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Host and Defense > Week 10 and 11 > Flashcards

Week 10 and 11 Flashcards

1
Q

True or false… CD8 T cells have repeated activity until inhibited

A

True

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2
Q

True or false… some CD4 T cells have direct effector function and can kill

A

True

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3
Q

Which T cell kills virus-infected cells?

A

CD8 cytotoxic T cells

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4
Q

Which T cell activates infected macrophages and provides help to B cells for antibody production? They target microbes that persist in macrophage vesicles and extracellular bacteria

A

CD4 Th1 cells

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5
Q

Which T cells enhance neutrophil response and promote barrier integrity? They target klebsiella pneumoniae and fungi

A

CD4 Th17 cells

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6
Q

What T cells provide help to B cells for antibody production, especially isotype switching to IgE? They target helminths and parasites.

A

CD4 Th2 cells

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7
Q

Which T cells help B cells with isotype switching and antibody production?

A

TfH cells

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8
Q

Which T cells function to suppress other T cell responses?

A

Treg

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9
Q

True or false… CD8 T cells do not form memory cells

A

False, they do

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10
Q

___ are the most common T cell activator. They must be activated. Presentation occurs in the ___

A

Dendritic cells

Secondary lymphoid organs

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11
Q

How do dendritic cells uptake antigen? Describe their MHC expression and co-stimulation delivery.

A

Antigen uptake - macrophinocytosis and phagocytosis

MHC expression - low on immature dendritic cells, high on dendritic cells in lymphoid tissues

Co stimulation delivery - constitutive by mature, nonphagocytic lymphoid dendritic cells.

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12
Q

Dendritic cells mature through ______. Immature dendritic cells in the peripheral tissues encounter pathogens and are activated by ____. ___ signaling induces ___ and enhances processing of pathogen-derived antigens. ____ directs DC migration into lymphoid tissues and augments expression of co-stimulatory molecules and MHC molecules. The mature DC in T cell zone primes ____.

A

Antigen activation

PAMPS

TLR

CCR7

CCR7

Naive T cells

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13
Q

Antigen presenting cells distribute differently in lymph nodes. Describe where the different cells are found.

A

DCs - T cell areas

Macrophages - all areas

B cells - B cell areas

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14
Q

True or false… cross presentation of antigen via MHC 1 and MHC 2 is critical for CD8 T cell activation

A

True

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15
Q

Circulating naive T cells are exposed to antigen in _____. the naive T cells can get there by two routes. What are they?

A

Lymph nodes (they travel from node to node to survey lots of antigen)

Blood

Afferent lymph coming from an upstream lymph node

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16
Q

T cell activation requires three signals. What are they and what do they cause?

A

T cell receptor - activation

Co-stimulatory molecules - survival signal

Cytokines - differentiation, propagation

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17
Q

Co-stimulatory signals are required for T cell activation. ___ on APCs bind to ____ on T cells.

A

B7

CD28

(This gives a survival signal)

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18
Q

Which cytokine involved in T cell activation gives a propagation/clonal expansion signal?

A

IL-2

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19
Q

Naive T cell TCR activation in the absence of co-stimulation leads to ___

A

Anergy

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20
Q

Activation of T cells causes changes. Name 5 potential changes

A

Differentiation

Clonal expansion

Changes in surface protein expression

Migration to target tissues (lymph nodes or sites of infection/damage)

Effector functions

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21
Q

Resting T cells express a _____-affinity IL-2 receptor. Activated T cells express a ___-affinity IL-2 receptor. IL-2 signals in an ____ fashion.

A

Moderate

High

Autocrine

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22
Q

____ inhibits continued T cell activation and proliferation. Describe how. Why is this important?

A

CTLA-4

CTLA-4 (on T cell) binds B7 (on APC) more strongly than CD28. This will deliver inhibitory signals.

T cells dont die after their effector functions, thus must be inhibited. Binding an APC after activation will lead to inhibition.

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23
Q

What are the two ways naive CD8 T cells can be activated?

A

Dendritic cell sends strong enough signal to induce the CD8 T cell to produce IL-2, to cause it to proliferate and differentiate. Note that costimulatory receptors CD28 and B7 are necessary

Dendritic cells can activate CD4 T cells which will produce IL-2 to cause the CD8 T cell to become activated.

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24
Q

True or false… secondarysignals are necessary for CD8 T cell activation but not for active CD8 T cells to kill

A

True

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25
Q

The only cells that kill via perforin and granzyme are ___ and ___ cells

A

NK

CD8 T cells

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26
Q

Th1 cells are involved in ____ immunity whereas Th2 cells are involved in ___ immunity

A

Cellular

Humoral

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27
Q

Differentiation of T helper cells involves what three things?

A

Cytokine induction

Transcription factors

Effector cytokines

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28
Q

What two cytokines induce differentiation into Th1 cells? What is the function of these cells?

A

IL-12

IFN-gamma

Function: activate macrophages

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29
Q

What three cytokines induce differentiation into Th17 cells? What is the function of these cells?

A

IL-16
TGF-beta
IL-23

Function: enhance neutrophil response

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30
Q

What cytokine induces differentiation into Th2 cells? What is the function of these cells?

A

IL-4

Activate cellular and antibody response to parasites

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31
Q

What two cytokines induce the differentiation into TFH cells? What are these cells’ function?

A

IL-6
IL-21

Activate B cells. Maturation of antibody response.

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32
Q

What cytokine induces differentiation into Treg cells? What is a function of these cells?

A

TGF-beta

Function: suppress other effector T cell function

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33
Q

Th1 cells activate macrophages. What do activated macrophages do? (4 things)

A

Express co-signaling ligands

Kill intracellular pathogens

Release cytokines and antimicrobial effectors

Present antigen

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34
Q

____ T cells form granulomas when pathogen cannot be cleared? What are granulomas?

A

Th1

A compact aggregate of leukocytes that sequester pathogen. Involved in chronic inflammation, may be infectious or no infectious agents, several types of granulomas

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35
Q

True or false… pyrogenic granulomas are true granulomas

A

False

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36
Q

True or false… Th1 cytokines enhance the induced immune response to increase inflammation

A

True

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37
Q

How do Th2 cells promote tissue protection and repair?

A

Recruitment and activation of mast cells and eosinophils

B cell activation (different than Th1)

Cytokine release

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38
Q

True or false… TFH cells activate B cells and induce class switching

A

True

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39
Q

True or false… Treg cells suppresses other T cells, but must be interacting with the same APC in order to do so

A

True

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40
Q

What four things do Treg cells do?

A

Prevent T cell activation in the lymph node

Stops adaptive immune response

Prevents autoimmunity

-TGF beta differentiation

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41
Q

Describe how Th17 and Treg cells regulate mucosal inflammation

A

Th17 is involved in tissue repairs, neutrophil recruitment, antimicrobial peptide production

Treg cells inhibit mucosal inflammation

Persistent Th17 function will result in autoimmunity

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42
Q

What is hypertrophy?

A

Increase in cell size

Atrophy - decrease in cell size

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43
Q

What is hyperplasia?

A

Increase in cell number

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44
Q

What is metaplasia?

A

Replacement of one type of cell with another type

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45
Q

What is dysplasia?

A

Disordered growth

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46
Q

Describe how hypertrophy in the heart can result in ischemia?

A

Blood vessels are more widely dispersed in the heart, limiting the dispersement of blood flow

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47
Q

Atrophy can be caused by…

A 
Lack of hormonal signals 
Loss of innervation
Lack of use
Loss of blood supply 
Starvation
Individual cell death

Note that dementia is atrophy in the brain

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48
Q

What is cachexia?

A

Fatty atrophy

(Starvation)

Fatal at 68% of normal body weight

49
Q

Where is a common place where hyperplasia occurs?

A

Prostate

(Also liver, kidney, breast, endometrium)

Note that hyperplasia and hypertrophy often occurs together

50
Q

Name three examples of metaplasia

A

Smoker’s airways

Cervix

Barrett’s esophagus

51
Q

Define dysplasia

A

Disordered hyperplasia without maturation

Preneoplastic

52
Q

Name three examples of dysplasia

A

Uterine cervix

Bowel in inflammatory bowel disease

Esophagus with Barrett’s

53
Q

What types of cells are most prone to injury? Give examples

A

High metabolic activity (cardiac myocytes, renal tubular cells, hepatocytes)

Rapidly proliferating (testicular germ cells, intestinal epithelium, hematopoietic cells)

54
Q

What are the two degrees of cell injury? Define them and give some examples

A

Reversible - damage not enough to kill cell (toxic liver injury, severe exercise, hypoxia (loss of ATP), anaerobic glycolysis with lactate and acidosis)

Irreversible - apoptosis or necrosis. More severe damage involving holes in membranes, long calcium influx, mitochondria loss

55
Q

True or false… apoptosis is energy-requiring programmed cell death that usually only involves one cell at a time and does not involve inflammation

A

True

56
Q

How does apoptosis work?

A

Caspase cascade is initiated because cytochrome C is released from mitochondria. Cytochrome C activates P53 which will then go to activate the caspase cascade.

57
Q

What is the TdT stain used for?

A

Identifying DNA

58
Q

True or false… apoptosis results in a shriveled cell with a pyknotic nucleus, with peripheral clumping of chromatin

A

True

59
Q

What are the early events of necrosis?

A

Cell membrane disruption, calcium signal depletion, loss of ATP (loss of ions will cause cells to swell)

Cell contents leak and cause acute inflammation.

60
Q

What is gangrene?

A

Necrosis of whole anatomical areas

61
Q

Describe the cellular changes in necrosis

A

Cytoplasm is deeper red (loss of mRNA). Cells swell. Nuclei not basophilic. Hemorrhage, acute inflammation, then chronic inflammation and fibrosis

62
Q

What are the three different types of nuclear changes in cell death? Describe them

A

Nuclear pyknosis - shriveled and dark

Karyolysis - digested, pale nucleus

Karyorrhexis - nuclear fragmentation

63
Q

Name 6 different patterns of necrosis. Describe them

A

Coagulative - with ischemia - makes infarct

Liquefactive - loss of substance - in brain or lung abscess

Fat necrosis - necrosis in fat

Caseous necrosis - necrotizing granulomas - combination of liquefactive and coagulative fungal TB infection

Gangrenous necrosis - necrosis of anatomic area

Fibrinoid necrosis

64
Q

Coagulative necrosis is common in the ___

A

Heart

Forms a scar or thin area - leads to ventricular anuersym

-note that in the last stage of coagulative necrosis, it is fibrous

65
Q

Name some differences between necrosis and apoptosis

A 
Necrosis:
Injury-induced uncoordinated death
Early cell membrane disruption 
Cell swelling 
Cells die in large groups 
Acute inflammation
Always pathological 
Apoptosis:
Programmed cell death
Activation of caspases 
No swelling 
Usually one cell at a time
No inflammation involved
Can be a normal phenomenon
66
Q

What are three brown storage products?

A

Lipofuscin - degraded lipid lysosomes.

Bilirubin - hemoglobin breakdown product

Hemosiderin - iron containing pigment

67
Q

What is hemosiderin?

A

Hemochromatosis. Hereditary iron storage disease

68
Q

What is anthracosis?

A

Carbon pigment

Mostly in or near lungs

(Coal worker’s lung. “I have the black cough. *cough cough” - zoolander)

69
Q

What is the role of macrophages, platelets, lymphocytes, and other blood cells in tissue healing?

A

Make proper cytokines to promote healing (TGF -beta)

Matrix metalloproteinases

Macrophages phagocytose and eliminate foreign material

70
Q

What are the roles of fibroblasts in tissue healing?

A

Make collagen and rest of extracellular matrix

Contractile myofibroblasts shrink wound

71
Q

What are the roles of endothelial and epithelial cells in tissue healing?

A

Endothelial cells - make new blood vessels

Epithelial cells - migrate and proliferate to cover wound or regenerate organ

72
Q

What are the steps in tissue healing?

A

Inflammatory response and clot formation

Fibroblasts, endothelial cells, and others migrate to clot and form granulation tissue and new epithelium

Granulation tissue matures forming a scar with mature vessels and abundant collagen (10% strength at week 1)

Scar matures - collagen remodeling and loss of excess blood vessels (occurs in months to years. ~80% of normal strength at 3 months

73
Q

Repair after an inflammatory process may form a cavity in the ___ or in the ___. In other locations, it may form a scar because…

A

Brain

Lung

The damage is too severe for simple regeneration

74
Q

Typically in tissue healing, ~____% of strength is achieved in the first week. After about three months ~___% of strength is achieved.

A

10

70-80

75
Q

What happens if tissue repair is too much or too little?

A

Too much - hypertrophic scar formation, keloid formation (extends beyond site of injury), Desmond/fibromatosis ( a benign neoplasm)

Too little - infection or mechanical stress

76
Q

What are some things that can lead to too little tissue healing?

A

Steroids, poor perfusion, diabetes, malnutrition (especially vitamin C)

77
Q

What are the three patterns of inflammation? Describe them.

A

Acute - begins almost immediatly, lasts minutes to days. Includes neutrophils, vessels, mast cells

Chronic - begins at least 6 hours (to days) later. Includes lymphocytes, macrophages and plasma cells

Granulomatous - variant of chronic inflammation. Aggregates of epithelium histiocytes/macrophages, giant cells, lymphocytes

Note that mixes of all three of these can occur

78
Q

What are the five clinical signs of inflammation?

A 
Rubor - redness
Tumor - swelling
Calor - warmth
Dolor - pain 
Loss of function
79
Q

What causes the pain in inflammation?

A

PgE2

Bradykinin

Substance p

80
Q

What is exudate

A

Fluid coming from vessels into the site of inflammation. Fluid rich in protein (such as clotting factors, Ig, complement, etc.)

81
Q

Which has a lower specific gravity, exudate or transudate?

A

Transudate (Lower specific gravity, protein, and LDH than exudate)

82
Q

If you have leukocytosis with neutrophilia, what should you suspect?

A

Bacterial infection

83
Q

If you have leukocytosis with lymphocytosis, what should you suspect?

A

Viral infection

84
Q

If you have eosinophilia, what should you suspect?

A

Parasitic infection, autoimmune, or allergic

Causes a type 2 response

85
Q

How many mm of RBCs sink in one hour in a vertical capillary tube, normally?

A

less than 20mm

86
Q

What are the laboratory signs of inflammation?

A

Increased sedimentation rate

Because…

Increased plasma fibrinogen, red cells clump and sink faster

Fibrinogen is an acute phase reactant made in liver

Nonspecific disease indicator

Index of activty of a known disease

87
Q

What are some other acute phase reactants? Describe them.

A

CRP - c reactive protein. Becomes abnormal faster than sedimentation rate. Can increase up to 1000 fold. Mild increases in otherwise healthy subjects indicate risk of atherosclerosis

Procalcitonin - specific for bacterial infection. Can help determine if antibiotics are needed

SAA (serum amyloid A protein)

Ceruloplasmin (copper binding protein)

88
Q

What are the cells involved in chronic inflammation?

A

Lymphocytes (sometimes plasma cells too)

Macrophages

Fibroblasts and new vessels in tissue repair

89
Q

Giant cells are involved with…

A

TB granuloma

90
Q

True or false… granulomas can calcify

A

True

Calcification often develops in areas of necrosis

91
Q

What is a type two immune response?

A

A response that involves Th2 lymphocytes, eosinophils, mast cells and basophils

This is a reaction to parasites, allergies, and allergic-like diseases

92
Q

True or false… basophils are the rarest type of blood cell. Like mast cells, they are coated with IgE, and are involved in allergies and responses to parasitic infection

A

True

93
Q

Is appendicitis acute inflammation or chronic inflammation?

A

Acute

94
Q

True or false… asthma is an allergic-like disease involving a type 2 response

A

True

95
Q

What is the definition of SIRS in kids?

A

Core temp >38.5 or <36C

Tachycardia (> 2 SD above normal for age) or bradycardia (<10th percentile for age)

Mean respiratory rate > 2 SD above normal for age

High or low WBC, or >10% immature neutrophils

96
Q

How is T cell function different in infants?

A

Anti-inflammatory cytokine production diminished

Less Immunoglobulin synthesis (B cells)

Neutrophils differ from adult functional capacity

97
Q

At what months of life are children at an increased risk for serious bacterial infection?

A

0-3 months

98
Q

What is an SBI?

A

Serious bacterial infection

Such as…
Meningitis, bacteremia, UTI, pneumonia, osteomyelitis,

99
Q

____ accounts for most of the SBIs infants within their first 3 months of life

A

UTIs

100
Q

What are the three most common bacterial pathogens of neonatal SBI?

A

Group B streptococcus (S. Agalactiae)

E. Coli (and other gram negative enteric bugs)

Listeria monocytogenes

101
Q

What are the most common viral causes of neonatal sepsis?

A

HSV 1 and 2

VZV

Enteroviruses

Influenza

Adenoviruses

RSV

102
Q

True or false group B strep is alpha hemolytic and are common colonizers of the pharynx

A

False.. it is beta hemolytic and they are not common colonizers of pharynx (they colonize the GI and GU tracts)

103
Q

What are some important virulence factors of group B strep?

A

Pilus-like structures

Alpha C surface protein

Beta-hemolysis/cytolysin

Capsular polysaccharides

104
Q

What are the clinical manifestations of GBS infection? What is the onset for early-onset, late-onset, late, late-onset?

A

Early-onset = <7days

Late-onset = 7-89 days

Late,late-onset = 90+ days

105
Q

Early-onset GBS infection is commonly associated with maternal OB complications, and has the highest morality rate of 5-10%. What are some symptoms of this disease?

A

Respiratory distress, poor feeding, bradycardia, lethargy

106
Q

What is the number one cause of early neonatal morbidity and mortality in the US?

A

GBS

107
Q

Universal screening for GBS occurs in all pregnant women in __ - ___ weeks gestation using a vaginal-rectal specimen.

A

35-37

108
Q

What is the drug of choice for treating neonatal GBS?

A

Penicillin

109
Q

True or false… intrapartum antibiotic prophylaxis (IAP) only reduces early-onset GBS

A

True

110
Q

True or false… listeria monocytogenes has incomplete beta-hemolysis, grows well at refrigerator temps, and has polar flagella, and is a gram positive rod

A

True

111
Q

True or false… it is ok to narrow your antibiotics based on your gram stain

A

False

112
Q

How is early-onset sepsis or late-onset meningitis acquired regarding listeria monocytogenes?

A

Early-onset: aquired in utero. Associated with prematurity

Late-onset meningitis: onset about 2 weeks of age, acquired via birth canal

113
Q

What is the drug of choice for treating neonatal listeria infection? Do cephalosporins work well?

A

Ampicillin (plus gentamicin)

Cephalosporins dont have activity!!!

114
Q

Think ____ with E.coli sepsis

A

Galactosemia

115
Q

What is the best choice for empiric antimicrobial therapy for a febrile neonate?

A

Ampicillin, cefotoxamine, gentamycin

Also note that you use acyclovir for HSV

116
Q

What is the number one case of neonatal conjunctivitis?

A

Chemical irritation from silver nitrate

117
Q

True or false… chlamydia trachomonas is the number one reportable STD in the US. 50% of infants are born to infected mothers. They will either develop conjunctivitis or pneumonia

A

True

118
Q

What is the treatment give to prevent neonatal conjunctivitis?

A

Erythromycin (taken orally, not ocularly!!!)

Host and Defense (17 decks)

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