2 Flashcards
(24 cards)
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%
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
White blood cell counts
RBC’s -> 5-7 million per mm3
WBC’s 5-10 thousand per mm3
Platelets -> 250-400 thousand per mm3
Terms
____cytosis -> elevated Coyne
____penia -> depressed count
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
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
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)
Hemostasis
- 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
- 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 ^^)
- seratonin
Platelets stick to the would and each other, called -> platelet adhesion
- attract more platelets
- platelets pipe up
- > platelet aggregation
- 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
Two pathways
Intrinsic pathway
-> requires only blood (slow)
Extrinsic pathway
-> requires stuff not found in blood (fast)
(stuff -> damaged endothelium)
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
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
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)
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
Why doesn’t blood clot?
Heparin
-> from basophils - inhibits clogging
Free moving blood resists clotting
Platelets + endothelial cells are both positively charged
-> require activation
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)
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
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 procoagulentsBlood 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
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
Velocity of blood flow
Blood moves fastest in the aorta
Blood moves slowest in the capillaries
Blood speeds up again in the systemic veins
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
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)
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
Circulatory routes
Systemic circulation
- hepatic portal circulation
Pulmonary circuit
Coronary circuit
—-
Hepatic portal circulation:
- stomach
- small intestine
- large intestine
- spleen
-»_space; hepatic portal vein
- > liver
- > hepatic veins (different ^)
- > inferior vena cava
