antibody exists,

lymphocytes are sensitized and aid in damaging myelin

Inflammation

myelin sheath

Edema

Degeneration of myelin sheath

/ Demyelination

Nerve and damaged myelin sheath

The demyelinating form of Guillain-Barre syndrome destroys the protective covering

f the peripheral nerves (myelin sheath), preventing the nerves from transmitting signals to the brain

Signs and symptoms

• Weakness/paresis (partial paralysis), paralysis

progressing upward from lower extremities to total

paralysis requiring ventilatory support

• Paresthesias (numbness and tingling) and pain; muscle

aches, cramping, and nighttime pain

• Respiratory compromise and/or failure:

dyspnea, diminished vital capacity,

breath sounds,

decreasing O2 saturation,

abnormal blood gases;

• Autonomic dysfunction:

-Orthostatic hypotension (lowered BP and dizziness with

sudden position changes)

-Hypertension

-Change in heart rate (bradycardia, heart block, asystole or

tachycardia),

-Bowel and bladder dysfunction

-Flushing and diaphoresis

MYASTHENIA GRAVIS

(“grave muscle weakness”)

https://www.youtube.com/watch?v=np6g2mwHKcw

Myasthenia gravis (MG), which literally means “grave muscle weakness,” is an autoimmune neuromuscular disease.

1. Pathophysiology

● In myasthenia gravis, the immune system mistakenly attacks the acetylcholine receptors (AChRs) at the neuromuscular junction. The neuromuscular junction is the site where nerve impulses are transmitted from motor neurons to muscle fibers. Acetylcholine (ACh) is the neurotransmitter that binds to AChRs on the muscle side of the junction, triggering muscle contraction. ● When autoantibodies against AChRs are present, they block, damage, or destroy these receptors. As a result, the number of functional AChRs is reduced, and the transmission of nerve impulses from the nerve to the muscle is impaired, leading to muscle weakness.

2. Clinical Manifestations

● Ocular Symptoms: Ptosis (drooping of the upper eyelid) and diplopia (double vision) are the initial and common manifestations. ● Facial and Bulbar Muscles: Weakness of the facial muscles can cause a mask-like appearance, difficulty in smiling, and problems with chewing and swallowing. Weakness of the muscles involved in speech can lead to dysarthria (slurred speech).

● Respiratory Muscles: In severe cases, weakness of the respiratory muscles (such as the diaphragm and intercostal muscles) can lead to respiratory distress or failure, which is a life-threatening complication known as myasthenic crisis. ● Limb Muscles: Proximal muscle weakness, especially in the arms and legs, is also common. The weakness typically worsens with repetitive use of the muscles and improves with rest.

3. Diagnosis

● Clinical Evaluation: A detailed medical history and physical examination, focusing on the characteristic pattern of muscle weakness that worsens with activity and improves with rest, are important. ● Blood Tests: Detection of autoantibodies against AChRs, MuSK, or LRP4 in the blood can confirm the diagnosis. However, in some cases, patients may be seronegative (i.e., no detectable antibodies). ● Edrophonium Test: Also known as the Tensilon test, edrophonium is a short-acting acetylcholinesterase inhibitor. When injected intravenously, it temporarily blocks the breakdown of ACh. ● Electromyography (EMG): Repetitive nerve stimulation studies can show a decremental response in muscle action potential amplitude with repeated stimulation, which is characteristic of MG.

(Containing Acetylcholine)

2. The symptoms increase with exertion and improves with

rest; eventually leads to fatigue without relief from rest

3. Characterized by unpredictable remissions and

exacerbations

4. Affects women 3 times more than men until after age 50

with onset usually between ages 20-30 years