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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
s%eat
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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
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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@
1 %ee& 1
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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.
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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
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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)
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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)
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COURSE STUDY GUIDE
LEARNING GUIDE, PRECEPTOR GUIDELEU?EMIA
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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&!!*
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"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)
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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
"tudents should be able to:
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
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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!
"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
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)
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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
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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!
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:
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
3. S0!eome'a!&rocedure of spleen e*amination:
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
belo% a possibly enlarge spleen.
-. 0s& the patient to ta&e a deep breath.
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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
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, parotid, subma*illary,
sublingual, a*illary, 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 are
normal 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 matted
Aodes usually malignant.
5arge, %arm, soft, tender nodes
usually indicate acute infection.
Firm, rubbery nontender nodes are
more common %ith leu&emia.
Firm nodes that adhere to each other
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.
5ocal adenopathy usually
indicates local infection but may be a sign
of
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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
SOME IN-ORMATION -OR PRECEPTORS
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
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> 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%)
($armening 2==2, p 2
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Pa"o'ee*&* of !euBem&a
he origin of leu&emia at the genetic le#el in most cases appears to be related to
mutation and altered e*pression of oncogenes and tumor suppressor genes. ost
oncogenes regulate cell proliferation and differentiation. 0bnormal oncogene ortumor suppressor gene e*pression induced by translocation and genetic fusion or
mutation often results in unregulated cellular proliferation. 0lthough the e#ents that
lead to this are not entirely understood, a number of host and en#ironmental factorsha#e been identified that are associated %ith increased ris& of leu&emic
transformation. ($armening 2==2, p 2
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'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
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'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 ($armening 2==2, p 2?4>
2?/)
he treatment of this patient (05) may consist of cytoto*ic chemotherapy alone or
marro%8stem cell transplantation after chemotherapy.
0dministration of cytosine arabinoside, usually in con-unction %ith an anthracyclinehas been the cornerstone of chemotherapy in 05 for o#er 2/ years.
herapy can be di#ided into t%o phases: induction and postremission therapy. he
initial goal of therapy is induction of a complete remission ('B). 'B is defined by
normaliation of neutrophil counts (at least 1./*1=@85) and platelet counts (more than1==* 1=@85), and a marro% aspirate and biopsy that demonstrate at least 2=D
cellularity, less than /D blasts, and no 0uer rods, as %ell as absence of
e*tramedullary leu&emia.
ostremission therapy may consist of maintenance, consolidation, or intensificationtherapy. (introbe 1@@@, p 22@=>22@B, d, 5ymphoid, B>1
'ytogenetics
3@
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COURSE STUDY GUIDE
LEARNING GUIDE, PRECEPTOR GUIDE
MALIGNANT LYMP/OMA
MALIGNANT LYMP/OMA
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Ra"&oa!e
n ndonesia, malignant lymphoma and leu&emia are the si*th most commonmalignancies. 5ymphoma can be cured if it is detected in early stage. "tudents are
e*pected to generate a prioritied differential diagnosis of lymph nodes
enlargement
Pree@u&*&"e
rior &no%ledge of the :
anatomy and physiology of lymph node
etiology of lymph node enlargement
pathogenesis, etiology, pathological feature of malignant lymphoma
?o!ed'e
"tudents should be able to :
E*plain the definition of malignant lymphoma istinguish the types of malignant lymphoma into 2 categories
utline the signs and symptoms of alignant 5ymphoma
escribe the classification of Aon>$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&!!*
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"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&!!*
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"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
"tudents should be able to:
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/
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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!
"pontaneously or after some specific
e#ent!
$o% has it changed or progressed!
hat ma&es it %orse or better!
3. 'onclude the history and fit it %ith somepattern of disease that %e recognie.
Sym$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
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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!
he li#er is normally not palpable or
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.
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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
3. S0!eome'a!&rocedure of spleen e*amination:
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
belo% a possibly enlarge spleen.
+. 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
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, parotid, subma*illary,
sublingual, a*illary, 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 diameter
are usually normal in these areas9
n the cer#ical and inguinal
regions, nodes up to 1 cm in diameter are
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normal until age 12 years.
Aodes that bare in the anterior
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.
5arge, %arm, soft, tender nodes
usually indicate acute infection.
Firm, rubbery nontender nodes are
more common %ith leu&emia.
Firm nodes that adhere to each other
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.
5ocal adenopathy usually
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
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SOME IN-ORMATION -OR PRECEPTORS
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
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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
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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 /
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COURSE STUDY GUIDELEARNING GUIDE, PRECEPTOR GUIDE
SINDROMA ?ORONER A?UT
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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
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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&