Med Surg

NSG 338: Exam 4
Chapter 35: Assessment of Immune Function

Immunity: the body’s specific protective response to a foreign agent or organism;
resistance to disease, specifically infectious disease.
Anatomy
■ epitope: any component of an antigen molecule that functions as an
antigenic determinant by permitting the attachment of certain antibodies
■ antigenic determinant: the specific area of an antigen that binds with an
antibody combining site and determines the specificity of the antigenantibody reaction

The immune systems is composed of

bone marrow, lymphoid tissue, and RBCs

WBCs involved in immunity are primarily
produced in the:

bone marrow

T lymphocytes, descendents of stem cells, mature
in the:

Thymus

Granulocytes, which fight invasion by releasing
histamine, do not include:

Lymphocytes

The leukocytes that arrive 1st at a site of
inflammation are:

neutrophils

WBCs that function as phagocytes are:

monocytes

The body’s first line of defense is:

phagocytic immune response

The primary cells responsible for recognition of
foreign antigens are:

lymphocytes

Antibodies are believed to be a type of

protein

A deficient immune system response that is
congenital in origin would be classified as a ____
disorder.

natural deficiency

During what stage of an immune response do
lymphocytes interfere with diseases by picking up
specific antigens from organisms to alter their
function?

proliferation

NSG 338: Exam 4
Table 35-1 Immune System Disorders
■ Autoimmunity: normal protective immune response paradoxically turns
again or attacks the body, leading to tissue damage
■ Hypersensitivity: body produces inappropriate or exaggerated responses to
specific antigens.
■ Gammopathies: Overproduction of immunoglobulins.
■ Immune deficiencies Primary: deficiency results from improper
development of immune cells or tissues; usually congenital or inherited.
■ Secondary: deficiency results from some interference with an already
developed immune system; usually acquired later in life.
Function of the Immune System
■ The basic function is to remove foreign antigens
■

Natural Immunity
■ non-specific
■ provides a broad spectrum of defense
■ considered the first line of defense

What does cellular membrane damage result from? activation of complement, arrival of killer T cells,
and attraction of macrophages
How do effector T cells destroy foreign
organisms?

4 ways that disorders of the immune system occur

by altering the antigens cell membrane, causing
cell lysis, and producing lymphokines, which
destroy invading organims
1.
2.
3.
4.

natural vs acquired (active and passive) immunity

excesses or deficiencies of
immunocompetent cells
alterations in cellular functioning
immunologic attack on self antigens
inappropriate or exaggerated responses to
specific antigens

NATURAL=nonspecific, present at birth.
ACQUIRED=more specific, develops thru out life.
-active: defenses developed by self
-passive temporary protection transmitted from
another source that has developed immunity thru
previous disease or immunization.

NSG 338: Exam 4
1.
2.
1.

What is a complement?
How is it formed?
How does it function?

circulating plasma proteins that are made in the
liver and activated when an antibody couples with
an antigen.
Defends the body against bacterial IxN, bridges
natural and acquired immunity, and disposes of
immune complexes and byproducts associated
with inflammation.

How do biological response modifiers (BRMs)
affect the immune response?

suppress antibody production and cellular
immunity

What age related changes affect immunological
function?

(Table 35-4)

What effects do adrenal corticosteroids,
antimetabolites, and antibiotics have on the
immune system?

(Table 35-5)

IgA

-protects against resp. infections
-prevents absorption of antigens from food

IgD

possible influence on B-lymphocyte differentiation

IgE

helps defend against parasites

IgG

-enhances phagocytosis
-activates complement system

IgM

appears in intravascular serum

cyclosporine

leukopenia, T cell inhibition

dactinomycin

agranulocytosis, neutropenia

indomethacin

agranulocytosis, leukopenia

methotrexate

leukopenia, aplastic bone marrow

mustargen

agranulocytosis, neutropenia

propylthiouracil

agranulocytosis, leukopenia

vancomycin

transient leukopenia

NSG 338: Exam 4
REVIEW:
- what does the first line of defense, or the PHAGOCYTIC IMMUNE RESPONSE,
involve?
• primarily the WBCs (granulocytes and macrophages), which have the ability to
ingest foreign particles and destroy invading agent; eosinophils are only weakly
phagocytic. Phagocytes also remove the body’s own dying or dead cells. dying cells
in necrotic tissue release substances that trigger inflammatory response.
- What is the 2nd protective response, or the HUMORAL IMMUNE RESPONSE?
- What is the 3rd mechanism of defense, or the CELLULAR IMMUNE RESPONSE?

■ Chapter 36: Care of the Patient with Immunodeficiency Disorders
■ Managing an Intravenous Immunoglobulin Infusion

Primary Immunodeficiency
genetic in origin

Secondary Immunodeficiency
result from external factors such as infection

result from intrinsic defects in the cells of the
immune system

■ Immunodeficiency Disorders
■ caused by: defect in or a deficiency of phagocytic cells, B/T lymphocytes,
or the complement system
■ cardinal symptoms: chronic or recurrent and severe infections, infections
caused by unusual organisms that are normal body flora, poor response to
standard Tx of infections, and chronic diarrhea
■ susceptible to a variety of 2ndary disorders (autoimmune disease and
lymphoreticular malignancy)

NSG 338: Exam 4
■ MOST COMMON CAUSE WORLDWIDE=severe malnutrition
■ Primary Immunodeficiency
■ Genetic
■ Predispose people to 3 conditions: infections, cancer, and
autoimmunity
■ Male to female 5-1
■ 5 common PIDs: humoral immunity, T cell defects, combined B- and
T cell defects, phagocytic disorders, complement production
■ May affect phagocytic function, B cells or T cells, or the
complement system
■ Usually seen in infants and young children
■ common primary immunodeficiencies:
■ Manifestations: vary according to type, severe or recurrent
infections, failure to thrive or poor growth, positive family history
■ Potential complications: recurrent, severe, potentially fatal
infections; related blood dyscrasias or malignancies
■ Treatment: varies by type; treatment of infection, pooled plasma or
immunoglobulin, granulocyte colony stimulator, thymus graft, stem
cell or bone marrow transplant
■ Warning Signs of Primary Immune Deficiency

i.

Immune Component
Phagocytic cells

i.

Disorder

Hyperimmunoglobu
linemia (E
syndrome)

Major Symptoms

Treatment
i.

antibiotics and
treatment for viral
and fungal
infections
ii. granulocytemacrophage colonystimulating factor
iii. granulocyte colony
stimulating factor

NSG 338: Exam 4
B lymphocytes

i.

Sex-linked
agammaglobulinem
ia (Brutons)
ii. Common Variable
Immunodeficiencyhypogammaglobuli
nemia (CVID)
iii. IgA deficiency
iv. IgC2 deficiency

i.

T lymphocytes

i.

Thymic hypoplasia
(DiGeorge
syndrome)
ii. Chronic
mucocutaneous
candidiasis

i. Thymus graft
ii. Antifungal Agents:

B/T lymphocytes

i.

i.

Complement system

Ataxiatelangiectasia
ii. Nezelof’s syndrome
iii. Wiskott-Aldrich
syndrome
iv. Severe combined
Immunodeficiency
disease (SCID)

-passive pooled
plasma or gammaglobulin
ii. IVIG,
Metronidazole
(Flagyl), Quinacrine
HCL (Atabrine),
Vitamin B12,
Antimicrobial
therapy
iii. none
iv. pooled
immunoglobulin

Antimicrobial
therapy;
management of
presenting s/s; fetal
thymus transplant;
IVIG

ii.

i.

Angioneurotic
edema
ii. Paroxysmal
nocturnal
hemoglobinuria

■ Phagocytic Dysfunction
■ affect the natural (innate) immunity
■ neutrophils cannot reach site->abnormal inflammatory response
■ CHARACTERIZED BY DISEASE-SPECIFIC IXNs (chronic
granulomatous disease)
■ Manifestations:

NSG 338: Exam 4

■
■
■

■

■ increased increased fungal (candida), bacterial, and viral (herpes
simplex/zoster) infections
■ recurrent bacterial ixns of the skin and lungs; abnormalities of the
connective tissue, skeleton, vascular system, and dentition; and
elevated levels of IgE!
■ severe neutropenia (AT RISK FOR-developing severe infections)
■ accompanied by mouth ulcers, gingivitis, stomatitis, and
cellulitis
Chronic granulomatous disease is resistant to aggressive treatment with
antibiotics
DIAGNOSIS: hx, s/s, and NITRO-BLUE TETRAZOLIUM REDUCTASE
TEST (shows self destruction of phagocytic cells)
WARNING SIGN!!
■ 4 or more new ear ixns within 1 year
■ 2 or more serious sinus IxNs within 1 year
■ 2 or more months on antibiotics with little effect
■ two or more pneumonias within 1 year
■ failure of an infant to gain weight or grow normally
■ recurrent, deep skin or organ abscesses
■ persistent thrush in mouth or fungal infection on skin
■ need for IV antibiotics to clear infections
■ two or more deep-seated infections including septicemia
■ a family hx of PI
TREATMENT FOR PRIMARY PHAGOCYTIC D/O: IV immunoglobulin
(IVIG)

■ B Cell Deficiencies
■ The 2 typles of inherited B cell deficiencies result from lack of
differentiation of B cells into:
■ MATURE B CELLS & PLASMA CELLS
■ X linked agammaglobulinemia (Bruton’s disease)
■ a complete absence of antibody production
■ B cells and IgG, -M, -A, -D, and -E are low or absent in peripheral
blood
■ infants suffer early with severe IXNs
■ males at high risk if has an affected MALE relative
■ USUALLY BECOME SYMPTOMATIC AFTER THE NATURAL
LOSS OF MATERNALLY TRANSMITTED IMMUNOGLOBULINS,
WHICH OCCURS AT ABOUT 5-6 MONTHS OLD. (RECURRENT
PYOGENIC INFECTIONS USUALLY OCCUR)
■ autosomal agammaglobulinemia=transient form of antibody
deficiency (IgG levels rise eventually)

NSG 338: Exam 4
■ [S/S]:
■ DX marked by deficiency or complete absence of all serum
immunoglobulins
■ Hypogammaglobulinemia
■ B cells do not differentiate into plasma cells
■ diminished antibody production
■ CVID:
■ most common in adults (either gender)
■ normal B cell lymphocytes (cells are diverse and immature)lack ability to become memory B cells and mature plasma
cells
■ MORE THAN 50% OF CVID PATIENTS develop
PERNICIOUS ANEMIA (if s/s of pernicious anemia are
displayed-h&h levels are assessed)
■ T-cell deficiencies
■ lead to opportunistic IXN
■ genetic
■ DIGEORGE SYNDROME-THYMIC HYPOPLASIA:
■ (only ID d/o) manifests IMMEDIATELY after birth
■ CHRONIC MUCOCUTANEOUS CANDIDIASIS:
■ rare
■ autosomal recessive
■ affects both genders
■ leads to endocrine dysfunction
■ B- and T-cell deficiency
■ Deficiencies of the complement system
■ Secondary Immunodeficiency
■ Acquired (natural is also affected)
■ known as ―immunocompromised hosts‖
■ ex: HIV which causes AIDS
■ Related to underlying disorders, diseases, toxic substances, or medications
■ also chronic stress, burns, uremia, diabetes, AI disorders, viruses
■ More common than primary immunodeficiencies
■ Occur as a result of underlying disease processes or treatment
■ Best-known secondary immunodeficiency is human immunodeficiency
virus (HIV)
■ Affect both natural and acquired immunity
■ Known as immunocompromised hosts

NSG 338: Exam 4
■ IMMUNE COMPONENTS OF IMMUNODEFICIENCY D/O
■ B lymphocytes→bruton’s disease
■ T lymphocytes→DiGeorge syndrome
■ Complement System→Angioneurotic edema
■ Phagocytic Cells→hyperimmunoglobulinemia E
■ Nursing Management for immunodeficiencies
■ Monitor for signs and symptoms of infections
■ Note symptoms of inflammatory response may be blunted
■ Monitor lab values
■ Promote good nutrition
■ Address anxiety, stress, and coping
■ Strategies to reduce risk of infection
■ Handwashing and strict aseptic technique
■ Patient protection and hygiene measures: skin care, promote normal
bowel and bladder function, pulmonary hygiene
■ Nursing Management
■ Chart 36-3 Assessing for infection
■ Hx of infections, frequency, kinds
■ Skin, respiratory, oral, gastro, genitourinary
■ Assess for subtle and unusual signs
■ Patient Teaching
■ Signs and symptoms of infection
■ Medication teaching
■ Prevention of infection
■ Handwashing
■ Avoid crowds and persons with infections
■ Hygiene and cleaning
■ Nutrition and diet
■ Lifestyle modifications to reduce risk
■ Follow-up care

■ Chapter 37: Care of the Patient with HIV Infection and AIDS
■ National HIV/AIDS Strategy
■ President Obama ( 2010)
■ Reduce number of people who become infected

NSG 338: Exam 4
■ Increase access to care; optimize outcomes
■ Reduce HIV related health disparities
■ What is HIV
■ HIV stands for human immunodeficiency virus. It is the virus that can lead
to acquired immunodeficiency syndrome, or AIDS. Unlike some other
viruses, the human body cannot get rid of HIV. That means that once you
have HIV, you have it for life.
■ Infectious disease
■ HIV belongs to a group of viruses known as:
■
■ Retroviruses; target cells with CD4 receptors
■ HIV → AIDS
■ HIV affects specific cells of the immune system, called CD4 cells, or T
cells. Over time, HIV can destroy so many of these cells that the body can’t
fight off infections and disease. When this happens, HIV infection leads to
AIDS.
■ Transmission of HIV
■ 2 MAJOR MEANS OF HIV TRANSMISSION ARE:
■
■
■ 5 TYPES OF BODY FLUIDS THAT CAN TRANSMIT HIV-1:
■
■
■
■
■
■ Transmitted by body fluids containing HIV or infected CD4 lymphocytes
■ Blood, seminal fluid, vaginal secretions, amniotic fluid, and breast
milk
■ Most prenatal infections occur during delivery
■ Casual contact does not cause transmission
■ Breaks in skin or mucosa increase risk
■ Prevention for Health Care Providers
■ Hand hygiene
■ Personal protective equipment (PPE)
■ Soiled patient care equipment handling
■ Environmental control

NSG 338: Exam 4
■
■
■
■

Textiles and laundry
Needles and other sharps
Patient resuscitation
safe sexual behaviors that nurses should educate patients on include:
■

■ Health Care Provider Treatment
■ Postexposure prophylaxis
■ Vaccination
■ Assessment and Diagnostic Findings
■ The standard new HIV testing method now used when info about HIV status
is needed STAT (ED, labor, and delivery) is:
■
■ HIV1/2 antigen antibody combination immunoassay ( 4th generation)
■ HIV1, HIV 2 differentiation assay
■ ( according to CDC this is more effective than the Western blot test)
■ CD4 & CD8 count
■ Viral load:
■ The goal of HIV treatment is to help move your viral load down to
undetectable levels. In general, your viral load will be declared
"undetectable" if it is under 40-75 copies in a sample of your blood
■ Stages of HIV Infection
■ Table 37-1
■ Once you have achieved a stage you can’t back down
■ Who Should be Tested?
■ Who is at Risk?
■ Gerontology Considerations
■ One quarter of people living with HIV are older than age 50 years.
■ Reasons
■ Unprotected intercourse
■ Do not consider themselves at risk
■ Social bias toward homosexuality
■ May use IV drugs
■ May have received HIV-infected blood before 1985
■ Reduction in immune system function

NSG 338: Exam 4
■ Treatment
■
■
■ ART or HAART Table 37-3 page 1007
■ Non-Adherence is a major problem
■ Common adverse effects
■ Hepatotoxicity
■ Nephrotoxicity
■ Osteopenia
■ Cardiovascular disease
■ Drug Resistance:
■ IRIS
■ Nursing Process: The Care of the Patient With HIV/AIDS—Diagnosis
■ Impaired skin integrity
■ Diarrhea
■ Risk for infection
■ Activity intolerance
■ Disturbed thought processes
■ Nursing Process: The Care of the Patient With HIV/AIDS—Assessment
■ Assess physical and psychosocial status
■ Identify potential risk factors: IV drug abuse, risky sexual practices
■ Immune system function
■ Nutritional status
■ Skin integrity
■ Respiratory status and neurologic status
■ Fluid and electrolyte balance
■ Knowledge level
■ Clinical Manifestations of HIV/AIDS: Respiratory
■ Pneumocystic carinii pneumonia (PCP):
■ Most common life-threatening infection
■ Initial symptoms may be nonspecific and may include nonproductive
cough, fever chills, dyspnea, and chest pain
■ If untreated, progresses to pulmonary impairment and respiratory
failure
■ Treatment: TMP-SMZ or pentamidine, prophylactic TMP-SMZ
■ Mycobacterium avium complex (MAC)
■ Tuberculosis
■ Clinical Manifestations of HIV/AIDS: GI
■ Oral candidiasis

NSG 338: Exam 4
■ a fungal infection present in nearly ALL patients with AIDS
■ May progress to esophagus and stomach
■ Treatment with Mycelex troches or nystatin, ketoconazole
■ Diarrhea related to HIV infection or enteric pathogens
■ Octreotide acetate for severe chronic diarrhea
■ Wasting syndrome
■ 10% weight loss and chronic diarrhea or chronic weakness and fever
with absence of other cause
■ Protein energy malnutrition
■ Anorexia, diarrhea, GI malabsorption, and lack of nutrition may
contribute
■ Manifestations of HIV/AIDS: Neurologic
■ Peripheral neuropathy
■ HIV encephalopathy
■ Progressive cognitive, behavioral, and motor decline
■ Probably directly related to the HIV infection
■ Cryptococcus neoformans
■ Progressive multifocal leukoencephalopathy
■ Other neurologic disorders
■ Depression
■ Clinical Manifestations of HIV/AIDS: Oncologic
■ Kaposi's sarcoma
■ Cutaneous lesions but may involve multiple organ systems
■ Lesions cause discomfort, disfigurement, ulceration, and potential
for infection
■ A recommended chemo agent for Kaposi’s sarcoma is:
■
■ B-cell lymphomas: the second most common malignancy with AIDS
■ Nursing Process: The Care of the Patient With HIV/AIDS—Planning
■ Goals may include
■ Achievement and maintenance of skin integrity
■ Resumption of usual bowel patterns
■ Absence of infection
■ Improved activity tolerance
■ Improved thought processes
■ Improved airway clearance
■ Increased comfort, improved nutritional status
■ Increased socialization
■ Expression of grief
■ Increased knowledge regarding disease prevention and self-care

NSG 338: Exam 4
■ Absence of complications
■ Nursing Process: The Care of the Patient With HIV/AIDS—Interventions: Skin
■ Frequent routine assessment of skin and mucosa
■ Encourage patient to maintain balance between rest and activity
■ Reposition at least every 2 hours and as needed
■ Pressure reduction devices
■ Instruct patient to avoid scratching
■ Use gentle, nondrying soaps or cleansers
■ Avoid adhesive tape
■ Perianal skin care
■ Nursing Process: The Care of the Patient With HIV/AIDS—Interventions: Bowels
■ Assess bowel pattern and factors that may exacerbate diarrhea
■ Avoid foods that act as bowel irritants, such as raw fruits and vegetables,
carbonated beverages, spicy foods, and foods of extreme temperatures
■ Small, frequent meals
■ Administer medications as prescribed
■ Assess and promote self-care strategies to control diarrhea
■ Nursing Process: The Care of the Patient With HIV/AIDS—Interventions:
Respiratory/ pain
■ Improving airway clearance
■ Position in semi-Fowler's or high Fowler’s position
■ Pulmonary therapy; coughing and deep breathing, postural drainage,
percussion, and vibration
■ Ensure adequate rest
■ Pain
■ Medications as prescribed
■ Skin and perianal care
■ Nursing Process: The Care of the Patient With HIV/AIDS—Interventions:
Nutrition
■ Monitor weight, I&O, dietary intake, and factors that interfere with nutrition
■ Dietary consult
■ Control of nausea with antiemetics
■ Oral hygiene
■ Treatment of oral discomfort
■ Dietary supplements
■ May require enteral feedings or parenteral nutrition
■ Nursing Process: The Care of the Patient With HIV/AIDS—Interventions:
Isolation

NSG 338: Exam 4
■
■
■
■
■
■

Promote an atmosphere of acceptance and understanding
Assess social interactions and monitor behaviors
Allow patient to express feelings
Address psychosocial issues
Provide information related to the spread of infection
Educate ancillary personnel, family, and partners

■ Nursing Process: The Care of the Patient With HIV/AIDS—Interventions:
Thoughts
■ Assess mental and neurologic status
■ Use clear, simple language if mental status is altered
■ Establish and maintain a daily routine
■ Orientation techniques
■ Ensure patient safety and protect from injury
■ Strategies to maintain and improve functional ability
■ Instruct and involve family in communication and care
■ Managing Potential Complications and Collaborative Care
■ Opportunistic infections
■ Respiratory failure
■ Cachexia and wasting
■ Medication side effects
■ Educate about self-care
■ Community support systems
■ Emotional and ethical concerns
■ Health Promotion
■ Chart 37-2
Chapter 38:Allergic Disorders

IgE Mediated

Non-IgE Mediated

NSG 338: Exam 4
■ Allergic Rhinitis
■ Hay fever, seasonal allergy
■ Allergic rhinitis more persistent than viral, seasonal
■ Early spring: tree pollen
■ Early summer: rose, grass pollen
■ Early fall: weed pollen ( ragweed)
■ Allergic Rhinitis Clinical Manifestations
■ Sneezing
■ Nasal congestion
■ Clear watery nasal discharge
■ Nasal, throat and soft palate itching
■ Clear throat, cough
■ Diagnosis
■ History
■ Physical
■ In particular resp
■ Nasal smears
■ Total serum IgE
■ RAST
■ Food elimination
■ Challenge
■ ↑ eosinophils
■ How would this make you feel
■ Atopic Dermatitis
■ Type I immediate hypersensitivity
■ Atopic eczema
■ Pruritus and hyperirritability of the skin
■ Can lead to asthma and allergic rhinitis
■ Chronic remissions and exacerbations
■ Treatment
■ Decreasing itching/scratching
■ Wear cotton fabrics
■ Mild detergent
■ Humidifying dry heat in winter
■ Room tem 68-72
■ Using antihistamines ( Benadryl)
■ Avoid: animals, dust, spray, perfume

NSG 338: Exam 4
■
■
■
■

Skin moisturized daily baths
Topical corticosteroids
Antibiotics for skin infections
Drugs called calcineurin inhibitors — such as tacrolimus (Protopic) and
pimecrolimus (Elidel) — affect your immune system. Applied to the skin,
they help maintain normal skin, control itching and reduce flares of atopic
dermatitis.

■ Medical Management
■ Avoidance
■ Air conditioners
■ Air cleaners
■ Humidifiers/ dehumidifiers
■ Removal of dust catching furniture, carpets,drapery
■ High efficiency particulate air filters and vacuum cleaner filter
■ Pharmacological Therapy
■ Antihistamine
■ H1 first generation sedating
■ Benadryl
■ H1 second generation non-sedating
■ Zyrtec, Allegra, Claritin
■ Can be combined with decongestant ( D)
■ Adverse effects
■ Antihistamine contraindicated
■ Third trimester
■ Narrow angle glaucoma
■ BPH
■ HTN
■ Don’t drink ETOH
■ Pharmacological Therapy
■ Mast Cell Stabilizer
■ Reduces release of histamine by stabilizing cell
■ Used prophylactically
■ Intranasal cromolyn (NasalCrom)
■ Intranasal Corticosteroids
■ Indicated for cases don’t respond to above meds
■ May take 2 weeks to work
■ Beconase, Rhinocort, Nasacort, Flonase
■ Systemic affects more likely with Rhinocort
■ Risk for infection
■ (patients with TB and lung infections should avoid)

NSG 338: Exam 4
■ Immunotherapy
■ Allergen desensitization
■ Administration of gradually increasing quantities of specific
allergens
■ Must continue therapy for several years
■ Patient must remain in office 30 min past injection
■ HCP must be prepared for anaphylaxis
■ Dermatitis Medicamentosa
■ Drug rash
■ Type 1 hypersensitivity
■ Appear suddenly
■ Vivid in color
■ Disappear when drug is removed
■ Patient teaching:
■
■ Food Allergy
■ IgE mediated food allergy
■ Genetic predisposition and exposure to allergens early in life
■ Common culprits
■ Seafood, legumes, seeds, tree nuts, berries, egg white, buckwheat,
milk and chocolate
■ Peanut and tree nut responsible for most severe food allergies
■ Pregnant and breast feeding mothers with family history of allergy should
avoid peanut butter, peanuts
■ Can be hidden within foods, combinations
■ Food allergy
■ Symptoms
■ Classic allergic symptoms
■ What are they??????
■ Diagnosis
■ Detailed allergy history
■ Physical exam
■ Skin testing
■ Treatment
■ Avoidance
■ Must carry epi-pen especially with nuts and seafood
■ May outgrow it
■ Nursing: important to indicated on records

NSG 338: Exam 4
■ Latex Allergy
■ Rhinitis, conjunctivitis, contact dermatitis, urticaria
■ Greatest risk
■ You, patients with atopic allergies, multiple surgeries, factories, food
handlers, hairdressers, automobile mechanics, police officer, patients
with spina bifida
■ Cross reactions to
■ Kiwis, bananas, pineapples, mangoes, passion fruit, avocados, and
chestnuts
■ Latex allergy
■ Cutaneous, percutaneous, mucosal, parenteral, or aerosol
■ More likely with mucous membrane and parenteral
■ Most common with cutaneous (wearing latex gloves)
■ Mucosal exposure from :Condom, catheters, airways and nipples
■ Powder in gloves can be inhaled
■ Parenteral: IV lines, dialysis
■ Manifestations
■ Table 38-6
■ Assessment
■ Physical, skin test
■ Management of Latex allergy
■ Avoidance
■ Epipen
■ Antihistamines
■ Medic alert
■ Carry own supply of gloves
■ Nursing
■ Assess all patient
■ Be alert to s/s
■ Instrumental in establishing a latex free environment
■ Allergy management
■ Chart 38-6
■ Chart 38-7
Chapter 39:
PEDS

NSG 338: Exam 4

FLUID AND ELECTROLYTES:
Chapter 13 (p. 237-51)
Fluid Volume Disturbances
Fluid Compartments
Hypovolemia
Don’t confuse with dehydration
◦ This is loss of water only
Occurs when loss of ECF is greater than intake of fluid
Causes
◦ Vomiting
◦ Diarrhea
◦ GI Suctioning
◦ Sweating
◦ Decreased intake
◦ Third space shift
◦ Hemorrhage
Hypovolemia Clinical Manifestations
Acute weight loss
↓ skin turgor
Oliguria, concentrated urine
↓ CVP and B/P, however ↑ pulse
Flattened neck veins
Dizziness, weakness
Thirst

NSG 338: Exam 4
Confusion
Hypovolemia: what labs look like
↑ H&H, serum and urine osmolality, specific gravity
↑ BUN and creatinine
Nursing Management
I&O
1 1lb represents fluid loss of 500ml
Assess for
◦ Rapid pulse
◦ Orthostatic hypotension
◦ Tongue turgor
◦ Tissue turgor
◦ Urine specific gravity should be 1.020
◦ delirium
Correcting Hypovolemia
Oral fluids first
Then isotonic fluids if necessary
Hypervolemia Clinical Manifestations
Acute weight gain
Peripheral edema
Ascites
DJV
Crackles
↑ CVP & BP
SOB
Contributing Factors
Heart failure
Renal failure
Cirrhosis
Excessive sodium intake ( oral, parenteral)
Hypervolemia: What diagnostics look like
↓ H&H
↓serum and urine osmolality
↓ urine sodium and specific gravity
CXR
Correcting Hypervolemia
Correcting underlying cause
Diuretics
◦ Thiazide
◦ Loop diuretics
● Hypokalemia
◦ Aldactone
● Hyperkalemia

NSG 338: Exam 4
◦ Hyponatremia
◦ Hypomagnesemia
◦
◦
Correcting Hypervolemia
Dialysis
Nutritional Therapy
◦ Foods low in sodium
◦ Avoid seasonings
◦ Watch out for salt substitutes
◦ Assess sodium in water in community
◦ Monitor protein ( why?)
Nursing Management
I&O
Weighed daily
Assess breath sounds
Degree of edema
◦ How do we do that?
Teach sodium restricted diet
Teach about OTC medications
Monitor parenteral fluid therapy
Administer appropriate medications
◦ you would expect to see
Nursing Management
Assess skin
◦ Why?
Position
How do we evaluate all of the above
Educating Patients About Edema
Teach s/s
Localized
Generalized
Treat cause
Restrict fluids and or sodium
Elevation of the extremities,
TED Hose
Dialysis

Hyponatremia
Serum sodium less than 135 mEq/L
Causes: adrenal insufficiency, water intoxication, SIADH or losses by vomiting,
diarrhea, sweating, diuretics

NSG 338: Exam 4
Manifestations: poor skin turgor, dry mucosa, headache, decreased salivation,
decreased blood pressure, nausea, abdominal cramping, neurologic changes
Medical management: water restriction, sodium replacement
Nursing management: assessment and prevention, dietary sodium and fluid intake,
identify and monitor at-risk patients, effects of medications (diuretics, lithium)
Hypernatremia
Serum sodium greater than 145 mEq/L
Causes: excess water loss, excess sodium administration, diabetes insipidus, heat
stroke, hypertonic IV solutions
Manifestations: thirst; elevated temperature; dry, swollen tongue; sticky mucosa;
neurologic symptoms; restlessness; weakness
Note: thirst may be impaired in elderly or the ill
Medical management: hypotonic electrolyte solution or D5W
Nursing management: assessment and prevention, assess for OTC sources of
sodium, offer and encourage fluids to meet patient needs, provide sufficient water
with tube feedings
Hypokalemia
Below-normal serum potassium (<3.5 mEq/L), may occur with normal potassium
levels with alkalosis due to shift of serum potassium into cells
Causes: GI losses, medications, alterations of acid–base balance, hyperaldosterism,
poor dietary intake
Manifestations: fatigue, anorexia, nausea, vomiting, dysrhythmias, muscle weakness
and cramps, paresthesias, glucose intolerance, decreased muscle strength, DTRs
Medical management: increased dietary potassium, potassium replacement, IV for
severe deficit
Nursing management: assessment, severe hypokalemia is life-threatening, monitor
ECG and ABGs, dietary potassium, nursing care related to IV potassium
administration
Hyperkalemia
Serum potassium greater than 5.0 mEq/L
Causes: usually treatment related, impaired renal function, hypoaldosteronism,
tissue trauma, acidosis
Manifestations: cardiac changes and dysrhythmias, muscle weakness with potential
respiratory impairment, paresthesias, anxiety, GI manifestations
Medical management: monitor ECG, limitation of dietary potassium, cationexchange resin (Kayexalate), IV sodium bicarbonate, IV calcium gluconate, regular
insulin and hypertonic dextrose IV, β-2 agonists, dialysis
Hyperkalemia (cont’d)
Nursing management: assessment of serum potassium levels, mix IVs containing K+
well, monitor medication affects, dietary potassium restriction/dietary teaching for
patients at risk
Hemolysis of blood specimen or drawing of blood above IV site may result in false
laboratory result

NSG 338: Exam 4
Salt substitutes, medications may contain potassium
Potassium-sparing diuretics may cause elevation of potassium
◦ Should not be used in patients with renal dysfunction
Hypocalcemia
Serum level less than 8.6 mg/dL, must be considered in conjunction with serum
albumin level
Causes: hypoparathyroidism, malabsorption, pancreatitis, alkalosis, massive
transfusion of citrated blood, renal failure, medications, other
Manifestations: tetany, circumoral numbness, paresthesias, hyperactive DTRs,
Trousseau’s sign, Chovstek's sign, seizures, respiratory symptoms of dyspnea and
laryngospasm, abnormal clotting, anxiety
Hypocalcemia (cont’d)
Medical management: IV of calcium gluconate, calcium and vitamin D
supplements; diet
Nursing management: assessment, severe hypocalcemia is life-threatening, weightbearing exercises to decrease bone calcium loss, patient teaching related to diet and
medications, and nursing care related to IV calcium administration
Trousseau’s Sign
Hypercalcemia
Serum level greater than10.2 mg/dL
Causes: malignancy and hyperparathyroidism, bone loss related to immobility
Manifestations: muscle weakness, incoordination, anorexia, constipation, nausea
and vomiting, abdominal and bone pain, polyuria, thirst, ECG changes,
dysrhythmias
Medical management: treat underlying cause, fluids, furosemide, phosphates,
calcitonin, biphosphonates
Nursing management: assessment, hypercalcemic crisis has high mortality,
encourage ambulation, fluids of 3 to 4 L/d, provide fluids containing sodium unless
contraindicated, fiber for constipation, ensure safety
Hypomagnesemia
Serum level less than 1.3 mg/dL, evaluate in conjunction with serum albumin
Causes: alcoholism, GI losses, enteral or parenteral feeding deficient in magnesium,
medications, rapid administration of citrated blood; contributing causes include
diabetic ketoacidosis, sepsis, burns, hypothermia
Manifestations: neuromuscular irritability, muscle weakness, tremors, athetoid
movements, ECG changes and dysrhythmias, alterations in mood and level of
consciousness
Medical management: diet, oral magnesium, magnesium sulfate IV
Hypomagnesemia (cont’d)
Nursing management: assessment, ensure safety, patient teaching related to diet,
medications, alcohol use, and nursing care related to IV magnesium sulfate
Hypomagnesemia often accompanied by hypocalcemia
◦ Need to monitor, treat potential hypocalcemia

NSG 338: Exam 4
Dysphasia common in magnesium-depleted patients
◦ Assess ability to swallow with water before administering food or medications
Hypermagnesemia
Serum level greater than 2.3 mg/dL
Causes: renal failure, diabetic ketoacidosis, excessive administration of magnesium
Manifestations: flushing, lowered BP, nausea, vomiting, hypoactive reflexes,
drowsiness, muscle weakness, depressed respirations, ECG changes, dysrhythmias
Medical management: IV calcium gluconate, loop diuretics, IV NS of RL,
hemodialysis
Nursing management: assessment, do not administer medications containing
magnesium, patient teaching regarding magnesium-containing OTC medications

Osmosis:
Diffusion:
Filtration:
Active Transport:
Role in regulating the body’s composition and volume:
-kidney:
-lungs:
-endocrine glands:
Effects of aging of fluid and electrolyte regulation:
-Younger ppl have a higher percentage of body fluid than older adults
IMBALANCES:
Fluid volume excess:
Fluid volume deficit:
Sodium excess:
Sodium deficit:
Potassium excess:
Potassium deficit:
■ Body Fluids
■ Third Space Fluid Shift (third spacing):
■ Loss of the ECF into a space that does not contribute to equilibrium between the ICF
and the ECF
■ S/S=decrease in urine output (despite normal intake)
■ Increased heart rate and body weight, decreased bp and central venous pressure,
edema, and imbalances in I&O=FLUID VOLUME DEFICIT (FVD)
■ Occurs in Patients with:
■ hypocalcemia

NSG 338: Exam 4
■
■
■
■
■
■
■
■

decreased iron intake
severe liver disease
alcoholism
hypothyroidism
malabsorption
immobility
burns
cancer
■ Electrolytes

REG. OF BODY FLUID COMPARTMENTS
■ Osmosis/Osmolality
■ Diffusion
■ Filtration
■ Na-K Pump
SYSTEMIC ROUTES OF GAINS AND LOSSES
■ Kidneys
■ daily volume losses thru urine in adults=1-2L/day
■ output=1 mL/kg/hr for ALL AGES!
■ Skin
■ Sensible perspirations: visible water and electrolyte loss thru the skin
(sweating)
■ chief solutes in sweat=Na+, Cl-, & K+
■ sweat loss=0-1000 mL/hour
■ continuous water loss by evaporation=500 mL/day (insensible)
■ water loss increases with fever and loss of natural skin barrier (e.g. burns)
■ Lungs
■ eliminate water vapor (insensible loss)↑ WITH
■ 300 ml q day
■ ↑ WITH ↑RR OR DEPTH, OR IN A DRY CLIMATE!
■ GI Tract
■ Loss of 100-100 mL daily
■ 8 L of fluid flows thru GI q 24 hours
■ diarrhea and fistulas cause large fluid losses
LAB TESTS FOR FLUID STATUS
■ osmolality
■ measures the solute concentrations per kg in blood and urine
■ reflects the concentration of Na (BUN and glucose also play role)
■ determined by urea, creatinine, and uric acid.

NSG 338: Exam 4

■

■

■

■

■

■

■ URINE+SERUM OSMOLALITY=MOST RELIABLE INDICATOR OF
URINE CONCENTRATION!
■ reported as milliosmoles/kg of water (mOsm/kg)
■ NORMAL SERUM OSMO=270-300 mOsm/kg
■ FACTORS THAT INCREASE OSMO:
■ FACTORS THAT DECREASE OSMO:
■ measured thru lab tests or by doubling the serum Na level
■ Na+=Approximate value of serum osmolality
osmolarity
■ describes the concentration of solutions
■ measured in milliosmoles per liter (mOsm/L)
■ usually within 10 mOsm of the value of osmolality
Urine Specific Gravity
■ measures the kidneys ability to excrete or conserve water
■ normal range=1.010-1.025
■ measured at bedside by putting a hydro-or urinometer in 20 ml of urine;
also using refractometer or dipstick
■ inverse relationship with fluid volume (LARGE VOLUME OF
URINE=LOW SPECIFIC GRAVITY)
■ factors that increase/decrease are same as those for urine osmolality
BUN
■ made up of urea (end product of protein metabolism by the liver)
■ normal BUN=10-20 mg/dL (3.6-7.2 mmol/L)
■ increasing factors: ↓ renal function, GI bleed, dehydration, ↑ protein intake,
fever, sepsis
■ decreasing factors: end stage liver disease, low protein diet, starvation, any
d/o that results in ↑ fluid volume (pregnancy)
Creatine
■ end product of muscle metabolism
■ better indicator of renal Fx than BUN (doesnt vary with protein intake and
metabolic state)
■ Normal serum levels=0.7-1.4 mg/dL (62-124 mmol/L
■ Levels increase when renal fx decreases
Hematocrit
■ measures the volume % of RBCs in whole blood
■ normal ranges:
■ male=42-52%
■ female=35-47%
■ dehydration and polycythemia INCREASE hct
■ overhydration and anemia DECREASE hct
Urine Na
■ ↑ Na intake=↑ excretion
■ as the circulation fluid volume ↓=Na is conserved

NSG 338: Exam 4
■ Normal Levels=75-200 mEq/24 hrs (75-200 mmol/24 hrs)
■ used to assess volume status and dx of hyponatremia and acute renal failure
HOMEOSTATIC MECHANISMS
● Kidney Functions
● Heart and Blood Vessel Functions
● Lung Functions
● Pituitary Functions
● Adrenal Functions
● Parathyroid Functions
● Baroreceptors:
● Renin-Ang.-Aldost.-System
● ADH and Thirst
● Osmoreceptors
● Natriuretic Peptides
GERONTOLOGIC CONSIDERATIONS

HYPOVOLEMIA

HYPERVOLEMIA

NSG 338: Exam 4

GASTRO-INTESTINAL SYSTEM
Chapter 44
Care of Clients with Gastric/Duodenal Disorders
Gastritis
•
•
•
•

Inflammation of the gastric/stomach mucosa
2million people
Acute/chronic
Non-erosive

NSG 338: Exam 4
•
too much acid production
•
Erosive
• NSAID
• ETOH Abuse
• Recent exposure to radiation therapy
•
More severe form
• Patients who ingest acid/alkali ( poison)
•
Path
•
Edematous
•
Hyperemic
• Can’t produce acid but large amounts of mucous are formed
•
Superficial erosion
•
Erosion could lead to ulceration-hemorrhage
Clinical Manifestations
•
Acute
• Rapid onset of symptoms
• Abdominal pain, H/A, lassitude, nausea, anorexia, vomiting, and
hiccupping, which last few hours/few days
• Erosive may cause bleeding
• What does this look like
Assessment
•
Clinical Manifestations
•
Achlorhydria ( lack of HCL)
•
Endoscopy
• Histological examination
Medical Management
•
Mucosa can repair itself past acute episode
•
Generally one day
•
Patient teaching
• refrain from alcohol and food until symptoms subside
• Non-irritating diet
•
May have to have IV fluids
•
NG
•
Medications
Medications
•
Antacids
•
Histamine 2 blockers
• Pepcid, Zantac
•
Proton Pump Inhibitors
• Prilosec, prevacid
Nursing Management
•
Reduce anxiety ( ingested)
•
Optimal nutrition

NSG 338: Exam 4
•
•

Physical/emotional support
Manage symptoms
• n/v, heartburn, fatigue
• No fluid/foods for several days (IV)
• Monitor lytes
• Progress diet
• Discourage caffeine, ETOH
• Discourage smoking
Nursing Management
•
Priority Assessment
• Assess for hemorrhage
• What would this look like
•
Pain management
• What pain medications would you avoid
Medical Management Continued
•
Extreme cases
• Surgery may be required to remove gangrenous/perforated tissue
•
Chronic
• Diet
• Rest
• Decreasing stress
• Avoid NSAID, ETOH
• Antacids, H2 blockers, PPI
Peptic Ulcer Disease
•
Epidemiology
• 14.5 million Americans
• 1.4 million outpatient visits
• 489,000 inpatient hospitalizations
•
Gastric, esophageal, duodenal
•
Peptic Ulcer
•
Erosion can include one or more layers
•
Peptic ulcers more likely to occurs in duodenum than in stomach
•
Rates are decreasing middle age
•
Rates are increasing older adult
•
Most common cause gram neg bacteria
• H. pylori
• Acquired: food, water, person to person through close contact and exposure to
emesis
Peptic Ulcer
•
Risk factors
• NSAID
• Zollinger-Ellison syndrome

NSG 338: Exam 4
• Questionable smoking, ETOH
Peptic Ulcer
•
Pathophysiology
• Gastoduodenal mucosa
• ↑ acid
• ↓mucous
• NSAIDS decrease mucous production
•
ZES
• Suspected with multiple peptic ulcers don’t respond to treatment
• Hypersecretion of gastric juice
• Steatorrhea, epigastric pain
•
•
Stress ulcer :
• Acute mucosal ulceration of the duodenal/gastric area after physiological
stress events
• Most common in ventilator-dependent patients after trauma/ surgery
Peptic Ulcer
•
Manifestations
•
last fore few days, weeks months, come and go
•
Complains of dull gnawing pain
•
Burning pain midepigastrium or the back
•
Gastric immediately after eating
• 30-40% wake with pain
•
Duodenal 2-3 hours past eating
5080% wake with pain
•
Pyrosis (heartburn)
Peptic Ulcer
•
manifestations
• Epigastric tenderness
• Abdominal distension
•
Diagnostic
• Endoscopy
• Bx
•
Other methods of assessing for h.pylori
• Serum for antigen
• Urea breath test
Peptic Ulcer
•
Medical management
• Irradiate h. pylori, manage gastric acidity
• Pharmacological
• Antibiotics, proton pump inhibitors, bismuth salts 10-14 days
• Table 47-2
• Smoking Cessation
• Dietary modification

NSG 338: Exam 4
• Surgical Management
• Follow up
Peptic Ulcer
•
Nursing Care
• Assessment
• History
• pain
• Vital signs
• Vomiting
• Lifestyle
Peptic Ulcer
•
Nursing Diagnosis
•
Acute pain related to the effect of gastric acid secretion on damaged tissue
•
Anxiety related to an acute illness
•
Imbalanced nutrition: less than body requirements related to changes in diet
•
Collaborative problems
• Hemorrhage
• Perforation
• Penetration
• Gastric outlet obstruction
Peptic Ulcer
•
Nursing Interventions
• Pain relief
• Reducing anxiety
• Maintaining optimal nutritional status
• Monitoring/Managing potential complications
• Gastritis
• Hemorrhage
• Vital signs
• What do you look for?
• Assess emesis
Peptic Ulcer
•
Nursing Interventions
• Perforation: erosion of the ulcer through the gastric serosa into the peritoneal
cavity
• Sudden severe pain upper abd pain
• Vomiting
• Collapse
• Extremely tender and rigid abdomen
• Hypotension and tachycardia
Peptic Ulcer
•
Penetration: erosion of the ulcer though the gastric serosa into adjacent structures
such as the pancreas biliary tract

NSG 338: Exam 4

•
•
•

•
Back and epigastric pain
•
Not relieved by medication
•
Requires surgical intervention
•
Monitor care postoperatively
Gastric Outlet Obstruction:
•
Area distal to the pyloric sphincter becomes scarred and stenosed from spasm
or edema or scar tissue

Gastric Outlet Obstruction continued
• First consideration NG tube
• Residual of 400 or greater suggest obstruction
• Upper GI or Endoscopy to confirm
• Balloon dilatation may be helpful
Gastroeosphageal Reflux Disease (GERD)
•
Backflow of gastric or duodenal contents into the esophagus
• Risk factors
• Incompetent lower esophageal sphincter
• Pyloric stenosis
• Hiatal hernia
• Motility disorder
• Increases with age
GERD Symptoms
•
Pyrosis
•
Dyspepsia
•
Regurgitation
•
Dysphagia
•
Hypersaliviation
•
esophagitis
GERD Diagnosis/Management
•
Diagnosis
• Endoscopy
• Barium swallow
• 12-36 hour capsule monitoring
•
Management
• Avoid situations that decrease lower esophageal sphincter pressure or cause
esophageal irritation
• Low fat diet
• Avoid caffeine
GERD
• Tobacco
• Beer
• milk
• Foods containing peppermint or spearmint, and carbonated beverages

NSG 338: Exam 4
•
•
•
•

Avoid eating/drinking 2 hours before bedtime
Maintain normal body weight
↑ HOB 6-8 inches on block
↑upper body on pillows

GERD
•
Medications
• Antacids
• H2 antagonist/blockers
• Pepcid
• Axid
• Zantac
• Proton Pump Inhibitors
• Prevacid
• Nexium
• Prilosec
• Protonix
GERD
•
Medications
• Increase motility
• Urecholine
• Motilium
•
If nothing works may need surgical correction

FUNCTION OF GI TRACT:
◆ digestion
◆ absorption
◆ elimination
GASTRIC FUNCTION
● Gastric secretions
● 2.4L/day
● HCL
● TWO FUNCTIONS=breaks down food and destroys ingested bacteria
● Pepsin-important enzyme for protein digestion
● Intrinsic factor-combines with B12 so it can be absorbed

NSG 338: Exam 4
Acute
Gastritis
Patho

inflammation of the
stomach mucosa

Etiology

acute
-diet (eating
irritating food
highly seasoned or
that is infected)
-acute illness
-excessive aspirin
or NSAID use
-MAY BE 1ST
SIGN OF ACUTE
SYSTEMIC IXN!
chronic
-benign or
malignant ulcers of
the stomach
-bacteria
(helicobacter
pylori)
nonerosive
erosive

Risk Factors

-effects both
genders equally
-more common in
OLDER adults

Manifestations
Assessment and
Dx Findings
Medical
Treatment
Nursing
Management

Chronic
Gastritis

Chronic Peptic
Ulcer Disease

NSG 338: Exam 4

CH. 46: GERD
■ gastroesophageal reflux-backflow of gastric or duodenal contents into esophagus
■ Increased with aging
■ can be r/t barrets
■ Manifestations:
■ mimic a heart attack
■ pyrosis
■ dyspepsia
■ regurgitation
■ dysphagia
■ odynophagia
■ hypersalivation
■ esophagitis
■ Diagnostics:
■ endoscopy/barium swallow
■ ambulatory 12 to 36 hour esophageal pH monitoring
■ AVOID tobacco, caffeine, milk, beer, products with peppermint or spearmint; do
not drink 2 hours before bedtime; eat a lowfat diet, maintain normal body weight
■ elevate head of bed 6-8 inches and elevate upper body with pillows
CH. 48 (p. 1285-1292, 1293-1294, 1296-1299, 1301-1315, 1328-1330)
Care of Patients with Intestinal & Rectal Disorders
Physical Assessment:
Look, Listen & Feel
Mouth
Abdomen
◦ masses
◦ Peristaltic waves
◦ Symmetry

NSG 338: Exam 4
◦
◦
◦

Skin color
Distension
Auscultate
● Character/frequency of sounds
● Normal sound heard every 5-20 seconds
● Hypoactive ( 1 or 2 sounds in 2 minutes)
● Hyperactive (5-6 sounds in less than 30 seconds)

Medications
Bentyl: decreases gastric emptying
Opioids: slow peristalsis
Anticholinergic drugs: inhibit secretions, decrease peristalsis
NSAID: GI irritation-GI Bleeding
ASA: GI Bleeding
H2 antagonist: suppress secretion of acid
Common Bowel Elimination Problems

Constipation
◦

◦

S&S
◦ Infrequent bowel movement less than 3/week
◦ Difficulty passing stools
◦ Excessive straining
◦ Hard feces
◦ Can’t defecate at will
Causes
◦ Medications
● CNS depressants, anticholinergic, diuretic, opioids
◦ Hemorrhoids
◦ Neurological disorders
◦ Obstruction
◦ Weakness, Immobility, Fatigue, Inability to increase intra-abdominal pressure
◦ Ignoring the urge
◦ Dietary habits
Gerontological considerations
◦ See chart 48-1 page 1287
◦ The ―10 Ds of Constipation‖
1. side effects of Drugs
2. defecatory dysfunction
3. degenerative disease
4. decreased diet intake, mobility, and privacy
5. dementia
6. dependence on others assistance
7. dehydration
8. depression

NSG 338: Exam 4
Complications
◦ Hemorrhoids-dilated portions of anal veins
◦ Fissures-normal or abnormal fold, groove, or crack in body tissue
◦ Hypertension
◦ Valsalva (forcibly exhaling while glottis is closed)
● Flow of venous blood to chest impeded
● This pressure can collapse the large veins in chest
● Atria and ventricles receive less blood
● Less blood is ejected by the left ventricle
● Cardiac output decreased, results in hypotension
● Immediately following increase in arterial pressure is elevated higher than
original pressure : can rupture artery
Impaction
Collection of hardened feces wedged in the rectum
◦ May result in bowel obstruction
◦ Inability to pass a stool for several days despite the urge
◦ Oozing which might be confused with diarrhea
◦ Gently perform a digital examination of the rectum
Patients at greatest risk
◦ Debilitated,
◦ Confused,
◦ unconscious
Treatment of Constipation
Target underlying cause
Medical management
◦ Table 48-1
Education
◦ Chart 48-2
Exercise
Diet
Gastrocolic reflex-peristaltic movements of the large bowel occurring five to six
times daily that are triggered by distention of the stomach
attempt to defecate following a meal and a warm drink
Nursing Management
Nursing history
Patient education
Health promotion
Nursing History
Elimination pattern
Usual stool characteristics
Routines which promote normal elimination
Use of artificial aids

NSG 338: Exam 4
Presence/status bowel diversions
Change in appetite
Diet history
Daily fluid intake

Diarrhea
Diarrhea
◦ Increase in the number of stools, more than 3/day
◦ Passage of liquid unformed feces
Acute
often associated with infection
self-limiting 7-14 days
Chronic
persists for more than 2-3 weeks
medications
metabolic disorders
Viral /bacterial infections
Dysentery
Nutritional malabsorption
◦

Passage occurs too quickly through GI
● Anal bag
● Results in electrolyte /fluid imbalance
● Skin breakdown

Types of Diarrhea
Secretory
◦ High volume, bacterial toxins & neoplasams
Osmotic
◦ Water pulled into the intestine by osmotic pressure; lactase deficiency,
pancreatic dysfunction, intestinal hemorrhage
Malabsorptive
◦ combination of biochemical, mechanical , low albumin levels,
Infectious
● C-Diff
Exudative
◦ Loss of mucosal integrity, epithelial loss, Radiation/ chemo
Diarrhea
◦ Clinical manifestations
◦ Abdominal cramps
◦ Distension

NSG 338: Exam 4
◦
◦
◦
◦

Borborygmus ( gas)
Anorexia
Thirst
Tenesmus (straining)

Diarrhea by location/time/character
Small bowel: watery
Large bowel: loose semisolid
intestinal malabsorption: voluminous, greasy
Enteritis/colitis: blood pus mucus
Pancreatic insufficiency: oil droplets on water
Nocturnal diarrhea: diabetes
Assessment
CBC
Chemistry
Urinalysis
Stool examination
Stool for parasite, toxin blood fat, lytes, WBC’s
Endoscopy
Complications
Cardiac dysrhythmias-loss of fluid and electrolytes ( low K)
Metabolic acidosis (loss of bicarb)
Urinary output less an 0.5ml/kg/h for 2-3 consecutive hours, muscle weakness,
paresthesia, hypotension, drowsiness, anorexia with K of less than 3.5
Management of Diarrhea
Treat underlying issues
Controlling symptoms
Preventing complications
Use contact precautions until C-diff ruled out
Imodium
Probiotics (lactobacillus species)
Nursing Management
Health history
Recent illness
Recent travel
Assess for skin breakdown
Diet
◦ Increase liquids and floods low in bulk during acute phase: then bland diet
progressing to solid as tolerated
◦ Avoid caffeine, carbonated beverages, very hot/cold foods, restrict milk, fat,
whole-grain, fruits, vegetable

NSG 338: Exam 4
Nursing Management
Rehydration (IV)
Monitor lytes ( which ones?)
Monitor for dysrhythmia
Skin assessment
Cleanse and apply barrier cream

Fecal Incontinence
Involuntary passage of stool from rectum
Factors of influence
◦ Ability of rectum to sense and accommodate
◦ Amount and consistency of stool
◦ Integrity of sphincter, musculature
◦ Rectal motility
Fecal incontinence
Trauma ( post op)
Neurological disorders
Inflalmmation
Infection
Chemo
Radiation
Fecal impaction
Diagnostic
Assess for underlying etiology
Rectal exam
Sigmoidoscopy
x –ray
Barium enema
Medical Management of Fecal Incontinence
Assess for fecal impaction
Assess drug regimen, may need to alter
Biofeedback
Bowel training
Surgical interventions
Nursing Management
Fecal Management System
Celiac Disease
http://celiac disease/
Inflammatory Bowel Disorders

NSG 338: Exam 4
Diverticular Disease
Ulcerative colitis
Crohns’s Disease
Diverticulosis
Diverticula congenital or acquired
Pouch like herniations of the mucosa; non-inflamed
◦ Typically in sigmoid
Diverticulitis inflammation of diverticulum
Diverticular Disease
Etiology
◦ Diets low in fiber: constipation
◦ Obesity
◦ Weakening of the bowel wall; ↑ intraluminal pressure
◦ Common in both men and women ↑45
◦ 80% of those ↑ 85
Diverticular Disease
Clinical Manifestations for Diverticulitis
◦ Abdominal pain
◦ Localized left lower quadrant
◦ Low grade to elevated temp
◦ N/V
Examination
◦ Distension,
◦ Tenderness
◦ Vital signs
Diverticular Disease
Examination cont’d
Diverticulosis generally found during colonoscopy
◦ ↑ WBC ↓H&H, + FOBT
◦ Alteration in bowel status
◦ CT with contrast agent diagnostic test of choice
◦ Colonoscopy is contraindicated in acute diverticulitis
Diverticular Disease
Medical Management
◦ Symptomatic treatment
● Rest
● Medications: analgesics, antispasmodics, antibiotics
● Initial diet liquid, when inflammation subsides
● High fiber ,low fat diet
● Prevention of constipation

NSG 338: Exam 4
● Bran
● Bulk laxatives
● Instruct patient to notify MD of any bowel change
● Bowel Rest
● NPO
● ? NG
● IV’s, Meds
Diverticular Disease
Medical Management Cont’d
◦ Surgical management: emergency situations
● Hemorrhage
● Obstruction
● Abscesses
● Perforation/peritonitis
◦ One stage resection
◦ Multiple stage resection: results in colostomy
Nursing Care
Page 1299
Nursing Management
Patient Education
◦ High Fiber diet
● 25-35 grams of fibers daily
● Fresh fruits and vegetable
◦ Avoid
● ETOH
● Foods containing seeds
◦ Prevent constipation
Note: Avoid high-fiber diet with diverticulitis
Inflammatory Bowel Disease
30,000 new cases each year
Cost’s between 1.8 and 2.6 billion dollars
15-30 / 50-75
More prevalent when of Jewish decent
Positive family history most significant
Table 48-4 page 1302
Symptoms
◦ Diarrhea
◦ Abdominal pain
◦ GI bleeding
◦ Fatigue
◦ Weight loss/ or growth failure in children

NSG 338: Exam 4
Diagnostic Test
Barium enema with air contrast
Colonoscopy with biopsy
↑ ESR
Crohn’s Disease
Etiology
◦ ? Mycobacterium paratuberculosis
◦ ? Genetic predisposition,
● appears in clusters, twins
◦ Immunoregulation
◦ Peak incidence is 15-30
◦ Seen more in smokers than non-smokers
Crohn’s Disease
Disease of chronic inflammation of GI Tract
Characterized by remission/exacerbations
May involve both the large and small bowel
Involves multiple layers of the bowel
Thickening inflamed mucosa: cobblestone
Slowly progressive
Involvement of multiple regions
Deep fissure and ulcerations form
Granulomas form
Crohn’s Disease
Becomes fibrotic, intestinal lumen narrows bowel loops can begin to adhere to other
loops
Clinical Manifestations
◦ Right lower quadrant abdominal pain
◦ Cramping pain occurs after meals
◦ Diarrhea
◦ Low-grade fever,
◦ Steatorrhea
◦ Bright red blood is rare
◦ 80% experience weight loss, malnutrition, anemia
◦ Irritating discharge into colon
Diagnosis of Crohns
Complications of Crohns
Intestinal obstruction
Stricture formation
Perianal disease
Fluid and electrolyte imbalance
Fistula; enterocutaneous fistula

NSG 338: Exam 4
abscess
Ulcerative Colitis
Etiology; unknown
◦ ? Genetic basis
● Seen in families, twins, and ethnic groups
● 4-5X more common among peoples of Jewish origin
● Females more affected than men
Immunologic hypotheses
◦ Autoimmune dysfunction
Associated with colon cancer
Ulcerative Colitis
Affects the colon only
Multiple ulcerations
Lesions are contiguous
Tends to start at the rectum and extend proximally
Limited to mucosal/submucosal lining
Increased cancer risk
Inflammatory infiltrate : crypt abscess
Characterized by remissions and exacerbations
Ulcerative Colitis
Clinical Manifestations
◦ Left lower abdominal pain
◦ Diarrhea; up to 20 liquid bloody stools, mucous , pus
◦ Tenesmus (uncontrollable straining)
◦ Weight loss
◦ Systemic or Extraintestinal manifestations include skin lesions
◦ Hypocalcaemia, anemia
Diagnosis of Ulcerative Colitis
Assess for tachycardia, Hypotension, Tachypnea, Fever, Pallor
Nutritional status
Stool positive for blood
What lab values?
Abdominal x-ray
Sigmoidoscopy, colonoscopy barium enema
Complications of Ulcerative Colitis
Toxic megacolon
◦ Colonic distention, fever, abdominal pain, distension, vomiting, and fatigue
◦ If doesn’t respond to medical treatment surgery needed: illeostomy
Perforation
Bleeding
High risk of colon cancer

NSG 338: Exam 4
Non Surgical Management for UC and Chron’s
Drug Therapy
◦ Salicylate compounds: antiinflammatory
● Azulfidine, Dipentum
●
◦ Corticosteroids: severe disease, po or IV
◦
◦ Immunosuppressive Drugs
● Immuran, methotrexate
●
◦ Biological therapies: Crohns: Remicade, Humira
◦ UC: infliximab
◦
◦ Antidiarrheal Drugs
◦ Noncompliance with medications is huge problem
Nursing Management
What is overall goal?
Maintain normal elimination pattern
Relieving pain
Maintaining fluid intake
Maintaining optimal nutrition
Promote rest
Reduce anxiety
Enhancing coping measure
Prevent skin break down
Monitor/manage complications
Non-Surgical Management Cont’d
Rest
Complementary & Alternative therapies
Pain management
Nutrition
◦ Oral fluids, low-residue, high protein, high calorie diet with vitamin
supplements
Cold foods and smoking avoided
Surgical Management
Ileostomy
Kock pouch
Restorative proctocolectomywith Ileal Pouch and anal anastomosis
Review care of the patient with an ostomy
Anorectal Abscess
Obstruction of anal gland= infection

NSG 338: Exam 4
◦ Crohn’s disease, AIDs
◦ Foul smelling pus
◦ Painful, swelling, tenderness
Palliative therapy
◦ Sitz baths, analgesics
Treatment of choice
◦ Surgery, also may excise fistula
◦ Wound is packed with absorptive dressing, heal by granulation
Anal Fistula
Tiny tubular fibrous tract extends from outside to inside of anal canal
Usually develop from infection
May develop from Crohn’s disease, trauma
Purulent drainage
Stool may leak from cutaneous opening
Flatus or feces from vagina/bladder
Antibiotics, anti-inflammatory agents
Recurrence is common
Fistulectomy
Wound packed with gauze
Anal Fissure
Longitudinal tear/ ulceration in lining
Trauma, passing of stool, childbirth
Extremely painful defecation, burning, bleeding
Typically treated conservatively
◦ Dietary modification, addition of fiber, stool softeners, increase in water, Sitz
bath
◦ Perianal,/intra-anal ntg ointment
Hemorrhoids
Dilated portions of veins in anal canal
50%
Causes:
◦ Shearing of mucosa during defecation
◦ Increased pressure during pregnancy
◦ Internal/external
Signs and symptoms
◦ Pain
◦ Itching
◦ Bright-red blood with defecation
Hemorrhoids
External
◦ Severe pain inflammation edema (thrombosis), ischemia necrosis

NSG 338: Exam 4
Internal
◦ Pain caused by bleeding or prolapse
Symptoms/discomfort relieved by
◦ Good hygiene
◦ Avoid excessive straining
◦ High residue diet
◦ Increased fluid
◦ Psyllium may help
◦ Warm compresses
◦ Sitz baths
◦ Witch hazel
Hemorrhoids
Treatment
◦ Rubber-band ligation
● Risk for perianal infection
◦ Cryosurgical
● Foul smelling discharge
◦ Laser
◦ Hemorrhoidopexy surgical staples
◦ Hemorrhoidecomy
● Gel foam applied to wound
Sexually Transmitted Anorectal Diseases
Proctitis
◦ Involves rectum
◦ Recent anal-receptive intercourse with infected partner
◦ Mucopurulent discharge, bleeding, rectal pain, and diarrhea
● Organism: gonorrhea, Chlamydia, herpes, Treponema pallidum
Sexually Transmitted Anorectal Diseases
Proctocolitis
◦ Involves rectum and lowest portion of the descending colon
● Water/bloody diarrhea, cramps, pain, bloating, and symptoms similar to
proctitis
Sexually Transmitted Anorectal Diseases
Enteritis
◦ Involves more of the descending colon
● Watery/bloody diarrhea, abdominal pain, weight loss
● Organisms: E. histolytica, Giardia lamblia, shigella, campylobacter
Treatment for STAD
◦ Sigmoidoscopy
◦ Antibiotics
◦ Acyclovir
◦ Antiamebic therapy

NSG 338: Exam 4
Pilonidal Sinus/ Cyst
Intergluteal cleft on posterior surface of the lower sacrum
◦ Theory: trauma causing penetration of hair in to epithelium; or congenital
Symptoms start in adolescence
◦ Initially antibiotics
◦ Once abscess has formed surgery
◦ Wound heals by granulation
◦ Absorptive dressings are used