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
PLASMA
is the liquid portion of the blood and consists primarily of water (92%) and plasma proteins (7%) Proteins - albumin, globulins, and fibrinogen

FORMED ELEMENTS

- solid component of the blood consisting of erythrocytes, leukocytes, 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 : 7m 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. 2. 3. 4.

5.
6.

Nutrional Anemia Hemolitik Anemia Defisiensi Anemia Renal Anemia Aplastik Anemia 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 TPRBPKerja 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 : 4.000 11.000

Jumlah Normal

< 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 Active phagocytes that ingest bacteria & cell fragments
Cytoplasm
Erythrocyte

Multi - lobed nucleus

GRANULOCYTES
2. Eosinophils
1 - 6% of leukocytes 10 - 14um diameter Bilobed nucleus Abundant large ovoid granules - stain bright red with eosin Phagocytes that ingest
Cytoplasmic granules

Bi - lobed nucleus

antibody + antigen complexes

Release histaminase that inhibits inflammation

GRANULOCYTES
3. Basophils
< 1% of leukocytes 10 - 16um diameter U- or S-shaped bi-lobed nucleus large blue cytoplasmic granules - exhibit basophilic
Cytoplasmic granules

Bi - lobed nucleus

staining
Granules contain materials that mediate inflammation - eg. histamine

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

Large
Small

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
individuals

whose 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