Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Semester 1 > Patho Exam 4-2 > Flashcards

Patho Exam 4-2 Flashcards

1
Q

What mediators are released when a mast cell degranulates ?

A
  • Cytokines (IL4 and TNF-a)
  • Histamine
  • Netrophil chemotactic factor (phagocytosis)
  • Eosinophil chemotactic factor (phagocytosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Common causes of mast cell degranulation

A
  • Physical injury
  • chemical agents (bee stings, venom, etc.)
  • Immunologic (anapalytoxins such as IgE)
  • Activation of TLR’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What attracts a neutrophil to the injury site?

A
  • Bacterial proteins
  • C3a and C5a
  • neutrophil chemotactic factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Roll of neutrophils in inflamation

A
  • Ist phagocyte to arrive (6-12 hrs)

- ingest bacteria, cellular debris and dead cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the main function of NK cells

A

To eliminate cells infected by viruses and cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Two functions of eosinophils

A
  • Primary against parasites
  • main regulator mast cell of the products released by mast cells (keep it isolated to the intended area) by enzymatic degradation of chemical mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the rolls of interleukins?

A
  • alteration of adhesion molecule expression
  • induction of leukocyte chemotaxis
  • proliferation and maturation of leukocytes in bone marrow
  • enhancement or suppression of inflamation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Rolls of interferons?

A

Protection against viruses: INF-a and INF-b are released by macrophages. INF-y is released by T Lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Roll of TNF-a

A

Locally it stimulates endothelial adhesion molecule expression and chemokine production by endothelial cells and macrophages.
Systemically 1. Fever, 2. proinflamatory liver proteins, 3. Muscle wasting and thrombosis (prolonged infection CA), 4. Death by shock of Gram -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What releases TNF-a

A
  • Macrophagres primary

- Mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Roll of chemokines

A
  • Chemotaxis of leukocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What releases chemokines?

A
  • macrophages
  • fibroblasts
  • endothelial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the types of chemokines?

A
  • CC (monocytes, lymphocytes, eosinophils)

- CXC (IL8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which complement fragments are chemotactic for neutrophils?

A
  • C3a and C5a
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which complement fragment is responsible for opsinization. (binds to receptors of phagocytes)

A

C3b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which complement fragments are anaphalytoxins?

A

C3a, C5a and C4a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

complement fragment vasodilates and capillary permeability?

A

C2b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In the alternative pathway C3b is protected by what?

A

Factor H and Factor I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In the alternative pathway C3b binds to what

A

Factor B which is activated by factor D. This forms C3bBb AKA C5 convertase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

The main purpose of the 3 complement pathways is?

A
  • opsonization (C3b)
  • mast cell degranulation (C3a, C5a and C4a)
  • Leukocyte Chemotaxis (C3a les arg, C5a les arg)
  • Cell lysis (C9)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Flow of the plasma kinin cascade

A
    1. Hageman Factor (XII) is activated producing XIIa
    1. XIIa converts prekallikrein into Kallikrein
    1. Kallikrein converts Kinogen into Bradykinin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Tissue factor (extrinsic) pathway is activated when

A

There is damage to the epithelial cells of blood vessels and thromboplastin (Tissue Factor) interacts with XIIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Contact factor (intrinsic) pathway is activated when

A

There is damage to the vessel wall and Hageman factor (XII) CONTACTS the subendothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does plasmin do?

A
  • Degrades fibrin and fibrinogen (clots)
  • Activates the Hageman factor
  • Activate C1. C3 and C5
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Activation of the Hageman factor has what 4 effects?

A
    1. Clotting cascade by activating X1
  • control of clotting by indirectly activating plasmin
  • Activation of the kinin system Hageman is (XIIa)
  • Activation of C1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Where are TLR’s found

A

On cells which encounter pathogens.

  • Mast cells
  • Macrophages
  • Epitheliall cells
  • Neutrophills
  • Dendritic cells
  • Lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Function of PAF

A

Similar to Leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Types of cytokines

A
  • chemokines
  • interleukins
  • lymphokines
  • tumour necrosis factor
  • interferons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Functions of lymphokines

A
  • Promote maturation of monocytes into macrophages.
  • Enhance macrophage migration.
  • Cause chemotaxis.
  • Induce production of lymphokines.
  • Produce lymphotoxins. (TNF-b)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are RANTES (b-chemokine)

A
  • Produced by T cells, endothelial cells, platelets during chronic inflammation.
  • Affects monocytes, NK cells, T cells, basophils, eosinophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Define Epitope

A

The antigenic determinant, the portion of the antigen which is configured for recognition and binding by an antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Define Paratrope

A

The section of the antibody or lymphocyte which matches to an antige’s epitope. AKA the antigen binding site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the membrane associated immunoglobulins on the surface of B Cells in the BCR?

A
  • mIgM

- mIgD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the function of Iga and Igb on a BCR

A

Intracellular signaling which communicates information to the nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the function of the CD3 proteins on the TCR

A

Intracellular communication to the nucleus of the T cell which stimulates differentiation and proliferation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Antigen presentation is the primary roll of what molecules?

A

MHC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What type of molecule is an MHC

A

Glycoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Function of IgG

A
  • 80% of the antibodies in the blood
  • is the most protective against infections
  • can cross the placenta
  • four subclasses of IgG numbered 1-4.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Function of IgM

A
  • large pentamer molecule

- produced first in response to antigen to provide the most rapid antibody response to infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Function of IgA

A

can be divided into two subclasses bound by a J chain

  • IgA1 is found in the blood
  • IgA1 is a monomer
  • IgA2 is found in body secretions.
  • IgA2 is called secretory IgA and is a dimer; it protects against penetration of organisms through mucous membranes
41
Q

Function if IgE

A
  • important in the defense against parasites
  • unfortunately is most often elevated in allergic disorders
  • least common of all the Ig’s
42
Q

Function of IgD

A
  • molecule found on the surface of immature B cells where it functions as an antigen receptor.
43
Q

Which cells are the professional APC’s

A
  • Dendritic cells
  • Macrophages
  • B lymphocytes
    (Dave Mathews Band)
44
Q

Which cells express MHC II cells.

A
  • Dendritic
  • Macrophages
  • B lymphocytes
45
Q

What are the 4 Th cell subsets and their functions

A
  • Th-1 cell - stimulates Tc cells (cellular immunity)
  • Th-2 cells- stimulates B cells (Humoral immunity)
  • Th-17 cells - stimulates inflammation
  • Treg cells - release immunosuppressive cytokines
46
Q

Where do superantigens bind?

A

To the MHC II and TCR’s outside of theire normal binding site.

47
Q

What effects can a SAG have?

A

Over production of inflammatory cytokines as a result of excess activation of T cells leading to

  • Fever
  • Low BP
  • Shock
48
Q

Examples of SAG’s

A
  • toxins of Staph A

- toxins of Strep Pyrogenes

49
Q

A naive B cell expresses which antibody?

A

IgM

50
Q

A mature B cell expresses which antibodies?

A

IgM and IgD

51
Q

How do antibodies directly prevent infection

A

By binding to the virus or bacterial toxin and inhibiting it from binding to its intended target receptor on the host cell.

52
Q

How do antibodies indirectly prevent infection

A

By activating the complement system or by stimulating phagocytosis

53
Q

What are the 3 signals for T cell maturation

A
  1. Antigen binding to CD4 and TCR
  2. Costimulation of CD80 and CD28
  3. Activation of IL 1 receptors
54
Q

Th 1 secretes what? Which does what?

A
  • Secretes INF-y

- Inhibits Th2

55
Q

Th2 secretes what? Which does what?

A
  • Secretes IL 4 and IL 10

- Inhibits Th1 and Th17

56
Q

Define allergy

A

The deleterious (harmful) effects of hypersensitivity to an environmental allergen.

57
Q

Define autoimmunity

A

A disturbance in the immunologic tolerance of self antigens.

58
Q

Define alloimmunuty

A

In immunologic response by an individual to the tissues of another

59
Q

Characteristics of Type I Hypersensitivity reaction

A
  • Mediated by IgE and the products of mast cells
  • Most occur due environmental factors (pollen)
  • Attracts Eosinophils (parasite eaters)
  • Develops immediately
60
Q

Characteristics of a Type II Hypersensitivity reaction

A
  • Tissue specific
  • Symptoms depend on which tissue is targeted
  • Some drugs target specific cells and cause a Type II
  • Can damage healthy tissue
  • Immediate
  • IgG and IgM
61
Q

5 Mechanisms of Type II Hypersensitivity reactions

A
  1. IgG or IgM activation of the complement system
  2. IgG and C3b are opsonis and promote phagocytosis
  3. Neutrophil mediated damage. Atibodies bind, start the complement system, chemotaxis for neutrophils, neutrophils bind to membrane and destroy healthy tissue
  4. ADCC- Antibodies bind to Fc receptors on NK cells
  5. Antibodies bind and block receptors (Graves and Myasthenia Gravis)
62
Q

What does ADCC stand for

A

Antibody Dependent Cellular Cytotoicity

63
Q

Characteristics of Type III Hypersensitivity reactions

A
  • Similar to neutrophil mediated damage in type II
  • Formed by antigen/antibody complexes formed in the blood and deposited later in the tissue or vessel.
  • Activates complement cascade
  • May lead to hypocomplementism
  • Serum Sickness, Raynauds, SLE
  • Immediate
64
Q

Characteristics of Type IV Hypersensitivity Reactions

A
  • Mediated by T lymphocytes (Tc, Th1 and Th17)
  • Th1 and Th17 produce cytokines which recruit macrophages
  • Graft rejections
  • Contact with poison ivy and metals
  • Hashimotos, Arthritis, DM1
  • Tb skin test
65
Q

4 types of Hypersensitivity Reaction

A

I - IgE Mediated
II - Tissue Specific
III - Immune Complex Mediated
IV - Cell Mediated

66
Q

Causes of autoimmune diseases

A
  • Breakdown of the barriers to immunologically privileged sites (Blood/brain, blood/ocular). Damage to one eye can spread may spread self antigens to the other
  • Molecular mimicry - Antigen closely resembles a host cell. Ex. Rheumatic fever after Group A Staph sore throat
  • Neoantigen (Haptens)
  • Forbidden clone - A lymphocyte with self recognition is accidently not deleted
  • Defective peripheral tolerance (deficient T reg cells)
67
Q

Define SLE

A

Systemic Lupus Erythematous. An autoimmune disease in which a large amount of autoantibodies are produced.

68
Q

Autoantibodies produced by SLE target what?

A
  • Nucleic acids (Most common)
  • Erythrocytes
  • coagulation proteins
  • phospholipids
  • lymphocytes
  • platelets
69
Q

2 Examples of Alloimmunity

A
  • Transient Neonatal diseases
  • Transplant rejection
  • Transfusion reactions
70
Q

What is the difference between Primary and Secondary Immune deficiency?

A
  • Primary is congenital

- Secondary is acquired

71
Q

What are the 5 primary immune deficiencies ?

A
  • B-lymphocyte deficiencies
  • T-lymphocyte deficiencies
  • Combined T- and B- lymphocyte deficiencies
  • Complement deficiencies
  • Phagocytic deficiencies
72
Q

Define hypogammaglobulinemia and agammaglobulinemia

A
  • Hypo is less than normal B Lymphocytes

- Agamma is none or almost no B lymphocytes

73
Q

Burton’s agammaglobulinemia

A
  • Burton’s agammaglobulinamia (X linked)
  • mutation on the gene for Burton’s tyrosine kinase
  • No nuclear communication in B Cells
  • B cells do not mature
  • T cells function normally
74
Q

Types of primary B cell deficiencies

A
  • Burton’s agammaglobiulinemia
  • autosomal agammaglobulinemia
  • X linked hyper- IgM syndrome
75
Q

Types of primary T cell deficiency

A
  • DiGeorge Syndrome

- Chronic mucocutaneous candidiasis

76
Q

Types of complement deficiencies

A
  • C3 deficiency most severe
  • MBL deficiency
  • Properdin deficiency
77
Q

Types of Phagocyte deficiency

A
  • Congenital neutropenias - caused by chronic bacterial infections
  • Leukocyte Adhesion deficiencies - results from mutations
  • C3 receptor deficiencies - recurrent bacterial infections
  • Chediak Higashi syndrome - defect in cytoplasmic granules
  • Chronic granulomatous disease
78
Q

Types of secondary immune deficiencies

A
  • Normal physiological conditions
  • Stress
  • Dietary insufficiencies
  • Malignancies
  • Metabolic or genetic disorders
  • Environmental
  • Physical trauma
  • Medical treatments
  • Infections
79
Q

Severe deficits in protein or calorie intake lead to

A
  • Deficiencies in T cell function and numbers.

- Complement activity, neutrophil chemotaxis, bacterial killing depressed

80
Q

Effects of Zinc deficiency

A
  • Profoundly depresses both T and B cell function.

- Zinc required as cofactor

81
Q

Deficiencies in pyridoxine, pantothenic acid, folic acid, vitamin A and E lead to

A

Severe depression in both B and T cell function.

82
Q

Acute Phase of HIV infection

A
  • Symptoms of acute viral infection
  • CD-4 T cell count normal.
  • Serologically negative.
  • Infectious to others in 2 weeks.
83
Q

Window phase of HIV infection

A

May not have antibody, but virus growing.
If Infected by blood:
- Antibody appears within 4-7 weeks.
If Infected by sexual exposure:
- May be seronegative for many months.
- May be infectious to others within 2 weeks

84
Q

Subclinical Phase of HIV infection

A
  • Seropositive for multiple antibodies against HIV-1.
  • Slight, chronic lymphadenopathy.
  • Virus replicating: Viral products released sporadically.
  • CD-4 T cell count decreasing.
85
Q

Intermittent stage of HIV infection

A
  • Early stages of HIV-1.
  • Acute viral infections without opportunistic infections.
  • CD-4 T cell count continues to drop.
  • Viral products released sporadically.
  • May last 10 years.
86
Q

AIDS phase of HIV infection

A
  • CD4/CD8 ratio
87
Q

Symptoms during the asymptomatic phase of HIV/AIDS

A
  • Mild symptoms
  • Night sweats
  • swollen lymph glands
  • diarrhea
  • fatigue
88
Q

Symptoms for seropositive stage of HIV/ AIDS

A
  • Opportunistic infections (Pneumocytis carinii pneumonia).
  • Atypical malignancies (Kaposi sarcoma).
  • Persistent lymphadenopathy.
  • Weight loss.
  • Recurrent fevers.
  • AIDS dementia complex.
89
Q

Definition of transformation

A

The process by which a normal cell becomes a cancer cell

90
Q

Define Anchorage- independence

A

Normal cells must be firmly attached to a surface in order to grow however CA cells can grow while suspended in a soft gel

91
Q

Define Anaplasia

A

Cancer cells do not differentiate into specialized functions. Anaplasia is recognized by a loss of organization and marked increase in nuclear size

92
Q

Define Plemorphic

A

Cancer cells are varying in size and shape compared to normal cells. Benign tumors will retain the ability to produce normal cells. A malignant tumor will rarely produce a normal cell.

93
Q

Define clonal proliferation (expansion)

A

A cancer cell can proliferate faster than its neighboring normal cells due to anchorage independence and lack of contact inhibition

94
Q

What are proto- oncogenes

A

Normal genes that participate in growth regulation such as

  • Growth factors receptors.
  • Transcription factors.
  • Nuclear protein receptors.
  • Cell signaling molecules.
95
Q

What are oncogenes

A

Mutant gene whose altered function or expression results in :

  • Abnormal stimulation of cell division.
  • Proliferation in absence of growth signals.
96
Q

What are tumor suppressor genes

A
  1. Facilitate neoplastic transformation via a cellular recessive model:
    - Loss of function of both alleles.
    - Function opposite proto-oncogenes.
  2. Gate-keeper genes:
    - Directly regulate cell cycle or growth inhibition.
  3. Caretaker genes:
    - Indirectly repair DNA and maintain genomic integrity.
97
Q

Characteristics of Benign tumors

A
  • Grow slowly
  • Well defined capsule
  • not invasive
  • well differentiated (look like the tissue they arose from)
  • low mitotic index (cell division is rare)
  • Do not metastasize
98
Q

Characteristics of malignant tumors

A
  • Grow rapidly
  • Not encapsulated
  • Invade local structure and tissue
  • poorly differentiated (may not be able to determine tissue of origin)
  • Highly mitotic (many dividing cells
  • Can spread distantly (through blood and lymph vessels)

Semester 1 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions