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Pathophysiology exam 1 > Blood and lymphoid tissue > Flashcards

Blood and lymphoid tissue Flashcards

1
Q

Albumin

A

Carrier protein
Stays in blood stream
Hydrophilic

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2
Q

Where do RBCs come from?

A

Reticulocytes

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3
Q

How do RBCs develop?

A

Cells in kidney can measure O2 in blood and will initiate erythropoiesis
Erythropoiesis
- Form reticulocyte in bone marrow
- Released into blood stream to mature

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4
Q

What are leukocytes made from?

A

Progenitor cells

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5
Q

Lymphoid progenitors

A

Differentiate into lymphocytes and released in bloodstream

Fully mature in lymphoid organs

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6
Q

What are the lymphoid organs?

A

Thymus, spleen

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7
Q

Myeloid progenitors

A

Differentiate into other WBCs
Monocytes released into blood stream and mature
Granulocytes mature in bone marrow
- Some immature ones are reserved in bone marrow and activated/released when needed

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8
Q

What are platelets formed from?

A

Megakaryocytes

Stimulated by thrombopoietin

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9
Q

Stages of hemostasis

A
  1. Vessel spasm to control blood loss
  2. Formation of platelet plug
    - Requires vWF
    - Fibrinogen
    - vWF binds to subendothelial portion of blood vessel
    - Hooks grab the platelets
    - Fibrinogen binds to 2B3A receptor on platelet and binds one to the next
    - Fibrin fills holes between
  3. Coagulation cascade
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10
Q

Coagulation cascade

A

Prothrombin -> thrombin

Thrombin converts fibrinogen -> fibrin

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11
Q

What is the intrinsic pathway stimulated by?

A

Blood injury

- Slower

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12
Q

What influences the intrinsic pathway?

A

Heparin

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13
Q

What is the extrinsic pathway stimulated by?

A

Tissue factor released by endothelial cells in response to injury or inflammatory process
- Faster

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14
Q

What influences the extrinsic pathway?

A

Coumadin

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15
Q

What should you check to evaluate the extrinsic pathway?

A

Prothrombin time

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16
Q

What should you check to evaluate the intrinsic pathway?

A

Partial thromboplastin time

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17
Q

What enzyme is important for clotting?

A

Ca++

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18
Q

What regulates coagulation?

A

Antithrombin III
Protein C
Protein S

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19
Q

What does Antithrombin III do?

A

Inactivates coagulation factors and thrombin

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20
Q

What does Protein C do?

A

Inactivates factors V and VIII

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21
Q

What does Protein S do?

A

Accelerates Protein C

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22
Q

Clot dissolution

A

Fibrinolysis causes plasminogen -> plasmin

  • Digests fibrin strands
  • Digests several clotting factors
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23
Q

What does TPA do?

A

Medication that speeds up plasminogen to dissolve blood clots

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24
Q

What is primary thrombocytosis?

A

An abnormally high level of free thrombopoietin due to abnormal thrombopoietin receptors on platelets

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25
Q

What is secondary thrombocytosis?

A

Increased production of thrombopoietin due to tissue damage

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26
Q

What is the job of thrombopoietin?

A

Regulate how many platelets one has

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27
Q

What happens when there’s an excess of thrombopoietin?

A

It will go into bone marrow and have it make more platelets, but abnormal receptors means there’s an excess of platelets and increased risk of developing a clot

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28
Q

What is Factor V Leiden mutation?

A

Factor V cannot be inactivated by Protein C

  • Venous thrombosis
  • Keeps stimulating coagulation cascade
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29
Q

Prothrombin gene mutation

A

Elevated prothrombin levels

- Venous thrombosis 3x greater than normal

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30
Q

What does Factor V do?

A

Factor V stimulates coagulation cascade

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31
Q

What does MI cause?

A

Venous congestion

Ventricle can’t squeeze effectively, leading backup of blood

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32
Q

How do hyper-estrogenic states/hormone based contraceptives affect clotting?

A

Increase synthesis of clotting factors

Reduce synthesis of Antithrombin III

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33
Q

What is Thrombocytopenia?

A

Reduced number of platelets

- Decreased production or survival

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34
Q

What is heparin-induced thrombocytopenia?

A

Reduction in platelets stimulated by heparin
Immune reaction against heparin-platelet factor 4 complex
Immune complexes activate platelets and leads to thrombosis
- Platelets release particles that activate thrombin

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35
Q

What does HIT lead to?

A

Thrombocytopenia due to overuse of platelets

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36
Q

What is Immune thrombocytopenic purpura?

A

Autoimmune disorder where antibodies are created against 2B3A receptors

37
Q

What happens in ITP?

A

Circulating immune complexes around platelet are created

More susceptible to phagocytosis and removal by spleen

38
Q

What does ITP lead to?

A

Drop of platelet count

39
Q

What is thrombotic thrombocytopenia purpura?

A

A deficiency of the enzyme that breaks down wVF

40
Q

What happens in TTP?

A

Platelets adhere and aggregate

41
Q

What is impaired platelet function?

A

Decreased activity of COX pathway
Decreased production of prostaglandin
Decreased production of thromboxane
Decreased platelet aggregation

42
Q

How do NSAIDs affect the COX pathway?

A

COX pathway is blocked

43
Q

What does the COX pathway produce?

A

Prostaglandins, which get converted into thromboxane

44
Q

What does the lipoxygenase pathway produce?

A

Leukotrienes

45
Q

What is Hemophilia A?

A

Coagulation factor deficiency
Genetic factor VIII deficiency
Can’t wind up with end factor of fibrin

46
Q

What is Hemophilia B?

A

Coagulation factor deficiency
Genetic factor IX deficiency
Can’t make fibring

47
Q

What is Von Willebrand disease?

A

Coagulation factor deficiency
Genetic deficiency or defect in vWF
Platelets cannot adhere to subendocardial membrane

48
Q

What is liver failure’s role in bleeding disorders?

A

Clotting factors are synthesized by the liver
Results in reduction of clotting factors
No clotting factors -> no coagulation cascade -> no fibrin

49
Q

What is disseminated intravascular coagulation?

A

Widespread coagulation and bleeding

50
Q

What is DIC caused by?

A

Endothelial damage

51
Q

What happens in DIC?

A

Widespread activation of coagulation response
Massive clot formation consumes all coagulation proteins and platelets
Hemorrhage follows
Pt initially clots and is followed by a risk of bleeding because the body uses all of its stores of platelets, fibrin, fibrinogen, etc

52
Q

What is hemolysis?

A

Premature destruction of RBC

53
Q

Where does hemolysis occur?

A

Can occur within or outside blood vessels

54
Q

What is sickle cell anemia?

A

Inherited abnormality in hemoglobin S synthesis

55
Q

What happens in sickle cell?

A

Deoxygenation and dehydration causes calls to sickle

Hemolysis and vascular occlusion occur

56
Q

What is Thalessemias?

A

Genetic disorder of hemoglobin synthesis

57
Q

What happens in Thalessemias?

A

Alpha or Beta chain deficiency

Results in small, pale cells

58
Q

In which population is Alpha-Thalessemia more common?

A

Asians, Africans

59
Q

In which population is Beta-Thalessemia more common?

A

Greeks and Italians, Africans

60
Q

What is Vitamin B12’s role in blood tissue?

A

Essential for DNA synthesis and nuclear maturation
Binds to intrinsic factor in the stomach, travels to intestine, is absorbed and used
Normally binds to intrinsic factor

61
Q

What happens after a Vit B12 deficiency?

A

Causes large cells due to excessive cytoplasmic growth

Short life span

62
Q

What is folic acid’s role in DNA and RBC?

A

Required for DNA synthesis and maturation

63
Q

How does one acquire a folic acid deficiency?

A

Reheating food

Drugs that interfere with absorption (seizure disorder drugs)

64
Q

What are the main branches of WBCs?

A 
Lymphoid line (B and T cells)
Myeloid line (all other WBCs)
65
Q

How does one get neutropenia?

A

Congenital
Acquired - SLE and RA
- Produce autoantibodies that target antibodies
Infection-/drug-related

66
Q

What happens in mono?

A

Virus binds to receptors on B lymphocytes
Virus kills host or incorporates into DNA
Produces easily detectable antibodies

67
Q

What is a malignant lymphoma?

A

Solid tumor composed of lymphocytes

68
Q

What is non-hodgkin lymphoma?

A

B (more common) or T cell neoplasms
Originate and lymph nodes and can spread
Remission in 60-80% of cases with chemo

69
Q

How does non-hodgkin lymphoma manifest?

A

Swollen, painless nodes

Constitutional symptoms

70
Q

What is hodgkin lymphoma?

A

Specialized form of lymphoma

71
Q

What cell rules hodgkin lymphoma?

A

Reed-Sternberg cells

72
Q

In which populations is Hodgkin lymphoma more common?

A

People <40 and >55

73
Q

How does hodgkin lymphoma manifest?

A

Painless enlargement of single nodes or group
Usually above diaphragm
Progressive spreading
Constitutional symptoms
5-year cure rate of 85% with radiation and chemo

74
Q

Hodgkin lymphoma

A 
Arises from single node or chain of nodes
Localized to head, neck, mediastinum
Orderly spread to contiguous nodes
Extranodal involvement is rare
Reed-Sternberg cell
75
Q

Non-Hodgkin’s lymphoma

A

May originate in extranodal site
More peripheral
Spread not often contiguous
Extranodal involvement is common

76
Q

What is leukemia?

A

Blood borne disorder

77
Q

What are characteristics of acute leukemia

A

From progenitor cells (less differentiated)
Sudden onset
Bone marrow crowds faster

78
Q

What are characteristics of chronic leukemia

A

Fully differentiated cells
Slow progression
No sudden bone marrow crowding

79
Q

What are characteristics of myeloblastic leukemia

A

Originating in myeloid (neutrophils) line

80
Q

What are characteristics of lymphoblastic leukemia

A

Originating in lymphoid (B&T cells) line

81
Q

Acute lymphoblastic leukemia

A

Most common in children
Fast, bone-marrow crowding, progenitor cells, B and T cells
Causes anemia, neutropenia, and thrombocytopenia
More cells in blood stream -> more viscous

82
Q

Acute Myeloblastic Leukemia

A

Most common adult leukemia
Fast, bone marrow crowding, progenitor cells, neutrophils
Bone marrow keeps spitting out new WBC into blood stream -> viscous
Increased numbers of undifferentiated blast cells, which crowd the marrow

83
Q

Chronic Lymphoblastic Leukemia

A

Slow, more fully differentiated, no bone marrow crowding, B and T cells affected
More common in older adults
Malignancy of B lymphocytes
Progressive infiltration of bone marrow and lymphoid tissues by neoplastic lymphocytes
Lymphocytosis noted on labs
Lymphadenopathy
Poor production of plasma calls -> v gamma globulinemia

84
Q

Chronic Myeloblastic Leukemia

A

Slow, more fully differentiated cells, no bone marrow crowding, neutrophils
Results in excessive production of marrow granulocytes and other blood cell precursors
Splenomegaly
Immature WBCs released into blood stream

85
Q

Which leukemia contains the Philadelphia chromosome?

A

Chronic Myeloblastic Leukemia

86
Q

What is multiple myeloma?

A

B-cell malignancy of terminally differentiated plasma cells
Proliferation of malignant plasma cells in bone marrow
Hyperviscosity of blood

87
Q

What happens in multiple myeloma?

A

Abnormal plasma cells secrete cytokines that activate osteoclasts -> bone resorption (punch lesions) -> ^ calcium in blood

88
Q

What is the Bence Jones protein associated with?

A

Diagnosing multiple myeloma

Pathophysiology exam 1 (3 decks)

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