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Medsurgultimate - Nurse Angie
Medical Surgical Nursing II (ECPI University)
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lOMoARcPSD|11334620
JULY 2020 | ISSUE NO. 7
MEDICAL SURGICAL
Nursing
1. NOTE TAKING
TEMPLATE
2. SMART GOALS
3. CONCEPT MAPS
4. NEURO
5. RESPIRATORY
6. CARDIAC
7. ONCOLOGY
8. BILIARY
9. RENAL
10. ELECTROLYTES
11. ENDOCRINE
12. EYE
13. GI
14. LIVER
"THE MEANING OF LIFE IS
TO FIND YOUR GIFT. THE
PURPOSE OF LIFE IS TO
GIVE IT AWAY." —WILLIAM
SHAKESPEARE
"When I think about all the patients and
their loved ones I have worked with
over the years, I know most of them
don't remember me, nor I them. But I
do know that I gave a little piece of
myself to each of them, and they to me,
and those threads make up the tapestry
that is my career in nursing." —Donna
Wilk Cardillo
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ADPIE
NOTE TAKING
METHOD
Assessment
Diagnosis
PATHOPHYSIOLOGY
Disease Process:
Planning
Interventions
Evaluation
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SMART GOALS FOR PLANNING PATIENT CARE
Specific
Who, what, where ,
when, which and why
Attainable
Measurable
Create criteria
SMART GOAL
Track progress
Develop attitudes,
abilities, skills
Plan your steps
Willing and able to
work towards the goal
Anchor your goal to a
specific date
Realistic
Timely
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Pathophysiology
Concept Maps
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Medical Surgical Nursing Concept Map
5
Disease & Pathophysiology
Assessment
Physical Findings
Causes
Risk Factors
Interventions
Medications
Monitoring
Prioritization
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lOMoARcPSD|11334620
Medical Surgical Nursing Concept Map
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Disease & Pathophysiology
Assessment
Physical Findings
Causes
Risk Factors
Interventions
Medications
Monitoring
Prioritization
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lOMoARcPSD|11334620
Medical Surgical Nursing Concept Map
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Disease & Pathophysiology
Assessment
Physical Findings
Causes
Risk Factors
Interventions
Medications
Monitoring
Prioritization
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Medical Surgical Nursing Concept Map
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Disease & Pathophysiology
Assessment
Physical Findings
Causes
Risk Factors
Interventions
Medications
Monitoring
Prioritization
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Medical Surgical Nursing Concept Map
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Disease & Pathophysiology
Assessment
Physical Findings
Causes
Risk Factors
Interventions
Medications
Monitoring
Prioritization
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Medical Surgical Nursing Concept Map
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Disease & Pathophysiology
Assessment
Physical Findings
Causes
Risk Factors
Interventions
Medications
Monitoring
Prioritization
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Medical Surgical Nursing Concept Map
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Disease & Pathophysiology
Assessment
Physical Findings
Causes
Risk Factors
Interventions
Medications
Monitoring
Prioritization
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Medical Surgical Nursing Concept Map
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Disease & Pathophysiology
Assessment
Physical Findings
Causes
Risk Factors
Interventions
Medications
Monitoring
Prioritization
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Medical Surgical Nursing Concept Map
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Disease & Pathophysiology
Assessment
Physical Findings
Causes
Risk Factors
Interventions
Medications
Monitoring
Prioritization
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lOMoARcPSD|11334620
Medical Surgical Nursing Concept Map
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Disease & Pathophysiology
Assessment
Physical Findings
Causes
Risk Factors
Interventions
Medications
Monitoring
Prioritization
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MEDICAL SURGICAL NURSING: NEURO 1.9.5
NURSE ANGIE 2018
Head Injury
Trauma to the skull such as jarring, shaking or laceration can lead to mild or extensive brain damage.
Assessment
Types
Concussion: A brain injury caused by a blow to the
head or a violent shaking of the head and body. This
is a closed type of head injury.
Contusion: Bruising or bleeding on the brain due to
localized trauma.This is also a closed head injury.
Closed head injury: Traumatic brain injury in where
the skull and dura mater remain intact. These are the
leading cause of death in children under 4 years old
and the most common cause of physical disability and cognitive impairment in young people.
Basilar Skull Fracture: Is a fracture of the base of the skull, typically involving the temporal
bone, occipital bone, sphenoid bone, and/or ethmoid bone. These are very uncommon. Can be a
closed fracture.
Epidural Hematoma: Bleeding occurs between the skull and the dura (the brain cover). The
bleeding is from an injury to a vein or a branch of the posterior meningeal artery. The most
dangerous type of hematoma
Subdural hematoma: Known as a subdural hemorrhage (SDH), is a type of hematoma, usually
associated with traumatic brain injury. Blood gathers between the inner layer of the dura mater and
the arachnoid mater.
Intracerebral Hematoma: Blood leaks into the brain as a result of head trauma or spontaneously.
Subarachnoid Hemorrhage: Bleeding into the subarachnoid space. Can be caused by ruptured
aneurysm or trauma
‣ Assessment finding will vary
depending on the type and severity
of the head injury.
‣ Increased ICP
‣ LOC changes
‣ Altered mental status
‣ Airway and breathing changes
‣ Vital signs will show increased
ICP
‣ Visual changes
‣ Pupillary changes and papilledema
‣ Nuchal Rigidity
‣ CSF drainage
‣ Weakness and paralysis
‣ Posturing
‣ Decreased sensation
‣ Reflex changes
‣ Seizure activity
Treatments
‣
Minor Injury: Repair CSF leak,
lacerations of the scalp
‣ Penetrating wounds: Surgical repair
and antibiotics
‣ Moderate to severe head injury:
supportive care, prophylactic
antiseizure medications, prevent and
control intracranial hypotension,
prevent brain damage from
hypotension , prevent anemia,
Increased arterial Carbon Dioxide
levels.
COMPLICATIONS
‣ Cerebral bleeding
‣ Hematoma
‣ Uncontrollable ICP
‣ Infections
‣ Seizures
‣ CSF leakage
EDUCATION
INTERVENTIONS
‣ Administer Glucocorticoids:
Dexamethasone, mannitol and
Educate the client and family
on possible behavior changes,
the long term effects of a
traumatic brain injury and
when to contact the HCP
‣ Monitor respiratory status and
maintain patent airway,
increased C02 levels cause
cerebral edema.
‣ Monitor vitals & Temperature
Monitor neuro status
‣ Monitor for signs of ICP
‣ Keep head elevated to reduce
venous pressure
‣ Prevent neck flexion
‣ Initiate normothermia measures.
‣ Assess for pain and restlessness.
‣ Monitor for CSF drainage
‣ Mental status changes
‣ Behavioral changes
‣ Cranial nerve deficits
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furosemide these are hypertonic
solutions that will pull fluid from the
brain and decrease intracranial
pressure.
‣ Barbiturate therapy: Decreases cerebral
metabolic weight.
‣ Morphine Sulfate: Decreases agitation
and restlessness, administer with
caution because it can cause respiratory
depression which will also cause ICP.
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MEDICAL SURGICAL NURSING: NEURO 1.9.1
NURSE ANGIE 2018
Hyperthermia
An elevated body temperature due to failed thermoregulation that occurs when a body produces or
absorbs more heat than it dissipates.
Pathophysiology
Assessment
A fever occurs when the body sets the core temperature to a higher temperature, through the action
of the pre-optic region of the anterior hypothalamus. In contrast, hyperthermia occurs when the
body temperature rises without a change in the heat control centers. temp above 105* increases
cerebral metabolism and increases the risk for hypoxia. Hyperthermia is different from a fever
because it is characterized by an uncontrolled increase in body temperature that exceeds the body’s
ability to lose heat. The setting of the hypothalamic thermoregulatory center is unchanged. In
contrast to fever in infections, hyperthermia does not involve pyrogenic molecules.
‣
‣
‣
‣
‣
‣
‣
‣
‣
Agitation
Confusion
Dizziness
Hypertension then
hypotension
Moist cool skin
Thready pulse
Seizures
Tachypnea
Arrhythmias
Medications
‣
‣
‣
‣
‣
Laboratory Findings:
‣
‣
‣
‣
‣
‣
‣
Interventions
Increased PaCO2
Increased CK
Increased plasma lactate
Decreased PaO2
acidosis
Hyperkalemia (potassium leaks out of the muscle cells)
Myoglobin in blood or urine (from cell death and rhabdomyolysis - precipitates
in renal tubules causes urinary obstruction and RF)
CAUSES
‣ Infection
‣ Salt and water deprivation in a
hot environment
Stages
‣ Mild: Temp over 99 degrees
to 102 degrees
‣ Moderate: up to 104 degrees
‣ Severe: temperature greater
than 105 degrees
Severity of symptoms are based
on the clients temperature.
Symptoms range from mild
confusion to critical
neurological and cardiovascular
issues including death.
Dantrolene: To lower temperature
and prevent seizures.
Bicarbonate: To reverse acidotic
state.
Glucose: Due to elevations in
insulin levels with higher body
temperatures
IV fluids: To replenish fluid loss
and reverse dehydration.
Chlorpromazine and diazepam:
To stop excessive shivering.
‣ Heat stroke
‣ Endocrine disorders
INTERVENTIONS
‣ Medications such as: diuretics,
‣
‣
‣
‣
‣
Oxygen therapy
Cvp monitoring
Intubation if needed
Continue vital sign monitoring
If you reduce the body
temperature too fast you can
cause vasoconstriction which
increases metabolic demand and
oxygen consumption from
shivering
‣ Monitor neuro and cardio status
anticholinergics, malignant
hyperthermia can result from
anesthesia or succinylcholine
due to a genetic issue.
‣ Remove clothing and avoid
shivering
‣ Apply hypothermic blanket
‣ Apply ice packs to the groin area
‣ Treatment continues until body
temperature has decreased to 102.2
Memory Trick
Some hot dude better give fluids
fast!
Stop triggering agents
Hyperventilate & give 100% 02
Dantrolene administration
Bicarbonate administration
Glucose and insulin
IV fluids and cooling blanket
Fluid intake & output
monitoring
‣ Exposure to high temps
‣ Dysfunction of
thermoregulatory centers
‣ Brain injury or trauma
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MEDICAL SURGICAL NURSING: NEURO 1.9.12
NURSE ANGIE 2018
Guillain barre syndrome
Disorder in which a person's immune system attacks the peripheral nervous system.
Pathophysiology
Assessment
Prior infection leads to an immune response. The immune response the cross-reacts with the
peripheral nerve components, causing segmental demyelination of
peripheral nerves. Preventing normal transmission of electrical
RISK FACTORS
impulses. Sensorimotor nerve roots are affected; autonomic nerve
‣ Recent surgery or transplant
‣ Diabetes mellitus
transmission may also be affected
‣ Rabies or swine influenza
vaccination
‣ Viral illness, most commonly
respiratory followed by
gastrointestinal infections
‣ Hodgkins. Meningococcal
vaccination
‣ Zika viral infection
‣ Meningococcal vaccination
‣ Zika viral infection
INTERVENTIONS
‣ Supportive measures
‣ Emotional support
‣ Maintenance of skin integrity
‣ Possible endotracheal
Laboratory Findings:
intubation or tracheotomy with
‣ Liver function levels: May be elevated.
‣ Creatinine phosphokinase level and erythrocyte sedimentation rate test: Results
may be elevated
‣ Cerebrospinal fluid (CSF) analysis: May show a normal white blood cell count,
an elevated protein count, and, in severe disease, increased CSF pressure.
‣ Electromyography: Demonstrates repeated firing of the same motor unit instead
of widespread sectional stimulation.
‣ Nerve conduction studies: Show prolonged F-wave latency initially, conduction
block, and marked slowing of
nerve conduction velocities.
CAUSES/COMPLICATIONS
Education
‣ Not to receive live vaccines
‣ Can get PPD
‣ Encourage coughing and deep
breathing
‣ Use TENS
‣ Home oxygen
ventilator support
‣ Cardiac monitoring
‣ Fluid volume replacement
‣ Urinary catheterization for
urine retention due to
autonomic neuropathy
‣ Plasmapheresis
‣ Transcutaneous electrical
nerve stimulation (TENS) for
‣ Can be a post infectious immunemediated disorder
‣ Campylobacter jejuni and
cytomegalovirus
‣ Paralysis
‣ Permanent residual weakness
‣ Arrhythmias, Urine retention
‣ Thrombophlebitis
‣ Pressure injury
‣ Contractures
‣ Muscle wasting, Aspiration
‣ Respiratory tract infections; adult
respiratory distress syndrome
‣ Life-threatening respiratory and
cardiac compromise
pain
‣ Occupational and speech
therapy
‣ Venous thromboembolism
(VTE) prophylaxis
‣ Adequate fluid and caloric
intake
‣ Enteral feedings if intubated
‣ Aspiration precautions
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‣ MS: Weakness of the limbs,
muscle weakness, Paralysis of
the ocular, facial, and
oropharyngeal muscles.
‣ GI/GU: Urinary retention or
difficulty with bowel and
bladder function, decreased
bowel sounds.
‣ Neuro: Sensory loss, usually
in the legs (spreads to arms),
difficulty talking, chewing,
and swallowing, sensory loss,
usually in the legs (spreads to
arms), Difficulty talking,
chewing, and swallowing,
facial flushing.
‣ RESP: oor inspiratory effort,
Diminished breath sounds,
respiratory failure, dyspnea on
exertion.
‣ Cardio: Tachycardia,
bradycardia, labile blood
pressure.
Treatments
‣ I.V. immune globulin
‣ Low-molecular-weight heparin :
Enoxaparin sodium (Lovenox) for
deep vein thrombosis prophylaxis
‣ Analgesics: Opioids for pain
control
‣ Laxatives: Constipation or ileus
due to autonomic neuropathy
‣ Tricyclic antidepressants, tramadol
hydrochloride (Ultram),
gabapentin(Neurontin),
carbamazepine (Tegretol), or
pregabalin (Lyrica) for long-term
management of pain; gabapentin
or carbamazepine for pain control
during the acute phase
‣ Oxygen
‣ I.V. fluids for volume expansion if
hypotensive
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MEDICAL SURGICAL NURSING: NEURO 1.9.13
NURSE ANGIE 2018
Alzheimer’s
Degenerative, irreversible disorder of the cerebral cortex.
Pathophysiology
The disease initially involves the parts of the brain that
control thought, memory, and language. Neurons involved
with communication, metabolism, and repair are
disrupted.Brain damage is caused by a substance called
amyloid. The disorder reveals three distinguishing features
of brain tissue: Neurofibrillary tangles, neuritic plaques, and
granulovacuolar degeneration
Assessment
‣ C:Cognitive changes
‣ O: Olfactory dysfunction ( loss
of smell)
‣ N: Not able to remember
recent events
‣ F: Frustration, irritability
‣ U: Unable to recognize self
‣ S: Steroidogenesis is impaired
‣ I: Incontinence
‣ O: organic brain disease
‣ N: Not able to walk steadily
Treatments
INTERNVENTIONS
Laboratory Findings:
‣ Positron emission tomography: Reveals metabolic activity of the cerebral cortex.
‣ Computed tomography scanning (brain): Shows excessive and progressive brain
atrophy and rules out other neurologic problems.
‣ Magnetic resonance imaging:Rules out intracranial lesions and detects
biochemical and anatomic changes, including generalized and focal atrophy.
‣ Cerebral blood flow studies: Reveal abnormalities in blood flow to the brain.
‣ Cerebrospinal fluid analysis: Shows chronic neurologic infection and possibly
elevated tau protein levels and low
amyloid protein levels.
‣ Electroencephalography: May show
slowing of the brain waves in late
stages of the disease.
‣ Preclinical Alzheimer disease:
‣ Neuropsychological tests may show
Evidence of measurable
impaired cognitive ability and
changes in brain biomarkers
reasoning.
years before any signs and
‣ Diagnosis is by exclusion; tests are
symptoms involving memory,
performed to rule out other diseases.
thinking, or behavior are noted
‣ Positive diagnosis is made on autopsy.
STAGES
CAUSES
‣ Abnormal processing of
amyloid-beta protein
‣ Acetylcholinesterase
inhibitors, such as donepezil
hydrochloride (Aricept),
rivastigmine (Exelon), and
galantamine hydrobromide
(Razadyne)
‣ Safe activities as tolerated
‣Selective serotonin reuptake
inhibitors (SSRIs), such as
(may need to be monitored)
sertraline hydrochloride
‣ Exercise to reduce restlessness
(Zoloft) and citalopram
‣ Participation in mental
hydrochloride (Celexa), for
depression
activities (patients with normal
‣Trazodone hydrochloride
or mildly impaired cognition)
(Oleptro), zolpidem tartrate
(Ambien), zaleplon(Sonata), or
‣ A home-based balanced
ramelteon (Rozerem) for
exercise program may
insomnia
‣Benzodiazepines, such as
decrease risk of falls.
lorazepam (Ativan) and
‣ Well-balanced (may need to be
buspirone
monitored)
hydrochloride(Aplenzin), or
SSRIs for moderate anxiety
‣ Avoidance of caffeineand restlessness
containing foods, such as
‣Antipsychotics, such as
coffee, tea, cola, and chocolate
risperidone (Risperdal) and
olanzapine (Zyprexa), or
‣ Nutritional supplements in
anticonvulsants, such as
later stages
carbamazepine (Tegretol) and
valproic acid(Depakene), for
‣ Behavioral interventions
severe aggressive agitation
(patient-centered or caregiver
‣Memantine hydrochloride
training) focused on managing
(Namenda) to help preserve
memory
cognitive and behavioral
‣Ginkgo biloba (conflicting
changes
results) to improve or preserve
memory
‣ Occupational therapy
‣ Music therapy
(being used primarily for
research purposes, not for
diagnosis)
‣ Mild cognitive impairment:
Noticeable mild changes in
memory and thinking that can
be measured using a mental
status examination Changes not
severe enough to affect the
person's daily functioning.
‣ Dementia due to Alzheimer
disease: Significant impairment
in memory, thinking, and
behavior. Impairments
impacting the person's ability to
function independently
‣ Advance directive planning
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MEDICAL SURGICAL NURSING: NEURO 1.9.8
NURSE ANGIE 2018
Amyotrophic Lateral Sclerosis
A degenerative disorder that is progressive in nature ALS is also known as Lou Gehrig’s disease.
Pathophysiology
Risk Factors
Excess glutamate causes progressive muscle weakness and atrophy
until flaccid tetraplegia occurs. As the disease progresses the
respiratory muscles become affected causing respiratory
compromise, pneumonia and eventually death.
‣ Age
‣ Family history
‣ Cigarette smoking
Assessment
P: Pneumonia
L: Loss of coordination
A: Atrophy of the muscles
Y: Young or old can get it
B: Bilateral weakness and
tetraplegia
Complications
‣ Respiratory tract
infections and
respiratory failure
‣ Complications of
immobility
‣ Aspiration
‣ Injury
‣ Pressure injury
‣ Pulmonary emboli
‣ Nutritional
deficiencies
‣ Death
A: Aspiration risk
L: Loss of energy , fatigue.
L: Loss of respiratory function
Treatments
‣ Riluzole (Rilutek) slows the
progression of ALS in some
patients, by reducing levels of
glutamate in the brain
‣ Edaravone (Radical) —
reduces the decline in daily
functioning associated with
ALS. It is given by intravenous
infusion (typically 10-14 days
Laboratory Findings:
in a row, once a month), and
‣ Electromyogram: Shows fibrillation and fasciculation. Motor conduction will be slow or slightly normal.
‣ CCK: elevation in creatinine Kinase from muscle changes.
‣ Respiratory: pulmonary function testing will show decreased vital capacity.
bruising, gait disturbance,
side effects may include
hives, swelling and shortness
of breath.
‣
EDUCATION
‣ Educate the caregiver on
suctioning to remove
secretions and reduce the risk
of aspiration.
‣ Educate the patient to tuck
their chin in while eating and
drinking to avoid aspiration.
‣ Patient may need thickened
liquids.
CAUSES
INTERVENTIONS
‣ Gene mutation.
‣ Chemical imbalance.
‣ Monitor respiratory status.
‣ Prevent aspiration.
‣ Prepare to begin respiratory
support.
‣ Administer spasmolytic agents
as ordered.
‣ BIPAP
‣ Refer to hospice.
‣ Monitor vitals and
cardiovascular status
‣ Assess gag reflex
‣ Disorganized immune
response.
‣ Protein mishandling.
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MEDICAL SURGICAL NURSING: NEURO 1.9.4
NURSE ANGIE 2018
Brain abscess
A lesion on the brain that is rare in healthy people.
Pathophysiology
Assessment
Infectious material that has collected in the brain mostly caused by accumulation of bacteria. The
most common cause of brain abscess is otitis media and rhino-sinusitis. Abscesses can also be a
result of intracranial surgery, penetrating head injury, and tongue piercings. Organisms can spread
from the lungs, gums, wound, heart, or tongue.
‣ S: severe headache
‣ T: total loss of
consciousness
‣ I: Impaired motor
function , nuchal rigidity.
‣ F: funky rash
‣ F: fever
Treatments
‣ Antibiotic agents that cross the
blood brain barrier.
‣ Penicillin G in combination with
a cephalosporin : ceftriaxone IV
within 30 minutes of hospital
arrival.
‣ Dexamethasone: adjunct therapy
in acute bacterial meningitis,
improves the outcome of adults.
Does not cause GI bleeding.
Laboratory Findings:
‣
‣
‣
‣
‣ Fluid replacement: treatment for
CT: Is mostly used to identify location and size of the abscess. Aspiration is also guided by CT or MRI.
Culture & Sensitivity: To identify the organism and how to treat it.
Chest X-Ray: Rules out prior lung infections.
EEG: To Localize the lesion.
dehydration and shock. With
fluid volume expanders.
Preventions
CAUSES
‣ Otitis media
‣ Tongue piercings
‣ Oral infections
‣ Cardiac infections
‣ Lung infections
‣ Mastoiditis
‣ Rhinosinusitis
‣ Systemic infections
Education
INTERVENTIONS
‣ Importance of immediately
reporting worsening of
symptoms
‣ need for continued follow-up
care, for at least 3 months to
evaluate the effectiveness of
treatment, identify any new
lesions, and manage any
complications
‣ Seek treatment immediately
for infections
‣ importance of adhering to the
prescribed medication regimen
to ensure complete resolution
of the infection
‣ Continuous neurological
monitoring
‣ Monitor vital signs
‣ Administer antibiotics
‣ Monitor for signs of ICP
‣ Monitor blood glucose and
Potassium when administering
corticosteroids.
‣ Initiate seizure precautions
‣ Keep patient safe and free of
falls
‣ Assess distress and ability to
cope with altered state.
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‣ Meningitis vaccine.
‣ Treatment of those who have
been exposed within 24 hours.
‣ Flu vaccine
‣ Pneumonia vaccine.
FACTS
Aminoglycosides, erythromycin,
tetracyclines, and first-generation
cephalosporins aren’t indicated
for use with brain abscess. These
agents don’t cross the blood-brain
barrier at concentrations that are
high enough to be effective.
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MEDICAL SURGICAL NURSING: NEURO 1.9.5
NURSE ANGIE 2018
Increased intracranial pressure
Pressure on the brain from increased swelling on the brain.
Assessment
Pathophysiology
Can be caused by trauma, intracranial hemorrhage, tumors, hydrocephalus, edema, or
inflammation. Increased ICP impaired cerebral circulation, decreases absorption of CSF,
affects the functioning of nerve cells and can lead to brain stem herniation or death.
Normal ICP ranges from 5-15 mmHg anything above 20 indicates immediate treatment.
INTERVENTIONS
•
•
•
•
•
!
•
CPP
• Pressure that pushes blood
to the brain.
• Normal CPP 60-100 mmHg
• When CPP falls too low <
50 mmHg brain death
occurs due to cerebral
hypoxia.
• CPP= MAP-ICP
INFLUENCING FACTORS
• Body temperature: Fever
• Oxygenation : Elevated C02
•
causes vasodilation or hypoxia
• Body position
• Arterial or Venous pressure
• Intra Abdominal or thoracic
pressure: vomiting, hip flexion
•
P: Position, elevate HOB
30-35 degrees, midline.
Avoid flexion of head or hips
R: Respiratory status
monitoring, prevent hypoxia
and hypercapnia.
Maintaining a PCO2 at 30-35
mmhg will decrease ICP by
causing vasoconstriction
Suction for only 15 seconds
at a time. Keep peep low
with mechanical ventilation.
E: Elevated temp, lower
body temp, prevent
shivering, this can increase
ICP. administer antipyretics,
cool blankets, decreased
room temp.
S: Systems to monitor,
frequent neuro checks,
glasgow coma scale,
S: Straining activities to
avoid: Vomiting, sneezing,
valsalva, keep a calm
environment and avoid
restraints.
U: Unconscious patient care:
avoid morphine to avoid
hypoxia, monitor lung
sounds, ROM, eye care,
blood clots.
R: RX: administer
vasopressors,IVF,
barbiturates to decrease
brain metabolism,
MAINTAIN SBP >90 <150,
anticonvulsants,
hyperosmotic drugs such as
mannitol to pull fluids from
the brain.
E: Edema management with
mannitol to dehydrate the
brain. Electrolyte monitoring
r/t fluid volume or depletion
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‣ Altered LOC ( earliest presenting
symptom)
‣ Headache
‣ Cheyne stokes
‣ Increased BP with
‣ widening pulse
‣ pressure
‣ Double vision
‣ Swelling of optic
‣ nerve
‣ Unequal pupils
‣ Fever
‣ Vomiting
‣ Pupil changes
Late signs
•Cushing's triad: increased
systolic pressure, bradycardia,
bradypnea.
•widened pulse pressure, decreased
CPP,
•Hemiplegia
•Posturing : Decorticate,
Decerebrate ( death)
•Seizures
•Papilledema
• Dolls eyes
Treatments
• Anticonvulsants: Prophylaxis against
seizures which increase ICP.
• Antipyretics/ Muscle relaxants:
Antipyretics prevent temperature
elevation & Muscle relaxants prevent
shivering
• Blood pressure drugs: Needed to
maintain BP of 90-150 mmHg to avoid
cerebral hypoxia.
• Corticosteroids: Stabilize the cell and
reduces leakage of fluids through the
blood brain barrier which, decrease
cerebral edema
• IV Fluids: Hypotonic fluids are
avoided due to risk of cerebral edema
• Hyperosmotic Fluids: Increase
intravascular pressure by drawing fluids
from the brain to the vasculature and
out via the kidneys. Monitor renal
function. Monitor intake and output
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MEDICAL SURGICAL NURSING: NEURO 1.9.2
NURSE ANGIE 2018
Encephalitis
An acute inflammatory process that affects the brain tissue, the cerebrum, brainstem, and cerebellum.
Pathophysiology
Assessment
Encephalitis is an inflammatory process caused by the herpes simplex virus or bites from a tick or
mosquito and causes necrotizing hemorrhage of the brain that becomes generalized and is followed
by edema. Encephalitis also can cause damage to nerve cell bodies.
•
•
•
•
•
•
•
•
•
•
•
•
H: Herpes Virus infection
E: Enterovirus infection
R: Rigidity
P: Populations with lots of disease
E: Extreme changes in LOC
S: Sores in the mouth
V: Varicella infection
I: Insect Bites
R: Really high fever
U: unilateral paralysis
S: Seizures
Lab studies
• MRI: Inflammation in the basal ganglia
•
•
•
•
•
•
( St. Louis) or periventricular area
( West Nile)
EEG: Abnormal brain waves.
CSF: Immunoglobulin M antibodies
will be present
Fungal Encephalitis
CSF: Elevated White cells and protein
or candida
Neuroimaging: Identifies CNS changes
MRI: Is the study of choice, identifies
hemorrhage, abscess or inflammation.
Treatments
Laboratory Findings:
‣ EEG: Diffuse slowing or focal changes in the temporal lobe.
‣ Lumbar Puncture: High opening pressure, normal glucose range,
high protein levels.
‣ Viral cultures: Usually negative
‣ Polymerase Chain reaction: Standard test for early diagnoses and
identifies the DNA of HSV-1, validity is highest on the 3rd and
10th day post symptom onset.
EDUCATION
‣ Encourage fluid intake
‣ Small frequent meals
‣ Educate the client on the
disease.
‣ Educate the client on the treat
regimens and when to call the
HCP.
INTERVENTIONS
‣ Assess neurological function
and for signs of ICP
‣ Assist client to Turn cough and
Deep breathe
‣ Elevate HOB 30-45 degrees
‣ Comfort measures to reduce
headache.
‣ Administer analgesia.
‣ Use opioids cautiously because
they can mask neurological
symptoms.
‣ Seizure precautions.
‣ Monitor Blood cultures.
‣ Monitor intake and output due
to possible renal impairment
from the antivirals.
‣ Initiate rehabilitation for motor
dysfunction
CAUSES
‣ Viral infection of HSV
‣ Mosquito bites
‣ Tick bites
‣ Bacteria
‣ Fungi
‣ parasites
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‣ Acyclovir: Antiviral agent ,
decreased dose if the patient has
a history of renal impairment.
‣ Ganciclovir: Antiviral Agent
‣ Starting antivirals early is well
tolerated and the patient should
continue treatment for up to 3
weeks.
‣ IV administration over 1 hour
prevents crystallization of the
medication in the urine.
‣ Interferon : St. Louis
Encephalitis
‣ Lumbar Puncture and Shunting:
Fungal encephalitis.
‣ Amphotericin B: Treats
progressive fungal infection.
May cause renal dysfunction
‣ Fluconazole: Treats fungal
infection and may cause bone
marrow depression
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MEDICAL SURGICAL NURSING: NEURO 1.9.3
NURSE ANGIE 2018
Meningitis
Inflammation of the meninges in the brain and spinal cord.
Pathophysiology
Assessment
Bacterial meningitis occurs as an opportunistic infection and is concentrated in the nasopharynx.
Transmission occurs by secretion or aerosol contamination. Once the organism is in the blood
stream it moves across the blood brain barrier and infiltrates into the CSF. this causes inflammation
in the sub arachnoid and pia mater causing ICP and meningeal inflammation.
• S: severe headache
• T: total loss of
consciousness
• I: Impaired motor function ,
nuchal rigidity.
• F: funky rash
• F: fever
Treatments
Laboratory Findings:
‣CT/MRI: Detects a shift in brain contents.
‣Lumbar Puncture: Culture is taken of the CSF to test strain and culture and
sensitivity of the bacteria.
CAUSES
‣ IBacterial : Streptococcus
pneumoniae
‣ Viral: Neisseria
meningitidis.
EDUCATION
INTERVENTIONS
‣ Remind the patient about the
importance of keeping
appointments and screening.
‣ Educate the client on the
disease process and how it's
transmitted.
‣ Educate the client on
treatments and the importance
of adhering to the
recommended treatment
regimens
‣ Finish all antibiotics.
‣ Educate the patient of asepsis
and preventing the spread of
meningitis.
‣ Institute infection control
precautions for 24hrs.
‣ Assist with pain management.
‣ Provide a restful environment.
‣ Administer antipyretics.
‣ Offer a cooling blanket.
‣ Encourage hydration.
‣ Monitor neurologic status.
‣ Monitor vitals.
‣ Initiate seizure precautions
‣ Keep the patient safe.
‣ Monitor daily weights
‣ Monitor electrolytes
‣ Obtain and monitor U/A results
‣ Maintain skin integrity by
providing immaculate skin care.
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‣ Antibiotic agents that
cross the blood brain
barrier.
‣ Penicillin G in
combination with a
cephalosporin :
ceftriaxone IV within 30
minutes of hospital
arrival.
‣ Dexamethasone: adjunct
therapy in acute bacterial
meningitis, improves the
outcome of adults. Does
not cause GI bleeding.
‣ Fluid replacement:
treatment for dehydration
and shock. With fluid
volume expanders.
Preventions
‣ Meningitis vaccine.
‣ Treatment of those who have
been exposed within 24 hours.
‣ Flu vaccine
‣ Pneumonia vaccine.
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MEDICAL SURGICAL NURSING: NEURO 1.9.10
NURSE ANGIE 2018
Multiple Sclerosis
A chronic and progressive disease of the CNS that causes demyelination of the neurons.
Pathophysiology
Assessment
Sporadic patches of demyelination occur in the central nervous system, resulting in
widespread and varied neurologic dysfunction. Typically progresses slowly; may progress
rapidly if diagnosed late, causing death within months. Occurrence is between 20 and 40 years
of age. MS is precipitated by a viral infection , pregnancy, immune response, fatigue, stress,
trauma, and infection.
‣
‣
‣
‣
W: Weakness
E: Electric shock sensations
A: Apathy and other mood changes
K: Killer pain
‣ V: Vision changes ( diplopia, nystagmus,
blurry vision)
‣ I: Incontinence
‣ S: Sensory loss
‣ I: Inability to swallow
‣ O: Optic neuritis
‣ N: Neuralgias
Treatments
‣ Symptomatic treatment for acute exacerbations
‣ Plasmapheresis (second-line treatment for
exacerbations that won't respond to
corticosteroid therapy; not indicated for chronic
or secondary progressive multiple sclerosis)
‣ Venous thromboembolism (VTE) prophylaxis
Laboratory Findings:
Education
‣ Nonpharmacologic pain
relief, such as imagery,
distraction, transcutaneous
electrical nerve stimulation,
heat, massage
‣ Physical therapy helps
maintain joint mobility and
prevent contractures;
‣Magnetic resonance imaging (MRI) of the neurologic system: The most
sensitive method of detecting multiple sclerosis focal lesions in the brain and
spinal cord.
‣Computed tomography scanning may reveal plaques.
‣Electroencephalography : Abnormalities occur in one-third of patients with
multiple sclerosis.
‣Evoked potential studies: Show slowed conduction of nerve impulses.
‣Lumbar puncture with cerebrospinal fluid analysis: Results show
mononuclear cell pleocytosis, an elevation in total immunoglobulin (Ig) G
levels, and the presence of oligoclonal IgG (used when MRI is inconclusive or
unavailable).
‣ Stress management
‣ Ensure safety
‣ Education on treatment
regimen
‣ Eye patch for diplopia
‣ Safety related to sensory loss
( no heating pads, monitor
water temperature.
‣ High-fluid and high-fiber (for
constipation)
acute attacks or exacerbations with full
recovery and no lasting disability and no
worsening of the disease between attacks
(approximately 85% of cases)
‣ Primary progressive: Steadily progressing
or worsening with minor recovery or
plateaus, possibly involving different brain
and spinal cord damage from other forms
occupational therapy; speech
therapy
Types
‣ Relapsing-remitting: Clear relapses or
CAUSES
‣ Autoimmune response
‣ Viral infection
‣ Genetic factors possibly
also involved
‣ Environmental factors
INTERVENTIONS
(approximately 10% of cases)
‣Secondary progressive: Beginning as a
pattern of clear-cut relapses and recovery
‣ Monitor activity and pain
but becoming steadily progressive and
‣ Monitor mobility
worsening between acute attacks
‣ Monitor medication response
(approximately 50% of cases of the
‣ Sensory function
relapsing-remitting type change to the
‣ Muscle function
secondary progressive type within 10 years
‣ Speech & Elimination
‣ Vision changes
of onset)
‣Progressive-relapsing: Steadily
‣ Energy level
progressing from onset but also involving
clear, acute attacks (less than 5% of cases)
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MEDICAL SURGICAL NURSING: NEURO 1.9.9
NURSE ANGIE 2018
Myasthenia Gravis
A neuromuscular disease that manifests as severe weakness and extreme fatigue of the voluntary
muscles.
Pathophysiology
Assessment
Blood cells and the thymus gland produce antibodies that block, destroy, or weaken neuroreceptors
that transmit nerve impulses, mainly acetylcholine. The number of acetylcholine receptors in the
postsynaptic muscle membrane is decreased, causing failure of transmission of nerve impulses at
the neuromuscular junction.
CAUSES/COMPLICATIONS
‣ Idiopathic
‣ Congenital
‣ Myasthenia crisis: Acute
exacerbation caused by rapid
unrecognized progression of
the disease, inadequate amount
Laboratory Findings:
Education
‣ Disease process
‣ Medications
‣ Symptoms are transient
‣ need to avoid strenuous exercise,
stress, infection, and unnecessary
exposure to the sun or cold
weather
‣ swallowing-therapy program
‣ danger signs and symptoms,
especially those of myasthenic
crisis and cholinergic crisis and
the need to report any to the
practitioner immediately.
Masklike expression
Diplopia
Decreased breath sounds
Ptosis
Weakness
Trouble swallowing
Treatments
‣ Anticholinesterase:
pyridostigmine bromide
(Mestinon) and neostigmine.
‣ Immunosuppressive drugs:
azathioprine (Imuran),
cyclosporine (Neoral),
cyclophosphamide (Cytoxan),
mycophenolate mofetil (CellCept),
and tacrolimus
‣ Corticosteroids prednisone
‣ I.V. immune globulin
‣ Stop triggering agents
‣ Plasmapheresis
‣ Emergency airway management
of medication, infection,
fatigue, or stress.
‣ Anti-acetylcholine receptor antibody: is positive in 80% to 90% of patients
‣ Anti–muscle-specific kinase antibody: 30% to 40% of patients
Anti Striated muscle antibody is present.
‣ Muscle-specific tyrosine kinase antibody: Is present in about 40% to 50% of
patients with generalized myasthenia gravis and is absent in patients with ocular
myasthenia gravis.
Tensilon test or endorphin test: Results are positive, showing temporary
improved muscle function and confirming the diagnosis.
‣ Ice pack test results: (for patients
for whom the Tensilon test is
contraindicated) reveal decreased
ptosis after ice is applied for 60
seconds to the closed eyelid.
‣
‣
‣
‣
‣
‣
Characterized by rapid pulse
rate, increased respirations,
dyspnea, anoxia, cyanosis,
bowel and bladder
incontinence, decreased urine
output, absent cough and
Risk Factors
‣ Systemic lupus erythematosus
‣ Thyrotoxicosis
‣ Autoimmune disorder
associated with the thymus
gland
‣ immune and thyroid disorders
causing secondary symptoms
swallow reflex.
‣ Interventions: increase anti
INTERVENTIONS
cholinesterase medications.
‣ Monitor respiratory status
‣ Monitor for respiratory failure
‣ Maintain patent airway and
suctioning.
‣ Thickened liquids
‣ Encourage the client to sit up
and eat.
‣ Assess musculoskeletal status.
‣ Plan short activities during
periods when the patient has the
most strength.
‣ Monitor for myasthenic and
cholinergic crisis.
IMPORTANT
‣ Cholinergic crisis:
Depolarization of motor end
plates. Characterized by
abdominal cramps, nausea,
vomiting, diarrhea, blurred
vision, pallor, facial muscle
Monitor the patient for signs
of impending myasthenic
crisis, including
increased muscle weakness,
respiratory distress, and
difficulty talking or chewing.
twitching, hypotension,
pupillary miosis.
‣ Interventions: Withhold anticholinesterase medications,
prepare to administer antidote
if ordered
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MEDICAL SURGICAL NURSING: NEURO 1.9.7
NURSE ANGIE 2018
Parkinson’s Disease
A slow progressive neurological disease that results in disability and long term self care deficits.
Pathophysiology
Assessment
S: Slow movements
A degenerative disease resulting from a depletion of dopamine and an imbalance of acetylcholine
which interferes in with the inhibition of excitatory impulses, thus causing the patient to shake and
tremor uncontrollably. The debilitation can cause self care deficits, falls, failure of body systems.
Later as the disorder progresses mental deterioration can occur.
GOALS
‣ Improving functional mobility
‣ Maintaining independence
‣ Maintaining acceptable
nutritional status
‣ Achieving adequate bowel
elimination
‣ Achieving effective
communication
‣ Develop positive coping
mechanism
H: Hypotension
A: Akinesia
K: Kinesis ( Brady)
Y:Yes they walk with forward
flexion
M: Mask like expression
A: Agitation
N: Not steady, tremors when at rest
Treatments
‣ PNo treatment cures the disorder.
‣ Treatment is individualized.
‣ Antiparkinsonian drugs: increase
dopamine and reduce
acetylcholine.
‣ Levodopa: Converted to
dopamine in the basal ganglia.
Laboratory
Findings:
‣ PET scans
INTERVENTIONS
‣ Assess neuro status
‣ Assess ability to swallow
‣ Provide high calorie, high
protein, high fiber, soft diet.
‣ Increase fluid intake to 2000
mL/day
‣ Monitor for constipation
‣ Promote independence and
avoid rushing the patient
‣ Promote safety
‣ Encourage the use of assistive
devices. Help with ambulation.
‣ Promote physical therapy and
rehabilitation.
‣ Position on a firm mattress,
prone without a pillow.
‣ Avoid foods high in VIT B, they
reduce the effects of
antiparkinsonian drugs.
‣ Administer antiparkinsonian
drugs as ordered.
‣ Use caution with MAOIs they
may cause hypertensive crisis.
See agency protocol.
CAUSES
‣ Depletion of dopamine,
‣ Early diagnosis is rare because
patients can rarely pinpoint when
symptoms started.
dopamine-generating cells,
known as dopaminergic
neurons (types of nerve
Education
‣ possible adverse effects of such
medications as levodopa
carbidopa or bromocriptine
‣ measures to prevent pressure
injury and contractures
‣ promote activity and
participation in self-care;
importance therapy
‣ household safety measures
dietary recommendations,
including the need for adequate
fiber and fluid intake
‣ methods to improve
communication
‣ swallowing therapy regimen
(aspiration precautions)
cells) in the substantia nigra
part of the brain have died.
Experts do not know why
these cells die.
Complications
‣ Injury from falls, Aspiration
‣ Urinary tract infections
Skin breakdown, Pneumonia
Anxiety, Depression,
psychosis
Dementia, Constipation
Sleep problems, sensory
issues
‣ Pain
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Levodopa is the post effective
treatment for parkinson's.
‣Antiviral agents: Reduce rigidity,
tremors, bradykinesia, and
postural changes
‣Dopamine Agonists: Secondary to
carbidopa/levodopa for early
stages.
‣MAOI: Inhibit dopamine
breakdown
‣Catechol-O-Methyltransferase
inhibitor: increases action of
carbidopa or levodopa, reduces
motor fluctuations in advanced
parkinson's.
‣Tricyclic antidepressants/SSRI :
Anticholinergic and
antidepressant
‣Antihistamines: may reduce
tremors.
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MEDICAL SURGICAL NURSING: NEURO 1.9. 10
NURSE ANGIE 2018
Spinal Cord Injury
Trauma to the spine that results in full or partial severance, this leads to loss of mobility
Emergency management
Pathophysiology
• Always suspect spinal injury
when trauma occurs
• Assess and maintain a patent
Trauma to the spinal cord causes disruption of the nerve
tracts and neurons. A spinal cord injury can result in edema,
total or partial severance of the cord causing paralysis.
Common affected vertebrae
• Cervical : C5-C7
• Thoracic: T 12
• Lumbar: L 1
airway and assess respirations.
• Prevent head flexion, extension
or rotation.
• Log-roll the client.
• Never twist or turn the client.
• Do not allow them to sit.
• In the emergency department,
place the patient immediately in
skeletal traction. To reduce
fracture and dislocation.
!
Assessment
•Cervical: injury at C2 or C3 is
fatal, injury above C4 causes
respiratory difficulty and paralysis
in all extremities. Client may move
shoulder and have decreased
respiratory reserve with injury to
C5-C8.
•Thoracic: Loss of movement in
the trunk, chest, bowel, bladder and
legs. Paraplegia may occur,
autonomic dysreflexia in injuries
above T6. Distended bladder or
impacted rectum, bradycardia,
hypertension and goosebumps.
• Lumbar: Loss of movement or
sensation in the lower extremities,
injury to S2 or S3 can cause
neurogenic bladder. Injury above
S2 in males enables them to still
experience erection but not
ejaculate due to sympathetic nerve
damage. Injury at S2-S4 will result
in inability to obtain an erection or
ejaculate.
Types
INTERVENTIONS FOR
AUTONOMIC
DYSREFLEXIA
• Raise the head of the bed
• Loosen tight clothes
• Administer
antihypertensives
• Document occurrence
treatment and response.
Autonomic dysreflexia:
•
•
•
•
•
Severe hypertension
bradycardia
severe headache
nasal stuffiness
and flushness.
SYNDROMES
INTERVENTIONS
• Immediately stabilize the spine
• Assess neuro function
• Assess respiratory function every
Central cord syndrome: Is a result
of a lesion on the central portion of
the spinal cord. Motor function loss is
apparent in the upper extremities,
some sensation remains intact.
Anterior syndrome: Results from
injury to the anterior portion of gray
and white matter. Motor function,
pain sensation and temperature are
lost below the area of injury.
Posterior Syndrome: Results from
damage to the posterior portion of the
gray and white matter in the spinal
cord. Motor function remains intact,
but the patient will experience a loss
of sense of vibration , crude touch,
and position sensation.
Brown-Sequard syndrome: Is a
result of a penetrating injury that
cause injury to half the cord.
Sensation, temperature and pain are
affected on the opposite side of
hour
• Monitor secretions and breath
sounds
• Monitor 02 saturation
• Assess cardiovascular function
every hour
• Monitor blood pressure
• If there is a pulmonary catheter in
•
•
•
•
•
•
•
the injury.
1
monitor inform the HCP of a
decrease in right atrial pressure,
pulmonary artery pressure,
systemic vascular resistance, or
pulmonary wedge pressure as this
could indicate neurogenic shock
Monitor GI status
Monitor intake and output
Avoid uriniary retention to avoid
autonomic dysreflexia
Monitor for dvt
Frequent skin assessments
Begin rehab as soon as possible
Provide emotional support
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‣Transection of the cord:
Complete severance of the spinal
cord, results in total loss of
sensation, movement, and reflexes.
‣Partial Transection : The cord is
partially severed, symptoms
depend on the extent of the
damage, early treatment may result
in avoidance of permanent damage.
Complications
• Respiratory failure
• Death
• Autonomic dysreflexia
• Spinal shock
• Extensive cord damage
Effects
• Tetraplegia: Injury between C1
and C2. paralysis involving all
extremities.
• Paraplegia: Injury between T1
and L4 paralysis only involving
lower extremities.
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MEDICAL SURGICAL NURSING: NEURO 1.9.6
NURSE ANGIE 2018
Stroke
Sudden loss of neurological function caused by cerebrovascular disease.
CAUSES
Pathophysiology
‣ Thrombosis
‣ Embolism
A stroke can be caused by an embolus in the peripheral
vasculature that breaks off and makes its way into the cerebral
vessels causing a blockage. This blockage causes cerebral
ischemia which leads to the death of cerebral cells and tissues
causing paralysis, weakness, impaired speech and possibly
death.
‣ Hemorrhage: Intracranial or
Subarachnoid
•D: Drooping of the face
•E: Extra high BP
• A: Apraxia
• D: Dysarthria
RISK FACTORS
‣
‣
‣
‣
‣
‣
‣
‣
‣
Laboratory Findings:
‣
‣
‣
‣
‣
‣
‣
‣
‣
Maintain a patent airway.
Position.
Monitor elimination patterns
Provide skin care.
Perform passive/Active ROM.
Move extremities that have been
affected slowly.
‣ Teach the use of supportive
device ( cane, walker,
commode)
‣ Address communication needs.
‣ Orient client to person, place
and time.
Smoking
Advanced age
Hypertension, Stress
TIA’s
Diabetes, Obesity
High Cholesterol
Oral contraceptives
Atherosclerosis
Anticoagulant therapy
Assessment of cranial
nerves
•V: Difficulty chewing.
•VII: Facial paralysis or paresis
•IX: Absent gag reflex
•IX & X: Dysphagia
•XII: Impaired tongue movement
Criteria for t-PA admin
‣18 yrs old
‣Clinical diagnoses of ischemic
stroke
‣ Time of onset of stroke under 3
hours
‣BP less than 185/110 mmHg
‣Not a minor or rapid resolving
stroke
‣No seizure at onset of stroke
Maintain a patent airway
‣Not on warfarin
Administer TpA within 6 hrs of
‣Prothrombin < 15 seconds
symptom onset, and not for
‣Not on heparin within the past
hemorrhagic stroke if indicated to
48 hrs.
break up a thrombus.
‣Platelet count > 10,000/mm3
Administer 02 as prescribed
‣No prior aneurysm, hemorrhage,
Monitor Vitals
or neoplasm
Maintain BP of 150/100 mmHg to
‣No major surgery in the last 14
maintain cerebral perfusion.
days.
Suction secretions as ordered. No
‣No stroke within 3 months
longer than 10 seconds to prevent
‣No GI or GU bleeding within 3
ICP.
months.
Monitor for increased ICP the
‣Dosage : 0.9mg/ kg not to
highest risk for ICP is within the
exceed 90mg. Given IV 10% as a
first 72 hours.
bolus over 1 min. The remaining
Position the client on the side with
IV over 1 hour pump.
the head of the bed elevated 15-30
degrees.
Monitor LOC, PERRLA.
Insert foley
Administer IV fluid.
PRIORITY INTERVENTIONS
CT scan
Electroencephalography
Cerebral arteriography
MRI.
NURSING INTERVENTIONS
POST ACUTE PHASE
Assessment
•B: Bothered field of vision
•R: Respiratory changes
•A: Agnosia
•I: Instant LOC changes
•N: Not able to speak clearly
‣
‣
EDUCATION
‣ Remind the patient about the
importance of keeping
appointments and screening.
‣ Educate the client on the
disease process and how it's
transmitted.
‣ Educate the client on
treatments and the importance
of adhering to the
recommended treatment
regimens
‣ Finish all antibiotics.
‣ Educate the patient of asepsis
and preventing the spread of
meningitis.
‣
‣
‣
‣
‣
‣
‣
‣
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MEDICAL SURGICAL NURSING: NEURO 1.9.11
NURSE ANGIE 2018
Trigeminal Neuralgia
A sensory disorder that affects the 5th cranial nerve.
Risk Factors
Pathophysiology
The trigeminal nerve has multiple branches. This nerve
affects movements and sensations of the face, scalp, and
teeth. Compression of the nerve root occurs from an
unknown cause. Demyelination occurs in the area of the
compression. An impulse triggers the area, and interaction or
short-circuiting of touch and pain fibers occurs.
Paroxysmal attacks causing excruciating facial pain
‣
‣
‣
‣
‣
‣
Herpes zoster
History of multiple sclerosis
Age over 50 years
Disorder of blood vessels
Female gender
Arteriovenous malformation
Complications
‣ weight loss
‣ Depression
Social isolation
Paresthesia
‣ loss of corneal reflex
Assessment
‣
‣
‣
‣
P: Pain on the lips, face & gums
A: Along the trigeminal nerve
I : Initiated by light touch
N: No impairment of sensory or motor
function
‣ E: Exacerbated by extreme temperatures
‣ D: Does Not shave or chew on the affected
side
‣
‣ F: Favors the affected side, splinting the
affected side
‣ A: A Draft or cold air can aggravate it
‣ C: Cold drinks and food can aggravate
‣ E: Eating, smiling, talking, and brushing
teeth can exacerbate the pain.
Treatments
‣ Anticonvulsants: Carbamazepine
(Tegretol) or oxcarbazepine, as a
first-line agent and phenytoin,
gabapentin, lamotrigine, or valproic
acid as a second-line agent;
tizanidine hydrochloride as
alternative agent
‣ Skeletal muscle relaxants: Baclofen,
Laboratory Findings:
as an adjunct to phenytoin or
‣ Skull radiography, computed tomography scanning (brain), and magnetic resonance imaging rule
out sinus or tooth infections and tumors.
carbamazepine
‣ Antidepressants: Amitriptyline
hydrochloride, fluoxetine
hydrochloride, or trazodone
Education
CAUSES
‣ Instruct the client to avoid hot
or cold food.
‣ Small frequent feedings of
‣ Compression of the nerve root
by: Middle fossa tumors,
posterior fossa tumors, vascular
lesions
‣ Afferent reflex phenomenon
soft food.
‣ Instruct client to chew food
hydrochloride, in conjunction with an
INTERVENTIONS
on unaffected side.
‣ Frequency of attacks
‣ effectiveness of medications
‣ Microvascular decompression
‣ Monitor CBC with tegratol
‣ Monitor post OP neuro
compresses the trigeminal nerve.
‣ Radiofrequency waveforms: Creates
function
‣ Administer anticonvulsants as
‣ Obtain informed consent for
ordered.
surgery
‣ Prepare for microvascular
‣ Focused pain assessments
‣ Wound assessment
decompression surgery if
indicated.
anticonvulsant
‣ Topical capsaicin cream
surgery: Relocates the artery that
lesions that provide pain relief.
‣ Rhizotomy: Resection of the
trigeminal nerve root.
‣ Glycerol injection: Destroys the
myelinated fibers of the trigeminal
nerve root.
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MEDICAL SURGICAL NURSING: RESPIRATORY 1.6.4
NURSE ANGIE 2018
Tuberculosis
A highly contagious communicable disease caused by mycobacterium tuberculosis.
Pathophysiology
Assessment
Multiplication of the bacillus Mycobacterium tuberculosis causes an inflammatory process where
deposited. A cell-mediated immune response follows, usually containing the infection in 2 to 8
weeks. The T-cell response results in the formation of granulomas around the bacilli, making them
dormant. This confers immunity to subsequent infection. Bacilli within granulomas may remain
viable for many years, resulting in a positive purified protein derivative or other skin test for TB.
Transmission occurs via airborne droplet nuclei when a
person with active disease coughs or sneezes.
Complications
Massive pulmonary tissue damage
Respiratory failure
Bronchopleural fistulas
Bronchiectasis
Hemoptysis
Pneumothorax
Pleural effusion
Pneumonia
Infection of other body organs by
small mycobacterial foci
‣ Liver involvement disease
secondary to drug therapy
‣
‣
‣
‣
‣
‣
‣
‣
‣
INTERVENTIONS
‣ Tuberculin skin test result is positive in active and inactive (latent) TB.
‣ T-SPOT TB test identifies interferon-gamma response to specific
Mycobacterium tuberculosis proteins to detect infection.
‣ QuantiFERON-TB gold test or interferon gamma release assay detects
latent TB infection.
‣ Stains and cultures of sputum, cerebrospinal fluid, urine, abscess drainage,
or pleural fluid show heat-sensitive, nonmotile, aerobic, acid-fast bacilli.
‣ Chest radiography shows nodular lesions, patchy infiltrates, cavity
formation, scar tissue, and calcium deposits; may be normal in primary
infection.
‣ Exposure to M.
tuberculosis
‣ Exposure to other
strains of mycobacteria
called mycobacteria
other than tuberculosis
(MOTT)
N: not able to sleep
I: intense chest pain
G: gross sputum( bloody)
H: history of influenza
T: travel to TB prevalent areas
‣ S: sweats at night
‣ W: weight loss
‣E: extra effort to breathe
‣A: anorexia
‣T: tightness in chest
Medical Treatment
‣ First-line drugs:
Antitubercular therapy for at
least 6-9 months isoniazid
( isonicotinic acid hydrazide)
(Isotamine), rifampin
(rifampicin) (Rifadin), and
pyrazinamide,plus ethambutol
hydrochloride (Myambutol) or
streptomycin in some cases
‣ Second-line drugs:
Laboratory Findings:
CAUSES
‣
‣
‣
‣
‣
‣ Isolate the patient in a quiet, properly
ventilated room.
‣ Institute airborne precautions for
pulmonary TB until the patient has at
least three consecutive negative
sputum cultures
‣ Properly dispose of secretions;
encourage respiratory hygiene
measures.
‣ Provide adequate rest periods.
Cluster activities to provide for
adequate rest.
‣ Provide well-balanced, high-calorie
foods & foods high in iron, vitamin c
and protein.
‣ Provide small, frequent meals.
‣ Perform chest physiotherapy.
Encourage frequent coughing and
deep-breathing exercises.
‣ Obtain specimens for laboratory
testing, such as sputum cultures, as
indicated.
‣ Notify the local health department if
required by state regulations.
EDUCATION
‣ Take all of your medications
‣ Wear proper PPE
‣ Appropriate infection control
precautions.
‣ Coughing and deep breathing
exercises
‣ Follow up
‣ TB medications can reduce the
effectiveness of birth control
‣ High calorie, high protein diet
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➢ Capreomycin (Capastat
Sulfate)
➢ Streptomycin
➢ Ethionamide (Trecator)
➢ Aminosalicylic acid (paraaminosalicylic acid [Parasol])
➢ Pyrazinamide
➢ Cycloserine (Seromycin)
‣ Alternative agents:
levofloxacin (Levaquin),
moxifloxacin
hydrochloride(oral; injection)
(Avelox), linezolid (Zyvox), or
meropenem-clavulanate for
treatment of multidrug or
highly drug-resistant TB
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MEDICAL SURGICAL NURSING: RESPIRATORY 1.6.12
NURSE ANGIE 2018
Pleural Effusion
Fluid accumulation between the visceral and parietal pleura of the lung
Pathophysiology
Assessment
Fluid and other blood components migrate through the walls of intact capillaries bordering the
pleura. Classified as transudative or exudative Usually unilateral but can be bilateral (usually due
to heart failure, kidney failure, liver failure, or malignant neoplasms).
‣ Shortness of breath, chest
pain; referred abdominal or
shoulder pain, malaise, cough,
productive or nonproductive,
weight loss, night sweats,
fever, trachea, mediastinum, or
both deviating from the
affected side . Dullness and
decreased tactile fremitus over
the effusion, diminished or
absent breath sounds,
tachypnea, bronchial breathing
or egophony, hemoptysis,
pleural friction rub, bronchial
breath sounds, peripheral
edema, distended neck veins,
and S3 gallop (suggesting
heart failure) foul-smelling
sputum (empyema)
Medical Treatment
‣Thoracentesis to remove fluid
CAUSES
Laboratory Findings:
‣ Pleural fluid analysis findings: May show empyema, elevated WBC,
elevated amylase or lipase if related to pancreatitis, elevated protein.
‣ Chest radiography may show pleural effusions; lateral decubitus films may
show loculated pleural effusions or small pleural effusions not visible on
standard chest radiography.
‣ Computed tomography scanning (thorax) shows pleural effusions.
‣ Transthoracic ultrasonography reveals the amount and level of fluid
accumulation.
‣ Pleural biopsy may be positive for carcinoma.
SURGICAL PROCEDURES
‣ Tube thoracostomy
‣ Pleuroperitoneal shunts (rare;
for
‣ recurrent effusions)
‣ Pleurodesis—chemical or
mechanical
‣ sclerosing agents under VATS
‣ Pleurectomy—radical total or
subtotal
‣ and decortication for malignant
‣ effusions
‣ Insertion of long-term tunneled
‣ indwelling pleural catheter to
allow for outpatient management
with recurrent
INTERVENTIONS
‣ Monitoring Vitals
‣ Coping
‣ Administer prescribed drugs and I.V.
fluids, initiate I.V. access, and
maintain I.V. patency. Provide I.V. site
care
‣ Give supplemental oxygen based on
oxygen saturation levels and arterial
blood gas results.
‣ Elevate the head of the bed at least 30
degrees
‣ Assist the patient with relaxation
measures to reduce oxygen demand
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
Empyema
Infected wound
Intra-abdominal infection
Lung abscess
Pulmonary infection
Thoracic surgery
Malignancy
Connective tissue diseases
Transudative Pleural Effusion
Cardiovascular disease
Hepatic disease
Hypoproteinemia
Renal disease
Exudative Pleural Effusion
Pleural infection
Pleural inflammation
Pleural malignancy (most
often occurring with lung or
breast cancer)
Pneumonia
Pulmonary embolism
Pancreatitis
Trauma
Drug use
Tuberculosis
Asbestos exposure
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‣Possible chest tube insertion
‣Possible chemical pleurodesis
‣Intrapleural fibrinolytic agents in
limited cases
‣Treatment of underlying condition
‣Antimicrobial therapy,: ampicillin
sodium imipenem–cilastatin
sodium clindamycin phosphate
(injection)(Cleocin Phosphate), or
piperacillin sodium–tazobactam
sodium (Zosyn), doxycycline
(Vibramycin), bleomycin sulfate,
or talc for chemical pleurodesis to
treat recurrent pleural effusions
‣Chemotherapy for malignancy
‣Corticosteroids and nonsteroidal
anti-inflammatory drugs for
effusions due to rheumatologic or
inflammatory causes
‣ Diuretics, such as furosemide
(Lasix), for effusions resulting
from heart failure and ascites
‣Oxygen
‣I.V. fluid therapy
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MEDICAL SURGICAL NURSING: RESPIRATORY 1.6.8
NURSE ANGIE 2018
S.A.R.S
Severe form of alveolar injury or acute lung injury
Assessment
Pathophysiology
Coronaviruses cause diseases in pigs, birds, and other animals. A theory suggests that a
coronavirus may have mutated, allowing transmission to and infection of humans.
Mucous membranes come in direct or indirect contact with infectious respiratory droplets
or fomites. The virus attaches itself to human receptor cells, initiating a nonspecific acute
lung injury. The result is diffuse severe alveolar
damage.
Risk Factors
‣ Close contact with
aerosolized (exhaled)
droplets and bodily
secretions from an
infected person
‣ Travel to endemic areas
‣ O:out of the country
‣ U:underdeveloped countries
‣ T: travel to endemic areas
‣ O: out of breath
‣ F: fever, fatigue
‣ B: bad muscle aches
‣ R: rhinorrhea/ respiratory
distress
‣ E: excess vomiting
‣ A: A sore throat
‣ T: tachypnea
‣ H: headache
Medical Treatment
Complications
Laboratory Findings:
‣ Respiratory difficulties
‣ Severe thrombocytopenia
(low platelet count)
‣ Heart failure
‣ Liver failure
‣ Death
‣ Arterial blood gas (ABG) analysis initially shows hypoxemia and
respiratory alkalosis
‣ ABG analysis later showed respiratory acidosis
‣ B-type natriuretic peptide assay result of less than 100 pg/mL suggests
ARDS.
‣ Gram stain and sputum culture and sensitivity show infectious organisms.
‣ Leukopenia or leukocytosis may be present in patients with sepsis.
‣ Blood culture reveals infectious
organisms.
‣ Chest radiography show early
bilateral infiltrates
‣
‣
INTERVENTIONS
CAUSES
‣ Coronavirus
known as
SARSassociated
coronavirus
(SARS-CoV
Education
‣
‣
‣
‣
‣
Monitor respiratory status.
Administer 02
Trach care if indicated
Conservative fluid management
Tube feedings or parenteral
nutrition as indicated
‣ Bed rest with frequent turning
and position changes
‣ Elevation of the head of the bed
to 45 degrees
importance of frequent
hand washing
importance of covering
the mouth and nose when
coughing or sneezing
avoiding close
personal contact with friends
and family
Report condition to CDC
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‣ Treatment of the
underlying cause
‣ Correction of electrolyte
and acid-base imbalances
‣ Mechanical ventilation
‣ Vasopressors if the patient
is hypotensive
‣ Antimicrobials if nonviral
infection is identified
‣ Inotropic agents
‣ Inhaled vasodilators
‣ Anxiolytics : lorazepam
(Ativan)
‣ Anti embolic
‣ Bronchodilators
‣ Paralyzing agents
‣Sodium bicarbonate
‣Sedatives
‣Opioids
‣Neuromuscular blocking
agents
‣Fluids and vasopressors if
hypotensive
‣ Antimicrobials if nonviral
infection is identified
‣Prone positioning to help
with perfusion of the lungs
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MEDICAL SURGICAL NURSING: RESPIRATORY 1.6.6
NURSE ANGIE 2018
COPD: Chronic Bronchitis
Progressive respiratory disease characterized by airflow limitation that is progressive, not preventable,
and not fully reversible.
Assessment
Pathophysiology
Changes associated with chronic bronchitis include hypertrophy and hyperplasia of the bronchial mucous
glands, increased goblet cells, ciliary damage, squamous metaplasia of the columnar epithelium, and chronic
leukocytic and lymphocytic infiltration of bronchial walls. Widespread inflammation occurs, leading to airway
narrowing and mucus within the airways. Producing resistance in the small airways and, consequently, a
severe ventilation-perfusion imbalance.
‣ Increased respiratory rate
‣ Increased hemoglobin
‣ Decreased breath sounds,
wheezes, crackles at the lung
bases
‣ Increased anteroposterior
diameter of the chest. Clubbing of
the nails.
‣ Acidosis, Hypoxia
‣ Hypercapnia, Tripod position to
assist in breathing, Full use of the
accessory respiratory muscles of
the neck and shoulders, Pursedlips expiration, Hoover sign
(paradoxical retraction of the
lower interspaces during
inspiration), Cyanosis.
‣ Asterixis due to severe
hypercapnia. Neck vein distention
(especially during expiration).
‣ Coughing and sputum production.
Medical Treatment
Laboratory Findings:
‣ Arterial blood gas analysis may reveal: mild or moderate hypoxemia
without hypercapnia in patients with mild COPD, and with hypercapnia
when the disease progresses and the hypoxemia becomes more severe..
‣ Hemoglobin level test shows an increased hemoglobin level late in the
disease
‣ Pulmonary function tests show increased residual volume, increased total
lung capacity, and decreased diffusion capacity as well as decreased vital
capacity, decreased forced expiratory flow, normal static compliance, and
normal diffusing capacity.
CAUSES
‣ Tobacco smoking
‣
‣
‣ Occupational exposure to dusts
and chemicals
‣ Indoor and outdoor air pollution,
including the use of biomass
fuel for heating and cooking
‣ Antiprotease deficiency (rare
inherited disorder known as
alpha-1-antitrypsin deficiency
Education
INTERVENTIONS
‣
‣
‣
‣
Monitor airway. Provide 02 as ordered
Clear secretions. Provide a high-calorie,
protein-rich diet to ensure adequate
nutritional status; offer small, frequent
meals to minimize energy expenditure.
Ensure adequate oral fluid intake to
maintain hydration and help mobilize
secretions.
Auscultate lungs for evidence of
adventitious breath sounds.
Elevate the head of the bed to ease the
work of breathing.
Coughing and Deep breathing
exercises
Chest physiotherapy
Energy conservation
Avoid triggers
Obtain vaccinations
Importance of balanced high protein
diet
Maintain adequate nutrition and
hydration
Perform chest physiotherapy to help
mobilize and remove secretions;
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‣ Influenza vaccine yearly;
pneumococcal vaccine at
diagnosis and again in 5 years if
first vaccine at < age 65
‣ Short-acting bronchodilators:
Anticholinergics (such as
ipratropium bromide[Atrovent]) or
beta-adrenergic agonists (such as
albuterol sulfate [Ventolin HFA]).
‣ Long-acting bronchodilators:
Anticholinergics (such as
tiotropium bromide [Spiriva]) and
long-acting beta-adrenergic
agonists (such as salmeterol .
‣ Inhaled glucocorticosteroids
(Flovent) for repeated
exacerbations
‣ long-term oxygen therapy
‣ Theophylline (Theolair)
‣ Combination of inhaled
corticosteroids, long-acting betaadrenergic agonists, and
anticholinergics for severe disease
‣ Low-dose macrolides
(clarithromycin [Biaxin] or
erythromycin) to decrease
inflammation
‣ Mucolytic agents to improve
secretions but not outcomes
‣ Systemic glucocorticosteroids for
5 to 10 days
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MEDICAL SURGICAL NURSING: RESPIRATORY 1.6.5
NURSE ANGIE 2018
Asthma
Airway inflammation, intermittent airflow obstruction, and bronchial hyper-responsiveness
Pathophysiology
Chronic inflammation of the airways that causes varying degrees of obstruction. Marked by
inflammation and hyper-responsiveness to a variety of stimuli “triggers”. Once a trigger has been
met the patient may wheeze, feel breathlessness, may feel tight chested and may cough , this is
associated with airway obstruction.
Complications
‣ Acute, severe asthma (formerly
known as status asthmaticus)
‣ Respiratory failure
‣ Pneumonia
‣ Atelectasis
‣ Air-leak syndrome (such as
pneumothorax)
‣ Death
Assessment
‣ C: chest tightness
‣ L: long exhalation
‣O: obstructed airway
‣S: sounds wheezy
‣E: expiratory wheezes
‣D: diminished breath sounds
‣
‣
‣
‣
‣
‣
T: tachycardia
H: has lots of sweat
R: restlessness
O: oh he’s blue
A: altered mental status
T : tachypnea
Medical Treatment
Laboratory Findings:
‣ Arterial blood gas analysis (ABG) provides the best indication of an attack's
severity and may reveal hypoxemia during an acute attack. A normal Paco2
during an acute attack may be a sign of impending respiratory failure.
‣ Complete blood count with white blood cell count and differential shows
increased eosinophil count in acute phases.
‣ Pulmonary function tests commonly show decreased peak flow rates and
forced expiratory volume in 1 second, low-normal or decreased vital
capacity, and increased total lung and residual capacities. However,
pulmonary function tests may be normal between attacks.
‣ Skin testing may identify specific allergens.
‣ Pulse oximetry measurements may show decreased oxygen saturation.
‣ Peak flow monitoring reveals a result of less than 80% of personal best; a
reading below 50% of personal best indicates a severe exacerbation.
CAUSES
‣ Sensitivity to specific
external allergens
(leading cause)
‣ Internal, nonallergenic
factors, such as genetic
factors and stress
EDUCATION
INTERVENTIONS
‣
‣
‣
‣
‣ Educate on the need for
long term management
‣ Identify triggers and have
the patient avoid them.
‣ Educate on medication
regimen.
‣ Educate on the correct use
of a peak flow meter.
Maintain patient airway
Monitor pulse ox
Monitor vitals
Monitor peak flow
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‣ Quick-relief bronchodilators,:
albuterol sulfate
‣ Quick-relief anticholinergics:
ipratropium bromid for relief of
bronchospasm
‣ Corticosteroids:
methylPREDNISolone,
prednisoLONE, and prednisone, to
prevent exacerbation during
moderate or severe exacerbations
‣ Corticosteroids for persistent
asthma : an inhaled corticosteroid
of fluticasone furoate,
beclomethasone dipropionate,
budesonide, or mometasone
‣ Long-acting beta-agonist or
combination drug: salmeterol
xinafoate inhaler, formoterol,
fluticasone furoate/ salmeterol
xinafoate inhaled or budesonideformoterol fumarate dihydrate
(Symbicort)
‣ Leukotriene antagonists
(antileukotrienes): montelukast
sodium(Singulair)
‣ Anticholinergic bronchodilators :
tiotropium bromide inhaled
(Spiriva)
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MEDICAL SURGICAL NURSING: RESPIRATORY 1.6.7
NURSE ANGIE 2018
COPD: EMPHYSEMA
The destruction of alveoli
Assessment
Pathophysiology
‣ Increased respiratory rate
Changes associated with emphysema include recurrent inflammation associated with the release of
proteolytic enzymes from lung cells that causes abnormal, irreversible enlargement of the air
spaces distal to the terminal bronchioles.The amount of alveolar surface area available for gas
exchange decreases. This enlargement leads to the destruction of alveolar walls in the distal or
terminal airways, which results in a breakdown of elasticity. Elastic recoil is reduced, limiting
airflow. Supporting
‣ Increased hemoglobin
‣ Decreased breath sounds, wheezes,
crackles at the lung bases
‣ Increased anteroposterior diameter
of the chest. Clubbing of the nails.
‣ Acidosis, hypoxia
‣ Hypercapnia, tripod position to
assist in breathing, full use of the
accessory respiratory muscles of
the neck and shoulders, pursed-lips
expiration, hoover sign, cyanosis.
‣ Asterixis due to severe
hypercapnia
‣ Neck vein distention
‣ Coughing and sputum production.
Medical Treatment
Laboratory
Findings:
‣Arterial blood gas analysis may reveal: mild or
moderate hypoxemia without hypercapnia in patients with mild COPD, and with hypercapnia when the disease progresses and
the hypoxemia becomes more severe..
‣ Hemoglobin level test shows an increased hemoglobin level late in the disease
‣ Sputum culture may reveal the number of microorganisms and neutrophils..
‣ Pulmonary function tests show increased residual volume, increased total lung capacity, and decreased diffusion capacity as
well as decreased vital capacity, decreased forced expiratory flow
‣ Influenza vaccine yearly
‣ Short-acting bronchodilators:
Anticholinergics
‣ Long-acting bronchodilators:
Anticholinergics and long
acting beta-adrenergic agonists
(such as salmeterol .
‣ Inhaled glucocorticosteroids
for repeated exacerbations
‣ Long-term oxygen therapy
‣ Theophylline (Theolair)
‣ Combination of inhaled
INTERVENTIONS
CAUSES
‣ Tobacco smoking
‣
‣ Occupational exposure to dusts
and chemicals
‣
‣
‣ Indoor and outdoor air pollution,
including the use of biomass
fuel for heating and cooking
‣
‣ Antiprotease deficiency (rare
inherited disorder known as
alpha-1-antitrypsin deficiency)
‣
EDUCATION
Monitor airway. Provide 02 as
ordered. Clear secretions
Provide a high-calorie, protein-rich
diet.
Ensure adequate oral fluid intake to
‣ Pursed lip breathing
‣ Use of incentive spirometer
‣ Eat frequent small meals
corticosteroids, long-acting
beta-adrenergic agonists, and
anticholinergics for severe
disease
‣ Low-dose macrolides,
maintain hydration and help mobilize
secretions.
clarithromycin
‣ Mucolytic agents to improve
Auscultate lungs for evidence of
adventitious breath sounds.
Elevate the head of the bed to ease
secretions but not outcomes
‣ Systemic glucocorticosteroids
for 5 to 10 days
the work of breathing.
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MEDICAL SURGICAL NURSING: RESPIRATORY 1.6.1
NURSE ANGIE 2018
INFLUENZA
Known as the “FLU” , a highly contagious acute viral respiratory infection.
Pathophysiology
Assessment
Virus invades the epithelium of the respiratory tract, causing inflammation and desquamation. After
attaching to the host cell, viral ribonucleic acid enters the cell and uses host components to
replicate its genetic material and protein, which are then assembled into new virus particles. Newly
produced viruses burst out to invade other healthy cells. Viral invasion destroys host cells,
impairing respiratory defenses (especially the mucociliary transport system) and predisposing the
patient to secondary bacterial
infection.
Usually, recent exposure
(typically within 48 hours) to
a person with influenza, No
influenza vaccine received
during the past season
CNS: Headache
MISC: Malaise, Fatigue,
listlessness, weakness,
Fever, Warm, hot skin, Red,
watery eyes; clear nasal
discharge, Erythema of the
nose and throat without
exudate
MS: Myalgia, Pain with eye
movement Fatigue,
listlessness, weakness
RESP: Sore throat,
Nonproductive cough,
Tachypnea, dyspnea,
cyanosis
Cardio: Tachycardia
Medical Treatment
Laboratory Findings:
‣ Immunodiagnostic techniques show viral antigens in tissue culture or in
exfoliated nasopharyngeal cells obtained by washings.
‣ White blood cell (WBC) count is elevated in secondary bacterial infection.
‣ White blood cell count and differential are decreased in overwhelming viral
or bacterial infection.
‣ Rapid influenza antigen tests are positive for the type of influenza (A or B).
‣ Chest radiography rules out pneumonia.
CAUSES
‣ Infection by the
orthomyxovirus, which
is transmitted by
inhaling a respiratory
droplet from an
infected person or by
indirect contact (such
as drinking from a
contaminated glass)
INTERVENTIONS
EDUCATION
Encourage rest
Encourage fluid intake
Monitor lung sounds
Administer medications as
prescribed
‣ Institute droplet
precautions
‣ Hand washing
‣ Cover your mouth when
you cough
‣ Influenza is a virus and
isn’t cured with
antibiotics.
‣ Drink fluids
‣
‣
‣
‣
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‣ TAntipyretics:
acetaminophen (Tylenol),
or nonsteroidal antiinflammatory drugs
(NSAIDs) such as
ibuprofen (Advil)
‣ Guaifenesin (Robitussin)
or expectorant
‣ Antivirals: oseltamivir
phosphate (Tamiflu) or
zanamivir (Relenza
Diskhaler) as
precautionary medications
to family members and
others not vaccinated and
who have been exposed
by the infected even if
they are not showing
signs or symptoms
‣ Influenza virus vaccine
(for prevention)
‣ Antibiotics for secondary
bacterial infections such
as bacterial pneumonia,
otitis media, or sinusitis
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MEDICAL SURGICAL NURSING: RESPIRATORY 1.6.2
NURSE ANGIE 2018
Pneumonia
Infection of the pulmonary tissue including the interstitial spaces, alveoli and bronchioles.
Pathophysiology
Assessment
The pulmonary tissue becomes infected causing edema which stiffens the lungs and decreases lung
compliance and vital capacity, this also causes hypoxemia. Pneumonia can be community acquired
or hospital acquired.
‣ NEURO: Chills & Fever, Loc
changes
‣ RESP: Tachypnea , pleuritic
pain, rhonchi, wheezes, use of
accessory muscles to breathe,
sputum production.
CAUSES
Aspiration pneumonia
‣ Caustic substance entering the airway
from either vomiting or impaired
swallowing
Bacterial and viral pneumonia
‣ Abdominal and thoracic surgery
‣ Alcoholism
‣ Aspiration
‣ Atelectasis
‣ Bacterial or viral respiratory infections
‣ Cancer
‣ Chronic illness and debilitation
‣ Chronic respiratory disease
‣ Endotracheal intubation or mechanical
ventilation
‣ Exposure to noxious gases
‣ Immunosuppressive therapy
‣ Influenza
‣ Malnutrition
‣ Sickle cell disease
‣ Tracheostomy
Medical Treatment
INTERVENTIONS
viral pneumonia; ribavirin
Laboratory Findings:
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
White blood cell count and differential identifies leukocytosis.
Blood culture tests are positive for the causative organism.
Arterial blood gas analysis (ABG) values may show hypoxemia.
Fungal or acid-fast bacilli cultures identify the etiologic agent.
Assay for Legionella-soluble antigen in urine detects the presence of the
antigen.
Sputum culture, Gram stain, and
smear reveal the infecting
organism.
Rapid antigen testing reveals the
causative organism.
‣ Turn cough deep breath
Chest radiography generally
shows patchy, interstitial, or
‣ Incentive spirometer as
lobar infiltrates (bilateral with
ordered
viral pneumonia; unilateral with
bacterial pneumonia).
‣ Increase fluids
Bronchoscopy or transtracheal
‣ Take medications as
aspiration specimens identify
the etiologic agent.
prescribed
‣
EDUCATION
‣
‣
‣
‣
‣
‣
‣
‣
Airway maintenance
Monitor vitals and Spo2
Institute incentive spirometry.
Monitor color, amount and
consistency of sputum.
Mechanical ventilation with low tidal
volumes (6 mL/kg) and positive endexpiratory pressure for respiratory
failure
Chest physiotherapy
Swallow evaluation if cause is
aspiration
Venous thromboembolism (VTE)
prophylaxis, if hospitalized
Nothing by mouth in cases of
respiratory failure or of aspiration
from impaired swallowing ability
High-calorie, high-protein
Soft, easy-to-chew foods
Adequate fluids
Tube feedings or total parenteral
nutrition if necessary
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‣Antibiotics: clarithromycin,
azithromycin (Zithromax),
azithromycin for Mycoplasma
pneumonia
‣Piperacillin sodium-tazobactam
sodium (Zosyn), imipenemcilastatin sodium (Primaxin),
clindamycin phosphate
(injection) (Cleocin), or
metronidazole hydrochloride
(Flagyl) and a respiratory
fluoroquinolone and
ceftriaxone sodium (Rocephin)
for aspiration pneumonia
‣Antiviral agents : (Tamiflu) for
(Virazole) for viral pneumonia
due to adenovirus; acyclovir
(Zovirax) for viral pneumonia
due to herpes simplex virus
‣ Humidified oxygen
‣ Antitussives
‣ Analgesics and antipyretics:
acetaminophen (Tylenol),
ibuprofen (Advil)
‣ Bronchodilators: albuterol
sulfate (AccuNeb), for
wheezing
‣ I.V. fluids
‣ Glucocorticoids to reduce
inflammatory response in
certain patients in the intensive
care unit.
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MEDICAL SURGICAL NURSING: RESPIRATORY 1.6.9
NURSE ANGIE 2018
Pneumothorax
Full or partial collapse of the lung
Assessment
Pathophysiology
Pneumothorax
Air enters the pleural space and accumulates and separates the visceral and parietal pleurae.
Negative pressure is eliminated, affecting elastic recoil forces. The lung recoils and collapses
toward the hilus, impairing lung expansion.
CAUSES
Spontaneous pneumothorax
‣ Rupture of bleb on lung
surface
‣ Emphysematous bullae
rupture
Closed pneumothorax
‣ Barotrauma
‣ Blunt chest trauma
‣ Clavicle fracture
‣ Congenital bleb rupture
‣ Emphysematous bullae
rupture
‣ Erosive tubercular or
cancerous lesions
‣ Interstitial lung disease
‣ Rib fracture
Open pneumothorax
‣ Penetrating chest injury
(stabbing, gunshot)
Iatrogenic pneumothorax
‣ Central venous catheter
insertion
‣ Chest surgery
‣ Percutaneous lung biopsy
‣ Thoracentesis
‣ Transbronchial biopsy
‣ Tension pneumothorax
‣ Chest tube occlusion or
malfunction
‣ High positive end-expiratory
pressures
‣ Lung or airway puncture
from positive-pressure
ventilation
‣ Mechanical ventilation after
chest injury
‣ Blunt or penetrating chest
wound
Laboratory Findings:
‣ Arterial blood gas analysis may show hypoxemia, hypercapnia, and
acidosis.
‣ Chest radiography shows air in the pleural space with a white visceral
pleural line defining the interface of the lung and pleural air, lack of lung
markings, and, possibly, a mediastinal shift.
‣ Ultrasonography reveals absence of lung sliding (movement of visceral
pleura against parietal pleura), absence of comet-tail artifact (vertical air
artifacts arising from the visceral pleural line), and presence of lung point
(location where lung sliding and absent lung sliding alternately appear).
INTERVENTIONS
‣ Maintain patent airway
‣ Monitor respiratory status & vitals
‣ Maintain a closed chest drainage
system;
‣ Monitor a chest tube unit for any kinks
or bubbling
‣ Stabilize the chest tube
‣ Maintain aseptic technique
‣ Oxygen therapy and mechanical
ventilation are prescribed as needed.
‣ Bed rest until lung re-expansion
‣ No air travel until chest radiography is
normal
EDUCATION
‣ Deep breathing exercises
‣ Incentive spirometer
‣ Causes and prevention
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‣ Tachypnea or bradypnea,
Respiratory distress,
Tachycardia, Pulsus
paradoxus, Asymmetrical
chest wall movement Overexpansion and rigidity on the
affected side, Possible
cyanosis, Subcutaneous
emphysema, Hyperresonance
on the affected side,
Diminished or absent breath
sounds on the affected side
Tension pneumothorax
‣ Distended jugular veins,
Pallor, Anxiety, Tracheal
deviation away from the
affected side, Weak, rapid
pulse, Hypotension,
Tachypnea, Cyanosis, Absent
breath sounds on the affected
side, Decreased cardiac
output, Chest pain, Cardiac
arrest.
Medical Treatment
‣ Chest tube insertion or
emergent needle thoracotomy
(cardiac arrest).
‣ One-way valve (such as
Heimlich valve) insertion.
‣ Video-assisted thoracoscopic
surgery (for recurrent primary
or secondary spontaneous
‣ pneumothorax)
‣ Thoracotomy, pleurectomy
(for recurrent spontaneous
pneumothorax)
‣ Repair of traumatic
pneumothorax
‣ Needle thoracotomy (tension
pneumothorax)
‣ Pleurodesis (for repeated
pneumothorax in patients who
are not surgical candidates)
‣ Resection of blebs or pleura.
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MEDICAL SURGICAL NURSING: RESPIRATORY 1.6.10
NURSE ANGIE 2018
Hemothorax
Blood accumulation in the pleural cavity that may result in respiratory distress
Pathophysiology
Assessment
Damaged intercostal, pleural, mediastinal, and sometimes lung parenchymal vessels cause blood to
enter the pleural cavity. The blood acts as a space-occupying lesion, leading to respiratory
difficulty. The amount of bleeding and its cause are associated with varying degrees of lung
collapse and mediastinal shift.
.
‣ Recent trauma, recent
thoracic surgery, metastatic
disease, chest pain,
dyspnea, tachypnea,
shallow respirations, cool,
clammy, dusky colored
skin, diaphoresis,
hemoptysis, restlessness,
anxiety, cyanosis, stupor,
expansion and stiffening of
the affected side, rising of
the unaffected side with
gasping respirations,
dullness over the affected
side, decreased or absent
breath sounds over the
affected side, symptoms
associated with blunt
trauma, such as bruising,
tachycardia, hypotension.
Medical Treatment
Laboratory Findings:
INTERVENTIONS
‣ Arterial blood gas (ABG) analysis may show increased partial pressure of
carbon dioxide and decreased partial pressure of oxygen.
‣ Serum hemoglobin level test may be decreased, depending on blood loss.
‣ Thoracentesis may yield blood or serosanguineous fluid.
‣ Chest radiography, computed tomography scanning (thorax), or chest
ultrasonography shows presence and extent of hemothorax and helps to
evaluate treatment.
CAUSES
‣ Blunt or
penetrating
chest trauma
‣ Anticoagulant
therapy
‣ Central venous
catheter
insertion
‣ Damaged
intercostal,
pleural, or
mediastinal
vessels
‣ Damaged
parenchymal
vessels
‣ Dissecting
thoracic
aneurysm or
internal
‣
‣
‣
‣
‣
‣
‣
‣
‣
mammary
artery
aneurysm
Heart or
thoracic
surgery
Hereditary
hemorrhagic
telangiectasia
Necrotizing
infections
Neoplasm
Pulmonary
arteriovenous
fistulas
Pulmonary
infarction
Thoracic
endometriosis
Tuberculosis
Spontaneous
pneumothorax
‣
Monitor Vital signs, Pain level and
effectiveness of interventions,
Intake and output, Chest tube
drainage, Cardiopulmonary status,
Closed drainage system function,
Hemodynamic parameters, ABG
results, Chest radiography results,
CBC results, Signs and symptoms
of infection, Skin integrity.
EDUCATION
‣
Medication regimen
Make follow up appointments
Prevention
Notify HCP if they experience s/
sx of infection
‣ Alcohol cessation if the incident
was alcohol related
‣ Counseling
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
Institute comfort measures and help
the patient relax.
Institute energy-conservation
measures.
Give prescribed oxygen based on
oxygen saturation levels.
Give prescribed I.V. fluids and
blood transfusions or
autotransfusion, if indicated.
Change the chest tube dressing and
provide chest tube care, as needed.
Prepare the patient for surgery, if
needed.
Obtain specimens for laboratory
testing, such as ABG analysis and
complete blood count (CBC).
1
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‣ Stabilization of the patient's
clinical condition with
cardiopulmonary
resuscitation, if necessary
‣ Stoppage of bleeding
‣ Thoracentesis
‣ Insertion of chest tube
‣ Autotransfusion of blood
loss approaches or exceeds
1L
Medications
‣ Oxygen
‣ Analgesics
‣ I.V. fluid therapy, especially
with hypotension
‣ Hormonal suppression for
thoracic endometriosis
Surgery
‣ Thoracotomy if a chest tube
doesn't improve the
condition and massive
hemothorax or persistent
bleeding are present
‣ Video-assisted
thoracoscopic surgery to
directly remove a clot and
allow for precise placement
of chest tubes
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MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.9
NURSE ANGIE 2018
Heart Failure: Left Side
Due to impaired pumping ability, the heart cannot maintain adequate cardiac output.
Cardiac Symptoms
Pathophysiology
Complications
•
•
•
•
•
The pumping ability of the left ventricle fails and cardiac output
decreases. Blood backs up into the left atrium and lungs, causing
pulmonary congestion. If untreated, left-sided heart failure will
lead to right-sided heart failure.
Respiratory failure
Pulmonary edema
Digoxin toxicity
Cardiogenic shock
Hypokalemia
‣ Decreased cardiac
output
‣ S3 / S4 gallop, Jugular
vein distention
Respiratory
Symptoms
‣ Dyspnea
‣ Tachypnea (30-40 /min)
‣ Orthopnea
‣ Pulmonary edema ‣
Cough
‣ Cheyenne Stokes
‣ Pleural Effusion
‣ Pink tinged sputum
CNS Symptoms
‣ Fear
‣ Anxiety ‣ Cerebral
Anoxia
‣ Fatigue
Labs & Diagnostics
‣ BNP elevated
Decreased Pa 02, increased C02 ( Acidosis)
‣ Chest X-ray may reveal
cardiomegaly and alveolar
edema
Medical Treatment
‣ BUN and Creatinine elevated
CAUSES
Atherosclerosis
‣ Fluid overload
‣ MI
‣ Valvular insufficiency
‣ Hypertension
‣ Cardiomyopathy
‣ Infection
‣ Autoimmune disorders
EDUCATION
INTERVENTIONS
‣ Low saturated fat, trans fat,
Low in sodium, and
‣ Low saturated fat &
cholesterol.
‣ The client should read
labels to
identify heart-healthy foods.
‣ Educate client about
disease
‣ Elevate HOB to SemiFowlers, Administer
cardiac glycosides
‣ Monitor vital signs
‣ Record I’s & O’s
‣ Perform daily weights
‣ Oxygen therapy
1
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‣ Digoxin
‣ Diuretics ‣ ACE
‣ ARB
‣ Low dose beta
blockers
‣ Vasodilators: nitrates,
Milrinone ‣ Morphine
sulfate
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MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.9
NURSE ANGIE 2018
Heart Failure: Right Side
The Hearts inability to properly pump blood to periphery to perfuse vital organs.
Pathophysiology
Heart failure is the inability of the heart to maintain adequate
cardiac output due to impaired pumping ability. Diminished
cardiac output results in inadequate tissue perfusion.
Complications
•
Acute: Occurs suddenly.
• Chronic: Develops over time, and can be accompanied by
acute episodes.
•
•
•
Labs & Diagnostics
Altered cardiac
function
Fluid overload
Myocardial Infarction
Death
‣ ABG my reveal Hypoxia‣
Elevated BNP/ Decreased Ejection fraction
‣ Elevated BUN & Creatinine
‣ CBC may show anemia
CAUSES
Atherosclerosis
‣ Fluid overload
‣ MI
‣ Valvular insufficiency
‣ Hypertension
‣ Cardiomyopathy
‣ Infection
‣ Autoimmune disorders
EDUCATION
INTERVENTIONS
‣ Low saturated fat, trans fat,
Low in sodium, and
‣ Low saturated fat &
cholesterol.
‣ The client should read
labels to
identify heart-healthy foods.
‣ Educate client about
disease
‣ Elevate HOB to SemiFowlers, Administer
cardiac glycosides
‣ Monitor vital signs
‣ Record I’s & O’s
‣ Perform daily weights
‣ Oxygen therapy
1
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Cardiac Symptoms
‣ Jugular vein distention
‣ Increased BP from fluid
volume
excess or decreased BP from
pump
failure
‣ Tachycardia, Dependent
edema
Respiratory Symptoms
‣ Chest pain
‣ Orthopnea
‣ Dyspnea
CNS Symptoms
‣ Fear and anxiety
GI/GU Symptoms
‣ Anorexia
‣ Weight gain
‣ Abdominal distention
Treatments:
‣ ACE
‣ ARB
‣ Digoxin
‣ Diuretics
‣ Low dose beta blockers
‣ Morphine sulfate
‣ Vasodilators: nitrates,
milrinone
‣ Human B natriuretic
peptide: acute
episodes
Medical Treatment
‣ Assess clients BP and HR
right
before administration.
‣ Evaluate clients BP 30
mins post
admin.
‣ Monitor for dizziness and
hypotension.
‣ Monitor labs, especially
potassium.
‣ Note interactions between
NSAIDS
and antihypertensive,
medications.
‣ Monitor labs and look for
signs of
digoxin toxicity.
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MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.6
OCTOBER 10, 2018
Angina
Transient ischemia of the heart muscle upon exertion.
Pathophysiology
Cardiac Symptoms
Ischemia of the heart results in chest pain from decreased blood and oxygen supply. Angina is
caused by an imbalance of oxygen supply and demand.
Types of Angina
‣ Stable: occurs with activity or
over exertion or stress.
Disappears with Nitro
‣ Unstable: occurs with an
Unpredictable amount of
exertion. Happens more
frequently and more severely
overtime.
‣ Variant: Prinzmetal’s Angina,
results from coronary artery
‣
‣
‣
‣
‣
‣
Tachycardia
Palpitations
Dizziness
Syncope
Sweating
Pallor
Respiratory Symptoms
‣
Chest pain
‣
Dyspnea
GI
‣ Digestive disturbances
spasm. Can happen at rest
Medical Treatment
‣ Nitrates: dilation of the
coronary arteries and
decrease preload and
afterload.
‣ Calcium channel
blockers: dilation of the
coronary arteries and
reduction of vasospasm.
‣ Beta Blockers: reduction
of BP for clients who are
hypertensive.
‣ Cholesterol lowering
meds : HMG-COA
reductase inhibitors,
reduce the development
of plaques.
Laboratory Findings:
‣
‣
‣
‣
Cardiac Enzymes are negative
EKG is normal until episode occurs, the ST Depression or T-wave inversion
Stress test will show changes in vital signs during episodes
Cardiac Catheterization provides definitive diagnoses
CAUSES
‣ Coronary artery blockage
‣ Coronary artery spasm
‣ Conditions increasing
myocardial oxygen
consumption
INTERVENTIONS
‣
‣
‣
‣
‣
‣
‣
EDUCATION
‣ Balance rest and activity
‣ Follow prescribed exercise
regimen
‣ Hot/Cold Temperature extremes
may induce angina
‣ Encourage use of emotional
support resources
‣ Avoid medications and OTC
medications that increase HR
‣ Stop smoking
‣ Diet: decreased saturated fat,
increased fiber, and (if indicated)
decreased calorie intake
Assess pain
Administer oxygen
Assess vitals
Provide cardiac monitoring
Administer Nitroglycerine
Elevate HOB
‣ Can Lead to MI
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MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.2
OCTOBER 10, 2018
Aortic Aneurysm
Pathophysiology
Cardiac Symptoms
Chronic inflammation which weakens the artery wall causing degenerative dilation, subsequent
plaque deposits, and weakness of aorta.
Risks
‣
‣
‣
‣
‣
‣
‣
Smoking
Hypertension
Advanced age
Male Gender
COPD
Genetic Disorders
Obesity
‣ Pulsation in the abdomen
& systolic bruit ( If AAA)
‣ Abrupt loss of femoral
and radial pulses
‣ Flatness heart over the
heart
Respiratory Symptoms
‣
‣
‣
Cyanosis
Dyspnea
Wheezing
CNS Symptoms
‣
‣
‣
Limb weakness
Transient paralysis
Neuro Deficits
Complications
‣
‣
‣
‣
‣
‣
‣
‣
‣
Aortic valve insufficiency
Stent fractures
Cardiac temperance
Rupture
Dissection
Hemorrhage
Heart failure
Impaired Kidney function
Stroke
‣ Atherosclerosis
‣ Bacterial infections
‣ atherosclerotic plaque
‣
Blunt chest trauma
‣
‣
‣
‣
Coarctation of the aorta
Marfan syndrome
Rheumatic vasculitis
Syphilis infection
‣
Congenital heart defects
Pallor
Perfuse sweating
If ruptured
‣
‣
‣
Hypotension
Tachycardia
Shock
‣ If rupture or dissection
occurs: Fluid replacement
‣ Airway management
‣ Cardiac Monitoring
‣ Smoking cessation
‣ Strict BP management
Decreased Hemoglobin Levels
X-Ray: Widening of the Aorta
MRI: Confirms location
EKG: Rule out MI
CAUSES
‣
‣
Treatments:
Laboratory Findings:
‣
‣
‣
‣
‣
Skin Symptoms
Medical Treatment
EDUCATION
INTERVENTIONS
‣ Low in sodium, and
‣ Low saturated fat, trans fat and
cholesterol.
‣ Strict blood pressure monitoring
‣ Signs and symptoms of rupture
or dissection: Sharp pain in the
back or neck.
‣ Medication Compliance
‣ Smoking cessation
‣ Weight loss
‣ Making all follow visits
‣ Administer antihypertensives: Beta
Blockers, ACE, ARBS.
‣ Monitor vitals and Cardiac status
‣ Monitor heart and lung sounds
‣ Assess peripheral pulses
‣ Assess for pain
1
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‣ Beta Blockers:
Metoprolol
‣ Negative Inotropes
‣ Morphine
‣ IV fluids or Blood
Transfusion
‣ Surgery
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44
MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.2
MAY 13, 19, 2:50 PM
CARDIAC TAMPONADE
a large amount of fluid inside the pericardial sac around the heart
Cardiac Symptoms
Pathophysiology
Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial
space, resulting in reduced ventricular filling and subsequent hemodynamic compromise. The
condition is a medical emergency, the complications of which
include pulmonary edema, shock, and death.
Increased jugular venous
pressure, hypotension, and
distant heart sounds, narrow
pulse pressure r/t decrease in
stroke volume
Rapid weak pulses
Cardiac arrest
Complications
Jugular vein distention
‣ Pulmonary edema
‣ Cardiogenic shock
‣ Pericardial constriction
Pulsus Paradoxus
Respiratory Symptoms
Chest pain
‣ Death
Dyspnea
CNS Symptoms
Confusion
Coolclammyextremities
Paleness
Swelling
Laboratory Findings:
Treatments:
Hemodynamic support
‣ Creatinine kinase and isoform tests are elevated
with myocardial infarction and cardiac trauma.
‣
‣
‣
‣
‣
Fluid therapy
Pulmonary artery catheterization
Chest CT or MRI of chest
Chest x-ray
Coronary angiography
ECG (non-diagnostic, used to rule-out other conditions)
Right heart catheterization
Venous thromboembolism
(VTE) prophylaxis
Cardiopulmonary resuscitation
Medical Treatment
Pericardial window
Pericardiocentesis
CAUSES
‣ Cardiac catheterization
‣ Acute myocardial infarction
‣ Cardiac surgery, Drug reaction
‣ Effusion in cancer, bacterial
infections, tuberculosis and,
rarely, acute rheumatic fever
‣ Hemorrhage from non-traumatic
cause. May be idiopathic
‣ Trauma, including blunt chest
trauma
Percutaneous balloon
EDUCATION
INTERVENTIONS
‣ Educate on treatment
‣ Hemodynamic monitoring
‣ Administer fluids IV
‣ Chest x-ray / echocardiogram
‣ Prepare the client for
pericardiocentesis
‣ Monitor for tamponade
‣ Educate on medication
regimen
pericardiotomy
Complete pericardectomy
Pericardio-peritoneal shunt for
malignant recurrent pericardial
effusions
Sclerosing of the pericardium for
‣ Educate on follow-up
care
recurrent effusion or tamponade
Video-assisted thoracoscopic
procedure to drain pericardial
‣ Renal failure
1
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MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.10
NURSE ANGIE 2018
Endocarditis
Infection of the endocardium, heart valves, or cardiac prosthesis caused by bacteria, viruses,
fungi, rickettsia, and parasites
Pathophysiology
Assessment:
Fibrin and platelets cluster on valve tissue and engulf circulating bacteria or fungi. This produces
vegetation, which in turn may cover the valve surfaces, causing deformities and destruction of
valvular tissue and may extend to the chordae tendineae, causing them to rupture, leading to
valvular insufficiency. Vegetative growth on the heart valves, endocardial lining of a heart
chamber, or the endothelium of a blood vessel may embolize to
the spleen, kidneys, central nervous system, and lungs.
INTERVENTIONS
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
Complete blood count
WBC count, and
differential
Electrolytes
‣
Creatinine
‣
Blood urea nitrogen
(BUN), glucose
‣
Coagulation panel
Monitor for signs of emboli,
splenic emboli will be evidenced by
abdominal pain radiating to the left
shoulder and rebound abdominal
tenderness.
Monitor mental status.
Assess for petechiae on skin oral
mucosa and conjunctiva.
Assess for Osler's nodes and Janeway
lesions.
Assess for clubbing.
Evaluate blood culture.
Administer antibiotics as ordered.
Prepare to dc client with IV line.
‣ Educate the client to maintain
aseptic technique.
‣ Instruct the client on how to
administer IV antibiotics
‣ Have the client record. temp daily
for six weeks.
‣ Encourage oral hygiene for six
weeks with a soft bristle toothbrush
2x daily.
‣ Have the client clean any skin
lacerations and apply antibiotic
ointment.
‣ Client should inform all HCP’s of
hx of endocarditis
‣ Client should use prophylactic
antibiotics for oral procedures.
‣ Tech the client the signs and
symptoms of emboli and HF.
CAUSES
‣ IV drug abuse
‣
Monitor cardiovascular status.
Monitor of signs of HF.
EDUCATION
Laboratory Findings:
‣
Provide adequate rest and balanced
activity, this prevents thrombus
formation.
Anti Embolism stocking.
‣ Rheumatic fever
‣ Infection
‣ Valve replacement
‣ Oral surgery ( 3-6 mos)
‣ Surgery
‣ IV line placement
1
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‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
Murmurs
Heart Failure
Fatigue
Anorexia
Splinter hemorrhage
in nail beds
Clubbing from
hypoxia
Osler's nodes
Janeway lesions
Blood clots
Petechiae
Fever
Splenomegaly
Treatments:
‣
‣
‣
‣
‣
INSAIDS
Corticosteroids
Analgesia
Diuretics
Digoxin
Medical Treatment
‣ Penicillin G at 12-18
million U/d IV by
continuous pump or in
six equally divided
doses for four weeks.
‣ Ceftriaxone at 2 g/d IV
for four weeks.
‣ Penicillin G and
gentamicin at 1 mg/kg
(based on ideal body
weight) every 8 hours
for 2 weeks
‣ Patients who are
allergic to penicillin,
use vancomycin at 30
mg/kg/d IV in two
equally divided doses
for four weeks.
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MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.9
NURSE ANGIE 2018
Cardiogenic Shock
Inadequate blood flow due to the dysfunction of the ventricles of the heart.
Risks
Pathophysiology
*
*
A drop in blood pressure resulting from dysfunction of the
ventricles of the heart. The blood pools in the left ventricle, which
then causes a backup of blood into the lungs causing pulmonary
edema. This causes an increased demand for oxygen.
*
*
Age over 65
History of heart
failure or previous MI
Coronary artery
disease
Hispanic or black
ethnicity
Cardiac Symptoms
•
•
•
•
•
Diminished peripheral
pulses, rapid irregular
pulses
Tachycardia
Hypotension
Cool, clammy, pale, skin
JVD
Respiratory Symptoms
Complications
*
Cardiovascular
•
•
•
•
Rapid, shallow breathing
Tachypnea
Cyanosis
Pulmonary crackles
accident
*
Acute respiratory
distress syndrome
*
Acute kidney injury
*
Cardiac arrest
*
Arrhythmias
*
Multiple organ
dysfunction syndrome
*
Labs & Diagnostics
•
•
Death
•
Troponin level test is elevated.
Arterial blood gas analysis respiratory and metabolic acidosis
and hypoxemia.
BUN & Creatinine
level (serum) test
results may be
elevated, indicating
reduced renal
perfusion.
Neuro Symptoms
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GI/GU Symptoms
Urine output less than 20 mL/hr
Medical Treatment
*
*
CAUSES
INTERVENTIONS
EDUCATION
*
*
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•
•
•
•
•
Acute mitral or aortic
insufficiency
Cardiac tamponade
cardiomyopathy
MI (most common)
Ventricular aneurysm
Ventricular septal
defect, ventricular
tachyarrhythmia
•
•
•
•
•
•
Oxygen
Monitor urine output
Iv fluid resuscitation
Electrolyte replacement
Elevate HOB to promote
lung expansion
Daily weights administer
diuretics
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Medications
Disorder
Possibility of death
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Fatigue
Anxiety
Decreased level of
consciousness
Norepinephrine or
dopamine: Gives
Vasopressor support
Milrinone: induces
peripheral vasodilation
Nitroglycerin: Decreased
preload and afterload
Aspirin: For patients with
MI
Amiodarone: for
sustained
tachyarrhythmias
Morphine: Decrease
oxygen demands
Diuretics: Decrease fluid
overload
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MEDICAL SURGICAL NURSING: CRITICAL CARE NURSING 3.1.1
NURSE ANGIE 2018
Septic Shock
Dysregulated response to infection resulting in acute organ dysfunction or tissue hypoperfusion
Pathophysiology
Risks
‣ Chronic diseases (acquired
immunodeficiency
syndrome, chronic
obstructive pulmonary
disease, diabetes, cancer)
‣ Communityacquired pneumonia
Intensive care unit admission
Immunosuppressive therapy
Previous hospitalization,
especially with Clostridium
difficile infection
Infection triggers pro-inflammatory and anti-inflammatory
mechanisms. An imbalance leads to tissue damage and increased
susceptibility to secondary infections. Organ dysfunction occurs,
partly due to impaired tissue oxygenation.Vascular endothelium is
damaged, leading to cell death.Altered coagulation leads to
impaired tissue oxygenation, micro thrombi, and endothelial
dysfunction and may lead to disseminated intravascular
coagulation.Systemic vasodilation and hypotension lead to tissue
hypoperfusion.Organ dysfunction and tissue hypoperfusion lead to
multi-organ failure.
Complications
‣
‣
Labs & Diagnostics
‣
‣
‣
White blood cell count > 12,000 or < 4,000 or > 10% immature
bands indicates infection and helps confirm the diagnosis.
‣
Arterial blood gas analysis may identify acidosis, hypoxemia, or
hypercapnia.
‣
Elevated lactate levels indicate organ dysfunction.
‣
Urinalysis may identify urinary tract infection.
‣
‣
‣
‣
Hospital-acquired infections,
especially catheter-related
blood stream infections,
pneumonia, or abdominal
infections
Respiratory failure
Disseminated intravascular
coagulation
Acute renal failure
Impaired hepatic function
Multi-organ failure
Death
‣ Blood culture results are positive for
bacterial organisms.
Assessment
‣ Temperature > 100.4° F
(38° C) or < 96.8° F
(36° C)
‣ Tachycardia
‣ Tachypnea
‣ Symptoms specific to
the infectious source
‣ Altered mental status
‣ Decreased capillary
refill time or mottling
‣ Pain and purulent
drainage in a surgical
wound
‣ Acute oliguria (urine
output < 0.5 mL/kg/
hour for 2 hours
despite adequate fluid
resuscitation)
Medications
‣ crystalloid IV fluids or
lactated Ringer
solution as a 30 mL/kg
bolus within 3 hours of
symptom identification
‣ Albumin
‣ IV antibiotics
‣ Vasopressors
‣ Dobutamine
‣ Tylenol
‣ Blood transfusion
‣ Corticosteroids
Monitoring
CAUSES
‣ Community-acquired and
health care-associated
infections
‣ Gram-positive and gramnegative bacteria; fungal
infections
‣ Pneumonia (most
common cause)
‣ Urinary tract and
abdominal infections
INTERVENTIONS
EDUCATION
‣ Oxygen
‣ Medication regimen
‣ Intubation
‣ Communication
‣ Ventilation
‣ Energy conservation
‣ Hemodialysis
‣ Disease process
‣ Fluids
‣ symptoms of infection
‣Vital signs
‣ Peripheral perfusion
‣
‣ When to call the HCP
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Lactate level
Goals of resuscitation:
MAP > 65 mm Hg
Lactate ≤ 2 mmol/L
Urine output > 0.5 mL/
kg/hour
Central venous
pressure = 8 to 12 mm
Hg
CV oxygen saturation
≥ 70%
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MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.5
NURSE ANGIE 2018
Coronary Artery Disease
Atheroscleros is caused by the narrowing or obstruction of one or more coronary
Pathophysiology
Cardiac Symptoms
Narrowing of the coronary arteries limits blood supply to the heart muscle causing angina
(chest pain due to the heart muscle ischemia).Atherosclerotic buildup will cause decreased
perfusion to the myocardial tissue leading to inadequate myocardial oxygenation thus
causing hypertension, angina, dysrhythmias, MI, HF or death.
‣ Chest pain
‣ palpitations
‣ Decreased peripheral
pulses
‣ Pedal edema
‣ Hypertension
Laboratory
Findings:
‣ Elevated triglycerides. Elevated
HDL and Decreased LDL
‣ C-Reactive protein may be elevated
‣ BNP may be elevated
Respiratory
Symptoms
‣
Dyspnea
‣
Cough
‣
Tachypnea
‣
Pulmonary congestion
Risks
‣
‣
‣
‣
‣
‣
‣
!
Complications
‣
‣
‣
‣
Cardiac arrhythmias
Myocardial infarction (MI)
Heart failure
Angina
Medical
Treatment
‣ Cardiomyopathy
‣ Sudden cardiac death
EDUCATION
INTERVENTIONS
CAUSES
‣ Atherosclerosis
‣ Dissecting aneurysm
‣ Coronary artery spasm
‣
‣
‣
‣
‣
‣
HDL < 40
LDL >130
Smoking
Hypertension
Diabetes
Contraception
Sedentary lifestyle
‣ Low in sodium, and
‣ Low saturated fat, trans fat and
cholesterol.
‣ The client should read labels to
identify heart-healthy foods
‣ Educate client to reduce stress
‣ Educate on the importance of
weight reduction
‣ Educate on the importance of
compliance with treatments
Monitor vital signs
Respiratory status
Edema of lower extremities
Monitor fluid status
Intake and output
Daily weights
‣ Congenital defects
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‣ Nitrates: dilation of the
coronary arteries and
decrease preload and
afterload.
‣ Calcium channel
blockers: dilation of
the coronary arteries
and reduction of
vasospasm.
‣ Beta Blockers:
reduction of BP for
clients who are
hypertensive.
‣ Cholesterol lowering
meds : HMG-COA
reductase inhibitors,
reduce the
development of
plaques.
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MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.2
OCTOBER 10, 2018
Hypertension
Blood pressure reading above the normal range of 120/80.
Pathophysiology
Cardiac Symptoms
A common condition in which the force of the blood against your artery walls is high enough that it
may eventually cause health problems, such as heart failure and organ damage.
‣ Tachycardia
‣ Flushing
‣ Epistaxis
Respiratory Symptoms
‣
Chest pain
‣
Dyspnea
CNS Symptoms
‣ Visual changes
‣ Dizziness
‣ Tinnitus
‣ Headache
Treatments:
‣ Initially lifestyle changes
‣ Beta blockers
Alpha Blockers
‣ Alpha 2 agonist
‣ Diuretics
‣ Vasodilators
‣ Calcium channel blockers
‣ ACE inhibitors
ARBS
!
‣ Renal angiography : Test for renal
disease.
‣ BUN and Creatinine
Laboratory Findings:
‣
‣
‣
‣
‣
‣
Urinalysis :Will detect protein, RBC, pus, and casts.
Blood count/ESR
Serum potassium, chloride and C02.
Urinary catecholamine metabolites: To dx pheochromocytoma.
Urine ketones
IV pyelogram, urine cultures, radioisotope.
CAUSES/COMPLICATIONS
‣ Primary: Caused by genetic,
race, or unknown cause.
‣ Secondary: Result of an
underlying condition such as
Diabetes.
‣ Risk factors: Stress, smoking,
diabetes, African American race,
high cholesterol, genetics
Medical Treatment
‣ Take clients BP and HR right
before medication
administration
‣ Assess clients BP ~30 mins
post admin.
‣ Monitor for dizziness and
hypotension.
‣ Monitor labs, especially
INTERVENTIONS
EDUCATION
‣ Document BP in the standing and
lying positions.
‣ Encourage weight loss if the client
is obese.
‣ Provide moderate salt restricted
‣ Low in sodium, and
‣ Low saturated fat, trans fat and
cholesterol.
‣ The client should read labels to
identify heart-healthy foods.
diet.
‣ Plan exercise regularly
‣ Encourage stress reduction
measures.
‣ Monitor s/sx of hypertensive crisis.
‣
potassium levels.
‣ Note interactions between
NSAIDS and antihypertensive
medication.
Educate on new medication
regimen
‣ Hypertensive Crisis
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MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.1
NURSE ANGIE 2018
Pericarditis
Normal amount of fluid in the pericardium is 30 mL
Pathophysiology
Causes
Infections
MI
Radiation
Immune disorders
Thyroid disorders
Acute or chronic inflammation of the pericardium. Thickening of
the pericardium causes constriction and compression of the heart.
Can result in loss of pericardial elasticity, cardiac tamponade, and
heart Failure.
Cardiac Symptoms
‣ Precordial chest pain that
radiates to the left side,
neck and shoulder.
‣ Pericardial friction rub
Respiratory Symptoms
‣ Grating pain with
Risks
‣
‣
‣
‣
‣
‣
‣
Chest trauma
Phenotoyin
Rheumatic fever
Autoimmune disease
Myxedema
MI
TB
breathing,
coughing, or
swallowing
‣ Exacerbation of pain in
the supine
position
‣ Tachypnea, dyspnea
Complications
‣
‣
‣
‣
‣
‣
Laboratory Findings:
Pericardial effusion
Cardiac tamponade
Recurrent
Constrictive pericarditis
Dressler syndrome
Hemodynamic instability
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
Arteriosclerosis
Raynauds
Buerger’s
Smoking
Diabetes
Hyperlipidemia
Hypertension
Obesity
Sedentary lifestyle
Age
‣
‣
‣
‣
Fever
Chills
Malaise
Fluid retention
‣ Possible elevated troponin
‣ Positive TB test is possible
‣ Elevated WBC count
‣ Elevated Erythrocyte sedimentation rate
CAUSES
Other Symptoms
Medical Treatment
INTERVENTIONS
EDUCATION
‣ Check extremities for paleness,
coolness or necrosis
‣ Do not cross legs
‣ Regular exercise
‣ No smoking
‣ Weight loss
‣ Educate on the importance of
care
‣ Educate on the medication
regimen
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‣ Pericardiocentesis to
identify the causative
agent.
‣ Manage the underlying
cause.
‣ NSAIDS: Ibuprofen
‣ Colchicine
‣ Indomethacin if allergic to
NSAIDS
‣ Corticosteroids:
prednisone
‣ Antibiotics or Anti-fungal
therapy
‣ Proton Pump Inhibitors
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MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.8
NURSE ANGIE 2018
Peripheral Vascular Disease: Venous
Pathophysiology
A narrowing of vessels that carry blood to the legs, arms, stomach or
kidneys. Refers to diseases of blood vessels outside the heart and brain.
Risks
‣
‣
‣
‣
‣
Diabetes
Obesity
High cholesterol
High blood pressure
Sedentary lifestyle
Complications
‣ PE: embolism in the lungs,
tachycardia, SOB, feeling of
impending doom.
‣ Embolism : stagnant
collection of blood in the
venous system.
‣ DVT: pain redness and
decreased pulse in lower
limb. Look for Homan’s sign.
‣ Cardiac enzyme levels: findings
are normal in angina
Labs & Diagnostics
‣ ECG: ST-depression or T-wave inversion during pain
‣ Cardiac catheterization: provides
a definite dx by monitoring
patency of coronary arteries.
‣ Stress Test: Changes in EKG or vitals could indicate ischemia
CAUSES
‣ Advanced age causes a
decreased competence of the
valves
‣ Advanced age causes a greater
incidence of varicose veins
and slower wound healing
‣ Thrombophlebitis
‣ Venous Stasis
‣ Hyper coagulability
‣ Injury to the venous wall
INTERVENTIONS
EDUCATION
‣ Avoid standing or sitting
‣ Educate on medication
regimen
‣ Avoid hot compresses, only
apply intermittent warm moist
packs
‣ Educate the client to
follow prescribed
anticoagulant therapy
‣ Elevate legs above heart
‣
Cardiac
Symptoms
‣ Normal or
decreased pulses
Respiratory
Symptoms
‣ Dyspnea
Neuro
Symptoms
‣ Numbness of the
legs or feet
‣ Weakness of calf
muscle
‣ Feeling coldness
in the feet or legs
Medications
‣ Anti-platelet
medications
Integumentary
‣ Cool brown skin,
edema, ulcers, pain
redness and
induration along
the vein, limb may
be warmer.
Musculoskeletal
‣ Deep muscle
tenderness
‣ Avoid
Monitor peripheral pulses
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Cardiovascular Disorders Overview
lOMoARcPSD|11334620
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More than 75 conditions and
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pregnancy, alcohol intake, viral
infection, chemo medications
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D – Drug abuser
R – Replacing cardiac valves
U – Untreated bacteremia;
G – Gram negative and positive
bacteria
S – STDs
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ONCOLOGY
Blood. Body. Adult. Pediatric
CONTENTS
Types of cancer
PATHOPHYSIOLOGY
Nurse Angie | 2020
Oncological
Emergencies
Pain Management
Grading, Staging, &
Diagnostics
Chemotherapy
Radiation therapy
Oncology is the study of complex disease processes that span across many
body systems as the result of mutations, malfunction, proliferation, or
destruction of genes and cells. There are over one hundred types of
cancer, and each has its pathophysiology, nursing Implications, and
treatments.
The main groups of tumors we study often include carcinoma, sarcoma,
leukemia, or lymphoma. Carcinomas develop from epithelial cells that
proliferate into the body tissues. Sarcomas are cancers that form that in
the bones, soft tissue, and connective tissues. Lymphomas and leukemias
are cancers that affect the blood and are common among children. One of
the main priorities when caring for the patient with cancer is emotional
support and pain management
Treatments of cancer vary depending on the type, aggressiveness, stage, and
receptiveness of the patient and family. Conventional treatments include
54
chemotherapy, radiation therapy, and bone marrow transplants.
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Oncology: Carcinomas
55
Patho
Carcinomas are cancers that affect the epithelial
tissues of various organs such as the skin, Intestines,
and blood vessels. After the initial invasion of the
healthy organ, carcinomas may spread to other
nearby structures; this is known as metastases.
Labs & Diagnostics
Computerized tomography (CT) scan
Bone scan
Magnetic resonance imaging (MRI)
Positron emission tomography (PET) scan
Ultrasound and X-ray
Biopsy by collecting a sample of cells for testing
Treatments
Chemotherapy targeted for the specific type of
carcinoma
Lymphnode dissection
Immunotherapy
Surgery
Radiation therapy
Types
Basal cell carcinoma
Squamous cell carcinoma
Renal cell carcinoma
Ductal carcinoma in situ (DCIS)
Invasive ductal carcinoma.Adenocarcinoma
Risks
Aging
Tobacco use
Sun exposure
Exposure to radiation
Exposure to chemicals
Viruses and bacteria
Hormones such as
estrogen
Family history
of cancer
Alcohol abuse
Poor diet
Being overweight
Interventions
Maintain nutrition
Prevent infection
Administer
chemotherapy
Control pain
Provide emotional
support
Monitor for infection &
signs of
decompensation
Education
The importance of
infection control
Side effects of
chemotherapy &
radiation treatment
The importance of a
healthy diet and
lifestyle
Community resources
for mental health and
support groups
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Oncology: Sarcoma
Patho
Treatments
Sarcoma's are rare cancers that manifest In the
bones, fat, nerves, arms, legs, and other types of
connective tissues. Sarcoma's are often treated
and cured by surgery, however, a small portion
of them can have lasting effects and are more
difficult to eradicate.
Surgery
Radiation therapy
Brachytherapy
Chemotherapy
Targeted therapy
Immunotherapy
Labs & Diagnostics
Types
Tissue Biopsy
Computerized tomography (CT) scan
Bone scanMagnetic resonance imaging (MRI)
Positron emission tomography (PET) scan
Ultrasound and X-ray
Risks
56
Previous radiation
therapy
Lymphedema
Being
Immunocompromised
Chemicals such as
agent orange or dioxin
Genetic
predisposition
Angiosarcoma: Effects the blood vessels
Osteosarcoma: Effects the bones
Chondrosarcoma: Effects the cartilage
Desmoid-type fibromatosis: Effects fibroblasts
Ewing's sarcoma: Effects the bones of children and
teens
Rhabdomyosarcoma: Effects skeletal muscle
Fibroblastic sarcoma: Effects fiborous tissues
Kaposi's sarcoma: Occurs as the result of AIDS
infection and effects the skin and mouth
Interventions
Maintain nutrition
Prevent infection
Administer
chemotherapy
Control pain
Provide emotional
support
Monitor for infection &
signs of
decompensation
Education
The importance of
infection control
Side effects of
chemotherapy &
radiation treatment
The importance of a
healthy diet and
lifestyle
Community resources
for mental health and
support groups
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Oncology: Leukemia
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Patho
Leukemia's are cancers that form in the bone marrow and
cause alterations in over production of faulty white blood
cells. They can be myleoid or lymphoid cells.
Treatments
Chemotherapy
Blood transfusions
Stem cell transplant
Radiation therapy
Labs
CBC: Decreased erythrocytes & platelets
Leukocyte count: Normal, high or low. You may see a lot
of baby WBC’S “ blast cells” and low adult WBC’s.
Electrolytes : Potassium & Phosphate are elevated
Uric acid: Elevated
Risks
Types
Acute lymphoblastic leukemia
Acute myeloid leukemia
Chronic lymphocytic leukemia
Interventions
High doses of radiation
Smoking
Benzene
Chemotherapy
Down syndrome
Human T-cell Virus
Decrease the risk of
infection
Place patient on
neutropenic precautions
Monitor the oral mucosa
for mucositis
Improve nutritional
intake
Mouth care, small
frequent meals, daily
weights, low microbial
diet such as, no fresh
fruit
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Education
Maintain nutrition
Prevent infection by
not eating fresh fruit ,
planting soil, and
avoiding unhealthy
environments
Side effects of
treatments
Signs of infection
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Emergencies:Spinal Cord Compression
58
Patho
A oncological emergency that manifests by
impeded blood flow to the spinal cord. This
occurs in 5-30% of cancer patients and is
caused by growth of a tumor or metastases.
Can cause paralysis If left untreated for a
prolonged period of time.
Labs
X-ray
MRI
Myelography with CT
Causes
Neoplasms
Spinal
tuberculosis
Trauma
Lesions
Presentation
Loss of sensation
Incontinence
Sexual Impotence
Paralysis
Muscle Atrophy
Back pain
Treatments
Dexamethasone
Surgery
Radiography
Chemotherapy
Analgesics
Disease Progression
Compression of blood supply to cord
Ischemia
Edema
Tissue death
Loss of function: Motor & Sensory
Interventions
Deep breathing
Incentive spirometry
Log rolling
Pain Control
Mobility
Safety & skin
complications
Provide encouragement
& support to patient &
family
Goals
Palliation of symptoms
Pain control
Prevention of permanent
disability
Avoid complications
Maximize function
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Emergencies: D.I.C
Patho
59
Assessment
The coagulation cascade is activated when blood is
exposed to tissue factor. In association with the
coagulation system, the fibrinolytic pathway is also
activated. DIC usually begins rapidly and causes
bleeding and microvascular occlusion, leading to
organ failure. DIC is not a disease process in itself.
DIC occurs as a complication of another disorder or
condition. Because of excess thrombin and fibrin,
blood coagulates within the entire vascular
compartment of the body, thus causing decreased
amounts of platelets, ultimately depleting them. The
depletion of platelets causes and increased risk of
hemorrhage. Microthrombi are formed throughout
the body as a result of the coagulation sequence
being activated. The microthrombi are made up of
coagulation proteins and platelets.
Labs
PT: Prolonged normal is 11-14 seconds
PTT: Normal or prolonged normal is 25 to 35
seconds
Platelet count: Decreased
Fibrin degradation products: Elevated
D-dimer: Possible elevation
Risks
B: Bleeding from puncture sites & wounds
L: Loses unexpectedly large amounts of blood
O: Oh so many mini clots
O: oozing blood from your gums or nose
D: Decreased platelets and RBCS
Y: You may see blood in the stool or urine
M: Mucosal bleeding
E: Epistaxis
S: Symptoms of anemia
S: Shock, sepsis, cancer, OB issues may be present
Interventions
OB complications
Neoplastic disease
Infection
Injury to RBC/platelets
Post trauma
Shock
Cancer
Sepsis
Treatments
Cefepime
Continuous infusion NS 100 cc administer
furosemide 40 mg IV after first unit .
Vasopressors/ Heparin Blood transfusion:
Packed RBC to replace loss from bleeding. Fresh
frozen plasma replaces deficits in coagulation
factor.
Platelets replace needed cells
Cryoprecipitate replaces fibrinogen
Anticoagulant therapy to decrease coagulation:
Heparin to interrupt the coagulation cascade and
to decrease the risk of venous thromboembolism
Complications
Monitor for bleeding
Avoid cleaning clots
from exposed areas
Educate the patient not
to shave or to use an
electric razor
Use a soft bristle
toothbrush
Do not floss.
Renal failure
Cardiac tamponade
Hemothorax
Intracerebral
hematoma
Stroke
Ischemic bowel
Multiple organ
dysfunction
syndrome
Death
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Emergencies: Tumor Lysis Syndrome
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Patho
Treatments
An oncological emergency where cancer cells
become destroyed and causing excess potassium
and uric acid to to be released into the serum
leaving the renal and cardiovascular systems
vulnerable to system failure.
Labs
Complete metabolic panel
LDH
Serum uric acid
Urinalysis
EKG
Complications
IV fluids
Allopurinol 300 mg BID
Daily labs
Rasburicase
Inpatient monitoring
Cardiac monitoring
Treatment of hyperkalemia
Dialysis may be required to remove potassium
and phosphate burden
calcium gluconate (decreases phos level
byincreasing calcium level)
Renvela (phosphate binder to decrease
phosphate level)
Kayexalate (binds to K+ and excretes through
stool)
Insulin and glucose to push potassium back Into
the cells
Acute renal failure
Cardiac arryhthmias
Seizures
Death (multi-organ failure)
Flank pain (nephrolithiasis)
Muscle weakness/tetany
Nausea & Vomiting
Lethargy
Risks
Interventions
High tumor burden
Elevated baseline SCr
(including
dehydration)
Elevated baseline uric
acid
Increase LDH
Anticipate at risk
patients
Vigorous hydration
Urinary alkalization
with sodium bicarballopurinol
Nursing
Monitor labs
Treatment of
electrolyte imbalance
Monitor I & O, weights,
vital signs
Complete nursing
assessment
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Oncology: Pain Management
61
Treatments
Patho
Pain is a subjective feeling that can be
nociceptive, somatic, or visceral as a result of
mixed mediums such as inflammation and cancer
mediated responses. Pain is different in every
patient and is what the patient says it is.
Clinicians should take special consideration when
caring for patients with pain associated with
cancer because it is chronic and cause
Comorbidities such as anxiety and depression.
Cancer Pain & Mental
Health
A patient's response to pain can be just as unique
and Individualized as the treatment provided for
it. Some patients will deny pain, but vital signs
and expressions verify that pain present. Some
patients will endorse pain but rate it lower than
what they feel while other patients will be stoic or
seem inappropriate with their pain response. No
matter how the patient is expressing their pain, It
Is vital to understand that whether acute or
chronic, pain can have devastating effects on
one's mental, spiritual, and emotional wellbeing,
which is why it is critical to provide holistic care
to address all of the patient's needs.
Treatments for cancer pain will vary depending
on the type, stage, and areas the cancer is
affecting. Treating cancer pain can involve oral,
IM, transdermal, and IV pain medication
administration. It is critical that the clinician
administering the medication know the potential
side effects and complications of analgesic
administration. For example, the nurse should
follow institution guidelines concerning
administering more than one opioid at a time.
Pharmacological Treatment
Common pain medications given to cancer
patients includes NSAID's or Tylenol mildmoderate pain. For severe pain opioids are given
such a codeine or morphine sulfate. Neuropathic
pain can be treated with anticonvulsants such as
Tegratol and antidepressants Cymbalta.
Gabapentin may also be prescribed for this
purpose also.
Alternative Therapies
While pharmacological treatments are the gold
standard for treating pain associated with cancer
it is vital the nurse understands that alternative
therapies such as healing touch, reiki, meditation,
and herbal suppliments have proven to have a
profound impact on the cancer patients
preception of pain and should be Included In the
plan of care if the patient requests and the
provider agrees that no harm will be caused.
Causes
Interventions
Bone pain
Organ obstruction
Necrosis
Fear & Anxiety
Inflammation
Infiltration of tissue
Nerve compression
Tissue distention
Monitor vital signs
Perform pre & post
pain assessments
Monitor respirations
Provide relaxation
Provide guided
imagery
Provide hot/cold
therapy
Provide emotional
support
Education
Educate on medications
Educate on the use
opioids
Educate on meditation,
relaxation, and other
ways to reduce pain
Provide materials on
support groups
Educate when to call
the provider
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62
Oncology: Diagnostics, Grading, & Staging
Diagnostics
Staging
Because there are so many forms of cancer there is
no one size fits all approach. However, there are
protocols and standards of care testing that are
placed once informed consent is obtained.
Common diagnostic tests and procedures include
Biopsy of tissue
Bone marrow
Chest CT
CBC & Liver function tests
MRI
Tumor markers
Radioisotope scanning
Stage 0: tumor In situ
Stage I: localized tumor cell growth limited to
one tissue area of origin
Stage II: spread locally but limited
Stage III: spread throughout the local and
regional areas
Stage IV: Metastasis in organs and tissues
distant from the origional area of growth
Surgery
Grading
Grade I : cells are well differentiated but look
mildly abnormal
Grade II : cells are more abnormal and slightly
differentiated
GradeIII: cells appear extremely abnormal and
are poorly differentiated
Grade IV: cells are not differentiated and
immature
Surgery is performed to stage, treat, and diagnose
cancer. Surgery can be prophylactic, curative,
palliative, or completed to control the growth of
the tumor.
Early Detection Warning signs Common Areas
Skin checks
Testicular exam
Breast exam
Mammogram
Rectal exams
Colonoscopy
Pap smear
Wounds that do not
heal
Sore throat that does
not go away
Changes in bowel and
bladder habits
Heartburn
Hoarseness & cough
Unusual bleeding
Lumps In breasts or
testicles
Wart & mole changes
Bladder cancer
Brain tumor
Breast cancer
Colorectal cancer
Lung cancer
Prostate cancer
Testicular cancer
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Oncology: Chemotherapy
63
Types
Definition
Chemotherapies are cytotoxic drugs that
target tumor cells systemically and are
treatment modalities prescribed by
oncologists to cure, palliate, maintain
remission, or as a prophylatic measure.
Mode of Action
Chemotherapy kills normals cells while
inhibiting the replication of abnormal cells
causing system effects such as alterations in
other areas of the body. Chemotherapy is
often prescribed as series and In combination
with other biotherapies to potentiate the
therapeutic response efficacy.
Routes of Administration
Topical
Oral
IV push (slow admin)
Infusion (most common)
IM/SQ
Intrathecal (spinal theca, lumbar puncture)
Intraventricular (brain)
What Alters Effects
Tumor cell burden
Tumor growth rate
Vascular supply
Pattern of cell division
Concentration of
chemotherapy
available for malignant
cells
Adjuvant
Neoadjuvant
High dose/ intensiveCombination therapy
Regimen changes
Alkylating Agents: Non-cell specific and used for
treatment in the resting cell phase. Examples Include
mustard gas derivatives, Ethylenimines,
Alkylsulfonates, Hydrazines, Nitrosureas, and Metal
salts
Plant Alkaloids: Derived from plants they treat various
stages of cell growth and are cell- specific. Examples
include Podophyllotoxins, Vinca alkaloids,
Camptothecan analogs, and Taxanes
Anti-tumor Antibiotics: Made from fungus are
considered cell-specific. Some examples include
Anthracyclines and Chromomycins
Antimetabolites: Component are similar to the cell.
Once infiltrated Into the cell they Inhibit the cancer
cell from dividing and are cell cycle specific. Some
examples include Folic acid antagonists, Pyrimidine
antagonists, Purine antagonists, and Adenosine
deaminase inhibitors
Topoisomerase Inhibitors: Control the enzymes that
alter the DNA during cellular replication. Some
examples include Topoisomerase I inhibitors &
Topoisomerase II inhibitors:
Interventions
Administer allopurinol
prior to chemo
administration to avoid
tumor lysis
Monitor IV access and
PICC line sites
Monitor for
nephrotoxicity by
assessing BUN and
creatinine
Practice safe handling
and disposal
Double flush the toilet
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Side Effects
Anorexia
Loss of taste
Aversion to food
Erythema
Painful ulcerations
Alopecia
Bone marrow
depression
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Oncology: Radiation Therapy
Patho
Radiation therapy is given because it only targets cancer
cells within its path and causes minimal damage to good
cells. Once the cells have received the radiation they die
and are no longer able to divide.
Nursing Management of
Dislodged Radiation
Implants
Types
Teleatherapy: Known also as external beam therapy is
administered externally to the patient which does not
emit radiation thus decreasing the risk of exposure to
others.
Brachytherapy: Radiation is administered directly to the
tumor tissue for a prescribed time and can be sealed or
unsealed. Because the radiation is within the patient,
the patient can pose a safety risk to those around them.
Sealed vs. Unsealed
Unsealed: When administering an unsealed radiation
source it is important to understand that the radiation
is not confined to one body area and can be excreted
via sweat, urine, or feces and can be hazardous to
others. Unsealed radiation can be administered via IV,
oral, or through body cavities.
Sealed: A sealed radiation source is typically implanted
into specific tumor tissues. The patient does emit
radioactivity when the implant is placed but does not
excrete radiation through bodily fluids.
Dose Parameters
Dose
Fractionation
Volume
Time
Chemotherapy
Adverse effects
64
Ensure the patients safety and have them lay
still
Use long forceps to gain access to the
source
Place the implant in a lead container
Contact the radiation oncologist
Document the incident and interventions
Nursing Actions
The patient must have a private room
There should be a sign placed on the
patients door
Limit visitors, no pregnant women or
children they should remain 6 ft away from
the radiation source
Cluster nursing tasks to minimize radiation
exposure
Rotate the patient assignment
Wear a radiation measurement device and
lead shield
The nurse should only be assigned to one
patient undergoing radiation at a time
Side effects
Localized skin
changes
Alopecia
Fatigue
Changes in taste or
smell
Education
Wash irradiated area
every day with warm
water and mild soap
Do not remove the
markings
Pat dry
Do not use ointment or
powders on the area
Avoid sun and heat
Wear soft loose
clothing
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65
MEDICAL SURGICAL NURSING: BILIARY 1.5.1
NURSE ANGIE 2018
BILIARY STRUCTURE AND FUNCTION
Biliary Pathway
Biliary Tree & Bile Pathway
‣
A pear shaped hollow sac-like organ under the inferior surface of the liver that holds and stores
30-50 mL of bile. Bile is mostly water that gets absorbed by the gallbladder, electrolytes, fatty
acids, bilirubin, and bile salts.
‣
‣
‣
‣
‣
‣
Biliary is made from the liver
and it travels through the
common hepatic duct.
Then through the cystic duct
and stored in the
gallbladder.
Cholecystokinin is released
when you et fats to tell the
gallbladder to contract.
Bile then travels through the
cystic duct to the common
bile duct and into the GI
tract through duodenum.
In the duodenum bile mixes
with fat and emulsifies with
bile salts and travels to the
ileum.
In the ileum bile salts and
fats get absorbed.
The remainder of the bile
salts travel back to the liver
for storage until the next
cheeseburger via
enterohepatic circulation or
get excreted in feces.
Exocrine Functions
The secretions of the exocrine
portion of the pancreas are
collected in the pancreatic duct
which joins the common bile
duct and enters the duodenum
at the Ampulla of Vater.
PANCREAS
Located in the upper
abdomen and functions as
an endocrine and exocrine
gland.
ENDOCRINE
FUNCTIONS OF THE
PANCREAS
ENZYMES SECRETED
BY THE PANCREAS
‣ Sphincter of Oddi: A
muscular valve that controls
the flow of digestive juices
(bile and pancreatic juice)
through ducts from the liver
and pancreas into the first
part of the small intestine
(duodenum.)
‣ Ampulla of Vater:
Hepatopancreatic Ampulla
or the hepatopancreatic duct,
is formed by the union of the
pancreatic duct and the
common bile duct.
‣ Beta cells: Secrete insulin
Cholecystokinin stimulates the
release of the pancreatic/
digestive enzymes.
to put glucose back into the
cells.
‣ Alpha cells: Secretes
glucagon to raise blood
glucose levels.
‣ Delta cells: Secrete
somatostatin to lower blood
glucose levels.
‣ Secretin:
Stimulates the release
of bicarb which
neutralizes he acidic
gastric juices that
enters the duodenum.
‣ Amylase: Breaks
down carbohydrates
‣ Trypsin: Breaks
down protein
‣ Lipase: Breaks down
fats/lipids
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MEDICAL SURGICAL NURSING: BILIARY 1.5.2
NURSE ANGIE 2018
Gallstones
A small, hard crystalline mass formed abnormally in the gallbladder or bile ducts from bile pigments,
cholesterol, and calcium salts. Gallstones can cause severe pain and blockage of the bile duct.
Pathophysiology
Assessment
Gallstones are the cause of acute cholecystitis. The process is caused by a physical obstruction of
the gallbladder by a gallstone, at the neck or in the cystic duct. There are two types of gallstones.
Pigment stones make up 10-25% of gallstone seen in the US. Pigment stones form when
unconjugated pigment is in the bile. Pigment stones must be removed surgically. Cholesterol stones
make up 75% of gallstones seen in the US. Cholesterol stones are insoluble in the water and are
caused by bile supersaturation with cholesterol which causes inflammatory changes in the
gallbladder. Usually found by secondary detection.
‣ GI: Mild GI symptoms,
epigastric distress, abdominal
distention, vague right upper
quadrant pain. Pain follows after
eating a meal high in fat or fried
foods. Pain and biliary colic.
Deep breathing increases pain.
‣ GU: Very dark urine, clay colored
stools.
‣ Endocrine: Deficits in vitamin
absorption KADE.
‣ DERM: Jaundice, pruritus.
Medical Treatment
‣ Open cholecystectomy:
Removal of gallbladder.
‣ Laparoscopic cholecystectomy:
Preferred removal method of the
gallbladder. Short recovery. There
is a risk of nicking the bile duct.
Get them upright and walking.
Control pain with heat or cold
15-20 minutes at a time.
Laboratory Findings:
‣ Percutaneous transhepatic
cholangiography: A needle
‣
‣
‣
‣
‣
‣
Cholecystogram: Visualizes gallbladder and bile duct
Cholangiogram: Visualizes gallbladder and bile duct
Laparoscopy: Visualizes the liver and gallbladder
Ultrasound: Visualizes abdominal organs and masses
CT/MRI: Visualizes neoplasms, cysts, and hematoma,
ERCP: Visualizes biliary structures and pancreas VIA endoscopy. Requires multiple
position changes, starts in the left lateral position.
‣ Serum alkaline phosphatase: Measures biliary tract obstruction
‣ GCT/GGTP/LDL: Markers for biliary stasis. Elevated in alcohol abuse situations.
‣ Cholesterol levels: Elevated in biliary obstruction. Decreased in liver dysfunction.
CAUSES/RISKS
‣
‣
‣ Ileal resection, High estrogen intake/
birth control
‣
‣
‣ Peritonitis, edema, gangrene, blood flow
backup.
‣
‣ Infection in the biliary tract
‣ Hemolysis, cirrhosis
vile and decompress the biliary
EDUCATION
‣
‣
‣
‣
‣
tract. Usually done for patients
allergic to anesthesia.
‣
‣
‣
‣
‣
‣
‣
‣
INTERVENTIONS
‣ Obesity, Diabetes mellitus, Cystic
fibrosis, Women over 40, Multipara and
Native American women
‣ Frequent or rapid weight loss and
changes
inserted into the liver to aspirate
Position changes give a temp fix
NG tube and NPO status until novel
sounds return.
Report peritonitis.
Monitor drains, monitor for bleeding,
assess pain, relieve pain.
Monitor intake and output, monitor
incision site.
Pillow or binder over incision.
Turn, cough, deep breathe.
Monitor respiratory status and implement
incentive spirometry.
Early ambulation. Maintain skin integrity.
Monitor GI symptoms, fever and infection,
nutrition status.
‣
‣
‣
‣
‣
Ambulation.
No bathing for 48hrs.
Do not drive for 4 days.
Avoid lifting heavy objects for 1
week.
Resume sex when ready.
Check wound site daily.
Wash with mild soap and water.
Allow adhesive to fall off do not
pull.
Normal diet, gradually add fatty
foods back as tolerated.
Sit upright in bed or chair.
Take pain medication as
prescribed, report pain if
unrelieved by analgesia.
Follow up 7-10 days.
Call if you have fever of 100 or
more x 2 days, nausea vomiting
or abdominal pain.
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‣ Bed rest, IV fluids, NG suction
‣ Anticholinergics: Do not give to
elderly. Give toradol instead.
‣ Analgesics: Morphine, dilaudid,
and fentanyl.
‣ Antibiotics
‣ Dietary altercation: low fat
‣ Ursodeoxycholic acid: Dissolves
stones does not allow new ones to
form, takes 6-12 month to achieve
‣ Chenodeoxycholic: dissolves
stones
‣ Lithotripsy: Shockwaves to
dissolve gallstones
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MEDICAL SURGICAL NURSING: BILIARY 1.5.3
NURSE ANGIE 2018
PANCREATITIS
Release of pancreatic enzymes in the pancreatic duct causing corrosion in the tissue.
Pathophysiology
Assessment:
Pancreas begins to eat itself by using trypsin. Most patients have a history of biliary tract ideas or
long term alcohol abuse issues. Gallstones enter the common bile duct and get stuck at the Ampulla
of Vater thus causing an obstruction of the flow of pancreatic juices or bile reflux. Activation of the
pancreatic enzymes cause vasodilation, vascular permeability and necrosis and possible
hemorrhage.
‣ Lipase 0-160: Elevation can
indicate and diagnose
acute pancreatitis.
Elevates in 24 hours
and remains up to 2
weeks.
‣ H&H: Hematocrit will be
elevated in
hypovolemia,
hemoglobin will
decrease with internal
bleeding.
‣ WBC: Show elevation
‣ Serum glucose: Hyperglycemia
‣ Chest & Abdominal X-Ray: to
diagnose pancreatitis.
‣ CT with contrast: Show structure
and increase in size of
the pancreas.
‣ Peritoneal fluid samples: Show
increased pancreatic
enzymes.
‣ Pancreatic enzymes: Decreased
‣ Bicarb: Decreased.
‣ Albumin: Decreased.
Laboratory Findings:
‣ Electrolytes: A low calcium level can indicate pancreatitis. The lower the
calcium the worse the pancreatitis. Ca binds the albumin.
‣ Serum amylase 23-85 U/L: Elevation within 24 hours of start of symptoms
and returns to normal within 24-72 hours.
Causes
‣ Mumps virus
‣ Spasm and edema of
ampulla of Vater
‣ Trauma
‣ Duodenitis
‣ Peptic ulcer
‣ Ischemic vascular disease
‣ Hyperlipidemia
‣ Hypercacemia
‣ Bacterial or viral infection
INTERVENTIONS
Education
‣ Respiratory care
‣ Biliary drainage
‣ Antacids, low fat low
protein diet.
‣ Monitor weight, TPN and
blood glucose.
‣ Skin assessments
‣ Monitor fluids and
electrolytes
‣ Small frequent meals
‣ Discontinue meds that
cause acute episodes.
‣ Caffeine and alcohol
cessation.
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‣
‣
‣
‣
‣
GI: Severe abdominal pain,
left upper quadrant pain that
radiates to the back and gets
worse after a fatty meal or
ingestion of alcohol and is
unrelieved by antacids,
abdominal distention. Worse
in supine position. Poorly
defined palpable abdominal
mass. decreased hypoactive
bowels. Vomiting that does
not relieve the pain or
nausea. Steatorrhea.
Abdominal guarding. Fat
malabsorption, starvation
edema.
Cardiac: Hypotension,
tachycardia, cyanosis.
CNS: Confusion
RESP: Hypoxia, respiratory
distress, dyspnea, tachypnea
DERM: Jaundice
Treatments:
‣ Enteral feedings/NPO status
‣ Pancreatic enzyme
administration: Take enzyme
before or with meals and
fluids.
‣ DO not give with Benadryl. Do
not chew. Do not give powder
with a protein.
‣ Give Tagamet and Zantac to
reduce pancreatic activity.
‣ Pain management: No opioids
due to irritation of sphincter of
Oddi. (morphine can be given
if needed.)
‣ Pancreatic Jejunostomy (Rouxen-Y)
‣ Whipple
‣ Endoscopic & laparoscopic
surgery
‣ If cysts are present, drain
them.
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MEDICAL SURGICAL NURSING: URINARY 1.7.3
NURSE ANGIE 2018
Chronic Kidney Disease
Irreversible progressive loss of kidney function with a GFR of less than 60mL/
Pathophysiology
Assessment
Chronic Kidney Disease is characterized as an irreversible progressive loss of kidney function with
a GFR of less than 60mL/ min. Chronic kidney disease occurs in stages and causes uremia and
eventually end stage kidney failure. The kidneys cannot filter wastes from the blood or concentrate
urine, not maintain acid base balance or regulate blood pressure. The waste and extra fluids build
up in the body causing uremia and electrolyte imbalances.
‣ 24 HR urine creatinine F: 85-125
ml/min M: 95-35 ml/min.: < 95%
decrease means acute damage has
limited the ability to clear
creatinine.
‣ Glomerular Filtration rate 125
mL/min: The amount of filtrate
formed by the kidneys. GFR
determines the stage of kidney
failure your patient is in.
‣ CBC: If blood counts are low,
kidney function is reduced.
Stages of CKD
Laboratory Findings:
‣ Acute Kidney Injury
‣
Oliguric phase: Give lasix, restrict
fluid intake if hypertension is
persistent.
‣
Diuretic phase: Administer IV
fluids and Electrolytes as prescribed
to replace excess fluid loss.
‣
Recovery phase: Monitor intake
and output..
‣ Diabetes
‣ Metabolic disorders
‣ Hypertension
‣ Recurrent infections
‣ ACE/ARBs : Treat
hypertension and helps
protect the kidneys.
‣ Diuretics: Controls fluid
1. At risk > 90 mL/min
2. Mild 60-89 mL/min
Phosphorus binders,
3. Moderate 30-59 mL/min
sodium bicarb,
4. Severe 15-29 mL/min
kayexalate. Help control
electrolyte imbalances.
‣ Erythropoietin: Increases
RBC production
‣ Corticosteroids: Decrease
inflammation and pain.
‣ Antihyperlipidemics: To
INTERVENTIONS
CAUSES
Medications
overload
‣ Supplements: Vit D, Ca,
5. ESKD < 15mL/min
‣ BUN 8-25 mg/dL: Indicates the renal clearance of waste products. If the
BUN is elevated this indicates that the kidneys aren't clearing waste as they
should.
‣ Serum Creatinine 0.7-1.4mg/dL: Creatinine is a breakdown of protein and
muscle metabolism. An elevated creatinine indicates renal disease and >
50% of kidney function has been lost.
H: Hypertension, hyperelectrolytes
Y: Your calcium is low
P: Pulmonary edema/
effusion
E: Edema in the periphery
R: Really confused
K: Kussmaul respirations
I: Itching, irritable,
imbalanced gait
D: Diluted urine, decreased
output
N: Not able to excrete waste
(Uremia)
E: Excess fluid volume
Y: Yellow gray skin (ESKD)
EDUCATION
‣
‣
‣
‣
‣
Medication routine
Dialysis
Fluid restrictions
Dietary restrictions:
Low phosphate, low potassium,
moderate protein and high
carbs.
‣ Avoid salmon and green leafy
veggies
‣ Reduce intake of milk, chicken,
beans and carbonated
beverages.
‣ Renal Artery occlusion
‣ Autoimmune disorders.
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decrease cholesterol and
lower BP.
Treatments
‣ Hemodialysis
‣ Kidney transplant
‣ Peritoneal Dialysis
‣ Diet restrictions
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MEDICAL SURGICAL NURSING: URINARY 1.7.3
NURSE ANGIE 2018
Cystitis -UTI
UTI that usually manifests when E.coli has been misplaced into the urinary tract.
Pathophysiology
Assessment
Inflammation of the bladder caused by obstruction, bacteria, or other irritants. The most common
bacteria found in cases cystitis include; E.coli, pseudomonas, and Enterobacter. Cystitis is more
common in women because they have a shorter urethra that is also positioned closer to the rectum.
Sexually active women and pregnant women are at an increased risk for cystitis.
C: Continual urge to pee,
cloudy urine
R: Really smelly pee
A: Lot of restroom trips
( frequency)
N: Not a lot of pee each
void
K: Killer pain when
urinating
Y: Yes I wipe the wrong
way
B: Bladder spasms
L: Lots of blood cells in
my pee
A: Always unable to go
( inability to pee)
D: Dark urine
D: Dude I have a fever
E: E Coli in my pee
R: Really cold, really
malaise
Medical Treatment
Laboratory Findings:
‣ Urinalysis :WBC’s will be present and elevated specific gravity will be
noted. Bacteria may be found indicating a need for a culture and sensitivity
to properly prescribe treatment.
CAUSES
‣ Irritants such as soap, sprays and
bubble bath.
‣ Bladder distention. Calculus
‣ Hormonal & vaginal flora changes
‣ Indwelling urinary catheters
‣ Microorganisms. Spermicides
‣ Ill-fitting vaginal diaphragms
‣ Synthetic underwear and
pantyhose
‣ Bathing suits that are wet and worn
for long periods of time.
INTERVENTIONS
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
EDUCATION
Obtain a culture & sensitivity prior
to administering antibiotic treatment.
Have the client increase fluids up to
3L /d especially with sulfonamides
Monitor urine PH.
Provide intermittent heat to the
abdomen.
Provide a sitz bath.
Perform meticulous peri care.
Perform catheter care as indicated by
facility.
Change the client's brief frequently.
Discourage use of caffeine.
‣ Wipe front to back
‣ Avoid tub baths and bubbles
baths
‣ Void every 2-3 hours
‣ Wear cotton underwear, avoid
tight clothes and pantyhose
‣ Avoid sitting in a wet bathing
suit
‣ Use water soluble lubricants for
intercourse
‣ Void, shower, and drink water
after intercourse.
‣ Avoid alcohol
‣ Take complete course of
antibiotics
‣ Repeat urine culture
Encourage good hygiene and
handwashing.
‣
‣ Antibiotic therapy: note
that if the patients is on
an aminoglycoside,
sulfonamide or
nitrofurantoin the
actions of these drugs
are decreased with
increased acidity of
urine.
‣ Antispasmodics
‣ Analgesia
‣ Antimicrobials
‣
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MEDICAL SURGICAL NURSING: URINARY 1.7.5
NURSE ANGIE 2018
Glomerulonephritis
A group of kidney disorders caused by an inflammation in the glomerulus.
Pathophysiology
Assessment
Most cases of glomerulonephritis are due to an immunologic response to any variety of etiologies.
The response then activates a biological process that in turn results in glomerular
inflammation and/or injury.
‣ ANA presence
‣ Electrolyte studies:
Hyperkalemia,
hyperphosphatemia,
hypocalcemia
Laboratory Findings:
‣
‣
‣
‣
‣
‣
‣
‣
Urinalysis (shows protein and RBCs)
GFR decreased
If indicated: blood, urine, or throat cultures
24 hr urine collection: For protein assay (increased in acute
glomerulonephritis, decreased in chronic glomerulonephritis)
Serum BUN and Creatinine increased
Antistreptolysin-O titers increased after GBS infection
C3 complement levels decreased
Cryoglobulins present
CAUSES
‣ Immunological diseases
‣ Previous hx of strep
infection
‣ Autoimmune diseases
‣ GBS infection of the
pharynx or skin
‣ H/o pharyngitis or tonsillitis
2-3 weeks before symptoms.
s
INTERVENTIONS
EDUCATION
‣ Coordinate nursing cares to
conserve energy.
‣ Be aware of potential fluid
restrictions ordered by
provider.
‣ Monitor BP, fluid and
electrolytes, and respiratory
status.
‣ Advise pt to complete full
course of antibiotics.
‣ Daily weights; report
increases to provider.
‣ Education regarding
dietary and fluid
restrictions.
‣ Infection control practices,
ie. Hand washing
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D: Dark colored urine,
Jugular vein distention.
A: Anorexia
R: Really high BP
K: Kind of short of breath
P: Proteinuria, pulmonary
HTN
E: Epigastric tenderness
E: Edema
GI/GU: Hematuria,
Oliguria or anuria, Smoky
or coffee-colored urine,
Sudden onset of
proteinuria, Nephrotic
syndrome, Sudden onset
of red blood cells (RBCs)
and casts in urine
RESP: Dyspnea,
MISC: Edema
(periorbital and facial
initially, then lower
extremities), Fatigue,
weakness (chronic),
Anorexia, weight loss
(chronic), Flank pain,
Headache
CARDIO: Increased
blood pressure,
hypertension, jugular vein
distention, pulmonary
edema, and epigastric
tenderness.
Medication
Treatments
‣ Medications:
Antibiotics,
Antihypertensives (to
control HTN associated
with disease process).
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MEDICAL SURGICAL NURSING: URINARY 1.7.6
NURSE ANGIE 2018
Nephrotic syndrome
A kidney disorder characterized by massive proteinuria, hypoalbuminemia, hypoproteinemia, and
edema.
Pathophysiology
Assessment
Renal glomerular damage leads to massive proteinuria, leading to hypoproteinemia. The low
protein in the blood leads to increased hepatic synthesis of proteins and lipids (leading to
hyperlipidemia) as well as decreased oncotic pressure. The decreased oncotic pressure leads to
edema, and then hypovolemia, which leads to decreased renal blood flow→ renin release→
vasoconstriction, or increased ADH/aldosterone→ Na+ and H20 reabsorption-> increased
hydrostatic pressure-> edema.
P: Periorbital edema
U: Urine has lots of
protein
F: fatigue/ lethargy
F: Frothy, dark urine
Y: Yes the edema is in the
AM
F: Facial, scrotal, edema
A: Ascites
C: Cankles ( edema on
the ankles)
E: Electrolyte imbalances
Laboratory Findings:
Medications
‣ Urine: specific gravity, proteinuria
‣ BUN, Creatinine: Elevated Albumin
‣ Electrolytes: Monitor sodium and potassium.
CAUSES
‣ Diabetes mellitus
‣ Focal segmental
glomerulosclerosis
‣ Membranous nephropathy
‣ Systemic Lupus Erythematosus
‣ Amyloidosis
Child gains weight
Periorbital/facial edema
more noticeable in
morning
Leg, ankle, labial, scrotal
edema
UOP decreases
Urine dark, frothy
Ascites
BP normal or slightly low
Lethargy
Anorexia
Pallor
Massive proteinuria
Hypoproteinemia
Elevated lipids
‣ Corticosteroids:
EDUCATION
INTERVENTIONS
‣ Instruct parents about
testing urine for protein.
‣ Importance of completion
of medication therapy.
‣ Monitor VS, I/O, daily
weights.
‣ Monitor urine (specific
gravity, protein).
‣ Monitor for edema.
‣ NAS diet
‣ Monitor for hyperglycemia
r/t use of corticosteroid use.
Decreases inflammation.
‣ Immunosuppressants
‣ Diuretics: Decrease fluid
build up
‣ Plasma expanders:
Increase volume
‣ Blood clot in a kidney vein
‣ Heart failure
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MEDICAL SURGICAL NURSING: URINARY 1.7.9
NURSE ANGIE 2018
Renal Calculi
Calculi (stones) are found anywhere in the urinary tract
Pathophysiology
Assessment
Calculi form when substances normally dissolved in the urine, such as calcium oxalate, malate, and
calcium phosphate, precipitate.Renal calculi can consist of calcium stones from calcium oxalate
and calcium phosphate or precipitate Large, rough calculi may occlude the opening to the
ureteropelvic junction.Dilation, stretching, and spasm from acute obstruction can lead to a coliclike pain. The frequency and force of peristaltic contractions increase pain, as do local
inflammation, irritation, and edema.
‣ White blood cell count may be
slightly increased.
‣ Kidney-ureter-bladder (KUB)
radiography or noncontrast
computed tomography scanning
(kidneys) reveals most renal
calculi.
‣ Excretory urography helps
confirm the diagnosis and
determines calculi size and
location.
‣ IV pyelography, computed
tomography scanning (abdomen
and pelvis), or magnetic
resonance imaging may reveal
stones or obstruction of the ureter.
‣ Ultrasonography, kidney and
perirenal structures can detect
obstructive changes and
radiolucent calculi not seen on
KUB radiography creatinine.
‣ Glomerular Filtration rate 125
mL/min: The amount of filtrate
formed by the kidneys. GFR
determines the stage of kidney
failure your patient is in.
‣ CBC: If blood counts are low,
kidney function is reduced.
Laboratory Findings:
‣ A 24-hour urine collection shows calcium oxalate, phosphorus, and uric
acid excretion levels.
‣ Urinalysis shows increased urine specific gravity, gross or microscopic
hematuria, crystals, casts, and pyuria.
‣ Urine pH of less than 5.5 suggests uric acid stones; pH greater than 7.0
suggests struvite stones.
CAUSES
‣ Family history of stone
formation.
‣ Diet high in calcium and Vit D,
oxalate, purines, alkali.
‣ Obstruction and urinary stasis.
‣ Diuretics
‣ UTI
‣ Prolonged urinary
catheterization.
‣ Immobilization.
‣ Hypercalcemia
‣ Hyperparathyroidism
‣ Elevated uric acid level
INTERVENTIONS
‣
‣
‣
‣
‣
‣
‣
‣
‣
S: Sharp pain
T: Temperature elevation
O: onset of pain is sudden
N: Noted urinary
frequency
E: Elevated RBC, WBC,
and bacteria in
the urine
D: Dull aching kidney
pain
Types
‣ Cystine stones caused
by an autosomal
recessive inherited
disorder involving an
excess of the amino
acid cystine
‣ Struvite stones, which
form when ammonium
magnesium phosphate
is precipitated in
women with urinary
tract infections
‣ Uric acid stones, which
form when purines are
broken down in
conditions such as gout
or during
chemotherapy.
EDUCATION
Monitor vitals and for temperature
elevation.Administer analgesia
Monitor intake & output
Assess for Fever, chills & infection.
Encourage fluid intake of 3L/day.
Administer IV fluids if indicated.
Provide warm baths and avoid
massage. Encourage ambulation.
Educate on proper diet for renal
calculi.
Prepare client for lithotripsy.
Prepare to administer antibiotics and
analgesia.
‣
‣
‣
‣
‣
Medication routine
Dialysis
Fluid restrictions
Dietary restrictions:
Low phosphate, low potassium,
moderate protein and high
carbs.
‣ Avoid salmon and green leafy
veggies
‣ Reduce intake of milk, chicken,
beans and carbonated
beverages.
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MEDICAL SURGICAL NURSING: URINARY 1.7.11
NURSE ANGIE 2018
Urethritis
Inflammation of the urethra, often d/t STI/STD, and may be concurrent with cystitis.
Pathophysiology
Assessment
Inflammation of the urethra occurs d/t gonorrhea or chlamydia in men; in women, inflammation
occurs d/t feminine hygiene sprays, perfumed feminine products, UTI, spermicidal jelly, UTI, or
changes in vaginal mucosal lining.
‣ Dysuria
‣ Urinary frequency,
urgency
‣ Nocturia
‣ Males: clear to
mucopurulent penile
discharge
‣ Female: lower abd pain
Treatments
‣ Antibiotics
‣ Urethral dilation
Laboratory Findings:
‣ UA/UC, STI/STD testing
INTERVENTIONS
CAUSES
‣ Inflammation results from
STI/STD in men or in
women: UTI, scented
feminine products, changes
in vaginal mucosal lining
‣
‣
‣
‣
‣
‣
EDUCATION
Encourage fluid intake
Prepare for STI testing.
Instruct pt in how to take a sitz/tub
bath
Istruct females to avoid perfumed
feminine products.
Instruct pt to avoid intercourse until
UTI tx is complete.
If STI is the cause, instruct pt on
future prevention (condom use,
potential for sterility with repeated
infections).
‣ Similar to interventionsinstruct pt to complete
abx course, safe sex
practices.
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MEDICAL SURGICAL NURSING: URINARY 1.7.10
NURSE ANGIE 2018
Urosepsis
A gram-negative bacteremia originating in the urinary tract.
Pathophysiology
Assessment
Most commonly caused by E-coli, and in the immunocompromised patient, from an
indwelling urinary catheter or untreated UTI. The greatest problem is the bacteria
developing abx resistance.
Fever is the most
common and earliest
manifestation.
Treatments
‣ IV, then oral abx once
discharged
Laboratory Findings:
‣ UA/UC prior to abx.
CAUSES
INTERVENTIONS
‣ Infection from indwelling
urinary catheter or
untreated UTI
‣ Obtain UA/UC before abx tx
is started, administer IV abx
as prescribed and provide
teaching regarding
importance of oral abx once
pt is home.
EDUCATION
‣ Finish antibiotics course
of treatment
‣ Increase fluid intake.
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MEDICAL SURGICAL NURSING: URINARY 1.7.2
NURSE ANGIE 2018
Acute Kidney Injury
A rapid loss of kidney function resulting from renal cell damage.
Pathophysiology
Assessment
Due to renal cell damage the kidney suddenly loses function from hypoperfusion and cell
death. Normal kidney function may resume gradually depending on the cause and condition
of the patient.
disease.
‣ BUN and Creatinine
‣ Oliguric phase: less than 400 mL/
d urine output, signs of fluid
volume excess, signs of uremia,
metabolic acidosis, kussmaul
respirations, tingling, drowsiness,
disorientation, coma, pericarditis.
‣ Diuretic phase: Urine output rises
slowly, followed by diuresis 4-5
L/d. This indicates damage to the
nephrons is healing and
recovering their ability to excrete
waste.
‣ Recovery phase: Slow process and
can take up to 2 years. Urine
volume returns to normal, memory
improves, strength increases.
‣ The signs and symptoms of Acute
Kidney injury are primarily
caused by the retention of
nitrogenous waste.
Nephrotoxic Meds
Laboratory Findings:
‣
‣
‣
‣
‣
Urinalysis :Will detect protein, RBC, pus, and casts.
Blood count/ESR
Serum potassium, chloride and C02.
Urinary catecholamine metabolites: To dx pheochromocytoma.
Urine ketones
‣IV pyelogram, urine cultures,
radioisotope.
‣Renal angiography : Test for renal
CASE
CAUSES
‣ Pre renal: Intravascular volume
depletion, dehydration,
decreased cardiac output,
decreased peripheral vascular
resistance, decreased blood flow
to the kidneys, infection outside
of the kidneys or obstruction.
‣ Intrarenal: Tubular necrosis,
prolonged renal ischemia,
intrarenal infection, obstruction,
nephrotoxicity.
‣ Post renal : Bladder neck
obstruction, bladder cancer,
calculi, post renal infection
(cystitis) .
INTERVENTIONS
‣
Oliguric phase: Give lasix,
restrict fluid intake if
hypertension is persistent.
‣
Diuretic phase: Administer
IV fluids and Electrolytes as
prescribed to replace excess
fluid loss.
‣
Recovery phase: Monitor
intake and output.
EDUCATION
‣ Decrease intake of
sodium, protein, fluid,
potassium, and
phosphorus.
‣ Take medication as
prescribed.
‣ Go to follow-up
appointments.
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Antibiotics:
‣ Ampocerin B ,Methicillin,
Polymyxin B, Rifampin,
Sulfonamides, Tetracycline
chloride, Vancomycin
Aminoglycosides
‣ Antineoplastics:
‣ Cisplatin, Cyclophosphamide,
Methotrexate
Nsaids:
‣ Celecoxib, flurbiprofen,
indomethacin, ketorolac,
meclofenamate, meloxicam,
nabumetone, naproxen, oxaprozin,
rofecoxib, tolmetin
Other Medications:
‣ Acetaminophen, captopril,
cyclosporine, fluorinated
anesthetics, penicillamine, quinine
Non-Pharmacological:
‣ Chemical agents, Radiographic
contrast, pesticides, fungicides,
Ethylene glycol.
Heavy metals:
‣ Arsenic, Bismuth, Copper sulfate,
Gold salts, Lead, Mercuric
Chloride
‣
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MEDICAL SURGICAL NURSING: URINARY 1.7.1
NURSE ANGIE 2018
Incontinence
Accidental or involuntary loss of urine from the bladder
Pathophysiology
Assessment
Incontinence occurs when the process of micturition, physiology, functional toileting ability,
has been disrupted. The underlying pathology varies among the different types of
incontinence (ie, stress, urge, mixed, reflex, overflow, and functional incontinence.
Types
D - Delirium
I - Infection, urinary
A - Atrophic urethritis or vaginitis
P - Pharmacologic agents
P - Psychiatric illness
E - Endocrine disorders
R - Reduced mobility or dexterity
S - Stool impaction
Medical Treatment
Laboratory
Findings:
‣ Stress: Urine leakage associated with
increased abdominal pressure from
laughing, sneezing, coughing,
climbing stairs, or other physical
stressors on the abdominal cavity
and, thus, the bladder.
‣ Urge: Involuntary leakage
accompanied by or immediately
preceded by urgency.
‣ Mixed: A combination of stress and
urge incontinence, marked by
involuntary leakage associated with
urgency and also with exertion,
effort, sneezing, or coughing.
‣ Overflow: The bladder becomes too
full and “ leaks”
‣ Functional: The inability to hold
urine due to reasons other than
neuro-urologic and lower urinary
tract dysfunction (eg, delirium,
psychiatric disorders, urinary
infection, impaired mobility).
‣ Bladder training: urinating only
every 2.5 to 3.5 hours.
‣ Double voiding: Double
voiding means urinating, then
waiting a few minutes and
trying again.
‣ Fluid and diet management
‣ Pelvic floor muscle exercises
‣ Anticholinergics: Oxybutynin.
Used to treat urge incontinence,
this medication relaxes the
bladder muscle and can increase
the amount of urine your
bladder can hold.
‣ Alpha blockers. In men with
urge or overflow incontinence,
these relax the bladder neck
muscles and muscle fibers in
the prostate and make it easier
‣ Urinalysis :Will detect UTI
to empty the bladder. Examples:
Tamsulosin (Flomax),
CAUSES
‣ Urinary tract infection.
Constipation. Pregnancy.
Childbirth. Changes with age.
‣ Menopause.
‣ Hysterectomy.
‣ Enlarged prostate.
‣ Prostate cancer. Obstruction.
INTERVENTIONS
‣ Keep skin dry.
‣ Clean peri area well and
frequently
‣ Take medications as
prescribed
‣ Implement a bladder
training routine.
‣ Assess for depression.
‣ Assess for signs of UTI.
EDUCATION
‣ Stay hydrated
‣ Encourage family
members to change the
patients pad every 2
hours to prevent bacteria
‣ Frequent perineal care
doxazosin (Cardura) and
terazosin.
‣ Topical estrogen. For women,
applying low-dose, topical
estrogen in the form of a
vaginal cream.
‣ Surgeries: Sling procedure,
bladder neck suspension,
prolapse surgery, artificial
urinary sphincter.
‣ Neurological disorders.
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MEDICAL SURGICAL NURSING: URINARY 1.7.13
NURSE ANGIE 2018
Uremic syndrome
An accumulation of nitrogenous waste products in the blood caused by the kidneys inability to
filter out waste products.
Pathophysiology
Assessment
Kidneys become damaged from disease process or injury causing inability to filter out nitrogenous
waste products. This causes a buildup of waste in the blood stream, electrolyte imbalances, altered
mental status and scanty output.
‣ Stool culture: Evaluate
especially for E coli and
Shigella bacteria.
W: Waves of nausea and
vomiting.
A: Altered Level of
conscious, anemia
S: Some blood in the
urine
T: Terrible BP
E: Extra waste in the
urine and blood
D: Dysrhythmias
Treatments
‣ Hemodialysis,
Peritoneal dialysis,
Hemofiltration, and
Renal replacement
therapy.
‣ Calcitriol, calcium
reducers,
erythropoietin.
‣ Kidney transplant.
‣
Laboratory Findings:
‣ Urinalysis: Mild proteinuria may be present; red blood cells
(RBCs) and RBC casts may be present.
‣ (BUN), serum creatinine, and serum electrolyte levels: Elevated.
‣ Hematologic determination: Severe anemia may be present.
‣ Hemolytic workup: Results may show anemia. Bilirubin levels
may be elevated. Lactate dehydrogenase (LDH) levels may be
elevated. Haptoglobin levels may be decreased.
CAUSES
‣ CKD
‣ AKI
‣ Diabetes
‣ Kidney trauma
INTERVENTIONS
‣
‣
‣
‣
‣
EDUCATION
‣ Educate the patient on
dialysis procedures.
‣ Educate the patient on
prescribed treatment
regimen.
‣ Educate the patient on
proper diet to reduce the
risk of recurrence.
Monitor VS for tachycardia,
hyper/hypotension and
dysrhythmias.
Monitor serum electrolyte
levels.
Monitor intake & Output
Provide a high protein diet.
Provide a limited sodium,
nitrogen, phosphate and
potassium diet.
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MEDICAL SURGICAL NURSING: URINARY 1.7.12
NURSE ANGIE 2018
Ureteritis
Inflammation of the ureter often associated with bacterial or viral infections and pyelonephritis
Pathophysiology
Assessment
Pathophys will be dependent upon causative disease process
‣ Dysuria
‣ Urinary frequency
‣ Clear to mucopurulent
penile discharge
Treatments
‣ Metronidazole (Flagyl) or
clotrimazole (Mycelex)
for Trichomonas
infection.
‣ Nystatin and Diflucan for
yeast infections.
‣ Doxycycline or
Zithromax for chlamydial
infections.
Laboratory Findings:
‣ Dependent upon causative organism (bacterial/viral
infections, pyelonephritis).
CAUSES
‣ Bacterial or viral infection
‣ Pyelonephritis
INTERVENTIONS
EDUCATION
‣ Identifying and treating
the underlying cause,
providing symptomatic
relief.
‣ Encourage pt to finish
abx treatment, safe sex
practices.
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Electrolytes
Introduction
Keeping The
Balance
Electrolyte Regulation in the Body
Electrolytes are minerals that come from dietary sources such as fruit,
vegetables, and salt. Proper electrolyte balance is vital to maintain homeostasis
and cellular regulation in the body.Each electrolytes has a specific function. For
example, some electrolytes aid in nerve conduction, muscular function, acid-
Potassium
Magnesium
Sodium
Calcium
Phosphate
Chloride
base balance, and water balance.
Electrolyte imbalances can have devastating effects on the body. Symptoms of
electrolyte imbalances range from mild with dizziness, weakness, or nausea.
Severe symptoms can include cardiovascular irregularities, tetany, and death.
Electrolyte regulation begins with the ingestion of sodium, potassium,
phosphate, chloride, calcium, or potassium. The kidneys filter electrolytes and
water by keeping what the body needs and excreting excess electrolytes and
water out of the body.
Electrolyte imbalances occur when the body is unable to excrete or hold on to
the appropriate amount of water and electrolytes due to kidney disease, cardiac
disease, or endocrine disorders. Excess amounts of electrolytes are classified as
HYPER while deficits of electrolytes are classified as HYPO. A way to remember
these is to learn how the body will present in presence of one of these
imbalances.
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ELECTROLYTE IMBALANCES
Potassium Excess : Hyperkalemia
Expected Laboratory Findings
Pathophysiology
Excessive amounts of potassium build up
outside of the cell. This can happen because of
trauma, metabolic dysfunctions such as
acidosis,kidney failure, blood transfusions, and
more. When the serum potassium level rises
and the body is unable to excrete the excess
potassium the patient may present with cardiac
arrhythmia, muscular dysfunction, and
eventually death if left untreated for long
periods.
Potassium level (serum) is greater than 5.5 mEq/L
Arterial blood gas analysis shows decreased pH
Complete blood count (CBC) with differential may
show a decreased hemoglobin
Creatinine Kinase Levels may be elevated
Assessment & Physical Findings
Cardiac: Tachycardia and later bradycardia
T wave elevation,Cardiac arrest (with levels >7
mEq/L), Ventricular arrythmia's
Musculoskeletal: Muscle weakness, flaccid
paralysis
GI: Nausea, diarrhea, abdominal
GU: Oliguria, anuria
Neuro: Hyperreflexia progressing to weakness,
numbness,tingling, flaccid paralysis, Metabolic
acidosis
Causes
Interventions
Kidney dysfunction or
failure
Adrenal gland insufficiency
Burns/crush injuries
Decreased urinary
excretion of potassium
Mass blood transfusion
Severe infection
Potassium Sparring
medications
Serum potassium levels
Cardiac status, including
cardiac rate and rhythm
Intake and output
Signs and symptoms of
hyperkalemia and
hypokalemia
Education
Decrease dietary intake of
potassium, no avocados or
green veggies or oranges.
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ELECTROLYTE IMBALANCES
Potassium Deficit: Hypokalemia
Expected Laboratory Findings
Patho
Slight deviations in serum levels can produce profound
clinical consequences. Deviations result from deficient
intake of potassium, increased excretion of potassium,
or a shift of potassium from extracellular to intracellular
space. Potassium imbalance can lead to muscle
weakness and flaccid paralysis because of an ionic
imbalance in neuromuscular tissue excitability.
Treatments
Potassium chloride, potassium
phosphate, potassium bicarbonate,
potassium citrate or IV infusion of
potassium
Magnesium sulfate
Potassium-sparing diuretics
Drugs That Cause Hypokalemia
Adrenergic drugs, such as albuterol
sulfate (Proventil-HFA) and
epinephrine
Digoxin potentiates hypokalemia
but causes hyperkalemia
Antibiotics, such as amphotericin B
deoxycholate, carbenicillin, and
gentamicin sulfate
cisplatin
corticosteroids
Diuretics, such as furosemide and
thiazide diuretics
Insulin
Laxatives
Causes
Acid-base imbalances
Cushing syndrome
Excessive GI or urinary
losses, such as from vomiting,
gastric suction, diarrhea,
dehydration, anorexia, or
chronic laxative abuse
Low-potassium diet
Hyperaldosteronism
Severe serum magnesium
deficiency
Potassium level (serum) is less than 3.5 mEq/L.
Arterial blood gas analysis shows elevated
bicarbonate and pH levels.
Serum glucose level is slightly elevated.
Magnesium level may be decreased
Assessment & Physical Findings
Cardiac: Dizziness, Hypotension,
Arrhythmias, flattened T
waves, elevated U waves,
decreased ST segments,
cardiac arrest with levels < 2.5
mEq/L
Musculoskeletal: Muscle weakness
and fatigue, leg cramps
GI: Nausea, vomiting, anorexia,
diarrhea, abdominal distention,
paralytic ileus or decreased
peristalsis
GU: Polyuria
Neuro: Malaise, irritability,
confusion, mental depression,
speech changes, decreased
reflexes, respiratory paralysis,
Metabolic alkalosis
Interventions
Monitor serum potassium
levels
Assess cardiac rate and
rhythm
Monitor Intake and output, i
Monitor vital signs
Maintain I.V access site
Monitor hypokalemia
Education
Increase dietary intake of
potassium
Educate on symptoms of
hypokalemia
Educate diabetics on risks of
hypokalemia when taking
insulin
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ELECTROLYTE IMBALANMCES
Calcium Excess: Hypercalcemia
Expected Laboratory Findings
Patho
Hypercalcemia occurs when the amount of calcium in
the blood stream becomes greater than the amount of
calcium that is normally excreted by the kidneys. This
can happen from a number of factors however,
hyperparathyroidism is the most common cause.
Treatments
I.V. fluid therapy with normal saline solution
Loop diuretics
Furosemide
Bisphosphonates
Alendronate sodium
Calcitonin
Cinacalcet hydrochloride: lowers PTH levels
PredniSONE : treats diseases related to
increased absorption of dietary calcium
Serum calcium level is greater than 10.2 mg/dL.
PTH level elevated.
Assessment & Physical Findings
Cardiac: Heart block, cardiac arrest,
hypertension
Musculoskeletal: Weakness, flaccidity,
hyporeflexia, bone pain
GI: Anorexia, nausea, vomiting, constipation,
dehydration, polydipsia
GU: Polyuria, pain in the kidneys, azotemia
Neuro: Drowsiness, lethargy, headaches,
depression, apathy, irritability, confusion
Drugs That Cause Hypercalcemia
Thiazide diuretics
Calcium-containing
antacids
Calcium preparations
Lithium
Vitamin A
Vitamin D
Theophylline
Anti-estrogens
Chlorthalidone
Causes
Hyperparathyroidism
Multiple myeloma or bone
tumors
Excess vitamin D or A intake
Addisonian crisis
Multiple fractures
Rhabdomyolysis
Acute kidney injury
Interventions
Vital signs
Pain level and effectiveness
of interventions
Cardiopulmonary status
Cardiac rhythm
Neurologic status
Seizures
Calcium levels
Hydration and fluid balance
Education
Reduction of calcium and
vitamin D
Adequate hydration-at least
6 to 8 glasses of water per
day
Avoid calcium containing
antacids
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ELECTROLYTE IMBALANCES
Calcium Deficit: Hypocalcemia
Expected Laboratory Findings
Patho
Calcium and phosphate together aid in the bone making
process. Calcium also affects the blood's ability to clot
and affects cardiac and smooth contraction. When
serum calcium is low it can have detrimental effects on
the heart and CNS as well as the muscular system.
Calcium level (serum) is less than 8.5 mg/dL.
Phosphate level (serum) may be elevated or
decreased, depending on the
underlying cause.
Serum magnesium level test may be low.
PTH levels may be low to normal
Treatments
Oral calcium (calcium carbonate, calcium citrate,
or calcitriol) and vitamin D supplements
Calcium chloride or. calcium gluconate IV (if
severe)
Magnesium sulfate (IV) if serum magnesium level
is less than 1 mg/dL
Ergocalciferol or cholecalciferol if vitamin D
deficiency is present
Drugs That Cause Hypocalcemia
Cinacalcet hydrochloride
Chemotherapy
Bisphosphonates
Anticonvulsants, and foscarnet sodium
Causes
Hypomagnesemia
Hypoparathyroidism
Hyperphosphatemia
Inadequate dietary intake of
calcium and vitamin D
Malabsorption or loss of
calcium from the GI tract
Overcorrection of acidosis
Pancreatic insufficiency,
acute pancreatitis
Liver disease & Kidney failure
Severe infections or burns
Sepsis &Rhabdomyolysis
‣ Vitamin D deficiency
Assessment & Physical Findings
Cardiac: Arrhythmias, hypotension, bradycardia
Musculoskeletal: Chvostek’s & Trossou's sign,
paresthesia, tetany, facial spasms, abdominal cramps,
muscle cramps,
spasmodic contractions
Resp: Dyspnea
GI: Increased GI motility, diarrhea
Neuro: Anxiety, irritability,
twitching around, mouth, laryngospasm,
Seizures
Interventions
Monitor Cardiac rate and
rhythm & respiratory status,
including airway
Monitor Serum electrolyte
levels, especially calcium,
phosphorus, and magnesium
Implement seizure precautions
Obtain IV access site
Monitor Signs and symptoms
of hypocalcemia and
hypercalcemia
Education
Proper administration of
calcium supplements
Ingest foods high in calcium
Frequent lab testing for
alterations in calcium levels
Increase vitamin D. This
promotes absorption of
calcium
Do not take OTC antacids or
laxatives without speaking to
your HCP
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ELECTROLYTE IMBALANCES
Magnesium Excess: Hypermagnesemia
Expected Laboratory Findings
Patho
Magnesium enhances neuromuscular integration and
stimulates parathyroid hormone secretion,
thus regulating intracellular fluid calcium levels.
Magnesium may also regulate skeletal muscles
through its influence on calcium utilization by
depressing acetylcholine release at synaptic
junctions. Magnesium almost always first effects the
muscles.
Treatments
Magnesium level test is greater than 2.5 mEq/L.
Potassium level (serum) may be elevated.
Calcium level may be decreased.
Creatinine clearance test result is less than 30
mL/minute
Arterial blood gas analysis may reveal respiratory
acidosis
Assessment & Physical Findings
IV fluids, such as normal saline
or lactated Ringer solution
Loop diuretics such as furosemide (Lasix)
Calcium gluconate to act as a magnesium antagonist
when symptoms are severe
IV glucose and insulin to shift magnesium into the
cells
Drugs That Cause Hypermagnesemia
Cardiac: Bradycardia, weak pulse, hypotension, heart
block, increased PR interval, QRS complex, and Q-T
interval , cardiac arrest
Musculoskeletal: Diminished reflexes, muscle
weakness, flaccid paralysis, respiratory
muscle paralysis, facial, paresthesia
Neuro: Drowsiness, flushing, lethargy, Confusion,
diminished sensorium, fixed and dilated pupils
Magnesium containing antacids
Laxatives that contain magnesium
Magnesium supplements
Lithium
Causes
Acid-base imbalances
Addison's disease
Adrenocortical insufficiency
Chronic renal insufficiency
Overcorrection of
Hypomagnesemia
Untreated diabetic
ketoacidosis
Hypothyroidism
Hypoparathyroidism
Lithium intoxication
Tumor lysis syndrome
Interventions
Monitor serum potassium
levels
Assess cardiac rate and
rhythm
Monitor Intake and output, i
Monitor vital signs
Maintain I.V access site
Monitor hypokalemia
Education
Decrease intake of
magnesium
Educate on the signs and
symptoms of magnesium
toxicity
Diet : avoids foods high in
magnesium
Avoid laxatives
Monitor lithium levels
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ELECTROLYTE IMBALANCES
Magnesium Deficit: Hypmagnesemia
Expected Laboratory Findings
Patho
Magnesium enhances neuromuscular integration and
stimulates parathyroid hormone secretion, thus
regulating intracellular fluid calcium levels. Magnesium
may also regulate skeletal muscles through its influence
on calcium utilization by depressing acetylcholine
release at synaptic junctions.
Treatments
Magnesium gluconate orally or
magnesium sulfate I.V.
Potassium and calcium
supplementation (if hypokalemia or hypocalcemia
is present)
Benzodiazepines
for
seizures
with
severe
hypomagnesemia
Calcium gluconate I.V. if overcompensation of
magnesium correction causes low calcium levels
Serum magnesium level test is less than 1.5 mEq/L.
Potassium level (serum) is below normal.
Calcium level is below normal.
EKG: Torsades de Pointes
Assessment & Physical Findings
Cardiac: Arrhythmias, vasomotor
changes, occasionally hypertension
Neuromuscular: Hyper-irritability, tetany, leg and foot
cramps
Neuro: Confusion, Delusions,
hallucinations, seizures
Drugs That Cause Hypomagnesemia
Aminoglycoside antibiotics
Amphotericin B deoxycholate
Cetuximab, panitumumab
Cisplatin
CycloSPORINE
Insulin
Laxatives
Loop or thiazide diuretics, such as
bumetanide, furosemide, or torsemide
Pentamidine isethionate
Causes
Acute injury
Chronic alcoholism, chronic
diarrhea, Diabetic acidosis,
excessive release of
adrenocortical hormones
Hyperaldosteronism,
Malabsorption syndrome,
nasogastric suctioning
Prolonged diuretic
therapy/Severe dehydration
Starvation or malnutrition
Interventions
Monitor Vital signs
Monitor serum electrolyte
levels, especially
magnesium,
calcium, and potassium
Monitor intake and output
Monitor cardiac rate and
rhythm
Monitor Neurologic status,
including level of
consciousness
Respiratory status
Education
Increase intake of foods
high in magnesium such
as: legumes, green leafy
veggies, nuts, seeds, whole
grains
Avoid over the counter
diuretics
Avoid alcohol
consumption
‣ Improve glucose control
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ELECTROLYTE IMBALANCES
Chloride Excess: Hyperchloremia
Expected Laboratory Findings
Patho
Chloride level (serum) is greater than 108 mEq/L.
Chloride accounts for two-thirds of all serum anions.
Chloride is secreted by the stomach mucosa as
hydrochloric acid; it provides an acid medium that aids
digestion and activation of enzymes. Chloride helps
maintain acid-base and body water balances. An inverse
relationship exists between chloride and bicarbonate.
When the level of one goes up, the level of the other goes
down.
With metabolic acidosis, arterial blood gas analysis
shows pH is less than 7.35, carbon dioxide level is less
than 22 mEq/L, and the anion gap is normal
Sodium level (serum) is greater than 145 mEq/L
Assessment & Physical Findings
Treatments
Sodium bicarbonate I.V.
I.V. fluid therapy with lactated Ringer solution
Loop diuretics to address fluid
overload
Mineralocorticoids for aldosterone
deficiency and to prevent heart failure
Cardiac: Pitting edema, Dyspnea, rapid deep breathing,
tachypnea, hypertension, signs of heart failure with
pulmonary edema
Musculoskeletal: Weakness, musculoskeletal
difficulties
Neuro: Agitation
Drugs That Cause Hyperchloremia
AcetaZOLAMIDE
Ammonium chloride
Sodium polystyrene sulfonate
Salicylates
Triamterene
Causes
Hypernatremia
Hyperparathyroidism
Loss of pancreatic secretion
Diabetes insipidus
Autoimmune disorders
Metabolic acidosis
Prolonged diarrhea
Renal tubular acidosis
Interventions
Serum electrolyte levels,
especially sodium, chloride,
and potassium levels
Respiratory status
Signs of metabolic alkalosis
Intake and output
Daily weight
Location and extent of edema
Neurologic status
Cardiopulmonary status,
including cardiac rhythm
ABG levels
Education
Avoid foods high in chloride:
tomato juice, bananas, dates,
eggs, cheese, milk, salty
broth,
canned veggies
Avoid free water w/out
electrolytes if excreting large
amount of chloride
(sweating)
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ELECTROLYTE IMBALANMCES
Chloride Deficit: Hypochloremia
Expected Laboratory Findings
Patho
Chloride accounts for two-thirds of all serum anions.
Chloride is secreted by the stomach's mucosa as
hydrochloric acid; it provides an acid medium that aids
digestion and activation of enzymes. It participates in
maintaining acid-base and body water balances,
influences the osmolality or tonicity of extracellular
fluid, plays a role in the exchange of oxygen and carbon
dioxide in red blood cells, and helps activate salivary
amylase.
Treatments
Fluid resuscitation with I.V normal saline solution
Electrolyte replacement therapy, including
potassium chloride (K-Lor) and sodium chloride
Nonsteroidal anti-inflammatory drugs (NSAIDs),
such as indomethacin(Indocin)
Carbonic anhydrase inhibitors such as
acetaZOLAMIDE (Diamox)
Chloride level (serum) is less than 98 mEq/L
Sodium level, serum, is less than 135 mEq/L
Potassium level (serum) may be decreased
Assessment & Physical Findings
Cardiac: Cardiac arrhythmias
Musculoskeletal: Muscle weakness, twitching, tetany,
hyperactive deep tendon reflexes, muscle cramps
Integumentary: Dry skin
Respiratory: Shallow, depressed
breathing
Drugs That Cause Hypochloremia
Loop Diuretics
Osmotic Diuretics
Thiazide Diuretics
Causes
Addison disease
Administration of dextrose
I.V. without electrolytes
Loss of hydrochloric acid in
gastric secretions due to
vomiting, gastric
suctioning, or gastric
surgery
Prolonged diarrhea or
diaphoresis
Diuretics
Salt-restricted diets
Interventions
Neurologic status assessment,
including level of
consciousness
Muscle strength and
movement
Cardiac rate and rhythm
Fluid balance
Serum electrolyte levels
Respiratory status
Signs and symptoms of
metabolic alkalosis and
metabolic acidosis
Respiratory status
Education
Increase foods high in
chloride and sodium tomato
juice, bananas, dates, eggs,
cheese, milk, salty broth, &
canned veggies
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ELECTROLYTE IMBALANCES
Phosphate Excess: Hyperphosphatemia
Expected Laboratory Findings
Patho
Functions of phosphate: Exists in combination with
calcium in teeth and bones. In extracellular fluid,
supports many metabolic functions (B vitamin use, acidbase homeostasis, bone formation, nerve and muscle
activity, cell division, transmission of hereditary traits,
and metabolism of carbohydrates, proteins, and fats.
Treatments
I.V. fluid hydration with normal
saline solution
Oral phosphate binders, such as
sevelamer hydrochloride (Renagel), sevelamer
carbonate (Renvela), or lanthanum carbonate
(Fosrenol)
Calcium-based phosphate binders such as
calcium carbonate or calcium acetate (PhosLo)
Aluminum salts (not given to patients with kidney
disease because they may contribute to
aluminum-related osteomalacia)
Loop diuretics with normal saline
Replacement to enhance urine excretion
Chloride level (serum) is less than 98 mEq/L.
Sodium level, serum, is less than 135 mEq/L.
Potassium level (serum) may be decreased.
Arterial blood gas (ABG) analysis may show metabolic
alkalosis: pH is greater than 7.45.
Bicarbonate level is greater than 26 mEq/L.
Assessment & Physical Findings
Cardiac: Hypotension
Musculoskeletal: Hyperreflexia, abdominal spasm,
Tetany
Neuro: Altered mental status, presence of Chvostek or
Trousseau sign, cataracts, visual impairment, seizure
Drugs That Cause Hyperphosphatemia
Enemas such as Fleet enemas
Laxatives containing phosphorus
or phosphate
Oral phosphorus supplements
Parenteral phosphorus supplements
(sodium phosphate, potassium
phosphate)
Vitamin D supplements.
Causes
Acid-base imbalance
Trauma, burns, crush
injuries,
or heat-related illnesses
Severe infections
Hypocalcemia
Hypoparathyroidism
Overuse of laxatives with
phosphates or phosphate
enemas
Kidney failure
‣ Acidosis
‣ Rhabdomyolysis
Interventions
Monitor vital signs
Monitor cardiac rhythm
Monitor phosphorus and
calcium levels
Monitor neurologic status
Monitor neuromuscular
status
Monitor intake and output
Monitor hydration
Monitor kidney function
Education
Decrease intake of phosphate
rich foods such as
Hard cheese
Meat, nuts, dried fruit and
Veggies, sardines, milk,
whole grains, & sweet bread
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ELECTROLYTE IMBALANCES
Phosphate Deficit: Hypophosphatemia
Expected Laboratory Findings
Patho
Phosphate level (serum) is less than 2.5 mg/dL
Decrease in phosphate levels may affect: Calcium in
teeth and bones. Metabolic functions such as
including use of B vitamins; acid-base homeostasis; bone
formation; nerve and muscle activity; cell division;
transmission of hereditary traits; and metabolism of
carbohydrates, proteins, and fats.
Treatments
Oral or I.V. phosphate salts (for
severe hypophosphatemia)
Vitamin D preparations, Cinacalcet
hydrochloride (Sensipar) for treatment of
hyperparathyroidism as the cause of
hypophosphatemia
Assessment & Physical Findings
Chest pain
Bone pain
Tissue hypoxia
Nystagmus
Paresthesia
Muscle weakness
Tenderness
Confusion
Seizures
Drugs That Cause Hypophosphatemia
AcetaZOLAMIDE
Thiazide diuretics
Loop diuretics
Antacids
Bisphosphonates
Cisplatin
Bevacizumab
Carmustine
Ifosfamide
Insulin
Laxatives.
Causes
Chronic diarrhea
Chronic use of antacids
containing
aluminum hydroxide
Hypomagnesemia
Inadequate dietary intake of
phosphorus
Intestinal malabsorption of
phosphorus related to
malnutrition resulting from a
prolonged catabolic state or
chronic alcoholism
Renal tubular defects
Interventions
Respiratory status
Neurologic status and
seizures
Serum phosphorus and
calcium levels
Nutritional intake
Intake and output
Signs and symptoms of
hypocalcemia,
hypercalcemia,
hypophosphatemia, and
hyperphosphatemia
Education
Increase intake of phosphate
rich foods such as ; hard
cheese, meat, nuts, dried fruit
and veggies, sardines, milk,
whole grains, sweet bread
Take Renvela with food
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ELECTROLYTE IMBALANMCES
Sodium Excess: Hypernatremia
Expected Laboratory Findings
Patho
Sodium is the major cation (90%) in extracellular fluid,
and potassium is the major cation in intracellular fluid.
Sodium cation functions include maintaining tonicity
and concentration of extracellular fluid, acid-base
balance (reabsorption of sodium ion and excretion of
hydrogen ion), nerve conduction and neuromuscular
function, glandular secretion, and water balance.
Treatments
Hemodialysis for serum sodium levels greater
than 200 mEq/L
Oral water if the patient is alert & responsive
Administration of salt-free
solutions (such as dextrose in
water), followed by infusion of
half-normal saline solution to
prevent hyponatremia
I.V. fluids for hydration: Isotonic saline or lactated
Ringer solution for hypovolemia
Hypotonic fluids for excess sodium
Desmopressin acetate (DDAVP) intranasally for
neurogenic diabetes insipidus
Chlorothiazide (Diuril) for nephrogenic diabetes
insipidus
Serum sodium level is greater than 145 mEq/L.
Urine sodium level is less than 40 mEq/24 hours, with
high serum osmolality
Assessment & Physical Findings
Cardiac: Hypertension, tachycardia, pitting
edema, excessive weight gain
Musculoskeletal: Flushed skin, dry, sticky membranes
Resp: Dyspnea, respiratory distress, death
GI: Rough, dry tongue, intense thirst
GU: Oliguria
Neuro: Fever, agitation, restlessness, seizures, gait
disturbances
Drugs That Cause Hypernatremia
Antacids with sodium bicarbonate
Antibiotics such as ticarcillin disodium-clavulanate
potassium
Salt tablets
Sodium bicarbonate injections
I.V. sodium chloride
Laxatives
Causes
Decreased ADH
Dehydration
Cushing syndrome
Excess hypertonic solution
infusion
GI fluid loss
Diabetes insipidus
Interventions
Serum sodium levels
Urine osmolality
Cardiopulmonary status
Renal function
Intake and output
Daily weight
Hydration status
Neurologic status
Education
Decrease sodium intake
Contact HCP if you feel dizzy,
have excessive weight gain,
or high heart rate
Avoid foods such as: Bacon,
butter, canned food, cheese,
frankfurters, ketchup, lunch
meat, milk, mustard,
processed foods, snack
foods, soy sauce, table salt,
white and whole wheat bread
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ELECTROLYTE IMBALANCES
Sodium Deficit: Hyponatremia
Expected Laboratory Findings
Patho
Sodium is the major cation (90%) in extracellular fluid
(potassium is the major cation in intracellular fluid).
During repolarization, the sodium-potassium pump
continually shifts sodium into the cells and potassium
out of the cells; the reverse occurs during depolarization.
Treatments
Sodium replacement
Demeclocycline: chronic hyponatremia due to SIADH
Vasopressin receptor antagonists:
conivaptan hydrochloride, tolvaptan for hypervolemic
hyponatremia and SIADH
Hypertonic saline solution (with serum sodium levels
below 110 mEq/L); isotonic saline solution for
hypovolemia
Drugs That Cause Hyponatremia
ANTICONVULSANTS
carbamazepine
ANTIDIABETICS
chlorpropamide & tolbutamide
ANTINEOPLASTICS
cyclophosphamide & vinCRIStine sulfate (VCR)
ANTIPSYCHOTICS
fluphenazine decanoate, thioridazine hydrochloride
thiothixene
DIURETICS
bumetanide, ethacrynic acid, furosemide, thiazides
SEDATIVES
barbiturates & morphine sulfate
Causes
Acid-base imbalances
Cushing syndrome
Excessive GI or urinary
losses, such as from vomiting,
gastric suction, diarrhea,
dehydration, anorexia, or
chronic laxative abuse
Low-potassium diet
Hyperaldosteronism
Severe serum magnesium
deficiency
Serum sodium level is less than 135 mEq/L.
Urine specific gravity is less than 1.010.
Osmolality (serum) is less than 280 mOsm/kg (dilute
blood).
Urine specific gravity: increased
Blood urea nitrogen-creatinine ratio is less than 20:1
in euvolemic
hyponatremia and greater than 20:1 in hypovolemic
hyponatremia.
Assessment & Physical Findings
Cardiac: Hypotension, Tachycardia, vasomotor
collapse, thready pulse
Respiratory: Cold, clammy skin, decreasing skin
turgor, Cyanosis
GI: Nausea, Vomiting, abdominal cramps
GU: Oliguria or anuria
Neuro: Anxiety, Headaches, muscle, twitching
weakness, seizures
Interventions
Restrict water intake as
appropriate; limit the patient's
free access to fluids.
Give prescribed IV fluids;
Ensure patent IV access.
Assess skin turgor and
mucous membranes
Assess the patient's
neurologic status closely and
frequently for changes.
Institute seizure precautions.
Education
Increase sodium intake
Eat foods high in sodium
Signs and symptoms of
hyponatremia
Medication regimen
Symptoms of hypernatremia
If on lithium educate on the
importance of a steady salt
intake
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.13
NURSE ANGIE 2018
ENDOCRINE DISORDERS: CUSHING’S DISEASE
A metabolic disorder characterized by Excess glucocorticoid secretion, increased secretion of
ACTH and large doses of corticosteroids.
Physiology
Assessment
When stimulated by ACTH, the adrenal gland secretes cortisol and other steroid hormones. ACTH
is produced by the pituitary gland and released into the petrosal venous sinuses in response to
stimulation by corticotropin-releasing hormone (CRH) from the hypothalamus.
S: High sugars
A: Androgen hormone increase
R: Resistance to infection low
A: Apple shape
H: Hypertension
I: Intense mood swings
S: Sodium increase
S: Serum calcium increased
A: A buffalo hump
L: Looks like the moon ( face)
T: Lines and striations on the
skin
Y: Yes they are obese in the
trunk
Derm: Purple striations on the
skin, poor resistance to
infections, moon face, buffalo
hump, easily bruised skin.
Heart: hypertension.
ENDO: Edema, truncal obesity,
hirsutism, hyperglycemia,
hypernatremia.
CNS: Mood swings.
MS: Muscle wasting,
weakness, osteoporosis, thin
extremities.
Laboratory Findings:
‣
‣
‣
‣
‣
‣
‣
‣
Skull films
CT
MRI
Serum sodium and glucose elevated
Serum potassium lowered
Plasma cortisol will be increased
ACTH stimulation test
Urinary hydrocortisone and ketocorticoids will be increased
CAUSES
‣ Tumor that grows on the
pituitary releasing ACTH.
‣ Adrenals release excess
amounts of cortisol.
‣ Stress and cortisol build
up from medications
( cushing's syndrome).
‣
‣
‣
‣
‣
‣
‣
‣
Treatments
INTERVENTIONS
Education
Monitor vital signs esp. BP
Monitor intake and output
Monitor labs esp. WBC
Meticulous skin care
Provide emotional support
Administer chemotropic agents
Prepare client for radiation
Prepare client for removal of
pituitary tumor if indicated Avoid
OTC.
‣ Eat a high fiber diet
‣ Notify HCP if you
notice sweet tasting
drainage
‣ Surgical removal of the
pituitary gland is the
treatment of choice.
‣ Hypophysectomy
‣ Adrenalectomy
‣ Ketoconazole
‣ Metyrapone
‣ Reduce steroid therapy
‣ Adhere to fluid and
sodium restrictions
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.14
NURSE ANGIE 2018
Adrenal cortex disorders: Primary Hyperaldosteronism
Hyper-secretion of aldosterone from the adrenal cortex of the adrenal glands.
Pathophysiology
Assessment
The pathophysiology of primary aldosteronism still remains unknown.
COMPLICATIONS
‣ Neuromuscular irritability,
tetany, and paresthesia
‣ Seizures
‣ Left ventricular
hypertrophy, heart failure,
and death
‣ Metabolic alkalosis,
nephropathy, and
azotemia
Laboratory Findings:
‣
‣
‣
‣
Decreased Serum potassium levels
Elevated Serum sodium levels
Urinary specific gravity increased
Metabolic alkalosis from elevated Bicarbonate levels
H: Hypertension
Y: Yes they drink a lot
P: Polyuria
E: Excretion of potassium
R: Reabsorption of sodium
GU: Low urine gravity,
increased aldosterone levels
Heart: Hypertension
ENDO: Symptoms of
hypokalemia and
hypernatremia
CNS: Paraesthesia, polydipsia
and polyuria, visual changes
Treatments
‣ Spironolactone to hold
potassium
‣ Potassium supplements
‣ Calcium channel blockers
‣ ACE inhibitors
‣ Thiazide diuretics
Surgery
‣ Adrenalectomy
INTERVENTIONS
Causes
‣ Bartter's syndrome
‣ Benign aldosteroneproducing adrenal adenoma
(in 70% of patients)
‣ Bilateral adrenocortical
‣
hyperplasia or carcinoma
(rarely)
Conditions that produce a
sodium deficit
‣
‣
‣
‣
‣
‣
‣
Education
Monitor vital signs especially BP.
Monitor intake and output.
Monitor potassium and sodium.
Monitor intake and output.
Monitor urine specific gravity.
Sodium restriction.
Administer glucocorticoid
therapy if ordered post
adrenalectomy. Avoid OTC
medications
‣ Use of diuretics
‣ Weight maintenance
‣ symptoms of
hyperkalemia
‣ Medication regimen
‣ When to call the doctor
Conditions that reduce
‣ renal blood flow and
extracellular fluid volume
(renal artery stenosis)
‣ Heart failure
‣ Hepatic cirrhosis with
ascitesNephrotic syndrome
‣
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.15
NURSE ANGIE 2018
Adrenal medulla disorders: Pheochromocytoma
A catchelcholemine producing tumor usually found in the adrenal medulla.
Pathophysiology
Assessment
Pheochromocytoma is usually a non malignant tumor that causes extreme elevations in blood
pressure. They secrete catecholamines from the medullary cells of the adrenal glands which
increase metabolism, increases thermogenesis, and heart rate. These patients feel they are in fight
or flight.
Heart: Paroxysmal HTN,
palpitations, chest pain.
CNS: Sweating, heat
intolerance, tremors and
headache, tinnitus, blurred
vision, air hunger,
impending doom.
GI: Abdominal pain, nausea
and vomiting.
ENDO: Hyperglycemia.
5 H’s:
Hypertension
Hypermetabolism
Hyperglycemia
Hyperhidrosis
Headache
Complications of
Pheochromocytoma
‣
‣
‣
‣
‣
Laboratory Findings:
‣ 24 h urine collection for vanillylmandelic acid
‣ Metanehpirne
‣ Cholecatchimines up to 14 mcg/100 ml of urine
‣
‣
‣
‣
CAUSES
INTERVENTIONS
Education
‣ PCCs cause the affected
adrenal gland to release
hormones that cause high
blood pressure. If left
untreated, a PCC can
harm the body, especially
the cardiovascular system.
‣ Monitor vitals
‣ Monitor BP
‣ No smoking, no caffeine, do not
change positions suddenly
‣ Prepare to administer beta
blockers
‣ Monitor serum glucose
‣ High calorie, vitamin, and
mineral diet Avoid OTC.
• Eat a high calorie diet
• Avoid caffeine and
Hypertensive crisis
Hypertensive retinopathy
Nephropathy
Heart failure
Increased platelet
aggregation
Stroke
Heart enlargement
MI
EKG changes
smoking because of
vasoconstriction
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.8
NURSE ANGIE 2018
Pancreatic Disorders: Diabetic ketoacidosis
A life threatening complication of type 1 diabetes. Develops when severe insulin deficits occur.
Pathophysiology
Assessment
Occurs when a person with type 1 diabetes becomes dehydrated. As the body produces a stress
response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down
muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel.
F: Fruity breath
R: Respirations ( kussmal )
U: Unbalanced electrolytes
I: Insulin low
T: Tachycardia
Treatment
Normal saline or 0.45%
NaCl
Regular insulin IV
Potassium as soon as kidney
function is satisfactory.
02 depending on respiratory
status.
Sodium bicarb pending
ABG’s.
Hyperglycemia
Laboratory Findings:
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
Can be caused by stress,
injury, infection, food, too
little insulin, thirst,
decreased BP, Loc changes,
hot dry skin, poor turgor,
fruity breath, potential
ketoacidosis
Serum glucose > 300 mg/dl
Osmolality: Varies
Serum ketones: Positive
Serum PH < 7.35
Serum HCO3 <15 mEq/ L
Serum NA : Low, normal or high
Serum K: Normal, elevated with acidosis and low with dehydration
BUN >20 mg/dl due to dehydration
Creatinine: >1.5mg/dl due to dehydration
Urine Ketones: Positive
CAUSES
‣ Infection
‣ Illness can cause your
body to produce higher
levels of certain
hormones, such as
adrenaline or cortisol.
‣ Pneumonia
‣ Urinary tract infections
EDUCATION
‣ Take insulin or oral anti
diabetic meds as prescribed
‣ Test urine ketones every 3-4
hours
‣ Soft foods 6-8 times a day
‣ Consume liquids every 30
minutes iv excess vomiting
or diarrhea occur
‣ Educate the client on the
signs and symptoms of
hyperglycemia
‣ Notify the HCP if blood
glucose levels exceed
250-300 mg/ dl
‣ Ketonuria over 24hrs
INTERVENTIONS
‣ Monitor vitals
‣ Monitor i&O
‣ Monitor potassium and
glucose
‣ Monitor for signs of ICP
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Hypoglycemia
Excess insulin, lack of food,
alcohol, overexertion.
Increased respirations,
decreased bp, increased HR,
hunger, anxiety, confusion,
cold and clammy skin,
weakness, blurred vision
seizures.
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.7
NURSE ANGIE 2018
pancreatic disorders: Diabetes mellitus
A permanent disorder of food metabolism where the amount of insulin required by the
body and the amount of insulin produced is inconsistent causing a rise in blood glucose.
Pathophysiology
Assessment
The beta cells of the pancreas produce insulin and protein where they are stored and released into
the bloodstream as blood glucose levels become elevated. When there is an insulin deficit essential
nutrients can not cross the cell membrane.
‣ Heart: CAD, PVD, HTN
‣ CNS: Retinopathy, cataracts,
paraesthesia
‣ RESP: Pulmonary edema,
frothy sputum, sob, infections,
decreased bronchomotor tone,
pulmonary HTN
‣ GU/GI: Kidney failure
‣ MS: Muscle wasting, weight
loss, thin limbs with fatty
deposits around the face , neck
and abdomen
‣ DERM: Feet and leg ulcers,
unhealed or infected wounds
‣ Reproduction: Erectile
dysfunction, decreased vaginal
lubrication, decreased libido
Medications
TYPES
‣ TYPE 1: Insulin dependent,
“juvenile” usually acute
onset, balance meds,
nutrition, activity and
accucheck QID.
‣ TYPE 2: Oral or injectable
insulin, may be regulated
with nutrition, gradual onset,
monitor BG as ordered.
‣ Gestational: Develops during
pregnancy from an increase in
the production of hormones.
‣ Surgical: Surgery on the
pancreas can cause organ
dysfunction.
Laboratory Findings:
‣
‣
‣
‣
Hemoglobin (A1C) Under 6%
Urinalysis: glucose in the urine
Random blood sugar test: Under 200 mg/dl
Fasting blood sugar test: Less than 100 mg/dL (5.6 mmol/L) is normal, If
it's 126 mg/dL (7 mmol/L) or higher on two separate tests, you have
diabetes.
‣ Oral glucose tolerance test: A reading of more than 200 mg/dL (11.1 mmol/
L) after two hours indicates diabetes.
3 P’s:
Polydipsia, polyuria, polyphagia
INTERVENTIONS
CAUSES
‣
‣
‣
‣
‣
Genetic
Autoimmune disorders
Lifestyle
Type 1: Contributed to an
autoimmune response causing
beta cells to not be produced
leading to no insulin
production.
Type 2: Onset is accelerated by
obesity and sedentary lifestyle,
there is little or no insulin
production.
EDUCATION
‣
‣
‣
‣
‣
‣
‣
‣
Eliminate smoking
Med administration
Rotate injection sites
Monitor blood glucose as ordered
Regulate diet
Skin and foot care
Sick days guidelines
Know s/s of hyper/
hypoglycemia
‣ Give regular insulin
‣ Balance fluids
‣ Electrolyte replacement
‣
‣
‣
‣
‣
‣
Calorie restriction
Count carbs 50-60%
Low protein low sodium
Artificial sweeteners
Increase fiber
For hypoglycemia give OJ,
graham crackers, sugar
candy
‣ Ensure your client eats a
carb after taking insulin &
before they workout
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SubQ
‣ Humalog, lispro : Rapid
acting, 15min onset, .5-1.5hr
peak, 2-6 hour duration give
5-15 min after meals.
‣ Humulin R, Regular: Short
acting, 30-60 min onset, 2-3
hr peak, 3-10 hr duration
give 30 min after meals.
‣ Humulin N, NPH:
Intermediate acting, 2-4 hr
onset, 3-10hr peak, 10-18 hr
duration.
‣ Lantus : All day insulin, no
peak, lasts 24 hr.
Oral
‣ Sulfonylureas: slows the
release of insulin from the
pancreas.
‣ Alpha-glucosidase
inhibitors: slows carb
breakdown in the small
intestine.
‣ Biguanides: Decrease
hepatic glucose output.
‣ Thiazolidinediones:
Decrease insulin resistance
‣ Byetta: used to improve
glycemic control.
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.9
NURSE ANGIE 2018
Pancreatic Disorders:Diabetic Hyperglycemic
Hyperosmolar Nonketotic Syndrome
A complication of type 2 Diabetes Mellitus. It involves extremely high blood sugar (glucose)
level without the presence of ketones.
Assessment
Pathophysiology
Ketosis and acidosis do not occur with HHNS. Enough insulin is made to prevent the breakdown
of fat, thus preventing ketosis.
‣ Blood sugar level of
600 milligrams per
deciliter (mg/dL) or
33.3 millimoles per
liter (mmol/L) or
higher.
‣ Excessive thirst.
‣ Dry mouth.
‣ Increased urination.
‣ Warm, dry skin.
‣ Fever.
‣ Drowsiness, confusion
‣ Hallucinations.
Laboratory Findings:
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
Serum glucose > 800 mg/dl
Osmolality: > 350 mOsm/ L
Serum ketones: Negative
Serum PH >7.4
Serum HCO3 >20 mEq/ L
Serum NA: Low, normal
Serum K: Normal, low
BUN >20 mg/dl
Creatinine: >1.5mg/dl
Urine Ketones: Negative
CAUSES
‣ Infection
‣ Illness can cause your
body to produce higher
levels of certain
hormones, such as
adrenaline or cortisol.
‣ Pneumonia
‣ Urinary tract infections
Treatment
EDUCATION
‣ Take insulin or oral
antidiabetic meds as
prescribed
‣ Test urine ketones every 3-4
hours
‣ Soft foods 6-8 times a day
‣ Consume liquids every 30
minutes iv excess vomiting
or diarrhea occur
‣ Educate the client on the
signs and symptoms of
hyperglycemia
‣ Notify the HCP if blood
glucose levels exceed
250-300 mg/ dl
‣ Ketonuria over 24hrs
INTERVENTIONS
‣ Monitor vitals
‣ Monitor i&O
‣ Monitor potassium and
glucose
‣ Monitor for signs of ICP
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‣ Normal saline or
0.45% NaCl
‣ Regular insulin IV less
critical role than in
DKA
‣ Potassium as soon as
kidney function is
satisfactory.
‣ 02 depending on
respiratory status.
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.10
NURSE ANGIE 2018
Pituitary Disorders:Diabetes Insipidus
Most common pituitary disorder resulting from a deficit of ADH.
Pathophysiology
Assessment
Diabetes insipidus is a dysfunction in levels of antidiuretic hormone (ADH), also known as
vasopressin. Produced in the hypothalamus and stored in the pituitary gland, ADH helps to regulate
the amount of fluid in the body. The disease cannot be controlled by limiting fluid intake, because
the high-volume loss of urine continues even without fluid replacement.
Complications
‣
‣
‣
‣
‣
‣
‣
‣
Hypovolemia
Hyperosmolality
Circulatory collapse
Loss of consciousness
CNS changes
Bladder distention
Hydroureter
Hydronephrosis
Laboratory Findings:
‣ ⬆Hemoglobin and Hematocrit.
‣ ⬆BUN.
‣ ⬆Urine output with low gravity less than 1.010.
‣ The fluid deprivation test is carried out by withholding fluids for 8
to 12 hours or until 3% to 5% of the body weight is lost
CAUSES
‣ Head injury
‣ Pituitary tumor
‣ Craniotomy
INTERVENTIONS
Education
‣ Monitor fluids and
electrolytes
‣ Prevent constipation
‣ Record strict intake and
output
‣ Monitor skin integrity
‣ Daily weights
‣ Monitor blood pressure,
pulse, and temp
‣ Signs and symptoms of
hyponatremia
‣ Signs and symptoms of
dehydration
‣ Monitor weight
‣ Drink water
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‣
‣
‣
‣
‣
‣
H: Hypotension
E: Excess urination
P: Poor turgor
E: Excess thirst
E: Extra dry mucous
membranes
‣ S: Skin turgor poor
Treatments
‣ Desmopressin acetate nasal
spray
‣ Vasopressin tannate: Sub Q
or IM injection
‣ Chlorpropamide
‣ Thiazide diuretics
‣ Prostaglandin inhibitors
Classifications
Nephrogenic diabetes
insipidus: Is the inability of the
kidneys to respond to AVP
results in functional AQP
deficiency. Resulting in affected
patients having constant diuresis
and producing large volumes of
dilute urine.
Primary diabetes insipidus:
Known as dipsogenic diabetes
insipidus or psychogenic
polydipsia. This can cause
excretion of large volumes of
dilute urine. Primary Polydipsia
can be the result of abnormal
thirst caused by damage to the
thirst mechanism, in the
hypothalamus.
Drug related diabetes
insipidus:
Some drugs, such as lithium or
antiviral medications such as,
cidofovir and foscarnet
(Foscavir) can also cause
nephrogenic diabetes insipidus.
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.11
NURSE ANGIE 2018
Pituitary Disorders: siadh
A condition in which excess ADH is released but not needed.
Pathophysiology
Assessment
A disorder of impaired water excretion caused by the inability to suppress the secretion of
antidiuretic hormone (ADH) causing electrolyte imbalances ( dilutional hyponatremia) & fluid
volume excess.
Complications
‣ Water intoxication
‣ Cerebral edema
‣ Severe
hyponatremia
‣ Heart failure
‣ Seizures
‣ Coma
‣ Death
B: Weight gain ( bloated)
L: Long time between voids
O: Overabundance ADH
A: Anorexia
T: Tachycardia
E: Electrolyte imbalance
D: Disorientation
Meds that cause
SIADH
‣
‣
‣
‣
Vinchristine
Phenothiazines
Nicotine
Thiazide diuretics
Medical
Management
‣
‣
‣
‣
Fluid restriction
IV Saline
Lasix
Demeclocycline
Laboratory Findings:
‣ Monitor fluid and electrolytes especially serum sodium < 115
mEq/L
‣
Monitor urine osmolality
CAUSES
‣ Trauma
‣ Stroke
‣ Lung or pancreas malignancies
‣ Medications
‣ Stress
INTERVENTIONS
Education
‣ Monitor fluids and
electrolytes
‣ Monitor vitals and neuro
status
‣ Provide a safe environment
‣ Strict intake and output
‣ Restrict fluid intake
‣ Monitor serum lithium
levels if indicated
‣ demeclocycline may take
up to 1 week to work
‣ Weigh self daily
‣ Alcohol withdrawal
‣ Hypothyroidism
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.1
NURSE ANGIE 2018
Thyroid disorders :Hypothyroidism
Disease of the thyroid characterized by low secretion of thyroid hormone and decreased
rate of metabolism
Pathophysiology
Assessment
Decreased thyroid hormone production is the most common cause of hypothyroidism. Decreased
production of T4 causes an increase in the secretion of TSH by the pituitary gland.
COMPLICATIONS
‣
‣
‣
Myxedema coma: Rare but serious.
Results from persistently low thyroid
production
Assessment: Hypotension,
bradycardia, hypothermia,
hyponatremia, hypoglycemia, general
edema, respiratory failure,
cardiovascular collapse, shock, coma.
Interventions: Maintain patent,
institute aspiration precautions, IV
hypertonic saline, administer
levothyroxine IV, IV glucose,
corticosteroids, assess hourly temp,
keep the client warm, monitor LOC
and electrolytes/ glucose.
‣ Atrophy of thyroid gland
‣
‣ Radioactive iodine, Iodine
compounds,Iodine
deficiency and iodine excess
‣
‣
‣ Thyroidectomy is the most
common cause.
‣
‣
‣
Treatments
‣ Hormone replacement
Synthroid, levothroid:
Monitor cardiovascular
status, can cause
dysrhythmias and
tachycardia.
Meds that can alter
Thyroid lab tests
INTERVENTIONS
‣
C: Constipation
O: Orbital edema
L: Lethargy / low BMR
D: Dry skin
‣ Lithium, Antithyroid
medications
‣ Radiation related to head
and neck cancers
‣ Infiltrative diseases of the
thyroid (amyloidosis,
scleroderma, lymphoma)
‣ T3 Resin Uptake Test: Indirect measure of unsaturated TBG Normal value:
25% to 35% < than 35% hyperthyroid, >25% hypothyroid.
‣ Thyroid Antibodies: Antibody titers are normally present in 5% to 10%.
Fine-Needle Aspiration Biopsy: Use of a small-gauge needle to sample the
thyroid tissue.
‣ Thyroid Scan, Radio Scan, or Scintiscan: Scintillation detector or gamma
camera moves back and forth across the area to be studied, commonly used
isotopes of iodine are 123 and iodine 131, helpful in determining the
location, size, shape, and anatomic function of the thyroid gland,
particularly when thyroid tissue is substernal or large.
‣ Serum Thyroglobulin: Used to detect persistence or recurrence of thyroid
carcinoma.
‣ Autoimmune disease
(Hashimoto’s thyroiditis,
post-Graves’ disease)
G: Goiter (maybe)
E: Edema
T: Temperature decrease
S: Alopecia
Meds that can cause
hypothyroidism
Laboratory Findings:
CAUSES
H: Heart failure
E: Enlarged heart
Education
Monitor vital signs esp. HR and
rhythm.
Administer thyroid medication and
monitor for OD.
Diet, low calorie, low cholesterol,
low saturated fat. Monitor for
constipation.
Provide a warm environment.
Avoid sedatives and opioids as these
worsen constipation
Support cardiac and respiratory
function.
Know medication interactions.
‣ Replacement therapy is
lifelong
‣ Levothyroxine is to be taken
in the AM prior to breakfast
do not skip doses
‣ Monitor blood glucose
‣ HRT’S potentiate
anticoagulants,
antidepressants , and digoxin
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‣
‣
‣
‣
‣
‣
‣
‣
‣
amiodarone
aspirin
cimetidine
diazepam
furosemide
Heparin
lithium
phenytoin
and other anticonvulsants
propranolol
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.2
NURSE ANGIE 2018
Thyroid disorders: Hyperthyroidism
Overproduction of thyroid hormones T3 and T4 and an increased basal rate of metabolism.
Pathophysiology
Assessment
Hyperthyroidism, also called thyrotoxicosis, excess production of thyroid hormone by the thyroid
gland.
S: Soft skin
H: Hypertension
E: Exophthalmos (pug eyes)
COMPLICATIONS
‣
‣
‣
Laboratory Findings:
‣ T3 Resin Uptake Test: Indirect measure of unsaturated TBG. Normal
value: 25% to 35% < than 35% hyperthyroid, >25% hypothyroid.
‣ Thyroid Antibodies: Antibody titers are normally present in 5% to 10%.
‣ Fine-Needle Aspiration Biopsy: Use of a small-gauge needle to sample
the thyroid tissue.
‣ Thyroid Scan, Radio Scan, or Scintiscan: Scintillation detector or gamma
camera moves back and forth across the area to be studied, commonly used
isotopes of iodine are 123I and iodine 131, helpful in determining the
location, size, shape, and anatomic function of the thyroid gland,
particularly when thyroid tissue is substernal or large.
‣ Serum Thyroglobulin: Used to detect persistence or recurrence of thyroid
carcinoma.
Thyroid storm: An acute life
threatening condition in a client
with uncontrolled
hyperthyroidism. Can be caused
by manipulation of the thyroid
gland during surgery. anti thyroid
meds, beta blockers
glucocorticoids can be given
before surgery to prevent
occurrence.
Assessment: Elevated temp,
tachycardia, systolic HTN, nausea
vomiting and diarrhea, agitation,
tremors, seizures, delirium, and
coma.
Interventions: Maintain open
airway and proper ventilation,
give antithyroid meds, beta
blockers, and glucocorticoids,
monitor vitals, monitor EKG for
dysrhythmias.
G: GI loss (diarrhea)
E: Enlarged thyroid gland
T: Temperature increases
S: Shakiness
H: High BMR
O: Overproduction of sweat
T: Thin (weight loss)
Medications that
alter Thyroid lab
tests
‣ amiodarone
‣ aspirin
‣ cimetidine
‣ diazepam
‣ furosemide
‣ Heparin
‣ lithium
‣ phenytoin
‣ and other anticonvulsants
‣ propranolol
Treatments
‣ SSKI
‣ methimazole
‣ Sodium or potassium
CAUSES
‣ Graves' Disease
‣ Functioning adenoma and toxic
multinodular goiter (TMNG)
‣ Excessive intake of thyroid
hormones
‣ Abnormal secretion of TSH.
‣ Thyroiditis (inflammation of the
thyroid gland)
INTERVENTIONS
‣
‣
‣
‣
‣
‣
‣
‣
Education
‣ Take medications with meals
‣ Medication should be taken at
regular divided doses
‣ Thionamides are taken for 1-2
years
‣ Report jaundice to the HCP
right away
‣ Follow instructions on intake
of iodine
Provide adequate rest
Administer sedatives as ordered
Make the environment cool and
quiet
Monitor daily weight
Do not give stimulants (caffeine)
Administer antithyroid meds as
ordered
Administer iodine preps as
indicated
Give propranolol for tachycardia
Iodide
‣ PTU
‣ Dexamethasone
‣ Beta blockers
‣ Propylthiouracil
‣ Irradiation
‣ Thyroidectomy
‣ Excessive iodine intake
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.3
NURSE ANGIE 2018
Thyroid disorders: Hypoparathyroidism
Decreased amounts of parathyroid hormone are secreted from the parathyroid gland.
Pathophysiology
Assessment
Hypoparathyroidism is caused by a parathyroid hormone (PTH) deficiency or resistance, leading to
hypocalcemia and hyperphosphatemia.
H: Hypotension
E: EKG changes
S: Spasms bronchus and
laryngeal
T: Trousseaus
I: Irritability
G: Great amount of
phosphate
H: Hypocalcemia
T: Tingling
Interventions
Laboratory Findings:
‣ Positive chvostek’s and trousseau's sign
“carpopedal spasm”
‣ Dangerously low calcium levels & High
phosphate levels.
‣ X-rays of bone show increased density
‣ Sulkowitch test: Tests for calcium in the urine
CAUSES
TREATMENTS
‣ Injury to or removal of the
parathyroid glands
‣ Radical neck dissection
‣ Parathyroidectomy
‣ DiGeorge syndrome, which is
a genetic disorder that affects
development of certain body
systems
‣ Genetics
‣ Autoimmune disease
‣ Cancer radiation treatment.
‣ Low magnesium levels
‣ Calcium Gluconate IV
1.5-3g/day
‣ Emergency tx: calcium
gluconate or chloride over iv
over 10-15 mins
‣ Vit D, Calcitriol,
ergocalciferol 50,000 to
400,000 units daily
‣ Phenobarbital
Education
‣ Take the prescribed
amount of vitamin D
‣ Avoid dark green veggies
and milk
‣ Increase intake of calcium
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‣ Quiet environment, no drafts
bright lights or sudden
movements.
‣ Diet high in vitamin D to
help absorb calcium, except;
No milk or Milk products, or
spinach as these contain high
amounts of phosphate.
‣ Diet high in calcium and low
in phosphate ( green leafy
veggies, tofu, soybeans.
‣ Have trach set and suction
equipment at bedside.
‣ Initiate seizure precautions.
‣ Prepare to administer
calcium gluconate IV.
‣ Prepare to administer
phenobarbital to decrease
neuromuscular excitability.
‣ Monitor voice for
hoarseness, this could
indicate damage to the
larynx which can be a
complication of removal of
the parathyroid glands.
Nursing Diagnosis
‣ Risk for injury
‣ Knowledge deficit
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.12
NURSE ANGIE 2018
Adrenal cortex disorders: Addison’s Disease
Adrenal insufficiency characterized by decreased secretion of adrenal cortex hormones.
Pathophysiology
Assessment
Addison's disease is caused by too little or absent cortisol release from the adrenal cortex.
Remember in Addison’s disease you add cortisol. Patients will also have low sodium and increased
potassium levels.
Medications that can
cause a need to increase
glucocorticoid dosage
‣ phenytoin (dilantin),
barbiturates, rifampin
‣ (Rifadin), and antacids. in
addition estrogen inhibits
steroid metabolism
H: Hypotension
E: Emaciation
S: Serum sodium and glucose
low
T: Tan skin
A: Alopecia
N: No feelings (depression)
Treatments
‣
‣
‣
‣
Hydrocortisone IV
5% dextrose in normal saline
Vasopressors
Antibiotics
Laboratory Findings:
‣
‣
‣
‣
‣
‣
‣
Skull films
CT
MRI
Elevated potassium levels
Plasma cortisol will be low
ACTH stimulation test
Urinary hydrocortisone and ketocorticoids will decrease
CAUSES
‣ Autoimmune disease
‣ Infections such
tuberculosis, HIV, or
fungal infections.
‣ Hemorrhage into the
adrenal glands
Complications
INTERVENTIONS
Education
‣ Monitor vital signs esp. HR and
rhythm and intake and output.
‣ Monitor WBC count.
‣ Monitor sodium, potassium and
glucose levels.
‣ High protein diet, high carbs and
high sodium and low potassium
diet. Avoid OTC.
‣ Monitor addisonian crisis caused
by stress, trauma or infection.
‣ Client will need life long
corticosteroid therapy.
‣ Adverse effects of
corticosteroid therapy
and prevention
techniques
‣ Special instruction for
patients who are
diabetics and
management of blood
glucose when taking
corticosteroids
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‣ ADDISONIAN CRISIS :
‣ Acute adrenal insufficiency
‣ Assessment: severe
Hypotension, shock, severe
lower back, abdominal and
leg pain. Severe headache.
‣ Interventions: prepare to
administer glucocorticoids
IV, hydrocortisone
succinate. Then oral
glucocorticoids and
mineralocorticoids. Monitor
BP and neuro status,
monitor I&O, monitor
sodium, potassium, and
glucose. IV fluids, bed rest
and quiet environment.
Prevent infection.
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.5
NURSE ANGIE 2018
Pituitary disorders: Hyperpituitarism
Acromegaly/Giantism
Hyper-secretion of growth hormone by the anterior pituitary gland.
Pathophysiology
Assessment
Acromegaly is characterized by hyper-secretion of growth hormone (GH), which is caused by the
existence of a secreting pituitary tumor in more than 95% of acromegaly cases. Leads to cushing's
diseases.
COMPLICATIONS
‣
‣
‣
‣
‣
ICP
Bleeding meningitis
Hypopituitarism
CSF leak
Infection
Laboratory Findings:
‣ Insulin-like growth factor-1 (IGF-1): Normally if this is high
the body stops producing growth hormone, if growth hormone
is present with a high GF1 reading then the client may have
acromegaly.
‣ Oral Glucose Tolerance Test (OGTT): Test results similar to
GF1 test, GH usually stops being produced when levels are
high unless, the client may be suffering from acromegaly.
‣ Pituitary tumor
T: Too much pain in joints
A: arthritis
L: Long hands and feet
L: Long protruding jaw
Treatments
‣ Hypophysectomy: First line
treatment.
‣ NSAIDs: For joint pain.
‣ Somatostatin Analogs
(SSAs): Somatostatin
analogs are synthetic (manmade) versions of the body's
natural hormone
somatostatin.
‣ Growth Hormone Receptor
Antagonists: They work by
blocking GH from doing one
of its jobs—making IGF-1.
‣ Dopamine Agonists: Works
by stopping the release of
GH from the pituitary tumor.
Hypophysectomy
Education
‣ Removal of a pituitary tumor
via craniotomy or
transsphenoidal approach.
‣ long-acting forms of
somatostatin analogues
require I.M. injection
approximately every 4
weeks for octreotide and
INTERVENTIONS
CAUSES
H: Hypertension
E: Enlarged organs
‘
S: Sweating and oily skin
‣
‣
‣
‣
Provide emotional support
Provide frequent skin care
Provide pain relief
Prepare the client for
radiation if planned
‣ Prepare the client for
hypophysectomy if planned
once every 7 to 14 days
for lanreotide
‣ potential adverse effects
of dopamine agonists
‣ Avoid activities that
increase ICP
‣ Breathe through the
mouth if nasal packing is
in place
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.6
NURSE ANGIE 2018
Pituitary Disorders: Hypopituitarism
Hypo-secretion of one or more of the following hormones: LH, FSH, GH, TSH, ACTH, ADH.
Pathophysiology
Assessment
A rare disorder usually caused by a tumor, where your pituitary gland either fails to produce one or
more of its hormones or doesn’t produce enough of them causing dwarfism in children.
H: Hypotension
O: Obesity
R: Really bad headaches
M: More tired
O: Output ( cardiac) decreased
N: Non fertile
E: Eating uncontrollably
S: Sexual dysfunction
Treatments
‣ Corticosteroids. These drugs,
such as hydrocortisone or
prednisone, replace the
adrenal hormones that aren't
being produced because of
an adrenocorticotropic
hormone (ACTH) deficiency.
‣ Levothyroxine (Levoxyl,
Synthroid, others).
‣ Sex hormone replacement.
‣ Growth hormone
replacement.
Dwarfism
‣ Synthetic thyrotropinreleasing hormone (TRH)
Laboratory Findings:
‣
‣
‣
‣
CT or MRI, with contrast
Free T4 and TSH levels
ACTH stimulation test
Insulin tolerance test
CAUSES
‣ Head trauma
‣ Pituitary tumors
‣ Encephalitis
‣ Autoimmunity
‣ Stroke
INTERVENTIONS
EDUCATION
‣ Provide emotional support.
‣ Client may need hormone
replacement.
‣ Monitor blood glucose for
hyperglycemia
‣ Monitor for pituitary
apoplexy
‣ Daily weights
‣ Prep for surgery if a tumor is
involved
‣ Children will reach their adult
height just at a slower pace
‣ Growth hormone is given
subcutaneously
‣
Educate the client on need
for extra cortisone if they
become over stressed or a
fever of over 101.1
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Dwarfism can be caused by any
of more than 200 conditions.
Causes of proportionate
dwarfism include metabolic and
hormonal disorders such as a
growth hormone deficit.
Dwarfism Assessment
‣ A large head with a
prominent forehead
‣ A flattened bridge of the
nose
‣ Protruding jaw
‣ Crowded and misaligned
teeth
‣ Forward curvature of the
lower spine
‣ Bowed legs
‣ Flat, short, broad feet
‣ "Double-jointedness"
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MEDICAL SURGICAL NURSING: ENDOCRINE 1.8.4ß
NURSE ANGIE 2018
Thyroid disorders: Hyperparathyroidism
Increased amounts of parathyroid hormone are secreted from the parathyroid gland.
Pathophysiology
Assessment
H: Hypertension
E: Epigastric pain
Hyperparathyroidism is caused by a parathyroid
hormone(PTH) overproduction leading to hypercalcemia
and hypophosphatemia.
Complications
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
Osteoporosis
Subchondral fractures
Traumatic synovitis
Renal calculi and colic
Renal insufficiency and failure
Cholelithiasis
Cardiac arrhythmias
Vascular damage
Hypertension
Heart failure
Muscle atrophy
Depression
F: Fatigue
E: Electrolyte imbalances
L: Low phosphate
L: Low bone density
F: Fractures
A: Anorexia
S: Stones ( renal)
T: Tender bones
Treatments
‣ IV furosemide and saline to
promote calcium excretion
‣ IV phosphate for rapid
lowering of calcium
‣ Bisphosphonate to increase
bone density
‣ Parathyroidectomy
Laboratory Findings:
‣
‣
‣
‣
‣
Dangerously high calcium levels above 10.2 mg/dl.
Decreased phosphate levels less than 4.5 mg/dl.
X-rays of bone show decreased density.
DEXA bone scan.
Sulkowitch test: test for calcium in the urine.
Nursing Diagnosis
INTERVENTIONS
CAUSES
‣ Benign tumor
‣ Vitamin D deficit
‣ Long term Kidney disease
Education
‣
‣
‣
‣
‣
‣
‣
‣
Relieve pain
Prevent formation of renal calculi
Increase fluid intake
Offer acid ash diet
Prevent fractures
Promote body alignment
Safety precautions
Monitor potassium levels
counteracts calcium on cardiac
muscles
‣ Parathyroidectomy care
‣ Increase fluids
‣ Decrease calcium intake
‣ Signs and symptoms of
hypercalcemia
‣ Symptoms of respiratory
distress
‣ Need for blood testing fro
electrolyte levels
‣ avoid calcium-containing
antacids and thiazide diuretics
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‣ Risk for injury
‣ Impaired urinary
elimination
‣ Nutrition less than body
requirements
‣ Constipation
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MEDICAL SURGICAL NURSING: EYES 1.8.1
NURSE ANGIE 2018
Legal Blindness
A visual acuity of 2/200 or less in the effected eye
Pathophysiology
Complications
‣ Injury
‣ Sensory deprivation
occurs when a person has central visual acuity
(vision that allows a person to see straight
ahead of them) of 20/200 or less in his or her
better eye with correction. With 20/200 visual
acuity, a person can see at 20 feet, what a
person with 20/20 vision sees at 200 feet.
CAUSES
‣ Glaucoma
‣ Cataracts
‣ Macular degeneration
‣ Head injury
‣ Hypertensive retinopathy
‣ Diabetic retinopathy
‣ Retinal vascular occlusion
‣ Increased intracranial
pressure
INTERVENTIONS
EDUCATION
‣ Use a normal tone of voice
‣ Speak before approaching
‣ Allow the patient to use
touch to orient to the room
‣ Use the clock to describe
placement on the plate at
meal times
‣ Provide radios, television
and clocks that tell time
orally provide a braille
watch
‣ Allow the patient to hold
on to you when
ambulating
‣ Instruct the client to use
assistive devices
‣ Support groups
‣ To sweep the cane
prior to taking a step
‣ Instruct on proper
cane use
General Eye
Assessment
‣ PERRLA
‣ Cardinal fields of
gaze
‣ Confrontation
‣ Visual acuity
‣ Accommodation
‣ Corneal light
reflex
‣ Sclera color
‣ Conjunctiva color
‣ Look for
strabismus and
nystagmus
‣ Eyebrows
‣ Eyelids and lashes
‣ Eyeballs
‣ Bulbar
Conjunctiva and
Sclera
‣ Palpebral
Conjunctiva
(stressful and
uncomfortable usually done only
if a complaint) Eversion of the
Upper Lid
‣ Lacrimal
Apparatus
‣ Use braille
‣ Provide a safe
environment by
removing trip
hazards
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MEDICAL SURGICAL NURSING: EYES 1.8.3
NURSE ANGIE 2018
Cataracts
Opacity of the lens that distorts the image projected into the retina
Pathophysiology
Risk Factors
The lens loses its transparency through
degenerative changes in the crystalline cell
structure. The clouded lens blocks light shining
through the cornea. Images cast onto the retina are
blurred. The brain interprets a hazy image.
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
Age
Smoking
Use of alcohol
Prolonged exposure to
sunlight
Intrauterine infection
Exposure to ionizing
radiation such as X-rays or
cancer radiation treatment
Occupation involving
infrared energy
Metabolic syndrome
Diabetes
Corticosteroid use
Long-term use of
antidepressants
Complications
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
Priority!
Assess for complaints of a sudden increase in
pain, accompanied by restlessness and
increased pulse rate, which may signal
increased intraocular pressure.
CAUSES
‣ Aging
‣ Heredity
‣ Trauma
INTERVENTIONS
Complete vision loss
Infection
Loss of vitreous fluid
Wound dehiscence
Hyphema
Pupillary block glaucoma
Retinal detachment
Macular or corneal edema
Bleeding
Dislocated intraocular lens
EDUCATION
‣ Lens extraction
‣ Extracapsular cataract
extraction
‣ Intracapsular cataract
extraction (rarely used in
the United States)
‣ Phacoemulsification
‣ Monitor for pain
‣ Monitor for increased
discharge
‣ Do not bend at the
waist
‣ Avoid sneezing
‣ Wear eye shield
‣ Do not touch eye
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Assessment
‣ Milky white pupil
on inspection with
a penlight
‣ Grayish white area
behind the pupil
Red reflex lost
‣ Change in color of
lens (may appear
slightly yellow or
brown) Poor
vision overall
(cloudy, blurred or
dim)
‣ Painless,
gradual vision loss
‣ Colors seem faded
‣ Blinding glare
from headlights
with night driving;
halo may appear
around lights
‣ Poor reading
vision
‣ Annoying glare
from sun or lights
‣ Poor vision in
bright sunlight
‣ Better vision in
dim light than in
bright light
(central opacity)
Medications
‣
‣
‣
‣
Corticosteroids
NSAIDS
Antibiotics
Mydriatics
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MEDICAL SURGICAL NURSING: EYES 1.8.1
NURSE ANGIE 2018
Refractive Errors
Refraction is the bending go light rays any problem with eye length can lead to reaction errors
Pathophysiology
Myopia: Near sightedness, refraction is too strong. Bent
images fall on the retina.
Risks
‣ Older age
‣ Young age
‣ Genetics
Astigmatism: irregular curvature of the cornea, images
are focused at two points in the retina
Hyperopia : farsightedness, refraction is too weak.
Image is focused behind the retina
Presbyopia: Loss of elasticity in the lens related to the
aging process. Images fall behind the retina
Complications
‣ Complications are
usually related to
surgery.
‣ Inability to read up
close or far away
‣ Fatigue
‣ Grades may go
down
Assessment
‣ Diagnosed with a
process known as
refraction.
‣ An eye chart is
viewed while
various lenses
with different
strengths are
systematically
placed in front of
the eye. Image
will sharpen or
blur
‣ decrease distance
visual acuity (VA)
‣ squinting
‣ near visual acuity
is often okay but
PT may need to
hold books closer
Surgical
intervention
CAUSES
The eyes inability to
bend light and focus
clearly on the retina
INTERVENTIONS
EDUCATION
‣ Eyeglasses
‣ Contacts
‣ Educate on post
operative
interventions
‣ Radial
keratotomy
‣ Photo refractive
keratotomy
‣ LASIK
‣ Corneal ring
‣ Avoid bright light
‣ Avoid sneezing
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MEDICAL SURGICAL NURSING: GASTROINTESTINAL 1.3.7
NURSE ANGIE 2018
Peritonitis
Acute inflammation of the peritoneum
Pathophysiology
Bacteria invade the peritoneum after inflammation and
perforation of the GI tract. Fluid containing protein and
electrolytes accumulates in the peritoneal cavity.Peristalsis
slows or stops.Respiratory problems can result from
abdominal distention caused by fluid shifts to the
peritoneal cavity.
Assessment
Risks
‣
‣
‣
‣
‣
‣
Peritoneal dialysis
History of cirrhosis
Appendicitis
Crohn disease
Peptic ulcer disease
History of peritonitis
‣
‣
‣
‣
‣
‣
‣
‣
‣
Complications
‣
‣
‣
‣
‣
‣
Abscess, fistula formation
Septicemia
Respiratory compromise
Bowel obstruction
Shock
Liver failure
‣
‣
Rigid board-like
abdomen
Fever
Tachycardia
Hypotension
Shallow breathing
Change in mental status
Signs of dehydration
Positive bowel sounds
(early); absent bowel
sounds (later)
General abdominal
tenderness
Rebound tenderness,
guarding
Typical patient
positioning: Lying very
still with knees flexed
Treatments
Labs & Diagnostics
‣
Abdominal x-ray
‣
Peritoneal lavage
Elevated WBC
Blood cultures
CAUSES
‣ Bacterial or chemical
inflammation
‣ GI tract perforation (from
‣ appendicitis, diverticulitis,
peptic ulcer, or ulcerative
colitis)
‣ Ruptured ectopic
pregnancy
‣ Peritoneal dialysis
INTERVENTIONS
EDUCATION
‣ Daily weights
‣ Pain management
‣ Monitor vitals
‣ Wound care, drains
‣ Monitor I & O
‣ Signs of infection
‣ Positioning
‣ Broad-spectrum I.V.
antibiotics based on
the infecting
organism
‣ Nasogastric (NG)
intubation
‣ Correction of the
underlying condition
Nothing by mouth
(NPO) until bowel
function returns
‣ Gradual increase in
diet
‣ Total parenteral
nutrition if necessary
Bed rest until the
condition improves
‣ Semi-Fowler position
‣ Avoidance of lifting
for at least 6 weeks
postoperatively
‣ Assess bowel sounds
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MEDICAL SURGICAL NURSING: GASTROINTESTINAL 1.3.6
NURSE ANGIE 2018
Appendicitis
Inflammation of the vermiform appendix, a bulge from the apex of the cecum
Pathophysiology
Risks
‣ Low fiber, high carbohydrate
diet
‣ Family history
‣ Gastrointestinal infection
‣ Inflammatory bowel disease
Mucosal ulceration triggers inflammation, which temporarily
obstructs the appendix.increasing pressure in the distended
appendix; the appendix then contracts. Fluids and mucus
continue to be secreted and stagnate. Continued
inflammation, pressure, and fluid collection can lead to
perforation and spillage of the appendiceal contents into the
peritoneal cavity.
Complications
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
Peritonitis (most common)
Wound infection
Dehiscence
Intra-abdominal infection
Fecal fistula
Intestinal obstruction
Incisional hernia
Paralytic ileum
Abdominal or pelvic abscess
Death (rare)
Labs & Diagnostics
‣ Elevated WBC count
‣ Ct showing enlarged appendix
‣ Ultrasound shows enlarged appendix
CAUSES
‣
‣
‣
‣
‣
‣
‣
‣
Barium ingestion
Fecal mass
Foreign body
Mucosal ulceration
Neoplasm
Stricture
Viral infection
Inflammatory bowel
disease
INTERVENTIONS
EDUCATION
‣ Monitor Vital signs
‣ Advance diet as tolerated
‣ Signs of shock
‣ Splinting surgical site
‣ Assess pain
‣ Turn cough deep breathe
‣ Monitor bowels
‣ Early ambulation
‣ Monitor surgical site
‣ I/S
Assessment
‣ Periumbilical
abdominal pain
‣ Rebound pain when
pressure on the
abdomen is
released quickly
‣ Guarding
‣ Rigidity
‣ Fever
‣ Nausea, vomiting
‣ Right lower
quadrant pain
Treatments
‣ Surgical removal of
the appendix
‣ NPO
‣ IV fluids
‣ Pain medication
( use cautiously to to
maintain awareness
of possible rupture)
‣ Antibiotic therapy
Never apply heat
to the right lower
abdomen; this can
cause the
appendix to
rupture.
‣ Monitor for signs of infection
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MEDICAL SURGICAL NURSING: GASTROINTESTINAL 1.3.5
NURSE ANGIE 2018
Ulcerative Colitis
Ulceration and inflammation of the bowel that causes poor absorption of nutrients
Pathophysiology
Risks
•
Ulceration and inflammation of the bowel that causes poor
absorption of nutrients. The colon becomes a rigid,
foreshortened tube.In severe ulcerative colitis, areas of hyperplastic growth occur with swollen mucosa surrounded by
inflamed mucosa with shallow ulcers.submucosa and circular
and longitudinal muscles may be involved.
•
•
•
•
Stress (may increase the
severity of an attack and
precipitate exacerbations)
Family history
Ashkenazi Jewish
ancestry
Nonsteroidal antiinflammatory drug use
Dairy products
Complications
•
•
•
•
•
•
•
•
•
•
•
•
Labs & Diagnostics
Nutritional deficiencies
Perineal sepsis
Anal fissure or fistula
Perirectal abscess
Perforation of the
colon
Hemorrhage
Anemia
Toxic megacolon
Cancer
Coagulation defects
Arthritic diseases
Death
‣ Perinuclear antineutrophil cytoplasmic antibody assay is positive
in 60% to 80% of patients with ulcerative colitis.
Medical treatment
‣ Hemoglobin : decrease
‣ Stool specimen analysis reveals blood, pus, and mucus, but no
pathogenic organisms and is done to exclude other causes.
‣ ESR: elevated
CAUSES
May be related to an
abnormal immune response
in the GI tract, environmental
factors, and possibly genetic
factors.
Assessment
‣ Liquid stools with visible
pus, mucus, and blood
‣ Possible abdominal
distention
‣ Abdominal tenderness
‣ Perianal irritation
‣ Jaundice
‣ Joint pain
‣ Tachycardia
‣ Fever
‣ Mild cramping and lower
abdominal pain
‣ Recurrent bloody
diarrhea as often as 25
times daily
‣ Nocturnal diarrhea
‣ Tenesmus
‣ Arthralgia
‣ Rectal urgency
‣ Occasional fecal
incontinence
MONITOR
EDUCATION
Vital signs
Patients with active signs and
symptoms of ulcerative colitis
shouldn't undergo barium
enemas because of the risk of
precipitating toxic megacolon.
•
Nothing by mouth (if
severe)
•
Well-balanced diet with
adequate fluid intake
•
Parenteral nutrition
(with severe disease)
Pain, infection
Fluid balance , nutritional status
Electrolytes
Bowel sounds , weights
Stool characteristics
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‣ 5-ASA: Aminosalicylates,
Sulfasalazine, Olsalazine,
Mesalazine, Balsalazide
‣ Corticosteroids:
Prednisone,
prednisolone
Methylprednisone,
hydrocortisone (IV
corticosteroid therapy)
‣ Immunosuppresants:
Azathioprine,
Cyclosporine
Hospitalization if drug
therapy does not work
Low residue diet
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MEDICAL SURGICAL NURSING: GASTROINTESTINAL 1.3.8
NURSE ANGIE 2018
Colon Cancer
Malignant tumor of the colon.
Pathophysiology
A premalignant lesion progresses to invasive
adenocarcinoma that most often involves genetic alterations.
Tumors tend to grow slowly and remain asymptomatic for a
long time.
Risks
Assessment
‣ Smoking or tobacco use
‣ Excessive intake of saturated
animal fat
‣ Age older than 50
‣ History of inflammatory
bowel disease
‣ Type 2 diabetes
‣ Family history of colon
cancer
‣ Low-fiber diet
‣ Diet high in red meat or
processed meats
‣ Obesity
‣ Sedentary lifestyle
‣ Alcohol use
‣ Black race
‣ Abdominal distention
or visible mass
‣ Enlarged abdominal
veins
‣ Abnormal bowel
sounds
‣ Abdominal mass
Generalized
abdominal tenderness
‣ Right colon cancers:
tend to be
asymptomatic until
palpable mass in
lower right quadrant
and blood mixed with
stool becomes visible
‣ Left colon tumors
produce pencil-
Complications
‣ Anemia
‣ Rectal bleeding
‣ Bowel obstruction (left-sided
tumors)
‣ Postoperative infection,
stricture, abscess formation,
pneumonia
‣ Adverse effects of
chemotherapy or radiation
Labs & Diagnostics
‣ Fecal occult blood test: may show blood in
stools,
‣ Carcinoembryonic antigen may be
elevated; permit patient monitoring before
and after treatment to detect metastasis or
recurrence.
CAUSES
‣ Genetics
‣ Ulcerative colitis
‣ Iron deficiency
anemia may be
present.
‣ Computed
tomography scanning (abdomen and
pelvis) determines stage. Transrectal
ultrasonography determines extent of
rectal lesions.
INTERVENTIONS
EDUCATION
‣ Monitor Stool
‣ Diet Education
‣ Adverse effects of
chemotherapy or radiation
‣ Diet high in whole grain fibers,
vegetables, and fruits and low
in processed meatsRadiation
preoperatively and
postoperatively to induce
tumor regression
‣ Radio-frequency or ethanol
ablation therapy
‣ Smoking cessation
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shaped stool
Treatments
‣ Chemotherapy, such as
fluorouracil, oxaliplatin,
irinotecan hydrochloride
‣ Targeted therapy:
bevacizumab,
ramucirumab, zivaflibercept
‣ Proctoscopy or
sigmoidoscopy (flexible)
permits visualization of
the lower GI tract and
can detect up to 66% of
colorectal cancers.
‣ Colonoscopy permits
visual inspection and
photography of the
colon up to the ileocecal
valve and provides
access for
polypectomies and
biopsies of suspected
lesions.
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MEDICAL SURGICAL NURSING: GASTROINTESTINAL 1.3.2
NURSE ANGIE 2018
Gastritis
Localized or patchy inflammation or erosion of the gastric mucosa
Pathophysiology
Localized or patchy inflammation or erosion of the gastric
mucosa.May be acute (erosive or non erosive) or chronic, reactive,
atrophic, reflux, hemorrhagic, or infectious. Most common
stomach disorder (acute). ACUTE: The protective mucosal layer is
altered due to a causative agent or factor. Acid secretion produces
mucosal reddening, edema, and superficial surface erosion.
CHRONIC: Gastric mucosa progressively thins and degenerates.
Assessment
Risks
Age older than 55
Exposure to toxic substances
Hemodynamic disorder
Alcohol abuse
Ingestion of NSAIDs, including
aspirin
‣ Smoking
‣ Stress
‣ Peptic ulcer disease
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
‣
Achlorhydria
Hypochlorhydria
Hyperchlorhydria
Grimacing
Restlessness
Pallor
Tachycardia
Hypotension
Abdominal distention,
tenderness, and guarding
‣ Normoactive to
hyperactive bowel sounds
‣ Possible positive fecal
occult blood test results
Medical Treatment
•
Complications
Hemorrhage, anemia
Dehydration
Obstruction
‣
‣
‣
Labs & Diagnostics
‣ Perforation
Peritonitis
‣ Gastric cancer
‣ Peptic ulcer
•
•
•
‣ Atrophic gastritis
‣ Occult blood found in vomitus or stools (or both) indicates gastric
bleeding.
‣ Hemoglobin (Hb) level and hematocrit may be decreased.
‣
Urea breath test or H. pylori stool antigen test indicates the
presence of H. pylori .
•
•
•
CAUSES
‣
‣
‣
‣
‣
Helicobacter pylori (H. pylori)
infection
Autoimmune response
Damage to the stomach lining
Crohn disease, sarcoidosis
food allergies
infections with viruses, parasites,
fungi, and bacteria
INTERVENTIONS
EDUCATION
‣ Nothing by mouth if bleeding
occurs
‣ Elimination of irritating foods,
‣
‣
‣
‣
‣ Elimination of irritating foods,
such as caffeine and spicy
foods
‣
prescribed drug therapy
‣
Avoidance of NSAIDS
‣
Antacids 1 hour after meals
‣
Avoid alcohol
‣
such as caffeine and spicy foods,
or of irritating drugs
Reduce anxiety
Maintain fluid balance
Pain relief
Nutritional support
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•
•
•
•
Elimination of cause
(such as treatment of
H. pylori with
antibiotic,
discontinuation of
NSAIDs)
Stomach acidreducing medications
Smoking cessation
Venous
thromboembolism
(VTE) prophylaxis if
the patient is
hospitalized
For massive bleeding:
Blood transfusion
Iced saline lavage
Angiography with
vasopressin
Histamine-2 (H2)
receptor antagonists,
such as cimetidine
(Tagamet), ranitidine
hydrochloride
(Zantac), famotidine
(Pepcid), and
nizatidine (Axid)
Antibiotics
Antacids, such as
aluminum and
magnesium
hydroxide
Sucralfate (Carafate)
Omeprazole
(Prilosec)
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MEDICAL SURGICAL NURSING: GASTRLOINTESTINAL 1.3.1
NURSE ANGIE 2018
GERD
Characterized by backflow of gastric contents into the esophagus.
Pathophysiology
Presenting Symptoms
Gastric motility is slowed which causes a delay in clearance of stomach acid. Gastric emptying is
delayed which causes an increased volume of gastric fluids.
Reflux occurs when the lower esophageal sphincter pressure
is deficient . The lower esophageal sphincter relaxes causes
Risks
regurgitation of stomach contents into the esophagus
Fatty foods
Alcohol
Anticholinergic drugs
Morphine
Calcium channel blockers
Nasogastric (NG) intubation for
more than 4 days
‣ Obesity, Smoking
‣ Connective tissue disorders
‣
‣
‣
‣
‣
‣
•
•
•
•
•
•
•
•
•
Pyrosis
Dyspepsia
Regurgitation
Dysphagia
Odynophagia
Hypersalivation
Esophagitis
Think burning and
trouble eating.
Symptoms may
mimic a heart attack
Complications
Peptic stricture
Reflux esophagitis
Esophageal stricture
Esophageal ulcer
Barrett esophagus
Anemia from esophageal
bleeding
‣ Reflux aspiration leading to
chronic pulmonary disease
‣
‣
‣
‣
‣
‣
Labs & Diagnostics
•
Esophageal acidity test reveals degree of gastroesophageal
reflux.
•
Esophagoscopy and biopsy results confirm pathologic
changes in the mucosa.
Esophagogastroduodenoscopy reveals evidence of
esophagitis.
•
CAUSES
‣ Laying flat
‣ Hiatal Hernia
‣ Pyloric surgery
‣ Pregnancy
INTERVENTIONS
Medications
•
Histamine h2
antagonist:
famotidine,
nizatidine,
ranitidine.
•
Proton Pump
Inhibitors:
lansoprazole,
rabeprazole,
esomeprazole are
used to decrease
gastric secretions
•
Prokinetic
agents: accelerate
gastric emptying.
Bethanechol,
domperidone
EDUCATION
‣ Elevate HOB 30 degrees
‣ No lying down for 2 to 3 ours
after eating
‣ Avoid late night eating
‣ Evaluation of effectiveness of
medications
‣ observing for adverse effects
of medications
‣
‣
Eat a diet low in fat and to avoid
caffeine,tobacco, milk, beer,
carbonated drinks, mint.
Avoid eating or drinking 2 hours
before bedtime
‣ Maintain normal body weight
‣ Avoid tight clothes
‣ Elevate the head of the bed and
upper body 6-8’’
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MEDICAL SURGICAL NURSING: GASTROINTESTINAL 1.3.3
NURSE ANGIE 2018
Irritable Bowel Syndrome
A widespread condition involving recurrent abdominal pain and diarrhea or constipation
Pathophysiology
Assessment
IBS manifests from a functional disorder of the bowel. Neuroendocrine changes may cause motility
issues within the intestines however, there is no inflammation or
tissue changes in the intestinal mucosa.
Risks
‣ Young age
‣ female gender
‣ family history
‣ Alternating between
constipation and
diarrhea
‣ Pain
‣
‣ mental health issues.
Complications
Poor quality of life
Diverticulitis
Hemorrhoids
Malnutrition
‣
‣
‣
‣
‣ Depression
Labs
•
•
•
Fecal occult blood test results are negative.
Stool examination for ova and parasites is negative.
Stool culture is negative for leukocytes and pathogenic
bacteria.
Complete blood count (CBC) with differential, serologic tests,
serum albumin level test, and erythrocyte sedimentation rate
test results are normal. Lactose tolerance blood test and
celiac testing may be performed.
•
•
CAUSES
•
GI motility
•
visceral hyperalgesia
•
psychopathology
INTERVENTIONS
‣
Weight
‣
Diet
‣
Bowel elimination pattern
Diet
‣ Initially, elimination diet
‣ Avoidance of sorbitol,
non-absorbable
carbohydrates, and
foods that contain
lactose or that are high
gas-forming
‣ Gradual increase in fiber
to prevent increased
intestinal gas production
‣ Increased fluid intake
(if constipation is
predominant)
‣ Avoidance of large
meals, fatty foods, and
caffeine, which can
exacerbate symptoms
‣ Small, frequent meals
‣ High-fiber diet
‣ Avoidance of alcohol,
artificial sweeteners,
and foods to which the
patient is intolerant
‣ Decreased dairy
EDUCATION
Because this patient is not
usually hospitalized
interventions focus on
teaching. Monitor:
‣
Bloating
‣ There is no cause or test for
IBS
‣ Drink 8-10 glasses of water a
day
‣ Implement relaxation
‣
Need for colorectal cancer
screenings
Medications
Fiber supplements
Lactase
Probiotics
Peppermint oil
Tricyclic
Antidepressants
‣ Anticholinergics
‣
‣
‣
‣
‣
and frequency of stool
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MEDICAL SURGICAL NURSING: GASTROINTESTINAL 1.3.9
NURSE ANGIE 2018
Peptic Ulcer
An excavated lesion of the mucosal wall of the esophagus, stomach, or duodenum
Risks
Pathophysiology
‣ Type A blood (for gastric ulcer)
‣ Type O blood (for duodenal
ulcer)
‣ Gastric or duodenal mucosal
defects
‣ Exposure to irritants
‣ Cigarette smoking or use of
smokeless tobacco
‣ High stress
‣ Family history
‣ Psychogenic factors
‣ Use of certain medications
‣ Normal aging
Results when gastric mucosal defenses become impaired and
longer protect the epithelium from the effects of acid and
pepsin. H. pylori bacteria releases a toxin that promotes
mucosal inflammation and ulceration.
Assessment
‣ Weight changes: loss
with gastric ulcer, gain
wire duodenal ulcer
‣ GI bleeding
‣ Coffee ground emesis
‣ Melena
‣ Perforation
‣ Tender, rigid board
like abdomen
‣ Hypovolemic shock
‣ Epigastric pain that is
worse with eating
Complications
‣ GI hemorrhage
‣ Abdominal or intestinal
infarction
‣ Ulcer penetration into attached
structures
‣ Increased risk of gastric
adenocarcinoma (in patients
with H. pylori)
‣ Obstruction from scarring or
acute inflammation
‣ Bowel perforation
‣ Peritonitis
‣ Anemia
Labs & Diagnostics
‣ Low hemoglobin from bleeding
‣ Occult blood in stool
‣ Positive test for H. Pylori
‣ Endoscopy and Colonoscopy will show ulceration
CAUSES
H. pylori
Nonsteroidal antiinflammatory drug
(NSAID) or glucocorticoid
use
‣ Pathologic hypersecretory
states (rare)
‣ Genetics
‣
‣
INTERVENTIONS
EDUCATION
‣ Monitor vitals
‣ Diet modifications
‣ Monitor I & O
‣ Avoid NSAIDS
‣ Monitor bowel sounds
‣ Smoking cessation
Treatment
‣ Histamine h2
blockers: Famotidine
‣ Proton pump
inhibitors:
omeprazole
‣ Mucosal barrier
fortifers: sucralfate
Prostaglandin analogue:
misoprostol
‣ Diet : avoid dairy,
spices, caffeine, and ,
alcohol
‣ NPO: if GI bleed is
present
‣ Monitor stools for blood
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MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.2
OCTOBER 10, 2018
Jaundice
Yellow or green tinged sclera and skin caused by elevated bilirubin levels.
Pathophysiology
Assessment:
If the flow of bile is impeded or if there is excess destruction of red blood cells as a consequence of
liver disease or bile ducts obstruction causes an increase in serum bilirubin. When serum bilirubin
levels become abnormally elevated all of the tissues in the body will turn yellow or green.
Complications
‣
‣
‣
‣
Kernicterus
Cerebral palsy
Epilepsy
Mental impairment
‣ Hemolytic: Usually
asymptomatic.
‣ Hepatocellular: Mild
or severe illness, lack
of appetite, nausea,
malaise, fatigue,
weakness and weight
loss, headache, chills,
and fever if the cause
is infectious.
‣ Obstructive: Light
gray or clay colored
stool, intense itching,
dyspepsia, and
intolerance to fatty
foods.
Treatments:
Laboratory Findings:
EDUCATION
‣ Educate the client on
treatment regimen
‣ GGT elevation
‣ Increased serum bilirubin
‣ AST and ALT elevation
‣ Signs and symptoms of
jaundice
‣ Encourage proper diet
‣ Encourage your client to keep
u with appointments and lab
CAUSES
‣ Increased production
‣ Decreased hepatic uptake
‣ Decreased conjugation
‣ Dysfunction of hepatocytes
work
INTERVENTIONS
‣ Causes of jaundice
‣ Interventions are
associated with the cause
of the jaundice.
‣ Long term jaundice can
cause pigment stones,
brain stem injury, and CNS
dysfunction.
‣ Slowing of bile egress from
the liver
‣ Encourage smoking and
alcohol cessation if
appropriate.
‣ Obstruction of extra-hepatic
bile flow
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‣ Jaundice itself requires
no treatment in adults,
if itching becomes an
issue, the HCP may
prescribe
cholestyramine 2 to 8 g
po bid. However,
cholestyramine is
ineffective in patients
with complete biliary
obstruction.
Medical
Treatments
‣ Jaundice induced by
anemia may be
treated by taking iron
supplements or eating
more iron rich foods.
‣ Jaundice induced by
hepatitis requires
steroid or antiviral
medications.
‣ Jaundice caused by an
obstruction can be
surgically resolved by
removing the
obstruction.
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MEDICAL SURGICAL NURSING: HEPATIC 1.4.3
NURSE ANGIE 2018
Ascites
Albumin rich fluid build up in the abdomen of 25 mL or more, caused by portal hypertension resulting in
increased capillary pressure and obstruction of venous blood flow.
Pathophysiology
Assessment:
Portal hypertension leads to vasodilation, which causes a decrease in effective arterial blood volume. As the
disease progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma volume
expands. This causes overflow of albumin rich fluid into the peritoneal cavity.
‣ Swollen, rounded abdomen,
bulging flanks in he supine
position
‣ Striae
‣ Weight gain
‣ Shortness of breath
‣ Distended veins
‣ Umbilical hernia
‣ Electrolyte and fluid
imbalances hypovolemia
Treatments:
Laboratory Findings:
‣ Protein concentration under <250 cells/ uL
‣ High serum-to-ascites albumin concentration gradient
≥ 1.1 g/dL
CAUSES
‣ Vasodilation of splanchnic
circulation. Changes in the
ability to metabolize
aldosterone which increases
fluid retention.
‣ Decreased albumin
synthesis. Decreased serum
osmotic pressure.
‣ Movement of albumin into
the peritoneal cavity, causing
a decrease in circulating
protein. Pericarditis.
Endocrine disorder
INTERVENTIONS
‣
‣
‣
‣
‣
‣
‣
‣
EDUCATION
‣
Daily weights.
Strict intake and output
monitoring.
Daily abdominal girth
measurements.
Monitor respiratory status.
Monitor serum ammonia,
creatinine, and electrolyte levels.
Monitor client's response to
therapy.
Monitor for signs of
encephalopathy. When potassium is
decreased ammonia is increased
causing encephalopathy.
‣
‣
‣
‣
‣
Educate the client on the plan of
treatment.
Avoid alcohol intake.
Importance of adhering to a low
sodium diet.
Take their medications as
ordered.
State the importance of daily
weights, more than 2kg a day is
too much loss.
Discuss the importance of
avoiding NSAIDS, cough
mixtures containing alcohol,
antibiotics or antacids that
contain salts.
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‣ Dietary restrictions: 2g
sodium per day restriction,
no salt substitutes because
they contain potassium and
ammonia.
‣ Bed rest: Semi fowlers.
‣ Diuretics: Spironolactone
to prevent potassium loss.
Lasix may be used
cautiously to avoid sodium
depletion.
‣ Paracentesis: removal of
excess abdominal fluid
under sterile conditions.
Can take up to 4 L of fluid
a day.have the client void
prior to procedure, obtain
baseline vitals, labs, weight
and abdominal girth.
Monitor for shock,
bleeding, hematuria. Send
Fluid to the lab. Apply
sterile dressing and
monitor vitals.
‣ Transjugular Intrahepatic
Portosystemic Shunt:
Cannula is threaded into
the portal vein to reduce
portal HTN.
‣ Administer salt poor
albumin.
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MEDICAL SURGICAL NURSING: CARDIOVASCULAR 1.2.2
OCTOBER 10, 2018
Cirrhosis
Chronic, slowly progressive, fibrotic liver disease.
Pathophysiology
Assessment
A chronic and progressive disease characterized by degeneration of hepatocytes. This destruction
then causes the liver to become fibrosed causing destruction of
liver lobules, leading to other complications.
Complications
Ascites
Muscle wasting
Coagulopathy
Portal hypertension
Bleeding esophageal
varices
‣ Hepatic encephalopathy
Hepatorenal syndrome
‣ Hepatocellular carcinoma
‣ Hepatic failure
Death
‣
‣
‣
‣
‣
Risk Factors
‣
‣
‣
‣
‣
Laboratory Findings:
‣
‣
‣
‣
‣
‣
‣
‣
‣
Albumin: Decreases
Serum AST, ALT, GGT: Increase
Serum cholinesterase: Decrease
Bilirubin: Increases
Prothrombin time: Prolonged
Ultrasound: Measures scar tissue.
CT, MRI: Give info about liver size and blood flow.
Liver biopsy: Confirms diagnosis
ABG: May reveal a ventilation perfusion imbalance and hypoxia.
Alcoholism
Toxins
Biliary obstruction
Hepatitis
Metabolic disorders
Heart failure
CAUSES
‣Excess alcohol consumption
INTERVENTIONS
‣Cellular necrosis
‣ Identify precipitating factors
‣Nutritional deficits
‣ Promote alcohol cessation. Improve
nutritional status, high calories, low
sodium.
‣Portal issues
‣ Frequent position changes. Prevent
falls and trauma. Daily weights.
‣Hepatotoxic medications
EDUCATION
‣ Low in sodium, and
‣ Low saturated fat, trans fat and
cholesterol.
‣ The client should read labels to
identify heart-healthy foods.
‣Hepatitis
‣Biliary obstruction.
‣ Vitamin supplements
‣ Monitor for infection, bleeding, and
fluid volume.
‣Bile stasis
‣Right sided heart failure
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‣ Organs: Liver
‣
‣
‣
‣
enlargement, portal
obstruction, firm enlarged
liver, splenomegaly.
GI/GU: Ascites, GI
varices, flatulent dyspepsia,
abdominal pain, ascites,
weight loss, gonadal
atrophy. steatorrhea.
Cardio: Portal obstruction,
anemia, clubbing,
hypotension, bleeding due
to decrease in Vitamin K.
CNS: Mental deterioration.
Misc: Vitamin ABD
deficits, intermittent fever,
red palms, jaundice, muscle
wasting, rash, itchiness,
sparse body hair, white
nails.
Medical Treatments:
‣ Antacids & H2 antagonists:
To relieve gastric distress.
‣ Vitamins: KADE to
promote healing of the
liver.
‣ Potassium sparing
diuretics: To decrease
ascites.
‣ Colchicine, angiotensin
system inhibitors, statins,
diuretics including
spironolactone (Aldactone),
immunosuppressants, and
glitazones such as
pioglitazone (Actos) or
rosiglitazone (Avandia):
Possess antifibrotic
properties for the treatment
of cirrhosis.
‣Milk thistle: Also is known
to be an anti-inflammatory
to treat jaundice and other
symptoms of hepatitis.
‣Ursodeoxycholic Acid:
Used to treat primary
biliary cirrhosis.
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MEDICAL SURGICAL NURSING: HEPATIC 1.4.4
NURSE ANGIE 2018
Esophageal varices
Varicosities in the esophagus caused by increased pressure from the portal vein.
Pathophysiology
Assessment:History
Esophageal varices develop when normal blood flow to the liver is blocked in the state of scar
tissue, cirrhosis, or a clot in the liver. Obstruction of portal venous flow results in increased portal
vein pressure. High pressure in the portal vein causes blood to be diverted into the smaller fragile
veins of the esophagus as well as the stomach and rectum. Increased pressure in the smaller veins
causes them to distend. Distended veins may rupture, which can cause life-threatening hemorrhage.
Complications
‣ Variceal hemorrhage
(may be fatal)
‣ Hypovolemic shock
‣ Encephalopathy
‣ Infection, sepsis
‣ Esophageal stricture
after surgery or
endoscopic therapy
‣ Aspiration pneumonia
‣ Acute kidney injury
‣ Acute or chronic liver
failure
‣ Hepatitis B surface antibodies
test and hepatitis C antibodies
test results may determine the
cause of liver disease.
Laboratory Findings:
‣ Complete blood count (CBC) with differential may reveal anemia,
leukopenia, and thrombocytopenia.
‣ Prothrombin time and partial thromboplastin time may be prolonged
because of liver failure.
‣ Liver function test shows mild elevation in aspartate aminotransferase and
alanine aminotransferase, which may occur because of cirrhosis.
‣ Blood urea nitrogen level test and creatinine level (serum) may be elevated.
CAUSES
‣ Cirrhosis
‣ Heart failure
‣ Blood clots such as portal vein
thromboses
‣ Sarcoidosis
‣ Schistosomiasis
‣ Wilson disease
‣ Hemochromatosis
‣ Weakness, tiredness, and
general malaise
‣ Anorexia
‣ Nausea and vomiting
‣ Hematemesis
‣ Weight loss
‣ Abdominal pain
‣ Jaundice or dark-colored
urine
‣ Ascites
‣ Pruritus
‣ Spontaneous bleeding
and easy bruising
‣ Muscle cramps
‣ Melena
Physical Findings
‣
‣
‣
‣
‣
‣
‣
‣
Pallor
Hypotension
Tachycardia
Dyspnea
Jaundice
Ascites
Palmar erythema
Spider nevi—clusters of
tiny vessels on the skin
resembling a spider
Treatments:
‣ Treat for shock
‣ Administer electrolytes
‣ Vasopressin
‣ Somatostatin and
octreotide
‣ Nitroglycerin with
INTERVENTIONS
‣ Elevate the head of the bed
‣ Monitor for orthostatic
hypotension.
‣ Monitor vitals and lung sounds.
‣ Administer O2 and IV liquids.
‣ Monitor hemoglobin, hematocrit
EDUCATION
‣ Educate patent to avoid
strenuous activities.
‣
vasopressin
‣ Beta-blockers
‣ Sengstaken-blackmore
tube
‣ Sclerotherapy
‣ Ligation
and coagulation factors.
‣ Gastric suctions.
‣ Start vitamin K therapy to
promote clotting.
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MEDICAL SURGICAL NURSING: HEPATIC 1.4.5
NURSE ANGIE 2018
Hepatic encephalopathy
A life threatening complication of liver disease that occurs in severe liver failure.
Pathophysiology
Assessment
Hepatic insufficiency may result in encephalopathy due to a diseased liver that is unable to detoxify toxic by
products of metabolism. Porto systemic shunting where collateral vessels are developed as a result of portal
‣
‣
‣
hypertension allows toxic substances extracted from the liver into the systemic circulation. Ammonia is
considered the main factor in the development of hepatic encephalopathy. Ammonia enters the brain and
excites benzodiazepine receptors causing CNS depression; which produce the sleep and behavior patterns
noted in hepatic encephalopathy. Ammonia from digestion of dietary and blood proteins in the GI tract.
‣
‣
‣
Increases in ammonia from these sources can cause GI bleeding (including varices).
‣
Complications
‣ Aspiration pneumonia
‣ Hepatorenal syndrome
‣ Irreversible coma
Cardiovascular collapse
‣ Cerebral edema
‣ Brain herniation
Death
Laboratory Findings:
‣ Serum ammonia level test results are elevated and, together with
characteristic clinical features, strongly suggest hepatic encephalopathy.
‣ Serum bilirubin level test results are elevated.
‣ Prothrombin time is prolonged.
‣ Serum electrolyte levels may reveal hypokalemia, altered calcium levels,
or hypomagnesemia.
‣ Chronic liver damage
‣ Suspected accumulation of
neurotoxic substances in the
brain due to inability of liver to
break down toxins
‣ Blockage of blood supply to the
liver
‣ Hepatitis B infection
(uncommon)
Treatments:
‣ Aimed at eliminating
precipitating causes and
minimizing potential
complications.
‣ Lactulose reduces serum
ammonia by trapping and
expelling it in feces. 2-3
soft stools a day is
indicative the lactulose is
having a therapeutic
effect.
‣ IV Glucose minimize
protein breakdown.
‣ Vitamins to correct
deficits and electrolyte
imbalances.
Incidence
INTERVENTIONS
CAUSES
‣
Mental status changes
Confusion
Sleepiness during the
day
May lapse into a coma
or have seizures
EEG changes
Asterixis “liver flap”
usually seen in stage 2
encephalopathy.
Hyperactive DTR’s in
early stages, flaccidity
in late stages.
Fetor hepaticus
EDUCATION
‣
‣
‣
‣
‣
Assess neuro status frequently
Keep a daily log of mental status
I&O, daily weights, and vitals q4.
Evaluate potential site of infection
Monitor serum ammonia,
electrolytes, and fluids.
‣ Discontinue sedatives, analgesics,
and tranquilizers. Reduce
ammonia levels by GI suctions,
enema, or antibiotics.
‣
‣
Educate on diet restrictions
Educate in medication
regimen
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‣ Hepatic
encephalopathy can occur
at any age.
‣ It occurs overtly in 30%
to 45% of patients
with cirrhosis; it will
develop to some degree in
up to 80% of patients
with cirrhosis.
‣ It is present in nearly half
of patients requiring liver
transplantation.
‣ It occurs in 24% to 50%
of patients with
transjugular intrahepatic
portosystemic shunts.
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MEDICAL SURGICAL NURSING: HEPATIC 1.4.5
NURSE ANGIE 2018
Hepatitis
An inflamation of the liver aused by drugs, alcohol use or a virus.
Pathophysiology
Assessment
There are three hepatitis viruses and they cause similar liver damage. The inflammation process is
initiated throughout the entire liver, and hepatocytes are destroyed by cytotoxic cytokines and
natural killer cells, both parts of the inflammation process. Cellular necrosis takes place. If
inflammation affects the periportal areas, cholestasis, or the interruption of the flow of bile takes
place. The liver is usually able to repair itself and regain complete function if no other
complications occur.
CAUSES/TYPES
‣ A: Infectious hepatitis
transmission is fecal oral route.
‣ Poor sanitation
‣ Person to person
Laboratory Findings:
‣ Water
‣ Food
‣ ALT: Elevated into the thousands. Normal 10- 40 U/L.
‣ AST: Elevated into the thousands. Normal 10-30 U/L.
‣ Ammonia : Elevated. May lead to encephalopathy. Normal
10 mcg/dl.
‣ Total Bilirubin levels: Elevated in serum urine. Normal is
lower than 1.5mg/dl.
Preicteric : No jaundice
yet, the patient will have flu
like symptoms.
‣ Malaise
‣ Fatigue
‣ Nausea, vomiting,
diarrhea
‣ Headache
‣ Muscle aches
‣ Polyartritis
‣ Elevated serum bilirubin
and enzyme levels
Icteric: Jaundice is present.
‣ Puritis
‣ Dark, tea colored urine
‣ Clay colored stools
‣ Decrease in pre-icteric
symptoms
‣ Posticteric: Increased
energy.
‣ Pain goes away
‣ Lessened GI symptoms
‣ Serum bilirubin and
enzyme levels return to
normal
‣ Possible contact with anal or
oral sex
‣ B/C: Hepatitis B virus transmitted
via blood.
‣ Sex
‣ Mother baby
Medical Treatment
‣ Hep B: Alpha interferon,
lamivudine (epivir),
adenovir, bed rest,
nutritional support, Hep B
‣ IV drug use
INTERVENTIONS
‣ Management usually
occurs at home.
‣ Help the patient cope with
fatigue.
‣ Have the patient contact
the HCP if symptoms
worsen..
EDUCATION
‣ Eat small frequent meals,
high in
‣ carbs, low in fats and avoid
animal fats.
‣ Do not donate blood.
‣ Avoid close personal contact
until results are negative.
‣ Alcohol cessation.
‣ Rest , increase activity
gradually.
‣ Blood work.
immune globulin, Hep B
‣ C: hepatitis C virus
vaccine. Do not give the
‣ Transmitted via blood
Hep B IG and vaccine in
‣ Blood transfusion
‣ Sex
‣ Drug paraphernalia
‣ D: Only those whom have
contacted
the same injection or the
same site.
‣ Hep C: Interferon,
Ribavirin, restrict animal
protein.
‣ Hep B are at risk.
‣ E: Hepatitis E. Transmitted via
fecal oral route.
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MEDICAL SURGICAL NURSING: HEPATIC 1.4.2
NURSE ANGIE 2018
Portal Hypertension
When the portal venous system is obstructed or stenosed it causes a rise in portal pressure
causing portal hypertension.
Assessment:
Pathophysiology
Obstruction of portal blood flow, such as cirrhosis or portal vein thrombosis. In liver cirrhosis,
increased intrahepatic vascular resistance to the portal flow elevates portal pressure and leads to
portal hypertension.
Complications
‣
‣
‣
‣
GI Bleeding
Varices rupture
Ascites
Hepatic Encephalopathy
‣ Varices
‣ Ascites
‣ Thrombocytopenia:
early indicator of
liver dysfunction
‣ Splenomegaly
Treatments:
‣ Endoscopic
therapy
‣ Esophageal
balloon
‣ Nonselective
beta-blockers
Laboratory Findings:
‣ CBC: Low platelets
‣ Hemoccult: yield GI bleeding
‣ H&H: Low
INTERVENTIONS
‣ Elevate the head of the bed to
minimize SOB.
‣ Restrict sodium intake.
‣ Administer diuretics.
‣ Monitor intake and output.
‣ Weigh the client daily.
‣ Monitor LOC.
‣ Administer blood products if
indicated.
‣ Monitor prothrombin time and
coagulation studies.
‣ Administer Vitamin K if
indicated.
‣ Administer lactulose if indicated.
‣ Avoid opioids, sedatives, and
barbituates.
EDUCATION
CAUSES
‣ Blood clots in the portal vein.
‣ Blockage of the veins that carry
blood from the liver to the heart.
‣ Focal nodular hyperplasia
usually seen in HIV.
‣ Parasitic infection,
schistosomiasis.
‣ Educate the client on the
importance of alcohol
cessation.
‣ Educate on medication
regimen
‣ Educate on dietary
restrictions
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‣
‣
‣
‣
Medical
Treatment
Surgery
Radiology
Dietary changes
Endoscopic
therapy
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