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NRSE 2121 Exam 4 Notes

Otitis Media, Visual Impairment
Otitis Media
 Inflammation of the middle ear
o Major reason for seeking medical treatment for peds
 Poor functioning of the eustachian tube
o Shorter, more flexible tube
o Negative pressure build up  prevention of drainage
 Risk factors
o Pacifiers
o Secondhand smoke
o Gastroesophageal reflux
 Incompetent esophageal sphincter
o Low socioeconomic status
o Daycare attendance
o Use of bottle in babies
o Males, Native Americans, Eskimo children
o Children with craniofacial abnormalities
o Children with down syndrome
Acute Otitis Media
 Sudden onset of ear pain
o Accompanies some sort of upper respiratory infection
 Usually of short duration
 Presentation
o Irritability, difficulty eating and sleeping
o Tugging at the affected ear as well as fever and pain
o Reddened tympanic membrane
 Poor mobility
 Bulging and ruptured
 Treatment
o Antibiotics
o “wait and see”
o Tubes
Chronic Otitis Media
 Inflammation in the middle ear
o > 12 weeks
 Prolonged inflammation  atrophy or perforation of tympanic membrane
o Scar tissue that latches onto membrane and pulls it back (inhibiting movement)
 Presentation
o Purulent drainage from ear
o Pain is atypical
o Hearing loss possible
Treatment – typically surgery
o To remove debris in middle ear
o Placement of ventilation
o Adenoidectomy
 Cloudiness or opacity of lens
o Painless, blurred vision, eventual loss of sight
 Increased glare at night, blurred vision, and altered color perception
o Due to refraction of light
 Cause
o Aging
o Trauma
o Congenital factors
o Metabolic disease
o Medications
 Surgical removal of the cataracts with replacement of lens
Age Related Macular Degeneration
 Central vision loss due to macular degeneration
o Risks
 Age, female gender, history of cigarette smoking, family history of AMD,
increased serum cholesterol level, hypertension, and previous cataract
 Oxidative stress and inflammatory chemicals may  retinal pigment epithelium decline
 impaired O2 delivery through epithelium  release of cytokines and growth factor
 new blood vessel growth
o Not competent vessels
 New vessels look  altered reception of light in retinal cells
 Two types of macular degermation
o Dry (atrophic)
 Most common
 One eye affected – progressively affects both eyes
 More gradual vision loss
 Outer retinal degermation + pigments layer + choroid
 Drusen accumulation (cell debris)
 Continued metabolic dysfunction of retina
 Presentation
 Ophthalmoscope shows yellow deposits
o Wet (exudative)
 More rapid visual loss
 Greater visual disruption earlier on
Barrier dysfunction  sub-retinal effusions
 Detachment
 Neovascularization
AMD Presentation
 Painless
 Atrophic AMD  blurred vision and acuity
 Greater light requirement
 Area of visual loos grows in size
 Wet-progressive blurring of vision  wavy vertical lines
o Due to fluid accumulation
AMD Diagnosis
 H&P
o History and physical
 Visual acuity
 Retinal examination
o See deposits
o Neovascular
 Amsler grid
 Fluorescein angiography
o Evidence of choroidal changes
 Problem maintaining pressure between and parts of eye
 Canal of Schlemm – channel that equalizes pressure
 Two types
o Chronic open angle
 Canal of Schlemm is normal
 Intraocular pressure increased by a decreased in the outflow of aqueous
humor  gradual loss of vision in periphery
 Field of vision gets narrower
 Cellular cause is death of retinal ganglion cells
 Optic disc becomes atrophic
 Subtle onset with constant elevated intraocular pressure
 Treatment
 Increasing aqueous humor drainage
 Decreased intraocular pressure: prostaglandin analogue eye drops
(first line)
 High interocular pressure
o Angle closure
 Angle between pupil and lateral space of cornea is narrow  blockage of
aqueous humor outflow when pupil dilated
 Severe eye pain
 Nausea and Vomiting
 Blurred vision with halos
 Red eye
 Dilated pupil nonreactive to light
Medical emergency
 Decreased intraocular pressure with carbonic anhydrase, miotics
Symptom of underlying problem
Divided into four stages
o Transduction
o Transmission
o Perception
o Modulation
 Conversion
 Nociceptors
o Transduce
 Chemical mediators after the membrane potential of the pain receptor
o Chemical mediators include K+, H+. lactate, histamine, serotonin, bradykinins,
and prostaglandins
o Released as result of injury
o Inhibit prostaglandin production by inhibiting cyclooxygenase (enzyme that
normally converts arachidonic acid to prostaglandins
 Stimulated nociceptors transmit impulses to the CNS by means of specialized sensory
 Primary sensory fibers include
o Aδ – large, myelinated fibers involved in transmission of sharp, stinging, localized
o C – small, unmyelinated fibers involved in transmission of more diffuse pain, dull,
 Most sensory afferent pain fibers enter the spinal cord by way of posterior nerve roots –
travel to the substantia gelatinosa.
 Pain signals enter SC via dorsal horn and eventually cross to anterolateral tract
Anterolateral (spinothalamic) tract has two divisions
o Neospinothalamic tract
 Thalamus to sensory cortex
o Paleospinothalamic tract
Lamina V – Key area for referred pain
o Numerous Aδ and C fibers deliver somatic input
 Mechanical, thermal, and chemical receptors
o Sensory afferent neurons from visceral receptors terminate in lamina V
 Somatic and visceral fibers CONVERGENCE might explain referred pain
 Pain from a visceral organ is perceived at body surface
Signals entering lower brain centers cause conscious perception of pain
Cortex interprets pain quality
Wind Up
 Many neurotransmitters and neuropeptides involved in synaptic transmission at the
spinal cord level
o Substance P, glutamate, GABA, cholecystokinin, and calcitonin gene-related
 Glutamate binding repeatedly conditions the receptor in C receptors
 Determine location of pain
 Transmission occurs in pathways that relate specific patterns of sensation
o Dermatomes
 Awareness + meaning of sensation
 Thresholds – when you notice it
 Tolerance – able to handle it
 Complex mechanisms whereby synaptic transmission of pain signals is altered
 Gate control theory
o Stimulate large myelinated fibers (Aδ)  “close the gate” on nociceptor
o Pain signals theoretically blocked in spinal cord and denied progression to brain
o Large “touch” neurons could inhibit the transmission of nociceptor impulses
o Rubbing, pressing, or shaking the painful area
 Modulated in brain/spinal cord
o Endogenous opioids (enkephalins, endorphins)
 Raphe magnus in the brain transmits to dorsal horn  release neurotransmitters 
inhabitation synaptic transmission of pain signals
Types of Pain
 Two major subtypes
o Physiologic pain: injury in tissue
o Pathologic Pain: occurs after tissue injury, but long-term changes occur within
the peripheral and CNS; changes occur along somatosensory from the periphery
to the cortex
 Classifications
o Duration (acute, chronic)
o Source (cancer, neuropathic, ischemic)
o Location and referral pain
Acute Pain
 Acute pain result from tissue injury and resolves when the injury heals
o Typically lasts less than 3 months
 Clinical manifestations
o Elevated heart rate, respiratory rate, and blood pressure
o Pallor
o Sweating
o Nausea
o Paving
o Grimacing
o Crying
o Moaning
 Short-term therapy with nonopioids and opioid medications to provide adequate relief
may prevent some types of chronic pain
o Risk if becoming dependent on drugs is minimal
Chronic Pain
 May be associated with a disease process
 Last longer than the expected healing time, >6 months
 Increased peripheral transduction sensitivity
o Greater sensitivity
 Central sensitization causes abnormal responsiveness (increased gain of the nociceptive
 Clinical manifestations
o Generally, not associated with signs and symptoms of sympathetic activity
o Psychological such as loos of job, irritability, and poor self-image
o Depression
 Significant factor of individuals with chronic pain
o Treatment
 Pain clinic with multimodal therapies
Neuropathic Pain
 Cause
o Tissue injury in which nerve become damaged/dysfunctional
o May result from altered central processing of nociceptive input (releasing NE
onto nociceptors)
 Presentation
o Constant aching sensations with intermittent sharp, shooting, burning, or shock
like pain
o Allodynia, hyperalgesia, atrophy of affected extremity, coldness in affected area,
dystrophic changes (hair loss, shiny appearance, of skin)
 Medications
o Antidepressants
o Anticonvulsants
Ischemic Pain
 Results from sudden or profound loss of blood flow to tissues
o Chronic ischemic pain associated with atherosclerosis
o Intermittent claudication
 Presentation
o Described as aching, burning, or tingling
 Management aimed at improving blood flow and reducing tissue hypoxia; removing clot
if needed
o Intermittent claudication; initial intervention may be rest
 Treatment
o Weight loss, smoking cessation, exercise, lipid-lowering medications
o Surgical
 Bypass procedures
 Placement of intravascular
Referred Pain
 Perceived in an area other than the site of injury
o Example
 Pain of MI  jaw or left arm
 Shoulder pain after pelvic procedure
 Result of convergence of visceral nociceptor activity with primary somatic afferents in
posterior horn
 Pain generally referred to other structures in the same sensory dermatome
Treatment Modalities
 Pain management interventions can be directed at three points
o Interrupting
 First step in control of pain
 Splinting helps reduce tissue injury
Application of heat or cold alters blood flow and reduces swelling
NSAIDs decreased prostaglandins thereby interrupting peripheral
 Local anesthetic agents by be used for localized pain
 Diminish or block nociceptive impulses by blocking sodium influx
through fast channels
o Modulating
 Cutaneous stimulation activates large sensory fibers that can block the
central progression of nociceptive transmission at the interneurons.
 Transcutaneous electrical nerve stimulation (TENS)
 Massage
 Acupuncture
 Heat/cold
 Therapeutic touch
 Epidural and intrathecal analgesia
 Dorsal column stimulators
o Altering the perception and integration
 Opioids
 Opioids work at specific receptor sites located throughout the
body but are highly concentrated in the brain
 Distraction
 Less able to integrate the pain experience when competition is
 Imagery
 Alters perception of painful stimuli in higher brain centers
 Produces relaxation as well as analgesia
 Relaxation
 Conditioned response
 Increases blood flow
 Biofeedback
 Increases endorphins
 Conditioned response
 Hypnosis
TBI, CVA, SCI, Parkinson’s, MS, MND, and Guillain-Barre Syndrome
Mechanism of Brain injury
 Primary injury
o Initial insult that is the cause
 Secondary injury
o Progressive damage resulting from physiologic to insult
o Body’s response to said primary injury
 Neurons are at major risk of death
o ATP depletion amount determines cell death/survival and the way in which cells
Ischemia – linked to cell energy failure
Hypoxia – linked to cell energy failure
o Hypoxia from ischemia  anaerobic metabolism  lactic acidosis  loss of
neural integrity (H+)
 Mitochondrial failure
 Ca+ overload  enzyme activation  more cell membrane
damage via lipid peroxidation
o Glutamate excess
 Excitatory neurotransmitter
 Result of impaired membrane integrity
 Encourages uptake of calcium ions  Ca+ overload injury (cytotoxic
edema and swelling)
o Other excitatory neurotransmitters
 NMDA receptor activation  increased production of reactive nitrogen
species acting as free radicals  damaged cellular components
o Reperfusion injury
 O2 reenters cells  reactive O2 (hydroxyl radicals, superoxide, peroxide)
 lipid peroxidation (causes membrane damage)
 Inflammatory cells can enter brain tissue
 Ischemia allows cells though BBB
o Inflammatory cytokines
 Platelet aggregation occurs as result of injury and inflammation
o Abnormal autoregulation
 Normally – cerebral blood flow is kept at a constant rate, within range
 Responds to CO2 and O2 levels (What are these responses)
 Cerebral edema is exacerbated by vasodilation – why is this? How does
this relates to PaCO2 and Ventilation rate?
 When autoregulation fails there is O2 supply/demand mismatch
 Key to keep demand lower than supply to avoid hypoxia
Increased Intracranial Pressure
o Volume of cranium composed of three elements
 Brain tissue
 Blood
o Monroe-Kellie Hypothesis
 An increase in one of the above components can be offset by volume
reduction of the other two.
 Skull is rigid – does not lend itself to compliance
 ICP can go up in a healthy person without consequence because it
returns to normal
 Injured – cannot compensate
o Increased ICP can occur with space occupying lesions, vasogenic or cytotoxic
edema, or with obstruction or excessive production of CSF
o Common Causes of increased intracranial pressure
 Increased brain tissue volume
 Tumor
 Hemorrhage
 Infection
 Cytotoxic edema
 Vasogenic edema
 Ischemia and necrosis
 Increase CSF volume
 Obstructive hydrocephalus
 Nonobstructive hydrocephalus
 Pseudotumor cerebri
 Increased blood volume
 Increased right atrial pressure
 Dural sinus thrombus
 High arterial PaCO2
 Acidosis
Cerebral Edema
 Component of Monroe-Kelly
o Tissue is swollen
 Vasogenic
o Interstitial
o Increased capillary pressure/damaged endothelium/BP beyond autoregulation
limits  extravasation of E+, fluid protein
o Localized to where BBB has damage
 Cytotoxic
o Intracellular (inside the cell)
o ATP deficit  tissue swelling
 Na+/K+ pumps don’t work
 Edema can be iterative
o Swelling leads to compression leading to ATP deficit and pump failure leading to
more swelling
Presentation of increased ICP
 Headache
 Vomiting
 ALOC (drowsiness)
 Blurry vision and edema of optic disk (papilledema)
 ICP rises to higher level
o Decreased LOC
Impaired pupil responsiveness
Altered respiratory patterns (decreased)
Unresponsive to stimulation
Unable to move, verbalize, or open the eyes
Mechanism of brain injury cont.
 Brain compression and hernitation
o ICP rises  compression of neuro/vascular tissue
o Herniation
 Subfalcine
 Tentorial
 Uncal
 Tonsillar
 Pushing out of cerebellum
o Severe consequence of increased ICP
 Level of consciousness
o Change in LOC
o State of alertness and attentiveness to one’s environment and situation
 RAS system  compression  declined brain activity
o LOC may fluctuate
 Important to monitor and treat changes
 Can be indicative of deterioration
o Complete loss of consciousness
 Coma
ALOC terms
 Confused
o Unable to think clearly or engage in effective problem-solving; orientation to
time, place, person impaired, easily aroused by verbal stimuli
 Delirious
o Restless and disoriented, may have hallucinations; easily aroused, but may have
difficulty with attention
 Lethargic
o Uninterested in surroundings or events; sluggish in thought and motor activities;
does not engage spontaneously in activities
 Obtunded
o Falls asleep unless stimulated; arousable with voice or touch, but quickly returns
to sleep
 Stuporous
o In a deep state of sleep; vigorous stimulation is required to arouse, and a
wakeful state is not maintained
 Coma
o Unable to be aroused, even with vigorous painful stimuli; motor responses, such
as withdrawal or posturing, may occur
Manifestations of Brain Injury:
 Glascow Coma Scale (box 44.2)
o Standardized tool
 Assess LOC in acutely brain-injured person
o Numeric scores given to
 Arousal-directed respoinse of eye opening
 Verbal response
 Motor response
 Mild (>12), moderate (9-12), to severe (<8)
o Motor response most powerful predictor of patient outcome
o Decorticate posturing
 Abnormal flexor
o Decerebrate posturing
 Abnormal extension
 Pupil Reflex
o Changes
 Size
 Shape
 Reactivity of the pupil
 Early indicator of ICP and possible brain herniation
o Failing response may be first indication of brain compression from increasing ICP
 Mild dilation with sluggish or absent light response = ominous (indicates
midbrain compression of optic nerve from herniation)
 Oculovestibular Reflex
o Doll’s-eye maneuver
 Normally eyes turn in in opposite direction of the head rotation
o Impaired reflex implies brainstem dysfunction
o C-spine must be cleared
Traumatic Brain Injury (TBI)
o Injury of brain tissues secondary to trauma
o Not the same as head injury, but has been used interchangeably
 Epi
o 50,000+ deaths per year
o Falls
o Sports
o Firearms
o Vehicular
 Severity of TBI is classified by the Glasgow coma scale (GCS) as
o Mild GCS score 13-15
o Moderate 9-12
o Severe 8 or under
Types of TBI
o Primary injury
 Result of injury trauma/injury on brain cells
 Focal
 Site of impact
 Polar (Coup contrecoup)
 Acceleration/deceleration movement of brain in skull
 Diffuse
 Movement of brain in skull  widespread axonal injury
 Shaken baby syndrome
 Intracranial hematomas
 Epidural
 Subdural
 Subarachnoid
 Concussion
 Mild TBI
 Alteration or loss of consciousness (<30 minute) but no evidence
of brain damage on CT
 HA, nausea, vomiting, dizziness, fatigue, blurred vision, cognitive,
and emotional disturbance
 Contusion
 CT or MRI reveals an area of brain tissue damage (necrosis,
laceration, bruising)
 Intracranial hematoma
 Localized collection of blood within the cranium
 Epidural hematoma
o Close to surface
o Typically, arterial
o Acute
o Impaired  lucid  deterioration
 Subdural hematoma
o Rigid/immobile vessels
o Venous = slow
o Large area affected = significant primary injury
 Subarachnoid hematoma
o Similar rigid vessel rupture
o Sometimes seen with trauma
o Seen with rigid aneurysms and AVM
o Secondary injury
 Response to initial injury
 Can cause more harm than the initial injury
 Ischemia
 Increased ICP
 Altered vascular regulation
 Concurrent trauma may complicate brain injury
 Cytotoxic or vasogenic edema
 Chest injury
o Lack of oxygen
o Poor blood flow
o Vasodilation
 Swelling in brain
o Treatment
 Cardiopulmonary stabilization
 Radiologic screening to evaluate need for emergent surgical management
 Maintenance of normal body temperature or mild hypothermia
 Normal PaCO2
 Normal serum glucose level
 Normal intravascular volume
 Acutely elevated ICP
 Administration of mannitol (osmotic diuretics)
 Sedation
 Hypothermia
 Mild hyperventilation
 Severely high ICP
 More aggressive measures
 Diuretics
 Hypertonic saline
 Moderate hyperventilation
 Barbiturate coma
 Base skull fractures
 CSF can seep out as clear fluid from the ears or nose (halo test)
 Bilateral periorbital hematomas (black eyes, raccoon sign)
 Bruising under the ear (battle sign)
Cerebral Vascular Accident (CVA)
 “Stroke is a term applied to cerebrovascular events that result in a localized area of CNS
infarction and was previously termed cerebrovascular accident (CVA). The term brain
attack has been popularized to educate the public about the importance of seeking care
early, as is recommended for heart attack.”
 Most stroke is ischemic
 Men more commonly affected
 Other risk factors
o Hypertension
o DM
o Hyperlipidemia
o Smoking
o Advancing age
o Family history
Ischemic CVA
o Thrombotic
 Carotids
o Embolic
 Typically, cardiac in origin (A-fib)
o Blockage  immediate ischemia  alterations specific to the area
communicating with blood vessel (<1 minute)
o If not reperfused  irreversible damage
 3-hour window
 Will see an infarct
o Sudden
o Numbness or weakness that is mostly unilateral
o Confusion
o Interpretive or expressive aphasias
o Visual disturbances
o Dizziness/loss of balance/difficulty walking
o Severe headache
o Seek immediate care
Hemorrhagic CVA
o Result of chronic HTN
o Primarily occurs in basal ganglia or thalamus
o Prognosis depends on age + location + speed of occurrence + size of bleed
 Morbidity is higher than ischemic strokes
o Cardiovascular stabilization
o Brain CT determines type and location
o ICP monitoring and management
o Ischemic stroke
 Tx: minimizing infarct size and preserving neurologic function
 Thrombolytics
 Anticoagulants
 Antiplatelets
 Endarterectomy
 Angioplasty
 Stents
o Hemorrhagic stroke
 BP management (keep mildly hypertensive at first)
 Keeps perfusion of affected area high
Sequelae: Motor deficits
o Initially motor deficits occur as flaccidity or paralysis
 Foot drop
 External rotation
 Dependent edema
o Recovery of motor function occurs with onset of spasticity
 Increased extensor tone – upper extremities
 Increased flexor tone – lower extremities
 ROM is critical – Why?
 Spasticity of muscle can contract
o Can lose function of muscle
Sequelae: Sensory deficit
o Infarction affects same region as motor – sensory follows same pattern
o Neglect
 Result of lack of sensory
o Homonymous hemianopia
 Contributes to lack of awareness of side that is lost
Language deficits: aphasias
o Integration disorder resulting in
 Reduced vocabulary
 Reduced verbal attention span
 Altered syntax
o Broca (expressive)
 Minimal vocabulary
 Poor articulation
o Wernicke (receptive)
 Impaired comprehension
 Fluent speech – may lack content
 Tangential speech
o Anomic aphasia
 Parietemporal lesion
 Have intact grammar
 Difficulty finding words
 Often very simple phrasing
o Conduction aphasia
 Arcuate fasciculus lesion
 Difficultly with repeating words
 Paraphrasic errors – unneeded syllables – cardiovascular might be
pronounced “bardiovascular”
o If dominant side of brain is affected – global aphasia results
Cognitive deficits
o Area of brain affected dictates presence and severity of cognitive impairments
Language impairments
Impaired spatial relationship skills
Short-term memory
Poor judgement
Reasoning may be impaired
May require rehabilitative services but in some cases, it may not be beneficial
Spinal Cord Injury (SCI)
 Younger people
 Males 3 to 4 time more likely
 Traumatic cause
o Falls
o Sports related injury
 Mechanisms
o Hyperextension
o Hyperflexion
o Compression
 Process
o Acute phase
 Mechanical trauma to the cord
 Blood flow is interrupted  ischemia
 Disruption of ionic balance
 Cytotoxic edema
 Disruption of ionic balance
 Invasion of granulocytes
 Neurotransmitter release with resultant excitotoxicity
 Free radical formation
o Subacute/intermediate
 7 days post injury (more oxidation, lipid peroxidation, and free radicals)
 Infiltration by macrophages/lymphocytes  increased cytokines =
 Promotes cell death outside of the area of injury
o Chronic
 Lasts for years after injury
 Death of cells that would possibly promote regrowth/recovery
 Non-somatic changes
o Spinal cord disconnected in terms of sensation and motor function +
 BP regulation altered
 Temperature regulation altered
 Glucose stabilization altered
Clinical manifestations
o Loss of function below injury
 Loss of pain
 Loss of proprioception
o Spinal shock
 Diminished reflexes below injury
o Return of spinal reflexes = cessation of spinal shock
 This will show the next development of paralysis – spastic with
 Can be flaccid paralysis if the lesion is at the correct spot
o Appropriate stabilization of spinal vertebrae
o Neurogenic shock
 Intensive care to maintain oxygenation and blood pressure
o High-dose methylprednisolone may be used to decrease secondary injury
o Intensive rehabilitation is required to maximize function and prevent
 Minimize spasticity
 Minimize contracture
o Chronic care
 Pressure reduction
 Prevention of resp. inf
 Prevention of UTI
 Prevention of septicemia
 Fecal impaction
Autonomic Dysreflexia
 T6 or above
 Acute reflexive response to sympathetic activation below the level of injury
o Visceral stimulation (full bladder or bowel)
o Activation of pain receptors
 Manifestations
o Headache
o Bradycardia
o Flushing above the level of injury
o Clammy skin below the level of injury
Parkinson’s Disease
 A neurodegenerative disorder of the extrapyramidal system associated with the
disruption of neurotransmission in the striatum
 Therapeutic goals
o Improve patient ability to carry out the activities of daily life
o The extent to which PD interferes with work, dressing, eating, bathing,
and other activities of daily living determines drugs and dosages
Dopamine/ACh imbalance in striatum
 Imbalance results from degeneration of the neurons that supply dopamine to
the striatum
Cardinal Symptoms of PD
 Dyskinesia
o Tremor at rest
o Rigidity
o Postural instability
o Bradykinesia (slowed movement)
o Tremor
 In addition to motor symptoms
o Autonomic disturbances
o Depression
o Psychosis and dementia
Chronic demyelinating disease of the CNS that primarily affects young adults
o Autoimmune disorder
o Demyelination can occur throughout the CNS
o Often affects the optic and oculomotor nerves and spinal nerve tracts
o Primarily unknown
o Genes – maybe
o Environment – maybe
o Impaired visual acuity or blurred vision
o Diplopia
o Weakness
 Deterioration of CNS
o Numbness
o Tingling
o Extreme fatigue
o Imbalance
 Vertigo
o Movement disorders
 Gait disturbance
o Spasticity
o Coordination difficulties
o Bowel and bladder disturbances
o Emotional disturbances
Amyotrophic Lateral Sclerosis (Lou Gehrig Disease, Motor Neuron Disease)
 Progressive disease affecting both the upper and lower motor neurons
 Causes unknown
o Genetic mutations possible
 Weakness and wasting of upper extremities  impaired speech/swallowing/breathing
 Occurs between 50-75 years
o Affects men more
 Clinical manifestations
o Weakness
o Atrophy
o Stiffness
o Cramps
o Fasciculation
o Hyperreflexia in weak, atrophied extremity (highly suggestive)
Guillain-Barré Syndrome
Inflammatory demyelinating disease
o Peripheral nervous system (lower motor neuron disorder)
Cause unknown
o Post-infectious immunologic mechanisms suspected
Spontaneous recovery usually occurs
Ascending muscle weakness
Spreads to proximal spinal neurons
o Progressive ascending weakness/paralysis, may affect respiratory muscles
Endocrine Function and Dysfunction
Hormones (lipid soluble)
 Travel – to target organ or cell
 Regulate – control and function of effector organ
o Reproduction
o Fluid imbalance
o Metabolism
o Stress response
 Activate
Mechanisms of Control: Negative feedback
 Aspect of the secreted hormone is sensed and regulates further secretion
o Decreased T4/T3  CNS detects  hypothalamus released TRH  TSH
production and release from anterior pituitary  increased production and
secretion of T3 and T4 > inhibition of TRH release
 Keeps hormone level and activity WNL
Endocrine Dysfunction
Basic Concepts
 Endocrine disorders occur from
o Hypersecretion – hyperfunction
 Secretion tumors
 Autoimmune disease
 Excessive stimulation of the gland by trophic signals
o Hyposecretion – hypofunction
 Failure or congenital absence of glandular tissue
 Autoimmune destruction
 Surgical removal of gland
 Lack of normal trophic signals
o Nonresponsiveness by target cells – hypofunction
 Target tissue dysfunction
 Clinically similar to hyposecretion
 Called tissue resistance
 Primary – intrinsic malfunction of the hormone producing gland
o Gland fails, inadequate hormone produced, low levels of circulating hormone
o Blood levels of the corresponding trophic pituitary hormone levels very elevates
o TSH – high
o Gland hormone – low
 Secondary – abnormal pituitary secretion of trophic signals
o Pituitary gland fails to release trophic hormone  reduced primary gland
o Trophic and primary hormone are low
Thyroid hormone disorders
 Thyroid hormone produced in follicular cells of thyroid
o Regulators of metabolism: required for normal growth and development of
 Thyroid hormones
o Triiodothyronine (T3)
o Thyroxine (T4)
o Regulated by thyroid-stimulating hormone (TSH) secretion from the anterior
 Etiology
o Majority are primary
 Due to intrinsic thyroid gland dysfunction
o Minority of cases are secondary
 Cranial/brain changes
 Trauma
 Surgery
 Cancer
o Congenital
 Congenital hypothyroidism (cretinism)
 Typically caused by thyroid dysgenesis  lack of development
 Malformed TSH receptors
 Abnormal T3/T4 production
o Acquired
 Radiation treatment of the thyroid
 Removal of glandular tissue
 I deficiency
o Most common cause of acquired hypothyroidism
 Lymphocytic thyroiditis (Hashimoto/autoimmune thyroiditis)
 Enlarged thyroid gland caused by lymphocytic infiltration
 T3/T4 production decreases  TSH release  elevated TSH
o Dyslipidemia
o Atherosclerosis
o Myxedema
o Loss of hair
 Coarse, brittle hair
o Periorbital edema
o Puffy face
o Normal or small thyroid
o Heart failure
o Constipation
o Cold intolerance
o Muscle weakness
o Edema of extremities
Other cases of hypothyroidism
o Congenital hypothyroidism
 Mental and physical dev. Defects
o Iodine deficiency hypothyroidism
 Iodine deficiency  T3/T4 def. thyroglob still produced  no TSH
inhibition  more thyroglob  increased gland size
Primary vs. secondary hypothyroidism
o Normal
 TSH – normal
 T4 – normal
o Hyperthyroidism
 TSH – low
 T4 – high
o Hypothyroidism primary
 TSH – high
 T4 – low
o Hypothyroidism secondary
 TSH – low
 T4 – low
o Goal to achieve euthyroid state
o Replacement
Complications: myxedema coma
o Risk factors
 Sepsis/trauma/medications
o Presentation
 Poor thermoregulation
 More generalized edema
 Hypotension
o Immediate treatment
Hyperthyroid Conditions
 Etiology
o Autoantibodies bind  stimulation of TSH receptors  diffuse toxic goiter
(graves disease)
o Thyroid destruction with release of performed T4 and T3 (hashimoto thyroiditis)
o Secondary – stimulation of TSH receptors by TSH (hypersecretion of TSH)
 Manifestations
o Autoantibody TSH receptors stimulation  increase in size of follicle and goiter
o Thin hair
o Exophthalmos
o Enlarged thyroid
 Diffuse (warm on palpitation)
 Nodular
 Solitary “toxic” nodule
o Heart failure (tachycardia)
o Weight loss
o Diarrhea
o Warm skin, sweaty palms
o Hyperreflexia
o Pretibial edema
o Insomnia
o Restlessness
o Tremor
o Irritability
o Palpations
o Heat intolerance
o Diaphoresis
o Inability to concentrate that interferes with work performance
o Enlarged thyroid gland
o Increased basal metabolic rate leads to weight loss
 Appetite and dietary intake increase
o Amenorrhea/scant menses
 Graves disease
o Immune cell infiltration  cytokines stimulate local cells to secrete excessive
glycosaminoglycans  tissue swelling
o Exophthalmos
o Pretibial myxedema
o Diagnostic studies
 Radioisotope iodine study – confirms
 Thyroid function test
 T4 – high
 TSH – looooooow
 TRH – low
A patient presents to a provider’s office with a complaints of weight loss despite
increased appetite, heat intolerance, and fatigue. Primary hyperthyroidism is suspected,
and thyroid function test is performed. Which results are consistent with
o High free T4, low TSH
o Pharmacologic
 Beta-blockers to block acute symptoms
 Antithyroid drugs, thionamides (propylthiouracil, methimazole)
 Radioisotope iodine
o Destroys part of thyroid for Graves’ Disease
o Surgery
 Malignancy is indication for thyroidectomy
Thyrotoxic crisis (thyroid storm)
o Exaggerated hyperthyroid condition – medical emergency
o Precipitating event: stress, gland manipulation
o Excessive amounts of thyroid hormones are acutely released into circulation
o Manifestations
 Elevated temperatures
 Tachycardia
 Arrhythmias
 Congestive heart failure
 Extreme restlessness/agitation/psychosis
o Treatment
 Aggressive management to achieve metabolic balance
 Antithyroid drugs are given followed by iodine administration
 Beta-blockers to alleviate cardiac symptoms
 Antipyretic therapy
 Fluid replacement
 Surgical removal of tumors
 Fatal if not treated
Adrenocortical Insufficiency
 Primary: Addison disease
o Autoimmune
 Secondary: hypothalamic-pituitary dysfunction
o Drugs – steroid therapy
 Congenital adrenal hyperplasia
 If the adrenal cortex does not respond sufficiently to ACTH, then how does is the
feedback system affected (picture is primary dysfunction)
What hormones will be low with adrenal insufficiency?
How does aldosterone work at the cellular level?
o Potassium is removed in urine
o If aldosterone is not secreted, we lose sodium and hold onto potassium
o Symptoms are result of too little cortisol and aldosterone
 Weakness (result of cortisol)
 Hypotension (result of aldosterone and cortisol)
 Hypoglycemia (result of aldosterone)
 Hyperpigmentation (Addison disease)
 Hyperkalemia (result of cortisol)
 Weight loss (result of cortisol)
Addison disease
o Destruction of all layers of the adrenal cortex by
 Autoimmune conditions
 Infections – tuberculosis, HIV, or fungal infections
 Hemorrhage into the adrenal glands
 Tumors
o Manifestations
 Deficiencies
 Mineralocorticoid (aldosterone)
 Glucocorticoid (cortisol)
 Excess
o Diagnosis
 History and physical
 Anorexia
 Weight loss
 Malaise
 Apathy
 Electrolyte imbalances
 Hyperpigmentation
 Laboratory findings
 ACTH provocation test
 Synthetic ACTH
 Serum samples of cortisol are measured 30 and 60 mins
 Serum cortisol levels should increase
 Imaging studies
 Gland size
o Will show further cause
o Treatment
 Replacement therapy
 Sick day treatment
Adrenal Crisis
o Life-threatening condition for those who has adrenal insufficiency
o Causes
 ACTH/cortisol deficiency  inadequate response with decreased vascular
tone, CO, and hypovolemia
o Manifestations
 NVD  dehydration
 Hypotensive + tachycardia
 Hypoglycemia
 Poor peripheral perfusion
o Treatment
 IV glucocorticoids
 Fluid replacement
o Prevention
 Stress dosing
Which laboratory results are consistent with an individual with untreated (or
undertreated) Addison’s disease? Select all that apply.
o Hyperkalemia
o Hyponatremia
o Low cortisol level
o Elevated ACTH level
o Decreased aldosterone level
o Low androgen level
Which laboratory results are consistent with an individual with untreated (or
undertreated) Addison’s disease? Select all that apply.
Cushing syndrome (clinical features of hypercortisolism)
 Etiology
o Primary
 Adrenal adenoma
o Secondary
 Anterior pituitary hypersecretion (ACTH)
o Tertiary
 Hypothalamic injury
o Medications
 Steroids
 Manifestations
o Relates to excess glucocorticoids secretion
o Stimulation of other adrenal cortex hormones
 Aldosterone
 Androgens
o Complications
 Hyperglycemia
 Risk of infections
 Hyperlipidemia
o Mood swings, insomnia, loss of libido
o Fine hair
o Moon fac and ruddy complexion
o Hirsutism
o Dorsocervical fat pad
o Supraclavicular fat pad
o Truncal obesity with pendulous breasts and abdomen
o Broad pubic and axillary hair in women
o Thinning extremities with muscle wasting and fat mobilization
o Ecchymoses
o Impaired wound healing and immune response
o Thin, fragile skin
o Slow healing
o History and physical
o Laboratory tests
 Where is the ACTH coming from?
 Primary or secondary?
o Primary – hypersecretion of cortisol, low ACTH
 Tumor on pituitary
o Secondary – hyposecretion of cortisol, high ACTH
 Tumor somewhere else
 Imaging studies
o Removing the cause
 Surgery
Antidiuretic Hormone (ADH) Disorders
 Diabetes Insipidus (DI)
o Neurogenic (central)
 Pituitary
o Nephrogenic
 Chronic renal disease
 Receptor defects
 Serum electrolytes
 Drugs (e.g., lithium)
o Manifestations
 Low or none ADH secretion without feedback
 Relate loss of pure water (without loss of Na+)
 Polyuria, polydipsia (hallmark)
 Low urine-specific gravity
 Nocturia
 Hypernatremia because of water deficit
 Dry mucous membranes, poor skin turgor, decreased saliva and sweat
 Disorientation, lethargy, seizures
 Manifestations from cell shrinkage
o Diagnosis
 History and physical
 Laboratory tests
 Serum
 Urine
 Deprivation test
 Central DI: urine concentration increases
 Nephrogenic DI: little or no response
o Treatment
Replacement of ADH (central DI) with a drug
Free access to water and urine
Thiazide diuretics
 Retain water
Syndrome of Inappropriate ADH (SIADH)
 Etiology
o Ectopic ADH secretion – small cell carcinoma of the lung, pulmonary tuberculosis
o Drug induced (e.g. carbamazepine, hydrochlorothiazide)
 Pathogenesis
o Hyponatremia
o High urine osmolality
o Low serum osmolality
o Weakness, muscle cramps, N/V, postural BP changes, poor skin turgor, fatigue,
anorexia, lethargy
o Confusion, hemiparesis, seizures, coma
o Asymptomatic until serum Na+ <115-120 mEq/L
o Symptomatic with Na levels >~115-120 mEq/L
o Low hematocrit
o Laboratory tests
 Serum
 Urine
o Rule out renal, adrenal, and thyroid diseases
o Imaging studies
o Treat the cause
o Fluid retention
o Increase salt intake (IV or oral) with a loop diuretic
o Pharmacologic
 Lithium (blocks ADH)