Brainscape's Knowledge GenomeTM

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


See full index

Physiology > IM > Flashcards

IM Flashcards

1
Q

Healthy immune system functions for: (3)

A
  1. Surveillance of the body
  2. Recognition of foreign material
  3. Destruction of entities deemed to be
    foreign
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

innate/Natural/Non-Specific Immunity:

A

Stimulated by structures common to groups of
related microbes; cannot distinguish between
fine differences of foreign substances.

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

Acquired Immunity:

A 
Very specific response 
to a distinct macromolecule, also has the 
ability to “remember” macromolecule and 
respond more vigorously to the second 
exposure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The two systems influence

each other:

A

Innate
stimulates adaptive;
adaptive utilizes innate
mechanisms.

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

Agranulocytes: (2)

A
  1. Monocytes/Macrophages

2. Lymphocytes

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

Granulocytes (3)

A

1 Neutrophils
2 Eosinophils
3 Basophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

order of prevalence of leukocytes (5)

A 
neutrophils
lymphocytes
monocytes
eosinophils
basophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Leukocytes or White Blood Cells

All are — and are larger and less
numerous (6000–10,000/μL) than
erythrocytes.

A

nucleated

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

Leukocytes or White Blood Cells

The granulocytes are —.

A

polymorphonuclear

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

Acute inflammation is protective; it (3)

A

neutralizes harmful
agents, removes dead tissue and initiates the tissue repair
process.

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

Damaged cells release inflammatory mediators, which (3)

A

stimulate the inflammatory process but they can also injure

normal tissue. The mediators can act locally or systemically.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cardinal Signs of Acute

Inflammation (5)

A 
1. Rubor (Red 
Discoloration)
2. Calor (Heat)
3. Dolor (Pain)
4. Swelling
5. Loss of Function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Phagocytosis (2)

A
  • Non-self or damaged particles are engulfed by cells.

* Essential part of inflammation and acquired immunity.

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

Innate Immunity

Accomplished primarily by neutrophils & macrophages.

A

Macrophages can phagocytize far more & larger material than neutrophils.
Macrophages are already in the tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Innate Immunity

How does a phagocyte recognize its “meal”? (4)

A 
1. Phagocytes contain Toll-Like Receptors (TLRs) that are capable of 
recognizing generic Pathogen-Associated Molecular Patterns 
(PAMPs) and Damage-Associated Molecular Patterns (DAMPs)
2. Rough surface
3. Native substances should 
have protein coats that 
repel phagocytes
4. If a target has an 
immunoglobulin/antibody 
attached to it, then it is 
marked for phagocytosis 
(opsonization)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Interferons (INF)

• Virally-infected cell secrete —.

A

INF

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

Interferons (INF)

Secreted INF cause uninfected
cells to

A

produce enzymes that
inhibit viral replication, which
prevents spread of the virus to
neighboring cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q 
Complement 
System• Consists of --- distinct 
components that are in plasma 
in an inactive form and must be 
cleaved to become active. 
Activated by
A

30
substances on the
surface of microbes.

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

Complement
System

Cascade of reactions leading to: (3)

A

(1) enhancement of inflammation,
(2) opsonization of pathogens,
(3) formation of a Membrane-Attack
Complex (MAC) that lyses
pathogens.

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

Complement
System

Also part of acquired immunity because

A

antibodies can activate the complement

system (Classical Pathway).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Acquired Immunity

A

very specific response to a distinct macromolecule (antigen), also has
the ability to “remember” macromolecule and respond more vigorously
to the second exposure. The process requires activation and
lymphocytes (B and T).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Antigens:

A

Each toxin or type of pathogen
contains one or more specific chemical
compounds in its make up that are different
(antigens). Antigens are molecules capable
of inducing an acquired immune response
by binding to B-cell and T-cell receptors and
the production of antibodies against them.
Antigens are usually surface peptides or
polysaccharides.

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

Antigen:

A

Peptides or
polysaccharide that are part
of a molecule on an
organism.

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

Epitope:

A

Molecular
group on the antigen
that is recognized by
the immune system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Antigen Presenting Cells
(APCs) present Antigens on
their surface via

A

Major
Histocompatability Complex
(MHC) Class II molecules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

APCs bind to and activate

A

T helper cells (CD4).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

T helper (CD4) cells activate
the two branches of Acquired
Immunity:

A
  1. Humoral

2. Cell-Mediated

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

APCs: (3)

A
  • Macrophages
  • Lymphocytes
  • Dendritic cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

• Macrophages

A

ingest the pathogen and
induce an inflammatory response, if
appropriate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

• Dendritic cells

A

ingest the antigen and

migrate to the nearest lymphoid organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Cell-Mediated Immunity

A

Activated T cells (Natural Killer and
Cytotoxic T, CD8) result in killing of
infected cells and stimulation of
phagocytosis of bacteria and fungi.

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

Humoral Immunity

aka Antibody-Mediated

A 
Activated B cells develop into 
Plasma cells that secrete 
Immunoglobulins. The antibodies 
neutralize toxins and viruses and 
enhancing phagocytosis of 
bacteria (opsinization)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Activated T & B cells interact with

pathogens & initiate a response in

A

secondary lymphoid tissues (e.g.
lymph nodes, spleen, nodules
(tonsils, mucosa-associated
lymphoid tissue, etc.)).

34
Q

After activation, T and B Lymphocytes
replicate a tremendous number of times
(= clones) and are secreted into the
lymphatic circulation. From there they

A

cycle through the blood, tissue, and back
to the lymph, working as effector cells to
eliminate the antigen for which they are
activated.

35
Q

Each B cell has ~—
antibodies in its membrane for a
single antigen.

A

100,000

36
Q

MHC Class II:

A

Found on Antigen Presenting Cells (macrophages, dendritic cells, etc.); involved in presenting antigens to T Helper cells for cell mediated immunity

37
Q

MHC Class I:

A

code for markers that display unique characteristics of self and foreign antigens when the cell is infected

38
Q

Antigen Presenting
Cell Membrane
(ex. Macrophage)

Interaction causes (2)

A

activation of the
T cell and
creation of T cell
clones.

39
Q

Cell Membrane of
All Nucleated Cells

Interaction causes

A

destruction of an
infected cell when it
presents a foreign
antigen

40
Q

T Helper Lymphocytes/Cells (CD4 Cells)
Activated by Antigen Presentation via
MHC Class II (4)

A 
1. Growth and proliferation of 
Cytotoxic and Suppressor T 
lymphocytes
2. Growth and proliferation of B 
lymphocytes 
3. Stimulates activation of more T   
Helper Cells 
4. Activation of macrophage system
41
Q
  1. Activation of macrophage system (2)
A 
a. Attract & slow/stop macrophage 
migration away from inflamed 
regions
b. Stimulate more efficient 
phagocytosis
42
Q

Cytotoxic T-Lymphocytes/Cells (CD8 Cells)

Activated by Antigen Presentation via MHC Class I. All nucleated
cells can present antigens to Cytotoxic T Cells because

A 
all cells 
(except RBCs) have MHC I.
43
Q
  1. After binding antigens, Cytotoxic T cells: (2)
A

a. Secrete perforin molecules that punch
holes in the membrane of the target. The
targeted cell will swell and lyse.
b. Release cytotoxic substances (granzymes)
into the target through perforin channels
that stimulate apoptosis

44
Q

After secreting substances, Cytotoxic

Cells can

A

unbind and move on to another

cell

45
Q

Suppressor T Cells (aka Regulatory T cells) (3)

A
  1. Capable of suppressing functions of both cytotoxic
    and helper T cells
  2. May be a separate type of cell, but they may not
    Many T cells may function as suppressors by
    secreting inhibitory cytokines
  3. These cells are very important as they limit the
    immune system’s ability to attack one’s own tissues
    —they add to immune tolerance
46
Q

B cells and the antibodies they secrete create humoral

immunity. (3)

A
  1. B Cells are activated by intact antigens but also by
    activated T helper cells.
  2. When B cells are activated, they enlarge and look
    like lymphoblasts
  3. Some B cells differentiate into plasmablasts which
    later become plasma cells
47
Q

Some B cells differentiate into plasmablasts which

later become plasma cells (3)

A 
a. One plasmablast will produce 500 
plasma cells in 4 days
b. A mature plasma cell can produce 
2000 immunoglobulins/second
c. Immunoglobulins are secreted into the 
lymph and carried into the blood for 
circulation.
48
Q

Fc Region (Constant Portion) determines
(3) The heavy chain also
determines (1)

A

diffusivity through membranes & tissue,
complement attachment, & other biological
properties.

Ig classification.

49
Q

Phagocytes have Fc receptors,
so antibody binding to an antigen
can lead to

A

enhanced phagocytosis (OPSONIZATION).

50
Q

Most abundant Ig in blood; crosses the placenta

A

IgG

51
Q

IgG (7)

A

– Most abundant Ig in blood; crosses the placenta
– Complement activation
– Opsonizes bacteria
– Neutralizes bacterial toxins and viruses
– Antibody-dependent cell-mediated cytotoxicity mediated
by NK cells & macrophages
– Primary antibody in the secondary response
– Mediates Type II (ex. blood transfusion reaction) and III
(ex. Grave’s Disease, Myasthenia Gravis, Lupus)
Hypersensitivity Reactions

52
Q

IgE (3)

A

– Mediates immediate (type I) hypersensitivity reactions
(asthma, hay fever, anaphalysix, food allergies, drug
sensitivity, etc.)
– Defends against parasitic infections
– Activates basophils, mast cells, and eosinophils

53
Q

IgA (3)

A

– Secretory Ig; synthesized by plasma cells in exocrine glands (saliva, tears, saliva, etc.)
– Most abundant Ig in the body (mucosal sites)
– Mucosal immunity and neonatal immunity (transfer via breast milk)

54
Q

IgM (4)

A

– Most potent activator of complement
– Largest of the immunoglobulins
– The first type produced in response to an antigen
– Membrane bound on B (monomer) but can also be
secreted as a pentamer

55
Q

Membrane bound on B (monomer) but can also be
secreted as a pentamer

B cells begin to express (2) when they reach
maturity. Expression of (2) antibodies on their
membrane surface allows the B cell to be able to

A

IgM and IgD
IgM and IgD

respond to
antigens.

56
Q

IgD (1)

A

– Membrane bound; Receptor on B lymphocytes
surface and aids in antigen recognition by B
lymphocytes

57
Q 
After activation by antigen, B cells undergo antibody class switching to produce (3)
antibodies. This allows daughter cells from the same activated B cell to produce
A

IgG, IgA or IgE

different types of
antibodies

58
Q

Mechanisms of
Immunoglobulin
Action (6)

A
  1. Neutralization
  2. Agglutination
  3. Precipitation
  4. Complement Fixation
  5. Opsonization
  6. Activation of NK Cells
59
Q

TOLERANCE (immunologic unresponsiveness to self antigens)
is vital for life and develops during preprocessing of T & B
lymphocytes. (2)

A
  1. Clonal deletion occurs within the fetal thymus & bone
    marrow (central tolerance).
  2. Clonal anergy (peripheral tolerance) is when cells that
    are self-antigenic become non-functional.
60
Q

If SELF tolerance fails =

A

autoimmune disease

61
Q

–% of
autoimmune
diseases occur in
women

A

90

62
Q

skipped
Theories for why immune tolerance
fails… (5)

A 
1. Failure of regulation of self-reactive 
lymphocytes
2. Exposure of T lymphocytes to 
antigens previously sequestered 
from the immune system
3. Molecular mimicry by invading 
pathogens.
4. Modification of self antigens
5. Inappropriate expression of Class II 
MHC Molecules (antigen-presenting 
molecules)
63
Q

skipped

  1. Molecular mimicry by invading
    pathogens. (2)
A 
a. Invading antigens have a similarity to 
self-antigens
b. Occurs in Rheumatic Fever:  
Streptococcal M protein resembles a 
portion of cardiac myosin
64
Q

skipped

Examples of Autoimmune Diseases (8)

A 
• Rheumatic Fever
• Myasthenia Gravis
• Systemic Lupus 
Erythematosus
• Rheumatoid Arthritis
• Sjogren’s Syndrome
• Multiple Sclerosis
• Type I Diabetes
• Graves’ Disease
65
Q

Treatment includes (2)

A

immunosuppression and/or plasmapheresis.

66
Q

mediator: Antibody (IgE)
type:
reaction:

A

I (immediate, anaphylactic)

IgE antibody is induced by allergen, binds to mast cells
and basophils. On succeeding exposures, the allergen
cross-links bound IgE and induces degranulation of mast
cells & basophils. Ex. Allergic and Anaphylactic reactions,
Asthma

67
Q

mediator: Antibody (IgG)
type:
reaction:

A

II (cytotoxic)

Antigens on a cell surface combine with antibody; this
leads to complement-mediated lysis.
Ex. Blood transfusion reactions, Hemolytic disease of the
newborn

68
Q

mediator: Antibody (IgG)
type:
reaction:

A

III (immune complex)

Antigen-antibody immune complexes are deposited in
tissues, complement is activated, and polymorphonuclear
cells are attracted to the site. They release lysosomal
enzymes, causing tissue damage. Ex. Systemic Lupus
Erythematous, Grave’s Disease, Myasthenia Gravis

69
Q

mediator: cell
type:
reaction:

A

IV (delayed)

Helper T lymphocytes sensitized by an antigen release
lymphokines upon second contact with the same antigen.
The lymphokines induce inflammation and activate
macrophages, which, in turn, release various mediators.
Ex. Contact dermatitis

70
Q

Immediate Hypersensitivity Reactions, Type I (5)

A

a. One of the most powerful immune reactions
b. Occurs when IgE stimulates mast cells and
basophils
c. Release of secretory products from mast cell
granules (ex. Histamine) causes:
d. Immediate Hypersensitivity begins within minutes of
antigen introduction
e. There is also a late phase reaction

71
Q

b. Occurs when IgE stimulates mast cells and

basophils (2)

A

• There is an extremely strong attraction between the two
(one mast cell/basophil can bind 500,000 IgEs)
• Mast cells & basophils are most concentrated in the lung,
skin, and GI tract

72
Q

c. Release of secretory products from mast cell

granules (ex. Histamine) causes: (2)

A

• Increases vascular permeability, vasodilation, bronchial and
visceral smooth muscle contraction, salivary and bronchial
secretions, and inflammation
• INCREASES respiratory resistance, DECREASES BP

73
Q

Can be life threatening if severe due to

bronchoconstriction and vasodilation -

A

ANAPHALYXIS

74
Q

d. Immediate Hypersensitivity begins within minutes of

antigen introduction

A

IgE-primed mast cells can remain in the tissues for years. A person retains the capacity to react immediately upon re-exposure. Next time allergen molecules contact the mast cells, they bind across adjacent receptors and stimulate degranulation

75
Q

e. There is also a late phase reaction (2)

A

• Inflammatory infiltration of eosinophils, basophils,
neutrophils, and lymphocytes 2-4 hours after degranulation
of mast cells & basophils
• This stage is capable of damaging tissue

76
Q 
Treatment and Prevention of Type I 
Allergic Response (3)
A
  1. Avoid the allergen
  2. Take drugs that block
    the action of
    lymphocytes, mast
    cells, or chemical
    mediators
  3. Undergo
    desensitization
    therapy
77
Q
  1. Undergo
    desensitization
    therapy (3)
A 
– Controlled injections 
of the antigen
– Works by producing 
IgG antibodies rather 
than IgE
– IgG considered to be 
“blocking antibodies”
78
Q

If you are “allergic”, you produce —
antibodies in response to environmental
allergens

A

IgE

79
Q

If you are “allergic”, you produce IgE
antibodies in response to environmental
allergens (6)

A 
• Hay Fever
• Asthma
• Drug hypersensitivity 
(penicillin)
• Food allergies (most common: 
peanuts, fish, cow milk, eggs, 
shellfish, soybeans)
• Urticaria (hives)
• Anaphylaxis
80
Q

Delayed –Type Hypersensitivity Reactions. Type IV

Hypersensitivity. Mediated by T cells (3)

A 
a.  The pathogen does not 
cause much damage to 
the tissue
b.   Instead, helper and 
cytotoxic T Cells are 
activated (increasingly 
so on repeat exposures)
c. Produce a cell-mediated 
immune reaction, 
stimulating macrophage 
recruitment and 
inflammation
d. Damage is delayed 1-2 
days
• Normally restricted to 
tissue area exposed to 
pathogen

Physiology (53 decks)

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