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1

White blood cells

Leukocytes

5 types:

Neutrophils
Eosinophils
Basophils
= granulocytes - visible granules
Lymphocytes
Monocytes
= agranulocytes - no visible granules

Neutrophils -> 65%
Lymphocytes -> 25%
Monocytes -> 7%
Eosinophils -> 3%
Basophils -> <1%

2

White blood cell functions

Lymphocytes - immunity

Basophils - in tissues
Mast cells: inflammation

Start: damaged tissues secrete LIF
LIF -> leukocytosis inducing factors
LIF targets bone marrow

Bone marrow
-> causes bone marrow to dump neutrophils into blood

Neutrophils from blood enter damaged tissue by diapedesis (cross through capillaries in the blood)

Neutrophils in damaged tissue:
- eat bad stuff
- sec compounds that stimulate CT repair
- sec compounds that attract more WBC’s

Over time of infection:
Monocytes enter damaged tissue by diapedesis

In tissue -> monocytes are macrophages

Macrophages
- do the same thing as neutrophils but better

Eosinophils
-> allergy
-> attack parasites

3

White blood cell counts

RBC’s -> 5-7 million per mm3

WBC’s 5-10 thousand per mm3

Platelets -> 250-400 thousand per mm3

4

Terms

____cytosis -> elevated Coyne

____penia -> depressed count

5

Counts

WBC’s
- 5-10 thousand
-> absolute count (all WBC’s together)

Differential count
- count of each of the five different types

- general increase in WBC count -> infection

Diagnostic generalities:
If: increased neutrophils
-> acute infection (new, raging)
If: increased monocytes
-> chronic infection (long time)
If: increased eosinophils
-> allergy, parasites

6

Leukemia

Bone marrow tumor cells produce excess numbers of one abnormal, non functioning WBC to the exclusion of the other formed elements
- spends resources that would otherwise be
used in other former elements

Symptoms:
- anemia
- immunosuppression
- increased bleeding

7

Thrombocytes

Platelets
- live for about 10 days
- destroyed in spleen

Functions:
1. Hemostasis
- the physiological events that stop bleeding
when blood vessels are damaged
Phases:
- vascular spasm (immediately)
- platelet plug formation (couple minutes)
- coagulation (5-10 min)

8

Hemostasis

1. Vascular spasm
a. damaged smooth muscle automatically contracts

b. damaged endothelial cells secrete compounds called endothelins
- endothelins -> stimulate smooth muscle contractions

c. pain
-> stress
- adrenal
-> epinephrine
-> stim vasoconstriction

2. Platelet plug formation
- damaged endothelial cells
- become sticky
- retract + expose collagen fibers in
basement membrane
(collagen fibers -> activate platelets)

Activated platelets
- become sticky
- secrete stuff
- seratonin
-> stim vasoconstriction spasm
- ADP
-> attracts more platelets to the area
- thromboxane A2
-> (does both ^^)

Platelets stick to the would and each other, called -> platelet adhesion
- attract more platelets
- platelets pipe up
-> platelet aggregation

3. Coagulation
- fibrinogen
-> soluble plasma protein
-> prod from liver

Fibrinogen
—converted into->
Insoluble fibrin web

an enzymatic cascade
-> a chain reaction, where the product of one redaction is an enzyme that catalyzes another reactions whose product is an enzyme that catalyzes another, etc.

The plasma proteins involved in the cascade are called Procoagulates
-> designated by Roman numerals or biochemical name
-> from liver
-> from platelets
-> from endothelial cells

9

Two pathways

Intrinsic pathway
-> requires only blood (slow)

Extrinsic pathway
-> requires stuff not found in blood (fast)
(stuff -> damaged endothelium)

10

Extrinsic pathway *see notes
- fast

Damaged tissue

Tissue factor
- ca++
- factor 7
-> tissue thromboplastin (enzyme)

Factor 10

—thromboplastin—>
(requires ca++)

Prothrombin activator (enzyme)

Prothrombin

—prothrombin activator—>

Thrombin (enzyme)

Fibrinogen

—thrombin—>
(requires ca++)

Fibrin web

*prothrombin activator and down is common pathway*

11

Intrinsic pathway *see notes
-slow

Platelets releases PF3 (platelet factor 3)

—longer cascade—>

Platelet thromboplastin (enzyme)

Factor 10

—platelet thromboplastin—>
(requires ca++)

Prothrombin activator (enzyme)

Prothrombin

—prothrombin activator->

Thrombin (enzyme)

Fibrinogen

—thrombin->
(requires ca++)

Fibrin web

*prothrombin activator and down is common pathway*

12

Clot retraction (shrinkage)

Platelets contain proteins called actomyosin

Actomyosin
-> shorten after 30-60 min
- pull clot smaller
- pulls wound shut
(requires less tissue repair need)
- squeezes out serum
serum- plasma minus clotting factors
(fibrinogen)

13

Clot destruction

Plasma contains a protein called Plasminogen

Plasminogen

—TPA (enzyme) —>

Plasmin (aka fibrinolyosin)
- clot buster, destroys clot

(TPA= tissue plasminogen activator)
* endothelial cells secrete TPA when those cells are exposed to fibrin
* plasminogen becomes trapped in the clot

14

Why doesn’t blood clot?

Heparin
-> from basophils - inhibits clogging

Free moving blood resists clotting

Platelets + endothelial cells are both positively charged
-> require activation

15

Unwanted clogging

Thrombus
- a clot that forms and is maintained in a unbroken blood vessel

Embolus
- “freely circulating” clot (a thrombus that has broken free)

Both ^^ have potential to block blood vessel
-> tissue down stream is starved for oxygen
- called Ischemia

Ischemia over time (minutes)
-> tissue death
- called Infarction (specific death)

MI
-> myocardial infarction (heart attack)

CVA
-> cerebral vascular accident (stroke)

Increased age
-> advancement of Atherosclerosis
Atherosclerosis
-> deposition if fiberous CT, smooth muscle, and lipids in the inner walls of blood vessels (arteries)

16

Other clots

Pulmonary embolism
-> thrombus forming in vein
- vein becomes embolus
- clogs branches of the pulmonary
artery -> shut off blood flow to parts
of the lung

Symptoms:
- chest pain
- rapid heart beat
- hypoxia
- shortness of breath
- death

Anticoagulant drugs
- heparin - prevents formation of thrombin (proteins)

- dicumerol - orally, blood thinner

- aspirin

- tPA - destroys blood clots

17

Clotting problems (decreased blood clotting ability)

Causes:
- decreased platelets
- liver damage
- most procoagulents are made in
the liver
- antibiotics
- can kill off bacteria that are the primary
source of vitamin K
(vit k - required to make procoagulents
- hemophilia + related disorders
- genetic -> individual can’t make one or
more of the procoagulents

18

Blood vessels *diagram side notes

Large arteries
-> elastic or conducting arteries
-> pressure buffers
- can give or squeeze

Medium + small arteries
-> muscular or distributing arteries

Small arteries + arterioles are the major modulators of blood pressure and blood flow

Vasoconstriction/vasodilation has several important functions
- can alter systemic blood pressure
- can alter the backload of the heart
- can shunt blood to where it is needed and away

19

Factors influencing flow + pressure of a liquid (blood) pushed through a system of tubes (BV’s) by a pump (heart) ** diagram

Pump
- the greater the pump output (volume/time), the higher the pressure
- the resistance of the tubes and liquid itself

Resistance
- increased viscosity of fluid -> increased resistance
- increased length of tubes -> increased resistance
- increased diameter of tubes -> decreased resistance

20

Velocity of blood flow

Blood moves fastest in the aorta

Blood moves slowest in the capillaries

Blood speeds up again in the systemic veins

21

Heart valves

Prevent backflow

Valve problems:

Valve does not open properly
-> valve stenosis
- causes increased resistance to flow
- heart must work harder to pump blood against resistance

Valve does not close properly
-> valve incompetence
- valve prolapse
- decreased output per contraction
- heart has to pump faster to maintain cardiac output

22

Common conduction problem

Heart block:

- occurs from damage to the AV node
- impulses can’t get through to ventricles
-> ventricles contract at own rate
(30-35 bpm) - too slow

Treated with:
- artificial pacemakers
- battery + clock
- fixed rate pacemakers (old - don’t account for changing heart rate)
- rate responsive pacemakers (new - sensors detect temperature, oxygen and carbon dioxide and adjusts rate)

23

Chemical control on diagram

If decreased oxygen and or increased carbon dioxide
- detected by chemoreceptors

- fired to -

Medulla oblongata

- increases cardio acceleratory centers

-> increased rate/ cardiac output

————————————————

If: increased oxygen, decreased co2

- chemoreceptors

-> medulla oblongata

-> cardio inhibitory center *

-> decreased rate/cardiac output

24

Circulatory routes

Systemic circulation
- hepatic portal circulation

Pulmonary circuit

Coronary circuit

—-
Hepatic portal circulation:

- stomach
- small intestine
- large intestine
- spleen
->> hepatic portal vein
-> liver
-> hepatic veins (different ^)
-> inferior vena cava