NSG 338: Exam 4

Chapter 35: Assessment of Immune Function

Immunity: the bodys 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 bodys 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 bodys 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. Nezelofs 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 (Brutons 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 lymphocytesbrutons disease
T lymphocytesDiGeorge syndrome
Complement SystemAngioneurotic edema
Phagocytic Cellshyperimmunoglobulinemia 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 cant
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 cant 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/AIDSDiagnosis
Impaired skin integrity
Diarrhea
Risk for infection
Activity intolerance
Disturbed thought processes
Nursing Process: The Care of the Patient With HIV/AIDSAssessment
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 Kaposis sarcoma is:

B-cell lymphomas: the second most common malignancy with AIDS

Nursing Process: The Care of the Patient With HIV/AIDSPlanning
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/AIDSInterventions: 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/AIDSInterventions: 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/AIDSInterventions:
Respiratory/ pain
Improving airway clearance
Position in semi-Fowler's or high Fowlers 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/AIDSInterventions:
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/AIDSInterventions:
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/AIDSInterventions:

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
Dont drink ETOH
Pharmacological Therapy
Mast Cell Stabilizer
Reduces release of histamine by stabilizing cell
Used prophylactically
Intranasal cromolyn (NasalCrom)
Intranasal Corticosteroids
Indicated for cases dont 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
Dont 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 acidbase 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, -2 agonists, dialysis
Hyperkalemia (contd)
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,
Trousseaus sign, Chovstek's sign, seizures, respiratory symptoms of dyspnea and
laryngospasm, abnormal clotting, anxiety
Hypocalcemia (contd)
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
Trousseaus 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 (contd)
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 bodys 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
Cant 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 dont 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
Cant 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, WBCs
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
Crohnss 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 contd
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
IVs, Meds
Diverticular Disease
Medical Management Contd
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
Costs 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
Crohns Disease
Etiology
? Mycobacterium paratuberculosis
? Genetic predisposition,
appears in clusters, twins
Immunoregulation
Peak incidence is 15-30
Seen more in smokers than non-smokers
Crohns 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
Crohns 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 doesnt respond to medical treatment surgery needed: illeostomy
Perforation
Bleeding
High risk of colon cancer

NSG 338: Exam 4

Non Surgical Management for UC and Chrons
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 Contd
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

Crohns 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 Crohns 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