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Pathophysiology > Exam 1 - 2nd Semester > Flashcards

Exam 1 - 2nd Semester Flashcards

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1
Q

Acute Phase response (i.e. systemic inflammation) effects include:

A.An elevation of core body temperature
B.Increased metabolism
C.Increased white blood cell count
D.All of the above

A

D. all of the above

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2
Q

Which of the following serves as the primary intracellular cue for the release of interferon by a virus infected cell?

A.The presence of MHC I
B.The presence of double-stranded RNA
C.The presence of single stranded DNA
D.The presence of intracellular viral protein

A

B.The presence of double-stranded RNA

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3
Q

As part of a systemic inflammatory response, the cytokines: _____, _____, and______ act on the ______ to increase the production of acute phase response proteins such as C-reactive protein and Mannose-binding lecithin.

A.IL-1, IL-6, and TNF- act on the liver
B.IL-1, IL-6, and TNF- act on the spleen
C.IL-12, IL-8, and interferon act on the liver
D.IL-1, IL-6, and interferon act on helper T cells

A

A.IL-1, IL-6, and TNF- act on the liver

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4
Q

Which of the following cytokines when released systemically, in high enough concentrations, is primarily responsible for bringing about a state of septic shock?

A.IL-12
B.IGF-beta
C.interferon-alpha
D.TNF-alpha

A

D.TNF-alpha

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5
Q

The effects of interferon α and β include:

A.Promotes the degradation of viral RNA
B.Increases production of MHC I
C.Activates surrounding NK cells
D.All of the above

A

D.All of the above

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6
Q

Acute phase response proteins such as CRP and MBL contribute to innate immunity by:

A.Activating macrophages
B.Direct phagocytosis
C.Contributing to activation of the Complement System
D.Acting as self-antigens

A

C. Contributing to activation of the Complement System

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7
Q

Which class of MHC is present on all cells (except for erythrocytes) and recognized by CD8 T cells and NK lymphocytes?

A.MHC I
B.MHC II
C. MHC III
D.None of the above

A

A.MHC I

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8
Q

Which of following can lead to chronic inflammation?

A.a superficial traumatic injury
B.elevated blood pressure during intense exercise
C.habitual cigarette smoking
D.eating a meal high in cholesterol

A

C.habitual cigarette smoking

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9
Q

In the process of the generation of clonal diversity (of B and T lymphocytes), successful “clonal deletion” is necessary for the development of:

A.Central Tolerance

B.Autoimmunity

C.Peripheral Tolerance

D.Alloimmunity

A

A.Central Tolerance

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10
Q

Immunoglobulins are secreted into circulation by which of the following cell types?

A.Helper T cells

B.Naïve B lymphocytes

C.Cytotoxic T cells

D.Plasma cells

A

D.Plasma cells

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11
Q

The avidity of antibodies refers to:

A.The strength of the bond between the antibody and the antigen
B.The number of binding sites between the antibody and the antigen
C.The speed with which antibodies are released
D.All of the above

A

B.The number of binding sites between the antibody and the antigen

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12
Q

The clinically designated “grade” of a cancer corresponds to:

A.The cancer’s degree of malignancy/aggressiveness
B.The rate of cell turnover in the tumor
C.The degree of anaplasia observed in the tumor
D.All of the above

A

D.All of the above

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13
Q

Which of the following routes of mutagenesis involves an exogenous source of oncogenes?

A.Gene-environment interactions
B.Inherited cancer genes
C.Direct mutagenesis by oncogenic viruses
D.Mutagenesis by oncogenic bacteria

A

C.Direct mutagenesis by oncogenic viruses

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14
Q

A loss of functional fibronectin is in part responsible for which of the following traits of cancer cells?

A.Mitotic division rate inhibited by tissue cell density

B.Greater cell motility

C.Loss of differentiation

D.Enzyme production

A

B.Greater cell motility

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15
Q

Compared to normal cells, cancer cells:

A.Have a more symmetrical shape
B.Have more amorphous shape with greater intracellular disorganization
C.Are smaller in shape
D.Have a more uniform morphology in tissue

A

B.Have more amorphous shape with greater intracellular disorganization

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16
Q

Which of the following are common characteristics of a malignant tumor?

A.Tumor cells fully encapsulated
B.Homogenous cells that correspond in type and organization to surrounding tissue
C.Expansive growth which displaces surrounding tissue
D.None of the above

A

D.None of the above

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17
Q

Which of the following statements is true about the development of antibiotic resistance?

A.The more wide-spread the use of an antibiotic is, the more resistance to that antibiotic we will observe.
B.Bacteria that develop resistance to an antibiotic can transmit those resistance genes to other bacteria.
C.The development of some degree of resistance is an inevitable consequence of the use of antibiotics.
D.All of the above

A

D.All of the above

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18
Q

A bacterial infection that cannot be treated with antibiotics can lead to:

A.Sepsis
B.Shock/multi-organ failure
C.Death
D.All of the above

A

D.All of the above

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19
Q

In what highly reputable medical journal did Dr. Andrew Wakefield publish his 1998 study suggesting a link between autism and the MMR vaccine?

A.The New England Journal of Medicine
B.The Lancet
C.JAMA
D.None of the above

A

B.The Lancet

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20
Q

Which of the following best describes the demographics of US regions with the highest rates of vaccine non-compliance (voluntary refusal to vaccinate)?

A.Low socio-economic status and poor access to healthcare
B.less likely to have completed higher levels of education
C.higher socio-economic status, highly levels of education completed
D.socially conservative and strictly religious

A

C.higher socio-economic status, highly levels of education completed

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21
Q

Currently in most states across the country parents can gain exception from mandated vaccinations for children attending public schools based on which of the following reasons.

A.Religious beliefs
B.Medical exception - ex immune-compromised or allergy
C.Person beliefs
D.all of the above

A

D.all of the above

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22
Q

Compare and contrast how the CDC VS WHO classify HIV infection.

A

Similarities: Both define HIV infection as including 1) a positive result on a HIV antibody test confirmed by a positive result on a second, different HIV antibody test AND/OR 2) a positive virologic test confirmed by a second virological test.

Differences: CDC case definition also classifies HIV infection based on the absolute CD4 cell count as stage 1 (CD4 cell count >500 cells/microL), 2 (CD4 cell count 200 to 499), or 3 (CD4 cell count

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23
Q

What is the Mode of acquisition for HIV?

A

usually acquired through sexual intercourse, exposure to infected blood, or perinatal transmission

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24
Q

What are the risk factors for HIV transmission?

A 
high viral load
certain sexual behaviors
presence of ulcerative sexually transmitted infections
lack of circumcision
host and genetic factors
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25
Describe the clinical presentation of acute retroviral syndrome.
``` fever lymphadenopathy sore throat rash myalgia/arthralgia headache ``` note: proportion of patients with early HIV infection will be asymptomatic In early HIV infection, the viral RNA level is typically very high (eg, >100,000 copies/mL) and the CD4 cell count can drop transiently
26
What is “Seroconversion”?
the development of detectable antibodies against HIV antigens most HIV-infected patients have documented seroconversion during early infection, ie, within the first six months after infection.
27
What is the “viral set point”?
When the plasma viremia has reached a steady state level by approx. 6 months closely associated with the rate of disease progression in the absence of antiretroviral therapy
28
What defines AIDS (i.e. defining conditions)?
AIDS-defining conditions are opportunistic illnesses that occur more frequently or more severely because of immunosuppression These opportunistic illnesses typically occur when the CD4 cell count has decreased
29
What are “Long-term nonprogressors”?
A minority of HIV infected patients who are not on antiretroviral therapy (ART) do not develop clinical progression and have stable CD4 cell counts and low levels of detectable viremia (
30
What are “Elite Controllers”?
a subset of long-term nonprogressors who have no detectable viremia, even on ultrasensitive diagnostic testing
31
If a pathogen manages to slip past an epithelial border without damage to tissue, what are the first cells that recognize it initiate an inflammatory response?
Macrophages residing in tissue
32
By what mechanism is the inflammatory response triggered?
Macrophages residing in tissue trigger inflammatory response via release of cytokines – IL 1, TNF alpha, IL 6, IL 8, IL 12 IL – activate and/or attract other lymphocytes TNF alpha – potent vasodilator, strongly increases permeability
33
What are the vascular and cellular events of acute inflammation and in what sequence do they occur?
Vascular: - Vasodilation - Increased permeability (redness, heat, edema) - Delayed vascular stasis Cellular: - Chemotaxis (migration of leukocytes to area)
34
What role do Mast Cells play in inflammation?
Reside in highly vascularized tissue at sites of potential infection Immediate response (“degranulation”) Long-term response (“synthesis”)
35
What are the relevant metabolites of Arachidonic Acid in relation to acute inflammation?
Leukotrienes and Prostaglandins
36
What's the function of Leukotrienes
sustain inflammatory reactions (chemotaxis of neutrophils), vasoconstriction, bronchospasm, increased permeability
37
What's the function of Prostaglandins
vasodilation, inhibit or promote platelet aggregation, potentiate edema
38
What is the complement system and what are the 3 possible pathways by which it can be activated?
A group of circulating plasma proteins that enhances the ability of antibodies and phagocytic cells to clear pathogens 3 pathways: 1. Classical – C1 directly or indirectly (through CRP or antibody) binds to pathogen surface 2. MB-lectin – MBL works like CRP (binds to pathogen surface to increase probability of complement activation) 3. Alternative – inactive C3 binds to pathogen surface
39
How does the complement system interact with both innate and acquired immunity?
Part of innate immunity Can be recruited and brought into action by the adaptive immune system In the classical pathway, C1 can bind to an antibody (body has already mounted adaptive response) – example of how adaptive immune system uses complement in a very targeted way
40
What cells function as the antigen-presenting cells?
Macrophages or dendritic cells Less typically – mature but naïve B cells travelling from bone marrow to secondary lymphoid tissue
41
What is the “generation of clonal diversity” with respect to B and T lymphocytes?
The process of developing a “library” of cells capable of responding to any antigen we may encounter  random reorganization of V, C and J genes to create a variety of different B and T cell receptors
42
When does “generation of clonal diversity” occur?
in the places where B and T cells mature – bone marrow and thymus
43
How do the central lymphoid organs ensure that no B or T lymphocytes carrying the self-antigen receptor survives?
Clonal deletion = elimination of auto-reactive B and T cells (cells with receptors to self antigens) Central tolerance – occurs before cells leave bone marrow or thymus
44
What cells in the immune system defend against extracellular pathogens?
Phagocytes (macrophages, dendritic cells, neutrophils), B cells (possible detection, antibody production)
45
What cells in the immune system defend against intracellular pathogens?
Natural killer cells (non-specific) and CD8 T-cells (specific)
46
By what 3 mechanisms do antibodies fight pathogens (i.e. what can they do to fight a bug)?
3 basic strategies: 1. Neutralization (IgG, IgA) 2. Opsonization (IgG) 3. Activation of complement system (IgM)
47
What is the “Acute phase response”? What triggers it?
The systemic inflammatory response to infection, which occurs once infection reaches some critical level IL1, 6 and TNF alpha are released in greater and greater amounts then enter circulation then act on distant tissue (ie. brain, bone marrow, liver) to bring about a variety of responses
48
What are the two acute phase response proteins that we spoke about in class and are their respective functions?
CRP and MBL are produced and released by the liver – act as opsons, increase likelihood that complement system is activated
49
Under what conditions are interferons released? From what cells?
Host cells infected by a virus detect presence of double stranded RNA, and they release interferon alpha and beta
50
What functions do the interferons perform?
- Host cell produces enzymes that degrade viral RNA, blocking production of viral protein - Increase production of MHC 1 (better antigen presentation) - Recruit NK cells (kill virus infected cells, release IF gamma which potentiates IF alpha and beta)
51
When someone is infected with a strain of virus for the first time, what parts of the immune system fight the infection before a T cell response can be mounted?
- NK cells – recognize non self-antigen on MHC 1 - Circulating B cells - Macrophages phagocytize circulating viruses
52
What part of the immune system is a natural defense against cancerous growth?
The NK cells of the adaptive immune system
53
What are the subtypes of T cells?
- CD4 (T-helper cell) - CD8 (cytotoxic T cell) - T regulatory cell
54
What is the function of CD4 (T-helper cell)?
doesn’t directly fight anything, recognizes antigens and activates B or T cell reaction, “gatekeeper” for all adaptive immune responses
55
What is the function of CD8 (cytotoxic T cell)?
operates like NK but with specificity, recognizes and destroys particular abnormal host cells (virus infected) and transformed cancerous cells
56
What is the function of T regulatory cell?
type of helper cell that recognizes attempt to activate inappropriate immune response ie. when CD4 tries to activate autoimmune attack
57
What are the four types of hypersensitivity reactions?
Type 1 – immediate: IgE production of antibodies against a typically non-harmful antigen (allergies) Type 2 – antibody mediated: Circulating IgM/IgG bind to antigen on target cell (autoimmune) Type 3 – immune complex mediated: Circulating antigen-antibody complexes insert themselves in tissue and cause local inflammatory effects (post strep glomerulonephritis) Type 4 – cell mediated: Antigen activation of T cells (graft or transplant, target is typically MHC of donor tissue)
58
The process of inflammation tends to bring about some degree of damage to otherwise healthy local tissue. What cells are responsible for this “collateral damage” ? What inflammatory mediators are responsible?
Neutrophils – first responders that dump ROS into interstitial space, which damages both bacteria and healthy tissue
59
What is “class switching” with respect to an antibody-mediated adaptive immune response? What purpose does it serve?
Switching between IgM and IgG to effectively rid body of pathogen
60
What are “plasma cells” and what role do they play in immunity?
Activated B cells, secrete antibodies
61
Explain a scenario in which a B lymphocyte could act as an antigen-presenting cell.
Mature, naïve B cells may encounter pathogen in circulation when leaving the bone marrow to sit in the lymphatic system
62
Which cytokines are primarily involved in mediating the acute phase response?
IL 1, TNF alpha, IL 6
63
For each cytokine (IL 1, TNF alpha, IL 6) briefly describe the: target organ/tissue and primary effect
IL 1: activates mast cells, vascular effects TNF alpha: potent vasodilator, strongly increases permeability IL 6: helps activate lymphocytes in area and increase antibody production
64
Describe the major differences in an antibody mediated response to a first exposure to an antigen compared to subsequent exposures to the same antigen.
IgM – acute phase IgG – delayed but remain elevated after first encounter Subsequent encounter -->  IgG reacts first and levels in circulation peak rapidly This “hides” the IgM response (feeling sick) because more antigen is “taken up” by IgG and less is available for IgM to bind to
65
What role does IgE play in type I hypersensitivity reaction
Sensitization of mast cells Antigen encountered and engulfed by APC --> presented to CD4 T cell Production of memory cells and plasma cells (which produce IgE) IgE attaches to mast cell --> now sensitized Next time antigen is encountered --> attaches to complementary IgE on mast cell --> degranulation --> release of vasoactive mediators --> vasodilation, increased permeability, etc.
66
What events can initiate a local inflammatory response?
Tissue damage or entry of pathogen Main players – macrophages and mast cells - Injured tissue releases cytokines that activate macrophages - Injury OR activated macrophages (through IL 1) stimulate mast cells to release pro-inflammatory mediators - Macrophages detect/ingest pathogen and release pro-inflammatory mediators
67
What are the Major Histocompatibility Complex molecules?
Self-antigens
68
Which cells possess class I and II MHCs?
I – all cells of your body except for RBCs | II – antigen presenting cells (macrophages, dendritic cells, B cells)
69
what function do class I and II MHCs play in immunity?
Any non-self protein will attach to MHC (virus, malignancy, bacterial antigens) and be presented on the cell membrane Abnormal MHC I killed by NK and/or CD8 cells Abnormal MHC II recognized by CD4 cells to mount adaptive response
70
What are “social control genes” and why are they important?
Social Control Genes are genes that codes for a protein that is someway involved in cell growth, division, or differentiation They are important because they direct, stimulate, inhibit, or regulate: - Cell Division - Cell Differentiation - Cell Growth - DNA repair - Cell mortality (number of times a cell can divide) - Apoptosis
71
What are Tumor-suppressor genes?
limit Normal cell division/ growth or promotes cell differentiation/ cell death ex. BRACA1 and 2
72
What are Proto-oncogenes?
they promote Normal cell division or growth ex. growth factors, cytokines that promote cell division
73
What is meant by the “transformation” of a cell in terms of cancer biology?
Altered growth-proliferation control (on genetic level) Transformation is the mutation of social control gene that results in UNREGULATED growth/division of social control mechanism The transformation of a cell into a cancer cell involves a mutation in a social control gene to form an oncogene.
74
Go over the cell cycle and be comfortable with what is happening in each stage
Beginning phase: G1 (most cells of the body are in this phase) - period of growth before DNA replication then, it moves into S phase (synthesis phase) where it actively replicates the DNA (chromosomes) G2 phase is the period after DNA is duplicated, when it’s making a copy of it’s intracellular material - final phase before cell division M phase (mitosis phase) is when nuclear division happens at the tail end of nuclear division is total cell division and production of 2 cells
75
What role does fibronectin play in normal cells?
In normal cells, cell adhesion molecules like fibronectin anchor cells to each other and to the extracellular matrix and helps maintain the integrity of the tissue —> when a tissue bed reaches an optimal cellular density, it shuts off (density- dependent growth)
76
How is fibronectin changed in cancer cells and what are the consequences of that change?
Cancer cells often lack adhesion molecules like fibronectin, which means the density of the tissue does NOT control their growth, and it also means that cancer cells in a tumor are NOT anchored to one another, making them much more mobile
77
Describe the sequence of events involved normal cell mortality.
Normally, cells can divide (double) about 50-60 times before growth shuts off — Senescence (the number of times the cell can make a copy of itself) Some escape Senescence and keep dividing. Eventually these cells will reach Crisis and start dying off in large numbers
78
Understand the Telomerase idea behind cell immortality.
Normal cells cannot divide indefinitely. The end of their chromosomes are controlled by telomeres. Telomeres get shorter with each division until the cells stop dividing. In cancer cells the telomerase gene is “switched on,” producing an enzyme that rebuilds the telomeres. Thus the cancer cells continue to divide indefinitely.

79
How can a virus cause cancer?
Direct (Insertional) Mutagenesis - most common Indirect Mutagenesis
80
How does Direct (Insertional) Mutagenesis cause cancer through a virus, and what's an example?
a virus infects a tissue bed and insert an oncogene into the cell’s genome that get’s propagated ex. HPV infecting cervical cells
81
How does Indirect Mutagenesis cause cancer through a virus, and what's an example?
the virus infects the person’s body, attacks a tissue bed, and essentially it contributes to a lack of immune regulation that would normally catch the mutation ex. KP sarcoma in AIDS patients - rare form of skin cancer that is caused when someone’s immune system is very weak and no longer regulation cell proliferation of the skin
82
What cancer types (based on body site of origin) would you think are sensitive to circulating sex hormones?
Breast cancer Cervical cancer Prostate cancer Ovarian cancer

Pathophysiology (5 decks)

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