m 5.

Blurred or double vision

CEREBRAL ANEURYSM 6. Loss of consciousness
 Cerebral aneurysm, also known as 7. Seizures
intracranial or brain aneurysm, refers to a 8. Focal neurological deficits (e.g.,
weakened area in the wall of a cerebral weakness, numbness)
artery, resulting in a localized, abnormal
dilation or ballooning of the blood vessel. MEDICAL MANAGEMENT:
This dilation poses a risk of rupture, leading
to potentially life-threatening intracranial 1. Diagnostic Imaging: CT angiography,
hemorrhage. magnetic resonance angiography
(MRA), or cerebral angiography to
RISK FACTORS: visualize the aneurysm.
1. Family history of cerebral aneurysms
2. Hypertension 2. Monitoring and Observation:
3. Smoking Continuous neurological assessments
4. Excessive alcohol consumption and vital signs monitoring.
5. Age (more common in individuals over
40) SURGICAL INTERVENTIONS:
6. Female gender  Clipping: Surgically occluding the
7. Connective tissue disorders (e.g., aneurysm with a metallic clip to prevent
Ehlers-Danlos syndrome, Marfan rupture.
syndrome)  Coiling: Endovascular procedure
8. Polycystic kidney disease involving the insertion of detachable
9. Cocaine or amphetamine abuse coils into the aneurysm to induce
thrombosis and occlusion.
PATHOPHYSIOLOGY:
Due to hemodynamic stress, genetic MEDICATIONS:
predisposition, or underlying vascular 1. Nimodipine (Brand Name: Nimotop):
abnormalities, chronic hypertension and Calcium channel blocker used to
atherosclerosis prevent and treat cerebral vasospasm
↓ following subarachnoid hemorrhage.
to the weakening of arterial walls. 2. Esmolol (Brand Name: Brevibloc):
↓ Beta-blocker administered to control
Arterial bifurcations or berry aneurysm, blood pressure and heart rate, reducing
characterized by a bulging sac-like structure. the risk of aneurysm rupture during
↓ acute hypertensive episodes.
Progressive thinning of the vessel wall and
degenerative changes further increase the risk NURSING DIAGNOSIS:
of rupture. 1. Risk for Impaired Tissue Perfusion
↓ related to cerebral artery compromise
When an aneurysm ruptures, blood spills into secondary to aneurysm formation.
the surrounding brain tissue, leading to 2. Anxiety related to the diagnosis of
intracranial hemorrhage and subsequent cerebral aneurysm and potential
neurological deficits. complications.

SIGNS AND SYMPTOMS: ESSENTIAL NURSING INTERVENTIONS:

1. Sudden, severe headache (often 1. Neurological Monitoring: Regular
described as "the worst headache of my assessment of Glasgow Coma Scale
life") (GCS), pupillary response, motor
2. Nausea and vomiting strength, and sensory function.
3. Stiff neck 2. Blood Pressure Management: Maintain
4. Photophobia (sensitivity to light) systolic blood pressure within the
 prescribed range to prevent aneurysm permeability, bleeding, and organ
rupture. dysfunction.
3. Pain Management: Administer
analgesics as ordered and provide Signs and Symptoms:
comfort measures to alleviate headache ● High Fever: Sudden onset of high fever.
and discomfort. ● Severe Headache: Intense pain behind
4. Emotional Support: Offer psychological the eyes.
support and education to the patient and ● Pain Behind the Eyes and Joints:
family regarding the condition, treatment Severe joint and muscle pain.
options, and potential outcomes.
● Fatigue: Overwhelming tiredness.
5. Seizure Precautions: Implement seizure
● Nausea and Vomiting: Often
precautions to prevent injury in patients
accompanied by abdominal pain.
at risk of seizures.
6. Prevention of Complications: Monitor for ● Bleeding: Manifestations may include
signs of vasospasm, infection, or other nosebleeds, gum bleeding, or easy
complications postoperatively and bruising.
intervene promptly. ● Plasma Leakage: Fluid accumulation
7. Health Promotion: Educate the patient leading to organ dysfunction and shock.
on lifestyle modifications, including
smoking cessation, blood pressure Diagnostics:
control, and stress reduction techniques, ● Clinical Evaluation: Based on the
to minimize the risk of aneurysm characteristic symptoms and travel
recurrence or rupture. history to dengue-endemic regions.
● Laboratory Tests:
○ Polymerase Chain Reaction
DENGUE HEMORRHAGIC FEVER (PCR): Detects viral RNA.
Description: Dengue Hemorrhagic Fever is a ○ Dengue Serology: Detects
severe form of dengue virus infection
antibodies against the virus.
characterized by bleeding, plasma leakage, and
○ Complete Blood Count (CBC):
organ impairment. It is caused by the dengue
Monitoring platelet count and
virus, transmitted primarily by Aedes
mosquitoes. hematocrit levels.

Etiology: Pharma:
● The dengue virus is transmitted to ● There is no specific antiviral treatment
humans through the bites of infected for dengue. Management is primarily
Aedes mosquitoes, primarily Aedes supportive. Pain relievers
aegypti and Aedes albopictus. (acetaminophen) are used to control
fever and alleviate pain. Nonsteroidal
Pathophysiology: anti-inflammatory drugs (NSAIDs) and
● Dengue virus has four serotypes aspirin should be avoided, as they can
(DENV-1, DENV-2, DENV-3, and increase the risk of bleeding.
DENV-4). Infection with one serotype
confers lifelong immunity to that specific Med. Mgt.:
serotype, but subsequent infections with ● Fluid Replacement: Intravenous fluids
a different serotype increase the risk of are administered to maintain hydration
severe disease. The pathophysiology and manage plasma leakage.
involves a complex interplay of viral ● Blood Component Transfusion: In
factors, immune response, and vascular severe cases with significant bleeding,
changes, leading to increased vascular platelet or blood transfusions may be
required.
 ● Pain Management: Analgesics for pain  The Ebola virus is believed to originate
relief. from fruit bats of the Pteropodidae
family, which are natural hosts of the
Nursing Interventions: virus.
● Fluid Monitoring: Regular assessment of
fluid balance and signs of dehydration.
● Vital Sign Monitoring: Frequent
monitoring of vital signs, especially
blood pressure and pulse. PATHOPHYSIOLOGY:
● Bleeding Precautions: Monitoring for Immune System
 Dendritic Cells activates the immune
signs of bleeding and implementing
system by sending message to other
precautions to prevent injuries.
WBC namely killer T cells, Helper T
● Pain Management: Administering pain
Cells, and B cells, to fight against
medications and providing comfort
pathogens.
measures.
● Patient Education: Educating patients Direct Contact of Bodily Fluids of infected person
and families about the importance of ↓
fluid intake, signs of worsening Ebola Virus enters primarily the dendritic cells
symptoms, and seeking prompt medical ↓
attention. Invades the cell’s DNA replication systems to
create more copy of the virus
(2-21 days)
EBOLA VIRUS ↓
 Ebola Virus Disease (EVD), also known as Apoptosis of cell due to overloading
Ebola hemorrhagic fever, is a severe, often ↓
fatal illness affecting humans and other Virus are then exposed to surrounding tissues
primates. The disease was first identified in and attacks other immune system cells
1976 during simultaneous outbreaks in ↓ ↓
Nzara, South Sudan, and Yambuku, Manipulates the Manipulates the vessels
Democratic Republic of Congo (DRC). Premature WBC to open to release fluid
To kill itself to the body
CAUSATIVE AGENT: The Ebola virus belongs ↓ ↓
to the family Filoviridae, genus Ebolavirus. There Decrease WBC Internal Bleeding
are five known species of Ebola virus, four of ↓ ↓
which cause disease in humans: Zaire Cytokine Storm Hemorrhage and Shock
ebolavirus (EBOV), Sudan ebolavirus (SUDV), ↓
Tai Forest ebolavirus (TAFV), and Bundibugyo Multiple Organ Failure and Death
ebolavirus (BDBV).
SIGNS AND SYMPTOMS:
MODE OF TRANSMISSION:  Fever
 Direct contact of bodily fluids  Severe headache
 Muscle pain
INCUBATION PERIOD:  Weakness
 2 to 21 days, with the average being 8 to  Fatigue
10 days. During this time, individuals  Sore throat
infected with the virus may not show any  Vomiting
symptoms.  Diarrhea
 Rash
POINT OF ORIGIN:
 Impaired kidney and liver function
  Internal and external bleeding (in Ebola virus disease can cause fear and
advanced stages) anxiety.
6. Education: Educate patients and caregivers
DIAGNOSTIC TESTS: about the mode of transmission, preventive
1. Reverse transcription-polymerase measures, and the importance of seeking
chain reaction (RT-PCR) assay medical care promptly.
 detect viral RNA in blood or 7. Environmental Cleaning: Ensure thorough
other bodily fluids disinfection of surfaces and medical
2. Antigen-capture enzyme-linked equipment to prevent the spread of the
immunosorbent assay (ELISA) virus within healthcare facilities.
 IgM and IgG antibodies
detection

MEDICAL MANAGEMENT: There is no specific GULLAIN BARRE SYNDROME.

antiviral treatment for Ebola virus disease.
 Galing Baba Symmetrical
 Acute ascending symmetrical Paralysis
Supportive Care
due to demyelination
 Fluid and electrolyte management
 Due to recent GI infection, J&J Covid Vac.
 Management of complications such as  Recovery is possible
bleeding and shock o Nerve cell bodies, axons, a Schwann
 Pain management cell are not destroyed unlike in MS
 Treatment of secondary infections o Only Demyelination
 Experimental therapies such as
monoclonal antibodies or antiviral drugs  Men & women both affected
under investigation  Idiopathic

NURSING DIAGNOSES:
1. Risk for Infection related to exposure to PATHOPHYSIOLOGY
Ebola virus and compromised immune
response. Immune cells → Schwann Cells← Immune cells
↓
2. Fluid Volume Deficit related to fever,
Demyelinating Disease of PNS
vomiting, diarrhea, and hemorrhage.
↓
Damages Cranial & Spinal Nerves.
ESSENTIAL NURSING MANAGEMENT: ↓
1. Infection Control: Strict adherence to Damages Neurons
personal protective equipment (PPE) ↓
protocols, hand hygiene, and isolation Communication Breakdown
precautions to prevent transmission.
2. Monitoring Vital Signs: Regular assessment S/Sx: Sensory, Motor, ANS Problems
of temperature, blood pressure, pulse, and
respiratory rate to detect early signs of
deterioration. SIGNS & SYMPTOMS
3. Fluid and Electrolyte Management: Monitor 1. Clumsiness (INITIAL SIGN)
2. Decrease DTR
intake and output, assess for signs of
3. Paresthesia
dehydration, and administer intravenous 4. Difficulty Breathing
fluids as prescribed. 5. Dysphagia
4. Symptom Management: Provide comfort 6. ANS
measures such as pain relief, antiemetics  Alternating APN to Hypotension
for nausea and vomiting, and oral hygiene. head to arrhythmia
5. Psychosocial Support: Offer emotional  Urinary Incontinence
support to patients and their families, as  Constipation
 ● Hepatitis A virus
DIAGNOSTIC TEST
1. CSF Analysis - Lia lumbar puncture RISK FACTOR
 Increase CHON but (N) WBC  Poor sanitation
 Flat on Bed post op  Hepatitis A outbreak
 prevent spinal headache  You live with someone who has hepatitis
 You recently had sexual contact with
MANAGEMENT someone who has hepatitis A
1. Maintain patent airway & adequate vent by:
 Assist in MV PATHOPHYSIOLOGY
 Monitor pulmonary function test
2. Monitor VS, I&O, neuro check, ECG Tracing
due to Arrhythmia
3. Maintain side rail
4. Prevent complications of inmobilit
5. Assist in passive Rom exercise
6. NGT feeding
a. Assist in plasmapheresis

PHARMACOLOGIC MANAGEMENT
a. Corticosteroids -suppress immune response
 prednisone
 dexamethasone
b. Immunoglobulins
 fight GBS antibodies HEPATITIS A
 widespread liver inflammation that
c. Anti-Arrhythmic Agents results in degeneration and necrosis of
 Amiodarone liver cells
 Lidocaine / Xylocaine  Hepatitis in its various forms is
 Bretylium preventable and treatable but not
necessarily curable
NURSING DIAGNOSIS  Although self-limiting, approximately
1. Ineffective Breathing Pattern related 20% of acute hepatitis B cases progress
to ascending paralysis
2. Risk for aspiration related to ETIOLOGY
esophageal muscle  caused by the viral infection hepatitis B
weakness/paralysis virus
 spread when blood, semen, or other
body fluids from a
HEPATITIS INFECCTION  person infected with the virus enters the
body of someone who is not infected
HEPATITIS A
 Mainly toddlers, adolescents and young RISK FACTOR
adults)  sexual contact, especially with multiple
 Hepatitis A is caused by a virus that partners
infects liver cells and causes  sharing needles
inflammation. The inflammation can  syringes or other drug-injection
affect how your liver works and cause equipment
other symptoms of hepatitis A.  mother to baby at birth
 The virus spreads when infected stool,
even just tiny amounts, enters the mouth PATHOPHYSIOLOGY
of another person (fecal-oral HEPATITIS B
transmission). ↓
Blood is exposed to Hepatitis B Virus (HBV)
ETIOLOGY ↓
 Body sends cytotoxic T cells and natural killer o Rationale: Many people with
cells to the virus and hepatitis A feel tired and sick
release inflammatory cytokines (body’s immune and have less energy.
response)  Get adequate food and liquid.
↓ o Rationale: Eat a balanced
Hepatocytes appear to have a “ground glass” healthy diet. Nausea can make
look due to the it difficult to eat. Try snacking
HBsAg infiltrating the cell’s cytoplasm throughout the day rather than
↓ eating full meals. To get enough
Hepatocytes are continually proliferating calories, eat more high-calorie
↓ foods. For instance, drink fruit
Virus is constantly being shed into the blood juice or milk rather than water.
↓  Drinking plenty of fluids is important to
chronic infection prevent dehydration, especially if
vomiting or diarrhea occurs.
CLINICAL FINDINGS  Avoid alcohol and use medications with
SUBJECTIVE care.
 Unusual tiredness and weakness o Rationale: Your liver may have
 Sudden nausea and vomiting and difficulty processing medications
diarrhea and alcohol. If you have
 Abdominal pain or discomfort, especially hepatitis, don't drink alcohol. It
on the upper right side beneath your can cause liver damage.
lower ribs, which is over your liver  Avoid sexual activity.
 Loss of appetite o Rationale: Avoid all sexual
 Joint pain activity if you have hepatitis A.
 Intense itching Many kinds of sexual activity
OBJECTIVE can spread the infection to your
 Clay- or gray-colored stool partner. Condoms don't offer
 Dark urine adequate protection.
 Yellowing of the skin and the whites of  Don't prepare food for others while
your eyes (jaundice) you're actively infected. You can easily
 Low-grade fever pass the infection to others.

DIAGNOSTIC PROCEDURE MEDICAL MANAGEMENT

● Blood Tests: Measure levels of liver  Antiemetics: metoclopramide (Reglan),
enzymes, antibodies, and viral antigens. trimethobenzamide (Tigan)
● Imaging Studies: Ultrasound, CT scan, o Given 1/2 hr before meals, may
or MRI to visualize the liver. reduce nausea and increase
food tolerance.
● Liver Biopsy: A sample of liver tissue
Prochlorperazine (Compazine)
may be collected for examination is contraindicated In hepatic
disease.
NURSING DIAGNOSIS  Antacids: Mylanta, Titralac
 Imbalanced Nutrition: Less Than Body o Counteracts gastric acidity,
Requirements as evidenced by loss of reducing gastric irritation and
appetite, nausea and vomiting risk of bleeding.
 Risk for deficient fluid volume
 Vitamins: B complex, C, other dietary
 Fatigue
supplements as indicated
 Risk for infection
 Corrects deficiencies and aids in the
healing process.
INTERVENTION
NURSING MANAGEMENT
GOAL
 Have an adequate Rest.
 Demonstrate progressive weight gain
toward goal with normalization of
laboratory values and no signs of
 malnutrition b) Western Blot test –used as confirmatory test
for HIV,. also detects HIV antibodies
c) Nucleic Acid Test or the Polymerase Chain
HIV/AIDS Reaction –detection of the virus (HIV)

RISK FACTORS NURSING DIAGNOSIS

● Sexual transmission 1. Imbalanced Nutrition: Less than Body
● Injecting drug use Requirements r/t decrease oral intake
● Mother to child transmission 2. Risk for infection r/t immunodeficiency
● Transmission of contaminated blood 3. Ineffective airway clearance r/t PCP,
increased bronchial secretions,
PATHOPHYSIOLOGY decreased ability to cough
Sexual Intercourse
↓ NURSING GOAL
HIV attacks immune system The client will be able to improve airway
↓ clearance, nutritional status, minimize
CD4+ cells and molecules get affected development of new infections
↓
HIV enters T-cells nucleus NURSING INTERVENTIONS
↓ ● Promote skin integrity. Patients are
Transcription and translating of new HIV encouraged to avoid scratching; to use
happens nonabrasive, nondrying soaps and apply
↓ nonperfumed moisturizers; to perform regular
RS strain of HIV gets into macrophages, oral care; and to clean the perianal area after
dendritic cells, & T-cells each bowel movement with nonabrasive soap
↓ and water.
Viral Infection increases and T-cells decreases ● Promote usual bowel patterns. The nurse
↓ should monitor for frequency and consistency of
AIDS stools and the patient’s reports of abdominal
pain or cramping.
SIGNS AND SYMPTOMS ● Prevent infection. The patient and the
Flu-like symptoms (headache, muscle ache, caregivers should monitor for signs of infection
fatigue, swollen lymph nodes, nausea and and laboratory test results that indicate infection.
vomiting, sore throat, diarrhea, fever, rashes) ● Improve activity intolerance. Assist the patient
in planning daily routines that maintain a balance
AIDS: CD4 T-cells falls below 200 between activity and rest.
● Being tired all of the time ● Maintain thought processes. Family and
● Swollen lymph nodes in your neck or groin support network members are instructed to
● Fever that lasts for more than 10 days speak to the patient in simple, clear language
● Night sweats and give the patient sufficient time to respond to
● Unexplained weight loss questions.
● Purplish spots on your skin that don't go away ● Improve airway clearance. Coughing, deep
● Shortness of breath breathing, postural drainage, percussion and
● Severe, long-lasting diarrhea vibration is provided for as often as every 2
● Yeast infections in your mouth, throat, or hours to prevent stasis of secretions and to
vagina promote airway clearance.
● Bruises or bleeding you can't explain ● Relieve pain and discomfort. Use of soft
cushions and foam pads may increase comfort
DIAGNOSTIC TESTS as well as administration of NSAIDS and
a) Enzyme Linked Immunosorbent Assay – opioids.
detects HIV antibodies in the blood, once ● Improve nutritional status. The patient is
positive a confirmatory test is ordered . encouraged to eat foods that are easy to
swallow and to avoid rough, spicy, and sticky DOB SOB Death
food items. Crackles Wheezing
Productive High Fever
MEDICAL MANAGEMENT cough
No known cure/ or vaccine for HIV/AIDS ↑ ↑ ↑
Anti-retroviral Signs and Symptoms

MERS-CoV DIAGNOSTICS:
● Polymerase Chain Reaction (PCR):
Description: MERS-CoV is a viral respiratory Detects the presence of MERS-CoV
illness caused by the Middle East Respiratory genetic material in respiratory samples.
Syndrome Coronavirus. It was first identified in ● Serology: Blood tests to detect
Saudi Arabia in 2012. MERS-CoV belongs to the antibodies against the virus.
same family of viruses as Severe Acute
Respiratory Syndrome Coronavirus (SARS-CoV)
and more recently, SARS-CoV-2, which causes
COVID-19.
MEDICAL MANAGEMENT
Etiology: ● Supportive Care: Management of
● MERS-CoV is zoonotic, meaning it is symptoms, including oxygen therapy
transmitted from animals to humans. and mechanical ventilation in severe
The exact source of the virus is believed cases.
to be dromedary camels. Human-to- ● Isolation: Infected individuals should be
human transmission occurs, primarily in isolated to prevent the spread of the
healthcare settings and close household virus.
contacts. ● Infection Control Measures: Strict
infection prevention measures in
Pathophysiology:
healthcare settings.
Direct Contact/Droplets
● Fluid and Electrolyte Management: To
↓
maintain hydration and address any
Virus enters the Eye, nose, mouth
↓ imbalances.
Lines and settles on respiratory tract
↓ NURSING INTERVENTIONS:
Attacks the ACE receptor cells ● Isolation Precautions: Implementing
↓ measures to prevent the spread of the
Invades the cell’s DNA replication to create more virus in healthcare settings.
copy of the virus ● Respiratory Monitoring: Frequent
(2-14 days) assessment of respiratory status and
↓ prompt intervention for respiratory
Apoptosis of cells distress.
↓ ● Hygiene Practices: Emphasizing hand
Release of virus to surrounding tissue hygiene and proper use of personal
↓ protective equipment.
Virus attacks more cells in the Respiratory Tract ● Emotional Support: Providing emotional
↓ ↓ ↓
support to patients and their families.
Increase Capillary Increase Lung
● Education: Educating individuals about
Permeability Inflammation Collapse
the importance of seeking medical care
↓ ↓ ↓
Increase Mucus Constriction Respiratory promptly and following infection control
Production of airway depression measures.
NURSING DIAGNOSIS
1. Ineffective airway clearance related to
increase mucus secretion RHEUMATOID ARTHRITIS
2. Infection related to failure to avoid - Arthritis due to immune system attacking the
pathogen s/c to exposure to virus synovium

RISK FACTORS:
● Family History
● Environmental influence such as diet or
geographic location, nulliparity
● Affects women more than women
● Occurs at any age 20-60 yrs
Modifiable factors:
● Smoking
● Obesity

PATHOPHYSIOLOGY
Autoimmune reaction
↓
Inflammation in the synovium (synovitis)
↓
Invasion of white blood cells
↓
Breaks down collagen, causing edema,
proliferation of the synovial membrane
↓
Formation of Pannus - layer of fibrous tissues
↓
Destroys cartilage and erodes bone
↓
Loss of articular surfaces and joint motion
↓
Muscle fibers undergo degenerative changes
↓
Loss of function of tendon and ligament elasticity
and contractile power

SIGNS AND SYMPTOMS

Seven S’s
● Sunrise stiffness gretater than 30 mins
● Soft, tender, warm joint
● Swellling in joint
● Symmetrical
● Synovium Inflamed
● Systemic
● Stages- synovitis, pannus, ankylosis

NURSING DIAGNOSIS
⮚ Acute pain related to the inflammatory
process as evidenced by swollen joints
⮚ Impaired physical mobility related to joint ⮚ Monitor the patient for any adverse drug
stiffness as evidenced by limitation or lack of reaction and administer the right doses of anti-
function due to pain inflammatory and analgesic medication as per
⮚ Risk for ineffective role performance possibly doctor's order.
evidenced by fatigue ⮚ Refer the patient to a dietitian to have a meal
plan that includes increases in vitamins, protein
DIAGNOSTIC TEST and iron for tissue building and repair
1. Initial Physical Examination ⮚ Instruct the patient to have a rest after doing
2. X-ray of involved joints light exercise to prevent straining their muscles
3. Radionuclide scans and to have a good body posture when using
4. Direct Arthroscopy assistive devices
5. Synovial membrane biopsy ⮚ Remind the patient and their family about the
6. CBC importance of the follow up health check ups
7. Erythrocyte sedimentation rate (ESR)
8. Immunoglobulin (Ig) (IgM and IgG) Test MEDICATIONS:
⮚ methotrexate (rheumatrex) non biologic
NURSING GOAL
immune suppression and affects DNA synthesis
After 3 days of nursing interventions the patient
⮚ Aspirin platelet aggregation inhibitors
will be able to incorporate relaxation skills and
diversional activities to control pain ⮚ choline trisalicylate (athropan, trilisate), anti-
inflammatory, analgesic, antipyretic
NURSING INTERVENTIONS ⮚ diclofenac (Voltron), ibuprofen (Motrin) - anti-
⮚ Demonstrate to the patient the use of pain inflammatory, analgesic, antipyretic, platelet
management techniques and provide a variety of aggregation inhibitors
comfort measures so they would not fully ⮚ hydroxychloroquine (plaquenil) – inihibits
depend on taking larger doses of pain lysosomal enzyme
medication.
⮚ Develop a plan based on the patient's
perceptions and priorities on how to establish RUBELLA (German Measles)
and achieve goals to meet self-care needs,
incorporating joint protection, and work RISK FACTORS
simplification concept 1) Lack of immunization against Rubella or
⮚ Note the patient's reports of pain, noting the immunosuppression; and
2) Exposure to an active case of rubella.
location and intensity using a pain scale as well
as nonverbal pain cues.. Educate the patient
PATHOPHYSIOLOGY
about preventive skin care measures to relieve
Measles virus enters mucosa
skin from itching and monitor skin status.
↓
⮚ Examine the patient's range of motion of the
Infect epithelial cells in the trachea or bronchi
affected joints and encourage the use of
↓
assistive ambulatory devices
H protein binds to a target receptor (CD46)
⮚ Help the patient recognize their weaknesses ↓
in self - care and the things that make it difficult F protein helps virus to enter cell
for them to engage in self-care activities. ↓
⮚ Encourage them to verbalize their concerns Translated into viral proteins
and provide them all the information they wanted ↓
to know. Spreads through local tissue
⮚ Inform the patient's family to give their ↓
emotional support and to help the patient in Picked up by dendritic cells and alveolar
doing some physical activity to prevent further macrophages
incidents. ↓
Carry virus to the lungs and local lymph nodes
 ↓ 9. The occurrence of complications must also be
Continuous to spread prevented
S/Sx 10. Encourage increased fluid intake
 Low grade fever MEDICAL MANAGEMENT
 Headache Administration of live attenuated vaccine (MMR)
 Malaise
 Mild coryza
 Conjunctivitis SEPTIC SHOCK
 Post-auricular, sub-occipital, and  is a life-threatening condition
posterior cervical lymphadenopathy (the characterized by systemic inflammation
presence of these swollen lymph nodes and widespread tissue damage resulting
distinguishes rubella from rubeola from an overwhelming immune
measles) from which occurs on the 3rd response to infection. It represents the
to the 5th days after onset most severe form of sepsis, a condition
 Forscheimer’s spot – pinkish rash in soft where the body's response to infection
palate causes organ dysfunction.

DIAGNOSTIC TESTS PATHOPHYSIOLOGY:

 Serological test for antibodies  Infection: Septic shock typically begins
with an infection, often bacterial, although it
 Mothers: Rubella antibody titer
can also be caused by fungi or viruses. The
infection triggers an immune response,
NURSING DIAGNOSIS
leading to the release of inflammatory
1. Hyperthermia r/t to infectious agents
cytokines.
2. Impaired social interaction r/t isolation
from friends  Systemic Inflammation: In response to the
3. Impaired skin integrity r/t presence of infection, the body's immune system
pruritus activates inflammatory pathways, resulting
in the release of pro-inflammatory cytokines
GOAL such as interleukin-1 (IL-1), interleukin-6
The patient will be able to have: (IL-6), and tumor necrosis factor-alpha
- Skin will stay clean, dry and intact. (TNF-alpha).
- Mucous membranes will stay moist, discomfort  Vasodilation: The inflammatory response
will stay within defined tolerable range by causes vasodilation, leading to a decrease
patient. in systemic vascular resistance and blood
- Patient will understand purpose of isolation, pressure. This results in poor tissue
cooperate and be free of distress. perfusion and impaired oxygen delivery to
organs and tissues.
INTERVENTIONS  Microvascular Dysfunction: Endothelial
1. The patient should be isolated dysfunction and damage occur, leading to
2. The patient should be advised to rest in bed increased capillary permeability and
until fever subsides leakage of fluid into the interstitial space.
3. The patient’s room must be darkened to avoid This contributes to tissue edema and organ
photophobia dysfunction.
4. The patient must take a mild liquid but  Organ Dysfunction: Inadequate tissue
nourishing diet. perfusion and oxygenation lead to multi-
5. The patient’s eyes should be irrigated with organ dysfunction, including acute
warm normal saline to relieve irritation respiratory distress syndrome (ARDS),
6. The ears must be taken care of. Do not apply acute kidney injury (AKI), hepatic
heat or cold compress unless ordered dysfunction, and coagulopathy.
7. Good ventilation is necessary
8. The spread of infection must be prevented CAUSES
  Bacterial, fungal, viral, parasitic drainage of abscesses, debridement of
infections infected tissue).

SIGNS AND SYMPTOMS: SURGICAL MANAGEMENT:

 Hypotension (systolic blood pressure Surgical intervention may be necessary to
<90 mmHg or a decrease of ≥40 mmHg address the source of infection and prevent
from baseline) further spread. This may include:
 Altered mental status  Drainage of abscesses or infected fluid
 Tachycardia collections
 Rapid, shallow breathing  Debridement of necrotic tissue
 Cool, clammy skin  Removal of infected implants or devices
 Decreased urine output  Repair of perforated viscera
 Lactic acidosis
 DIC NURSING DIAGNOSES:
 Signs of organ dysfunction (e.g., 1. Decreased Cardiac Output related to
confusion, oliguria, jaundice) decreased systemic vascular resistance
and hypotension.
DIAGNOSTIC TESTS: 2. Ineffective Tissue Perfusion related to
1. Blood cultures to identify the causative impaired oxygen delivery and multi-
organism organ dysfunction.
2. Complete blood count (CBC) to assess
for leukocytosis or leukopenia ESSENTIAL NURSING MANAGEMENT:
3. Serum lactate levels to evaluate tissue 1. Frequent Assessment: Regular
perfusion monitoring of vital signs, urine output,
4. Arterial blood gas (ABG) analysis to mental status, and laboratory values to
assess for metabolic acidosis detect changes in condition.
5. Imaging studies (e.g., chest X-ray, 2. Fluid Management: Monitor fluid
ultrasound) to identify the source of balance closely and administer
infection or assess for complications intravenous fluids as prescribed, while
being cautious to avoid fluid overload.
MEDICAL MANAGEMENT: 3. Vasopressor Support: Monitor the
1. Antimicrobial Therapy: Prompt initiation patient's response to vasopressor
of broad-spectrum antibiotics to target therapy, assess for complications such
the suspected or identified pathogen. as extravasation, and ensure proper line
2. Fluid Resuscitation: Aggressive fluid placement.
resuscitation with crystalloids (e.g., 4. Patient Positioning: Position the patient
isotonic saline, lactated Ringer's to optimize respiratory function and
solution) to restore intravascular volume prevent complications such as pressure
and improve tissue perfusion. ulcers and venous stasis.
3. Vasopressor Therapy: Administration of 5. Infection Control: Adhere to strict hand
vasopressor medications (e.g., hygiene and isolation precautions to
norepinephrine, dopamine) to increase prevent the spread of infection.
systemic vascular resistance and 6. Nutritional Support: Ensure adequate
maintain blood pressure. nutrition and hydration to support the
4. Corticosteroids: In some cases, body's metabolic needs and promote
corticosteroids may be used to modulate healing.
the inflammatory response. 7. Emotional Support: Provide emotional
5. Source Control: Identification and support to the patient and their family,
treatment of the source of infection as septic shock can be a frightening and
through surgical intervention (e.g., stressful experience.
8. Education: Educate the patient and
family about the condition, treatment
 plan, and signs of complications to
promote understanding and participation SIGNS AND SYMPTOMS
in care. ● Redness and Dryness of the eyes
● Sores or ulcers in the mouth
● Affects the brain, causing fatigue, memory
SYSTEMIC LUPUS ERYTHEMATOSUS loss, psychosis, seizures, and fevers
⮚ Affects multiple organs notably often causes ● Photosensitivity
reddening of the skin ● Skin rashes - butterfly rash, discoid rash
Autoimmune condition that causes inflammation. ● Alopecia
Body systems affected: Joints, ● Heart failure
Skin, Lungs, Heart, Kidneys, Brain, and Blood ● Chest pain/ pericarditis
system ● Heart murmurs
● Infections such as pneumonia
ETIOLOGY ● Lupus nephritis
● Genetic Predisposition ● Protein in urine
● Environmental Factors ● Retain fluid
● Susceptibility to certain viruses ● Hypertension
● Autoimmune/Idiopathic ● Renal Failure
● Risk of infections
RISK FACTORS ● Blood clots
● Hormonal abnormality ● Antiphospholipid syndrome
● UV radiation ● Swollen, painful joint
● Drug exposure ● Muscle aches & pains
● Low birth weight ● Raynaud’s Syndrome
● Preterm birth ● Blood clotting during pregnancy
● Exposure to farming pesticides
DIAGNOSIS
PATHOPHYSIOLOGY  4 or more criteria met: of the S/Sx
Apoptosis  Blood Test:
↓ o (+) antinuclear antibody
Formation of blebs o (+) Anti-smith
↓  Targets the
Apoptotic cells are not cleared efficiently by ribonucleoprotiens
macrophages o (+) Anti-dsDNA
↓  Targets the Double-
Cell material exposed to immune system stranded DNA
↓
Immune system forms Anti-nuclear antibodies NURSING DIAGNOSIS
↓ ● Acute pain related to inflammation
Attacks the nuclear antigens ● Impaired skin integrity related to chronic
↓ inflammation
It will lead to Immune complex ● Disturbed body image related to presence of chronic
↓ condition
Flow around the body and it can go collect in the
body systems GOAL OF CARE
↓ ● After 24 hours of nursing interventions, the client will
Activation of complement cascade report that the symptoms have been alleviated or
↓ reduced to a minimum level of discomfort
Inflammation
↓
Damage in any body systems
  The incubation period for tetanus
NURSING INTERVENTION typically ranges from 3 to 21 days, with
1. Assess the client’s description of pain and impact an average of 7 to 10 days. However, it
on ADLs can vary depending on factors such as
2. Teach the patient gentle ROM exercises the location and severity of the wound.
3. Assess for the signs of joint inflammation
4. Assess previous measures used to alleviate pain PATHOPHYSIOLOGY:
5. Encourage the use of ambulation aids when pain is GABA
related to weight-bearing ↓
6. Remind the client to avoid prolonged periods Binds to GABA Receptors
of inactivity ↓
7. Encourage the client to take a 15 minutes Allows the Negatively Chloride Ions to
warm shower or bath on arising enter the neurons
8. Encourage the use of non-pharmacological ↓
measures of pain control such as relaxation, Inhibits Neuron Transmission
distraction, or guided imagery ↓
9. Monitor for elevated BUN &Creatinine Decrease Response to Stimuli
10. Assess for proteinuria ↓
11. Measure UO Sedative Effect
12. Daily weights  Entry and Germination: Clostridium
13. Medication administration tetani spores enter the body through a
14. Educate the patient about the disease wound or injury. In anaerobic conditions,
the spores germinate and release
MEDICATIONS tetanospasmin toxin.
● NSAIDs as prescribed  Toxin Spread: Tetanospasmin toxin
● Hydroxychloroquine travels via retrograde axonal transport to
● Steroids the central nervous system (CNS),
specifically targeting inhibitory
interneurons in the spinal cord and
brainstem.
TETANUS (LOCK JAW)  Inhibition of Inhibitory
 Tetanus, also known as lockjaw, is a Neurotransmission: Tetanospasmin
serious bacterial infection caused by the inhibits the release of inhibitory
bacterium Clostridium tetani. It affects the neurotransmitters such as gamma-
nervous system and causes muscle aminobutyric acid (GABA) and glycine,
stiffness and spasms, often leading to life- which normally regulate muscle
threatening complications. contraction. This leads to uncontrolled
muscle contractions and spasms
CAUSATIVE AGENT: characteristic of tetanus.
 Clostridium tetani, a spore-forming
bacterium commonly found in soil, dust, SIGNS AND SYMPTOMS:
and animal feces. The bacterium 1. Muscle stiffness and spasms, often
produces a potent neurotoxin called starting in the jaw (lockjaw) and neck
tetanospasmin, which is responsible for muscles
the characteristic symptoms of tetanus. 2. Difficulty swallowing (dysphagia)
MODE OF TRANSMISSION: 3. Stiffness and rigidity of the abdominal
Common sources of infection include muscles (abdominal rigidity)
puncture wounds, burns, animal bites, 4. Painful muscle contractions, especially
and surgical or injection sites in the neck, back, and abdomen
contaminated with soil or feces. 5. Increased heart rate (tachycardia)
INCUBATION PERIOD: 6. Fever and sweating
7. Elevated blood pressure (hypertension)
 8. Spasms of respiratory muscles, 2. Risk for Aspiration related to dysphagia
potentially leading to respiratory failure and difficulty swallowing.

DIAGNOSTIC TESTS: ESSENTIAL NURSING MANAGEMENT:

 Clinical evaluation of symptoms and 1. Neurological Assessment: Regular
history of wound exposure assessment of muscle tone, strength,
 Laboratory tests to identify C. tetani and neurological status to monitor for
bacteria or tetanospasmin toxin in changes in symptoms.
wound samples 2. Pain Management: Administering
 Electromyography (EMG) to assess analgesics as prescribed to alleviate
muscle activity and confirm diagnosis muscle pain and discomfort.
 Imaging studies (e.g., MRI) to evaluate 3. Respiratory Support: Monitoring
for signs of CNS involvement respiratory status, providing
supplemental oxygen, and assisting with
MEDICAL MANAGEMENT: ventilation if necessary to prevent
 Wound Care: Thorough cleaning and respiratory compromise.
debridement of wounds to remove tetanus 4. Oral Care: Providing frequent oral care
spores and prevent further toxin production. and monitoring for signs of difficulty
 Tetanus Toxoid Vaccination: Administration swallowing or aspiration.
of tetanus toxoid vaccine to boost immunity 5. Positioning: Positioning the patient to
and prevent future infections. minimize muscle spasms and promote
comfort and respiratory function.
 Tetanus Immune Globulin (TIG):
6. Education: Educating patients and
Administration of TIG for passive immunity
caregivers about wound care, signs and
in individuals with high-risk wounds or
symptoms of complications, and the
incomplete immunization.
importance of completing the tetanus
 Muscle Relaxants: Medications such as
vaccination series.
benzodiazepines or baclofen to control
7. Psychosocial Support: Providing
muscle spasms and rigidity.
emotional support to patients and
 Antibiotics: Antibiotic therapy (e.g.,
families coping with the stress and
metronidazole, penicillin) to eradicate C.
uncertainty of tetanus infection.
tetani bacteria and prevent further toxin
production.
 Supportive Care: Monitoring and
management of complications such as
respiratory failure, autonomic dysfunction,
and cardiac abnormalities.

SURGICAL MANAGEMENT:
1. Wound Debridement: Surgical removal
of necrotic tissue and foreign material
from the wound to prevent ongoing toxin
production.
2. Tracheostomy: Surgical creation of a
tracheostomy tube to maintain airway
patency in cases of severe respiratory
muscle spasms or respiratory failure.

NURSING DIAGNOSES:
1. Impaired Physical Mobility related to
muscle stiffness and spasms.