Things to note

Somethings that came up on a test..

1. When you give the FIRST DOSE of captopril (ACE inhibitor) have your client lie down for about 3 hours because they will be hypotensive after.
2. Make sure you check your clients apical pulse before you give captopril because it can cause you client to be hypotensive, you need to make sure they are not bradychardic before you give the med to them. If they are bradychardic then hold the med according to hospital policy i think.
3. Pentam can make your client hypoglycemic
4. To test for cryptoccocal infection in HIV ask the client to put his chin to his chest if infected he/she will find it difficult because it causes a stiff neck
5. Before you do anything to a client with eye complaints assess for visual acuity
6. Assess for orthostatic hypotension after you give lisinopril
7. First priority in sickle cell crisis patient is pain second is risk of injury due to decreased oxygenation
8. No Benadryl with alchohol.
9. If you get a question that says whats the first thing the nurse should do always go for the answer with assess especially if theres only one asnwer with assess.
10. Hope this helps.

Care of the Patient With HIV Adult healthh 1

Care of the Patient With HIV Adult healthh 1 Lecture notes




Care of the Patient With HIV
Adult Health I

Human Immunodeficiency Virus Infection
 HIV varied course to AIDS
 AIDS is the End Stage of this chronic, progressive immune function disorder

Pathophysiology
 Retrovirus
 HIV is an RNA virus that replicates backwards
 Replicate within a living cell
HIV infects cells with CD4+T cells
 Lymphocytes, monocytes
 Normal CD4 +T cells = 800-1200cells/ul
 Live for 100 days, with HIV die after only 2
 Virus destroys 1 billion cells a day
 HIV cells destroys the bodies abilities to replace cells
 Decrease in immune capacity and
 Develop opportunistic infections

Transmission
 Fragile virus
 Specific conditions allow transmission
 Sexual intercourse with infected partner
 Blood and blood products
 Pregnancy during delivery
 Breast feeding
 It is not spread casually


Primary Infection: Acute HIV Infection
 The development of HIV antibodies or seroconversion:
 Symptoms 1-3 weeks after infection
 HIV level is ↑and CD4+T cell decrease but returns to normal
 Lasts 1-2 weeks
 Symptoms include:
 Flu like symptoms, ,Fever, enlarged lymph nodes, pharyngitis, headache, malaise, nausea and rash
 Symptoms can be misinterpreted

HIV Asymptomatic: CDC Category A
 Often asymptomatic
 Can develop symptoms: fatigue, headache, low grade fever, night sweats and lymphadenopathy
 Symptoms are vague and non specific
 People unaware of infection
 Continue high-risk behavior
 A1: CD4 ≥ 500/µL
 A2: CD4 = 200-499/µL
 A3: CD4 <>HIV Symptomatic: CDC Category B
 Development of 1 or more opportunistic infections
 B1: CD4 ≥ 500/µL
 B2: CD4 = 200-499/µL
 B3: CD4 <>AIDS: CDC Category C
 Development of opportunistic infections, cancers, wasting syndrome, HIV encephalopathy, etc
 Classified as having AIDS
 C1: CD4 ≥ 500/µL
 C2: CD4 = 200-499/µL
 C3: CD4 <>Diagnostic and Laboratory Studies
 Based on detection of HIV specific antibodies EIA – detects serum antibodies
 Western Blot - immunfluorescence assay
 ELISA enzyme-linked immunosorbent assay (detect antibodies that bind to HIV antigens)
 Viral Load
 Quantifies HIV viral load
 Lower level associated with longer survival time and longer delay in onset to AIDS
 Other pertinent lab data:
 WBC – neutropenia, thrombocytopenia
 Anemia – disease or drug related
 Abnormal LFT – disease or drug related

Aims of Collaborative Care
 Monitoring of disease progression
 Baseline assessment
 Patient education
 Psycho-social aspects
 Prevent opportunistic infections
 Monitoring antiretroviral treatment
 Management of signs and symptoms
 Prevent complications of treatment


Drug Therapy and Interventions
Three classifications of drug therapy
1. Inhibit the activity of reverse transcriptase
Zidovudine ( AZT, Retrovir)
Lamivudine (3TC, Epiver)
Stavudine (D4T, Zerit)
Combivir (lamivudine, zidovudine combination)


Drug Therapy and Interventions
2. Protease inhibitors
Indinavir (Crixivan)
Nelfinavir (Viracept)
Ritonivir ( Norvir)
3. Fusion inhibitors
Enfuvirtide (Fuzeon)


Use of Antiviral Drugs
 Multiple medications
 Rigid dosing schedule
 Multiple side effects:
 Nausea, vomiting, diarrhea
 Rash
 Liver function changes
 Peripheral neuropathy
 Taste changes

Preventive Prophylactic Interventions
 Hepatitis B vaccine
 Influenza Vaccine
 Pneumonia
 INH
 Zovirax
 PPD

Nursing Diagnosis
 Pain, neuropathy, arthralgia
 Anxiety
 Altered thought process r/t hypoxemia
 Altered nutrition less than body requirements
 Risk for activity intolerance
 Diarrhea
 Impaired gas exchange

Nursing Interventions
 Reduce Fear
 Prevent Infection
 Improve Nutritional status
 Relieve oral Discomfort
 Minimize effects of diarrhea
 Managing altered thought process
 Reducing a fever
 Improve breathing pattern
 Improve management of therapeutic regimen

Patient Teaching
 Perinatal Risks
 Occupational exposure Risks
 Reduce Risk-reducing behaviors
 Safe sex
 Drug paraphernalia
 Patient Teaching
 Side effects of drugs
 Alternate methods of pain relief
 Energy conservation
 Infection control measures
 Information about support groups and community resources


Transmission to Health Care Workers
 Use standard precautions with ALL patients
 Use needle safe devices
 If exposed, immediately wash area
 Report exposure
 Depending on level of exposure, may need Post exposure prophylaxis (PEP)
 Give ASAP, but more than 72h post-exposure
 Give for 4 weeks
 http://www.cdc.gov/MMWR/preview/mmwrhtml/rr5409a1.htm

Assessment and Management of Patients with Hypertension Adult Health 1

Assessment and Management of Patients with Hypertension Adult Health I


What is Blood Pressure?
Product of cardiac output x peripheral resistance

Hypertension
Defined by Seventh Report on the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC 7) as:
systolic blood pressure = or >140mmHg and/or diastolic blood pressure = or > 90mmHg
Requires 2 or more readings on 2 or more occasions
Affects 28% - 31% of adults in US

Classification of Hypertension
Types of Hypertension

Primary Hypertension
90% - 95% of all hypertension
No known cause
Secondary Hypertension
Remaining 5% - 10% of hypertension

HTN r/t other causes
Example: Pheochromocytoma


Facts About Hypertension
"The Silent Killer"
Incidence is greater in southeastern U.S. and among African-Americans
Other factors that influence HTN:
Increased sympathetic nervous system activity
Increased reabsorption of sodium, chloride and water by the kidneys
Increased activity of the renin-angiotensin system
Decreased vasodilatation
Insulin resistance


Recommendations for Follow-up Based on Initial BP Readings
Normal BP – recheck 2 years
Pre-hypertension – recheck 1 year
Stage 1 hypertension – confirm within 2 months
Stage 2 hypertension – evaluate or refer to source of care within 1 month
BP 180/100 or >, evaluate or refer for care within 1 week


Major Risk Factors
Elevated BP readings
Smoking
Obesity
Physical inactivity
Dyslipidemia
Diabetes mellitus
Microalbuminuria or GFR <60
Older age
Family history


Signs and Symptoms
Elevated bp readings
If any sx are reported:
Retinal changes
Headache
Dizziness
Epistaxis
Sx usually only reported in cases of hypertensive emergencies


Manifestations of Hypertension
Usually NO symptoms other than elevated blood pressure
Symptoms seen related to organ damage are seen late and are serious:
Retinal and other eye changes
Renal damage
Myocardial infarction
Cardiac hypertrophy
Stroke


Lifestyle Modifications
Weight loss
Reduced alcohol intake
Reduced sodium intake
Regular physical activity
DASH diet


DASH (Dietary Approaches to Stop Hypertension) Diet

Advantages of Lifestyle Modification
Weight loss of 10kg can reduce BP 5-20mmHg
Sodium reduction (2.4g/day) can reduce BP 2-8mmHg
Physical activity can reduce BP 4-9mmHg
Moderation of alcohol can reduce BP 2-4mmHg

Medications
Usually initial medication treatment is a diuretic, a beta blocker, or both
Low doses are initiated and the medication dosage is increased gradually if blood pressure does not reach target goal
Additional medications are added if needed
Multiple medications may be needed to control blood pressure
Lifestyle changes initiated to control BP must be maintained

Medication Therapy for Hypertension
Diuretic and related drugs
Thiazide diuretics (HCTZ)
Loop diuretics (Furosemide)
Potassium-sparing diuretics (Triamterene)
Aldosterone receptor blockers (Spironolactone)
Central Alpha2-Agonists and other centrally acting drugs (Clonidine)
Beta blockers (Atenolol)

Medication Therapy for Hypertension
Alpha and beta blockers (Carvidilol)
Vasodilators (Nitroglycerine)
Angiotensin-converting enzyme (ACE) inhibitors (Enalapril)
Angiotensin II antagonists (Valsartan)
Calcium channel blockers
Nondihydropyridines (Diltiazem)
Dihydropyridines (Amlodipine)

Nursing Assessment
History and risk factors
Assess potential symptoms of target organ damage
Angina, shortness of breath, altered speech, altered vision, nosebleeds, headaches, dizziness, balance problems, nocturia
Cardiovascular assessment: apical and peripheral pulses
Personal, social, and financial factors that will influence the condition or its treatment

Nursing Diagnoses
Knowledge deficit regarding the relation of the treatment regimen and control of the disease process
Noncompliance with therapeutic regimen related to side effects of prescribed therapy

Patient Centered Goals
Patient understanding of disease process
Patient understanding of treatment regimen
Patient participation in self-care
Absence of complications

Interventions
Patient teaching
Support adherence to the treatment regimen
Consultation/collaboration
Follow-up care
Emphasize control rather than cure
Reinforce and support lifestyle changes
A lifelong process

Gerontologic Considerations
Noncompliance
Include family
Understanding of therapeutic regimen
Reading instructions
Monotherapy

Hypertensive Crises
Hypertensive emergency
Blood pressure >180/120 and must be lowered immediately to prevent damage to target organs.
Hypertensive urgency
Blood pressure is very high but no evidence of immediate or progressive target organ damage.

Management of Hypertensive Emergency
Reduce BP 25% in first hour
Reduce to 160/100 over 6 hours
Then gradual reduction to normal over a period of days
Exceptions are ischemic stroke and aortic dissection
Medications
IV vasodilators: sodium nitroprusside, nicardipine, fenoldopam mesylate, enalaprilat, nitroglycerin
Need very frequent monitoring of BP and cardiovascular status

Management of Hypertensive Urgency
Patient requires close monitoring of blood pressure and cardiovascular status.
Assess for potential evidence of target organ damage.
Medications
Fast-acting oral agents: beta-adrenergic blocker- labetalol; angiotensin-converting enzyme inhibitors: captopril or alpha2-agonists-clonidine

Nursing Care of the Patient with Hematologic Problems: Adult Health I

Nursing Care of the Patient with Hematologic Problems

Definitions
Hematocrit:
Measure of packed cell volume of RBC expressed as a %
Women: 38-47%
Men: 40-54%
Hemoglobin
Measurement of gas carrying capacity of RBC
Men: 13.5-18g/dl
Women: 12-16g/dl
Neutropenia
abnormally low number of neutrophils in the blood
< 1500…normal 3000 – 7000mm³
Neutrophils, a type of white blood cell, help fight bacterial infections. Most abundant WBC
Side effects of medication, chemotherapy, viral infections

Reticulocytes
Are young red cells just released from the bone marrow. The Retic count tells us how the marrow factory is doing.
Immature RBC’s, less than 1%
Thrombocytopenia
Platelet counts are between 150,000-400,000ul
low platelets, below 100,000-150,000
Bleeding may occur
ESR Erythrocyte sedimentation rate
Indicative of inflammation
Increased ESR is common during acute and chronic inflammatory reactions
Women: 1-20mm
Men: 1-15mm



Anemias
A deficiency in the number of RBC, quantity of HgB and the volume of HCT
There is an abnormality with the structure or function or number of RBC’s
Anemia is not a disease, it is a manifestation of a pathologic process.
primary hematological problems
secondary to defects in other body systems
This can lead to hypoxia, a decrease in the oxygen carrying capacity of the blood.
The clinical manifestations anemia are primarily caused by the body’s responses to tissue hypoxia.

Clinical Manifestations of Anemia
Mild Anemia
10-14 Hgb.
Generally asymptomatic, symptoms can occur with disease or exertion
Moderate Anemia
Hgb 6-10
Cardiopulmonary symptoms may be increased and may be associated with rest as well as activity.
Palpitations, fatigue, dyspnea, & diaphoresis
Severe Anemia
Hgb less than 6.
Symptoms involve many body systems.
It is caused by severe tissue hypoxia. Pallor, chronic fatigue, chills, ↑ HR, murmurs, can lead to CHF, angina, MI
Cardiac effects when Hgb is too low.
Ischemia
Tissue hypoxia
Chronic fatigue
Sensitivity to cold
The blood is shunted to the major organs
Pallor – reduced hemoglobin and blood flow to skin
Decreased CO leads to Increased HR
Murmurs due to lack of blood volume
CHF can occur to the increased strain on the heart. In severe cases, angina and MI can occur.

Nursing and Gerontological Considerations
Anemia is common in older adults
Anemia of chronic disease
Nutritional deficiencies
Signs and symptoms unrecognized
Attribute them to the normal aging process
Common signs and symptoms include: pallor, confusion, ataxia, fatigue, worsening angina.

Nursing Implementation:
Dietary and lifestyle changes
Blood products
Blood transfusions
Drug therapy – Erythropoietin (Procrit, Epogen)
Oxygen therapy


Nutrients Needed for Erythropoiesis
Vitamin B12
RBC maturation – red meats
Folic Acid
RBC maturation – Green leafy vegetables, liver, meat, fish legumes, whole grains
Iron
Hemoglobin synthesis – liver and muscle meats, eggs
Vitamin B6
Hemoglobin synthesis – meats, legumes, potatoes
Amino Acids
Synthesis of nucleoproteins –eggs, meat, milk, poultry, fish
Vitamin C
Aids in iron absorption – citrus fruits, green leafy veggies, strawberries, cantaloupe

Anemia’s Related to Decreased Erythrocyte Production
Iron Deficiency Anemia
Found world wide due to poor nutrition
Inadequate dietary intake
Iron is obtained from food and dietary supplements
If you eat 12 mg. of iron per day only 10% is absorbed

Malabsorbtion
After GI surgery or malabsorbtion syndromes
Blood loss
Chronic GI bleed scan cause loss of 2-4mls
Black stools or melena requires 50 to 75ml of blood from UGI tract
At risk population:
Pregnancy because of increased iron needs
Pre-menopausal women
Low socioeconomic background
Older adults
Blood loss

Anemia's Related to Decreased Erythrocyte Production
Clinical Manifestations
Asymptomatic early in the disease
Chronic Symptoms:
Pallor – most common
Glossitis – inflammation of the tongue
Cheilitis – lesions of the corners of the lips
Headache, dizziness, parasthesias, DOE, burning sensation of the tongue…..all due to ↓ iron.

Diagnostics
Lab testing
Stool for occult blood
Colonoscopy
Take iron in an acidic environment, with OJ, empty stomach, one hour prior to breakfast. Don’t take with milk, reduces absorption. > fluids to prevent constipation.

Treatment
Goal: treat underlying cause Foods > in iron = liver, meat, eggs, dark green veggies, raisins, prunes, apricots, fortified cereals, breads.
Anemia's Related to Decreased Erythrocyte Production

Drug therapy
Oral Iron Replacement – Ferrous Sulfate
Iron is best absorbed from the duodenum
Enteric coated or SR and not wise choice
Dosage should be 150mg to 200mg TID
300mg of ferrous sulfate has 60mg of iron available
Best absorbed in an acidic environment
Take with OJ, empty stomach, one hour prior to breakfast.
Don’t take with milk, reduces absorption.
↑ fluids to prevent constipation.
GI side effects : heartburn, constipation and diarrhea
Diet teaching: Foods ↑ in iron: liver, meat, eggs, dark green veggies, raisins, prunes, apricots, fortified cereals, breads

Nursing Interventions
Obtain a history of symptoms, dietary intake and past hx of anemia
Possible sources of blood loss
Examination for: Tachycardia, pallor DOE, s/s of GI or other bleeding
Assess diet for inclusion of Iron rich foods
Assess level of fatigue and sleep
Assist in scheduling activities and rest patterns
Maximize tissue perfusion
Assess /Evaluate for palpitations, chest pain, dizziness and SOB….minimize activities which cause these symptoms
Elevate HOB and supplemental Oxygen

Education
Proper nutrition
Well balanced diet
Teach about Iron supplements
Take on empty stomach
Epigastric discomfort
Stool changes
Follow up lab studies

Vitamin B12 (Pernicious) Anemia
Gastric secretion of Intrinisic Factor(IF) is defective
IF is required for Cobalamin absorption
Impaired B12 absorption in the small intestine due to lack of IF or destruction of the parietal cells.

Clinical manifestations: as Anemia- normal levels 200-900ng/L
Sore tongue, anorexia, vomiting and abdominal pain
Neuromuscular manifestations-parasthesias, weakness
Low Hgb
Schilling test abnormal test = pernicious anemia
Indirect test of IF deficiency
Evaluates the ability to absorb vitamin B12

Nursing management
includes IM B12 1000mg weekly IM or intra-nasally.
B12 for the rest of their life due to lack of IF
Without vit B12 leads to macrocytic anemia, GI disorders, paresthesia, gait problems & death

Folic Acid Deficiency
Folic acid is necessary for DNA synthesis leading to RBC formation and maturation.
Common Causes:
Poor nutrition (lack of green vegetables, liver, fruits)
Malabsorption syndromes-small bowel disorder
Drugs, alcohol and hemodialysis (folic acid is lost).
Clinical manifestations are similar to vitamin B 12 deficiency

Treatment:
Folic Acid replacement: PO 1-5 mg/OD, standard dose is 1mg.
Vitamin C helps with development
Encourage liver, green veggies, legumes


Blood Loss
Acute Blood Loss
Trauma or Blood vessel rupture due to trauma

Complications of surgery
Diseases that disrupt vascular integrity i.e Shock, the body reacts by vasoconstriction.
30% blood loss
symptoms with exertion only
40% blood loss
rapid, thready pulse, CO low, clammy skin. Blood is being shunted centrally
50% Blood loss
shock & potential death
First identify the cause and stop bleeding
Expand blood volume, pain from organ displacement, check blood work, administer albumin, & colloids

Polycythemia Vera
Overproduction of RBC’s ↑ blood viscosity, volume
Myeloproliferative disorder – Chromosome mutation
Hgb to 18g/dl, RBC 6 million/mm, HCT > 55%.
Common in patients over 50
Splenomegaly and hepatomegaly – organ engorgement
Headache, ↑BP, vertigo, dizziness, angina
Increased uric acid production – gout
Plethora or ruddy complexion, pruritis
Hemorrhagic phenomenon
Nosebleeds, petichiae, thrombus-↑stroke risk

Treatment: aimed at ↓blood volume and viscosity
Phlebotomies to keep Hct < 45%
Allopurinol for uric acid
Teach S/S of bleeding & clotting, discourage smoking, low sodium diet, frequent rest periods
Myelosuppressive agents-Hydrea, Alkeran
Antiplatelet therapy – ASA
Chemotherapy-bone marrow suppression

Thrombocytopenia
Number of platelets is abnormally low
Below the normal of 150,000 to 400,000
Counts below 50,000 cause prolonged bleeding, below 20,000 life threatening
Platelets help the blood clot
Manifests as prolonged bleeding or spontaneous bleeding.
Petechiae = micro hemorrhages.
Purpura when petechaie are numerous, the resulting reddish skin bruise.
Ecchymosis larger purplish lesions that are caused by hemorrhage
Causes: Leukemia, Drugs-ASA, Infection, Lupus
Immune thrombocytopenia, patient makes antibiodies against their own platelets( survival is 1-3 days).

Thrombocytopenia Treatment Options:
Platelet transfusions
Steriod therapy
Splenectomy to reduce macrophages which destroy platelets.
Avoid sharp objects, razors, no contact sports, no IM’s, no rectal temps, oral care, no spicy foods.
If blood work, hold for 5 minutes or greater
Watch for hidden ASA in OTC
Periodic check for bleeding times and platelet counts…
NO ASA

DIC-Disseminated Intravascular Coagulation
Abnormal response of the clotting cascade
Small blood clots develop throughout the blood stream blocking small vessels depleting platelets and clotting factors needed to control bleeding
The clotting factors run out & there is excessive bleeding.

Clinical manifestations:
Bleeding -Pallor, petechiae, hematomas, GI bleeding, hematuria, dizziness, headache, musculoskeletal changes
Thrombosis- cyanosis, ischemia, pulmonary emboli, resp. distress
Life threatening, mortality is > 80%
Occurs with septic shock.
Bleeding out of every orifice, platelets are destroyed.
PT & PTT is increased, Platelets are decreased.

Medical Management:
Tx underlying cause
Heparin, Xigris

Nursing Management:
Early detection of bleeding

Neutropenia
Reduction in the neutrophils
Neutrophils play a role in phagocytosis of pathogenic microbes
Definition: neutrophil count of less than 1,000- 1,500/uL
Normal level: 4000-11,000/uL
It is not a disease, it is a syndrome that occurs with a variety of diseases
As a result of chemotherapy
Patient is predisposed to an infection:
Observe for chills, ↑temp, sore throat and cough
Abnormal s/s of inflammation
Minor infections can lead to sepsis
Good mouth care to prevent pneumonia.
Protective isolation, private room, limit visitors, handwashing.
Normal flora, transmission by hand, food
Neupogen – stimulates production of neutrophils

Leukemias
Acute Lymphocytic (ALL)
Most common in children
Malignant growth of Lymphoblasts
Large numbers of immature white blood cells
Proliferate the bone marrow and lose ability to mature
Chronic Lymphocytic (CLL)
Slow growth of lymphoid cells in lymph nodes, failure of bone marrow, invasion of malignant cells into the organs
Most age 50 > and men
Prognosis poor

Leukemias
Acute Myelogenous Leukemia (AML).
Make to many immature myeloblasts infiltrate organs
Normal cells turn in to granulocytes (WBC)… leukemia blast cells don’t
Most common adult (15-39) leukemia, exact cause is unknown
Prognosis generally poor

Chronic Myelocytic Leukemia (CML)
Slow abnormal growth of granulocytes
Chromosomal abnormality called Philadelphia chromosome.
Affect age 50 >, more males than females
Prognosis generally poor, worse if Ph chromosome present

Leukemia Signs & Symptoms
Eccymoses
Petechiae
Open infected lesions
Pallor
Bleeding gums
Anorexia
Weight loss
Enlarged liver and spleen
Hematuria

Leukemia Treatment
Chemotherapy
Bone Marrow Transplantation
Leukemia Nursing Interventions
Infection prevention
Injury prevention
Energy conservation
Blood replacement therapy
Psychosocial support
Home care education related to care of: CVC, diet, infection prevention, bleeding risk

Hodgkins & Non Hodgkins

Hodgkin’s disease
Malignant disorder of unknown cause
Reed sternberg cells invade lymph nodes
Gigantic atypical tumor cell which multiplies and replaces normal cells.
Painless superficial adenopathy or enlarged lymph nodes
Fever, night sweats, weight loss

Non Hodgkin’s Lymphoma
Malignancies of the lymphoid tissue
Abnormal lymphocytes invade lymph nodes organs bone marrow and blood.

Symptoms are the same
Treatment
Outpatient chemo & radiation
High risk for infection, as survival rate increases
Risk of secondary malignancy increases

Transfusions
Administration of blood or blood components
Need #20 or larger IV line
Establish IV access before getting blood from blood bank!
Check ABO compatibility
Inspect blood for abnormalities
Check pt ID
Stay with pt during first 15min of transfusion

Monitor vs per protocol
Monitor for s/s adverse reactions
PRBCs – give over 2h-4h (but not more than 4h)
FFP, Platelets- run in as quickly as possible

Transfusions
ABO Incompatibility
4 types of blood- A, B, AB, O
A carries A antigen, B carries B antigen, AB carries A&B antigens, O has no antigens
O- universal donor
AB+ universal recipient
Rh factor
- absent
+ present
Blood testing is done to determine compatibility

Transfusion Complications
Febrile non-hemolytic reaction
Temp rise 1°C or greater during infusion
Tx with antipyrectics
Consider use of leuko depleted blood for future transfusions

Acute hemolytic reaction
Life threatening
Cause- ABO incompatibility
s/s- fever, chills, back pain, nausea, chest tightness, dyspnea, anxiety
Stop blood immediately and start transfusion reaction protocol

Transfusion Complications
Allergic reaction
Cause- rx to proteins in blood
s/s- pruritis, hives (mild), to bronchospasm, laryngeal edema, shock (life threatening)
Tx- antihistamines, steroids, epinephrine
Circulatory Overload
Cause- too rapid infusion in vulnerable individual
s/s- dyspnea, tachycardia, anxiety, frothy pink sputum, crackles, JVD
Tx- give blood slowly, diuretics, O2, morphine if dyspnea severe

Transfusion Complications
Bacterial Contamination
s/s- fever, chills, hypotension
Tx- prevention is key; stop transfusion, broad-spectrum abt

Disease Acquisition
Hep B, Hep C, CMV, HIV, Creutzfeldt-Jakob Disease

Complication r/t Long-term Transfusions
Infection, sensitization to donor antigens, iron overload

Dermatologic Disorders in Adult Health for Nursing

Dermatologic Disorders Adult Health I Lecture notes

Pressure Ulcers
Causes
Pressure
Friction
Shear

Identify Risk Factors
Altered mobility
Altered mentation
Decreased sensory perception
Excess moisture
Poor nutrition

Braden Scale
Interventions for Patients at Risk
Use a scoring tool at regular intervals
Document skin condition on admission and daily
Turn and position q2h – use a turning schedule
Use lift sheets or lift devices
Moisturize dry skin
Use mild soaps and warm (not hot) water to bathe

Interventions for Patients at Risk
Heel/elbow protectors
Use moisture barrier creams
Keep linens dry and wrinkle-free
Do not massage over bony prominences
Diet rich in calories, protein, vitamin c, zinc, b vitamins
Use pillows to align properly and elevate limbs off bed
Use pressure-reducing mattress

Wound Assessment
Location
Size (length x width x depth)
Color
Exudate
Odor
Periwound condition
Tunnelling
Undermining
Presence of foreign bodies
Pain
Patient tolerance to procedure

Wound Assessment Documentation Example:
Stage IV sacral wound measuring 3cm x 2.8cm x1.7cm. 2cm tunnel at 5 o’clock. Small amount serous drainage, no odor present. Base of wound 90% granulation tissue, 10% yellow adherent slough tissue at 6 o’clock. Periwound skin intact. Wound irrigated with normal saline and wound filled with calcium alginate dressing and covered with transparent dressing. Patient denied pain, tolerated procedure without complaints. Nancy Nurse, RN.

Stage I
Redness that does not blanch
Skin intact
Stage II
Superficial break in the skin

Stage III
Extends to subcutaneous tissue but not into fascia
Crater-like appearance
Stage IV
Extends down into fascia and possibly bone
Undermining and tunnelling become more common

Transparent Dressings
Useful to prevent shearing and friction wounds or as a secondary dressing
Limited absorption

Hydrocolloid Dressings
Useful for wounds with some exudate
Can be left in place for several days
Can be used as a secondary dressing

Foam Dressings
Highly absorbent
Can be left in place for several days
Calcium Alginate Dressings
Easily applied
Requires secondary dressing
Highly absorbent
Can be left in place for few days at a time
Can be used for autolytic debridement

Hydrogel Dressings
Adds moisture to dry wounds
Can be useful to debride
Can cause maceration if not used properly
Requires secondary dressing
Hydrofiber Dressings
Easily applied and atraumatic
Requires secondary dressing
Highly absorbent
Can be left in place for few days at a time
Can be used for autolytic debridement

Gauze Dressings
Needs frequent changes
Can use with topical agents
Can use to debride
Readily available and cost effective

Wound Vac Therapy
Useful for chronic wounds and wounds preparing for flap/graft surgery

Debridement
Used to remove necrotic tissue

Flap – Graft Surgery Management

Fluidized air bed
Totally off flap surgical site
Drain care
Pain management
Assess site for viability
Monitor for infection
Prevent post-op complications

Cellulitis
Usually caused by Staph or Strep infections
Clinical Manifestations:
Erythema
Edema
Drainage
Pain

Treatment:
Antibiotics – oral or intravenous (reserved for severe cases)
PCNs, Cephalosporins, Quinolones
Herpes Zoster (Shingles)
Caused by reactivation of varicella-zoster virus

Clinical Manifestations:
Malaise
Tingling, pain in area
Unilateral rash along set of dermatomes
Raised cluster of erythematous vesicles

Treatment:
Pain management
Antiviral (ex: Valcyclovir)
Prevention: Zostivax – 60y and older

Psoriasis
Autoimmune disorder where rate of cell division is sped up and plaque formation develops
Clinical Manifestations:
Thickened red plaques with silvery white scales
Usually found bilaterally in elbows, scalp, trunk, knees, outside surfaces of limbs

Psoriasis Treatment:
Topical steroids
Topical tar
Ultraviolet light therapy
Methotrexate
Biologics
Raptiva
Enbrel

Skin Cancer
Health Prevention Strategies
Limit sun exposure between 11:00a – 3;00p
Wear sunscreen
Wear opaque clothing and sunglasses
Examine skin monthly for lesions

Seek medical advice if any of the following:

Asymmetry
Border irregularity
Color changes
Diameter >6mm
Elevation
Treatment
Nonsurgical
Topical 5-FU
Interferon
Radiation
Immunotherapy – experimental
Surgical
Cryosurgery
Excisioncurettage and electrodessication

Nursing care of clients experiencing sensory stressors of the eye and ear

Nursing care of clients experiencing sensory stressors of the eye and ear Lecture notes


Vision stressors
Cataracts
Glaucoma
Retinopathy
Macular degeneration

Cataracts Overview
gradual, progressive thickening of lens
Clouding, blurring of lens distorts image & color projected onto the retina.
As cataract matures, opacity makes it difficult to see the retina & Visual acuity is restricted.
one of the leading causes of blindness in the world today
Increased incidence with age

Etiology of cataracts
Age-Related Cataracts Lens water loss and fiber compaction
Traumatic Cataracts Blunt injury to eye or head • Penetrating eye injury • Intraocular foreign bodies • Radiation exposure, therapy
Toxic Cataracts Corticosteroids • Phenothiazine derivatives Miotic agents
Associated Cataract Diabetes mellitus Hypoparathyroidism • Down syndrome • Chronic sunlight exposure
Complicated Cataracts Retinitis pigmentosa Glaucoma • Retinal detachment

Clinical manifestations
Decreased visual acuity and glare
Photophobia
Decreased color perception
Painless loss of transparency
Diplopia
Absence of red reflex

SURGICAL MANAGEMENT
Intracapsular Cataract Extraction
Extracapsular Cataract Extraction
Intraocular Lens Implantation
Aphakia - absence of lens
Complications:
Secondary Glaucoma
Retinal Detachment

Post procedure complications
PC: ocular inflammation
Administer steroid vs. NSAID drops to affected eye as prescribed
PC: Increased intraocular pressure
Avoid physical activities that may increase pressure
PC:IOL migration
Report visual disturbances once eye is unpatched
Pain
Use Tylenol for pain
PC: surgical site infection
Report fever, drainage or swelling of eye
Risk for injury
Wear eye shield/sunglasses
Discharge instructions

Cataract surgery Do’s
Do use prescribed eye drops, as instructed.
Do wear glasses or eye shield at all times to protect eye from injury, at least for 1 - 2 weeks.
Do wash your eye lid gently with a cotton ball or clean facecloth soaked with luke-warm tap water. Your surgeon will discuss the of sterile water, if necessary.
Do wear eye shield when showering or bathing for one week. Let the water hit your back not your face.
Cataract surgery Do’s
Do ask a family member or friend to help you wash your hair the first time. Do not get operated eye wet.
Gradually increase your activity on the advice of your eye surgeon. Sit in a chair to put on shoes.
Do sleep on back or unoperated side (place a pillow between your knees to help avoid turning over during sleep).

Cataract surgery Don’t’s
Do not rub or bump the operated eye.
Do not get water in the eye.
Do not strain.
Do not get constipated.
Do not lift anything heavier than 20 lbs., for the first week, after surgery.
Do not go swimming until your eye surgeon says you can.
Do not play contact sports.
Do not put your head down below your waist for 2-3 days when bending over.

Health Teaching
Report to surgeon: sharp, sudden pain in the eye, bleeding or increased discharge, lid swelling, decreased vision, or flashes of light or floating shapes.
Avoid activities that might increase IOP.
Review procedure for use of eyedrops.

Glaucoma
Group of ocular diseases resulting in increased IOP and decreased visual acuity
Primary open-angle glaucoma(POAG)
Most common type, slow to develop
Acute angle-closure glaucoma (AACG) is an ocular emergency

Pathophysiology
compromised drainage of aqueous humor circulation and the subsequent increase in IOP

Etiology of Glaucoma

Primary Glaucoma

• Aging
• Heredity
• Central retinal vein occlusion

Secondary Glaucoma

• Uveitis
• Iritis
• Neovascular disorders
• Trauma
• Ocular tumors
• Degenerative disease
• Eye surgery

Associated Glaucoma

• Diabetes mellitus
• Hypertension
• Severe myopia
• Retinal detachment

Clinical Manifestations
Headache or brow pain, nausea and vomiting, colored halos around lights, and sudden blurred vision with decreased light perception
mid-dilated nonreactive pupil, and a firm globe.
Cupping & atrophy of the optic disc, disc wider, deeper, turns white or gray
Change in Visual field measurement

Diagnostic Tests
Tonometry
IOP>21
tonometry must be performed and must demonstrate increased IOP.
Ophthalmoscopic exam
Cupping and atrophy of optic disc

Drug Therapy
Inhibition of aqueous humor: timolol, levobunolol, beta blockers, carbonic anhydrase inhibitors
Pupillary constriction: miotics, pilocarpine hydrochloride after initial therapy
Pilocarpine must be used with caution
Osmotic drugs part of emergency treatment for rapid reduction of IOP
No epinephrine used in angle-closure glaucoma because it dilates the pupil

Management
Intravenous gamma globulin
High dose of ASA while in hospital
Low dose ASA upon discharge
Base-line echocardiogram to assess coronary artery status

Surgical Management
iridotomy (LPI) performed 24-48 hours after IOP is controlled

Hypertensive Retinopathy
In HTNR, retinal arterioles narrow, take on classic "copper wire" appearance.
Nicking or narrowing of the vessels occurs.
If blood pressure remains elevated, areas of ischemia or "cotton wool" spots, small hemorrhages, headaches, and vertigo occur.

Diabetic Retinopathy
Retinal blood vessel complication
Retinopathy worsened with poor glucose control
Diabetic education is key to minimizing complication
Managed with
Laser therapy
Vitrectomy

Macular Degeneration Overview
The macula—the area of central vision —deteriorates.
Degeneration can be atrophic age-related (dry) or exudative (wet).
Rod and cone photoreceptors die.
Central vision declines; client describes "mild blurring" and "distortion." leading to blindness
Diagnosed with Ophthalmologic exam and angiogram

Risk factors
Smoking, may increase the risk of AMD.
Obesity. Research studies suggest a link between obesity & progression of AMD
Race. Whites are much more likely to lose vision from AMD than African Americans.
Family history. Those with immediate family members who have AMD are at a higher risk of developing the disease.
Gender. Women >men.

Clinical manifestations
For dry AMD: the most common early sign is blurred vision.
-blind spot in the middle of their field of vision.
For wet AMD: the classic early symptom is that straight lines appear crooked.
A small blind spot may also appear in wet AMD, resulting in loss of one's central vision.

Testing
Visual acuity test. This eye chart test measures how well you see at various distances.
Dilated eye exam. Drops are placed in your eyes to dilate the pupils. Your eye care professional uses a special magnifying lens to examine your retina and optic nerve for signs of AMD and other eye problems. After the exam, your close-up vision may remain blurred for several hours.
Tonometry.

Macular degeneration Management
Laser surgery.
The risk of new blood vessels developing after laser treatment is high. Repeated treatments may be necessary. In some cases, vision loss may progress despite repeated treatments.
Injections.
Wet AMD can now be treated with new drugs that are injected into the eye (anti-VEGF therapy). Avastin (off label use) Macugen, Lucentis.
This drug treatment blocks the effects of the growth factor, impeding choroidal neovascularization (CNV). Source: Mayo Clinic

Macular degeneration Management
Photodynamic therapy.
Injected drug tends to "stick" to the surface of new blood vessels. Next, a light is shined into your eye for about 90 seconds. The light activates the drug. The activated drug destroys the new blood vessels and leads to a slower rate of vision decline.
Photodynamic therapy is relatively painless. It takes about 20 minutes and can be performed in a doctor's office.
Treatment results often are temporary. You may need to be treated again.

Interventions for Clients with Ear and Hearing Problems

Otosclerosis Overview
abnormal growth of bone of the middle ear.
Slowly progressive conductive hearing loss results.
Exact etiology unknown
Increased incidence with Family history
Viruses/measles?
Hormones?
Increased incidence in white middle aged women

Clinical manifestations
Hearing loss
Associated findings (may or may not be present)
Vertigo
Balance problems
Tinnitus
Tuning-fork examination reveals signs of conductive hearing loss.
Weber: lateralizes toward the poor ear
Rinne: BC=AC

Collaborative care
Non surgical management
Hearing aid
Surgical management
stapedectomy
bypasses the diseased bone with a prosthetic device that allows sound waves to be passed to the inner ear.
Complications:
Facial nerve palsy
Vertigo
Taste disturbance
infection

Nursing priorities
Injury, Risk for related to disturbances of balance and impaired ability to detect environmental hazards

Communication, Impaired Verbal related to difficulty understanding others secondary to impaired hearing

Risk for Social Interaction, Impaired related to difficulty in participating in conversations

Social Isolation related to the lack of contact with others secondary to fear and embarrassment of hearing losses

Acute Pain related to inflammation, infection, tinnitus, or vertigo

Therapeutic Regimen Management, Ineffective related to insufficient knowledge of condition, medications, prevention of recurrence, hazards (swimming, air travel, showers), signs and symptoms of complications, and hearing aids


Ménière's Disease Overview
increase in volume and pressure of the inner ear
Increased incidence with positive family history
Multiple episodes of vertigo and hearing loss eventually result in permanent damage to the vestibular and cochlear apparatuses
Falls and accidents are likely to occur

Ménière's Disease
Onset typically occurs in early- to mid-adulthood
fullness or blocked sensation in one ear
Tinnitus, vertigo occur in attacks that can last for several days.
Tuning fork examination reveals one-sided sensorineural hearing loss
Weber:
sound is heard better on the affected side
Rinne:
AC>BC

Collaborative care
Nonsurgical management includes:
slow head movements
Salt, sugar and fluid restrictions
cessation of smoking
Medications
Antihistamines to relive vertigo symptoms
Dramamine to manage nausea/vomiting
Scopolamine for motion sickness
Corticosteroids vs. mild diuretics to relieve pressure
diazepam.

Collaborative care (Continued)
Surgical management
last resort and consists of labyrinthectomy or endolymphatic decompression with drainage and shunt.
Hearing in the affected ear is often sacrificed.

Nursing priorities
PC: hearing loss
Injury, Risk for related to disturbances of balance and impaired ability to detect environmental hazards
Communication, Impaired Verbal related to difficulty understanding others secondary to impaired hearing

Nursing priorities (cont’d)
Risk for Social Interaction, Impaired related to difficulty in participating in conversations
Risk for loneliness related to the lack of contact with others secondary to fear and embarrassment of hearing losses
Therapeutic Regimen Management, Ineffective


Risk for Impaired Verbal Communication
Assistive devices for hearing compensation
Lip reading, sign language
Managing anxiety