MODUL-2 untuk Preceptor P3D-3.doc

8/10/2019 MODUL-2 untuk Preceptor P3D-3.doc

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COURSE STUDY GUIDE

LEARNING GUIDE, PRECEPTOR GUIDE

ANEMIA

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ANEMIA

Rationale

Anemia is a common finding, often identified incidentally in asymptomatic

patients. It can be a manifestation of a serious underlying disease. Distinguishingamong the many disorders that cause anemia, not all of which require treatment,is an important training problem for fifth-year medical students.

Knowledge

Students should be able to define, describe, and discuss the:

classification of anemias morphological characteristics, pathophysiology and relative prevalence of:

o iron deficiency and other microcytic anemias i.e., sideroblastic!

o macrocytic anemiaso anemia of chronic disease

o congenital disorders(i.e., sic"le cell,thalasemias!o hemolytic anemias

laboratory tests used in evaluating anemia -- normal and abnormal values indications, contraindications and complications of blood transfusion

Skills

Students should demonstrate specific s"ills, including:

History-Taking Skills: Students should be able to obtain, document, andpresent an age-appropriate medical history, that differentiates amongetiologies of disease including:

o constitutional and systemic symptoms: fatigue

weight loss

o #I bleeding

o abdominal pain

o medications

o diet

o menstrual history

o family historyo past medical history

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Physical Exam Skills: Students should be able to perform a physical

e$am to establish the diagnosis and severity of disease includinginspection of:

o s"in

o eyes

sclera con%unctiva

fundi

o mouth

o heart

o abdomen

o rectum

o lymph nodes

o nervous system

i!!erential iagnosis: Students should be able to:

o generate a list of the most important and most common causes of

anemiao recogni&e specific history and physical e$am findings that suggest

a specific etiology of anemia "a#oratory Inter$retation: Students should be able to recommend when

to order diagnostic tests and be able to interpret the following laboratorytest results:

o hemoglobin and hematocrit

o red cell indices

o reticulocyte count

o iron studies

serum iron

'I() ferritin

transferrin

o serum (*+ and folate

o D

o Schilling test

o hemoglobin electrophoresis

o blood smears

%omm&nication Skills: Students should be able to:o counsel patients and their families with regard to:

possible causes of the anemia

appropriate further evaluation to establish the diagnosis of

an underlying disease the impact on the family genetic counseling!

'asic and Ad(anced Proced&re Skills: Students should be able to:

o interpret a peripheral blood smear.

o assist in performing a bone marrow aspiration.

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Management Skills:Students should be able to develop an evaluation

plan to obtain appropriate diagnostic studies useful in establishing aspecific diagnosis including:

o #I blood loss

o hemolytic anemia

o pernicious anemiao chronic disease:

renal

thyroid

I

malignancy

inflammation

Students should be able to develop a treatment plan for thefollowing:

o iron deficiency anemia

Attit&des and Pro!essional 'eha(iors

Students should be able to:

recogni&e that constitutional symptoms, such as fatigue or malaise, may

be caused by depression, rather than any underlying anemia or dietarydeficiency.

appreciate that anemia is not a disease by itself, but rather a common

finding that requires further delineation and evaluation to identify the

casual disorder and therefore the most appropriate management.

Reso&rces

*. /introbe0s )linical ematology, **thedition, +112.

+. 3edoman Diagnosis dan 'erapi ematologi 4n"ologi 5edi" ,+116.

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"earning )&ide o! %linical Examination

Proced&re !or %linical ExaminationNo. Procedure Performace Sca!e Comme"

# $ 2

History Taking1. Find the chief complaint(s)of anaemia,

bleeding, and malignancy.

2. Each symptom is pursued for more details:

hen did it begin, suddenly or gradually!

"pontaneously or after some specific

e#ent!

$o% has it changed or progressed!

hat ma&es it %orse or better!

3. 'onclude the history and fit it %ith some

pattern of disease that %e recognie.

Sym$toms

Anaemia1. nterrogation along broad lines of symptoms

of decreased o*ygen deli#ery %ith associatedorgan dysfunction:

ea&ness, diiness, pale, irritability,

anore*ia, fatigue, decreased mentalconcentration

E*ertional dyspnea, palpitations,

orthopnoe, an&le edema, headache,urinary fre+uency

enstrual irregularities

2. nterrogation of the etiological factors:

$istory of prematurity (especially inchildren)

E*acerbation of pallor and -aundice

urpura, hematemesis, loss of blood

from the bo%el

nfestation %ith animal parasites,

allergy, ingestion of drugs or

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household products &no%n to depress

hematopoiesis or cause hemolysis,pica, e*posure to radiation.

Fre+uency of respiratory tract

infections and other infections,pree*isting cardiac, gastrointestinal,endocrine, or renal diseases, bone pain

and -oint s%elling

0 complete dietary history of food

(mil&, meats, #egetables, etc)

Family history of anaemia, bleeding,

and social history of ethnic,

geographic, socioeconomic, tra#ellingto endemic area of malaria

%!eed&'

1. nterrogation the manifestation of bleeding: superficial hemorrhage into the s&in

mucous membranes or massi#e

hemorrhage : petechiae, purpura,

ecchymoses, hematoma, hematuria,epista*is, hematemesis, melena,

hematocheia, hemarthrosis, gum

bleeding, subcon-uncti#al bleeding,menometrorrhagia

nset of bleeding : recurrent or not,

immediate, chronic or prolonged

bleeding from umbilical cord, after dentale*traction, tonsillectomy, circumcision,

surgery

"ingle site or multiple sites

2. he history of:

n-ury or trauma,

rolonged bleeding after circumcision,

dental e*traction or other trauma

Family history,

ast medical history (includingtransfusion)

Ma!&'ac

1. he symptoms of

allor, easy fati+uability, fe#er,

bleeding, easy bruising, infection, night

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5ymph node enlargement

0bdominal distension,

6one pain, arthralgia, abnormality of

gait or instability to %al&

7omiting, headache, respiratory

distress

ass(es) at particular region

5oss of consciousness

2. he history of

Family history

E*posure to drugs, radiation, and

chemicals

P*&ca! E+am&a"&o

Aaem&a

1. I&"&a! mea*ureme"

'areful obser#ation and loo& beforetouching the patient:

s the patient sic& or %ell! f

sic&, ho%

sic& is the patient! $o% is his8herposition!

5e#el of consciousness

6reathing ( respiration rate and effort,

cyanosis)9

'irculation (6lood pressure,

heart8pulse rate)

6ody temperature.

easurements of body %eight, length

or height.

2. -&d "e *&'* of aem&a

1. $air:

ry hair, easy to pull out (in ron

deficiency anemia)

2. he eye :

'on-uncti#a :

ale or not"mall hemorrhages in the con-uncti#a

may be significant signs of bleeding.

he sclera should be completely %hite.

;ello% sclerae may be the first sign ofclinical -aundice

3. outh:


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he color of the lips. ale or not.

ral mucosa : pale or not ongue: smooth and red (sign of

egaloblastic 0nemia)

"tomatitis angularis, oral patch (sign of

oral candidosis8candidiasis)

4. $eart:

dentify the sign of tachycardia.

he normal heart rate #aries from

14= beats8min at 1 year,

?=>13= beats8min at 2 years,?=>12= beats8min at 3 years and

11/ beats8min after 3 years

@= beats8min age 1= years ,adolescence decreases to

=.1== beats8min

0uscultation to find out a systolic

heart

murmur in all #al#e area as the

sign of se#ere anemia. 5isten %ith the

patients in the sitting and supinepositions.

/. Aail : pale, cyanosis or normal, spoon

nail (&oilonychia). almar: pale or normal


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massi#e bleeding

2. dentify the site of bleeding:

single or multiple, gum, nose bleed,

-oint, surgical %ound, circumcision, or

other locations.

"ymetric or asymmetric he mucous membrane, hemarthroses,

-oint deformity

Malignancy1. I&"&a! mea*ureme"

dentify the sign of :

fe#er, tachycardia, irritability,

anemia

bleeding

s&in infiltrates, periorbital edema,papiledema, adenopathy, e#idence of

mediastinal enlarhgement, hepatomegaly,splenomegaly, testicular enlargement, bone

paint, e#idence of infection, abdominal

mass and other mass(es)

2. /e0a"ome'a!

he li#er is normally not palpable or

could be palpable as a superficial mass 1>2cm belo% the right costal margin, %ith a

sharp margin. rocedure:a.lace your left hand behind the patient,parallel to and supporting the right 11thand

12thribs and ad-acent soft tissues belo%.

b. Bemind the patient to

rela* on your hand if necessary.c.6y pressing your left hand for%ard, the

patientCs li#er may be felt more easily by

your other hand.d. lace your right hand

on the patientCs right abdomen lateral to the

rectus muscle, %ith your fingertips %ellbelo% the lo%er border of li#er dullness.

e.0s& the patient to ta&e a deep breath.

f. ry to feel the li#er edge as it comes do%n

to meet yor fingertips.g. f palpable at all, the

edge of a normal li#er is soft, sharp and

regular, its surface smooth and maybe

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slightly tender.

3. S0!eome'a!&rocedure of spleen e*amination:

a. ith your left hand, reach o#er and around

the patient to support and press for%ard thelo%er left rib cage and ad-acent soft tissue.

b. ith your right hand belo% the left costal

margin, press in to%ard the spleen.c. 6egin palpation lo% enough so that you are

belo% a possibly enlarge spleen.

d. 0s& the patient to ta&e a deep breath.

e. ry to feel the tip or edge of the spleen as itcomes do%n to meet your fingertips.

f. Aote any tenderness, assess the splenic

contour.

4. Lm0 Node5ymph node are generally e*amined during

e*amination of the part of the body in%hich they are located.

Procedure

E*amine systematically occipital, post

auricular, anterior and posterior cer#ical,cer#ical,(figure 2), parotid, subma*illary,

sublingual, a*illary, epitrochlear and

inguinal nodes.

Aote sie, number, mobility,

tenderness and consistency of any glandsfelt.

"mall, discrete, mo#able, cool, non

tender nodes up to 3 mm in diameterare usually normal in these areas9

n the cer#ical and inguinal

regions, nodes up to 1 cm in diameter arenormal until age 12 years.

Aodes that bare in the anterior

cer#ical triangle or that enlarge slo%ly are

usually

benign.

Bapidly gro%ing nodes fi*ed to

underlying tissue, or hard, firm, or mattedAodes usually malignant.

5arge, %arm, soft, tender nodes

usually indicate acute infection.

Firm, rubbery nontender nodes are

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more common %ith leu&emia or sarcoid.

Firm nodes that adhere to each other

and the s&in are found in children %ithtuberculosis.

iscrete rubbery nodes are

found in $odg&in disease, and e*tremelyfirm, hard

nodes occur in metastases.

5ocal adenopathy usually

indicates local infection but may be a+ sign

ofgeneralied disease.

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SOME IN-ORMATION -OR PRECEPTORS

$. hat is the definition of anemia!

> 0nemia is a reduction belo% normal in the concentration of hemoglobin or red

blood cells or hematocrit (introbe 1@@@, p ?@ he mean normal #alues of hemoglobin, hematocrit and red blood cells count

depend on the age and se* of the sub-ects as %ell as their altitude of residence

(introbe 1@@@, p ?@ $ematology Beference 7alues in Aormal 0dults (introbe 1@@@, appendi* 0, p

2111/.3 g8d5 123>1/3 g85

$ematocrit ($ct) 41./>/=.4 =.41/>=./=4 3>4/ =.3>=.4/

Bed cell count 4./>/.@*1=8u5 4./>/.@*1=1285 4./>/.1*1=8u5 4./>/.1*1=1285

ean 'orpuscular 7olume ?=>@ f5 ?=>@ f5 ?=>@ f5 ?=>@ f5

ean 'orpuscular$emoglobin

233.2 pg 233.2 pg 233.2 pg 233.2 pg

ean 'orpuscular$emoglobin 'oncentration

33.4>3/./ g8dl 33.4>3/./ g8dl 33.4>3/./ g8dl 33.4>3/./ g8dl

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> $ematology #alues during nfancy and 'hildhood (introbe 1@@@, appendi* 0, p

22 " ean >2 " ean >2 " ean >2 " ean >2 " ean >2 "

6irth (cord 6lood) 1./ 13./ /1 42 4.< 3.@ 1=? @? 34 31 33 3=

1 to 3 days(capillary)

1?./ 14./ / 4/ /.3 4.= 1=? @/ 34 31 33 2@

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into the glomerular filtrate each time the blood passes through the capillaries.

herefore, for hemoglobin to remain in the blood stream, it must e*ist inside red

blood cell.he red blood cells ha#e other functions besides transport of hemoglobin. hey

contain a large +uantitiy of carbonic anhydrase, %hich catalyes the re#ersible

reaction bet%een carbon dio*ide and %ater, increasing the rate of this reaction se#eralthousand>fold. he rapidity of this reaction ma&es it possible for the %ater of the

blood to transport enormous +untitites of carbon dio*ide from the tissues to the lungs

in the form of the bicarbonate ion. 0lso, the hemoglobin in the cells is an e*cellentacid>base buffer, so that the red blood cells are responsible for most of the acid>base

buffering po%er of %hole blood (uyton 2===, p 3?2)

$emoglobin are tetramers comprised of pairs of t%o different polypeptide subunits.

he subunit composition of the principal hemoglobin are 22($b09 normal adult

hemoglobin), 22($bF9 fetal hemoglobin), 22(b029 a minor adult hemoglobin).

he primary structures of the , , chains of human hemoglobin are highly

conser#ed. $emoglobins bind four molecules of 2per tetramer, one per heme. 0molecule of 2binds to a hemoglobin tetramer more readily if other 2molecules are

already bound. ermed cooperati#e binding, this phenomenon permits hemoglobin to

ma*imie both the +uantity of 2loaded ath the o2of the lungs and the +uantity of2released at the o2of the peripheral tissues. 'ooperati#e interactions , an e*clusi#e

property of multimeric proteins, are critically important to aerobic life ($arper 2==3,

p 42).

. E*plain the erythropoiesis and %hat regulates this process!

n the red cell>producing bone marro% are cells called pluripotential

hematopoietic stem cells, from %hich all the cells in the circulating blood are deri#ed.Figure belo% sho%s the successi#e di#isions of the pluripotential cells to form the

different peripheral blood cells.

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Erythrocytes

'FG>6 'FG>E

('olony>forming ('olony>formingunit>blast) unit>erythrocytes) ranulocytes

(Aeutrophilis)

(Eosinophils) (6asophils)

onocytes

$"' 'FG>" 'FG>

(luripotent ('olony>forming ('olony>forming unit> acrocytes$ematopoietic unit>spleen) granulocytes, monocytes)

"tem cell)

ega&aryocytes

'FG>

('olony>formong unit latelets ega&arocytes)

lymphocytes

6 5ymphocytes

$"' 5"' (5yhmphoid stem cell)

0s these cells reproduce, contuining throughout life, a small portion of them

remains e*actly li&e the original pluripotential cells and retained in the boned maro% to

maintain a supply of these, although their numbers do diminish %ith age. he earlyoffspring cells still cannot be recognied as different from the pluripotential stem cell,

e#en though they ha#e already become commited to a particular line of cells and are

called commited stem cells

he different commited stem cells, %hen gro%n in culture, %ill produce coloniesof spesific types of blood cells. 0 commited stem cell that produces erythrocytes is called

a colony-forming unit-erythrocytes , and the abbre#iation 'FG>E is used to designation

'FG>, and so forth.ro%th and reproduction of the different stem cells are controlled by multiple

proteins called growth inducers. Four ma-or gro%th inducers ha#e been described, each

ha#ing different characteristic. ne of these, interleukin-3 , promotes gro%th andreproduction of #irtually all the different types of stem cells, %hereas the others induce

gro%th of only specific types of commited stem cells.

he gro%th inducers promote gro%th but not differentiation of the cells. his is

the function of still another set of proteins called differentiation inducers. Each of these

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causes one of type of stem cells to differentiate one or more steps to%ard a final type of

adult blood cells.

Formation of the gro%th inducers and differentiation inducers is itself controlled byfactors outside the bone marro%. For instance, in the case of red blood cells, e*posure of

the body to lo% o*ygen for a long time results in gro%th induction, differentiation, and

production of greatly increased numbers of erythrocytes (uyton 2===, p 3?3).

he term erythropoiesis identifies the entire process by %hich erythrocytes areproduced in the bone marro%. n response to er"ro0o&e"&, a gro%th factor that

stimulates the erythroid precursors, erythropoiesis occurs in the central sinus beds of

medullary marro% o#er a period of about / days through at least 3 successi#e reduction>

di#isions from rubriblast to prorubricyte to rubricyte, and finally to metarubricyte. ithsuccessi#e de#elopmental stages the follo%ing changes occur: reduction in cell #olume,

condensation of chromatin, decrease in A:' ratio, loss of nucleoi, decrease in ribonucleic

acid (BA0) in the cytoplasm, decrease in mitochondria, and gradual increase in synthesisof hemoglobin. emorie the follo%ing de#elopmental stages from Hmother cellI to

mature erythrocyte: rubriblast (pronormoblast) to prorubricyte (basophilic normoblast) to

rubricyte (polychromatophilic normoblast) to metarubricyte (orthochromatic normoblast).he nucleus of the metarubricyte is e#entually e*trude, lea#ing a non>nucleated

polychromatophilic (diffusely basophilic) erythrocyte, %hich is release into the

circulating blood to mature in 1 to 2 days. rogressi#e cellular di#isions of one rubriblast

results in production of 14 to 1 erythrocytes ($armening 1@@@=2)

atients %ith anemia usually see& medical attention because of decreased %or&tolerance, shortness of breath, palpitations, or other signs of cardiorespiratory

ad-ustments to anemia. 0t times, they feel fine,but their friends or family ha#e noted

pallor.he manifestations of anemia depend on fi#e factors: the reduction in the o*ygen>

carrying capacity of the blood, the degree of change in total blood #olume, the rate at

%hich the pre#ious t%o factors de#eloped, the capacity of the cardio#ascular and

pulmonary systems to compensate for the anemia, and the associated manifestationsof the underlying disorder that resulted in the de#elopment of anemia.

Cardiorespiratory systemn many patients, respiratory and circulatory symptoms are noticeable only after

e*ertion or e*citement9 ho%e#er, %hen anemia is sufficiently se#ere, dyspnea and

a%areness of #igorous or rapid heart action may be noted e#en at rest. hen anemiade#elops rapidly, shortness of breath, tachycardia, diiness or faintness (particularly

upon arising from a sittinf or recumbent posture), and e*treme fatigue are prominent.

n chronic anemia, only moderate dyspnea or palpitation may occur, but in some

patients, congesti#e heart failure, angina pectoris, or intermittent claudication can bethe presenting manifestation.

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The Skin

allor can be the most e#ident sign of anemia, but factors other than hemoglobinconcentration affect s&in color. hese factors include the degree of dilation of the

peripheral #essels, the degree and nature of the pigmentation, and the nature and fluid

content of the subcutaneous tissues.he pallor associated %ith anemia can be detected most accurately in the mucous

membranes of the mouth and pharyn*, the con-uncti#ae, the lips, and the nail beds. n

the hands, the s&in of the palms first becomes pale, but the creases may retain theirusual pin& color until the hemoglobin concentration is less than < g8d5. 0 satisfactory

interpretation cannot be made in the presence of cyanosis or abnormal

#asoconstriction.

Neuromuscular System

$eadache, #ertigo, tinnitus, faintness, scotomata, lac& of mental concentration,

dro%siness, restlessness, and muscular %ea&ness are common symptoms of se#ere

anemia. "ome of these signs may be manifestations of cerebral hypo*ia.

Retinopathy

'ertain ophthalmologic findings ha#e been obser#ed in anemic patients. 0bout

2=D of such patients ha#e flame>shaped hemorrhages, hard e*udates, cotton%oodspots, or #enous tortuousness affecting the retina. hese abnormalities are not clearly

related to the degree of anemia, and, for un&no%n reasons, are much more common in

men than %omen.

astrointestinal System

astrointestinal symptoms are common in anemic patients. "ome are

manifestations of the disorder underlying the anemia (such as duodenal ulcer orgastric carcinoma)9 others may be a conse+uence of the anemic condition, %hate#er

its cause. lossitis and atrophy of the papillae of the tongue commonly occur in

pernicious anemia and much less often in iron>deficiency anemia. ainful, ulcerati#e,and necrotic lesions in the mouth and pharyn* occur in aplastic anemia an in acute

leu&emia, usually reflecting the neutropenia accompanying these conditions.

ysphagia may occur in chronic iron>deficiency anemia.

enitourinary System

"light proteinuria is not uncommon in patients %ith significant anemia.

icroscopic hematuria occurs %ithout other e*planation in heteroygotes for sic&lehemoglobin.

!ther signsn se#ere anemia, the basal metabolic rate may be increase. hether the general

state of nutrition is preser#ed depends on the cause for the anemia. hen anemia is

se#er, fe#er of mild degree may occur %ithout other cause.

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Pa"o0*&o!o'

he #ital process of deli#ering o*ygen to the tissues consists of three components:the hemoglobin in red cells, respiration, and circulation. Each of the three can

compensate to some degree for deficiencies in the other components. he amount of

o*ygen deli#ered to the tissues by a gi#en #olume of blood is a function of theconcentration of hemoglobin, the degree to %hich the hemoglobin is saturated %ith

o*ygen, the affinitiy of hemoglobin for o*ygen, and the tissue o*ygen tension. hen

fully saturated %ith o*ygen, 1 g of hemoglobin binds 1.34 ml of o*ygen. 0t ahemoglobin concentration of 1/ g8d5, 1== m5 of arterial blood contains about 2= m5

of o*ygen, %hereas the same #olume of mi*ed #enous blood contains appro*imately

1/ m5. he difference results from the e*traction of o*ygen by the tissues. n an

anemic patients %ith a hemoglobin concentration of carrying effect of anemia because e#en though each unit +uantity ofblood carries only small +uantities of o*ygen, the rate of blood flo% may be increased

enough so that almost normal +uantities of o*ygen are actually deli#ered to the

tissues. $o%e#er, %hen this same person %ith anemia begins to e*ercise, the heart is

not capable of pumping much greater +uantities of blood than it is already pumping.'onse+uently, during e*ercise, %hich greatly increase tissue demand for o*ygen,

e*treme tissue hypo*ia results, and acute cardiac failure ensues (uyton 2===, p 3@=)

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4. hat is the classification of anemia!

Jinetic 'lassification of 0nemia (introbe 1@@@, p @=4>@=/)

Im0a&red er"roc"e 0roduc"&o (Re"&cu!oc"e Produc"&o Ide+5RPI 6 2)"ypoproliferative

ron>deficient erythropoiesis

o ron deficiency

o 0nemia of chronic disorders

Erythropoietin deficiency

o Benal disease

o Endocrine deficiencies

$ypoplastic anemia

o 0plastic anemia

o ure red cell aplasia

nfiltration

o 5eu&emia

o etastatic carcinoma

o yelofibrosis

Ineffective

egaloblastic

o 7itamin 612deficiency

o Folate deficiency

o ther causes

icrocytic

o halassemiao 'ertain sideroblastic anemias

Aormocytic

Icrea*ed er"roc"e 0roduc"&o (RPI 71)

"emolytic anemia

$ereditary

0c+uired

Treated nutritional anemias

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'lassification of 0nemia by B6' indices ($armening 1@@3) egaloblastic and

nonmegalobastic macrocytic

anemias (e.g.li#er disease,

myelodysplasias)

icrocytic (L?=) $ypochromic (32) ron deficiency, sideroblastic

anemia, thalassemia, lead

poisoning, chronic diseases,chronic infection or

inflammation, unstablehemoglobins


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ransport, storage, and metabolism of iron in the body are diagrammed in figure

belo%:

6ilirubin (e*creted)

T&**ue*

Ferritin

$emosiderin

Macro0a'e*

$eme

egrading hemoglobin Free iron Enymes

Free iron

$emoglobin ransferrin>Fe

Red Ce!!* P!a*ma

6lood loss M =.< mg Fe FeNNabsorbed Fe e*creted Mdaily in menses (small intestine) =.mg daily

hen iron is absorbed from the small intestine, it immediately combines in the

blood plasma %ith a beta globulin, apotransferrin, to form transferrin, %hich is then

transported in the plasma. he iron is loosely bound in the transferrin and, conse+uently,

can be released to any of the tissue cells at any point in the body. E*cess iron in the bloodis deposited in all cells of the body, but especially in the li#er hepatocytes and less in the

reticuloendothelial cells of the bone marro%. n the recei#ing cell cytoplasm, the iron

combines mainly %ith a protein, apoferritin, to form ferritin. 0poferritin has a molecular%eight of about 4=,===, and #arying +uantities of iron can combine in clusters of iron

radicals %ith this large molecule9 therefore, ferritin may contain only a small amount of

iron or a large amount. his iron stored as ferritin is called storage iron."maller +uantities of the iron in the storage pool are stored in an e*tremely

insoluble form called hemosiderin. his is especially true %hen the total +uantity of iron

in the body is more than the apoferritin storage pool can accommodate. $emosiderin

forms especially large clusters in the cells and, conse+uently, can be stained and obser#edmicroscopically as large particles in tissue slices. Ferritin can also be stained, but the

ferritin particles are so small and dispersed that they usually can be seen only %ith the

electron microscope.hen the +uantity of iron in the plasma falls #ery lo%, iron is remo#ed from

ferritin +uite easily but from hemosiderin much less easily. he iron is then transported

again in the form of transferring in the plasma to the portions of the body %here it isneede.

0 uni+ue characteristic of the transferrin molecule is that it binds strongly %ith

receptors in the cell membranes of erythroblasts in the bone marro%. hen, along %ith its

bound iron, it is ingested into the erythroblasts by endocytosis. here the transferrin

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deli#ers the iron directly to the mitochondria, %here heme is synthesied. n people %ho

do not ha#e ade+uate +uantities of transferrin in their blood, failure to transport iron to

the erythroblasts in this manner can cause se#er hypochromic anemia. hen red bloodcells ha#e li#ed their life span and are destroyed, the hemoglobin released from the cells

is ingested by the cells of the monocyte>macrophage system. here free iron is liberated,

and it is then mainly stored in the ferritin pool or reused for formation of ne% hemoglobin(uyton 2===, p 3??).

Bole of iron in erythropoiesis

ron, because of its electron state, is ideally suited to form chelates or comple*es %ith

heterocyclic rings and proteins. t is the ability of iron to chelate or form comple*es %ith

#arious molecules that enables its absorption, transport, storage, and function. heinteraction of iron %ith protoporphyrin allo%s the formation of heme. Ferrous iron

combines %ith protoporphyrin in the mitochondria of the B6' to form heme.

rotoporphyrin is produced through a se+uence of steps that starts %ith aminole#ulinic

acid (050) formation from glycine and succinyl coenyme 0. his is the rate>limitingstep in heme synthesis. %o 050 molecules combine to form porphobilinogen, and four

porphobilinogen molecules -oin together to form uroporphyrinogen . ecarbo*ylationof uroporphyrinogen forms coproporphyrinogen , %hich is o*idied to

protoporphyrin. 0lso %ithin the cytoplasm of the B6', alpha and beta globin protein

chains are synthesied. he t%o alpha and t%o beta globin protein chains combine %ithfour heme groups and four o*ygen molecules to form an intact functional hemoglobin

molecule ($armening 1@@. utline the pathogenesis of iron deficiency anemia including the stages in the

de#elopment of iron deficiency

ron deficiency usually is the end result of a long period of negati#e iron balance.

0s the total body iron le#el begins to fall, a characteristic se+uence of e#ents ensues.

First, the iron stores in the hepatocytes and the macrophages of the li#er, spleen, andbone marro% are depleted. nce stores are gone, plasma iron content decreases, and

the supply of iron to marro% becomes inade+uate for the normal regeneration of

hemoglobin. hen, the amount of free erythrocyte protoporphyrin

increases,production of microcytic erythrocytes begins, and the blood hemoglobinle#el decreases, e#entually reaching abnormal le#els.

his progression ser#es as a basis for definition of three recognied stages.

relatent iron deficiency or iron depletion refers to a reduction in iron stores %ithoutreduced serum iron le#els. etection of such a condition depends on the ability to

appraise iron stores by using biopsy techni+ues or the measurement of serum ferritin.

5atent iron deficiency is said to e*ist %hen iron stores are e*hausted but the bloodhemoglobin le#el remains higher than the lo%er limit of normal. n this stage, certain

biochemical abnormalities in iron metabolism are usually detected, particularly

reduced transferin saturation.

22


23/199

Finally, %hen the blood hemoglobin concentration falls belo% the lo%er limit of

normal, iron>deficiency anemia has de#eloped (introbe 1@@@, p @?1).

"e+uential steps in the de#elopments of ron>eficiency 0nemia

($armening 1@@deficiency anemiai. ecreased hemoglobin synthesis %ith anemia and significant

microcytosis (decreased '7)ii. 0nisocytosis of the B6's

iii. ncreased serum soluble transferring receptor le#els

1=. hat is the etiology of iron deficiency anemia!(introbe 1@@@, p @?3>@@1)

Ne'a"&e &ro :a!ace

#ecreased iron intake

nade+uate diet mpaired absorption

o 0chlorhydria

o astric surgery

o 'eliac disease

o ica (habitual ingestion of unusual substances: earth or clay

(geophagia), laundry starch (amylophagia), and ice

(pagophagia)Increased iron loss

astrointestinal bleeding

o "ite un&no%n

o $emorrhoidso "alicylate ingestion

o eptic ulcer

o $iatal hernia

o i#erticulosis

o Aeoplasm

o Glcerati#e colitis

23


24/199

o $oo&%orm

o il& allergy in infants

o ec&elCs di#erticulum

o "chistosomiasis

o richuriasis

E*cessi#e menstrual flo% 6lood donation

$emoglobinuria

"elf>induced bleeding

diopathic pulmonary hemosiderosis

$ereditary hemorrhagic teleangiectasia

isorders of hemostasis

'hronic renal failure and hemodialysis

BunnerCs anemia

Caused unknown $%idiopathic& hypchromic anemia'

Increased re(uirements nfancy

regnancy

5actation

5o% birth%eight and unusual perinatal hemorrhage are associated %ith

decreases in neonatal hemoglobin mass and stores of iron. 0s the high

hemoglobin concentration of the ne%born infants falls during the first 2>3months of life, considerable iron is reclaimed and stored. hese reclaimed

stores are usually sufficient for blood formation in the first >@ months of life

in term infants. n lo%>birth%eight infants or those %ith perinatal blood loss,stored iron may be depleted earlier and dietary sources become of paramount

importance. n term infants, anemia caused solely by inade+uate dietary iron

is unusual before months and usually occurs at @>24 month of age.

hereafter, it is relati#ely infre+uent. he usual dietary pattern obser#ed ininfants %ith iron Mdeficiency anemai is consumption of large amounts of

co%Cs mil& and of foods not supplemented %ith iron (Aelson 2==4, p 114)

24


25/199

11. hat are the signs and symptoms of iron deficiency anemia!

(introbe 1@@@, p @@1>@@/)

o ica (introbe 1@@@, p@?/)

Fatigue

rritability alpitations, diiness, breathlessness

$eadache

mpaired muscular performance

efecti#e structure or function of epithelial tissue:

o Aails: brittle, fragile, longitudinally ridged, thinning, flattening,

&oilonychias (spoon>shaped nails)

o ongue and mouth: atrophy of the lingual papillae, angular

stomatitis

o $ypopharyn*: dysphagia

o

"tomach: achlorhydria, gastritis

12.hat is the laboratory results of iron deficiency anemia!he serum iron decreased, 6' increased and Ferritin decreased

6one marro% smear sho%s erythroid hyperplasia n ron eficiency 0nemia, the

bone marro% is characteried by erythroid hyperplasia of a #ariable degree, butgenerally mild to moderate. f the nucleated cells in marro% aspirates from iron>

deficient patients, 2/N@.?D %ere erythroblast as compared +ith 1.@ N 2. Eliminate the source of bleeding> ral ron herapy: for adults the optimal response occurs %hen about

2==mg of elemental iron are gi#en each day. f patients cannot tolerate

2== mg8day of elemental iron as ferrous sulfate, a reasonable step is toreduce the dose to about 1== mg8day.

Begardless of the form of oral therapy used, an important step is to

continue treatment for 3 to months after the anemia is relie#ed. ftreatment does not continue, relapse is common. he continued

therapy allo%s for repletion of iron stores.

Side effects: astrointestinal symptoms (heartburn, nausea, abdominal

cramps, and diarrhea) (introbe 1@@@, p @@@>1===)> ndication of arenteral ron therapy (iron malabsorption (sprue, short

bo%el,etc), se#ere oral iron intolerance, as a routine supplement to

total parenteral nutrition, and in patients %ith renal disese %ho arerecei#ing erythropoietin (oodman illman 2==1, p 1/=1)

2/


26/199

COURSE STUDY GUIDE

LEARNING GUIDE, PRECEPTOR GUIDELEU?EMIA

2


27/199

LEU?EMIA

Ra"&oa!e

0cute leu&emias are hematological emergency. "tudents are e*pected to ma&eearly diagnostic and consultation %ith hematology consultant.

Pree@u&*&"e

rior &no%ledge of the :

structure and maturation of leucocytes

types of malignancy of the blood and pre>leu&emia condition

pathogenesis and etiology of leu&emia

?o!ed'e

"tudents should be able to : E*plain the definition of leu&emia

istinguish the types of leu&emia into 2 categories (acute and chronic)

E*plain the classification of acute myeloid leu&emia and acute non>

myeloid leu&emia (F06)

E*plain the symptoms and physical signs of leu&emia and its

pathophysiology.

E*amine the laboratory findings of leu&emia

E*plain the differential diagnosis of leu&emia

utline the treatment of leu&emia

utline the course and prognosis of leu&emia utline the diagnosis and treatment of oncologic emergencies related

to leu&emia ( massi#e bleeding, intracranial bleeding, leu&ostasis,

tumor lysis syndrome)

SB&!!*

/&*"or"aB&' *B&!!*

"tudents should be able to obtain, document, and present a medical history toestablish the diagnosis of acute leu&emia including:

- uration, progressi#ity of anemia, bleeding- ainless lymph node enlargement

- $epatomegaly- "plenomegaly- Fe#er> Family history

- E*posure to drugs, radiation, and chemicals

P*&ca! e+am *B&!!*

2


28/199

"tudents should be able to perform a physical e*am to establish the diagnosis and

se#erity of disease including:- 7ital signs- $igh and body %eight- E*amination of the head for :

0nemia 'on-uncti#al bleeding

um bleeding and hypertrophy

- E*amination of the nec& for : 5ymphadenopathy

- E*amination of the abdomen for : 0bdominal masses

$epatomegaly

"plenomegaly

- E*amination of the e*tremities for : 5ymphadenopathy

urpura, hematoma

D&ffere"&a! d&a'o*&*

"tudents should be able to generate a prioritied differential diagnosis recogniing

specific history and physical e*am findings that suggest a specific etiology.

La:ora"or e+am&a"&o

"tudents should be able to recommend and interpret diagnostic and laboratory

tests.

- "tudents should understand the rationale for and correctly identifyabnormalities detected by the follo%ing tests.

'omplete blood count

eripheral blood smear

6one marro% smear

Gric acid

Electrolyte

Benal function

'hest *>ray

Commu&ca"&o *B&!!*

"tudents should be able to:

- communicate the diagnosis, treatment plan, and prognosis of the disease topatients and their families, and consider the patientCs &no%ledge ofleu&emia and preferences regarding treatment.

- 'ommunicate the cost of treatment and ho% to get the fund (a&in)

2?


29/199

Maa'eme" *B&!!*

"tudents should be able to de#elop an appropriate e#aluation and treatment plan

for patients %ith:

- 0nemia and bleeding due to leu&emia- "tudents should be able to access and utilie appropriate information

systems and resources to help delineate issues related to leu&emia

A""&"ude* ad 0rofe**&oa! :ea&or


appreciate the importance of patient preferences and compliance%ith management plans for those %ith acute leu&emia

appreciate the importance of side effects of medications and their

impact on +uality of life and compliance ma&e appropriate referral to hematology consultant

get information of the economical status

Re*ource*

1. introbeCs 'linical $ematology, 11thedition, 2==4, p 2=3 M 2142

2. edoman iagnosis dan erapi $ematologi n&ologi edi& ,2==3, p 2/> 1

2@


30/199

Lear&' 'u&de

Proced&re !or %linical Examination

No. Procedure Performace *ca!e Comme"

# $ 2

Introd&ction1. ntroduce yourself.

History Taking

1. Find the chief complaint(s)of anemia,bleeding, and malignancy.

2. Each symptom is pursued for more details:

hen did it begin, suddenly or gradually!


e#ent!



3. 'onclude the history and fit it %ith some

pattern of disease that %e recognie.

Sym$toms

Anemia1. nterrogation along broad lines of symptoms

of decreased o*ygen deli#ery %ith associated

organ dysfunction:

ea&ness, diiness, pale, irritability,

anore*ia, fatigue, decreased mental

concentration

E*ert ional dyspnea, palpitations,orthopnoe, an&le edema, headache,

urinary fre+uency

enstrual irregularities

2. nterrogation of the etiological factors:

$istory of prematurity (especially in

children)

3=


31/199

E*acerbation of pallor and -aundice

urpura, hematemesis, loss of blood

from the bo%el

nfestation %ith animal parasites,

allergy, ingestion of drugs or

household products &no%n to depresshematopoiesis or cause hemolysis,pica, e*posure to radiation.

Fre+uency of respiratory tract

infections and other infections,pree*isting cardiac, gastrointestinal,

endocrine, or renal diseases, bone pain

and -oint s%elling

0 complete dietary history of food

(mil&, meats, #egetables, etc)

Family history of anaemia, bleeding,

and social history of ethnic,geographic, socioeconomic, tra#elling

to endemic area of malaria

ther symptoms : numbness,

stomatitis (sprue)

%!eed&'

1. nterrogation the manifestation of bleeding:

superficial hemorrhage into the s&in

mucous membranes or massi#e

hemorrhage : petechiae, purpura,ecchymoses, hematoma, hematuria,

epista*is, hematemesis, melena,hematocheia, hemarthrosis, gum

bleeding, subcon-uncti#al bleeding,

bleeding from umbilical cord, andmenometrorrhagia

nset of bleeding : recurrent or not,

immediate, chronic or prolonged

bleeding from umbilical cord, after dental

e*traction, tonsillectomy, circumcision,

surgery "ingle site or multiple sites

2. he history of:

n-ury or trauma,

rolonged bleeding after

circumcision, dental e*traction or other

trauma

31


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33/199

s&in infiltrates, periorbital edema,

papiledema, adenopathy, e#idence of

mediastinal enlargement ( dyspnea,#enectation, nec& s%elling), hepatomegaly,

splenomegaly, testicular enlargement, bone

paint, e#idence of infection, abdominalmass and other mass(es)

2. /e0a"ome'a!


could be palpable as a superficial mass 1>2cm belo% the right costal margin, %ith a

sharp margin.

rocedure:

h. lace your left handbehind the patient, parallel to and

supporting the right 11thand 12thribs and

ad-acent soft tissues belo%.i. Bemind the patient to rela* on your hand if

necessary.

-. 6y pressing your left hand for%ard, thepatientCs li#er may be felt more easily by

your other hand.

&. lace your right hand

on the patientCs right abdomen lateral to therectus muscle, %ith your fingertips %ell

belo% the lo%er border of li#er dullness.

l. 0s& the patient to ta&e a deep breath.

m. ry to feel the li#eredge as it comes do%n to meet yor

fingertips.n. f palpable at all, the

edge of a normal li#er is soft, sharp and

regular, its surface smooth and maybeslightly tender.

h. 0ssess li#er enlargement ( in cm) belo%

costal margin processus *yphoideus


g. ith your left hand, reach o#er and aroundthe patient to support and press for%ard thelo%er left rib cage and ad-acent soft tissue.

h. ith your right hand belo% the left costal

margin, press in to%ard the spleen.i. 6egin palpation lo% enough so that you are


-. 0s& the patient to ta&e a deep breath.

33


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&. ry to feel the tip or edge of the spleen as it

comes do%n to meet your fingertips.l. Aote any tenderness, assess the splenic

contour.

m.0ssess spleen enlargement( "chuffner >

7)4. Lm0 Node

5ymph node are generally e*amined during


Procedure


auricular, anterior and posterior cer#ical,cer#ical, parotid, subma*illary,

sublingual, a*illary, and inguinal nodes.

Aote sie, number, mobility,

tenderness and consistency of any glandsfelt.


tender nodes up to 3 mm in diameterare usually normal in these areas9


regions, nodes up to 1 cm in diameter are

normal until age 12 years.


cer#ical triangle or that enlarge slo%ly are

usually

benign.

Bapidly gro%ing nodes fi*ed to

underlying tissue, or hard, firm, or matted

Aodes usually malignant.




more common %ith leu&emia.


and the s&in are found in children %ith

tuberculosis. iscrete rubbery nodes are

found in alignant lymphoma, ande*tremely firm, hard nodes occur in

metastases.


indicates local infection but may be a sign

of

34


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generalied disease.

9I. Cr&"er&a of Per*oa! Performace Ea!ua"&o

Sca!e Performace Ac&eeme"

=. f student doesnCt perform the tas&

1. f student performs the tas& incorrectly8 incompletely

2. f student performs the tas& correctly completely


5eu&emia and lymphoma are common $ematopoietic and 5ymphoid Aeoplasm

(introbe 1@@@, p 1@@3>1@@2333)

LeuBem&a &* a ma!&'a" d&*ea*e of ema"o0o&e"&c "&**ue, characteried byreplacement of normal bone marro% elements %ith abnormal (neoplastic) blood cells.

hese leu&emic cells are fre+uently (but not al%ays) present in the peripheral bloodand commonly in#ade reticuloendothelial tissue, including the spleen, li#er, andlymph nodes. hey may also in#ade other tissues, infiltrating any organ of the body

($armening 2==2, p 2


36/199

> 0cute nonlymphocytic leu&emia (0A55) or acute myeloid leu&emia

(05)

055 has a pea& in childhood and 05 in adult age. he o#erlap is such thatage is not useful criterion in classifying leu&emia.

b. 'hronic leu&emia :4. 'hronic myeloid leu&emia ('5) is a clonal stem cell disorder

characteried by increase proliferation of myeloid elements at all stages of

differentiation . (introbe 1@@@, p 2342)/. 'hronic lymphocytic leu&emia ('55) is characteried by the

accumulation of non proliferating mature>appearing lymphocytes in the

blood, marro%, lymph nodes and spleen. (introbe 1@@@, p 24=/)

Te c!a**&f&ca"&o of acu"e me!o&d !euBem&a ad acu"e !m0oc"&c !euBem&a :a*ed

o -rec Amer&ca %r&"&* (-A%)

($armening 2==2, p 2


37/199

Pa"o'ee*&* of !euBem&a

he origin of leu&emia at the genetic le#el in most cases appears to be related to

mutation and altered e*pression of oncogenes and tumor suppressor genes. ost

oncogenes regulate cell proliferation and differentiation. 0bnormal oncogene ortumor suppressor gene e*pression induced by translocation and genetic fusion or

mutation often results in unregulated cellular proliferation. 0lthough the e#ents that

lead to this are not entirely understood, a number of host and en#ironmental factorsha#e been identified that are associated %ith increased ris& of leu&emic

transformation. ($armening 2==2, p 2


38/199

'ongenital 'hromosomal 0bnormalities

mmunodeficiency

'hronic arro% ysfunction

En#ironmental factors:

oniing radiation

'hemical and drugs

7iruses

Te 0a"o0*&o!o' of "e *m0"om* ad *&'* of !euBem&a

he ma-ority of patients %ith acute leu&emia display clinically abrupt onset of signs

and symptoms of only a fe% %ee&s duration. atients often see& medical attention

because of %ea&ness, bleeding abnormalities, or fluli&e symptoms. heseabnormalities reflect the failure of the bone marro% to produce ade+uate numbers of

normal cells and are caused by the proliferation and accumulations leu&emic cells in

the marro%. 5eu&emic replacement e#entually results in marro% failure and theresultant life>threatening complications of anemia, thrombocytopenia,

granulocytopenia, and their se+uelae. 0nemia, the most consistent presenting feature,

is associated %ith fatigue, malaise, and pallor. $emorrhagic complications related to

thrombocytopenia and, in some cases, to disseminated intra#ascular coagulation arealso common. hese may be mild and restricted to easy bruising, petechiae, and

mucosal bleeding9 or they may be more se#ere, in#ol#ing gastrointestinal tract,

genitourinary tract, or central ner#ous system hemorrhage. nfections result fromse#ere granulocytopenia. 6acterial infections are common (e.g Staphylococcus)

*seudomonas) +scherichia coli)and,lesiella) but fungal infections also occur (e.g.

Candida and.spergillus). 7iral infections are less fre+uent.

nfiltration of other tissues, especially organs that play a role in fetal hematopoiesis, is

often manifested by hepatosplenomegaly or lymphadenopathy, particularly in 055and acute monoblastic leu&emia (0o5) subtype of 05. 0 mediastinal mass

resulting from thymic in#ol#ement is a hallmar& of >cell 055. ingi#al hypertrophy

and oral lesions are primarily seen in 0o5. 6one or -oint pain, caused by pressure

of the e*panding leu&emic cell population in the marro% ca#ity, commonlyaccompanies the acute leu&emias. 5eu&emic infiltration of the central ner#ous

system, an ominous feature infre+uently obser#ed at initial presentation, is associated

%ith signs and symptoms of increased intracranial pressure (nausea, #omiting,headache, papilledema) or cranial ner#e palsies ($armening 2==2, p 22


39/199

'hemotherapy is the mainstay of treatment, although bone marro% transplantation is

being used more fre+uently. Badiotherapy is used as an ad-unct to chemotherapy in

patients %ho ha#e localied tissue in#ol#ement that may be targeted %ith irradiation,and has been used for central ner#ous system prophyla*is ($armening 2==2, p 2?4>

2?/)

he treatment of this patient (05) may consist of cytoto*ic chemotherapy alone or

marro%8stem cell transplantation after chemotherapy.

0dministration of cytosine arabinoside, usually in con-unction %ith an anthracyclinehas been the cornerstone of chemotherapy in 05 for o#er 2/ years.

herapy can be di#ided into t%o phases: induction and postremission therapy. he

initial goal of therapy is induction of a complete remission ('B). 'B is defined by

normaliation of neutrophil counts (at least 1./*1=@85) and platelet counts (more than1==* 1=@85), and a marro% aspirate and biopsy that demonstrate at least 2=D

cellularity, less than /D blasts, and no 0uer rods, as %ell as absence of

e*tramedullary leu&emia.

ostremission therapy may consist of maintenance, consolidation, or intensificationtherapy. (introbe 1@@@, p 22@=>22@B, d, 5ymphoid, B>1

'ytogenetics

3@


40/199

COURSE STUDY GUIDE

LEARNING GUIDE, PRECEPTOR GUIDE

MALIGNANT LYMP/OMA

MALIGNANT LYMP/OMA

4=


41/199

Ra"&oa!e

n ndonesia, malignant lymphoma and leu&emia are the si*th most commonmalignancies. 5ymphoma can be cured if it is detected in early stage. "tudents are

e*pected to generate a prioritied differential diagnosis of lymph nodes

enlargement

Pree@u&*&"e

rior &no%ledge of the :

anatomy and physiology of lymph node

etiology of lymph node enlargement

pathogenesis, etiology, pathological feature of malignant lymphoma

?o!ed'e

"tudents should be able to :

E*plain the definition of malignant lymphoma istinguish the types of malignant lymphoma into 2 categories

utline the signs and symptoms of alignant 5ymphoma

escribe the classification of Aon>$odg&in alignant 5ymphoma

(or&ing Formulation)

escribe the clinical stages of $odg&in and Aon>$odg&in alignant

5ymphoma (0nn 0rbor classification)

utline the treatment of malignant lymphoma

utline the course and prognosis of malignant lymphoma

utline the diagnosis and treatment of oncologic emergencies related to

lymphoma(tumor lysis syndrome)

SB&!!*

/&*"or"aB&' *B&!!*"tudents should be able to obtain, document, and present a medical history to

establish the diagnosis of malignant lymphoma including:- uration, progressi#ity of lymph node enlargement- painless lymph node enlargement- lymph nodes enlargement in other sites- 0bdominal masses

- $epatomegaly- "plenomegaly- 6 symptoms : night s%eats, %eight loss, fe#er> Family history

- E*posure to drugs, radiation, and chemicals- rugs abuse, promiscuity

P*&ca! e+am *B&!!*

41


42/199

"tudents should be able to perform a physical e*am to establish the diagnosis and

se#erity of disease including:- 7ital signs- $igh and body %eight- E*amination of the head for :

0nemia- E*amination of the nec& for :

5ymphadenopathy

- E*amination of the abdomen for : 0bdominal masses

$epatomegaly

"plenomegaly

- E*amination of the e*tremities for : 5ymphadenopathy

D&ffere"&a! d&a'o*&*

"tudents should be able to generate a prioritied differential diagnosis recogniingspecific history and physical e*am findings that suggest a specific etiology.

La:ora"or e+am&a"&o

"tudents should be able to recommend and interpret diagnostic and laboratorytests.

- "tudents should understand the rationale for and correctly identifyabnormalities detected by the follo%ing tests.

'omplete blood count

Gric acid

5$

'hest *>ray

0bdominal ultrasound or ' "can

5ymph node biopsy

Commu&ca"&o *B&!!*

"tudents should be able to:- communicate the diagnosis, treatment plan, and prognosis of the disease to

patients and their families, and consider the patientCs &no%ledge ofmalignant lymphoma and preferences regarding treatment.

- 'ommunicate the cost of treatment and ho% to get the fund (a&in)

Maa'eme" *B&!!*

42


43/199

"tudents should be able to de#elop an appropriate e#aluation and treatment plan

for patients %ith:

- lymph node enlargement- "tudents should be able to access and utilie appropriate information

systems and resources to help delineate issues related to malignant

lymphoma

A""&"ude* ad 0rofe**&oa! :ea&or


appreciate the importance of patient preferences and compliance

%ith management plans for those %ith malignant lymphoma

appreciate the importance of side effects of medications and their

impact on +uality of life and compliance ma&e appropriate referral to hematology consultant

get information of economical status of patients

Re*ource*

3. introbeCs 'linical $ematology, 11thedition, 2==4, p 23=1 M 241=

4. edoman iagnosis dan erapi $ematologi n&ologi edi& ,2==3, p 132>1/

43


44/199

Lear&' 'u&de

Proced&re !or %linical Examination

No. Procedure Performace *ca!e Comme"

# $ 2

Introd&ction1. ntroduce yourself.

History Taking1. Find the chief complaint(s)of anemia,

bleeding, and malignancy.

2. Each symptom is pursued for more details: hen did it begin, suddenly or gradually!


e#ent!



3. 'onclude the history and fit it %ith somepattern of disease that %e recognie.

Sym$tomsMa!&'ac

/. he symptoms of

allor, easy fati+uability, fe#er,

bleeding, easy bruising, infection, nights%eat, %eight loss

5ymph node enlargement

0bdominal distension,

6one pain, arthralgia, abnormality of

gait or instability to %al&

7omiting, headache, respiratory

distress ass(es) at particular region

5oss of consciousness

. he history of

Family history

E*posure to drugs, radiation, and

chemicals

44


45/199

P*&ca! E+am&a"&o

1. I&"&a! mea*ureme"

'areful obser#ation and loo& beforetouching the patient:

s the patient sic& or %ell! f

sic&, ho%sic& is the patient! $o% is his8her

position!

5e#el of consciousness

6reathing ( respiration rate and effort,

cyanosis)9

'irculation (6lood pressure,

heart8pulse rate)

6ody temperature.

easurements of body %eight, height.

Malignancy1. I&"&a! mea*ureme"

dentify the sign of :

fe#er, tachycardia

anemia

bleeding

s&in infiltrates, periorbital edema,

papiledema, adenopathy, e#idence of

mediastinal enlargement ( dyspnea,

#enectation, nec& s%elling), hepatomegaly,splenomegaly, testicular enlargement, bone

paint, e#idence of infection, abdominal

mass and other mass(es)

2. /e0a"ome'a!


could be palpable as a superficial mass 1>2

cm belo% the right costal margin, %ith asharp margin.

rocedure:

o. lace your left hand

behind the patient, parallel to andsupporting the right 11thand 12thribs and

ad-acent soft tissues belo%.

p. Bemind the patient torela* on your hand if necessary.

+. 6y pressing your left

hand for%ard, the patientCs li#er may befelt more easily by your other hand.

4/


46/199

r. lace your right hand on the patientCs right

abdomen lateral to the rectus muscle, %ithyour fingertips %ell belo% the lo%er border

of li#er dullness.

s.0s& the patient to ta&e a deep breath.

t. ry to feel the li#er edge as it comes do%nto meet yor fingertips.

u. f palpable at all, the

edge of a normal li#er is soft, sharp andregular, its surface smooth and maybe

slightly tender.

h. 0ssess li#er enlargement ( in cm) belo%costal margin processus *yphoideus


n. ith your left hand, reach o#er and around

the patient to support and press for%ard thelo%er left rib cage and ad-acent soft tissue.

o. ith your right hand belo% the left costalmargin, press in to%ard the spleen.

p. 6egin palpation lo% enough so that you are


+. 0s& the patient to ta&e a deep breath.r. ry to feel the tip or edge of the spleen as it

comes do%n to meet your fingertips.

s. Aote any tenderness, assess the spleniccontour.

t. 0ssess spleen enlargement( "chuffner >7)

4. Lm0 Node5ymph node are generally e*amined during


Procedure


auricular, anterior and posterior cer#ical,cer#ical, parotid, subma*illary,

sublingual, a*illary, and inguinal nodes.

Aote sie, number, mobility,tenderness and consistency of any glandsfelt.


tender nodes up to 3 mm in diameter

are usually normal in these areas9


regions, nodes up to 1 cm in diameter are

4


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normal until age 12 years.


cer#ical triangle or that enlarge slo%ly areusually

benign.

Bapidly gro%ing nodes fi*ed tounderlying tissue, or hard, firm, or mattedAodes usually malignant.




more common %ith leu&emia.


and the s&in are found in children %ith

tuberculosis.

iscrete rubbery nodes are

found in alignant lymphoma, and

e*tremely firm, hard nodes occur inmetastases.


indicates local infection but may be a sign

ofgeneralied disease.

9I. Cr&"er&a of Per*oa! Performace Ea!ua"&o

Sca!e Performace Ac&eeme"

=. f student doesnCt perform the tas&

1. f student performs the tas& incorrectly8 incompletely

2. f student performs the tas& correctly completely

4


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5ymphomas are a heterogeneous group of malignancies of 6 cells or cells thatusually originate in the lymph nodes (nodal) but may originate in any organ of the

body (e*tranodal).

Te e"&o!o' of ma!&'a" !m0oma> En#ironmental factors:

o 6enene

o $erbicides

o Badiation

> nfectious agents:

1. $uman >cell leu&emia>lymphoma #irus 1 ($57>1)2. Epstein>6arr #irus

3. $elicobacter pylori

> mmunosuppression:ndi#iduals %ho are immunosuppressed by drugs follo%ing organ transplantation

ha#e a range of abnormalities from benign proliferation of E67>infectedpolyclonal 6 cells to aggressi#e malignant lymphoma.

> 'hromosomal abnormalities

alignant lymphomas are distinguished into 2 categories : (Bobbin 2==3, p 433)

/od'B& ad No/od'B& Ma!&'a" Lm0oma

'linical differences bet%een $odg&in and Aon>$odg&in 5ymphomas

$odg&in lymphoma Aon>$odg&in 5ymphomasore often localied to a single a*ial

group of nodes ( cer#ical, mediastinal,para>aortic)

rderly spread by contiguity

esenteric nodes and aldeyer ringrarely in#ol#ed

E*tranodal in#ol#ement uncommon

ore fre+uent in#ol#ement of

multiple peripheral nodes

Aoncontiguous spread

aldeyer ring and mesenteric nodescommonly in#ol#ed

E*tranodal in#ol#ement common

4?


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he signs and symptoms of $odg&in and Aon>$odg&in alignant 5ymphoma

(6eutler 2==1 p 121@, 122=, 123@):> night s%eats, fe#er (el Ebstein fe#er in $odg&in disease), %eight loss

> lymphadenopathy: nontender, firm, rubbery

Te c!a**&f&ca"&o of N/ML ( or&ing Formulation) (6eutler 2==1 page 12=? ,

Bobin 2==3 , p 421)

orB&' -ormu!a"&o( 1@?2)

5o% rade"mall lymphocytic %ith or %ithout plasmacytoid differentiation

Follicular, small clea#edFollicular, mi*ed small clea#ed and large cell

ntermediate rade

Follicular, large celliffuse, small clea#ed

iffuse, mi*ed , small and large cell

iffuse, large cell

$igh rade 5arge cell, immunoblastic

5ymphoblastic ( con#oluted or noncon#oluted)

"mall nonclea#ed cell thers

$airy cell, cutaneous >cell, histiocytic neoplasia, plasmacytic, etc.

Te c!a**&f&ca"&o of /od'B& d&*ea*e( $ classification) (6eutler 2==1 p , 1211,

121)

Aodular lymphocyte predominant $odg&in lymphoma

'lassic $odg&in lymphoma

5ymphocyte> rich

Aodular sclerosis ( grades and )i*ed cellularity5ymphocyte depletion

escribe the clinical stages of $odg&in and Aon>$odg&in alignant 5ymphoma(0nn 0rbor classification) (6eutler 2==1, p 1221 and 124=, Bobbins 2==3, p432)

"tage istribution of disease

4@


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7

n#ol#ement of single lymph node region () or in#ol#ement of a single

e*tralymphatic organ or tissue (E)n#ol#ement of t%o or more lymph node regions on the same side of the

diaphragm alone () or %ith in#ol#ement of limited contiguous

e*tralymphatic organs or tissus ( E)

n#ol#ement of lymph node regions on both side of diaphragm (),%hich may include the spleen ( "), limited contiguous e*tralymphatic

organ or site ( E), or both ( E")ultiple or disseminated foci or in#ol#ement of one or more

e*tralymphatic organs or tissues %ith or %ithout lymphatic in#ol#ement.

0ll stage are further di#ided on the basis of the absence (0) or presence (6) of thefollo%ing systemic symptoms : significant fe#er, night s%eats, une*plained loss of

more than 1=D of normal body %eight.

Trea"me" recommeda"&o

No /od'B& Ma!&'a" Lm0oma &"ermed&a"e ad &' 'rade

"tadium herapy

0, 0 non bul&y (L 1= cm),

including E

> (bul&y), , 7

3>4 cycles of '$ chemotherapy

follo%ed by FB or

>? cycles of '$ N radiotherapy

>? cycles of '$

No /od'B& Ma!&'a" Lm0oma !o 'rade ( &do!e")

"tadium herapy

,

, 7

FB

ithout treatment ( in asymptomatic cases) )

"ingle agent or combined chemotherapy

onoclonal antibody

/od'B& !m0oma

"tadium herapy

,

, 7

EFB or

4> chemotherapy cycles N FB

>? chemotherapy cycles N B in residual site and bul&y

disease

/=


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'$ O cyclophosphamide, do*orubicin, onco#in, prednisone

FB O in#ol#ed field radiotherapy

EFB O e*tended field radiotherapy B O radiotherapy

he prognosis is +uite good, if sho%ing a good response. Belaps could be treated.

rognosis of A$5 is usually determined by a combination of specific factors

( 6eutler 2==1, p 124>124 or high>ris& lymphomas that typically ha#e a more aggressi#e

clinical course than de no#o intermediate or high>ris& disease.

he nternational Aon>$odg&inCs lymphoma prognostic factor inde*o 0ge ( L = #s K = )

o "erum 5$ ( L 1 * normal #s. K 1 * normal )

o erformance status ( = or 1 #s 2>4 )

o "tage or #s. or 7

o E*tranodal in#ol#ement ( L 1 site #s. K 1 site )

nternational nde* Ao. of ris& factor

5o% = or 1

5o%>ntermediate 2$igh>ntermediate 3

$igh 4 or /

/1


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COURSE STUDY GUIDELEARNING GUIDE, PRECEPTOR GUIDE

SINDROMA ?ORONER A?UT

/2


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SINDROMA ?ORONER A?UT

La"ar :e!aBa'

"indroma &oroner a&ut ("J0) merupa&an &eadaan darurat yang harus cepat di&enali

dan mendapat&an pera%atan yang optimal untu& menghindari &ompli&asi bah&an

&ematian. "aat ini penya&it -antung is&emi& menempati urutan pertama sebagai

penyebab &ematian di seluruh dunia. emahaman patofisiologi, pemeri&saan danpenanganan yang tepat a&an sangat berperan dalam menurun&an ang&a &ematian pasca

"J0.

Tuua 0em:e!aara umum

ada a&hir masa &epaniteraan, mahasis%a diharap&an mempunyai pengetahuan danpengalaman dalam menentu&an diagnosa banding, menega&&an diagnosis, mela&u&an

stratifi&asi resi&o dan merencana&an tatala&sana "J0.

Pe'e"aua a' d&0er!uBa *e:e!um me'&Bu"& Be0a&"eraa

0natomi pembuluh darah &oroner serta fa&tor fa&tor yang mempengaruhi

aliran darah pembuluh darah &oroner Jeadaan yang mengatur metabolisme mio&ard serta fa&tor fa&tor yang

menentu&an &ebutuan8 &onsumsi o&sigen

embentu&an, e#olusi dan &ompli&asi ateros&lerosis

$ubungan antara terhentinya aliran darah &oroner dan sindroma &linis yang

ter-adi

Jeadaan yang mencetus&an ter-adinya "J0

erubahan patologis yang ter-adi pada mio&ard yang mengalami infar& serta

respon &ardio#as&ular saat "J0

enilaian dan inter#ensi fa&tor resi&o penya&it -antung &oroner

ende&atan terhadap penderita dengan nyeri dada: penyebab, diagnosis banding

dan &emung&inan "J0

enanganan medi&al dan in#asif untu& &asus "J0

Tuua 0em:e!aara Bu*u*

1.engetahuan ahasis%a mampu:

membeda&an antara "J0 dan penya&it -antung is&emi& &roni&

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menerang&an patofisiologi ter-adinya "J0

menerang&an manifestasi &linis dan -enis "J0

membuat diagnosis dan diagnosis banding

menerang&an stratifi&asi resi&o

menerang&an tatala&sana medi&al dan prosedur tinda&an in#asif

menerang&an ri%ayat per-alanan penya&it dan prognosis

2. Jeterampilan

a) 0namnesisahasis%a mampu mengumpul&an, mendo&umentasi&an , menya-i&an data serta

analisa ri%ayat medis untu& mengetahui fa&tor resi&o, pencetus ter-adinya "J0,

menega&&an diagnosis dan diagnosis banding, serta rencana penatala&sanaannya

Ayeri dada

> embeda&an antara &eluhan angina pe&toris dan &eluhan yang setara

(e(uivalent) angina pe&toris

> embeda&an antara nyeri dada is&emi& dan nyeri dada &ardia& non>is&emi&

> embeda&an nyeri dada &ardia& dan nyeri dada non>&ardia&

> enerang&an nyeri dada pada penderita "J0> engetahui a%itan (onset) timbulnya "J0

> embeda&an antara nyeri dada pada penya&it -antung &oroner &roni&

dan nyeri dada pada "J0

enyulit

> enyulit is&emi&:

nfar& ulang

0ngina pasca infar&

> 0ritmia

0ritmia #entri&ular dan supra#entri&ular

6lo& dan gangguan &ondu&si

> Jematian mendada&> e&ani&

agal -antung dan ren-atan

0neurisma

Bupturfree wall, septum dan mus&ulus papilaris

> 5ain lain

Emboli sistemi&8 paru

Fa&tor resi&o dan penya&it penyerta

> ero&o& > islipidemia

> iabetes melitus

> $ipertensi> Bi%ayat &eluarga berpenya&it -antung &oroner

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e-ala penyerta

> ingsan

> alpitasi (bradi&ardia, ta&hi&ardia, e&strasistol, atrial fibrilasi,gangguan &ondu&si)

> Bespon simpatis lain pada "J0

> agal -antung

Fa&tor pencetus

> $ipertensi

> 0nemia

> Jer-a fisi&8 olah ragab) emeri&saan fisi&

ahasis%a mampu mela&u&an pemeri&saan fisi& untu& mendete&si adanya

&ega%atdaruratan medi&al, penya&it penyerta non &ardia&, serta &ompli&asi "J0

Gmum

> anda #ital

> Jepala: ar&us &ornea, anemia> 5eher: P7, nadi &arotis (amplitudo dan contour), thrillsdan ruit

di pembuluh darah &arotis

> ora&s: titi& impuls ma&simal> Julit: *antoma

> E&stremitas: nadi arteri brachialis, tanda penya&it pembuluh darah

perifer (peripheral vascular disease)

Pantung

> alpasi8 per&usi batas -antung> 0us&ultasi: "uara -antung ("1, "2, "3, "4), parado/ical splitting

dari "29 e0ection click9 murmur

aru: ron&hi dan whee1ing

c) emeri&saan penun-ang

1. E' istirahatahasis%a mampu membaca E' istirahat untu& membuat diagnosis

sindroma &oroner a&ut.

rama

0*is gelombang QB"

Fre&uensi gelombang QB" dalam 1 menit

elombang

nter#al B elombang QB"

"egment "

elombang

E&strasistol

angguan &ondu&si

2. emeri&saan laboratorium

//


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ahasis%a mampu menginterpretasi&an hasil laboratorium untu& membuat

diagnosis sindroma &oroner a&ut dan mendete&si fa&tor resi&o.

enanda -antung untu& ne&rosis

islipidemia

ula darah

Faal gin-al

3. emeri&saan foto tora&sahasis%a mampu menginterpretasi&an foto tora&s untu& menentu&an

penya&it penyerta -antung dan &ompli&asi

> Jardiomegali> 6endungan paru

d) Bencana penatala&sanaan

> ahasis%a mampu menentu&an stratifi&asi risi&o penderita "J0

> ahasis%a mampu merencana&an tatala&sana termasu& mengetahui saatyang tepat untu& meru-u& penderita "J0

> ahasis%a mampu mengamati dan menilai hasil tatala&sana penderita "J0 atala&sana &ega%atdaruratan pada "J0

atala&sana medi&amentosa nyeri dada dan tatala&sana untu&

mengurangi is&emia mio&ardium.

atala&sana re#as&ularisasi medi&al dan in#asif

atala&sana untu& mempertahan&an fungsi -antung

atala&sana fa&tor risi&o8 penya&it penyerta

e) Jomuni&asi

ahasis%a mampu

meng&omuni&asi&an diagnosis, rencana pemeri&saan lan-utan, rencana

pengobatan dan prognosis &epada penderita dan &eluarganya

meng&omuni&asi&an usaha pencegahan penya&it -antung &oroner

meng&omuni&asi&an efe& samping obat yang mung&in ter-adi

meng&omuni&asi&an perlunya &epatuhan terhadap pengobatan

3) ing&ah la&u dan si&ap profesional

ahasis%a mampu

be&er-a sama dengan semua piha& (mahasis%a, do&ter

ruangan, pera%at, tenaga &esehatan lain dan penderita termasu& &eluarganya)dengan tu-uan memberi&an pelayanan &esehatan yang sebai&>bai&nya bagi

penderita mela&u&an pe&er-aannya sesuai eti&a &edo&teran

Jepusta&aan

/


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Rippes , 5ibby , 6ono% B, 6raun%ald E (ed). 6raun%aldSs $eart isease: 0

e*t 6oo& of 'ardio#ascular edicine


58/199

Pedoma Be"eram0&!a aame*&* da 0emer&B*aa f&*&B

Ao LANG?A/5TUGAS 1 2 3 4 /

A.PER?ENALAN

1. 6eri salam pada penderita dengan ramah dan per&enal&an diri sendiri

2. erang&an pada penderita tentang segala sesuatu yang a&an dila&u&an

selama anamnesis dan tu-uan anamnesis

3. dentifi&asi data penderita

%. ANAMNESIS

1 Jeluhan utama: nyeri dada atau dada terasa tida& ena&

2. Bi%ayat penya&it se&arang

> Jualitas dan intensitas

> 5o&asi

> a&tu (onset, lama berlangsung, fre&uensi)

> era-at (grade) angina pe&toris sesuai dengan the CanadianCardiovascular Society

> Fa&tor pencetus

> Jeluhan lain yang muncul bersama nyeri dada

> Bi%ayat pengobatan sebelunnya dan responnya (bila ada)(nama, dosis, fre&uensi dari obat)

3. Bi%ayat penya&it dahulu

> Bi%ayat angina berulang > Bi%ayat cardiac event

> Bi%ayat pe&er-aan

4. Bi%ayat fa&tor resi&o mayor untu& penya&it -antung &oroner

> ero&o&

> $ipertensi > islipidemia > iabetes mellitus

> Bi%ayat &eluarga berpenya&it -antung &oroner

C PEMERI?SAAN -ISI?

1 6eritahu penderita tentang pemeri&saan fisi& yang a&an dila&u&an

2 6antu penderita untu& berbaring di atas me-a peri&sa

3 'uci tangan dengan air dan sabun dan &ering&an dengan &ain8handu& atau

pengering tangan (hand drier)

4 emeri&sa berdiri di sebelah &anan penderita (untu& mere&a yang be&er-adengan tangan &anan)

Tada 9&"a!1 engu&ur te&anan darah

2 enghitung la-u -antung, nadi

3 enghitung la-u pernafasan

?e0a!a

1 enilai con-ungti#a

2 elihat &emung&inan adanya sianosis perioral

/?


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Leer1 Jugular Venous pressure (JVP)

> 6uat penderita merasa nyaman

> erguna&an bantal untu& menai&&an &epala sehingga otot

sternomastoideus tida& tegang

> Aai&&an tempat tidur pada bagian &epala sebesar 3==dan

paling&an sedi&it &epala pasien &e arah berla%anan dari tempatpemeri&sa

> 5a&u&an identifi&asi #ena -ugularis internaT8 e&sterna dan titi&

pulsasi tertinggi di #ena -ugularis internaT8 e&sterna &anan didaerah setengah ba%ah leher

T)0ika vena 0ugularis interna tidak terlihat) dapat digunakan

vena 0ugularis eksterna

> 5eta&&an sebuah benda persegi pan-ang atau &artu secara

horisontal dari titi& tersebut dan sebuah penggaris (sentimeter)

secara #eri&al dari angulus sternalis

> G&ur -ara& #erti&al dalam sentimeter di atas angulus sternalis di

mana benda persegi pan-ang bertemu dengan penggaris.

> "ecara &asar, angulus sternalis berada / cm di atas atrium &anan.e&anan dicatat sebagai /N U.. cm$2

> Para& yang teru&ur adalah P7

2 Nad& Baro"&*

> Ailai simpangan (amplitude) dan garis bentu& (contour)

enderita dalam posisi berbaring dengan bagian &epala

dari tempat tidur tetap dalam posisi dinai&&an (3==>4/=)

erhati&an pulsasi &arotis di leher

5eta&&an -ari inde&s dan -ari tengah &iri (atau -empol

&iri) di atas arteri &arotis &anan di sepertiga bagian

ba%ah leher, te&an &e arah posterior dan rasa&an

pulsasinya Gntu& arteri &arotis &iri guna&an -ari atau -empol &anan

ing&at&an te&anan sampai terasa pulsasi ma&simal dan

garis bentu&nya (contour).

P0A0A mene&an &edua arteri &arotis secara

bersamaan

> etaran (thrills) dan ruits

"elama palpasi, tentu&an ada atau tida&nya of #ibrasi

yang berderum (humming) atau getaran

5a&u&an aus&ultasi di &edua arteri &arotis mema&ai

bagian diafragma dari stetos&op untu& mendengar ruit > 5eta&&an bagian diafragma dari stetos&op di atas

arteri &arotis

> intalah penderita untu&

menahan nafas

Le'a

/@


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1 Ar"er& :rac&a!&*> 5engan penderita dalam &eadaan santai, si&u e&stensi dan telapa&

tangan menghadap &e atas

> era&&an si&u beberapa &ali &e posisi fle*i agar ter-adi rela&sasi otot

yang optimal

> angan pemeri&sa dileta&&an di ba%ah si&u penderita.

> una&an -ari telun-u& dan -ari tengah untu& meraba pulsasi (medial daritendon bisceps)

ToraB*

1 T&"&B &m0u!* maB*&ma!

A"EJ"

> $arus dila&u&an di ruang dengan penerangan yang

cu&up> entu&an lo&asi titi& impuls ma&simal. Aormalnya di

garis mid>&la#i&uler, ruang sela iga 7)

050"

> una&an telapa& -ari untu& meraba impuls

> mpuls #entri&el dapat mendorong atau mengang&at -ari pemeri&sa> eri&sa adanya thrill dengan sedi&it mene&an dada, mengguna&an

telapa& tangan

iti& impuls ma&simal di area #entri&el &iri

'obalah menilai titi& impuls ma&simal saat penderita dalam posisi

telentang. Pi&a gagal, ubah posisi men-adi de&ubitus lateral &iri.

erintah&an penderita mengeluar&an seluruh nafas dan berhenti

bernafas sebentar

Pi&a yang diperi&sa adalah seorang %anita: dorong buah dada &iri &e

atas atau &e arah lateral

entu&an lo&asi titi& impuls ma&simal: normalnya

terleta& di ruang sela iga 7 atau 7 Ailai diameternya: pada posisi telentang, biasanya &urang dari

2,/cm dan menempati satu ruang sela iga.

Ailai amplitudonya: umumnya &ecil dan terasa seperti sentuhan atau

&etu&an

Ailai lama berlangsungnya: umumnya sampai 283 pertama sistole

iti& impuls ma&simal di area #entri&el &anan

asien dalam posisi telentang, miring 3==

5eta&&an u-ung -ari (-ari dalam posisi fle&si) di sela iga , 7 dan

7

Baba impuls sistoli& #entri&el &anan

EBJG"

engan per&usi yang cermat, umumnya dapat di&etahui apa&ah

-antung dalam u&uran normal atau membesar

5a&u&an per&usi yang seringan mung&in dan, se-alan dengan

pengalaman, rasa&an terus sensasi #ibrasi dari per&usi

Gntu& menentu&an batas &iri -antung, per&usi dimulai dari lateral &e

=


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arah sternum. "uara ma-al (dullness) biasanya terdengar sepan-ang

garis mid>&la#i&uler.

6atas &anan -antung umumnya di linea sternalis &anan dan batas

atas (basis -antung) di ruang sela iga &iri

Au*Bu!a"a*& a"u'

Suara a"u' 0er"ama(S$), Be dua (S2), Be "&'a (S1) da Be em0a" (S)

S$

> engar di seluruh daerah pre&ordium dengan penderita dalam posisi

terlentang.

> "1 ter-adi bersamaan dengan a%al impuls ape&s dan berhubungan

dengan permulaan sistol #entri&el. "1 terdiri dari 2 &omponen:

&omponen pertama disebab&an oleh penutupan &atup mitral dan

&omponen &e dua disebab&an oleh penutupan &atup tri&uspid.

Gmumnya &edua &omponen tersebut tida& dapat dibeda&an. "1

terdengar lebih dalam dan pan-ang dari "2

> Aadi &arotis dapat diguna&an sebagai penun-u& %a&tu ter-adinya "1

&arena ter-adi segera setelah "1.

S2

"2 -uga terdiri dari 2 &omponen: &omponen pertama disebab&an oleh

penutupan &atup aorta dan &omponen &e dua disebab&an oleh penutupan

&atup pulmonal. Jomponen aorta mendahului &omponen pulmonal.

S1

> "3 merupa&an temuan normal pada orang de%asa muda (di ba%ah 4=

tahun)

> erdengar setelah "2 saat fase diastoli&

> 5eta&&an bagian ell dari stetos&op di ape&s dengan memberi sedi&it

te&anan.

> "3 adalah suara dengan fre&uensi yang sangat rendah.

S

> "4 mendahului "1

> empunyai fre&uensi yang sangat rendah dan terdengar paling -elas di

ape&s, de&at *iphoid atau disuprasternal notch

?ATUP FANTUNG

> 0rea &atup mitral terleta& di ruang sela iga 7, garis mid>

&la#i&uler &iri.

> 0rea &atup pulmonal terleta& di ruang sela iga 2, garis

parasternal &iri.

> 0rea &atup aorta terleta& di atas iga &anan dan ruang sela iga, garis parasternal &anan.

> 0rea &atup tri&uspid terleta& di pertemuan &orpus sternum

dengan prosesus *iphoideus

Murmur

Jeti&a mendengar murmur -antung, tentu&an dan terang&an:

> a&tu ter-adinya

T entu&an murmur (systoli& atau diastoli&)

1


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T urmur sistoli&

MODUL-2 untuk Preceptor P3D-3.doc

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