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ANP 1105 > Lecture 9 - Blood > Flashcards

Lecture 9 - Blood Flashcards

1
Q

What is the movement of O2 in the body?

A

from blood to tissues

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2
Q

What is the CO2 movement in the body?

A

from tissues to the blood

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3
Q

What is the blood made of?

A

-formed elements (45% mostly RBC)
-plasma (55%)

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4
Q

What are the formed elements in blood?

A

-erythrocytes (RBCs)
-leukocytes (WBCs)
-platelets

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5
Q

What does hematocrit mean?

A

the # RBCs in the total volume of blood

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6
Q

What should the blood pH be?

A

7.35-7.45

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7
Q

What is the temperature of the blood?

A

38º C, warmer than the body temp

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8
Q

Average blood volume
-male
-female

A

-5-6L
-4-5L

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9
Q

What is the general pathway for O2 distribution by the blood?

A

from lungs to heart to target

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10
Q

How do nutrients get distributed by the blood?

A

the digestive tract to target

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11
Q

How does metabolic waste get distributed by the blood?

A

lungs and kidneys to the esophagus to uruter

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12
Q

How do hormones get distributed by the blood?

A

from endocrine glands to target

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13
Q

What does blood regulate?

A

-body temp
-pH in tissues (bicarbonate ions)
-fluid volume (osmotic pressure)

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14
Q

What and how does the blood protect the body?

A

-blood loss = proteins + platelets clot to stop bleeding
-infection = antibodies, proteins, and leukocytes stop the spread of viruses

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15
Q

What are the main plasma proteins?

A

-albumin
-alpha globulins
-beta globulins
-y globulins

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16
Q

What are plasma waste products?

A

-lactic acid
-urea
-creatine

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17
Q

What are the plasma’s organic nutrients?

A

-glucose
-carbohydrates
-amino acids

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18
Q

What are the electrolytes found in the plasma? (5)

A

-Na+
-K+
-Ca2+
-Cl-
-H3CO2

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19
Q

State the 2 respiratory gases found in the plasma

A

-O2 & CO2

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20
Q

What is special about the structure of an erythrocyte?

A

has no nucleus

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21
Q

How do erythrocytes transport gas?

A

O2 binds to iron on the heme on the polypeptide of the hemoglobin
-always at full capacity

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22
Q

What is the erythrocyte plasma membrane made of?

A

spectrin

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23
Q

What makes an erythrocyte so flexible?

A

-spectrin, actin and myosin

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24
Q

How do RBCs not consume the O2 it carries?

A

The ATP of the RBC is made anaerobically

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25
Q

Why are hemoglobins not free in circulation?

A

many negative consequences
-increase osmotic pressure
-lose Hb to tissues
-increase blood viscosity
-damage kidneys

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26
Q

What is the structure of hemoglobin (Hb)?

A

1 Hb
= 2 alpha polypeptide + 2 beta polypeptide chains
= 4 heme groups
= 4 iron
= 4 O2

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27
Q

How does the affinity O2 affinity increase/decrease?

A

once one O2 bind/unbind, the affinity increase/decreases to bind/unbind the rest

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28
Q

What are oxyhemoglobin and deoxyhemoglobin?

A

-with O2 from lungs
-no O2 from tissues

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29
Q

What is carbaminohemoglobin?

A

a compound of Hb and CO2 where the CO2 binds to the peptide backbone

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30
Q

What does CO2 get converted to?

A

HCO3 in erythrocytes by carbonic anhydrase

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31
Q

What is the word for blood cell formation?

A

hematopoiesis

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32
Q

Where does hematopoiesis occur in the body?

A

-red bone marrow
=axial skeleton + girdles (hips)
=humerus + femur (largest bones)

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33
Q

How much hematopoiesis in mL is made a day?

A

30mL/day

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34
Q

What is erythropoiesis?

A

production of RBCs

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35
Q

What are the steps of erythropoiesis?

A
  1. hemocytoblasts (formed elements)
  2. proerythroblasts
  3. early erythroblasts (ribosome synthesis)
  4. late erythroblasts (Hb accumulation)
  5. normoblasts
  6. reticulocytes (ejection of the nucleus)
  7. erythrocytes
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36
Q

How long is the process of erythropoiesis?

A

15 days

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37
Q

What is it called when there are too few RBCs?

A

-tissue hypoxia
=run out of O2 in the tissues

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38
Q

What happens when there are too many RBCs?

A

-increase in blood viscosity
=make blood flow hard, too thick

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39
Q

How is erythropoiesis controlled and maintained?

A

-hormonally controlled (erythropoietin)
-relies on iron, amino acids, vitamin B

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40
Q

Where is erythropoietin made?

A

kidneys

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41
Q

Why would erythropoietin be released?

A

-hypoxia (O2 levels low, demand more O2)

42
Q

What would an increased amount of erythropoietin do?

A

-increase RBCs in circulating blood
-increase O2 carrying ability
-increase reticulocyte count = rate RBC synthesis

43
Q

What is the homeostatic response to low O2 levels in blood?

A
  1. kidney release EPO
  2. stimulate red bone marrow
  3. enhanced erythropoiesis = increase RBC count
  4. increase O2 carrying
  5. increase until normal
44
Q

Why do dialysis patients become anemic?

A

no EPO is produced so there is no RBC production

45
Q

What does erythropoiesis require to function?

A

-proteins, lipids, carbohydrates
-iron, vitamin B12, folic acid

46
Q

Where does the body store iron?

A

-hemoglobin (65%)
-liver
-spleen
-bone marrow

47
Q

Where is the intracellular iron?

A

-ferritin
-hemosiderin

48
Q

Where is circulatory iron?

A

loosely bound to transferrin or eaten by haptoglobin

49
Q

What is the lifespan of an erythrocyte?

A

100-120 days

50
Q

Why do RBCs become rigid and fragile?

A

degeneration of backbone with no regeneration

51
Q

Where do dying RBCs go?

A

trapped in spleen and eaten by macrophages

52
Q

What happens to the heme of the hemoglobin when RBC is eaten?

A
  1. degraded to bilirubin
  2. liver bilirubin into intestine bile
  3. intestine bile metabolizes into urobilinogen
  4. urobilinogen to stercobilin feces leaves the body
53
Q

What happens to the globin of hemoglobin when RBC is eaten?

A

-metabolized into amino acids and released into circulation

54
Q

What happens to the iron from hemoglobin when RBC is eaten?

A

-salvaged for reuse, attach to ferritin and hemosiderin

55
Q

What happens to the hemoglobin released into the blood?

A

captured and phagocytized by haptoglobin

56
Q

What is anemia?

A

-erythrocyte disorder
-low O2 carrying ability

57
Q

What are the signs/ symptoms of anemia?

A

-fatigue, paleness, shortness of breath, chills

58
Q

What are the types of anemia where there is insufficient RBCs + explanation?

A
  1. hemorrhagic (acute/chronic blood loss)
  2. hemolytic (prematurely ruptured RBC)
  3. aplastic (destruct/inhibit red bone marrow)
59
Q

What are the types of anemia where there is decreased hemoglobin content + explanation?

A
  1. iron-deficiency (loss iron, no intake, no absorption)
  2. pernicious (no B12, no intrinsic factor)
60
Q

What are the types of anemia where there is abnormal hemoglobin + explanation?

A
  1. thalassemias (faulty globin of Hb)
  2. sickle-cell (defective gene)
61
Q

What is polycythemia?

A

-excess RBC = increased blood viscosity

62
Q

What are the 3 main polycythemia conditions + definitions?

A
  1. polycythemia vera = naturally make too much
  2. secondary polycythemia = smoker/burn victim
  3. blood doping/EPO abuse = drugs/ enhancers
63
Q

What are leukocytes?

A

-white blood cells
-a complete cell that is <1% blood volume
-responds to bacterial or viral invasion

64
Q

What are platelets?

A

-megakoryocytes
-clotting factors and enzymes

65
Q

What regulates platelets?

A

thrombopoietin

66
Q

What inactivates platelets?

A

nitric oxide (NO) and prostacyclin

67
Q

What is the genesis of platelets?

A

-hemocytoblast
-megakaryoblast
-promegakaryocyte
-megakaryocyte
-platelet

68
Q

How is blood homeostasis maintained?

A
  1. vascular spasms
    -smooth muscle contract
    -vasoconstriction
  2. platelet plug
    -collagen exposed
    -platelet adhere
  3. coagulation
    -fibrin mesh
69
Q

How is the platelet plug only formed where it is needed?

A

-Nitric oxide (NO) and prostacyclin (PGIs) stop spreading
-swift removal by normal blood flow
-inhibition of activated clotting factors

70
Q

What are the steps to platelet plug formation?

A
  1. damage to blood vessel
  2. release von Willebrand factor (VWF) = adhere to collagen
  3. release thromboxane A2
  4. stick to exposed collagen
  5. release serotonin and ADP = attract more platelets
71
Q

What kind of homeostatic process is the platelet plug formation?

A

positive feedback chain

72
Q

What is the process of homeostatic coagulation?

A
  1. intrinsic/extrinsic pathway
  2. prothrombin activator (PA)
  3. prothrombin to thrombin
  4. thrombin catalyzes fibrinogen to fibrin mesh
73
Q

What is special about the intrinsic pathway of coagulation?

A

-occurs in the blood itself
-occurs without the addition of anything
-small events
-multiple steps = slower

74
Q

What is unique about the extrinsic pathway of coagulation?

A

-requires tissue factor
-for larger events and vessel damage
-less steps = much faster

75
Q

Draw out the diagram of phase 1 of coagulation

A

-intrinsic
-extrinsic
-(X -> Xa)
-Ca2+, (V -> Va), PF3 (platelet factor 3) addition to Xa = prothrombin activator (PA)

76
Q

Draw out phase 2 and phase 3 of coagulation

A

phase 2 [
-Prothrombin + PA = thrombin
]

phase 3 [
-Fibrinogen + thrombin = fibrin
-(XIII -> XIIIa)+ Ca2+ + thrombin + fibrin = cross-linked mesh
]

77
Q

How does clot retraction work?

A

-pull together and stabilize the clot by squeezing serum out

78
Q

What are the 3 clot repair options and how?

A

=promote healing vessel wall (platelet-derived growth factor)
=CT patch-up (fibroblasts)
=restore endothelial lining (vascular endothelial growth factor)

79
Q

How does clot removal work?

A

-digestion = plasmin (plasminogen) which is activated by tissue plasminogen activator (tPA) and released by endothelial cells

80
Q

What causes the inhibition of clotting factors? (2 things)

A

-fibrin + thrombin = anticoagulant
-antithrombin III = thrombin inactivator

81
Q

What causes an increase in antithrombin III activity?

A

-heparin

82
Q

What is the name of a common thromboembolic condition and its definition?

A

thrombus
-clot develops and persists in unbroken bv
-causes a block in circulation

83
Q

What is the name of a type of thrombus?

A

embolus
-free floating thrombus in the blood
-can block and get stuck in smaller vessels

84
Q

How do you prevent undesirable clots? (3 drugs)

A

-aspirin (inhibit thromboxane A2)
-heparin (inhibit thrombin)
-warfarin (inhibit vitamin K)

85
Q

What is the bleeding disorder where there are insufficient platelets?
-definition
-cause
-symptoms
-treatment

A

=thrombocytopenia
-not enough platelets in circulation
-destruction/ suppression of bone marrow
-bruising
-whole blood transfusion

86
Q

What is the bleeding disorder where there is an inability to synthesize procoagulants?
-definition
-cause
-symptoms

A

=liver disease
-inability to make procoagulants
-liver disease, no procoagulants synthesize, no absorb fat
-vitamin k deficiency, hepatitis and cirrhosis

87
Q

What is a bleeding disorder where there is a lack of clotting factors?
-how is it passed down
-treatments

A

=hemophilias
A - no factor VIII (most common/ severe)
B - no factor IX (more severe)
C - no factor XI (mild type)
- A and B are X-linked, C is autosomal recessive
- blood transfusions, injection of missing factors

88
Q

Why is hemophilia C a more mild form of the disease in comparison to Hemophilia A/B?

A

Hemophilia C lacks factor XI which is where the extrinsic pathway can help the intrinsic pathway.
Hemophilia A and B lack factors VIII and IX which cannot be helped and therefore cause a larger problem.

89
Q

When are blood transfusions used?

A

-blood loss is substantial (15-30% weakness + 30% shock)

90
Q

How do the human blood groups differ?

A

-by the presence or absence of glycoprotein antigens on the surface of the RBC membranes
-unique to the person
-foreign if transfused
-30 varieties

91
Q

What blood groups are used for legalities?

A

M, N, Duffy, Kell, Lewis

92
Q

For ABO blood groups where are the following located?
-antigens
-agglutinins (antibodies)

A

-antigens A/B located on the surface of RBC
-anti- A/B located in the plasma

93
Q

Draw out the ABO blood group table
-blood group (4)
-RBC antigens (agglutinogens)
-illustration
-plasma antibodies (agglutinins)
-blood that can be recieved

A

look at notes

94
Q

How many Rh agglutinogens (antigens) are there?

A

50 different

95
Q

What are the 3 most common Rh blood groups?

A

C, D, E

96
Q

How do you know there is an Rh agglutinogen present on the RBC?

A

Rh+

97
Q

How are anti-Rh antibodies formed?

A

-not spontaneous
-Rh- individual receives Rh+ blood

98
Q

What causes a transfusion reaction in Rh blood groups?

A

a 2nd exposure to Rh+ blood

99
Q

What is the hemolytic disease of the newborn?

A

=erythroblastosis fetalis
-Rh- mom
-> 1st child (Rh+) = okay
-> 2nd child (Rh+) = antibodies attack

100
Q

What is the treatment for hemolytic disease of the newborn?

A

=RhoGAM drug (passively immunize Rh- mom)
-pre-birth transfusions
-after-birth exchange transfusions

101
Q

What happens when mismatched blood is infused?

A

=transfusion reactions
-donor cells attached by host agglutinins
-diminished O2 carrying
-clot = no flow
-free Hg in bloodstream = kidney

ANP 1105 (12 decks)

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