Exam 2 Flashcards
Nociceptors
“pain/sensory” receptors that are activated by noxious stimuli that damage or threaten the body’s integrity.
What are noxious stimuli?
harmful or potentially damaging stimuli that can cause pain, injury or discomfort
Where are nociceptors located?
Everywhere (skin, muscles, joints, bones, internal organs)
Most sensitive areas: fingertips (there are a lot located here)
Least sensitive area: cartilage (none, so no direct pain)
Acute Pain - Definition & Source
a protective mechanism to warn of actual or impending injury
- External agent or internal disease usually known
Acute Pain- Duration
Transient (up to 6 months)
Acute pain: Clinical signs
Sympathetic response:
- increased HR
- Increased BP
-increased RR
- diaphoresis/sweating
-dilated pupils
Acute pain: Prognosis
complete relief is likely
Chronic Pain: Source
Unknown; if known, treatment is prolonged or ineffective
Chronic Pain: Duration
Prolonged and persistent (months to years)
Chronic Pain: Clinical Signs
Response patterns very; fewer overt signs, sympathetic unresponsiveness (adaptation).
Usually, no increase in HR or BP and calm d/t adaptation
Chronic Pain: Prognosis
Complete relief usually not possible
Temperature regulation: Protective mechanism/hyperthermia
Moderate fever helps the body respond to infectious processes.
However, extreme, prolonged hyperthermia can produce complications such as nerve damage, coagulation of proteins, convulsions, and even death
Temperature regulation: Pyrogens
a substance that can cause a fever
Pyrogens: Sources
1) Exogenous pyrogens are produced by pathogens
2) Endogenous pyrogens are produced primarily by phagocytic cells (prostaglandin, interleukins)
Benefits of Fever
- Kills pathogens & stunts growth: Raising body temperature kills many pathogens and adversely affects their growth and replication.
- Decreases bacterial replication: Higher body temperatures decrease serum levels of iron, zinc, and copper—minerals needed for bacterial replication.
- Increased temperature causes lysosomal breakdown and auto destruction of cells, preventing viral replication in infected cells.
- Heat increases lymphocytic transformation and motility of polymorphonuclear neutrophils, facilitating the immune response.
- Phagocytosis is enhanced, and production of antiviral interferon is augmented.
Phagocytosis
process where immune cells, neutrophils & macrophages, “eat” and destroy harmful invaders
ex. bacteria, viruses, dead cells
antiviral interferon
interferons (IFN) special proteins made by immune system to help fight viruses = warning signals
polymorphonuclear neutrophils
type of WBC that help fight infections especially bacterial
Effects of Fever at the Extremes of Age
Infection and fever responses in older adults and children may vary from those in normal adults
Effects of Fever at the Extremes of Age
Older Adult Persons
Subtle or atypical responses to infectious fever are often accompanied by dehydration, and in severe systemic infection there may be no fever.
Symptoms can include feeling cold or warm, having strange body sensations, headache, vivid dreams, and hallucinations.
Severe systemic infections may cause alternating hypothermia and high fever in a 24 h period.
Effects of Fever at the Extremes of Age
Infants and Children
Infected babies may not develop infectious fever in the first few days of life.
Young infants (less than 60–90 days of age) often present with fever and no other symptoms, making differential diagnosis difficult.
Children develop higher temperatures than adults for relatively minor infections, and any skin vasoconstriction can lead to a rapid increase in body temperature.
Severe systemic infections may cause alternating hypothermia and high fever in a 24 h period, the same as elderly adults.
Sleep: Obstructive sleep apnea syndrome (OSAS)
- Most commonly diagnosed sleep disorder
- Occurs in all age groups
- incidence of OSAS increases w. age 60>
OSA: Risk Factors
“STOP-MAC”
🔹 S – Sex (Male) – Males are at higher risk
🔹 T – Tonsillar & adenoid enlargement – Large tonsils/adenoids can block airflow
🔹 O – Obesity – Excess weight increases airway collapse
🔹 P – Postmenopausal (without hormone therapy) – Higher risk in postmenopausal women
🔹 M – Maturity (Older Age) – Risk increases with age
🔹 A – Anomalies (Craniofacial) – Structural issues like a small jaw
🔹 C – Collapsed airway – Any condition leading to airway narrowing
OSA: Causes
- partial or total upper airway obstruction to airflow recurring during sleep w/ continuous respiratory efforts made against a closed airway.
Obstructive sleep apnea happens when the airway gets partially or completely blocked during sleep, making it hard to breathe. The body keeps trying to breathe, but the blocked airway stops airflow.
OSA: Symptoms
- Loud snoring
- Gasping
- Multiple apneic episodes that last > 10 seconds
Central sleep apnea: Cause
happens when the brain temporarily stops telling the body to breathe during sleep. This happens because the brain doesn’t respond properly to changes in oxygen and carbon dioxide levels, and the muscles that keep the airway open don’t work as well.
OSA: Obesity hypoventilation syndrome (OHS)
happens when being overweight makes it harder to breathe properly, especially during sleep. This leads to too much carbon dioxide (hypercapnia) in the blood and disrupted breathing patterns.
Over time, the irregular breathing causes frequent wake-ups during sleep, making it difficult to get enough deep sleep, especially REM sleep. This leads to poor sleep quality, daytime tiredness, and low oxygen levels, which can cause serious health problems if not treated.
Obesity hypoventilation syndrome (OHS): Can Cause
“PPP SLEEP DR” 💤🚑
🔹 P – Polycythemia (Increased red blood cells due to low oxygen)
🔹 P – Pulmonary Hypertension (High blood pressure in the lungs)
🔹 P – Peripheral Edema (Swelling in the legs and feet)
🔹 S – Systemic Hypertension (High blood pressure in the body)
🔹 S – Stroke (Increased risk due to low oxygen and high blood pressure)
🔹 L – Liver Congestion (Blood flow issues affecting the liver)
🔹 E – Enlarged Right Heart (Right-Sided Congestive Heart Failure)
🔹 E – Elevated Cyanosis (Bluish skin from poor oxygen circulation)
🔹 P – Poor Heart Rhythm (Dysrhythmias) (Irregular heartbeats)
🔹 D – Decreased Oxygen Levels (Causing long-term damage)
🔹 R – Right-Sided Heart Failure (Heart struggles to pump blood)
Memory Trick:
Think “PPP SLEEP DR” – because sleep apnea “puts you in the doctor’s office” for serious health issues! 😴🚑
Hearing: Conductive hearing loss - Cause
Occurs when there is interference in air conduction
Conductive hearing loss - Cause
- impaired cerumen
- forieng bodies lodges in ear canal
- benign tumors of the middle ear
-carcinoma of the external auditory canal or middle ear
Conductive hearing loss - Symptoms
- diminished hearing
-soft speaking voice b/c usually hear voice, conducted by bone, as loud - people usually hear better in a noisy environment than in a quiet one
Conductive hearing loss - Treatment
of underlying cause generally improves hearing
-hearing aid can improve quality of life
Sensorineural hearing loss: Causes
- impairment of the organ of corti or its central connections
- congenital & hereditary factors
- noise exposure
-aging - ototoxicity (damage to the ear)
- systemic disease (syphilis, Paget disease, collagen diseases, diabetes mellitus)
Sensorineural hearing loss: Organ of Corti
The Organ of Corti is the hearing center inside the inner ear. It sits in the cochlea and is responsible for converting sound waves into nerve signals that the brain can understand.
Presbycusis
age-related hearing loss, mainly affecting high-frequency sounds.
It is the most common type of sensorineural hearing loss, especially in older adults.
Presbycusis: Causes
Causes:
* Damage to the Organ of Corti (loss of auditory receptors)
* Poor blood flow (vascular changes)
* Stiffening of the basilar membrane
Presbycusis: Symptoms
- Gradual hearing loss over time
- Difficulty hearing high-pitched sounds (e.g., birds chirping, phone ringing)
- Trouble understanding speech, especially in noisy places
Presbycusis: Additional Risk
Certain ototoxic drugs (e.g., antibiotics, aspirin, mercury, tobacco, alcohol) can worsen hearing loss by damaging auditory function.
Glaucoma
leading cause of vision loss and blindness due to increased intraocular pressure (IOP).
This happens when the aqueous humor cannot drain properly through the trabecular meshwork or canal of Schlemm, causing pressure buildup.
Glaucoma: Open-angle glaucoma
Open-angle glaucoma is the most common type.
* Chronic high IOP damages the optic nerve and kills retinal ganglion cells.
* Early symptoms: Peripheral vision loss (tunnel vision), later progressing to central vision loss and blindness.
* Risk Factor: Family history (can be inherited).
Glaucoma: Cause of Vision Loss
Optic nerve damage from high pressure leads to gradual loss of visual acuity.
Multiple Sclerosis (MS)
Chronic autoimmune inflammatory disorder that destroys the myelin sheath, disrupting nerve signal transmission.
Multiple Sclerosis (MS): Pathophysiology:
- Demyelination leads to nerve signal disruption → causes motor symptoms, weakness, and slurred speech.
- Plaques form in the central nervous system (CNS) due to inflammation, scarring, and axon loss.
- B-cells produce myelin-specific antibodies.
- T-cells recognize myelin as an autoantigen, triggering an immune response.
Multiple Sclerosis (MS): Cause
Autoimmune attack on myelin in genetically susceptible individuals.
Guillain-Barré Syndrome (GBS): Definition
- Autoimmune disorder where the immune system attacks healthy nerves in the peripheral nervous system (PNS).
- Often triggered by a bacterial or viral infection.
- Vaccinations can also act as a trigger.
Guillain-Barré Syndrome (GBS) : Onset
Symptoms usually appear days to weeks after an infection or vaccination.
Guillain-Barré Syndrome (GBS): Immune System Role
- Normally, antibodies and white blood cells attack bacteria and viruses.
- In GBS, the immune system mistakenly targets healthy nerve cells.
- This may happen because bacterial and viral surface chemicals resemble nerve cell structures (molecular mimicry).
- The immune system fails to distinguish between pathogens and nerve cells, leading to an autoimmune attack.
Guillain-Barré Syndrome (GBS): Nerve Damage & Symptoms:
- The myelin sheath (protective nerve covering) is damaged, and in some cases, the axons are also affected.
- Impaired nerve signal transmission leads to:
- Muscle weakness
- Loss of coordination
- Reduced ability to respond to brain commands
Amyotrophic Lateral Sclerosis (ALS): Definition
- ALS is a motor neuron disease that leads to degeneration and death of upper and lower motor neurons.
- Formerly known as Lou Gehrig’s disease.
- Affects the neuromuscular junction (NMJ), preventing signals from reaching muscles.
Amyotrophic Lateral Sclerosis (ALS): Pathophysiology
- “Amyotrophic” → Lower motor neuron (LMN) involvement → Muscle wasting (atrophy).
- “Lateral Sclerosis” → Upper motor neuron (UMN) involvement → Scarring of the spinal cord.
- As motor neurons degenerate and die, they stop sending signals to muscles → muscle weakness, twitching (fasciculations), and atrophy.
- The brain loses the ability to control voluntary movements.
Amyotrophic Lateral Sclerosis (ALS): Symptoms & Progression
Bulbar onset ALS progresses more rapidly and affects:
* Speech (dysarthria)
* Swallowing (dysphagia)
* Saliva control
Respiratory failure is the most common cause of death.
Most patients die within 3–5 years, but 10% survive over a decade.
Amyotrophic Lateral Sclerosis (ALS): Risk Factor
Family history (genetic predisposition).
Parkinson’s Disease: Primary
Primary PD:
* Exact cause unknown (idiopathic).
* Caused by degeneration of the basal ganglia, affecting:
* Corpus striatum
* Globus pallidus
* Subthalamic nucleus
* Substantia nigra
Hallmark pathology: Dopaminergic deficiency in the striatum, brainstem, and cortex.
Parkinson’s Disease: Secondary PD
Caused by other neurodegenerative or acquired disorders, such as:
* Drugs (antipsychotics).
* Repeated head trauma (e.g., boxing).
*Toxic exposure (pesticides, heavy metals, herbicides).
Parkinson’s Disease (PD): Diagnosis
Caused by other neurodegenerative or acquired disorders, such as:
* Drugs (antipsychotics).
* Repeated head trauma (e.g., boxing).
*. Toxic exposure (pesticides, heavy metals, herbicides).
Parkinson’s Disease (PD): Clinical Manifestations/ Motor Symptoms
- Resting tremor – “Pill-rolling” hand tremor.
- Bradykinesia/Akinesia – Slow or absent movement (poverty of movement).
- Rigidity – Muscle stiffness, resistance to passive movement.
- Postural abnormalities – Impaired balance & stability.
Parkinson’s Disease (PD): Characteristic Appearance
Facial expression:
* Wide-eyed, unblinking, and staring appearance.
* Facial muscles appear smooth and immobile.
* Drooling from slightly open mouth.
Parkinson’s Disease (PD): Gait (Pathognomonic Features)
- Slow, short, shuffling steps.
- Arms flexed, abducted, and held stiffly at the side.
- Trunk bent slightly forward.
- May spontaneously break into a run when pushed forward or backward.
- Postural instability → Falls to the side due to poor balance control.
Myasthenia Gravis (MG): Definition & Pathophysiology
- Chronic autoimmune disease affecting the neuromuscular junction.
- Mediated by acetylcholine receptor (AchR) antibodies, which block or destroy receptors needed for muscle contraction.
- Results in impaired nerve-to-muscle communication, leading to muscle weakness.
Myasthenia Gravis (MG): Onset & Triggers
- Gradual (insidious) onset.
- Symptoms may first appear:
- During pregnancy.
- Postpartum period.
- After administration of certain anesthetic agents.
Myasthenia Gravis (MG): Hallmark Symptoms
Exertional fatigue & muscle weakness:
* Worsens with activity.
* Improves with rest.
* Returns with resumption of activity.
- Common complaint: Fatigue after exercise.
- History of recurring upper respiratory tract infections.
Myasthenia Gravis (MG): Affected Muscles & Clinical Manifestations: First Affected
Extraocular (eye) muscles → Diplopia (double vision), ptosis (drooping eyelid), ocular palsies.
Myasthenia Gravis (MG): Affected Muscles & Clinical Manifestations: Next Affected
Muscles of facial expression, mastication, swallowing, and speech → Difficulty smiling, chewing, and talking.
Delirium
Age: Usually older
Onset: Acute—common during hospitalization
Associated conditions: Urinary tract infection, thyroid disorders, hypoxia, hypoglycemia, toxicity, fluid-electrolyte imbalance, renal insufficiency, trauma, multiple medications
Course:Fluctuating; remits with treatment
Alertness: Impaired
Orientation: Impaired
Dementia
Age: Usually, older
Onset:insidious
Associated conditions: May have no other conditions
Course:Chronic slow decline
Alertness: Normal
Orientation: Intact early; impaired late
Alzheimer disease (AD) : Definition
Also called Dementia of Alzheimer Type (DAT) or Senile Disease Complex.
Leading cause of dementia and a major cause of severe cognitive dysfunction in older adults.
Alzheimer disease (AD): Pathophysiology
- Causes progressive deterioration of cognition, memory, and judgment.
- Exact cause unknown; the disease process is complex and not fully understood.
Alzheimer disease (AD): Risk Factors
- Age – Most significant risk factor.
- Family history – Genetic predisposition.
- More common in males.
Alzheimer disease (AD): Diagnosis
- First step: Rule out all other causes of dementia.
- Comprehensive evaluation includes:
- Clinical history – Behavioral and cognitive changes.
- Cognitive testing – Memory, reasoning, and problem-solving skills.
- Course of illness – Symptom progression over time.
- Laboratory tests & brain imaging – To exclude other conditions (e.g., stroke, tumors, metabolic disorders).
Focal Brain Injury
Focal brain injury is a traumatic brain injury (TBI) that affects a specific area of the brain rather than the entire brain.
Types of Focal Brain Injury: Direct Impact Injury (Contusion)
- Caused by a direct blow to the head (e.g., fall, gunshot wound, blunt trauma).
- May or may not involve loss of consciousness.
- Most common type of TBI—can range from mild to fatal.
Types of Focal Brain Injury: Acute Ischemic Stroke (Focal Brain Ischemia with Infarction)
- A stroke is considered a type of focal brain injury
Types of Acute Ischemic Stroke (T.H.E)
- Transient Ischemic Attack (TIA) – A temporary blockage, often called a “mini-stroke.”
- Hemorrhagic Stroke – Bleeding in the brain due to a ruptured blood vessel.
- Embolic Stroke – A clot travels to the brain, blocking blood flow.
Acute Ischemic Stroke: Effects
Can lead to cell death, motor impairment, sensory deficits, cognitive dysfunction, and infarction.
Acute Ischemic Stroke: Causes
- Arterial obstruction of blood flow to the brain.
- Blood flow below 25% of normal or lasting more than 30–60 minutes can cause infarction.
Acute Ischemic Stroke: Risk Factor
- High blood pressure (hypertension) is the leading cause of stroke.
- Hypertension can weaken or block arteries, increasing stroke risk.
Diffuse Axonal Injury (DAI) – Widespread Brain Damage: Cause
Caused by rapid acceleration-deceleration of the head (e.g., whiplash from a car accident).
- Shearing forces damage axons at the junction of gray and white matter in the brain.
Major cause of diffuse brain injuries in motor vehicle accidents.
Diffuse Axonal Injury (DAI): Leads to
- Axonal injury
- Vascular damage
- Brain swelling (edema)
Closed Head Injuries: Definition
- Closed head injuries involve specific, visible damage to the skull and brain at a precise location.
- The dura mater remains intact, meaning brain tissues are not exposed to the environment.
Closed Head Injuries: Blunt Trauma & Severity
- 75% to 90% of blunt trauma injuries are mild, but more severe cases can involve:
- Damage to the cranial vault (skull).
- Injury to blood vessels.
- Disruption of supporting brain structures.
Closed Head Injuries: Types
- Coup Injury
- Occurs directly at the site of impact (e.g., hitting the forehead in a fall).
- Contrecoup Injury
- Occurs on the opposite side of the initial impact.
- Caused by brain rebounding within the skull or force transmission through cerebrospinal fluid (CSF).
Secondary Brain Injury:
Indirect results of primary brain injury (trauma, stroke syndromes)
Triggered by a cascade of cerebral and molecular events lasting hours to days after the initial injury
Secondary Brain Injury: Causes
- Inflammatory mediators
- decreased cerebral perfusion pressure (CPP)
Secondary Brain Injury: Systemic Processes Risk Factors
- Hypotension
- Hypoxia
- Anemia
- Ischemia
- Hypercapnia (increased CO2 levels)
- Hypocapnia (decreased CO2 levels)
Migraines: Type
Vascular headache (trigeminovascular system activation)
Migraines: Pathophysiology
- Changes in brain metabolism and blood flow.
- Inflammatory mediators cause sterile meningeal inflammation and blood vessel edema.
- Neurotransmitter release contributes to pain.
Migraines: Theories
- Neurologic
- Vascular
- Hormonal
- Neurotransmitter involvement
Migraines: Key Features
- Throbbing pain
- More common in females
Migraines: differ from
- Cluster headaches (steady pain)
- Tension headaches (non-vascular origin)
Cluster Headaches Vascular headache (trigeminal autonomic cephalalgia): Pathophysiology
- Trigeminovascular system activation → release of vasoactive peptides and neuroinflammation (similar to migraines).
- Trigeminal-autonomic reflex activation leads to:
- Sympathetic underactivity
- Parasympathetic activation
Cluster Headaches: Key Features
- Steady pain
- Autonomic symptoms (e.g., lacrimation, nasal congestion)
Tension Headaches (TTH): Non-vascular headache: Pathophysiology
- Central and peripheral mechanisms involved.
- Peripheral sensitization of myofascial nociceptors → muscular hypersensitivity.
- Pericranial muscle tenderness from peripheral nociceptor activation around:
- Blood vessels in striated muscle
- Tendon insertions
- Fascia
Tension Headaches (TTH): Non-vascular headache: Key Features
- Steady pain
- Muscle tenderness
CHARACTERISTICS OF COMMON HEADACHES
MIGRAINE WITH OR WITHOUT AURA CLUSTER HEADACHE TENSION TYPE OF HEADACHE
Gender Female Male Not gender specific
Family history of headaches Yes No Yes
Onset and evolution Slow to rapid Rapid Slow to rapid
Time course Episodic Clusters in time Episodic, may become constant
Quality Usually throbbing Steady Steady
Location Variable, often unilateral Orbit, temple, cheek Variable
Associated features Prodrome, vomiting Lacrimation, rhinorrhea, Horner syndrome None
Schizophrenia: Cause
Combination of genetic and multiple factors (multifactorial).
Schizophrenia: Brain Structure Changes
- Enlarged lateral and third ventricles.
- Weakened amygdala connections → affects emotional processing and social judgment.
- Frontal lobe shrinkage over time → leads to cognitive decline.
Schizophrenia: Neurotransmitter Changes
- Dopamine pathway dysfunction (not just high dopamine levels, as previously thought).
- Still being studied, but linked to altered brain signaling
Anxiety Disorders: Definition
Characterized by excessive and persistent worry that interferes with daily functioning.
Anxiety Disorders: Prevalence
- Most common psychiatric illness.
- Affects 10%–30% of the general population.
- High comorbidity with major depression, suggesting a shared neural pathophysiologic basis.
Types of Anxiety Disorders
- Panic Disorder (PD)
- Social Anxiety Disorder (SAD)
- Generalized Anxiety Disorder (GAD)
- Posttraumatic Stress Disorder (PTSD)
Anxiety: Complications
Agoraphobia (common in panic disorder) → phobic avoidance of situations where escape or help is difficult.
Avoided situations include:
- Being away from home
- Standing in line or in a crowd
- Traveling by train, plane, or automobile
Severe cases: Individuals may become housebound.
Neuro Disorders in Peds:
Congenital Hydrocephalus
Definition: Excess cerebrospinal fluid (CSF) accumulation in ventricles.
Congenital Hydrocephalus: Causes
- Overproduction of CSF.
- Obstruction of CSF flow.
Congenital Hydrocephalus: Pathophysiology
- The brain is enclosed within the skull (fixed container).
- Increased CSF or brain edema → ↑ pressure on the brain → affects:
- Blood flow
- Oxygen delivery
- Nerve transmission
Neural Tube Defects (NTDs): Causes
- No identified gene; appears multifactorial (genetic + environmental).
- Folic acid deficiency is a major risk factor.
- Folate fortification (U.S., 1996) significantly reduced NTDs.
Types of NTDs: Meningocele
- Sac protrudes from spinal column.
- Sac contains spinal fluid, but no neural tissue.
- May be covered by skin or meninges.
Types of NTDs: Myelomeningocele (severe form)
- Spinal cord, meninges, spinal fluid, and nerves develop outside the body in a fluid-filled sac.
Symptoms:
- Muscle weakness/paralysis below the sac.
- Bowel and bladder dysfunction.
- Hydrocephalus (excessive brain fluid).
Types of NTDs: Encephalocele (rare)
- Part of skull fails to close during pregnancy.
- Brain tissue and spinal fluid protrude, forming a sac-like bulge.
Seizures: Causes
- Brain structural abnormalities
- Hypoxia
- Intracranial hemorrhage
- CNS infection
- Traumatic brain injury
- Electrolyte imbalance
- Inborn metabolic disorders
- Familial Link: Some seizures have a genetic component.
Seizures: Febrile Seizures
- Most common childhood seizure.
- Benign; DO NOT cause epilepsy
Childhood Epilepsy: Cause
Unknown (presumed genetic).
Childhood Epilepsy: Pathophysiology
- Overexcited neurons discharge abnormally, leading to seizures.
- Clinical manifestations depend on the location and spread of abnormal electrical activity.
- May involve motor, sensory, autonomic, behavioral, or consciousness changes.
Childhood Epilepsy: Diagnosis
≥2 unprovoked seizures occurring >24 hours apart
