Lecture 2 ** Flashcards

1
Q

Fibrinolysis

A

removal of clot when no longer needed

steps:
tPA is released from surrounding healthy cells
tPA activates plasminogen =>plasmin
plasmin breaks clot down

begins w/in 2 days

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2
Q

in general, mechanism to control size of clot

A

remove coagulation factors
inhibit activated clotting factors

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3
Q

Factors limiting clot growth/formation, gen

A
  1. blood washes procoagulants away normally.
  2. thrombin is absorbed into fibrin threads
  3. any escaping thrombin is deactivated by antithrombin III
  4. antithrombin III and protein C inactivate many intrinsic pathway procoagulations
  5. heparin enhances antithrombin III and stops intrinsic pathways
  6. smooth lining of normal vessels prevent un needed clotting
    also NO and prostacyclin
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4
Q

thromboembolytic

A

undesirable intravascular clotting

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5
Q

thrombi

A

stationary unnecessary clot, uncomfortable/dangerous, block blood circulation

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6
Q

why might a thrombus form, if not needed

A

staying stationary for long period of time, blood stasis, blood not moving fast enough,

high bp can push too forcefully against the walls of the vessels, epi cells peel off, exposure to collagenn

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7
Q

embolus

A

thrombus or part of thrombus that escaped can get restuck in a more critical/smaller vessel

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8
Q

treatment

A

tPA = which is usually released by healthy surr cells around a cut

streptokinase = bacteria enzyme that activates plasminogen

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9
Q

why is aspirin a good preventative therapy for heart attack patients

A

baby aspirin inhibits production of thromboxane which is what makes platelets sticky and clump together

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10
Q

thrombocytopenia

A

penia = fewer than normal
so less thrombin and les platelets, all stem cells commit to everything put platelets

any condition harmful to bone marrow (radiation, drugs,

we give whole blood transfusions for temp relief bc platelet life span is approx 10 days.

petechiae = bruise easy, small red dots = small breaks in caps, but body can’t even repair that

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11
Q

impaired liver function

A

liver disease/liver failure
procoagulants come from liver
coagulants promote clotting

also, liver makes bile,
bile needed for absorbing vitamin K
why? bc is a fat solute vitamin and bile emulsifies fats
imp bc? K is needed fro production of procoag.

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12
Q

Hemophilias

A

genetic bleeding disorder, lacking some factors of intrinsic pathways

12 or 9, A or B

Women can’t have it, only carry it or not at all
men can’t carry it, only have it ot not at all.

is sex linked

on X chromsonee,

women have 2, so if given bad X from mom, still has good X from dad, so they carry it but still healthy

men have 1 X, so if given bad X from mom, has hemophilia

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13
Q

how does the body compensate by blood loss

A

vasoconstriction to dec blood vessel volume

inc rate of RBC production, erythropoises

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14
Q

15% loss, more than 30% =

A

15-30 = weaknesss
more than 30 = induce shock

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15
Q

when given whole blood transfusion

A

substantial blood loss or thrombocytopenia
or packed cells for anemia

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16
Q

antibodies

A

a protein produced by the immune system to recognize and neutralize foreign substances found in the body when they shouldnt be

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17
Q

antigen

what do RBC antigens do

A

ea molecule or substance, on surface of the blood cell, that triggers the immune system to produce the antibodies.

they promote agglunation

18
Q

why is type O the universal donor

A

bc it has no antigens, so the immune system of the recipient won’t attack the blood

the recipient’s immune system doesn’t recognize any foreign antigens to attack.

19
Q

why is AB the universal recepient

A

bc has no antibodies, nothing will be there to recoginize the foreign blood type, so immune system doesn’t attack

20
Q

most/least common type

A

most = O+
least = AB-

21
Q

Rh Blood groups

A

Rh + = have Rh antigen/D antigen
Rh - = don’t have Rh antigen

22
Q

heart
what
where
layers

A

is a transport system pump, w hollow vessels for delivery routes

where = enclosed w/in mediastinum
oblique/diagonal placement

layers = pericardium, myocardium, endocardium

23
Q

pericardium

A

double walled, fibre-serous sac

a)fibrous pericardium
protects and anchors the heart, prevents overfilling

b)serous pericardium
parietal and visceral layers (epicardium)
and fluid filled pericardial cavity so can slide w/o friction

24
Q

myocardium

A

cardiac muscle, bulk of heart
connective tissue wrapping of bundles of muscle cells

CT wrapping
= provides support to vessels and valves
=directs spread of AP
=anchors muscle fibres

25
endocardium
layers of endothelium + CT layer of inner myocardial surface continuous e endothelium of vessels leaving and entering the heart
26
structure, components, grooves, compartments,
2 atria, 2 ventricles inter arterial septum = seperate 2 atriums inter ventricular septa = sep 2 ventricls ******don't want O2 rich/poor blood to mix**** coronary sulcus = atrioventricular groove = groove in bn A and V anterior-posterior interventricular sulcus = runs down the middle
27
Atria
receiving chamber small, thin walled, no P, just convey blood to vent deox. blood enters R atrium via Sup. vena cava = head, neck, upper limbs, thorax inf. vena cava = abdomen, lower limbs, pelvis coronary sinus = from myocardium, from walls of heart oxygenated blood to L atrium from lungs via 4 pulmonary veins
28
pectinate muscles
horizontal ridges esp in R atrium, muscle bundles
29
foramen ovale
hole in fetal heart, bn L and R atrium
30
fossa ovalis
indent on R atrium, remneant of foramen ovale
31
ventricles which V to what and diff types of muscle bundles
the true pumps of the heart, walls much thicker, esp L V R V = O2 poor blood to pulmonary trunk, to lungs L V = O2 rich blood to aorta to rest of body trabecular carneae = bundles of muscle w CT wrapping papillary muscles = reach out to valve, keep closed and make sure they open in right direction and link to chord tendinae chordae tendinae = att valves to papillary mucles "heart strings"
32
Valves
keep blood moving in a unidirectional flow chondrae tendinae and papillary muscles keep valves closed and open in the right direction
33
atrioventricular valves
paired, bn atria and ventricles open down to V from A 1. tricuspid valves, R A to R V 2. Bicuspid /mitral = L A to L V
34
Semilunar valves
paired from ventricles to pulmonary/systmeic circuits 1. pulmonary valve = RV to pulmonary trunk 2. aortic valve = LV to aorta
35
valve problems
valvular insufficiency = valves don't close 100% , blood flows backwards, more workload on heart, pumps same amount of blood multiple times valvular stenosis = valves are stiff , don't open 100%, maybe 85%, asking heart to work harder bc of damage or calcification
36
full pathwaty
blood goes from SVC, IVC, and coronary sinus fills up R A w O2 poor blood blood gets through tricuspid valve enters R V goes through pulmonary semilunar valve to pulmonary trunk to lungs pulmonary capillaries = site of gas exchange to heart by 4 pulmonary veins fill up L A w O2 rich blood goes through mitral valve (bicuspid valve) fills up L V goes through aortic semilunar value to aorta to body to systemic capillaries to body tissues = gas exchange O2 poor back to heart
37
Pulmonary and systemic circuits
equal volume pumped into both circuits, but 2 ventricles have unequal workloads pulmonary (Right vent) = low pressure, short circulation systemic (Left vent) = high P, long circulation, 5X the resistance so walls of L V are thicker (X3)
38
coronary circulation
shortest but most important circulation provides O2 to heart to keep pumping in coronary sulcus/atrioventicular groove = L and R coronary arteries, branch from aorta, encircle the heart gets blood when heart is relaxed bc when contracted, the vessel is closed shut
39
many anastomes
alternate pathways if some vessels are blocked for nourishment if an artery begins to be occluded total occlusion = heart attack
40
diseases of coronary vessels
angina pectoris literally chest pain vessels are narrow, so uncomfortable, as not enough O2 to heart muscles myocardial infraction vessels are completely blocked off = heart attack