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
Coagulation
Clot Formation
25
Anti-Coagulation
Blockage of Clotting Factors
26
Fibronolysis
Breakdown of Clots
27
Thrombosis
Occlusion of blood vessel caused by over clotting
28
Epithelial Hemostasis
Vasoconstriction - Increases tissue pressure
29
Platelet Plug Adhesion
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
30
Platelet Plug Activation
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
31
Platelet Aggregation
Recruited platelets attach to one another and form a thrombus
32
Coagulation Cascade Pathways
Intrinsic Extrinsic and Common
33
Intrinsic Pathway
Blood comes into contact with a negatively charged surface
34
Extrinsic Pathway
Blood contacts material from damaged tissue
35
Common Pathway
Where the intrinsic and extrinsic pathways meet
36
Factors in the Intrinsic Pathway
Collagen Kallikrein HMWK XII XI IX VIII
37
Factors of the Extrinsic Pathway
III Tissue Factor VII
38
Factors of Common Pathway
X V II Thrombin I Fibrin XIII
39
Tenase
Scaffolding for IXa and VIIIa activation of X
40
Prothrombin
Scaffolding for Xa and Va activation of II to IIa Thrombin
41
Activated Protein C
Inhibits Va VIIIa
42
Antithrombin
Inhibits Thrombin and Xa
43
Vitamin K Dependent Factors
II Prothrombin VII IX X
44
Activated Partial Thromboplastin Time
Measures Intrinsic and Common
45
Prothrombin Time
Measures Extrinsic and Common
46
Thrombin Time
Measures Fibrinogen to Fibrin
47
Thrombin Feedback
Increases: XIa VIIIa Va Decreases: Thrombomodulin
48
Fibrinolysis
Plasminogen reacts with t-PA or U-PA to become plasmin which causes stable fibrin to breakdown
49
Inhibitors of Fibrinolysis
PAI-1 PAI-2 and Alpha 2 AP
50
Preload
Load present prior to contraction EDV
51
Contractility
Change in force at any given sarcomere length
52
Afterload
Force resisting outflow from ventricle or shortening Mean Arterial Pressure measures afterload
53
Work Done by Heart
Heart energy expenditure is mainly from isovolumetric contraction and therefore the tension heat produced can measure cardiac output
54
Endocardium Isovolumic Contraction
Clockwise Shortening of inner fibers
55
Epicardium Ejection
Counterclockwise All heart fiber layers activate and shorten
56
Endocardium Isovolumic Relaxation
Clockwise Postsystolic shortening from a rebound like effect which stretches the epicardial fibers
57
Endocardium Filling
Clockwise All fibers are stretched to allow filling
58
Myocytes during Systole
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
Myocytes during diastole
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
Serca Pump Inhibitor
Un Phosphorylated Phospholamban
61
Beta - Adrenergic Signaling
Beta Adrenergic Receptors increase PKA
62
PKA Phosphorylation
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
Inotropy
Strength of Contractions
64
Frank Starling Law
Increased Sarcomere Length increases force generation Increased EDV -> Increased Fiber Length -> Increased Fiber Tension -> Increase Stroke Volume
65
Sarcomere Length and Force Generation
Increased Length Decreased inter filament spacing closer cross bridge more Tnc affinity for Ca Increased interaction of myosin and actin
66
Inotropy and contraction
More intracellular calcium or adrenergic agonist the stronger the contraction
67
Conduction Pathway
SA Node -> AV Node -> Bundle of His -> Purkinje Fibers -> Ventricular Myocytes
68
Slow Action Potentials of SA and AV Nodes
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
If Channel
Funny channel that lets Sodium and Potassium move into the cell
70
Fast APs of the ventricular myocytes
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
Calcium Chelator
Causes serum and plasma seperation
72
Intrinsic Factors associated with bleeding
XIII IX XI 8 9 11
73
Gp 1B
Binding site of platelet at the start of clot formation
74
Protein C
Promotes bleeding by inhibiting some coagulation factors
75
T PA
Tissue Type Plasminogen activator is a protein that breakdowns blood clots
76
Plasminogen to Plasmin
T-pa or U-Pa
77
Plasmin
Breakdown fibrin
78
Fibrinolysis Inhibitors
PAI-1 PAI-2 Alpha2 AP
79
Contractility effect on stroke volume
Increase Stroke volume
80
Extracellular Ca effect on SV
Increase SV
81
Extracellular Na effect on SV
Decrease SV
82
Phospholamban
Inhibits SERCA Pump
83
Beta Adrenergic Stimulation activates what GPCR Pathway
Gs
84
Isoelectric Lead
Q and R are same height
85
ESPVR Contractility
Slope of Ejection
86
Activating what receptors increases cAMP and PKA
Beta 1 and 2 Adrenergic
87
EKG Heart Rate Calculation
1500/R to R small squares 300/R to R big squares
88
Irregular Heart beat heart rate EKG
Count QRS in 15 big squares x 20
89
Normal Heart Rate
60-100 BPM
90
Funny Current If
Slow AP Phase 4 Activated via hyper polarization
91
Voltage Dependent Current Ica
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
Delayed Potassium Rectifier Current
Slow activation by depolarization Ikr Iks
93
Fast AP Inward Rectifier
Ikr Channel Sets resting potential for myocytes turns off upon depolarization
94
K+ Channels in Ventricle
Kir2 Ik1 Kv4 Ikto Kv10 (HERG) Ikr Kv7 Ik
95
Kir2 Ik1
Inward Rectifier Open at rest phase 4 closes during AP
96
Kv4 Ikto
Transient Outward Rapid activation and inactivation Contributes to phase 1 fast partial AP repolarization
97
Kv10 HERG Ikr
Rapid delayed rectifier Phase 3 repolarization
98
Kv7 Iks
Slow delayed rectifier contributes to phase 3 repolarization