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N339 > N339 Exam 2 from Fall cohort > Flashcards

N339 Exam 2 from Fall cohort Flashcards

1
Q

What do fibroblasts do?

A

Synthesize collagen and form new connective tissue

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2
Q

What are systemic manifestations of inflammation?

A

Fever; neutrophilia, lethargy, muscle catabolism

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3
Q

What is the erythrocyte sedimentation rate indicative of?

A

Presence of inflammation

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4
Q

When does autoimmunity occur?

A

When the immune system recognizes the own person’s cells as foreign and an immune system response is initiated

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5
Q

What are three factors that are involved in autoimmunity?

A

Gender
Genetic factors
Environmental factors

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6
Q

What is the mechanism for type 1 reaction?

A

IgE mediated

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7
Q

What are examples for mechanisms for type 1 reaction?

A

Hay fever, asthma, anaphylaxis

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8
Q

What is the mechanism for type II reaction?

A

IgG and IgM

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9
Q

What are examples for mechanisms for type II reaction?

A

Autoimmune hemolytic anemia; hemolytic disease of newborn; Goodpasture disease
Myasthenia Gravis

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10
Q

What are the mechanisms for type III reaction?

A

IgG, IgM, IgA

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11
Q

What are examples for mechanisms for type III reaction?

A

Lupus, arthritis

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12
Q

What are the mechanisms for type IV reaction?

A

T lymphocytes release cytokines and produce T-cell mediated cytotoxicity

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13
Q

In a type I reaction, what detects the antigens?

A

CD4-T cells

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14
Q

What occurs during a type I reaction?

A

Release of histamine
Release of membrane phospholipids
Release cytokines which recruit and activate other inflammatory cells

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15
Q

Is anaphylaxis a systematic or localized response?

A

Systematic response

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16
Q

What does anaphylaxis cause in relation to blood pressure?

A

Drop in BP and vasodilatation

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17
Q

What medications can cause human anaphylaxis?

A

Penicillin, radiographic contrast media, aspirin

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18
Q

What biological agents cause anaphylaxis?

A

Insulin, vaccines, local anesthetics, insect stings

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19
Q

What foods cause human anaphylaxis?

A

Nuts, shellfish, eggs, strawberries

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20
Q

In type II (cytotoxic hypersensitivity reaction), describe three mechanisms by which the cell destructs?

A

Direct cell destruction

Activation of complement can cause membrane lysis OR opsonization and phagocytosis

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21
Q

What is opsonization?

A

The coating of cells with complement; coating enhances phagocytosis

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22
Q

What does acetylcholine do?

A

Activates muscle contraction

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23
Q

What occurs in myasthenia gravis?

A

Acetylcholine cannot be received by muscle due to the antibodies blocking the receptors.

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24
Q

Name three diseases associated with type II hypersensitive.

A

Type 1 Diabetes
Myasthenia gravis
Graves disease

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25
Q

What occurs in Type III complex mediated hypersensitivy?

A

Antibodies bind to antigens and then they fall to the cell walls which initiate inflammatory response and cells will migrate to complement and destroy cell wall

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26
Q

What do antigen presenting cells synthesize?

A

T lymphocytes

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27
Q

In type IV (delayed hypersensitivy), how do the T lymphocytes react?

A

Either kills cells directly or release cytokines

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28
Q

Examples of type IV reaction?

A

TB; poison ivy

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29
Q

What are histoplasmosis and coccidiomycosis due to?

A

Fungal spores

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30
Q

What granulomatous disease is transmitted from animals?

A

Brucellosi

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31
Q

How is tularemia transmitted?

A

Rabbits, hares, ticks, flies

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32
Q

What is severe combined immunodeficiency disorder due to?

A

The failure of white blood cells to develop and there are no B or T lymphocytes

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33
Q

What does the lack of B/T lymphocytes indicate?

A

No immune response

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34
Q

What is DiGeorge syndrome?

A

Due to partial or total loss of thymus

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35
Q

What does a protein or general caloric deficiency do to the production of T lymphocytes?

A

T lymphocytes decreased

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36
Q

What are examples of secondary immunodeficiency disorders?

A

Severe burns; severe trauma; sickle cell anemia; malignancies and severe infection

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37
Q

What do lymphoid stem cells give rise to?

A

NK/B/T cells

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38
Q

What do T-cells function as?

A

Antigen presenting cells

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39
Q

What do Myeloid Stem Cells give rise to?

A

Neutrophil (Granulocytic Leukemia)
Monocyte (Monocytic Leukemia)
RBC (PV/Erythroid Leukemia)
Megakaryocyte (Essential thombrocythemia/megakaryocytic leukemia)

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40
Q

Where do lymphoid cells begin development?

A

Bone marrow

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41
Q

What are common manifestations of hematoligic malignancies?

A 
Anemia
Thrombocytopenia
Leukopenia
Pain
Infection
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42
Q

What is epistaxis and why does it happen?

A

Nose bleed

Thrombocytopenia

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43
Q

Acute Leukemia Age Range?

A

All ages

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44
Q

Chronic Leukemia Age Range?

A

Adult

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45
Q

What is the clinical onset of acute leukemia?

A

Sudden

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46
Q

What is the clinical onset of chronic leukemia?

A

Insidious

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47
Q

What is the course of untreated disease in acute leukemia?

A

Weeks to month

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48
Q

What is the course of untreated disease in chronic leukemia?

A

Months to years

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49
Q

What are the predominant cells for acute leukemia?

A

Blasts, some mature forms

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50
Q

What are the predominant cells for chronic leukemia?

A

Months to years

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51
Q

How severe is the anemia/thrombocytopenia in acute leukemia?

A

Mild-severe

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52
Q

How severe is the anemia/thrombocytopenia in chronic leukemia?

A

Mild

53
Q

What is the white blood cell count like in acute leukemia?

A

Variable

54
Q

What is the white blood cell count like in chronic leukemia?

A

Increased

55
Q

What is the age onset and what is exhibited in chronic myeloid leukemia?

A

Average age onset is 40-50 years

Majority of cases exhibit malignant granulocytes that carry Philadelphia chromosome

56
Q

What is the age onset and what is exhibited in acute myeloid leukemia?

A

Median age is 64 years

Causes bone pain, anemia, thrombocytopenia, an increased susceptibility to infection

57
Q

What is a neoplasm?

A

Benign or malignant growth

58
Q

What lymphoid neoplasm is often asymptomatic and has a malignant b-cell precursor?

A
  • Chronic Lymphoid Leukemia
59
Q

What lymphoid neoplasm is primary a disorder of children? What is the peak age?

A
  • Acute Lymphoblastic Leukemia/Lymphoma

- Peak age is 3-7 years old

60
Q

What is a rare, chronic type of leukemia?

A
  • Hairy cell leukemia
61
Q

What is the median age of presentation and gender incidence?

A
  • 55 years old; higher incidence in men
62
Q

What lymphoid neoplasm is due to a mutation of mature plasma cells that occurs primary in adults?

A
  • Plasma Cell Myeloma (multiple myeloma)
63
Q

What is the bone breakdown/lysis caused by in plasma cell myeloma?

A
  • osteoclasts cause bone breakdown which causes pain
64
Q

What are beence-jones proteins?

A
  • large protein molecules that circulate through the blood and become lodged in the kidney
65
Q

What is the age effected for Hodgkin’s Disease?

A

50% of individuals effected are between 20 and 40 years old

66
Q

Is the incidence higher in men or women in Hodgkin’s Disease?

A

Higher in men than women

67
Q

Hodgkin’s Disease represents what percent of all malignant lymphomas?

A

30%

68
Q

What is found in the blood work of someone with Hodgkin’s Disease?

A

Reed-Sternberg Cells

69
Q

What cells give rise to Non-Hodgkin’s Disease?

A

B/T/NK cells

70
Q

When does the mutation occur in Non-Hodgkin’s disease?

A

Earlier in cell development

71
Q

Are reed-sternberg cells present in non-hodgkin’s disease?

A

No

72
Q

Upon diagnosis, which type of Lymphoma (Hodgkin/Non Hodgkin) usually metastasizes by the time of diagnosis?

A

Non-hodgkins disease

73
Q

What is the pattern of spread for Hodgkin Disease?

A

Contiguous spread

74
Q

What is the pattern of spread for Non-Hodgkin Disease?

A

Noncontiguous spread

75
Q

Is extranodal involvement common/uncommon in Hodgkin Disease?

A

Uncommon

76
Q

Is extranodal involvement common/uncommon in NonHodgkin disease?

A

Common

77
Q

Where is the site of disease in Hodgkin Disease?

A

Mediastinal involvement common

78
Q

Where is the site of disease for Non Hodgkin Disease?

A

Liver involvement common

Bone marrow involvement common

79
Q

Is the extent of disease localized or unlocalized in Hodgkin Disease?

A

Often localized

80
Q

Is the extent of the disease localized or unlocalized in Non Hodgkin Disease?

A

Rarely localized

81
Q

What two viruses can cause AIDS?

A

HIV type 1 and HIV type 2

82
Q

Which type of HIV is milder and less virulent?

A

HIV type 2

83
Q

What is the hallmark of HIV infection?

A

Defective cell mediated immunity
HIV infects T-cells which causes immunodeficiency
CD4 die off

84
Q

What are modes of transmission for the HIV virus? (And how?)

A 
Sexual transmission (semen/vaginal/cervical secretions) 
Parenteral transmission (via blood/blood products)
Perinatal transmission (in utero, during delivery, breast milk)
Accidental exposure of healthcare workers
85
Q

What does the cell direct in a retrovirus?

A

Immune response

86
Q

What kind of virus is HIV?

A

Retrovirus

87
Q

What kind of virus is HIV?

A

Retrovirus

88
Q

What cell does HIV infect?

A

T-Cell (CD4 Lymphocytes)

89
Q

Once the virus enters the body, what does the t-cell do?

A

Picks up the virus

Presents virus to other t-cells (to helpt hem focus on antigen)

90
Q

What solutions carry HIV but don’t transmit the virus?

A 
Urine
Saliva 
Tears
Cerebral Spinal Fluid 
Feces
Coughing/Sneezing
91
Q

Who is at high risk for HIV (population)?

A 
Bisexual / homosexual males
Intravenous drug users 
Sex partners of high risk groups
Infants born to HIV infected mothers 
Accidently exposed health care workers
92
Q

What is the word for preventive medicine/ “before it happens?

A

Prophylaxis

93
Q

What is given to a person after exposure to the HIV virus?

A

Anti viral medications

94
Q

How does bi-layer viral envelope bind with CD4 cells?

A

The viral envelope has protein receptors on its surface

95
Q

What is binding also referred to as?

A

Fusion

96
Q

After HIV fuses to the membrane, what occurs?

A

Viral RNA is injected into the cytoplasm of the CD4 cell

97
Q

What does the CD4 transform?

A

RNA into DNA

98
Q

What is DNA the roadmap of?

A

Production of proteins of a cell

99
Q

What happens when the viral RNA migrates to the membrane?

A

Protease breaks down viral proteins to form viral RNA

Components of the cell membrane create a new shell which forms HIV Viron

100
Q

What does viron mean?

A

Newly formed virus

101
Q

Why does the host cell die?

A

The membrane is being punctured by the production of new virons

102
Q

What is the hallmark of HIV (not infection)?

CD4 die off before infection phase

A

CD4 die off before infection phase

103
Q

Why is HIV not initially detected by tests?

A

Lacks the antibody to the virus that has been formed

104
Q

When do flu like symptoms occur in HIV patients?

A

Serconversion

105
Q

When are antibodies produced?

A

During seroconversion

106
Q

Where do the antibodies go once in circulation?

A

Some go to hypothalamus

Some act as pyrogen (molecules that cause fever)

107
Q

What happens after the initial symptoms? There is a period of what?

A

Dormancy

108
Q

How long does it take for serconversion to HIV+ take place?

A

Usually occurs between 3 and 6 months

109
Q

What is an opportunistic infection?

A

Organisms have a greater chance of multiplying if the immune system is compromised

110
Q

When are you considered to have AIDS?

A

When the CD4 cell count is less than 200 cells per microliter

111
Q

What are systemic manifestations? (basic definition)

A

Manifestations that occur throughout the body

112
Q

What is the most common/significant systemic manifestation of AIDS?

A

Cachexia or malnutrition

113
Q

What is a gastrointestional manifestation of AIDS?

A

Chronic diarrhea (opportunistic fungal infection)

114
Q

What is the most common pulmonary manifestation of AIDS?

A

pneumocystis carinii pneumonia (PCP) AKA pneumocystis jiroveci pneumonia (new name change)
Tuberculosis (TB)

115
Q

What are mucocutaneous manifestations of AIDS?

A

Typically consists of rashes and viral/bacterial infection

116
Q

What are three gynecoligcal manifestations of AIDS?

A

Vaginitis (of yeast origin)
Cervical dysplasia (cervical neoplasia)
Pelvic Inflammatory Disease (PID)

117
Q

What are signs of nueroligcal manifestations of AIDS?

A

Encephalopathy – increased intracranial pressure can lead to behavioral/personality/cognitive changes (AIDS Dementia)

118
Q

What are ocular manifestations of AIDS?

A

Retinitis which is caused by cytomegalovirus

119
Q

How does AIDS progress in children versus adults (speed)?

A

Progresses faster

120
Q

Why is there a rapid progression of AIDS in children?

A

Children have underdeveloped immune system

121
Q

What are two major opportunistic infections of AIDS in children?

A

PCP and Chicken Pox (severe)

122
Q

What does the central nervous system involvement look like in children with AIDS?

A

Impaired cognition and impaired motor function

Increased intracranial pressure inhibits proper circuit formations

123
Q

What neoplastic disease are children with AIDS more suspetible to?

A

Kaposi Sarcoma: effects children’s skin and mucous membranes and internal organs

124
Q

What three ‘stages’ are focused in the treatment of HIV?

A

Fusion Inhibitors
Reverse Transcriptase Inhibitors
Protease Inhibitors

125
Q

In the fusion inhibitor stage, what two things occur?

A

Prevents fusion between virus and host cell membrane

Blocks receptors so the virus cannot fuse

126
Q

What occurs during the reverse transcriptase inhibitor phase of HIV treatment?

A

Viral RNA will not convert to DNA and then it cannot function in the cell’s nucleus

127
Q

What occurs in the protease inhibitor stage of HIV treatment?

A

Interrupts formation of new virus at the end of the cell cycle
Inhibits protease which converts proteins to viral proteins

128
Q

What is considered a “cocktail” for HIV?

A

Combination of all three treatment focuses

N339 (7 decks)

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