D115 Unit 3 Videos: Bacterial Meningitis & Neurologic System Alterations
Bacterial Meningitis
What is Bacterial Meningitis?
Bacterial meningitis is an inflammatory condition affecting the meninges, specifically the pia mater and arachnoid mater membranes surrounding the brain and spinal cord. This inflammation can result from infections caused by bacteria, viruses, fungi, parasites, toxins, or even from noninfectious sources.
Which Pathogens Are Most Common?
The leading bacterial pathogens responsible for meningitis are:
| Pathogen | Notes |
|---|---|
| Neisseria meningitidis | Most common cause in many populations |
| Streptococcus pneumoniae | Increasingly drug-resistant |
Who is at Risk?
Certain groups are more vulnerable to bacterial meningitis, including:
Infants under one year of age
Adolescents
Adults older than 40 years
High-risk environments prone to outbreaks include college dormitories, military bases, and the Sub-Saharan African region.
What Are the Predisposing Factors?
Factors increasing susceptibility to bacterial meningitis include:
Otitis media or sinusitis
Pneumonia
Immunocompromised states
Post-splenectomy status or sickle cell disease, particularly increasing the risk from pneumococcal infection
How is Bacterial Meningitis Transmitted?
The infection spreads through respiratory droplets or saliva, commonly by close contact such as coughing, sneezing, kissing, or sharing food and drinks. Individuals who are asymptomatic carriers may also transmit the bacteria.
What Happens in the Body? (Pathophysiology)
The bacteria typically enter through the respiratory tract or bloodstream and cross the blood-brain barrier. Once in the cerebrospinal fluid (CSF), they multiply and release toxins that increase vascular permeability, resulting in cerebral edema. The obstruction of CSF flow raises intracranial pressure, potentially leading to brainstem herniation and death.
What Are the Clinical Features?
| Symptom Category | Symptoms |
|---|---|
| Systemic Signs | Fever, chills, tachycardia |
| Meningeal Signs | Severe headache, photophobia, neck stiffness (nuchal rigidity), positive Kernig and Brudzinski signs |
| Neurologic Signs | Altered consciousness, seizures, hemiparesis, confusion, projectile vomiting, papilledema, petechial rash, bulging fontanels in infants, opisthotonic posturing in children |
How is Bacterial Meningitis Diagnosed?
Diagnosis involves performing a lumbar puncture to analyze CSF, showing elevated white blood cells. Blood cultures are also used to identify the specific causative bacteria.
What is the Treatment?
Empiric intravenous antibiotics should be administered immediately, with adjustments made based on culture results. Dexamethasone is recommended particularly for pneumococcal meningitis. Supportive care plays an essential role alongside antibiotic therapy.
What Complications Can Occur?
Serious complications include septic shock, disseminated intravascular coagulation (DIC), purpura fulminans, and multi-organ failure.
How Can Bacterial Meningitis Be Prevented?
Vaccination is crucial for prevention, targeting meningococcal, pneumococcal, and Haemophilus influenzae type B bacteria.
Guillain-Barré Syndrome (GBS)
What is Guillain-Barré Syndrome?
GBS is an acute autoimmune disorder that targets the peripheral nervous system, causing demyelination and progressive ascending muscle weakness.
What Causes GBS?
It often follows infections or immune activation triggered by pathogens such as Campylobacter jejuni, cytomegalovirus (CMV), Epstein-Barr virus (EBV), influenza virus, Mycoplasma pneumoniae, and Zika virus. Surgery and immunizations may also precipitate GBS.
What is the Underlying Mechanism?
Molecular mimicry leads to antibodies attacking peripheral nerve myelin or axons. Complement activation further disrupts nerve conduction.
What Are the Subtypes of GBS?
| Subtype | Description |
|---|---|
| Acute inflammatory demyelinating polyneuropathy | The most frequent variant |
| Acute motor axonal neuropathy | Affects motor nerves |
| Acute motor-sensory axonal neuropathy | Affects both motor and sensory nerves |
| Miller Fisher syndrome | Rare; involves ataxia, ophthalmoplegia, and areflexia |
What Symptoms Does GBS Present?
Patients experience ascending flaccid paralysis, paresthesia, muscle weakness, loss of reflexes (areflexia), autonomic instability, and may develop respiratory muscle paralysis within two weeks.
How is GBS Diagnosed?
Diagnosis requires progressive weakness in at least two limbs, areflexia, and symptoms progressing over fewer than four weeks.
What Treatment Options Exist?
Treatment includes intravenous immunoglobulin (IVIG), plasmapheresis, and intensive rehabilitation to regain muscle strength and function.
What is the Prognosis?
Recovery spans from weeks to months and sometimes extends to two years. Approximately 30% of patients may have residual weakness.
Multiple Sclerosis (MS)
What Defines Multiple Sclerosis?
MS is a chronic autoimmune disorder characterized by demyelination within the central nervous system (CNS).
What is the Pathophysiology?
Activated T-cells penetrate the blood-brain barrier and release cytokines that damage oligodendrocytes. This results in demyelinated plaques, which can be visualized through MRI. While early remyelination may occur, this capacity declines over time.
Who is at Risk?
Risk factors include:
Female gender
Presence of the HLA-DR2 gene
Vitamin D deficiency
Living at higher latitudes (farther from the equator)
What Types of MS Exist?
| Type | Description |
|---|---|
| Relapsing-remitting | Most common form; episodes of flare-ups followed by remission |
| Secondary progressive | Initially relapsing-remitting, then steady progression |
| Primary progressive | Continuous worsening from disease onset |
| Progressive-relapsing | Steady decline with acute relapses |
What Are Common Symptoms?
Typically affecting individuals between ages 20 and 40, symptoms include motor dysfunction (weakness, tremors, spasticity, ataxia), sensory disturbances (numbness, paresthesia), visual problems (optic neuritis, diplopia), speech difficulties (dysarthria), autonomic dysfunction, cognitive impairment, and depression. Charcot’s triad — dysarthria, nystagmus, and intention tremor — is a classic clinical sign.
How is MS Diagnosed?
Diagnosis is based on MRI findings showing CNS plaques, cerebrospinal fluid (CSF) analysis revealing oligoclonal bands, visual evoked potentials, and clinical evidence of symptoms separated by time and space.
What Treatments Are Available?
Acute attacks are treated with corticosteroids, IVIG, or plasmapheresis. Long-term disease-modifying therapies include interferon-beta and immunosuppressive drugs. Rehabilitation addresses ongoing symptoms and functional impairments.
Myasthenia Gravis
What is Myasthenia Gravis?
This chronic autoimmune disorder leads to fluctuating skeletal muscle weakness caused by impaired neuromuscular transmission.
What Causes It?
Autoantibodies attack and destroy acetylcholine receptors at the neuromuscular junction, disrupting the communication between nerves and muscles.
What Symptoms Are Characteristic?
Symptoms include ptosis, diplopia, facial weakness, difficulty chewing, swallowing, and speaking, limb and neck weakness. These symptoms typically improve with rest.
How is Diagnosis Made?
| Diagnostic Tool | Purpose |
|---|---|
| Acetylcholine receptor antibodies | Detect presence of autoantibodies |
| Anti-MuSK antibodies | Detect alternative autoantibodies |
| Electromyography (EMG) | Evaluate neuromuscular transmission |
| Edrophonium test | Assess temporary symptom improvement |
| CT/MRI | Identify thymoma presence |
What Are Treatment Approaches?
Treatment includes anticholinesterase medications, immunosuppressants, thymectomy (if thymoma is present), and IVIG or plasmapheresis during exacerbations.
Diabetes Mellitus
Overview
Diabetes Mellitus is a metabolic disorder characterized by chronic hyperglycemia due to insufficient insulin secretion or resistance to insulin.
How Is Blood Sugar Regulated?
Blood glucose is lowered by insulin and raised by glucagon, both produced by pancreatic islets.
Type 1 Diabetes Mellitus
Caused by autoimmune destruction of pancreatic β-cells, resulting in absolute insulin deficiency. It is linked to HLA-DR3 and DR4 genotypes. Symptoms include polyphagia, polyuria, polydipsia, and glycosuria. Diabetic ketoacidosis (DKA) is a critical complication. Lifelong insulin therapy is necessary.
Type 2 Diabetes Mellitus
Characterized by insulin resistance and relative insulin deficiency, often associated with obesity and genetic predisposition. A major complication is the hyperosmolar hyperglycemic state (HHS). Treatment includes lifestyle modification, oral antidiabetic drugs (e.g., metformin), and insulin if required.
How is Diabetes Diagnosed? (WHO Criteria)
| Test | Diagnostic Threshold |
|---|---|
| Fasting glucose | ≥126 mg/dL |
| Random glucose | ≥200 mg/dL |
| Oral glucose tolerance test (OGTT) | ≥200 mg/dL at 2 hours |
| HbA1c | ≥6.5% |
Hyperparathyroidism
What is Hyperparathyroidism?
This disorder is marked by excessive secretion of parathyroid hormone (PTH), leading to hypercalcemia.
What Are the Types?
| Type | Cause |
|---|---|
| Primary | Parathyroid adenoma or hyperplasia |
| Secondary | Chronic hypocalcemia due to chronic kidney disease or vitamin D deficiency |
| Tertiary | Autonomous PTH secretion after prolonged secondary hyperparathyroidism |
What Symptoms Occur?
Symptoms include kidney stones, bone pain, fractures, osteoporosis, gastrointestinal complaints (constipation, nausea), neuropsychiatric symptoms, polyuria, and polydipsia.
How Is It Managed?
Primary hyperparathyroidism is primarily treated surgically. Secondary hyperparathyroidism involves correcting vitamin D and phosphate levels and medications such as calcimimetics (e.g., cinacalcet).
Thyroid Disorders
Hyperthyroidism (Graves’ Disease)
Caused by autoimmune stimulation of thyroid-stimulating hormone (TSH) receptors. Clinical features include weight loss, tremor, anxiety, and heat intolerance. Laboratory findings show decreased TSH and elevated T3/T4. Treatments involve antithyroid medications, beta-blockers, and surgery. Thyroid storm is a severe, life-threatening complication requiring intensive care.
Hypothyroidism (Hashimoto’s Thyroiditis)
Characterized by autoimmune destruction of the thyroid gland, presenting with fatigue, weight gain, and cold intolerance. The mainstay of treatment is levothyroxine replacement therapy.
Otitis Media
What is Otitis Media?
Otitis media is inflammation of the middle ear, predominantly affecting children.
How is It Diagnosed?
Diagnosis is made by observing reduced mobility of the tympanic membrane, confirmed through tympanometry or pneumatic otoscopy.
What is the Treatment?
High-dose amoxicillin is the preferred initial treatment. Mild cases may be managed with watchful waiting.
Mental Health Disorders
| Disorder | Definition | Treatment |
|---|---|---|
| Depression | Depressed mood or loss of interest for ≥2 weeks | SSRIs, psychotherapy, or combination |
| Generalized Anxiety Disorder (GAD) | Excessive worry for ≥6 months | Cognitive Behavioral Therapy (CBT), SSRIs/SNRIs |
| Schizophrenia | Psychotic disorder with positive, negative, and cognitive symptoms | Antipsychotics and psychosocial therapy |
References
American Diabetes Association. (2023). Classification and diagnosis of diabetes. Diabetes Care, 46(Supplement_1), S19–S33. https://doi.org/10.2337/dc23-S002
Kumar, V., Abbas, A. K., & Aster, J. C. (2020). Robbins Basic Pathology (10th ed.). Elsevier.
Harrison, T. R. (2018). Harrison’s Principles of Internal Medicine (20th ed.). McGraw-Hill Education.
Jameson, J. L., Fauci, A. S., Kasper, D. L., Hauser, S. L., Longo, D. L., & Loscalzo, J. (2018). Harrison’s Manual of Medicine (19th ed.). McGraw-Hill Education.