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Pathophysiology exam 1 > Blood and lymphoid tissue > Flashcards

Blood and lymphoid tissue Flashcards

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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
What is secondary thrombocytosis?
Increased production of thrombopoietin due to tissue damage
26
What is the job of thrombopoietin?
Regulate how many platelets one has
27
What happens when there's an excess of thrombopoietin?
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
28
What is Factor V Leiden mutation?
Factor V cannot be inactivated by Protein C - Venous thrombosis - Keeps stimulating coagulation cascade
29
Prothrombin gene mutation
Elevated prothrombin levels | - Venous thrombosis 3x greater than normal
30
What does Factor V do?
Factor V stimulates coagulation cascade
31
What does MI cause?
Venous congestion | Ventricle can't squeeze effectively, leading backup of blood
32
How do hyper-estrogenic states/hormone based contraceptives affect clotting?
Increase synthesis of clotting factors | Reduce synthesis of Antithrombin III
33
What is Thrombocytopenia?
Reduced number of platelets | - Decreased production or survival
34
What is heparin-induced thrombocytopenia?
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
35
What does HIT lead to?
Thrombocytopenia due to overuse of platelets
36
What is Immune thrombocytopenic purpura?
Autoimmune disorder where antibodies are created against 2B3A receptors
37
What happens in ITP?
Circulating immune complexes around platelet are created | More susceptible to phagocytosis and removal by spleen
38
What does ITP lead to?
Drop of platelet count
39
What is thrombotic thrombocytopenia purpura?
A deficiency of the enzyme that breaks down wVF
40
What happens in TTP?
Platelets adhere and aggregate
41
What is impaired platelet function?
Decreased activity of COX pathway Decreased production of prostaglandin Decreased production of thromboxane Decreased platelet aggregation
42
How do NSAIDs affect the COX pathway?
COX pathway is blocked
43
What does the COX pathway produce?
Prostaglandins, which get converted into thromboxane
44
What does the lipoxygenase pathway produce?
Leukotrienes
45
What is Hemophilia A?
Coagulation factor deficiency Genetic factor VIII deficiency Can't wind up with end factor of fibrin
46
What is Hemophilia B?
Coagulation factor deficiency Genetic factor IX deficiency Can't make fibring
47
What is Von Willebrand disease?
Coagulation factor deficiency Genetic deficiency or defect in vWF Platelets cannot adhere to subendocardial membrane
48
What is liver failure's role in bleeding disorders?
Clotting factors are synthesized by the liver Results in reduction of clotting factors No clotting factors -> no coagulation cascade -> no fibrin
49
What is disseminated intravascular coagulation?
Widespread coagulation and bleeding
50
What is DIC caused by?
Endothelial damage
51
What happens in DIC?
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
What is hemolysis?
Premature destruction of RBC
53
Where does hemolysis occur?
Can occur within or outside blood vessels
54
What is sickle cell anemia?
Inherited abnormality in hemoglobin S synthesis
55
What happens in sickle cell?
Deoxygenation and dehydration causes calls to sickle | Hemolysis and vascular occlusion occur
56
What is Thalessemias?
Genetic disorder of hemoglobin synthesis
57
What happens in Thalessemias?
Alpha or Beta chain deficiency | Results in small, pale cells
58
In which population is Alpha-Thalessemia more common?
Asians, Africans
59
In which population is Beta-Thalessemia more common?
Greeks and Italians, Africans
60
What is Vitamin B12's role in blood tissue?
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
What happens after a Vit B12 deficiency?
Causes large cells due to excessive cytoplasmic growth | Short life span
62
What is folic acid's role in DNA and RBC?
Required for DNA synthesis and maturation
63
How does one acquire a folic acid deficiency?
Reheating food | Drugs that interfere with absorption (seizure disorder drugs)
64
What are the main branches of WBCs?
``` Lymphoid line (B and T cells) Myeloid line (all other WBCs) ```
65
How does one get neutropenia?
Congenital Acquired - SLE and RA - Produce autoantibodies that target antibodies Infection-/drug-related
66
What happens in mono?
Virus binds to receptors on B lymphocytes Virus kills host or incorporates into DNA Produces easily detectable antibodies
67
What is a malignant lymphoma?
Solid tumor composed of lymphocytes
68
What is non-hodgkin lymphoma?
B (more common) or T cell neoplasms Originate and lymph nodes and can spread Remission in 60-80% of cases with chemo
69
How does non-hodgkin lymphoma manifest?
Swollen, painless nodes | Constitutional symptoms
70
What is hodgkin lymphoma?
Specialized form of lymphoma
71
What cell rules hodgkin lymphoma?
Reed-Sternberg cells
72
In which populations is Hodgkin lymphoma more common?
People <40 and >55
73
How does hodgkin lymphoma manifest?
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
Hodgkin lymphoma
``` 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
Non-Hodgkin's lymphoma
May originate in extranodal site More peripheral Spread not often contiguous Extranodal involvement is common
76
What is leukemia?
Blood borne disorder
77
What are characteristics of acute leukemia
From progenitor cells (less differentiated) Sudden onset Bone marrow crowds faster
78
What are characteristics of chronic leukemia
Fully differentiated cells Slow progression No sudden bone marrow crowding
79
What are characteristics of myeloblastic leukemia
Originating in myeloid (neutrophils) line
80
What are characteristics of lymphoblastic leukemia
Originating in lymphoid (B&T cells) line
81
Acute lymphoblastic leukemia
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
Acute Myeloblastic Leukemia
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
Chronic Lymphoblastic Leukemia
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
Chronic Myeloblastic Leukemia
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
Which leukemia contains the Philadelphia chromosome?
Chronic Myeloblastic Leukemia
86
What is multiple myeloma?
B-cell malignancy of terminally differentiated plasma cells Proliferation of malignant plasma cells in bone marrow Hyperviscosity of blood
87
What happens in multiple myeloma?
Abnormal plasma cells secrete cytokines that activate osteoclasts -> bone resorption (punch lesions) -> ^ calcium in blood
88
What is the Bence Jones protein associated with?
Diagnosing multiple myeloma

Pathophysiology exam 1 (3 decks)

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