Comprehensive Study Guide (Neuro + Endocrine + Fluid & Electrolyte Integration)

Exam 2 Comprehensive Study Guide (Neuro + Endocrine + Fluid & Electrolyte Integration)

Neurophysiology & Neurological Disorders

1. Brain Structures & Functions

  • Cerebral Cortex

    • Role: Large part of the brain involved with higher cognitive functions.
    • Clinical Presentation of Damage: Damage to the cerebral cortex presents based on the specific area affected (hemisphere or lobe). For example, damage to the temporal lobe may lead to problems with language comprehension or expression.

  • Basal Ganglia

    • Role: Group of subcortical structures that assist in initiating and smoothening voluntary movement through dopamine; they suppress involuntary movement via acetylcholine.
    • Clinical Presentation of Dysfunction:
    • Parkinson’s Disease: Slow initiation of movements due to dopamine deficiency.
    • Tourette’s Syndrome: Tics or inability to suppress movements due to broken signalling pathways.
    • Autism: Related to issues with motor learning and emotional regulation.

  • Limbic System

    • Role: Regulates emotion and memory storage.
    • Amygdala: Acts as a “panic button” for fear, emotional aggression, stimulates SNS, and is involved in trauma response and addiction.
    • Hippocampus: Primarily responsible for memory formation and storage.
    • Hypothalamus: Maintains hormonal balance and links the endocrine and nervous systems.
    • Clinical Presentation of Dysfunction:
    • Anxiety and PTSD: From an overactive amygdala.
    • Alzheimer's Disease: Atrophy of the hippocampus leads to memory loss.
    • Endocrine and Sleep Disorders: Result from damage to the hypothalamus.

  • Brainstem

    • Role: Functions as a conduit between the brain and spinal cord controlling vital bodily functions (breathing, blood pressure, reflexes, etc.).
    • Clinical Presentation of Damage: Damage can cause life-threatening conditions such as respiratory failure, loss of gag reflex, and brain death.

  • Movement Disorders:

    • Most associated with Huntington’s Disease, characterized by chorea (uncontrolled movements), muscle rigidity, and slow or unusual eye movements.

2. Pain Physiology & Management

  • Acute vs Chronic Pain

    • Acute Pain:
    • Duration: Transient, short-lived.
    • Purpose: Protective mechanism related to recent injury meant to alert for prompt attention.
    • Physiological Response: Somatic pain (from skin, joints, muscles) or visceral pain (throbbing/aching from internal organs).
    • Chronic Pain:
    • Duration: Lasts longer than expected healing time, often >3-6 months.
    • Physiological Response: Leads to behavioral and psychological changes, can lead to comorbidities such as depression due to stress.

  • Types of Pain:

    • Nociceptive Pain: Caused by mechanical injury, transduction of noxious stimuli activates nociceptors.
    • Neuropathic Pain: Happens from nerve damage without stimulation, described as burning, shooting, or tingling sensations.
    • Referred Pain: Pain felt in an area distant from its origin, often linked to organ issues.
    • Example: Gallbladder pain manifesting as pain in the right shoulder.

  • Sympathetic Nervous System Activation During Acute Pain:

    • Results in peripheral inflammation, high blood pressure, and heart rate due to nociceptive activation and descending inhibition.

  • Treatment Options for Neuropathic Pain:

    • Pharmacologic: Anticonvulsants like Gabapentin and Pregabalin.
    • Gabapentin (Neurontin): Off-label use with side effects including drowsiness and dizziness.
    • Pregabalin (Lyrica): Controlled substance with potential for hypersensitivity reactions.
    • Non-Pharmacologic: TENS, exercise, acupuncture, physical therapy, heat/cold applications.

  • Multimodal Pain Control:

    • Combining different medication classes (e.g., NSAIDs, opioids, local anesthetics, acetaminophen) allows smaller doses of multiple medications to address different pain types without high doses of a single drug.

  • Adverse Effects and Safety Considerations:

    • NSAIDs: Risk for gastric ulcers, bleeding, renal impairment, hypertension; should be taken with food and monitored for low platelets.
    • Acetaminophen: Risk for hepatotoxicity; maximum dose limits depending on liver function.
    • Lidocaine: Risk for arrhythmias, avoid in broken skin due to systemic toxicity.
    • Morphine: Risk for respiratory depression and constipation; fall precautions and fluid improvement necessary.

3. Opioids & Their Clinical Management

  • Typical Effects of Opioids:

    • Respiratory depression, sedation, constipation, and pruritus.

  • Opioid-Related Conditions:

    • Overdose/Toxicity: Manage with Naloxone (Narcan); monitor respiratory status.
    • Tolerance and Dependence: Tolerance can lead to dependence and addiction; explore non-pharmacologic methods and manage opioid-induced constipation.
    • Withdrawal Symptoms: Present flu-like symptoms, body pain indicative of autonomic overactivity, anxiety, irritable behavior.

4. Extrapyramidal Symptoms (EPS)

  • Definition of EPS:

    • Movement disturbances resulting from dopamine receptor blockage. Symptoms include:
    • Akathisia: Restlessness.
    • Dystonia: Muscle spasms.
    • Pseudo-Parkinsonism: Mimicking Parkinson’s symptoms.
    • Tardive Dyskinesia: Involuntary facial and jaw movements.
    • Bradykinesia: Slow movements.
    • Tremor: Shaky movements.

  • Common Medication Causes of EPS:

    • Typically associated with dopamine-receptor blockers, notably antipsychotics.

5. Seizure Disorders

  • Pathophysiology of Seizures:

    • Abnormal or uncontrolled neuronal discharges due to imbalances of excitatory (high glutamate) and inhibitory (low GABA) signals.

  • Trigger Factors: Genetic predisposition and environmental factors can overstimulate brain activity.

  • Medications:

    • Status Epilepticus Medications:
    • Benzodiazepines (e.g. Lorazepam): CNS depressants that enhance GABA, potential respiratory depression.
    • Barbiturates (e.g. Phenobarbital): Control seizures by altering GABA action.
    • Maintenance/Prophylaxis Medications:
    • Hydantoins: Such as Phenytoin, require careful monitoring due to narrow therapeutic range; can cause side effects like ataxia.

  • Safety and Teaching:

    • Adherence is critical to prevent rebound seizures; risks associated with medications, especially teratogenic effects and potential CNS depression.

6. Neurodegenerative & Neuromuscular Disorders

  • Common Danger of ALS, Guillain-Barré, and Myasthenia Gravis:

    • Diaphragmatic paralysis leading to respiratory failure.

  • IVIG Usage in GBS and MG:

    • Effective for B-cell mediated conditions; works by flooding the body with antibodies to suppress harmful auto-antibodies.

  • Multiple Sclerosis (MS) Treatment Goals:

    • Early treatment of flares, reduce severity, preserve neuro function and prevent diaphragmatic paralysis.

7. Parkinson’s Disease

  • Neurochemical Imbalance:

    • Dopamine shortage and Acetylcholine excess in the basal ganglia’s substantia nigra causing motor issues.

  • Motor Symptoms:

    • Progressive symptoms such as tremors, rigidity, and bradykinesia developing over time.

  • Orthostatic Hypotension: Results from autonomic dysfunction tied to Parkinson's.

  • Medication Goals:

    • Levodopa-carbidopa to improve dopamine levels; Benztropine to reduce tremors and rigidity.
    • Non-Pharmacologic Strategies: Implement safety assessments to manage fall risks.

8. Alzheimer’s Disease

  • Therapeutic Goals:

    • Aim to slow disease progression using cholinergic drugs; no cure currently exists.

  • Stages of Manifestations:

    • Early Stage: Forgetfulness, misplacing items, and impairment in decision-making; opportunity for advanced directives.
    • Middle Stage: Increased confusion, agitation, weight loss due to poor nutrition.
    • Late Stage: Inability to perform ADLs, loss of bowel and bladder control, reliance on caregivers.

  • Caregiver Support and Environmental Modifications: Important for managing the unique challenges at each disease progression stage; opportunities for respite care.

Endocrine & Fluid-Electrolyte Regulation

9. Posterior Pituitary Disorders

  • Diabetes Insipidus (DI):

    • Mechanism: Lack of Antidiuretic Hormone (ADH) availability.
    • Lab Findings: High serum sodium, high osmolality; low urine specific gravity; increased urine output.

  • SIADH:

    • Lab Values: Low sodium, low serum osmolality, high urine specific gravity, and low urine output (fluid overload).

  • Desmopressin:

    • Action: Synthetic ADH that promotes water reabsorption in kidneys.
    • Therapy Monitoring: Effective therapy indicated by decreased urine output and decreased serum osmolality.

10. Thyroid Function Disorders

  • Hypothyroidism vs Hyperthyroidism:

    • Lab Patterns:
    • Hypothyroidism: High TSH, low T3/T4.
    • Hyperthyroidism: Low TSH, high T3/T4.
    • Clinical Manifestations:
    • Hypothyroidism: Fatigue, cold intolerance, constipation, weight gain.
    • Hyperthyroidism: Anxiety, irritability, weight loss, fever, palpitations.

  • Thyroid Storm:

    • Definition: A severe emergency state due to physiological stress leading to increased T3/T4 effects.
    • Symptoms: High fever, severe tachycardia, hypertension.
    • Management: IV beta blockers, PTU to block hormone synthesis, use of cooling measures.

11. Adrenal Disorders

  • Addison’s vs Cushing’s Syndrome:

    • Hormone Levels:
    • Addison’s: Low cortisol, high aldosterone.
    • Cushing’s: High cortisol, normal aldosterone.
    • Physical Findings:
    • Addison’s: Hyperpigmentation, fatigue, weight loss; low sodium and blood pressure.
    • Cushing’s: Truncal obesity, thin extremities; high BP and blood glucose levels.

  • Cortisol Excess Effects:

    • Impacts metabolism, immune system, and mood stability during stress.

  • Addisonian Crisis:

    • Can cause life-threatening hypotensive shock; priority treatment is fluid resuscitation and high-dose steroids.

12. Parathyroid Disorders

  • Hyperparathyroidism:

    • Lab Values: High PTH, high calcium, low phosphate in blood.
    • Risks: Increased fragility in bones leading to fractures.

  • Hypoparathyroidism:

    • Lab Values: Low PTH, low calcium, high phosphate in blood.
    • Risks: Neuromuscular issues due to calcium imbalances.

13. Glucose Regulation

  • Chronic Hyperglycemia Effects:

    • Microvascular complications including retinopathy, nephropathy, neuropathy.
    • Macrovascular complications including accelerated atherosclerosis increasing chances of MI, stroke, and peripheral artery disease.

  • DKA vs HHS:

    • DKA: Labs show metabolic acidosis, blood glucose >200 mg/dL with marked dehydration.
    • HHS: High serum osmolality, blood glucose >600 mg/dL, mild acidosis.

  • Electrolyte Replacement:

    • Especially potassium is critical during treatment to prevent complications.

14. Polycystic Ovarian Syndrome (PCOS)

  • Pathophysiology: Hormonal imbalance and insulin resistance.
  • Signs/Symptoms: Irregular periods, fertility issues, weight difficulties impacting overall health.

15. Electrolyte Relationships & Clinical Manifestations

  • Calcium–Phosphate Inverse Relationship: Imbalances can lead to various clinical manifestations.
  • Potassium–Hydrogen Relationship in Acid–Base Disorders: Essential to understand for diagnosis and treatment.
  • Magnesium–Potassium–Calcium Interdependence: Magnesium must be corrected first in hypomagnesemia.
  • Key Manifestations of Imbalance:
    • Na⁺: Neuro disturbances.
    • K⁺: Cardiac arrhythmias.
    • Ca²⁺: Tetany, pseudopregnancy.
    • Mg²⁺: Impact on cardiac conduction and muscle excitability.

16. Fluid Balance & RAAS

  • Fluid Compartments: Differentiate between intracellular, extracellular, and intravascular compartments.
  • RAAS Functionality: Raises blood pressure through sodium/water retention and vasoconstriction.
  • Dehydration Lab Changes: Elevated serum sodium, increased osmolality, and altered urine specific gravity measurement.
  • Challenge: Compare dehydration labs to DI and SIADH patterns.

Study Tips

  • Utilize matrix tables for visual learning and comparisons.
  • Use the ‘teach-back’ technique to explain imbalances, ensuring comprehension.
  • Continuously revisit medication rationales and associated adverse effects.
  • Cluster conditions based on shared risks (e.g., respiratory compromise, fluid imbalance).
  • Prioritize safety assessments focusing on airway, breathing, circulation, mental status, and electrolyte stability.