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Physiology III - Freedman > Unit 1: Cardiac Physiology- Physiology III Pt. 1 > Flashcards

Unit 1: Cardiac Physiology- Physiology III Pt. 1 Flashcards

1
Q

What is the #1 cause of death in U.S.? What is the main underlying cause?

A

cardiovascular disease

due to ischemia

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2
Q

What causes ischemia?

A
  1. atherosclerosis (plaque buildup)
    - white thrombus
    - red thrombus
  2. artery spasm
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3
Q

What has been linked to causing atherogenesis?

A
  • high blood cholesterol

- leukocyte recruitment and expression of pro-inflammatory cytokines

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4
Q

Inflammatory mechanisms has coupled what to artheroma formation?

A

dyslipidemia (aborm. amounts of lipids)

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5
Q

Inflammatory pathways promote __________, which is responsible for ____ and ____.

A

thrombosis; myocardial infarctions and most strokes

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6
Q

What can aid in modulating inflammation?

A

the nervous system. primarily the vagus nerve

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7
Q

What is hemostasis and what is the mechanisms of it?

A 
= prevention of blood loss
Mechanism:
- vascular spasm (limits and prevents blood movement)
- formation of platelet plug
- blood coagulation 
- fibrous tissue growth to seal 
(Ca2++ is important in clotting)
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8
Q

What is first to occur when there is trauma to a vessel wall? And what three aspect aid in it?

A

vasoconstriction

  1. Neural reflexes – SNS induced constriction from pain
  2. Local myogenic spam— responsible for most of the constriction
  3. Local humoral factors– thromboaxane A2 from platelets, esp. important in smaller vessels
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9
Q

T/F. The degree of spasm is proportional to severity of the trauma.

A

True

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10
Q

Are platelets whole cells? Can platelets divide?

A

Yes, they are whole cells

No, they cannot divide

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11
Q

What three things do platelets contain that are our focus?

A

ADP, Thromboxane A2, and serotonin

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12
Q

Describe the appearance of an inactive vs active platelet.

A 
Inactive = smooth
Active = spiky and will degenerate and release substances to promote clotting
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13
Q

What two things does a platelet’s cell membrane contain?

A
  1. glycoproteins that avoid normal endothelium, but adhere to damaged area
  2. Phospholipids containing platelet factor 3—AKA thromboplastin
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14
Q

What does thromboplastin do?

A

initiates clotting

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15
Q

What four steps occur when a Platelet contacts damaged area and becomes activated?

A
  1. swell
  2. irregular form w/ irradiating processes protruding form surface
  3. contractile proteins contract causing granule release
  4. secrete ADP, Thromboxane A2, and Serotonin
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16
Q

What does Thromboxane A2 cause?

A
  1. vasoconstrictior

2. Potentiates the release of granule contents

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17
Q

T/F. Thromboxane A2 is essential for release of granule contents to occur.

A

False– if block Thromboxane A2, granule contents can still be release, it is not essential for release to occur

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18
Q

What primarily eliminates platelets and where are they located?

A

macrophages–greater than 1/2 are all in spleen

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19
Q

What are two roles of the endothelium?

A

Prevents platelet aggregation
- produces PG12 (prostacyclin) (inhibits platelet aggregation)
Produces factor VII (clotting)

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20
Q

What are three effecs of PG12 (prostacyclin) produced by endothelium?

A
  1. vasodilator
  2. stimulates platelet adenyl cyclase, which suppresses release of granules
  3. limits platelet extension
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21
Q

What is the precursor for all prostaglandins (PGG2 and PGH2)? And what enzyme is used?

A

Arachidonic acid

Enzyme: Fatty Acid cyclooxygenase (COX)

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22
Q

What enzyme is used in platelets to produce Thromboxane A2? And what are the effects of Thromboxane A2?

A

COX1 (cyclooxygenase)

Effects:

  • vasoconstriction
  • potentiates platelet degranulation
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23
Q

What enzyme is used in Endothelium to produce Prostacyclin? And what are the effects of Prostacyclin?

A

COX2

Effects:

  • vasodilator
  • inhibits platelet degranulation
  • Cardioprotective
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24
Q

What do Aspirin and Ibuprofen block?

A

Fatty acid cyclooxygenase (COX)– which converts Arachidonic acid into prostaglandins–PGG2 and PGH2 (intermediates)
- therefore blocking production of thromboxane A2 and prostacyclin

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25
Q

Why do individuals take aspirin to prevent heart attacks?

A

low dose aspirin targets (inhibits) primarily COX1, ass. with platelets, which inhibits production of thromboxane A2

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26
Q

What are NSAID and what are they used for?

A

Nonsteroidal anti-inflammatory drug, used to control pain and inflammation
- COX inhibitors are a type of NSAIDs

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27
Q

What is the primary effect of inhibition of COX 1? COX 2? Examples of each.

A

inhibit COX 1–>effect on platelet and decrease Thromboxane A2 (Ex: Aspirin)

inhibit COX2–> effect on endothelium and decrease PGI2 (Ex: Celebrex, Vioxx)
–has less GI risk (bleeding ulcers) than COX 1 inhibitors

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28
Q

Compare anticoagulants vs lysis of clots.

What enzyme is used in lysis of clots?

A

Anticoagulants –> prevents clots from forming

Lysis of Clots–> dissolves clots that have already formed, use Plasmin (from plasminogen)

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29
Q

These are types of Anticoagulants. Tell me what they do.

  1. chelators
  2. heparin
  3. dicumarol
A

all prevent clots from forming…
1. tye up calcium (ex: citrate, oxylate)

  1. complexes with Antithrobin III
  2. inhibition of Vit. K dependent factors (Ex: cumadin, warfarin)
30
Q

What is the inactive form of plasmin that circulates in the blood?

A

plasminogen

31
Q

Where are Endogenous Activators of Plasminogen found?

A

tissues, plasma, urine

recall plasminogen = inactive form of plasmin, and plasmin is involved in lysis clots

32
Q

What are Exogenous Activators of plasminogen?

A

(aka drugs)
- streptokinase

  • *tPA (tissue plasminogen activator)–> 3 hr window for MI and stroke
33
Q

What causes most of the frank tissue damage associated with infarctions? Why?

A

reperfusion; b/c ass. with formation of highly reactive oxygen species with unpaired electrons = “free radicals” –> which are generated when pressure on tissues is relieved

34
Q

What is collateralization?

A

the ability to open up alternate routes of blood flow to compensate for a blocked vessel

  • Angiogenesis
  • Vasodilation
  • Role of SNS–> vasoconstriction
35
Q

What is the role of the SNS in relation to collateralization?

A
  • may impede(delay/prevent) via vasoconstriction (ass. with NT Norepinepherine)
  • may augment (make greater by adding to it) via release of neuropeptide Y (NPY)
36
Q

How is the creation of a thrombosis done by the Extrinsic mechanism?

A

initiated by chemical factors released by damaged tissues

37
Q

How is the formation of a thrombosis done by the Intrinsic mechanism?

A

requires only components in blood and trauma to blood or exposure to collagen (or foreign surface)

38
Q

What are hepatocytes role in clotting?

A

hepatocytes = liver cells

Live synthesizes 5 clotting factors:

  • I (fibrinogen)
  • II (prothrombin)
  • VII (SPCA)
  • IX (AHF B)
  • X (Stuart factor)
39
Q

What does Coumarin (warfarin or cumadin) due to liver formation of factors II, VII, IX, and X? How?

A

depresses liver formation of them by blocking action of vitamin K

40
Q

What is Hemophilia? And what is the defect in 85% of cases, 15% of cases, and <1% of cases?

A

a sex linked X chromosome disorder (blood doesn’t clot properly)–varies in degree

  • 85% cases = defect in factor VII
  • 15% of cases = defect in factor IX
  • <1% of cases = defect in factor XI
41
Q

What steps of blood coagulation do not require Ca2++?

A

first two steps in intrinsic steps, formation of Factor XII and Factor XI

42
Q

At formation of what factors do the intrinsic and extrinsic blood coagulation pathways come together?

A

factor V and X

43
Q

What is the key step in clotting of blood?

A

conversion of fibrinogen to fibrin, by thrombin

44
Q

What is Antiphospholipid antibody syndrome?

A

Autoimmune disorder where body makes antibodies against phospholipids in cell membranes —> causes abnormal clots to form

45
Q

What is an amino acid in the blood that may irritate blood vessels, promoting atherosclerosis, and can make blood more likely to clot?

A

homocysteine

46
Q

What can homocysteine cause cholesterol to change into?

A

oxidized LDL

47
Q

How can you reduce high levels of homocysteine in the blood?

A

by increasing intake of folic acid, B6 and B12

48
Q

What are the two particular antigen sets likely to cause blood transfusion reactions if mismatched?

A

O-A-B and Rh

49
Q

What blood types, O-A-B, cause most blood transfusion reactions and why?

A

Type A or B. They have A and B antigens on the RBCs known as agglutinogens b/c they can trigger agglutination
(O is essentially functionless)

50
Q

What are the possible allele combinations of blood types?

A

OO, OA or AA, OB or BB, and AB

51
Q

List the blood types in order form most common to least common?

A

O, A, B, AB

52
Q

Simply,
What are agglutinogens?
What are agglutinins?

A 
agglutinogens = surface markers
agglutinins = soluble anitbodies
53
Q

Which blood types have agglutinogens and what types do they have?

A 
O = none
A = A
B = B
AB = A and B
54
Q

Which blood types have agglutinins and what types do they have?

A 
O = Anti-A and Anti-B
A = Anti-B
B = Anti-A
AB = none
55
Q

T/F. Agglutinins for O-A-B blood types are produced spontaneously after birth (2-8months)

A

True

56
Q

When do antibody titers peak?

A

about 10 years of age and then decline throughout life

57
Q

T/F. Anti-A titiers are 2x Anti-B titers in respective blood type.

A

True

58
Q

In a mismateched transfusion, which is more common, immediate or delayed hemolysis?

A

immediate (less common)

delayed (more common)

59
Q

What causes the lysis of RBCs and how?

A

antibodies (primarily IgM), by activating compliment system which releases proteolytic enzymes rupturing cell membrane

60
Q

T/F. When hemolysis occurs in mismatched transfusions, it occurs to the recipients blood.

A

False. It occurs to the donor’s RBCs

61
Q

What blood type is the universal donor? The universal recipient?

A 
donor = O- 
recipient = AB+
62
Q

What is the most lethal effect of a blood transfusion reaction? Why/how does it occur?

A

Kidney failure:

  • toxic substances released form hemolysed RBC’s
  • Circulatory shock
  • hemoglobin from lysed RBCs precipitates and blocks renal tubules
63
Q

T/F. Spontaneous agglutinins for Rh factor arises after birth.

A

False!! spontaneous agglutinins for Rh factor never arises (this is unlike O-A-B system)

64
Q

What are the 6 common Rh antigens (Rh factors) on RBC’s? And which makes you Rh+ or Rh-?

A

C D E c d e

D = MC and most antigenic (Rh+) at 85% of population

Lacking the D antigen (Rh-), as in have either C, E, c, d, e

65
Q

When Rh+ RBCs are infused into a person who is Rh-, what occurs?

A

it will stimulate production of anti-Rh antibodies, but they develop slowely and will reach max. conc. 2-4 months later—> therefore is exposed again later a strong hemolysis rxn can occur

66
Q

What is the disease that is charactized by agglutination and hemolysis of the fetus’ RBCs by the mother’s anti Rh agglutinins?

A

Erythroblastosis Fetalis (AKA “Hemolytic disease of the Newborn”)

67
Q

What occurs during Erythroblastosis Fetalis

A

causes agglutination of fetal blood, therefore release Hgb which is converted by macrophages into bilirubin —> cause JAUNDICE (yellow)

68
Q

Most cases of erythroblastosis fetalis, mother is Rh- and fetus inherits Rh+ from father. What occurs and when does the problem occur?

A

mother develops anti-Rh agglutinins from exposure to fetus’ Rh+ antigen

symptoms usually don’t occur with initial pregnancy, but will occur whith 2nd (3%) or 3rd (10%) pregnancy where fetus is Rh+

69
Q

What happens in the fetus when erythroblastosis fetalis occurs?

A

after birth the anti Rh agglutinins from mother circulate for another 1-2 months destroying more neonate RBCs –> lead to anemia

Neonates liver and spleen enlarge

70
Q

In erythroblastosis fetalis, the potential for bilirubin to precipitate in neurons of the brain and causing mental impairment could occur. What is that called?

A

kernicterus

71
Q

What is the treatment option for Erythroblastosis fetalis?

Prevention?

A

replace neonate’s blood with Rh- blood

administer Rh immunoglobulin globulin (RhoGAM), an anti-D antibody, to mother at 28-30 weeks of gestation

Physiology III - Freedman (18 decks)

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