characteristies: #MATOCRIT

Bright red-OXYGENATED
packed Cell Volume
·

-aka
· Dark Red/ Purplish -
DEOXYSENATED

· Denser than H2O

·
pH= 7.35 to 7.45 CALRALINES

a
slightly warmer; 160.4 F/3802
·
Male: 5.6L
Female:4-5L

08% of BW
O

1* papara layer antic

 BLOOD COMPOSITION

• PLASMA 155% )

1. Plasma proteins 17% )

• Albumin 160 %) → osmotic pressure l retains Hao in BV )

→ transports lipids ; steroid hormones

→ produced by LIVER
-
MOST ABUNDANT PROTEIN IN THE BLOOD

• Globulin 5 1 35 %) pm transport
-
ions , hormones 4 lipids
Fx
→ Immunologic
• N , B -

from liver ; transports 1ipids4FatsoHb

vitamins
•
Y -

From lymphoid tx
;1MMUHEDEFEHS
•
Fibrinogen 14° Iu) → BLOOD CLOTTING

→ converted to insoluble fibrin

in LIVER
→ synthesized

•
regulatory proteins 11 %) -

enzymes , pro envy mesh

hormones
?⃝
 2. Other solutes 11% )

•
Electrolytes _

pm vital cellular act .

→ cations It) ; Anions t )

→ Hat Kt Cart Eli Hcoj , Hpoy " 504

, ,
"

, , ,

•
Organic Nutrients -
☆
for ATP production , growth and maintenance

→ lipids ( FA ,
choicest .
, glyceride)
carbohydrates 1 glucose etc)
vitamins
minerals

•
organic wastes -
excreted / removed

_p Area : catabolism of PROTEIN

Uric Acid : cat

op HUUEOTIDES
.

• GASES -

pm 02 , CO2 H2

3. Water 192%) -
r transports organic 4 inorganic molecules , formed
elements and heat .

• FORMED ELEMENTS 145% )

I thrombocytes )
1. Platelets → Fragmentation of Act -
pm aka PCV ; indicator

2 . WBC go.ly .
megakaryooyte
→ Granular : BEN
op anemia , polycythemia
1 → A granular : LM And others
Leukocytes)

3 .
RBC 99.9% -
A O2 and CO2 transport
1 Erythrocytes ) -

A
Hgb : buffer the blood
Functions of Blood
It

• Distribution and transport

→ 02 :
Lungs to
Body cells
-

p Coz : Body cells to Lungs

→ nutrients from 61 to
body cells
→ nitrogenous waste to
kidneys
→ hormones from
glands to body calls

•
Regulation or Maintenance of Homeostasis

normal circulatory 1 interstitial fluid body temperature

→
body pH , ,

o protection
-
p platelets and proteins : seal vessel damage → CLOTTING FACTORS 4 PITS

→
from foreign materials :
leukocytes ,
Ab and complement proteins

Hematopoiesis -

pm begins 20th week of life of Fetus

-8
 site of Blood Cell Formation
site of BC production
week yolk sac
Early : _

bones : 15 noy to
long
-

2nd trimester : liver , spleen , lymph node

•
Flat bones : 730 y to

3rd trimester : bone marrow

Growth Inducers → controls growth and reproduction of stem cells

Interleukin -3 :
promote growth and reproduction of 5C ; others induce
•
growth
of committed so

•
Differentiation inducer : causes csc to differentiate into mature cell
type
Factors that Influence t tension I t oxygenation → release erythropoietin )
• GI :
oxygen
↑ demand

Infections

stem cells

stem cell
theory all blood cells are produced by bone marrow
-

MYELOID SERIES → From bone marrow

pluripotent 5C
LYMPHOID SERIES → From lymphoid tx

Properties :

•
Capable of self renewal
-
And SHOULD NOT BE USED UP

•
capable of differentiating to mature cells

of cell 01 HAHA
COMMITTED 5C → diff . to 1- type -
A yiee loyal yarn Sana

{
involved in

hematopoiesis PLURIPOTENT SC than 1 di to bat boo !

→ diff .
to more → loyal ganon

1- 01-1 POTENT SC → diff . to

any type
-
di Siya choosy !
Progenitor cells → committed cells lost self renewal capability → IRREVERSIBLE COMM ITED

→ can either PROLIFERATE or UNDER 60 MATURATION

can no back to PSC

→ longer go

Hematopoietic Process

STAGE 1 : STAGE 2 : STAGE 3 :

Hemopoieticsc Precursor cells

committed progenitors
•
self renewal
-

Directional Differentiation undergo development

•
•

•
steady # ( CFU GEMM' CFU El CFU-6M
-

to mature cows
-

• Active differentiation
CFU MK-

, CFU TB )
-

RBC
Young RBC Mature
-

Mega karyocyte → platelets

CSC of Myeloid series -8 macrophages neutrophils eosinophils basophils

, , ,

Csc of lymphoid series DM

stay in BM ~
B-
lymphocyte
-

or

migrate to
thymus ~ t -

lymphocyte

Erythropoiesis -

Erythropoietin 5C ~ Mature RBO

Erythropoietin LEPO ) land liver )

pm from kidney
- -

phases of RBC Maturation

Hemocyte blast → Pro erythroblast

of Ribosomes
I.
Synthesis
2. Synthesis of Hemoglobin
* Diapedesis → leave BM as reticuiocytes and
3. Extrusion of nucleus 4 reduction in
mature in bloodstream to become
retiouti -
RBC Wto nucleus
ERYTHROCYTES .

organguys ,
 RED BLOOD CELLS
_÷-

7.5 micron diameter ; 2. Omicron thick are v01 90 to 95 cubic micrometer

;
-

• - .

• Biconcave disc shape -

for gas exchange

•
lifespan -
120
days

concentration of RBC Quantity of Hgb

in cells

RBC 1- %
Daily prod
-

• .

Healthy men → 5,200,000 It / -

goo , ooo ) / cc
in 100mL blood
•
Hgb -

94g
4,700,00011-1-4001000) / cc
Healthy women → •
Act -

info to 45%
* ↑ altitude ,
more # of RBCs • Each
gofltgb combine with

1. 34 mL of 02 .

Characteristics of Human Red Cells

|
MALE FEMALE
47 42
Act %
142 -

50 ) 136 -
45)

5.4 4.8
RBC 106 / UL
µ, .
, ,, ,,, ,
,,,

16 14
Itgb 91dL 114 -
17.5 ) 112 -
15.6 )

MCV IFL ) 87 180 -

96.1 )

MCH lpg ) 19 127.5 -

33)

MCHC lgldh) 94 13%4-35.5)

MCD 1mm)
7- 5
 ANEMIA
Hemoglobin 1 Agb
- =

Hematocrit * Het = anemia, bloodloss, RBC production

↑ Act =
polycythemia, 4EPO, t destruction of RBC

too much
*
Rolygthemia rera-causes bone manow to produce
RBC W
thickening of Hood is
stowblow
-

RBC Indices

· Mer (mean Corpuscular v01.) - Microcytic (80FL)

- Normochromic
Het x 15
Mildo Ma
RBC (100 / ML) - Macrocytic (795f2)

Mex 1 mean Corpuscular Agb)

· -
Hypochromic
Ab x10 Normochromic My to Hyp
RBC (10:/ M1) -
Hyperchromic

MCIe / Mean Corpuscular Agh concentration)

·
-
Hypochromic (25 gldL
Hb 100

Hormochromic
x
No
If of Hy one
· McD I mean cell Diameter) - small cell diameter:
Microcytic Anemia

Formation
ofAgb
Red
Oxygen-carrying pigment in RBCs
- Globular Transport Protein w/ 4 subunits
- synthesis begins in PROERYTROBLAST and continues

to Reticulocyte stage
of chain in 1gb
sub unit 1 1 Heme, 1
polypeptide chain polypeptide
2 & chains
1 Agb
subunit 2 1 Heme, 1
0

polypeptide chain
Subunit 3 1 Heme, 1
a
1b chains
polypeptide chain
s ub unit i 1 Heme, 1 chain
polypeptide
 Agb-A2- 2.5% OF ADULT H6B
2 ALD
I alpha, I delta chains

Agh -FFEAALASB
-- major Agb present during gestation
-2 alpha 2 1 gamma chains
2A26
For O2 @ A months
old
-↑
Affinity
lycated Age to 6% Agb are glycated; *G% =
POORLY CONTAINED DIABETES OR
HYPERGLYCEM IA

Agb. At most common in adult

IA LB
alpha and 1 beta chains

- Slycine and succinyl-CoA are the PRECRSORS

Function Catabolism of Hemoglobin

Hemoglobin
& enescent old RBC
o Transport of O2 5 CO2

destroyed by
the macrophages of the RES
·
Binding of Agb with On is LOOSE
----
G REVERSIBLE

Agb destruction
· Factors that affects the
affinity of AgD W/On:
V
a) pH
hense f globin
b.) temperature
c) [1,3- Biphospho glycerate] ↓ iliverdin iron 80 degraded by peptidases
I /
~

jo bilirubin
↑ [2, 3-BP6]

Acidic envi

↑ [H]
3 ↓ dFfinity of On to
Agb = P release of On bile
Iron Metabolism

in the
the Iron:
4-5 total
quantity body
- G5% -

nemogrobin
- 4% -myoglobin
1% compounds (ex.
name
Cytochrome P450)
-

0.1%
=> -
transferrin
to 15-30%-stored in RES and liver in the
Form OF FERRIAN

Free Iron -
For synthesis ofheme

Iron bound to transferrin to transport protein

Ferritin a
storage form of iron as stored in the tissue in the form of HEMOSIDERIN

:
In menstration, women lose 0.5
mg of iron
daily.

Regulation ofRBC Production

-> fissue oxygenation Hematopoietic SC

-
Erythropoietin stimulates RBC production
↳ formed in response mypoxia kidney
to
Proery throblast
↳ 90% formed in the
dney, the next in the h
tire
Erythropoietin
RB C

decreases

Tissue oxygenation
Decreases

↑ actors of t oxygenation:
· A Blood volume
· Anemia
·
A Agb
·
Poor blood flow
·
Pulmonary Disease
 Maturation of RBC
A need for vit Bly and Folic acid
-
essential for DNA synthesis

- For thymidine triphosphate synthesis

Lack of VitB12 and FA -> impairment of Abnormal

-> DNA - produce macrocytes w/ irregoval shaped cells
is F-T synthes

Clinical Disturbances
Red Cell Abnormalities

in S12E
Anisocytosis change -

change in color

I normal: about 7um)

O O
O O O

microcyte hypochromic spherocytes

normal macrocyte
caused I round with more (dark color)
I caused by defin 1 less in color by
vit BIL a FAC ↓ in heme synthesis (

Poikilo cytosis -
Change in SHAPE
Immature cells Other disturbances

so
normo blast sickle cells

B
·
a

a
megaloblast a
w/ inclusion bodies
I
echinocyte O
Chistocytes
a
reticulocytes · W/ parasites like malaria

burn cells, created RBCs) (Fragmented RBCs)

RBC Destruction

-> 90% are EXTRAVASCULAR

-
phagocytized by RES -
digested by LISOSOMES

- 5-10% INRAVASCULAR

"no Fe-> always passed back into the blood

excretory factor of
n* papara layer antic
 Anemia

Due to Insufficient RBC count

·
Hemorrhagic Anemia
- loss
of blood from bleeding; Acute or chronic - microcytic
less
or

color, smaller
hypochromic anemia

RBC; Can't Form

Agb

·
Hemolytic Anemia - premature RBC destruction -

secondary to:
Agb abnormalities, transfusion runs, IFX

·
Aplastic Anemia -
From bone marrow aplasia or destruction of hematopoietic cells in BM
I exposure to
gamma ray radiation, industrial chemical drugs -

Chemotherapy (

Due to Decrease in Agb

· Iron -

Deficiency Anemia & Felevels a

secondary to:poor diet, poor absorption of iron in a tract, or acute
bleeding

·
Megaloblastic Anemia - slow reproduction of erythroblast in BM

-def, in vitBl2, folic acid and intrinsic Factor (secreted in the stomach for
absorption of
vit Bl2)

Due to Abnormal Agb (Genetic)

Malassemia due to detect in
regulatory portion inAgb
· to
of globin heme -> t chains
-
RBC easily rupture
A
-> instead of Agb
a sickle-cell Anemia -
presence of Aghs containing faulty chains in Agb

Poly cy the mid

excess RBC produced in response to
- are
hypoxia

types:
a
secondary Polycythemia - altitude, a atmospheric oz

·
Polycythemia vera to
genetic abberation in hematocytoplastic cells

- A in total blood volume, a HOFRBC, a

viscosity
 WEBLOOD CELLS

a K a. Lenkocytes
- Bone marrow: granulocyte, monocytes, Few lymphocytes B
->activated by lymphocytes; produce Ig and Ab

Lymph tissue:
lymphocytes (I-cell G B-cell), and plasma cells

Granu1o cytes (polymorphonudear lymphocytes (

B asophil
Lifespan:4 to ours in tingblood
E osinophil

Neutrophil
3) 4-5 days O
in tissues

Neutrophil - 61% of total WBC

-a other name:
Polymorphonuclear

⑱
"
phagocytosis
- Gugh in vessels, diapedesis, chemotaxis and
> 3-5 nucleus

A leaves BM via diapedesis - site of infix the chemotaxis process

to contains hydrolytic enzymes that

destroys invading org.

Eosinophil
- 1.3% oftotal WBC

T
granules stained PINKISH
by ACIDICDYE
-a an -

limits and modulates the

--
effect of basophil on FAST ALLERSIRXN

Histaminase
release that
destroys histamine released by basophic.
a parasitic inFx

Basophil
* 0.4% total WBC
of

⑱
" WI BASOPHILIC SRANULES
&
chemotactic Factors a chronic material
PMN - contains heparin, histamine,

allergie rxn (IgE mediated)

1* papara layer antic

 A granulocytes

Monocyte
Lymphocyte

Monocyte 5.3% oftotal WBC

·

⑧ 3
Life span:
kidney shaped nuclei
a t w/ non-specific lipase and proteases
10-cours in blood

Phagocytosis

Lymphocyte
30% of total WBC

3
*

⑧
Life span:
to large round nuclei
weeks to months
- Ex: Immune
system

Neutrophils and Macrophage

i'
Neutrophils
-

phagocytize 3 to 20 bacteria
·
Defensive Properties Tissue Macrophage -
100 bacteria
cells MORE POWERFUL
-Phagocytic -

attack and
destroy invading organism
-o
MONOCYTE-MACROPHASE SYSTEM CRES)
a
squeeze than PORES
by DIAPEDESIS ·
macrophages that become attached to fissues for
months/years
-> move
by AMOEBOID MOTION are called to
perform specific Local Protective FX

-> CHEMOFAXIS skin-histiocytes ·

Liver kupFFer cells
-

nodes macrophages
·
spleen and bone marrow
Lymph
-
·

Response During Inflammation

CNS a Brain microglial cells
Lungs areolar macrophages · -

·
0
-

-1st line MSSUE MACROPHASE

ofDefense:
Whin mins MACROPHAGE ENLARE -
BREAK ATTACHMENT -
become MOBILE

-2nd Line of Defense: NEUTROPHILIC INVASION & the site of infx)

w/in Istur NEUT -> Inflamed area -> leave capillaries thru diapedesis -> site of MFx Cenemotaxis)
-> 3rd Line ofDefense:and MACROPHAGE INUASION

-> inflamed fissue -> MACROPHAGE

monocyte
-> ith Line of Defense: 4 PROD. OF SRAAMLO CHE a MOMOCYEE INBM
stimulation of granulate and monocyte by cells progenitor
Clinical conditions

Leukemia
- uncontrolled WBC production
prods in
·
Lymphocytic Leukemia - Cancerous lymphoid cells

in myelogenous cells
·
Myelogenous
Lakemia
- Cancerous pod,

PLATELITS
a product of Fragmentation ofmegakaryocyte
to a Ka. AROMBOCYTES
-
A lack nuclei

- 150,000 +

400,000 per cubic millimeter

mechanism
-* Hemostasis; activate blood dotting
Alpha Sramples:
Factors UWE
·
Clotting
-

·
PDCF
- Dense Granules:
· Cart, ADP, At-source of
energy
Thromboxane Al-potent vasoconstrictor
·
Clotting Promoting Enzymes
Thrombopoietin:influences prod. Of PCT

↳ produced by liver
DTYPES
·
Agglutinogen present on RBC surface; promoter ofagglutination
·
Agglutinin - antibodies in the plasma

E E FIT * ET E LEV E
EEBE:

Agglutinogen
o
Agglntinins

anti- B

B anti A
B -

AB
A and B no anti-A, no anti-B

O A and
no no B anti-A, anti-B

Mt GI M BAMTA -

BMC ALAM in in 11 MB (
0
I
"
a
d
"
Rh system HDN

Ru Factor-C, D, E Ags Mother RhE) RUCt

Baby
·

·
fgD- most antigenic 1st born:mom is exposed -> develops anti-
·
Ruct -

C) agglutinogen D no HDN
-

·
RGC) -

G) agglutinogen D and born: mom's anti-D attacks RBCS IF

the RUCt
baby; HN
develops