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MED PHYS > B3W2 > Flashcards

B3W2 Flashcards

1
Q

Blood Makeup

A

Plasma
Erythrocytes RBC
Leukocytes WBC
Thrombocytes

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1
Q

Blood viscosity

A

1.1-1.2 centipoise

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2
Q

Blood volume

A

70ml/kg 7% body weight

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3
Q

Hematocrit

A

Volume of RBC/Total blood Volume

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4
Q

Isolation of Plasma

A

Add calcium chelator to block coagulation so that coagulation factor remains dissolved

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5
Q

Isolation of Serum

A

Centrifuge without adding calcium chelator

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6
Q

Plasma

A

Electrolytes Proteins Carbohydrates lipids and coagulation factors

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7
Q

Serum

A

Same as plasma without coagulation factors

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8
Q

CSF

A

Colony Stimulating Factors

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9
Q

G-CSF

A

Granulocytes Colony Stimulating Factors
Basophil Neutrophil Eosinophil

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10
Q

M-CSF

A

Monocyte Colony Stimulating Factors
Macrophage

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11
Q

EPO

A

Makes RBC

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12
Q

TPO and IL11

A

Make Platelets

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13
Q

Erythropoiesis

A

EPO made in the kidneys stimulate progenitor cells to become RBCs

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14
Q

RBC Energy

A

Glycolysis and pentose phosphate shunt

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15
Q

Sequence of Hematopoiesis First Step

A

Hematopoietic Stem Cell -> Common Lymphoid or Common Myeloid Progenitor

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16
Q

Sequence of Hematopoiesis Common Myeloid Progenitor

A

Common Myeloid Progenitor becomes Megakaryocyte - Erythroid Progenitor or Myoblast

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17
Q

Sequence of Hematopoiesis Myoblast

A

Becomes Basophil Neutrophil Eosinophil or Monocyte

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18
Q

Sequence of Hematopoiesis Megakaryocyte - Erythroid Progenitor

A

Becomes Megakaryocytic Cell which becomes platelets or Red Blood Cells

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19
Q

Neutrophils

A

Has Granules
Phagocytose Bacteria
Most Common WBC

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20
Q

Eosinophils

A

Has Granules
Response to parasites and Allergies

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21
Q

Basophils

A

Has Granules
Stimulates lymphocytes immune response and allergic reactions
Least Common WBC

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22
Q

Monocytes

A

No Granules
Turn into macrophages and phagocytize pathogens

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23
Q

Hemostasis

A

Cessation of Bleeding

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24
Q

Coagulation

A

Clot Formation

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25
Q

Anti-Coagulation

A

Blockage of Clotting Factors

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26
Q

Fibronolysis

A

Breakdown of Clots

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27
Q

Thrombosis

A

Occlusion of blood vessel caused by over clotting

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28
Q

Epithelial Hemostasis

A

Vasoconstriction - Increases tissue pressure

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29
Q

Platelet Plug Adhesion

A

vWF released from endothelial cells in response to stress binds to GpIb receptor to catch platelets

Allows fibronectin and laminin to attach to other platelets

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30
Q

Platelet Plug Activation

A

Binding of collagen Fibronectin and laminin triggers activation of PLC and an influx of Ca 2+

Exocytosis of dense granules and alpha granules release recruitment chemicals

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31
Q

Platelet Aggregation

A

Recruited platelets attach to one another and form a thrombus

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32
Q

Coagulation Cascade Pathways

A

Intrinsic Extrinsic and Common

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33
Q

Intrinsic Pathway

A

Blood comes into contact with a negatively charged surface

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34
Q

Extrinsic Pathway

A

Blood contacts material from damaged tissue

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35
Q

Common Pathway

A

Where the intrinsic and extrinsic pathways meet

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36
Q

Factors in the Intrinsic Pathway

A

Collagen Kallikrein HMWK
XII
XI
IX
VIII

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37
Q

Factors of the Extrinsic Pathway

A

III Tissue Factor
VII

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38
Q

Factors of Common Pathway

A

X
V
II Thrombin
I Fibrin
XIII

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39
Q

Tenase

A

Scaffolding for IXa and VIIIa activation of X

40
Q

Prothrombin

A

Scaffolding for Xa and Va activation of II to IIa Thrombin

41
Q

Activated Protein C

A

Inhibits Va VIIIa

42
Q

Antithrombin

A

Inhibits Thrombin and Xa

43
Q

Vitamin K Dependent Factors

A

II Prothrombin
VII
IX
X

44
Q

Activated Partial Thromboplastin Time

A

Measures Intrinsic and Common

45
Q

Prothrombin Time

A

Measures Extrinsic and Common

46
Q

Thrombin Time

A

Measures Fibrinogen to Fibrin

47
Q

Thrombin Feedback

A

Increases:
XIa
VIIIa
Va

Decreases:
Thrombomodulin

48
Q

Fibrinolysis

A

Plasminogen reacts with t-PA or U-PA to become plasmin which causes stable fibrin to breakdown

49
Q

Inhibitors of Fibrinolysis

A

PAI-1 PAI-2 and Alpha 2 AP

50
Q

Preload

A

Load present prior to contraction
EDV

51
Q

Contractility

A

Change in force at any given sarcomere length

52
Q

Afterload

A

Force resisting outflow from ventricle or shortening
Mean Arterial Pressure measures afterload

53
Q

Work Done by Heart

A

Heart energy expenditure is mainly from isovolumetric contraction and therefore the tension heat produced can measure cardiac output

54
Q

Endocardium Isovolumic Contraction

A

Clockwise
Shortening of inner fibers

55
Q

Epicardium Ejection

A

Counterclockwise
All heart fiber layers activate and shorten

56
Q

Endocardium Isovolumic Relaxation

A

Clockwise
Postsystolic shortening from a rebound like effect which stretches the epicardial fibers

57
Q

Endocardium Filling

A

Clockwise
All fibers are stretched to allow filling

58
Q

Myocytes during Systole

A

Action potential -> Activates T Tubule -> Opens L Type Calcium Channels -> Calcium in opens RYR on SR to release more calcium -> Calcium Binds to troponin C -> Tropomyosin Moves -> actin/myosin bind

59
Q

Myocytes during diastole

A

Calcium has to leave the cell via:
NCX Sodium/Calcium Exchanger
PMCA Plasma Membrane Calcium ATPase

Calcium has to go back into the SR via:
Serca Pump

60
Q

Serca Pump Inhibitor

A

Un Phosphorylated Phospholamban

61
Q

Beta - Adrenergic Signaling

A

Beta Adrenergic Receptors increase PKA

62
Q

PKA Phosphorylation

A

Increase:
L Type Calcium Channels
RYR Calcium
SERCA pump (by phosphorylating Phospholamban)
TnI Calcium dissociation to cause relaxation
MyBP-C to accelerate crossbridge formation

63
Q

Inotropy

A

Strength of Contractions

64
Q

Frank Starling Law

A

Increased Sarcomere Length increases force generation
Increased EDV -> Increased Fiber Length -> Increased Fiber Tension -> Increase Stroke Volume

65
Q

Sarcomere Length and Force Generation

A

Increased Length
Decreased inter filament spacing
closer cross bridge
more Tnc affinity for Ca
Increased interaction of myosin and actin

66
Q

Inotropy and contraction

A

More intracellular calcium or adrenergic agonist the stronger the contraction

67
Q

Conduction Pathway

A

SA Node -> AV Node -> Bundle of His -> Purkinje Fibers -> Ventricular Myocytes

68
Q

Slow Action Potentials of SA and AV Nodes

A

Phase 4
If activated
Ik deactivates
Icat depolarize

Phase 0
Ica L type calclium channel depolarizes the cell

Phase 3
Inactivate Ica
Activate Ikr or HERG and Iks

69
Q

If Channel

A

Funny channel that lets Sodium and Potassium move into the cell

70
Q

Fast APs of the ventricular myocytes

A

Phase 4
Iki Activated

Phase 0
Ina major
Ica minor

Phase 1
Ina Inactivation
Ik to rapid open/close

Phase 2
Plateau
Ica active
Ik active

Phase 3
Ik HERG and Iks activation

71
Q

Calcium Chelator

A

Causes serum and plasma seperation

72
Q

Intrinsic Factors associated with bleeding

A

XIII IX XI
8 9 11

73
Q

Gp 1B

A

Binding site of platelet at the start of clot formation

74
Q

Protein C

A

Promotes bleeding by inhibiting some coagulation factors

75
Q

T PA

A

Tissue Type Plasminogen activator is a protein that breakdowns blood clots

76
Q

Plasminogen to Plasmin

A

T-pa or U-Pa

77
Q

Plasmin

A

Breakdown fibrin

78
Q

Fibrinolysis Inhibitors

A

PAI-1 PAI-2 Alpha2 AP

79
Q

Contractility effect on stroke volume

A

Increase Stroke volume

80
Q

Extracellular Ca effect on SV

A

Increase SV

81
Q

Extracellular Na effect on SV

A

Decrease SV

82
Q

Phospholamban

A

Inhibits SERCA Pump

83
Q

Beta Adrenergic Stimulation activates what GPCR Pathway

A

Gs

84
Q

Isoelectric Lead

A

Q and R are same height

85
Q

ESPVR Contractility

A

Slope of Ejection

86
Q

Activating what receptors increases cAMP and PKA

A

Beta 1 and 2 Adrenergic

87
Q

EKG Heart Rate Calculation

A

1500/R to R small squares
300/R to R big squares

88
Q

Irregular Heart beat heart rate EKG

A

Count QRS in 15 big squares x 20

89
Q

Normal Heart Rate

A

60-100 BPM

90
Q

Funny Current If

A

Slow AP Phase 4
Activated via hyper polarization

91
Q

Voltage Dependent Current Ica

A

Slow AP Phase 0
Activated by depolarization
L type primary deactivates during phase 0
T Type stays open but does not contribute as much

92
Q

Delayed Potassium Rectifier Current

A

Slow activation by depolarization
Ikr
Iks

93
Q

Fast AP Inward Rectifier

A

Ikr Channel
Sets resting potential for myocytes
turns off upon depolarization

94
Q

K+ Channels in Ventricle

A

Kir2 Ik1
Kv4 Ikto
Kv10 (HERG) Ikr
Kv7 Ik

95
Q

Kir2 Ik1

A

Inward Rectifier
Open at rest phase 4
closes during AP

96
Q

Kv4 Ikto

A

Transient Outward Rapid activation and inactivation
Contributes to phase 1 fast partial AP repolarization

97
Q

Kv10 HERG Ikr

A

Rapid delayed rectifier
Phase 3 repolarization

98
Q

Kv7 Iks

A

Slow delayed rectifier
contributes to phase 3 repolarization

MED PHYS (26 decks)

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