case study rheumatic

Pamantasan ng Lungsod ng MarikinaCollege of Nursing

Marikina City

A CASE STUDY ON AMANG RODRIGUEZ MEMORIAL HOSPITAL

RHEUMATIC HEART DISEASE

In Partial Fulfillment of the Academic RequirementsIn Related Learning Experience,

Presented to the College of NursingSY 2010-2011

Submitted to:

VICTORIA BEDONIA, R.N. M.A.NClinical Instructor

Submitted by:

Balderosa, Jill Anne S.

Benitez, Mercedes F.Bielza, Mary Grace S.Boco, Carlito S.Calitis, Reymin J.Capada, Shiela Marie B.

Cascano, Jhonnylyn Ver S.Cereza, Janice B.Condino, Monalisa S.Cruz, Geneva C.David, Maria Socorro S.De Dios, Mark Lester O.

GROUP 2

BSN3-1M

TABLE OF CONTENTS

PAGE

GOALS AND OBJECTIVES ------------------------------------------------------------------- -- 1

INTRODUCTION --------------------------------------------------------------------------------- 2

PATIENT’S PROFILE ----------------------------------------------------------------------------- 3

PHYSICAL ASSESSMENT -----------------------------------------------------------------------

PERSON GORDON’S APPROACH ------------------------------------------------------------

COURSE IN THE WARD ------------------------------------------------------------------------

LABORATORIES ----------------------------------------------------------------------------------

ANATOMY AND PHYSIOLOGY ---------------------------------------------------------------

PATHOPHYSIOLOGY ---------------------------------------------------------------------------

PRIORITIZATION ---------------------------------------------------------------------------------

NUSRING CARE PLANS -------------------------------------------------------------------------

DRUG STUDY -------------------------------------------------------------------------------------

DISHARGE PLANNING -------------------------------------------------------------------------

GOALS AND OBJECTIVE

Goal

The purpose of the study is to let the student nurses gain more knowledge about the disease

process of rheumatic heart disease, ascites, pleural effusion, to know the causes, how it is acquired and

prevented, and to render proper nursing care through a systematic nursing process and examinations.

Obejctives:

To assess the patient condition / health status through interview, physical assessment, and

interpretation of laboratory findings.

To discuss the anatomy and physiology of the cardiovascular system and immune system.

To trace and discuss the pathophysiology of rheumatic heart disease and other complication.

To learn the indications of the different diagnostic exam and test done to the patient. Also, to

identify the different drugs administered to the patient and will be able to discuss their

corresponding side effects, interventions of a nurse to be considered and contraindications.

To formulate and apply nursing care plans utilizing the nursing process.

To learn new skills as well as sharpen the student nurses’ clinical skills required in the management

of the patient with rheumatic heart disease.

To be able to impart health teaching for the prevention of the recurrence of the disease to other

family member.

To develop sense of unselfish love and empathy in rendering nursing care to the patient so that the

student nurses’ may be able to serve future patient with higher level of holistic understanding as

well as individualized care.

INTRODUCTION

Rheumatic fever is a descending infection that develops as a consequence of a streptococcus

throat infection that has progressed and been left untreated. Rheumatic heart disease occurs as a

consequence of rheumatic fever, (autoimmune disease) which is an inflammatory condition affecting

many of the body’s tissues including the heart, brain and joints. It can affect anyone of any age or

background but is more commonly seen in children.

Rheumatic fever typically follow streptococcal infection by about 2-3 weeks. Fever and

migratory joint pain are often initial manifestations. It has the potential of leading to rheumatic heart

disease meaning that the valves of the heart can become diseased by the disorder and may become so

inflamed that they cannot close fully or open properly due to stiffness. This can cause the blood in flow

ineffectively through the valves and can also contribute to blood leaking backwards through the valves

resulting in an accumulation of fluids. These fluids can cause enlargement of the heart and can lead to

fluid buildup in the lungs and on the limbs causing swollen ankles. As the condition affects mainly the

valves of the heart, the symptoms are similar to those with other conditions of the valves and can

include dizziness, chest pain, shortness of breath, tiredness, tachycardia, irritability and on auscultation

S3 and/or heart murmurs may be heard. For some there may be no symptoms initially, but they can

develop over time and must be treated when necessary.

The cause of rheumatic fever is still not entirely understood. It is known that rheumatic fever is

always preceded by an invasion of bacteria belonging to the group A beta hemolytic streptococcus

family. Sooner or later, everybody has a streptococcus infection, such as a streptococcus throat. Most of

us get over it without any complications. But in 1 out of every 100 children the strep infection produces

rheumatic fever a few weeks later, even after the streptococcus attack has long since subsided. There

are several risk factors for streptococcal infection including environmental and economical factor such

as crowded living conditions, malnutrition, immunodeficiency, poor food handling, poor sanitation and

poor access to health care (lack of immunization).

The invasion of streptococcus sparks the production of protective agents called antibodies. For

some reason, in a kind of biological double cross, the antibodies attack not only the strep but also make

war on the body's own tissues—the very tissues they are called upon to protect. Researchers are now

suggesting the possible reason, although all the evidence is not yet in. According to a widely held theory,

the strep germ possesses constituents ( antigens ) that are similar in structure to components of normal,

healthy cartilage and connective tissues—found abundantly in joints, tendons and heart valves—in

susceptible individuals. Failing to distinguish between them, the antibodies attack both. The result:

rheumatic fever involving joint and valve inflammation and, perhaps, permanent scarring.

Rheumatic heart disease (RHD) continues to be a common health problem in the developing

world, causing morbidity and mortality among both children with a median age of 10 years, although it

also occurs in adults (20% of cases). Although little longitudinal data are available, evidence suggests

that there has been little if any decline in the occurrence of RHD over the past few decades. Recent

reports from the developing world have documented rheumatic fever (RE) incidence rates as high as

206/100 000 and RHD prevalence rates as high as 18.6/1000. The high frequency of RHD in the

developing world necessitates aggressive prevention and control measures. The major interventions for

prevention and control include: (1) reduction of exposure to group A streptococci, (2) primary

prophylaxis to prevent initial episodes of RF, and (3) secondary prophylaxis to prevent recurrent

episodes of RE. Because recurrent episodes of RE cause increasingly severe cardiac complications,

secondary prophylaxis is the most crucial feature of an effective RHD programme.

PATIENT’S PROFILE

A. Demographic dataPatient R is a 15 year old male born on April 9, 1995 at Quezon City. He is the third child

among his five siblings. He was admitted at Pedia ward ARMMC last September 15, 2010 with a

chief complaint of difficulty of breathing, edema and mild ascites and was diagnosed with

Pleural Effusion left, Rheumatic Heart Disease under the service of Dra. Pasala as his attending

physician. He weighs 50 kgs and stands 1.56 meters. His vital signs upon admission are BP

110/70 mmHg, CR 100 bpm, RR 36 bpm and have a temp of 36⁰C.

B. History of past illness

Patient R was known to have on and off fever accompanied by sorethroat. It was

noticed to occur for at least 5 to 6 times per year since he was 5 years old. No consultations are

done because Paracetamol was noted to relieve the fever.

C. History of present illness

Present condition started 2 months PTA when patient was noticed to have on and off

Fever accomp[anied by abdominal pain, joint pain,swelling which is relieved by Paracetamol

intake. Consultation to a private Medical doctor and was diagnosed to have acute gastritis

with sore throats. Unrecalled medications were given.

1 month PTA, patient was noticed to have facial edema, DOB and easy fatigability.

Parents prompted to consult a private clinic and diagnosed to have RHD. He was then referred

to Philippine Heart Center for further management. Laboratories were requested and done.

He was treated for RHD one week PTA. He was then subsequently admitted in the institution

due to progression of DOB and edema. Due to financial constraints, patient was referred and

transferred at ARMMC.

D. Environmental history

Patient R was living with his family. He is residing at Rodriguez Rizal. The place is

somehow congested. They are living in a bungalow type of house. The house is made up of

wood and concrete. Electricity came from Meralco and water is supplied by Maynilad.

E. Socio-cultural and economic factors

Patient’s family is in good terms with their neighborhood. He strives hard in school

believing he can finish his studies to further help his family. Being a Filipino family, patients

family also believes in herbolaryos but seldom consult them. Their family is being supported

the father who is working as construction worker and earns around Php5,000. The mother

claimed to spend this earnings for food, school needs, electrical and water bills, and some

other family needs. No earnings was done for future hospitalization and health maintenance.

F. Religious Factors

Patients family were all Roman Catholics. They usually go to church every Sunday

believing that God will help them in their everyday living.

PHYSICAL ASSESSMENT

Assessment Normal Actual RemarksVital signs: Temp: RR: PR:

BP:

36.5 – 37.5 °C15 – 20 cpm60 – 90 bpm

120/80 mm Hg

36⁰C10036

140/120

Increase RR due to impaired gas exchanged

Due to aortic regurgitation

Weight:

Head: Facial movements: Hair: Scalp:

SymmetricalFine and equally

distributedClean without

dandruff and thick lice

SymmetricalFine and equally

distributed with lice with dandruff

NormalDue to Unhygienic

practicesDue to Unhygienic

practices

Eyes: Pupil: Conjunctiva: Sclera: Visual Acuity:

PERLLA ( 3 – 7mm)Pinkish

AnictericGrossly normal

PERRLA (4mm)Pale

AnictericGrossly normal

Normal↓tissue perfusion

NormalNormal

Ear: Gross Hearing: External Canal:

gross hearingno discharge

Grossly normalToo many ear wax

NormalDue to Unhygienic

practicesNose: Septum: Gross Smell: Sinuses:

MidlineNormal

(-) tenderness

Midline Normal

(-) tenderness

Normal NormalNormal

Mouth: Lips: Mucosa: Teeth: Gums: Tongue:

PinkishPinkish

No carries (32 teeth)Pinkishmidline

CyanoticPale

w/ caries (30 teeth)pale

midline

Due to ↓oxygenation↓tissue perfusion

Unhygienic practices↓tissue perfusion

Normal Pharynx: Uvula: Tonsils:

MidlineNot inflamed

MidlineNot inflamed

NormalNormal

Skin: Gen. Color: Texture: Temp:

Turgor:Wound/Dreesing/drains:

PinkishSmooth

Warm

Suppleno

duskySmooth

Cold clammy

Suppleno

Due to ↓oxygenationNormal

Due to response of SNS; vasoconstriction

NormalNormal

Abdomen: Configuration:

Bowel sounds:

Flat not tender

5-20/min, tympanic upon percussion

Distended abdomen

3/min,

Due toaccumulation of fluid in the

peritoneal cavityDue to stimulation of

SNS

Cardiovascular: Heart Sounds: Peripheral Pulse: Capillary Refill: Orthostatic hypotension:

regular

Equal and strong

1-3 secondsnone

Murmur sound with S3

fast bounding pulse

4 secs.Orthostatic

hypotension

Due to regurgitation of blood

Congestion of peripheral tissue

Dec. tissue perfusionDec. cardiac output

Respiratory: Breathing Pattern:

Shape of the chest: Tactile fremitus:

Breath sound:

Regular, w/o cough

1:2Symmetric

No adventitious sound

Difficulty of breathing

1:2Dec. vibration to both

lungsDiminished breath

sound

Due to pulmonary congestion

NormalAccumulation of fluid in the pleural spaceDue to pulmonary

congestion and pleural effusion

Back and Extremities: ROM: Spine: Gait: Muscle Tone:

full ROMstraight

CoordinatedEqually strong

Dec.ROMStraight

CoordinatedWeak muscle

Due to joint painNormalNormal

Due to fatigue and inc. workload of the

heart.

PERSON GORDON’S APPROACH

Before Hospitalization During HospitalizationPsychological:

Self Perception “dati nakakatulong ako sa gawaing bahay at nagaalaga sa mga kapatid ko”

“madali na akong napapagod kaya di na ako nakakatulong sa kanila.”

Description of self “masigla ako dati” “ngayon hindi na”Body Image “medyo payat ako dati ” “tumaba ako dahil sa

pamamanas”Role Relationship Pattern:

Support System “tatay ko ang sumusuporta sa amin”

“siya pa rin ang sumusuporta samin.”

Family Function “nakakatulong ako dati sa kanila” “pabigat na lang ako ngayon ”Sufficiency of Income “dati ngpakakasya nmin ang

suweldo ni tatay ”“din a kasya ung kinikita ni ni tatay dahil lagi n akong nasa ospital”

Accessibility of health care and nutritional resources

“hindi kami ngpapacheck-up at di kami umiinom ng kahit anong vitamins dahil di n sapat ang pera ”

“lagi na akong nasa ospital ”

Cognitive Perceptual Pattern:Hearing/visual Problem “maayos naman ang paningin at

pandinig ko”“maayos pa naman din ang paningin at pandinig ko””

Changes in memory “matalas ang aking memorya at nakakasagot pa nga ako sa eskwela eh”

“wala naman ganung pagbabago”

Pain management “dati tinutulog ko lang kapag may sakit akong nararamdaman”

Value Belief Pattern:Things and personal values held

important“ang mahalaga sa akin ay ang aking pag-aaral ”

“ngayon ang mahalag sa akin ay ang gumaling”

Family and social values that affect life

“dati gusting gusto ko agad makatapos ng pag-aaral para makatulong sa pamilya ko”

“ngayon gusto lang ay gumaling para di madagdagan ung gastos”

Spirituality “lagi kami nagdadasal ng sabay-sabay tuwing gabi”

“di na namin nagagawa iyon”

Religious practices that affect hospitalization

“lagi kaming nagsisimba tuwing linggo”

“hindi n kami nakakapagsimba tuwing lingo dahil inaasikaso nila ako”

Elimination:Bowel movement pattern (time,

frequency and amount)“ngayon 2x akong dumudumi at tuwing umaga at hapon”

“dati 1x ako dumudumi tuwing umaga”

Urinary Pattern (time, frequency, amount and color)

“Dati madalas akong umiihi at marami un”

“ngayon konti lang ang naiihi ko at din a madalas”

Use of Aids (fluid, medication and food)

“Umiinom lang ako ng maraming tubig”

Furosemide as diuretics

Rest and Sleep Pattern: 6-8 hrs 3-5 hrsActivities of Daily Living:

Feeding “makaisa ako nakakain” “kailangan ko na ng katulong”Toileting “makaisa ako dumumi ” “kailanagan ko ng katulong”

Bed Mobility “kayang kaya ko naman dati ” “kaya kong gumalaw kaya lang nahihirapan ako”

Gen. mobility “nakakakilos naman ako pero di ako masyadong nagpapagod”

“madali na akong napapagod kahit sa konting kilos lang”

Hygiene “pag may pasok lang ako naliligo”

“ngayon pinupunasan ako”

Circadian RhythmsSleep Concerns “madali lang ako nakakatuog

dati”“nahihirapan na akong maktulog dahil sa sakit”

Nutrition:Daily food intake (quality,

frequency, amount and quantity)“Magana naman ako kumain at kahit ano nakakain ko.”

“ngayon wala na kong masaydong gana”

COURSE IN THE WARD

On the day of admission, admitting impression was Pleural Effusion left, Rheumatic

Heart Disease. He has a chief complain of dyspnea. He was put on a DAT. Laboratories were

requested. Venoclysis of PNSS was started and IV meds (Pen G 1.2 M “U” Q6H, Captopril

25mg/tab ½ tab BID, Furosemide 40mg/tab 1 tab BID, Prednisone 20 mg/tab 1 tab TID after

meals, Lanoxin 0.25mg/tab ½ tab BID, INH 200 mg/tab 1 tab OD). Vital signs are monitored

Q1H. Intake and output were monitored every 4 hous. He was positioned on modified high

back rest. He was also hooked to oxygen inhalation via nasal cannula at 2-3 lpm.

On 2nd HD, Thoracentesis was also ordered which is not done.

On the 3rd HD, Furosemide was shifted to 40mg TIV Q12H. He was ordered for repeat

CXR. Thoracentecis was temporarily hold.

On the 4th HD, he was ordered to have PPD and sputum AFB tests.

On the 5th HD, IVF was maintained at same rate. Same day, IVf was shifted to heplock.

Furosemide was again increased to 40mg Q8H via heplock. CBC and APC was repeated.

On the 6th HD,patient complained of abdominal pain hence given Ranitidine 40 mg TIV.

CXR result revealed massive pleural effusion hence referred to Pulmo service. He was ordered

for TPAG, Thoracentecis was ordered. Furosemide was then again increased to 40 mg Q6H.

On 7th HD, Patient was seen by Cardiologist. Repeat serum K and Na was ordered.

Albumin infusion was ordered and Furosemide drip was started. Captopril was increased to

30mg ½ tab BID. Pen G was shifted to Cefuroxime 1.5 TIV Q8H. Repeat CXR is ordered after 48

hours (due 24 September 2010). Intake and output were strictly monitored. Blood Pressure is

140/20 to which the doctor prescribed Dopamine drip. Dyspneic episodes prompted physicians

to bring patient to PICU at around 4pm.

On the 8th HD, at about 4 am patient expired with Final Diagnosis of Congestive Heart

Failure 20 RHD, Tricuspid and Aortic Regurgitation.

LABORATORIES

Serology(September 09, 2010)

Result Normal Values

C – Reactive Protein CRP 33.7 H mg/dL 0.0 to 10.0 mg/dL

Anti – Streptolysin O Titer (ASO)

302.5 mg/dL (0.0-200.0)

Analysis: CRP is elevated during active inflammatory process. ASO titer is increased. This test is a test for streptococcal antibodies. Streptococcus can be acquired by living in a crowded place where in close contact to infected person is evident. It rises within 2 months of the onset and it is positive in most clients with rheumatic heart disease.

HEMATOLOGY (September 08,2010)

Results Normal Values

WBC 15.00 H 10 g/L 5.00-10.00

RBC 5.00 10-12 L 4:50-5.20

Hgb 125L g/L 140-170

Hct 0.39 L 0.42-0.51

platelet 351 10g/L 200-400

MCV 78 L 80-96

MCH 25.0 L 27.5-33.2

MCHC 320 L g/L 334-355

RDW 18.0 H % 12.6-14.6

ESR 19 mm/hr 0-10 mm/hr

Analysis: Supporting the serology result, WBC is increased contributing to the inflammatory process. Erythrocyte sedimentation rate is elevated. It is the measurement of the rate at which RBC’s “settle out” of anticoagulated blood in an hour. It is usually elevated in infectious heart disorders. MCV, MCH, MCHC determines relative volume, size, weight and the saturation of RBC.

Urine Microscopy

(IU) (hpf) Normal values

RBC 21 ≤17 ≤ 3

WBC 4 1 ≤28 ≤5

UrinalysisActual Values Normal values

Physical Analysiscolor straw Yellow

transparency slightly cloudy Clearspecific gravity 1.010 1.015-1.025

Chemical AnalysispH 5.0 4.6-8.0

protein negative Negativesugar negative Negative

bilirubin negative Negativeurobilinogen negative Negative

blood trace Negativenitrites negative Negative

leukocytes negative NegativeKetones negative Negative

Analysis: This test is performed to assess the effects of cardiovascular diseases on renal function and the existence of concurrent renal or systemic diseases like glumerulonephritis. In this result, there is the presence or traces of blood. This may indicate malfunctioning of glomerulus and or inability of the kidney to filter blood.

2D Echo

Binary Pressure Gradient Regurgitant fx

pulmonic valve .91 3

tricuspid valve .84 3 311

mitral valve 1.6 11

aortic valve 1.4 8 571

Analysis: The mitral valve is located between the left ventricle and left atrium. It is supported by the chorda tendinae during ventricular systole to prevent valvular proplase into the atrium. The aortic valve lies between the left ventricle and the aorta. These valves open during ventricular systole and they close during ventricular diastole

X-RAY REPORT (September 08, 2010)

Chest AP There is opacification of the right hemithorax spacing the upper lung with

obscuration of the right heart border bilateral hemidiaphragm, moderate to massive pleural effusion suggest follow up check up.

True cardiac size is difficult to assess but appears enlarge.Aorta is unremarkable

Left costophrenic sulcus is intactNo other remarkable finding

Analysis: Chest Xray suggest that the patient has pleural effusion. The test also suggests that the heart is quite enlarge and could be possibly because of the congestion. The inability of the heart to pump normally and allow normal flow of the blood is impaired and tries to accommodate those extra volumes of blood.

ANATOMY AND PHYSIOLOGY

LYMPHATIC SYSTEM

I. Body Defense System

A. Nonspecific defense system

- Mechanical barriers that cover body surfaces (skin and mucous membranes) and cells and

chemicals that acts to protect the body from invading pathogens.

- Responds immediately to protect the body from all foreign substances.

- Reduces the workload of the specific defense system by preventing entry and spread of

microorganisms throughout the body.

1. Surface body defense

- Body’s first line of defense against invasion of disease-causing microorganisms.

- Physical barriers:

Skin

Mucous membranes

- Chemical barriers:

Skin – skin acidity (acid pH) inhibits bacterial growth and sebum are toxic to

bacteria.

Stomach mucosa – secretes HCl acid and protein-digesting enzymes.

Oral cavity – saliva contains lysozyme that destroys bacteria.

Vagina – highly acidic secretions that destroys bacteria.

2. Cells

1) Phagocytes

- confronts pathogens that make it through the mechanical barriers in nearly

every body organ.

- Types:

1) Macrophage

2) Neutrophil

2) Natural Killer (NK) cells

- Unique group of defensive cells running in the blood stream and lymph that can

lyse and kill cancer cells and virus-infected body cells before the immune system

are enlisted in the fight.

INFLAMMATORY RESPONSE:

- Body’s second line of defense, triggered when body tissues are injured.

- Cardinal signs:

1) Redness (rubor)

2) Heat (calor)

3) Pain (dolor)

4) Swelling (tumor)

- Process of inflammation

INJURY

Damaged cells secretes inflammatory chemicals (histamine and kinins)

Dilatation of blood vessels ↑ capillary permeability (“leaky”) Attraction of phagocytes and WBC into the injured area (chemotaxis)↑ blood flow into the area

Leak of plasma from the blood stream into the tissue spaces

Entrance of clotting proteins from the blood into the area

Removal of damaged / dead tissue cells and pathogens from the area.

Redness Heat

↑ O2 & nutrient supply

↑metabolic rate of tissue cells

Edema

Swelling

Activation of pain receptors

Pain

Possible temporary limitation of joint movement

Fibrin barrier formation

Walls off the damaged area to prevent the spread of pathogen

FEVER

- A systemic response to invading microorganisms.

- Pyrogens reset the normal setting of the thermostat to high levels.

- Pyrogens = chemicals secreted by WBC and macrophages exposed to foreign

cells or substances in the body.

- Good effects of fever: (Low and moderate)

1. Prevents/retards bacterial proliferation

– fever causes liver and spleen to gather iron and zinc during fever,

since bacteria require large amounts of iron and zinc to multiply.

2. Facilitation of repair

- Fever increases metabolic rate of tissue cells.

B. Specific defense system

(Immune system)

- Attack against particular foreign substances

- Considered as functional system rather than an organ/anatomical system because it

recognizes antigens and abnormal cells to inactivated or destroy it.

- Body’s third line of defense.

- Types of Immunity:

1. Humoral Immunity (Antibody-mediated Immunity)

- Provided by antibodies present in the body’s fluids (humor)

Healing

2. Cellular Immunity (cell-mediated immunity)

- Protection provided by the lymphocytes (because the protective factor is living

cells).

Immune Response

- Immune system’s response to threat that tremendously increases

- Provides protection that is carefully targeted against specific antigen.

3 important Aspects of Immune Response:

1. Antigen specific – it recognizes and acts against particular pathogens.

2. Systemic – immunity is not restricted to the initial infection site.

3. Presence of “Memory” - it recognizes and mounts even stronger attacks on previously

encountered pathogens.

Antigens

- any substance capable of exciting the immune system and provoking an immune response.

Types:

non-self antigens –

self-antigen –protein molecules of own body cells.

- Do not trigger an immune response in own body, but strongly antigenic to other

people

Hapten (incomplete antigen) – troublesome small molecule causing an immune

response in the body

- But when small molecules link with the bodies proteins, the immune system

recognizes the combination as foreign and mount an attraction that is harmful

rather than protective.

Types of lymphocytes

a. B cells- resides in the lymph nodes, spleen, and other lymphoid tissues.

- Forms plasma cells and memory cells

- Descendants:

- Plasma cell- production of antibodies

- Memory cell- quick and efficient reaction to subsequent infections or

meetings with the same antigen

b. T cells- becomes immune competent in the thymus gland and can differentiate to the

several types of effector cells.

- Types:

1. Helper T cell- to stimulate production of killer T cells and B cells

2. Cytotoxic T cell- produce by helper T cell during cellular immunity.

- killing virus infected cells, and foreign graph cells

3. suppressor T cell- slow or stops the activity of B or T once the infection has been

conquered

- helps prevent uncontrolled unnecessary immune system activity by winding

down and finally stopping the immune system after an antigen has been

successfully destroyed.

4. Delayed hypersensitivity T cells- plays a major role in cell mediated allergies and

inflammation

- Promotes intense inflammatory response

Macrophages

- Engulf foreign particles and present fragments of the engulfed antigens under

surfaces, where they can be recognized by immuno competent T cells

- Remain fixed in the lymphoid organ

CARDIOVASCULAR SYSTEM

Four compartments

The heart is divided into 4 chambers: 2 on the right hand side and 2 on the left. Each upper

chamber is known as an atrium and each lower chamber as a ventricle. The 4 compartments are

known as: the right atrium; the right ventricle; the left atrium and the left ventricle. Blood comes

into the heart via the atria, which are the smaller chambers, and is pumped out via the larger

ones — the ventricles.

The right atrium,

Located in the upper right side of the heart, and a small appendage, the right auricle, act as a

temporary storage chamber so that blood will be readily available for the right ventricle.

Deoxygenated blood from the systemic circulation enters the right atrium through three veins,

the superior vena cava, the inferior vena cava, and the coronary sinus.

The right ventricle

is the pumping chamber for the pulmonary circulation. The ventricle, with walls thicker and

more muscular than those of the atrium, contracts and pumps deoxygenated blood through the

three-cusped pulmonary semilunar valve and into a large artery, the pulmonary trunk. The

pulmonary trunk immediately divides into two pulmonary arteries, which lead to the left and

right lungs, respectively.

The left atrium

and its auricle appendage receive oxygenated blood from the lungs though four pulmonary

veins (two from each lung). The left atrium, like the right atrium, is a holding chamber for blood

in readiness for its flow into the left ventricle. When the ventricles relax, blood leaves the left

atrium and passes through the left AV valve into the left ventricle. The left AV valve is also called

the mitral or bicuspid valve, the only heart valve with two cusps.

The left ventricle

is the pumping chamber for the systemic circulation. Because a greater blood pressure is

required to pump blood through the much more extensive systemic circulation than through the

pulmonary circulation, the left ventricle is larger and its walls are thicker than those of the right

ventricle. When the left ventricle contracts, it pumps oxygenated blood through the aortic

semilunar valve, into a large artery, the aorta, and throughout the body. The following events

occur in the left ventricle, simultaneously and analogously with those of the right ventricle.

Interventricular septum - Muscle that separates two ventricle from each other.

Interatrial septum -Cardiac Muscle that separates two atrium from each other.

Coronary sulcus (artioventricular groove) - marks the junction of the atria and ventricles.

Anterior interventricular sulcus and posterior interventricular sulcus- mark the junction of the

ventricles on the front and back of the heart, respectively.

Superior and inferior vena cava

These are the 2 large veins which enter the heart on the right hand side and bring blood low in

oxygen into the right atrium. The superior (top) vena cava brings in blood from the head and

arms and upper body; the inferior (lower) vena cava brings in blood from the trunk and legs —

the lower body.

Arteries

Carry blood away from the heart. They are the thickest blood vessels, with muscular walls that

contract to keep the blood moving away from the heart and through the body.

Arterial walls have three layers:

The endothelium is on the inside and provides a smooth lining for blood to flow over as it moves

through the artery.

The media is the middle part of the artery, made up of a layer of muscle and elastic tissue.

The adventitia is the tough covering that protects the outside of the artery.

Types of arteries:

a. Coronary arteries

The heart is just a big muscle which pumps blood around the body. This oxygen is brought to the

heart by the coronary arteries. The right and left coronary arteries branch off the aorta — the

large main blood vessel which leaves the heart with fresh oxygen-rich blood — so they are

ensured of a good blood supply rich in oxygen.

b. Pulmonary arteries

The right and left pulmonary arteries branch off the main pulmonary trunk. Blood that needs

oxygen is pumped into them from the right ventricle and they take it to the lungs where it is

loaded up with oxygen.

Veins

Carry blood back to the heart. They're not as muscular as arteries, but they contain valves that

prevent blood from flowing backward. Veins have the same three layers that arteries do, but are

thinner and less flexible. The two largest veins are the superior and inferior vena cava.

Pulmonary veins

The right and left pulmonary veins bring the oxygen-rich blood back from the lungs to the heart

into the left atrium.

Aorta

The aorta is the largest artery in the body. Fresh blood full of oxygen is pumped by the left

ventricle into the aorta, round the aortic arch and out into the upper body via the 3 main

arteries branching off the aortic arch and into the thorax, trunk and lower body via the

descending aorta.

Valves

Valves are one-way doors. There are valves separating the chambers of the heart. As the heart

beats, the valves open and blood is pumped from one chamber to another chamber.

Layers of the heart

Pericardium

The pericardium is the double walled sac that contains the heart and the roots of the great

vessels that leave from or enter the heart. There are two layers of the pericardial sac, which are

the fibrous pericardium and the serous pericardium. The serous pericardium is further divided

into two layers, which are the parietal pericardium and the visceral pericardium. The parietal

pericardium is inseparably fused to the fibrous pericardium, while the visceral pericardium is

actually a part of the epicardium, which is the outermost single layer of the pericardium. The

visceral layer extends into the starting point of great vessels, thus, becoming one with the

parietal layer of the serous pericardium.

Myocardium

The myocardium is the basic muscle that makes up the heart. This muscle is involuntary and,

this is striated in nature. The cardiac muscle structure consists of basic units of cardiac muscle

cells known as myocytes. Coordinated contraction of the cardiac muscles is what makes the

heart propel blood to various parts of the body.

http://www.buzzle.com/articles/cardiac-muscle-structure.html

Endocardium

The endocarium is the innermost, thin and smooth layer of epithelial tissue that lines the inner

surface of all the heart chambers and valves. This layer is made of thin and flat cells that are in

direct contact with the blood that flows in and out of the heart. Each heart valve is formed by a

fold of endocardium with connective tissue between the two layers.

Blood flow

Superior and inferior vena

cava

Right atrium

Right ventricle

Pulmonary semi lunar

Tricuspid

Pulmonary trunk

Pulmonary vein

Lung tissue (pulmonary circulation)

Pulmonary arteries

Left atrium

Aorta Aortic semilunar

valve

Left ventricl

Bicuspid valve

Body tissue (systemic

circulation)

Valves begin to heal w/ scar tissue formingInflammation subsides

Heart valve tissues become inflamed

Unmanaged, subsequent exposure to the antigen

PATHOPHYSIOLOGY

Predisposing factors:

- 15 yrs. Old- Exposure to GABHS (his auntie

has the same dse)- (-) immunization

Precipitating factors:

- Malnutrition- Poor living conditions- Congested neighborhood- Improper food handling

Presence of Group A beta-hemolytic streptococcus

Attach to epithelial cells of the upper respiratory tract

Activated antigen-presenting cells present the bacterial antigen to helper T-cells.

Activated B-cells

Production of antibodies against the cell wall against of streptococcus

Antibodies cross react with cardiac myosin and antigens of tissue glucoprotein in the joints, skin, brain and other connective tissue.

Induces cytokines release

Inflammatory response

↑ WBC count

FEVER

ARTHRALGIA

↑ ESR

Activity intolerance

Restriction of leaflet motion

Impeding to full swing action

Aortic Valvular stenosis

↑ blood volume to LV

Leaflets may become deformed by healing tissue

Valve fails to close completely

Aortic Regurgitation

↑blood volume and pressure in the LA ↓cardiac output

↑pulmonary venous blood flow & pressure

Pulmonary congestion

Stimulate SNS

Release of epinephrine and norepinephrine

vasoconstriction

Further damage to the heart

muscles

↑ Capillary permeability

Plasma leaked out

Accumulation of excessive fluid in the pleural space

Release of renin by kidneys

Dyspnea

Non productive cough

Pleural effusion

Orthopnea

Impaired sleepGITSkin Kidney

Cold clammy, pallor

↑ HR & Contractility

↓ gastric secretions

↓ digestion

↓ BM

↓ Renal perfusion

Formation of angiotensin I

S3 Heart sound

↑ blood volume to RV

Continuous flow of blood from the CVC

↑ blood volume of RV and RA

Tricuspid regurgitation

Wide pulse pressure

cyanosis

Murmurs

↑ RR

Use of accessory muscles

↑ RBC

Impaired gas exchange

Pulmonary hypertension

Respiratory failure

ACE converts angiotension I to II

Promotes the release of aldosterone

R Ventricular failure

Congestion of the viscera and peripheral tissue

Blood backs to hepatic veins

↑ Pressure w/in portal vessels

Promotes retention of Na+ and water

Fluid volume overload

Portal hypertension

Forced fluid into the abdominal cavity

Ascites

Anorexia

Abdominal pain

Nausea

Development of ↑ pressure

↑ Preload and afterload

Further ↑stress on the ventricular wall

Further ↑ in the workload of the heart

↑ Thickness of the heart muscle

↑ventricular pressure and resistance to ventricular filling

Subsequent ↓ in cardiac output

JVD

Dec. vocal tactile

fremitusDullness

when percussed

Weight gain

↑ workload of the heart

↑ contraction

↓ Elasticity

Fatigue↓ oxygenation in brain tissues

-dizziness, light-headedness

Activity intolerance

Stimulates ADH production

Peripheral edema

Fail to contract

Death

↑bp

↓ UO

Fast, bounding pulse

Weakness

s/sx:

fever, chills, pleuritic chest pain, dyspnea

Cyanosis, pallor

↓ lung expansion

PRIORITIZATION

Diagnosis Scientific explanation Rationale Score

Impaired gas exchange related to fluid shifting in

the pleural space secondary to pulmonary

congestion

It is the deficit in oxygen and carbon dioxide elimination at the alveolar capillary

membrane due to accumulation of fluid in

the pleural space

It is first prioritized problem because certain

vital tissues such as those of the brain and

the heart cannot survive for a long without

continuous supply of oxygen if gas exchange is impaired, it could lead to life threatening condition

of the patient

1st

Decrease cardiac output

The amount of blood pump by each ventricles

during a given period, cardiac output must be

responsive to changes in metabolic demands of

the tissue

It is our second prioritized problem

because decrease cardiac output may lead to

diminish ability of the patient to response to

stress

2nd

Excessive fluid volume related to sodium and

water retention

It is refers to an isotonic expansion caused by

abnormal retention of water and sodium. This

may be related to simple fluid overload or

diminished function of homeostatic mechanism responsive for regulating

fluid balance

This is our third prioritized problem, because retention of fluid and sodium can lead to more severe

complication that could be life threatening to the

patient. The goal of treatment is to preserve

or restore the intravascular fluid

volume and treating the cause of fluid retention

3rd

NURSING CARE PLANS

Diagnosis Goals and Objective Intervention Rationale Evaluation

Assessment

Diagnosis

Goals

Intervention

Rationale

Evaluation

Subj:“Hindi siya masyado makakilo

Decrease cardiac output related

After 2° of nursing intervention

Independent:-

Monitor VS, note for

- Provide baseline data for compa

GOAL PARTIALLY MET After 2° of n

Assessment

Subjective:“sobrang nagmamanas na nga ako, mula mukha hanggang paa ko” as verbalized by the patient

Objective: Edema Weight gain Abdominal girth

of 30cm Urine output:

Excess fluid volume related to increased ADH production and sodium/water retention as manifested by pitting edema (grade 3) and weight gain from 35-40 kgs.

Analysis

Goal: After 8hrs of continuous nursing intervention the patient will be able to reduce recurrence of fluid excess as manifested by decrease abdominal girth, reduce edema from (+3) to (+1).

Objective: To be able to

reduce accumulation of fluid (edema) on feet and different part of the body

To be able to increase output.

Independent: Monitor VS.

Note presence of underlying condition that potential fluid excess

Note presence of edema and calculate its grade

Measure abdominal girth everyday

Note pattern of urination

Elevate edematous part (feet) and change position frequently

Measure I and O

Promote ambulation

Dependent: Restrict Na and Fluid

as indicated Administer diuretics as

prescribed

Collaborative: Assist with procedure

as indicated (paracentesis)

Establish baseline data for further comparison

To assess precipitating factor

To evaluate degree of edema

To evaluate changes that may indicate increase fluid retention

To know if there is fluid retention in the body

To reduce tissue pressure and decrease risk of skin breakdown

To measure intake of fluids accurately

To promote circulation and to mobilize excess fluid

GOAL METAfter 8 hrs of continuous nursing intervention, patient was able to reduce recurrence of fluid excess as manifested by decreased abdominal girth and decreased edema from grade 3 to grade 1.Low cardiac output

Renal perfusion

Vasoconstriction

Release of renin by the kidney

Formation of angiotensin I

Convert to angiotensin II

Release of aldosterone

Sodium/water retention

ASSESSMENT DIAGNOSIS GOALS AND OBJECTIVES INTERVENTION RATIONALE EVALUATIONS: “Nahihirapan akong huminga” as verbalized by the patient

Objective data: Respiratory rate of

33 bpm Cyanosis Use of accessory

muscle Orthopnea Crackles Non-productive

cough

Impaired gas exchange related to fluid shift on alveoli secondary to pulmonary edema as manifested by respiratory rate of 33 bpm and cyanosis

GOALS:After 1 day of nursing intervention, the patient will improve respirationOBJECTIVES: To be able to

decrease respiratory rate from 33 bpm to atleast 30 bpm by positioning the patient in semi fowler position and administration of oxygen inhalation

To be able to change cyanosis to pinkish skin, lips and nail bed color by providing adequate oxygen for better circulation of blood

Monitor vital sign

Monitor color of the skin, use of accessory muscle oxygen saturation, depth, pattern and rate of respiration

Position patient in semi fowler position

Secure oxygen at bedside

Minimize activities and energy expenditures by assisting ADL’s

DEPENDENT Give oxygen as

prescribed by the physician

Give bronchodilator as prescribed by the physician

COLLABORATIVE Review laboratory and

diagnostic results such as ECG, Chest –xray, CBC, Blood chemistry

For baseline data and for further comparison

This assessment data alert the healthcare provider to potential hypoxemia or hypercapnea

To promote lung expansion and decreasing the work of breathing

Oxygen support alveolar gas exchange and improve oxygen in blood and tissue

Rest is vital to reduce oxygen and energy demand

Oxygen support alveolar gas exchange and improve oxygen in blood and tissue

It relaxes bronchial smooth muscle leading to brochodilation

To note any incongruence and alteration in the results

Goal partially met.After a day of nursing intervention the patient respiratory rate decrease from 33 bpm to 30 bpm but the skin, remain cyanosis

INFERENCE

Pulmonary congestion

Pulmonary edema

Increase capillary pressure

Plasma leak out

Accumulation of excessive fluid in the alveoli

Impaired gas exchange

DRUG STUDY

Name of drug,route, dose and indications

Mechanism of Action Contraindications Adverse Reactions Nursing Responsibilities

Dopamine drip D5W 92.8 cc

Indications:Correction of hemodynamic imbalances present in the shock syndrome due to MI, trauma, endotoxic septicemia, open heart surgery, renal failure and chronic cardiac decompensation in CHF.

Drug acts directly and by the release of norepheniphrine from sympathetic nerve terminals; dopaminergic receptors mediate dilation of vessels in the renal and splanchnic beds, which maintains renal perfusion and function; alpha receptor which are activated by higher doses of dopamine, mediate vasoconstriction, which can override the vasodilating effects; beta 1 receptors mediate a positive inotropic effect on he heart

>Contraindicated with pheochromocytomas, tachyparrythmias, ventricular fibrillation, hypovolemia (dopamine is not a substitute for blood, plasma, fluids, electrolytes, which should be restored promptly when loss as occurred), general anesthesia with halogenated hydrocarbons or cyclopropane, which senthesize the myocardium to catecholamines.>use cautiously with atherosclerosis, arterial embolism, Raynoud’s disease, cold injury, frost bite, diabetic endarteritis, Burger’s disease (monitor color and temperature of the extremities), pregnancy, lactation

CV: ectopic beats, tachycardia, anaginal pain, palpitations, hypotension, vasoconstriction, dyspnea, bradycardia, hypertension, widened QRS.GI: nausea and vomitingOther: headache, piloerection, azotemia, gangrene with prolonged used.

>Monitor body weight, skin color, urine output, serum electrolytes, Hct and ECG.>Drug should always be diluted before use if not prediluted.>Monitor cardiac output and BP closely during infusion.



captopril

Capoten, Novo-Captopril(anti-hypersensitive)

25 mg/tab ½ tab BID

Indication :>hypertension>CHF>left ventricular dysfunction (LVD) after MI>diabetic nephropathy

Selectively suppresses reninangiotensin-aldosterone system, inhibits ACE; prevents conversion of angiotensin I to angiotensin II.

>hypersensitivity>pregnancy (2nd/3rd trimester)>lactation>heart blockChildren>K-sparing>diuretics>bilateral renal artery stenosis

CNS: fever, chillsCV: hypotension, postural hypotension, tachycardia, anginaGI: loss of taste, liver function testsGU: impotence, dysuria, nocturia, proteinuria, nephrotic syndrome, acute reversible renal failure, polyuria, oliguria frequencyHEMA: neutropenia, agranulocytosis, pancytopenia, thrombocytopenia, anemiaINTEG: rashMISC: angioedema, hyperkalemiaRESPI: bronchospasms, dyspnea, cough

>may be crushed or mixed with food>monitor blood studies; decrease platelet count, and WBC with different baseline and periodically q3 months, if neutrophils <1000/mm^3, d/c treatment.>monitor BP, check for orthostatic hypotension, syncope, and if changes occur dosage change may be required.>monitor renal studies; protein, BUN, creatinine; watch for decrease levels that may indicate nephritic syndrome and renal failure; monitor renal symptoms: polyuria, oliguria frequency, dysuria>established baseline and renal, liver function tests before therapy begin and check periodically; monitor for increase liver function studies, watch for increase uric acid, glucose>check K levels throughout treatment, although hyperkalemia rarely occurs>check regularly for

edema in feet and legs; monitor weight daily in CHF>assess for allergic reactions; rash, fever, priritus, urticaria; drug should be d/c if antihistamine failed to help>reach pt. not to use OTC products (cough, cold,allergy) unless dictated by prescriber; serious side effects can occur; xanthines such as coffee, tea, chocolate, cola can prevent action of drug>teach patient to notify prescriber of mouth sores, sore throat, fever, swelling of hands or feet, irregular heartbeat, chest pain, coughing, SOB.>caution patient to report excessive perspiration, DHN, vomiting, diarrhea: may lead to fall in BP.>caution patient that drug may cause dizziness, fainting, lightheadedness; may occur during first few days of therapy, to avoid activities that may be hazardous.



Ranitidine hydrochloride 40 mg TIV now.

Indication:>Short-term treatment of active duodenal ulcer.>Maintenance therapy for duodenal ulcer at reduced dosage.>Short term treatment of GERD.>Treatment of heartburn, acid indigestion, sour stomach.

Competitively inhibits the action of histamine at the H2 receptors of the parietal cells of the stomach, inhibiting basal gastric acid secretion and gastric acid secretion that is stimulated by food, insulin histamine, cholinergic agonists, gastrin and pentagstrin

>Contraindicated with allergy to ranitidine, lactation.>Use cautiously with impaired renal or hepatic function, pregnancy

CNS: headache, malise, dizziness, somnolence, insomnia, vertigo.CV: tachycardia, bradycardia, PVC’s (rapid IV administration).DERM: rash, alopecia.GI: constipation, diarrhea, nausea, vomiting, abdominal pain, hepatitis, increased ALT levels.GU: gynecomastia, impotence or decreased libido.HEMA: leukopenia, granulocytopenia, thrombocytopenia, pancytopenia.LOCAL: pain at IM site, local burning or itching at IV site.OTHERS: athralgias

>Administer oral drug with meals at bedtime.>Decrease doses in renal and liver failure.>Provide concurrent antacid therapy to relieve pain.>Arrange for regular follow-up including blood tests, to evaluate effects.>If you are also using an antacid, take it exactly as prescribed, being careful of the times of the administration.>Report sore throat, fever, unusual bruising or bleeding, tarry stools, confusion, hallucinations, dizziness, severe headache, muscle or joint



Apo-Furosemide, Furoside Lasix, Lasix Special, Myrosemide (Loop diuretics)40 mg tab BID

Indication >edema in CHF, nephritic syndrome, ascites, caused by hepatic disease, hepatic cirrhosis; may be used alone or adjunct with antihypertensives such as spirolacone, triamference, should not be used with ethacrynic acid.

Acts on the ascending loop of Henle in the kidney, inhibiting reabsorption of electrolytes sodium chloride causing excretion of Na, Mg, Cl, H2o and some K; reabsorption of sodium chloride and and decrease excretion of K in the distal tubule of the kidney; responsible for slight antihypertensive effect and peripheral vasodilation.

>Hypersensitivity to sulfonamides, anuria, hypovolemia, infants, lactation, electrolyte depletion

CNS: fatigue, weakness, vertigo, paresthesias.CV: orthostatic hypotension, chest pain, ECG changes, circulatory collapse EENT: loss of hearing, ear pain, tinnitus, blurred vision.ELECT: hypkalemia, hypochloremic alkalosis, hypomagmesemia, hyperuricemia, hypocalcemia, hyponatremia, metabolic alkalosis.ENDO: hyperglycemiaGI: nausea and vomiting, diarrhea, dry mouth, anorexia, cramps, orpancreatitis.GU: plyuria, renal failure, glycosuria.HEMA: thrombocytopenia, agranulocytosis, leukopenia, neutropenia, anemia.INTEG: rash, pruritus, purpura, Steven’s Johnson Syndrome, sweating, photosensitivity, urticaria.MS: cramps, stiffness.

>assess patient for tinnitus, hearing loss, ear pain, periodic testing of hearing is needed when high doses of this drug are given by IV route.>monitor for renal, cardiac, neurologic, GI, pulmonary manifestations of hypokalemia: acidic urine, reduced urine osmolality, nocturia, polyuria and polydypsia; hypotension, broad T wave, U-wave, ectopy, tachycardia, weak pulse; muscle weakness, altered LOC, drowsiness, apathy, lethargy, confusion, depression, anorexia, nausea, cramps, constipation, distention, paralytic ileus, hypoventilation, respiratory muscle weakness.>monitor for CNS, GI, CV, integumentary and neurologic.



Cefuroxime 1.5 grm. TIV q8

Indication:> Pharyngitis, tonsillitis caused by streptococcus pyogenes.>Otitis media>Lower respiratory infection.>UTI>Uncomplicated gonorrhes.>Skin and skin structure infections, including impetigo>Treatment of early Lyme disease.>Meningitis>Septicemia

Bactericidal. Inhibits synthesis of bacterial cell wall, causing cell death.

>Contraindicated with allergy to cephalosporins or penicillins.>Use cautiously with renal failure, lactation, pregnancy

CNS: headache, dizziness, lethargy, paresthesias.GI: nausea and vomiting, diarrhea, anorexia, abdominal pain, flatulence, pseudomembranous colitis, hepatotoxicityGU: nephrotoxicityHEMA: bone marrow depression (decrease WBC, decrease platelets, decrease Hct,)LOCAL: pain, abscess at injection site, phlebitis, inflammation at IV site.OTHER: superinfections, disulfiram-like reaction with alcohol.

>Assess skin status, LFTs, renal functions tests, culture of affected area, sensitivity tests,>Culture infection, and arrange for sensitivity tests before and during therapy if expected response is not seen.>Give oral drug with food to decrease GI upset and enhance absorption.>Give oral drugs to children who can swallow tablets; crushing the drug results in a bitter, unpleasant taste.>Have vitamin K available in case hypoprothrombinemia occurs. >Discontinue if hypersensitivity reaction occurs.>Teach patient to report severe diarrhea with blood, pus or mucus; rash; DOB; unusual tiredness, fatigue; unusual bleeding or bruising; unusual

itching or irritation.



prednisone 20 mg/tab 1 tab TID after meals

Indication>Replacement therapy in adrenal cortical insufficiency.>Hypercalcemia associated with cancer.>Short term management of various inflammatory and allergic disorders such as rheumatoid arthritis, collagen disease, dermatologic diseases, status asthmaticus, and autoimmune disorder.>Hematologic disorders.>Ulcerative colitis, acute exacerbations of MS, and palliation and some leukemias and lymphomas.>Trichinosis with neurologic or myocardial involvement.

Enters target cells and binds to intracellular corticosteroid receptors, initiating many complex reactions that are responsible for its anti-inflammatory and immunosuppressive effects.

>Contraindicated with infections especially tuberculosis, fungal infection, amoebiasis, vaccinia and varicella, and antibiotic resistant infections, lactation.>Use cautiously with renal or liver disease hypothyroidism, ulcerative colitis with impending perforation, diverticulitis, active or latent peptic ulcer, inflammatory bowel disease, heart failure, hypertension, thromboembolic disorders, osteoporosis, seizure disorder, DM, hepatic disease, pregnancy (monitor infants for adrenal insufficiency).

CNS: vertigo, headache, paresthesias, insomnia, seizures, psychosis, cataracts, increase IOP, glaucoma (long term therapy), euphoria, depressionCV: hypotension, shock, hypertension and heart failure secondary to fluid retention, thromboembolism, thrombophlebitis, fat embolism, cardiac arrhytmiasELECTROLYTES IMBALANCE: Na + and fluid retention, hypokalemia, hypocalcemiaENDOCRINE: amenorrhea, irregular menses, growth retardation, decrease CHO tolerance, DM,Cushingoid state (long term effect), increase blood sugar, increase serum cholesterol, decreased T3 and T4 levels, HPA

>administer once a day doses before 9 AM to mimic normal peak corticosteroid blood levels>increase dosage when pt. is subject to stress>do not stop taking the drug without consulting your health care provider; take once daily doses at about 9 AM>avoid exposure to infections>report unusual weight gain, swelling of the extremities, muscle weakness, black or tarry stool, fever, prolonged sore throat, colds or other infections, worsening of the disorder for which the drug is being taken

suppression with systemic therapy longer than 5 daysGI: peptic esophageal ulcer, pancreatitis, abdominal distention, nausea, vomiting, increase appetite, weight gain (long term therapy)HYPERSENSITIVITY: hypersensitivity on anaphylactoid reactionsMS: muscle weakness, steroid myopathy, loss of muscle mass, osteoporosis, spontaneous fractures (long term therapy)OTHER: immunosuppression aggrevation or masking of infections; impaired wound healing; thin fragile skin; petechiae, ecchymosis, purpura, striae, subcutaneous fat atrophy



Lanoxin 0.25 mg/tab ½ tab BID

Indication:>heart failure>atrial fibrillation

Increases intracellular calcium and allows more calcium to enter the myocardial cell during depolarization via a Na-K pump mechanism; this increases force of contraction (positive inotropic effect), increases renal perfusion (seen as diuretic effect in patients with heart failure), decreases heart rate (negative chronotropic effect), decreases AV node conduction velocity

Increases intracellular calcium and allows more calcium to enter the myocardial cell during depolarization via a Na-K pump mechanism; this increases force of contraction (positive inotropic effect), increases renal perfusion (seen as diuretic effect in patients with heart failure), decreases heart rate (negative chronotropic effect), decreases AV node conduction velocity

>CNS: Headache, weakness, drowsiness, visual disturbances, mental status change.>CV: Arrhythmias>GI: GI upset, anorexia

> Assess patient for allergy to digitalis preparations.> Monitor apical pulse for I min. before administering; Hold dose if pulse is lower than 60 in adults and 90 in infants. Notify prescriber if the same PR was assessed after 1 hr.> Check dosage and preparations carefully> Avoid IM injections; w/c may be very painful.> Avoid giving with meals; This will delay absorption.> Have emergency equipment ready; have K+ salts, lidocaine, phenytoin, atropine, and cardiac monitor readily available in case toxicity develops.> Advise patient not to stop taking this drug without notifying the healthcare provider.> Advise patient to report slow or irregular pulse, rapid weight gain, loss of

appetite, nausea, diarrhea, vomiting, blurred vision and DOB.



IsoniazidIsotamine, NydrazidAntituberculotic200mg/tab 1 tab OD

Indication:> Tuberculosis, all forms in w/c organisms are susceptible.> Prophylaxis in specific patients who aretuberculin reactors or household members of recently diagnosed tuberculars or who are considered to be a high risk.

> Bactericidal: Interferes with lipids and nucleic acid biosynthesis in actively growing tubercle bacilli.

> Contraindicated in patients with allergy to isoniazid, isoniazid-associated hepatic injury or other severe adverse reactions to isoniazid, acute hepatic disease.> Use cautiously with renal impairment, lactation, pregnancy

> CNS: Peripheral neuropathy, seizures, toxic encephalitis, and optic neuritis.> GI: nausea, vomiting, epigastric distress, biliribinemia, elevated AST and ALT levels and hepatitis> Hema: Agranulocytosis, haemolytic or aplastic anemia, thrombocytopenia, eosinophilia, hyperglycemia and metabolic acidosis.> Hypersensitivity: Fever, skin eruptions, lympadenopathy, vasculitis.> Other: Gynecomastia, rheumatic syndrome.

> Assess patient for any allergy to isoniazid.> Give drug on an empty stomach, 1 or 2 hr before meal: May be given w/ food if GI upset occurs.> Decrease foods containing histamine in patient’s diet.> D/C drug if signs of hypersensitivity occur.> Monitor Liver and kidney function; risk of serious fatal hepatitis.> Advise strict compliance to pharmacological therapy.> Instruct patient to report any signs of weakness, fatigue, loss of appetite, nausea and vomiting, jaundice, darkening of urine.

DISCHARGE PLANNING

D- Diet

Encourage patient to eat nutritious foods, limiting intake of food and sodium.F- Follow- up

Instruct patient to have a follow-up visit after 1 week at his doctor’s clinic.A- Activity Level

Encourage following activity with restrictions, resuming activity gradually, and resting whenever tired.

Advise patient to have assistance and support as tolerated when ambulating and to perform ADL’s involving hygiene and self-care, with support if needed.

T- Treatment

Emphasize the importance of prophylaxis against recurrent streptococcal pharyngitis and continuous therapy to prevent recurrent rheumatic fever and rheumatic heart disease.

D- Discharge Plan

Explain to the patient and parents the disease process and its treatment to promote understanding of acute and lifelong prophylactic treatment.

Teach patient and parents to prevent further streptococcal infections b good hand washing and avoiding people with sore throat.

Encourage the patient and parents to contact the primary healthcare provider if a sore throat occurs.

Advise patient to return to physical education classes gradually, with the guidance of the physician.

Encourage patient to take frequent naps and rest periods. Encourage relaxing environment using relaxation techniques, listening to music and quiet

activities Teach patient and parents about the importance in keeping their environment clean and

practicing proper food handling and sterilizing kitchen utensils. Advise the parents that child cannot return to school until health care provider assesses that all

disease activity is gone. Parents may need to discuss with teachers how the child can catch up with school..

M- Medications

Make sure that the patient understands the purpose, dosage, route, and possible side effects of all prescribed home medications.

Instruct patient and the family to strictly follow the orders for take home meds upon discharge as prescribed by the physician.

case study rheumatic

Documents

semi fowler

vena cava

negative chronotropic

inferior vena

positive inotropic

aortic semilunar

health care

left av valve