DARAH

Dr. YETTY MACHRINA

BAGIAN FISIOLOGI FK USU
Tujuan Objective

1. Mampu memahami fungsi dasar darah

2. Mampu mengenal komponen-komponen darah

beserta fungsinya masing-masing
 Fungsi Darah

 Distribusi
oxygen, CO2, nutrien, hormone, waste
product/sisa metabolisme

 Regulasi
Body temperature, pH

 Proteksi
Melindungi tubuh dari kehilangan cairan
Melindungi tubuh dari infeksi
DARAH
 Merupakan jaringan tubuh
 Volume 6 – 8 % BB
 To 38oC, pH 7,35 – 7,45
 Terdiri dari plasma darah dan komponen
padat
Components of Blood
is the liquid portion of the blood and
PLASMA consists primarily of water (92%) and
plasma proteins (7%)
Proteins - albumin, globulins, and
fibrinogen

•- solid component of the blood

FORMED consisting of erythrocytes, leukocytes,
ELEMENTS and platelets

 BLOOD =
55% plasma + 45% formed elements
 PLASMA DARAH

 90 % air

 7 % protein : albumin, globulin, fibrinogen,

protrombin

 3 % bahan organik : lipid, garam, nutrien,

waste product
FUNGSI TIAP KOMPONEN

 Air
 Protrombin
 Fibrinogen
 Albumin
 Globulin
Hematocrit
When whole blood is spun
down in a centrifuge is
seperates into three distinct
components: plasma, white
blood cells combined with
the platelets, and the red
blood cells.
About 55% of the blood
is plasma and about 45%
are cells –( males generally having
a higher percentage of cells than females).
If the percentage of cells
becomes too low the person
is said to have anemia.
 Blood Plasma
 Blood is composed of cellular and non-cellular elements.
 If the cellular components are removed: plasma remains.
 HEMATOCRIT

 Perbandingan sel eritrosit terhadap volume

darah dalam bentuk persentase.
 Pria : 42% - 54%
 Wanita : 39% - 48%

 Ht < = Anemia
 Ht > = Polycytemia, perembesan
plasma,dehydrasi (polisitemia relatif)
KOMPONEN ELEMEN
 Sel darah merah (eritrosit
fs : 99% mengangkut O2 dari paru ke
seluruh tubuh dan CO2 dari jaringan
tubuh ke paru.
 Sel darah putih (leukosit)
fs : Melindungi tubuh dari infeksi dan
kanker
 Platelet (trombosit)
fs : Pembekuan darah
SEL ERITROSIT
• Bentuk cakram, biconcave dengan bagian tepi
lebih tebal.
• diameter : 7m
• Umur : 120 hari
• Jumlah normal : 5. 106 / mm3
• Dibentuk di red bone marrow, dihancurkan/
dirombak di hati dan limpa
• Eritropoeisis dipengaruhi oleh eritropoeitin hormon.
• Pembentukan eritosit juga dipengaruhi oleh vit B12,
AA , ferum, testosteron
Here is a picture of some blood - most all the cells you
see are erythrocytes - probably the easiest cell to identify
in all anatomy and physiology.
  Each RBC can contain up to 250 million
hemoglobin molecules!

Erythrocytes have a bi-concave disc shape - they look like donuts - their
shape optimizes their ability to carry oxygen
Red blood cells
Regulation of Erythropoiesis
 Erythropoiesis = formation of
erythrocytes
 the body must produce about 2.5 million new RBCs every
second
 in adults, erythropoiesis occurs mainly in the marrow of
the sternum, ribs, vertebral processes, and skull bones
 begins with a cell called a hemocytoblast or stem cell (below)
 rate is regulated by oxygen levels:
 hypoxia (lower than normal oxygen levels) is detected by
cells in the kidneys
 kidney cells release the hormone erythropoietin into the
blood
 erythropoietin stimulates erythropoiesis by the bone
marrow
Red blood cells
Haemoglobin
 Haemoglobin is a molecule specialised for transport of oxygen,

 composed of globin (made up of 4 highly folded

polypeptide chains) + 4 heme groups (with iron)
 each molecule can carry 4 molecules of oxygen
 called oxyhemoglobin when carrying oxygen &
called reduced hemoglobin when not carrying
oxygen
 can also combine with carbon dioxide & helps HAEM
transport carbon dioxide from the tissues to the
lungs
  Each RBC can contain up to 250 million
hemoglobin molecules!

Jumlah Hb normal ; 12 – 14 g/dl (wanita), 13 – 16 g/dl (pria)

ANEMIA
 Bila dilihat dari RBC : (< 5.106 )
A. Anemia
A. Hemorrhage
A. Hemolitik

 Bila dilihat dari Hb deficiensi : ( <10 g/dl)

Pernicious deficiensi
Iron deficiensi
 Bila dilihat dari penyebabnya:

1. Nutrional Anemia
2. Hemolitik Anemia
3. Defisiensi Anemia
4. Renal Anemia
5. Aplastik Anemia
6. Pernicious Anemia
Sickle Cell Anemia
 POLYCYTHEMIA
 Jika erytrosit > 5.106
 Dibagi atas : Polisitemia primer ( P. vera )
Polisitemia sekunder

 Polisitemia primer
 Ht dapat mencapai 70% - 80%
 Viskositas menjadi lebih besar (5 -7x normal)
sehingga aliran darah menjadi lambat. O2 carry
menurun.
 Viskositas  TPRBPKerja jantung
 Polistemia sekunder
 Merupakan mekanisme adaptif yang diinduksi
oleh eritropoeitin untuk meningkatkan kapasitas
darah mengangkut O2 sebagai respon terhadap
penurunan penyaluran O2 ke jaringan yang
berkepanjangan.
 Pada orang yang tinggal di dataran tinggi
 Penderita penyakit paru kronik atau gagal
jantung
 Eritrosit naik 6.106 – 8. 106
 SEL DARAH PUTIH (LEUKOSIT)
Mempunyai inti
Terbagi atas : Agranular leucocyte
Granular leucocyte

Jumlah Normal : 4.000 – 11.000

< 4.000 = Leukponenia
> 11.000 = Lekositosis

• Leukopoesis dipengaruhi oleh banyaknya jumlah

bakteri yang masuk ke dalam tubuh
 White Blood Cells
Leukocyte

Agranulocyte Granulocyte

Monocyte Basophil
Lymphocyte Eosinophil Neutrophil
 GRANULOCYTES

1. Neutrophils

• 40 - 75% of leukocytes
• 10 - 14um diameter
• Exhibit multi - lobed nuclei
• Cytoplasm lightly stippled with
indistinct granules
- represents large lysosomes
Erythrocyte
• Active phagocytes that ingest
Cytoplasm Multi - lobed
bacteria & cell fragments nucleus
 GRANULOCYTES

2. Eosinophils Bi - lobed
Cytoplasmic
nucleus
granules
• 1 - 6% of leukocytes
• 10 - 14um diameter
• Bilobed nucleus
• Abundant large ovoid granules
- stain bright red with eosin
• Phagocytes that ingest
antibody + antigen complexes
• Release histaminase that
inhibits inflammation
 GRANULOCYTES
Cytoplasmic Bi - lobed
granules
3. Basophils nucleus

• < 1% of leukocytes
• 10 - 16um diameter
• U- or S-shaped bi-lobed
nucleus
• large blue cytoplasmic
granules
- exhibit basophilic
staining
• Granules contain materials
that mediate inflammation
- eg. histamine
 AGRANULOCYTES

1. Lymphocytes
Large
• 20 - 30% of leukocytes Small
• 6 - 9um diameter (small)
• 9 - 15um diameter (large - 3%)
• Round, densely stained nuclei
• Pale non-granular cytoplasm
Rounded
• Small lymphocytes have nuclei
relatively little cytoplasm
- attack pathogens & regulate
immune responses
• Large lymphocytes make
antibodies
 AGRANULOCYTES

2. Monocytes

• 2 - 10% of leukocytes
• 14 - 24um diameter
• Large, often indented, nuclei
• Abundant grey-blue cytoplasm with
fine granules
• Cytoplasmic vacuoles often evident
• Highly motile
• Differentiate into macrophages
which phagocytose
pathogens & dead tissue
 TROMBOSIT (PLATELET)
 Mempunyai inti
 Umur 7 – 10 hari
 Dibentuk oleh megakaryosit di sstlg
 Berperan pada proses pembekuan darah
 Jumlah normal : 150.103 – 450.103
 Bila < 150.103 = trombositopenia
> 450.103 = trombositosi
 Platelets (or thrombocytes)

• Small cell fragments

• Possess granules
• 2.5 to 5 x 105/mm3(250,000 -500.000
per cubic millimeter )
• Produced by megakaryocytes in
marrow.
• Regulated by thrombopoietin.
• Contain granules.
• Role in clotting
•remain functional for about 7 - 10 days
(after which they are removed from the
blood by macrophages in the spleen &
liver)
Hemostasis - prevention of blood loss from broken vessel

 1 - Vascular spasm - vasoconstriction of injured

vessel due to contraction of smooth muscle in
the wall of the vessel. This 'spasm' may reduce
blood flow & blood loss but will not stop blood
loss.
 2 - Formation of a platelet plug - platelets
aggregate at the point where a vessel ruptures.
This occurs because platelets are exposed to
collagen (a protein found in the connective
tissure located just outside the blood vessel).
Upon exposure to collagen, platelets release
ADP (adenosine diphosphate) & thromboxane.
These substances cause the surfaces of nearby
platelets to become sticky and, as 'sticky'
platelets accumulate, a 'plug' forms.

 3 - Blood coagulation (clotting):
 The result of all of this is a clot -
formed primarily of fibrin threads (or
polymers), but also including blood
cells & platelets.

Blood clots in the right places

prevent the loss of blood from
ruptured vessels, but in the wrong
place can cause problems such as a
stroke (see below under
inappropriate clotting).
 
 Clot retraction:
 "tightening" of clot
 contraction of platelets trapped
within clot shrinks fibrin
meshwork, pulling edges of
damaged vessel closer
together

 Over time (with the amount of
time depending on the amount
of damage), the clot is
dissolved and replaced with
normal tissue
 COAGULATION PATHWAYS

There are three pathways to consider:-

1. Extrinsic pathway

2. Intrinsic pathway

3. Common pathway
EXTRINSIC PATHWAY

When tissue or endothelial cells are damaged they release tissue factor, which combines
with two clotting factors to make the enzyme tissue thromboplastin
INTRINSIC PATHWAY

The aggregated platelet

plug releases
platelet factor 3, which
combines with two
clotting factors to
make the enzyme
platelet thromboplastin
 COMMON PATHWAY

The common pathway begins once either of the two types of thromboplastin are formed.
When this happens, prothrombin is converted into the enzyme thrombin. Thrombin then
takes the final step in the coagulation process by converting fibrinogen into fibrin.
 Blood Groups - Typing
 Blood is typed into groups depending upon the
type of agglutinogens (antigens) present on the
red blood cell surface
 The plasma may contain genetically determined
agglutinins or antibodies against the blood group
antigens that they DO NOT have
 The ABO and Rh system are based upon antigen-
antibody type responses
 Blood Typing
ABO system -
•people who posses the A antigen on the RBC surface are type A;
•if you posses the B antigen you are blood type B;
• if both A and B are present you are type AB;
• if neither A or B antigens are present, your blood type is O

Type O - universal donor, can give blood to anyone

Type AB - universal recipient, can receive blood from
any blood type

Rh system
Rh system –
 individualswhose red blood cells possess the Rh
antigen are Rh+ (Approx 85%)
Antibodies against Rh antigens are not present
at birth but are stimulated by exposure

Hemolytic Disease of the Newborn

Only in Rh- mothers and an Rh+ child, after
exposure.

•RhoGam - medication given to prevent

sensitization of Rh- mother