B

• Abdominal Pain
• Guarding
• Rigid board-like Abdomen (peritonitis)
• Hypotension or Shock

SIGNS AND SYMPTOMS OF PANCREAS

• Fluid and electrolyte disturbances
• Necrosis of the pancreas
• Shock
• Multiple organ dysfunction syndrome
• DIC

Collaborative Problems and Potential Complications PANCREAITIS

• Cardiovascular Failure
• ARDS
• Renal Failure
• Hemorrhage
• Infection

PANCREAITIS

• Serum Amylase, Lipase
• X-Ray
• CT
• Ultrasound

DIAGNOSTIC TESTS

Chronic Pancreatitis

• IV Fluids/TPN
• Blood Products PRN
• Oxygen
• Analgesics, Antianxiety Agents
• NPO
• NG Suction

Histamine Antagonists

THERAPUTIC TX

Chronic Pancreatitis

• Pathophysiology
• Progressive Fibrosis
• Obstructed Ducts
• Ulceration
• Etiology
• Alcohol
• Biliary Disease

Chronic Pancreatitis

• Remissions and Exacerbations
• LUQ Pain and tenderness : “burn-out”
• Anorexia
• Malabsorption, Weight Loss, muscle wasting
• Steatorrhea and foul smelling stools
• Diabetes Mellitus
• Jaundice

Chronic Pancreatitis: SIGNS AND SYMPTOMS

• Pancreatic Enzymes Normal
• High Fecal Fat Level
• Changes on CT

DIAGNOSIS Chronic Pancreatitis

• Analgesics
• Pancreatic Enzyme Replacement
• Surgery

Chronic Pancreatitis TX

What is a major symptom of chronic pancreatitis?

A.Recurrent attacks of severe upper abdominal and back pain accompanied by vomiting

B.Fever, jaundice, confusion, and agitation

C.Ecchymosis in the flank or umbilical area

D.Abdominal guarding

A.Recurrent attacks of severe upper abdominal and back pain accompanied by vomiting

Chronic pancreatitis has recurrent attacks of severe upper abdominal and back pain accompanied by vomiting. Acute pancreatitis presents with fever, jaundice, confusion, agitation, ecchymosis in the flank or umbilical area, and abdominal guarding.

COPD

refers to diseases that obstruct air flow and commonly includes chronic bronchitis and emphysema (airflow limitation)

Exacerbation and co-morbidity contributes to the clinical manifestations

contributes to the clinical manifestations

Presents with 3 cardinal signs and symptoms

–Dyspnea

–Chronic cough

–Sputum production

Less common signs

• Wheezing
• Chest tightness

COPD SIGNS AND SYMPTOMS

cigarette, air pollution, allergy, autoimmunity, infection, occupational exposure, aging etc.

Excessive mucous production resulting in chronic cough is characteristic of chronic bronchitis.

RISK FACTOR FOR COPD

Inflammatory changes leads to mucociliary dysfunction & bronchial constriction

Increase production of mucus with a chronic cough that persists for at least 3 months of the year for 2 consecutive years

With continued irritation epithelial cells die, destroying their Celia

Goblet cells hypertrophy creating more tenacious mucus

The inability to clear the airway of excess mucus causes susceptibility to infections

CHRONIC BRONCHITIS

Repeated infections lead to airways showing scarring, stenosis and obstruction

• Because of the loss of alveolar walls and the capillaries surrounding them, there is increased pressure in the pulmonary circulation.
• This, along with thickening of the blood vessels, results in pulmonary hypertension.
• Which in turn leads to right side heart failure /cor pulmonale.
• Common characteristics
  • Mucus hypersecretion
  • Dysfunction of cilia
  • Hyperinflation of lungs
  • Gas exchange abnormalities

CHRONIC BRONCHITIS

Productive cough, exertional dyspnea, and wheezing

Over time, hypoxemia (PaO2 <60 mm Hg or O2 saturation <88%) may develop with hypercapnia (PaCO2 >45 mm Hg) leading to respiratory acidosis.

Because of their reduced oxygen saturation they start to retain fluid.

polycythemia develops as a result of increased production of red blood cells as the body attempts to compensate for chronic hypoxemia.

the resp. acidosis , polycythemia and < O2 leads to the constant cyanosis and bloated appearance and that’s why chronic bronchitis is referred to as “blue bloaters”

CLINICAL MANIFESTATIONS COPD

Degenerative, nonreversible disease characterized by

–Destruction of the alveoli

–Enlargement of the distal airspaces

–Breakdown of alveolar walls leads to loss of alveolar recoil+ decrease ventilation

Breathing out is the main problem

Pulmonary Emphysema

Thin, emaciated body frame

Dyspnea on exertion, later at rest

Shortness of breath and “air hunger”

Chronic productive cough

Classic “barrel chest” indicating constant lung over inflation and overwork of chest muscles used for breathing (diaphragm).

Dilatation and destruction of lung tissue distal to terminal bronchioles.

It leads to air trapping and an increase in total lung capacity.

There is also a loss of alveolar tissue, reducing capacity for gas exchange.

Carbon dioxide clearance is not impaired to the same extent as chronic bronchitis, usually because patients increase their respiratory effort and ventilation, the pt. Is not usually cyanotic

Instead you will observe a pinkish skin color and that is why they are called “pink puffers”

Clinical Manifestations:

Pulmonary Emphysema

H&P

CXR, CT scan

Pulmonary function tests

ABGs

Pulmonary test to rule out TB or malignancy

Diagnostic Eval. Of COPD

Elevated Hct - to low oxygenation levels

Hypoxemia-low PO2 less than 80mmHg

Hypercapnia- high PCO2 -45 mmHg

Resp acidosis

LABS COPD

The nurse reviews the arterial blood gases of a patient. Which result would indicate the patient has later stage COPD?

pH 7.32, PaCO2 58 mm Hg, PaO2 60 mm Hg, HCO3 30 mEq/LnpH 7.30, PaCO2 45 mm Hg, PaO2 55 mm Hg, HCO3 18 mEq/L

pH 7.40, PaCO2 40 mm Hg, PaO2 70 mm Hg, HCO3 25 mEq/L

pH 7.52, PaCO2 30 mm Hg, PaO2 80 mm Hg, HCO3 35 mEq/L

ABGS COPD

Answer: A

Rationale: In later stage COPD, the patient will have a low or low normal pH, a high normal or above normal PaCO2, and a high normal or above normal HCO3-. This indicates compensated respiratory acidosis, as the patient has chronically retained CO2 and the kidneys have conserved HCO3- to increase the pH to near or within the normal range.

This image shows multiple cystic areas caused by destruction of lung tissue typical of emphysema.

Lung Severe Emphysema:

The chest cavity is opened at autopsy to reveal numerous large bullae apparent on the surface of the lungs in a patient dying with emphysema.

Bullae are large dilated airspaces that bulge out from beneath the pleura.

Emphysema is characterized by a loss of lung parenchyma by destruction of alveoli so that there is permanent dilation of airspaces

BULLAE

nCan improve survival in patients with advanced COPD who have hypoxemia, (low blood oxygen levels)

nThis treatment can improve a patient's exercise tolerance and ability to perform on psychological tests which reflect different aspects of brain function and muscle coordination

HOME OXYGEN THERAPY COPD

Increasing the concentration of oxygen in blood also improves the function of the heart and prevents the development of Cor pulmonale.

Monitor amount of oxygen given. No more than 3L is recommended. Why?

Some patients cannot maintain this effort and their carbon dioxide levels rise. This stimulates respiratory drive for a time, but then they become desensitized to it and they depend on hypoxemia to drive ventilation.

Oxygen can also lessen sleeplessness, irritability, headaches, and the overproduction of red blood cells.

n Continuous oxygen therapy is recommended for patients with low oxygen levels at rest, during exercise, or while sleeping.

nReview Oxygen delivery system (NC, Mask etc..)

Suppressed respiratory drive and low O2

Fire

Oxygen toxicity

COMPLICATIONS OF OXYGEN THERAPY

COPD MEDICATIONS

Bronchodilators

Methylxanthines

Corticosteroids or Steroids

Antibiotics

Expectorants

Diuretics

Digitalis

Leukotriene Inhibitors

Tranquilizers

Pain meds

Cough suppressants (codeine, etc.)

Sleeping pills (barbiturates, etc.)

• The choice of bronchodilator depends on the patient’s response. However, when the patient has mild COPD or fewer symptoms, a short-acting bronchodilator is used as needed.
• Albuterol or ipratropium (Atrovent) may be used as single agents, but combining bronchodilators improves their effect and decreases the risk of adverse effects. These two agents (albuterol and ipratropium) can be nebulized together (DuoNeb) or delivered by one MDI (Combivent Respimat).
• In the moderate stages of COPD, a long-acting bronchodilator may be used in addition to a short-acting rescue bronchodilator, such as salmeterol (Serevent) or formoterol (Foradil).

Surgical removal of large air spaces called bullae that are filled with stagnant air

May be beneficial in selected patients

Recently, use of lasers to remove bullae has been suggested

BULLECTOMY

nHas been successfully employed in some patients with end-stage COPD.

n In the hands of an experienced team, the 1-year survival in patients with transplanted lungs is over 70 percent.

LUNG TRANSPLANT

Help to overcome the conditions which cause dyspnea, anxiety and allergic reactions

Smoking cessation

Oxygen therapy

Breathing retaining

Airway clearance techniques

Improve capacity for physical exercise and activities of daily living

Frequent rest periods

Diet : Offer small frequent meals;

high calorie, high protein

2-3L fluid unless contraindicated IV/PO

Daily weights

n Intermittent mechanical ventilatory support relieves dyspnea and rests respiratory muscles in selected patients.

nPurse lip breathing techniques

PULMONARY REHABILITATION

Continuous positive airway pressure (CPAP) is used as an adjunct to weaning from mechanical ventilation to minimize dyspnea during exercise.

Relaxation techniques may also reduce the perception of ventilatory effort and dyspnea

Breathing exercises and breathing techniques, such as pursed lips breathing and relaxation

Place in high Fowler’s position or seated on the bedside with the arms folded on the over bed table to promote full lung expansion (Tripod)

Keeping air passages reasonably clear of secretions is difficult for patients with advanced COPD.

Re: Some commonly used methods for mobilizing and removing secretions are already discussed.

nAvoid smoking environment

nBreathing toxic fumes such as glue, paint etc.

nAerosol products other than meds

nGoing to places with polluted atmosphere

nAvoid people with infections etc..

C: IS FOR CONTROLLED ENVIROMENT

Highly communicable disease

Caused by mycobacterium tuberculosis

–Rod shaped, gram+, acid fast bacillus (AFB)

http://en.wikipedia.org/wiki/Mycobacterium

WHAT IS TB?

Spread by airborne droplet from an affected person during

–Coughing

–Speaking

–Laughing

–Sneezing

Another person breathes in the bacteria & becomes infected

Close quarters

TRANSMISSION OF TB

The tuberculosis bacterium invades the alveoli and begins to multiply forming a tubercle lesion

The body’s defense mechanism encapsulate the tubercle leaving a scar.

May continue to grow to form granulomas or cheese like mass called caseation

This is what is seen on a CXR and is called the Ghon tubercle or primary lesion

Primary lesions form, they may become dormant, but can be reactivated and become a secondary infections when re-exposed to the bacterium

Pathophysiology TB

www.anatomy.unimelb.edu.au/museum/collection.html

Dissected, preserved lung with tuberculosis TB

Close contact with infected person

Live in areas where TB in common

HIV infections, immune system diseases

The elderly

Homeless, poor, crowded living conditions

Poor access to heath care

Illicit drug use

Health care professional

WHOS AT RISK TB

TB has an insidious onset and many pts are not aware of the symptoms until the disease is well advanced

Fever, night sweats, malaise

Anorexia and weight loss

Cough non productive at first, but later produces yellow mucoid sputum

Hemoptysis

Pleuritic chest pain and tightness

Dyspnea if severe lung involvement

CLINICAL MANIFESTATIONS OF TB

H&P especially for pts at risk

Tests: Sputum smear and C&S

–AFB x 3 samples are usually obtained for an acid-fast smear . (May aspirate gastric fluid if unable to obtain specimen)

–The sputum test confirms the diagnosis of TB because

Chest X-rays

–Determines the presence of Ghon tubercles or lesions on the lungs and the extent of the disease (cheesy caseations)

–Indicates presence and extent of disease process but cannot differentiate active from inactive form

–

WBC and ESR increased

A + reaction is noted if the induration is greater than 5mm

This means that the patient has had contact with tubercle bacillus.

It does not mean that active disease is present in the body . (antibodies are now present)

Check for vaccination with BCG

DIAGNOSTIC TESTS TB

¨Goal of treatment is to prevent transmission, control symptoms, and prevent progression of the disease

¨6-12 months, may be as long as 24 months

¨2-4 meds Given concurrently

¨Mycobacteria grow slowly, resistance is common

vImproper or noncompliant use of treatment programs may cause the development of mutations in the tubercle bacilli resulting in a multidrug resistant strain of TB (MDR-TB

(+) Mantoux test, (-) CXR, and at risk for the disease are treated prophylactically to prevent development of active TB

Isoniazid (INH) for 9-12 months

Medical management TB

Combination drug therapy is most effective

–It destroys the organism and minimize development of multiple drug resistant strain of the bacilli

–After TB meds have been given for 2-3 weeks, the risk of transmission is reduced greatly

ACTIVE TB

Drug of choice

Take with meals if GI upset otherwise take one hr before or 2hr after meals. Absorption is decreased if given with food

Avoid antacids exp. Aluminum based – decrease absorption

Peripheral neuritis

– drug is usually given with Vitamin B6 (Pyridoxine) to prevent this side effect

Hepatitis

Nausea, vomiting, diarrhea, stomach pain

Avoid foods with tyramine

– aged cheese, smoked fish, tuna, sauerkraut, avocado etc.

Combined with INH will make you sicker

Drugs for TB : INH Isoniazid

150-300mg , maximum dose 600mg /day

S/S: hepatotoxicity, hepatitis, blood dyscrasias

Steven Johnson’s syndrome

Red/orange stain to urine, feces, saliva, skin, sputum, sweat and tears ..

Rifampin (+ INH)

15mg/kg po daily or 50mg /kg twice weekly when use in combination with other TB drugs. Max. 1200mg/day

S/S: optic neuritis leading to color blindness (exp.Red- Green)

Peripheral neuritis; GI irritation

Gouty arthritis from ^ uric acid levels

Ethambutol/myambutol

Bactericidal. Kills mycobacterium present in macrophages

S/S: hepatotoxicity, thrombocytopenia

Hyperuricemia- gout (hot painful, swollen big toe, ankle or knee)

Gi irritation

Pyrazinamide (PZA

Not used as much theses days; has now been replaced by Ethambutol

S/S GI upset, fever, rash, hepatitis

Fluid retention because of high sodium content

150mg/kg/day

Para-Aminosalicylic Acid

Antibiotics- aminoglycosides

IM/ IV

S/S: nephrotoxicity

8th cranial nerve damage- ototoxicity

Streptomycin

Maintain prescribed isolation precautions

Diet high carbohydrate, protein, iron & Vit. C.

Small frequent meals. Stress food & meds combinations

Check for vaccination with BCG vaccine (Bacille Calmette-Guerin Vaccine)

Lifestyle changes

Review other nursing measures in the Hinkle chapter.

NURSING MANAMGEMENT TB

Rheumatoid arthritis (RA) is a chronic disease in which various joints in the body are inflamed, leading to swelling, pain, stiffness, and the possible loss of function.

Rheumatoid arthritis should not be confused with other forms of arthritis, such as osteoarthritis or arthritis associated with infections.

Rheumatoid arthritis is an autoimmune disease in which the body's immune system attacks joints and other tissues.

The pattern of joints affected is usually symmetrical, involves the hands and other joints, and is worse in the morning.

Rheumatoid arthritis is a systemic (body-wide) disease, involving other body organs, whereas osteoarthritis is limited to the joints. Both forms of arthritis can be crippling.

Synovitis

Synovium Thickens, Fluid Accumulates

Destructive Pannus Erodes Joint Cartilage, Destroys Joint Bone

Pannus Converted to Bony Tissue

Joint Deformity

Other Connective Tissue Affected

RHEUMATOID ARTHRITIS

Early Symptoms

Bilateral, Symmetrical Joint Inflammation

Reddened, Warm, Swollen, Stiff, Painful

Stiffness After Resting

Activity Decreases Pain and Stiffness

Low Grade Fever, Weakness, Fatigue, Anorexia

Late Symptoms

Joint Deformity

Secondary Osteoporosis

SIGNS AND SYMPTOMS RA

Unknown

Genetic Predisposition

Environmental

Abnormal Autoimmune Response – Antibodies (Rheumatoid Factor)

some environmental or biologic trigger, such as a viral infection or hormonal changes

ETIOLOGY RA

Health history: include onset of and evolution of symptoms, family history, past health history, and contributing factors

Functional assessment

Arthrocentesis

X-rays, bone scans, CTs, and MRIs

Tissue biopsy

Blood studies

Patient Assessment and Diagnostic Findings RA

Rheumatoid Factor (RF)

Red Blood Cell (RBC)

C4 Complement Decreased

Erythrocyte Sedimentation Rate (ESR)

Antinuclear Antibody (ANA)

C-reactive Protein (CRP)

DIAGNOSIS RA

Medication

Disease-modifying Antirheumatic Drugs (DMARDs)

Sulfasalazine (Azulfidine)

Leflunomide (Arava)

Etanercept (Enbrel)

Adalimumab (Humira)

Methotrexate -antineoplastic

Gold salts- antiflammatory effect

Prednisone

NSAIDs – Indocin, motrin, naprosyn etc.

Salicylates -ASA

COX -2 Inhibitor- Celebrex

Heat/Cold

Balanced Rest and Activity

Surgery – Total Joint Replacement

Therapeutic Interventions RA

Acute Pain

Disturbed Body Image

Fatigue

Self-care Deficit

Impaired Physical Mobility

Deficient Knowledge

Ineffective coping

NURSING DIAGNOSIS RA

Disease Process

Medication Management

Rest and Exercise

Vocational Counselor

Community Resources

PATIENT EDUCATION HR

Major goals may include:

Relief of pain and discomfort

Relief of fatigue

Promotion of restorative sleep

Increased mobility

Maintenance of self-care

Improved body image

Effective coping

Absence of complications

Nursing Process: The Care of the Patient with a Rheumatic Disease—Planning

Autoimmune Disease

More than 80 autoimmune diseases

75% of autoimmune diseases affect women

One of the top 10 causes of death in women 65 and younger

Lupus: Wolf

Systemic Lupus Erythematosus (SLE)

1.4 million cases of lupus in the USA

90% are women

80% diagnosed between 15 and 45 years of age

50% have organ-threatening disease to kidneys, heart, lungs, liver, CNS, and hematopoetic system.

INCIDENCE OF LUPUS

Definition:

Chronic, inflammatory disturbance caused by an exaggerated production of “auto-antibodies.”

Immune complexes and fibrin deposit in blood vessels, collagen, and in organs

Can result in necrosis of glomerular capillaries

Systemic Lupus Erythematous

Abnormal Antibodies

Immune Complex Formation

Complement System Activation

Affects Connective Tissue

Pathophysiology

SYSTEMIC LUPUS ERYTHEMATOUS

Disturbance is probably caused by some combination factors of:

1. Genetic

2. Hormonal

3. Environmental

Immuno-Regulatory

SYSTEMIC LUPUS ERYTHEMATOUS

Genetics: Occurs in families by no gene isolated yet.

Hormonal: Estrogen metabolism is abnormal, flares with pregnancy and post-partum and post-menopausal HRT

Environmental: Sunlight, stress, burns, infection, antibiotics

SYSTEMIC LUPUS ERYTHEMATOUS

Drugs:

Hydralazine (Apresoline)

Procainamide (Pronestyl)

Isoniazid (INH)

Chloropromazine (Thorazine)

Anticonvulsants

NOTE: Usually if taken away, process goes away.

SYSTEMIC LUPUS ERYTHEMATOUS

Systemic Lupus Erythematous (SLE)

Multiple organs affected

1 test will not diagnose – Watch

signs/symptom

Discoid Lupus erythematous

Mild involving skin of face, neck, cheeks, etc..

Rarely progresses to Systemic Lupus

Drug induced lupus

Symptoms go away when triggering drug is

removed

TYPES OF LUPUS

NOTE: Not a specific syndrome – varies from patient to patient

• Can be insidious or acute
• Can be mild or rapidly progression to organ failure
• Characteristically has exacerbations (flares)
• Has times of remission
• Presents with vague, nonspecific symptoms
• Fever
• Fatigue
• Weight Loss
• Arthralgia
• Malaise Note: Symptoms usually precedes or precipitates an exacerbation Many patients are undiagnosed for years !!

HISTORY/PHYSICAL LUPUS

Note: 4 or more symptoms simultaneously or

serially

Most common sites are:

Cutaneous

Muscle Tissue

Lining of the lungs (pleurisy)

Pericarditis

Nervous system

Kidneys

CLINICAL MANIFESTATIONS LUPUS

80% have Skin Manifestations:

Skin: butterfly rash across the cheeks and bridge of the nose (40% of patients)

Diffuse maculopapular rash upon sun exposure (flat pimple like)

Discoid lesions (round like coins)

Both can itch, burn and cause “red palms”

Alopecia

Ulcers (Nasal or oral) - 35% of patients

Pruritus

ASSESSMENT LUPUS

Polyarthralgia
Morning stiffness (95%)
Migratory without signs of overt
inflammation
Usually involves hands, feet,a dn knees
Usually symmetrical
Deformity is rare

MUSCOSKELETAL LUPUS

Atherosclerosis
Pericarditis (25%)
Pleurisy (50%)
Raynaud’s Syndrome (20%) – Patriotic fingers
Pleural Effusions

Cardiovascular disease – Cardiac Precautions

CARDIOPULMONARY LUPUS

Renal Disease (50% of patients)

50% with proteinuria, cellular casts
Microscopic hematuria
Elevated serum creatinine
Ankle edema,
Frequent UTI’s
10% develop renal failure

RENAL LUPUS

Lupus Nephritis – leading cause of death followed by cardiac involvement

Develop High Blood Pressure
Must monitor lab values (BUN/CR), electrolytes, blood chemistry.

Lupus Nephritis

Seizures (15%)
Headaches
Dizziness
Strokes
Organic Brain Syndrome (memory loss, disorientation, depression)
Psychosis

CENTRAL NERVOUS SYSTEM LUPUS

Caused by antibodies attacking blood cells

Anemia (98%) with reticulocytosis (excessive RBC’s, but immature)

Leukopenia (80%) – Highly prone to infections (lymphs <4000
Note: Carries a 30% mortality

Thrombocytopenia (36%) platelets <100,000

Hematologic LUPUS

Dysphagia
Anorexia
Diarrhea
Vomiting
Hemorrhage (upper of lower GI Bleed)
Pain

GI SYMPTOM LUPUS

Biopsy
Erythrocyte Sedimentation Rate
Immunological Tests
Antinuclear Antibody Titers
Antibodies Against SR Proteins

DIAGNOSTIC TESTS LUPUS

Fatigue

Fever without infection

Weight Loss

ASSOCIATE SYMPTOMS LUPUS

ELEVATED:
Sed Rate: Erythrocyte Sedimentation Rate (ESR)
(measures the rate of the fall of RNC suspended in plasma)

Note: Falls faster when lots of antibodies (gamma globulins) are attached.

Positive Serum Tests:

High + ANA (occurs when the body is fighting own DNA – in autoimmune diseases)

+LE Prep – 75% of those with lupus will have these cells-lots of false+ tests.

DIAGNOSTIC STUDIES LUPUS

• Infection or Injury
• Immunity
• Fatigue
• Stress
• Tissue Integrity & Clotting
• Thermoregulation
• Gas Exchange

• Inflammation