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Advanced Pathophysiology > Unit 2 > Flashcards

Unit 2 Flashcards

1
Q

Triggers the production of B lymphocytes, leading to destruction of the invader

A

Antigens

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2
Q

Type of immunity mediated by B-cell activation

A

Humoral immunity

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3
Q

Type of immunity mediated by T-cells, responsible for defense against intracellular microbes

A

Cell-mediated immunity

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4
Q

Low-molecular weight molecules that may contain antigenic determinants but may not be able to stimulate an immune response

A

Haptens

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5
Q

These molecules enable lymphocytes to responds to a limitless number of antigens but also recognize and ignore self-antigens expressed on tissues

A

Major Histocompatability Complex Molecules (MHC)

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6
Q

Most abundant Ig
o Possess antiviral, antibacterial and antitoxin properties
o Present in all body fluids, enters all tissues and is capable of crossing the placenta (passive immunity)
o 4 subclasses with specificity for certain types of antigens

A

IgG- gamma globulin

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7
Q

Second most abundant Ig- two identical molecules- second most common
o Secretory- found in saliva, tears, colostrum and bronchial, GI, prostatic and vaginal secretion
o Major function is local immunity on mucosal surfaces- prevents attachment of viruses and bacteria to epithelial cells
- acts locally rather than systemically

A

IgA

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8
Q

Ig- 5-membered macromolecule with identical heavy and light chains
o Agglutinating antibody- stimulating clumping of organisms for eventual lysis and elimination
o First antibody to be produced by the developing fetus and by immature B lymphocytes
- first to appear in response to an antigen
- effective in gram negative infection
-bound to B lymphs
-activates complement

A

IgM

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9
Q

Ig found on cell membranes of B cells
o Functions as a receptor for antigen
o Circulates in the serum in extremely low levels where its function is essentially unknown but may play a role in B-cell differentiation
- found primarily on cell membranes of B lymphs

A

IgD

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10
Q

Ig- least common serum IgE because it binds tightly to Fc receptors on basophils and mast cells
o Involved inflammation and allergic responses by causing mast cell degranulation and release of chemical mediators including histamine
o Essential for combating parasitic infections

A

IgE

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11
Q

The central event in initiation of humoral and cell-mediated immune responses

A

Activation of helper T Cells

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12
Q
  • Function to control immune system responses
A

Regulatory T Cells

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13
Q
  • CD 8- monitor the activity of all cells in the body and destroy any that threatens the integrity of the body
A

Cytotoxic T Cells

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14
Q

Central organs for immune system

A

Bone marrow and thymus

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15
Q

Responsible for T cell maturation

A

Thymus

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16
Q

Classic allergic response

A

Type I- IgE mediated hypersensitivity d/o

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17
Q

Release of histamine is associated with which cells

A

Mast cells and basophils

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18
Q

A prostaglandin released from platelets that plays a role in platelet aggregation

A

Thromboxane (TXA2)

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19
Q

This clotting factor is produced in the endothelial cells of blood vessels and circulates in the blood as a carrier protein for coagulation factor VIII- required for platelet adhesion

A

von Willebrand factor

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20
Q

Most platelet defects result in ______

A

Bleeding

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21
Q

Cyclooxygenase-1 (COX-1) inhibitors prevent clot formation by inhibiting prostaglandin synthesis, including TXA2- what is an example of this?

A

Aspirin

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22
Q

In liver damage, bleeding is more likely to occur because of lack of _______ synthesis

A

Prothrombin

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23
Q

Clotting pathway- Slow process, begins in circulation with activation of factor XII

A

Intrinsic

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24
Q

Clotting pathway-must faster (can cause clotting in 15 seconds)- begins with trauma to the blood vessel or surrounding tissues and release of tissue factor or tissue thromboplastin

A

Extrinsic

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25
Q

Both pathways terminate at the same step-activation of factor ___, which helps convert _____ to ______

A

X, prothrombin to thrombin

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26
Q

Proenzyme for fibrinolytic process is converted to its active form, plasmin- also, what’s the drug we use???

A

Plasminogen, tissue plasminogen activators (TPA!)

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27
Q

Causes activated Protein C Resistance (clotting d/o)

A

Factor V Leiden

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28
Q

Activates other lymphocytes and phagocytes

A

Helper T cells

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29
Q

Keeps cells in check to that an exaggerated immune response does not occur

A

Regulatory T cells

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30
Q

Activation of t-lymphocytes (t-helper and t-cycotoxic)- responsible for body’s defense against intracellular microbes like viruses

A

Cell-mediated Immunity

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31
Q

B-lymphocyte activation and antibody production

A

Humoral Immunity

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32
Q

Mature in bone marrow and secrete antibodies

A

B cells

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33
Q

Derived from the stem cell

A

Lymphocytes

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34
Q

Type of cell for humoral immunity

A

B cells

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35
Q

Type of cell for cell-mediated immunity

A

T cells

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36
Q

Also known as gamma globulins or immunoglobulins

A

Antibodies

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37
Q

The activated B cell divides and undergoes maturation into a ______, which produces thousands of antibodies and releases them into the blood and lymph to bind to and remove their antigen

A

Plasma cells

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38
Q

Orchestrate and control immune response/ direct the action of the immune response

A

Regulatory cells (t helper, t suppressor, and antigen presenting cells)

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39
Q

Cells that are able to attack the antigen and destroy it

A

Effector cells (t cytotoxic, B cells to produce antibodies, and leukocytes)

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40
Q

Immune response- when body first encounters the antigen- slower response, B cells need to proliferate and differentiate into plasma cells to produce the antibody

A

Primary Immune response

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41
Q

Immune response- memory cells are available, rise in antibody is more rapid because memory cells don’t have to differentiate

A

Secondary Immune response

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42
Q

Hypersensitivity Reaction:IgE mediated
o Against environmental antigens (allergens)
o IgE binds to receptors on surface of mast cells
o Histamine release causing itching, urticaria, conjunctivitis, rhinitis, hypotension, bronchospasm, dysrhythmias, GI cramps and malabsorption
o First, sensitizing event or exposure causes no symptoms, second event causes rapid reaction (immediate- within minutes)
o Can be inherited, called atopic

A

I

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43
Q

Hypersensitivity Reaction Type:tissue specific- cytotoxic
o Antibody attaches directly to an antigen in the target tissue (usually a cell membrane)
o Circulating IgG antibodies react with the antigen, causing destruction of the cell, either by releasing cytolytic enzymes related to complement activation or by phagocytosis
o ABO incompatible blood transfusion or myasthenia gravis autoimmune response

A

II

44
Q

Hypersensitivity Reaction Type:immune complex mediated
o Antigen-antibody complexes are formed in circulation and later deposited in vessel walls or extravascular tissues, causing activation of complement
o Not organ specific
o Immune complex clearance
o cause of most autoimmune diseases
1. RA, SLE- complexes form againt collagen and cellular DNA, and deposit in multiple sites throughout the body

A

III

45
Q

Hypersensitivity Reaction Type:T-cell mediated- does not involve antibody
o Cytotoxic (CD8) or helper (CD4) cells are activated by antigen, leading to destruction of the cells involved
o Often against virally-infected cells and can lead to extensive tissue damage
o Reactions are delayed, can take 24-72 hours to develop
o Poison ivy or oak, tuberculin skin test

A

IV

46
Q

3 factors of hemostasis

A
  1. blood vessel integrity
  2. platelet plug formation
  3. coagulation factors
47
Q

3 steps to formation of platelet plug

A
  1. activation using collagen from damaged endothelial tissue
  2. adhesion using vWF and factor VIII
  3. aggregation by secretion of ADP, TXA2, epinephrine and platelet activating factor to recruit more platelets to the area
48
Q

Steps to clot formation

A
  1. prothrombin activator (via extrinsic or intrinsic pathway) is formed in response to damage.
  2. catalyzes conversion of prothrombin into thrombin
  3. thrombin acts as an enzyme to convert fibrinogen into fibrin threads
49
Q

All clotting pathways end at this factor, which is responsible for converting prothrombin into thrombin

A

Factor X

50
Q

Which clotting factor?slow process, begins in circulation with activation of factor XII

  1. activated when blood comes in contact with collagen in the injured blood vessel wall
  2. produces clot in 1-6 minutes post initiation
  3. more complex and powerful
A

Intrinsic

51
Q

Which clotting factor?much faster (can cause clotting in 15-20 seconds)- begins with trauma to the blood vessel or surrounding tissues and release of tissue factor (aka tissue thromboplastin)

  1. activated when blood is exposed to tissue extracts
  2. activation of factor VII
  3. tissue thromboplastin is found in most tissue with high amounts in brain, lung, bone marrow, kidney and placenta
A

Extrinsic

52
Q

Extrinsic pathway uses factor _____

A

VII

53
Q

Intrinsic pathway uses factor _____

A

XII

54
Q

All clotting factors merge at Factor …..

A

X

55
Q

Factor IV is ____

A

Calcium

56
Q

o Associated with autoantibodies (primarily IgG) directed against protein-binding phospholipids- resulting in increased coagulation activity
o Common feature is venous and arterial thrombi, recurrent fetal loss, and thrombocytopenia
o Can be primary (in isolation) or secondary (associated with systemic lupus erythematosus)

A

Antiphospholipid Syndrome

57
Q

Triad of Virchow…

A
  1. abnormalities of blood flow
  2. endothelial injury
  3. hypercoagulability
58
Q

form under condition of high blood flow, composed mainly of platelet aggregates held together with fibrin- related to endothelial trauma

A

Arterial Thrombosis

59
Q

low flow conditions- mostly RBCs with fibrin, increased RBC mass and viscosity, small vascular caliber, and low levels of proteins related to coagulation/fibrinolysis

A

Venous Thrombosis

60
Q

reduction in platelet number (<150k)

  1. Loss of bone marrow function (from aplastic anemia)
  2. Replacement with malignant cells from bone marrow in leukemia
  3. XRT/drug therapy that suppresses bone marrow function
  4. HIV/CMV
  5. Splenomegaly- excessive pooling of platelets
  6. Drug-induced- aspirin (9-10 days), ibuprofen (half life of drug), heparin
A

Thrombocytopenia

61
Q

high platelets, usually has to be over 1mil to lead to clotting

A

Thrombocythemia

62
Q

• Spontaneous nosebleeds, mouth, GI, menstrual flow
• Presence of normal platelet count
• Types 1 and 2 are mild and require no treatement- usually diagnosed during surgery or dental extraction because of prolonged bleeding
• Tyle 3- severe GIB and joint hemorrhage
• Avoidance of ASAmarked as low levels of factor VIII
3. abnormal platelet aggregation and abnormalities in the way small blood vessels constrict

A

von Willebrand Disease

63
Q

o X-linked recessive disorder, primary affects males
o It is hereditary but 30% of people have no family history, there is possibly a new gene mutation from factor VIII gene
o 90% of people produce insufficient quantities of factor VIII and 10% produce a defective form
o Can be mild-moderate- bleeding doesn’t occur unless theres a trauma
o Severe- bleeding can be spontaneous and severe- can be several times a month
o Clinical manifestations
1. Bleeding of soft tissues, GI, joints (hip, knee, elbow and ankle joints)
• Can occur in joints when child learns to walk
• Acute pain and swelling

A

Hemophilia A

64
Q

_____ can lead to vitamin K deficiency, prothrombin cannot be created and bleeding can occur

A

Liver damage

65
Q

Necessary for synthesis of factors II, VII, IX, and X, prothrombin and protein C

A

Vitamin K

66
Q

Most clotting factors are synthesized in the ____

A

Liver

67
Q

How many molecules of oxygen can be carried by one molecule of hemoglobin?

A

4 (2 alpha chains, 2 beta chains, each able to carry one molecule of oxygen)

68
Q

RBCs (erythrocytes) are made in the _____ and destroyed in the ______.

A

Bone marrow, spleen

69
Q

Erythropoietin (stimulates bone marrow to produce RBCs) is made in the ______.

A

Kidneys

70
Q

RBCs break up in the _____, and their hemoglobin is processed as _______ in the _____.

A

Spleen, bilirubin, liver

71
Q

Measure of hgb content of blood (and normal values)

A

Hemoglobin
13.5-17.5 men
12-16 women

72
Q

Percentage of blood that is taken up by RBCs (and normal values)

A

Hematocrit
41-50 men
36-46 women

73
Q

Provides an index of the rate of RBC production

A

Reticulocyte count

1-2% of RBCs

74
Q

High reticulocyte count is what kind of anemia

A

Hemorrhage/hemolytic anemia

Low levels of RBC stimulates production of RBCs

75
Q

Normal or low retic count is characteristic of what kind of anemia

A

Production/synthesis of RBCs (iron, B12, folate)

76
Q

Reflects the volume (or size) of red cells; most commonly used index for identifying whether a cell is of normal, small, or large size, clinically used to categorize anemia

A

Mean corpuscular volume (MCV)

Normal 87-103 fl/red cell

77
Q

Concentration of hgb in the RBC

A

Mean corpuscular hgb concentration (MCHC)

Normal 31-35 g/dL

78
Q

Four symptoms of anemia

A

Fatigue, weakness, dyspnea and pallor

79
Q

Always check a ______ level for unexplained dementia.

A

Vitamin B12

80
Q

How to differentiate between pernicious (B12) and folic acid anemias

A

Pernicious has neurologic side effects, folic acid deficiency does not

81
Q

Refers to the size of the RBC

A

“Cytic”

82
Q

Refers to the concentration of hgb in the RBC

A

“Chromic”

83
Q

Microcytic/hypochromic anemia resulting from a disturbance of hemoglobin synthesis

A

Iron deficiency anemia

84
Q

Type of anemia c/w disturbance of DNA synthesis, megaloblastic, increased MCV, normal MCHC, with neurologic symptoms

A

Pernicious anemia (Vit B12)

85
Q

Type of anemia c/w disturbance of DNA synthesis, megaloblastic, high MCV, normal MCHC, absence of neurologic symptoms

A

Folic Acid Deficient Anemia

86
Q

Type of anemia c/w premature destruction of RBCs- normocytic, normochromic, high retic count

A

Hemolytic Anemia

87
Q

Type of hemolytic anemia- defects in RBC membrane, RBCs are shaped in tight sphere, can carry O2 but deformable and damaged by spleen easily, jaundice is main sign, splenectomy is treatment

A

Hereditary spherocytosis

88
Q

Type of hemolytic anemia– autosomal recessive d/o with defective hemoglobin gene (Hgb S)

A

Sick cell anemia

89
Q

Type of hemolytic anemia- makes RBCs more vulnerable to oxidants, causes oxidation of hgb to methemoglobin, which denatures hgb molecule to form Heinz bodies, can be drug-related

A

G6PD disease- inherited enzyme defects

90
Q

Type of hemolytic anemia- agents extrinsic to RBCs like drugs, bacteria, toxins, antibodies, and physical trauma

A

Acquired forms

91
Q

Type of anemia c/w decrease in response to erythropoiesis, not enough erythropoietin produced due to differentiation problems (patients with chronic renal failure, for ex.)

A

Chronic disease anemia

92
Q

Type of anemia where deformed RBC obstructs microcirculation, leading to tissue hypoxia and painful tissue ischemia, premature destruction of RBCs and hemolysis

A

Sickle Cell Anemia

93
Q

Stimuli for sickling of RBCs in Sickle Cell Disease (5)

A

Hypoxia, exposure to cold, stress/anxiety, exertion, and infection (especially bacterial)

94
Q

Abnormally high RBC leading to increased viscosity of the blood (Hct >55%)

A

Polycythemia

95
Q

Type of polycythemia- secondary to loss of plasma without corresponding decrease in RBCs from dehydration, water deprivation, excess use of diuretics and GI losses

A

Relative Polycythemia

96
Q

Type of polycythemia- proliferative disease of pluripotent cells of bone marrow, leading to increased RBC mass and elevated WBC and platelets, increased blood viscosity, more common in men

A

Primary polycythemia (polycythemia vera)

97
Q

Type of polycythemia- physiologic increase in level of erythropoietin as a compensatory response to hypoxia (from living at high altitudes, chronic heart or lung disease, and smoking)

A

Secondary polycythemia

98
Q

Treatment of relative polycythemia

A

Fluids

99
Q

Treatment of primary polycythemia

A

phlebotomy to reduce RBC volume and chemo/XRT to induce bone marrow suppression

100
Q

Treatment of secondary polycythemia

A

Continuous low-flow O2 to relieve palm HTN and polycythemia and delay onset of cor pulmonate

101
Q

Type of anemia c/w bone marrow depression (normocytic/normochromic) resulting in pancytopenia, petechiae and purpura

A

Aplastic Anemia

102
Q

Decrease in O2 content in the body = _____ of RBC production

A

Increase

103
Q

Inherited disorders of hgb synthesis leading to decreased synthesis of either alpha or beta globing chains of HgbA

A

The Thalassemias

104
Q

Present on all cells except RBCs and present antigens only to cytotoxic T cells to kill the infected cell before it can infect other cells

A

Major Histocompatibility Complex (MHC) I Molecules

105
Q

Help the body discriminate between molecules that are native to the body and those that are harmful to the body

A

MHC molecules

106
Q

Cell surface glycoproteins that contain a groove that interacts with T cytotoxic cells and activate them when presented with a foreign antigen peptide

A

MHC I Complex

Advanced Pathophysiology (4 decks)

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