histo re block 3 Flashcards

1
Q

resp system, where cilia but no goblet?

A

respiratory

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2
Q

Which gland contains both mucous and serous adenomeres? submandible or parotid?

A

submandibular

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3
Q

Which structure is partly encapsulated and covered by nonkeratinized stratified squamous epithelium? 1 of three types of tonsils?

A

Palatine tonsil

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4
Q

nail matrix?

A

Where your fingernails and toenails start to grow. The matrix creates new skin cells, which pushes out the old, dead skin cells to make your nails. As a result, injuries to the nail bed or disorders that affect the matrix can affect your nail growth.

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5
Q

he pulmonary (functional) and bronchial (nutrient) arterial systems enter the lungs separately through the hilus but anastomose into a single system at which level?

A

respiratory bronchiole

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6
Q

anaphylaxis shock? C3a C5a, IgE

A

Anaphylaxis is a type 1 hypersensitivity reaction mediated by binding of the anaphylatoxins C3a and C5a to immunoglobulin E (IgE) on mast cells.

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7
Q

M cells?

A

are epithelial - work with Peyer’s Patches

M cells is that they transport antigens from the lumen to cells of the immune system, thereby initiating an immune response or tolerance.

Peyer’s Patches: These are lymphoid follicles similar in many ways to lymph nodes, located in the mucosa and extending into the submucosa of the small intestine, especially the ileum. In adults, B lymphocytes predominate in Peyer’s patches. Smaller lymphoid nodules can be found throughout the intestinal tract.

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8
Q

B cell activation? CLONAL expansion after approval by T cells (co stim - c28/B7 - c3a? - IL 4, 5?

Create plasma cells (creating antibodies)

Create memory cells

A

B-cells are activated by the binding of antigen to receptors on its cell surface which causes the cell to divide and proliferate. Some stimulated B-cells become plasma cells, which secrete antibodies. Others become long-lived MEMORY B-cells which can be stimulated at a later time to differentiate into plasma cells.

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9
Q

What is the difference between B lymphocytes and T lymphocytes?

A

The main difference between T cells and B cells is that T cells can only recognize viral antigens outside the infected cells whereas B cells can recognize the surface antigens of bacteria and viruses

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10
Q

T cells?

A

Their roles include directly killing infected host cells,

activating other immune cells,

producing cytokines and

regulating the immune response.

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11
Q

Homing mechanism of leukocytes?

C3b

A

chemotaxis (chemoattraction) C3b is potent in opsonization: tagging pathogens, immune complexes (antigen-antibody), and apoptotic cells for phagocytosis

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12
Q

What are chemokines?

a large family of cytokines

A

any of a class of cytokines with functions that include attracting white blood cells to sites of infection.

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13
Q

What calls forth the integrins to bind?

A

C5a

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14
Q

Where is P selectin normally found

A

Weibel Palade bodies in endothelial cells

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15
Q

IL1 - TNF?

A

Cytokines IL-1 and TNF Induce PRODUCTION of E-selectin, ICAM-1, &; VCAM-1 in Endothelial Cells

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16
Q

Margination is caused by what two forces?

C5a

A

mechanical and chemo

c5a, leukotriene B4, bacterial products

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17
Q

do eosinophils cause asthma?

A

Eosinophilic asthma is a form of asthma associated with high levels of a white blood cell called eosinophils. In the United States (U.S.), an estimated 25.7 million people have some form of asthma, and 15 percent of these people have severe asthma that is difficult to control with standard medications.

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18
Q

Leukocyte adhesion Deficiency? LAD?

A

asso w/ recurrent bacterial infections

LAD type 1 - defective synthesis of integrins on leukocytes (CD11/CD18)

LAD type 2 - Lack of sialyl lewis on leukocytes (fecosyl transfease reqd for synthesis of sialylated oligosacchardide ))

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19
Q

Chemotaxis - factors needed for neutrophils?

A

N-formyl-methionine
Leukotriene LTB4
c5a complementary system
chemokines -IL 8

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20
Q

macrophages secrete what once out of blood stream to keep neutrifills homing?

A

TNFL and IL -1 Beta to keep neutriphils homing.

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21
Q

What is leukocyte activation?

A

is mediated through several signaling pathways that interact to produce changes in the affinity of binding protein on the surface of neutrophils, to mobilize the cytoskeleton for chemotaxis and phagocytosis, and ultimately to trigger a respiratory burst and degranulation

22
Q

Neutrophils - ROS?

A

rapidly release a large amount of reactive oxygen species (ROS) into the phagosome to kill ingested bacteria

need oxygen and NADPH

23
Q

4 steps of phagocytosis?

A
  1. recognition and attachment
  2. engulfment
  3. Killing and degradation
  4. degranulation of phagolysososme
24
Q

What are the 3 pathways of complement activation?

A

There are three pathways of complement activation: the classical pathway, which is triggered directly by pathogen or indirectly by antibody binding to the pathogen surface; the MB-lectin pathway; and the alternative pathway, which also provides an amplification loop for the other two pathways.

25
complement system?
With the antigen coated in opsonins, binding to immune cells is greatly enhanced. The function of opsonins is to react with bacteria and make them more susceptible to ingestion by phagocytes. Opsonization of bacteria may occur by three different mechanisms. First, specific antibody alone may act as an opsonin. Opsonization, or enhanced attachment, refers to the antibody molecules IgG and IgE, the complement proteins C3b and C4b, and other opsonins attaching antigens to phagocytes. 2. The Fab portions of the antibody IgG react with epitopes of the antigen
26
epitope?
the part of an antigen molecule to which an antibody attaches itself. light chain?
27
Granulomatous disease - ? X linked recessive disease characterized by absence of NADPH oxidase activity Marked by Phagocytic cells that ingest but do not kill certain microorganisms CATALASE positive (Staph.aureus): ingested but not killed Enzyme deficient & cannot produce H2O2 H2O2 not available as a substrate for MPO MPO-halide system of bacterial killing fails ``` Catalase negative (Streptococci): ingested and killed Streptococcus produce sufficient H2O2 to permit MPO-halide system to proceed ```
failure to produce enough oxygen so killing power reduced NADPH absense - deficient respiratory burst Children with these diseases - recurrent infections.
28
Oxygen burst mechanism Oxygen Burst
H2O2-MPO-halide system
NADPH -> superoxide -> hydrogen peroxide -> halide -> MPO -> Hypochlorous acid Following Phagocytosis, there is Rapid Activation of NADPH oxidase, which oxidizes NADPH and, in the process converts oxygen to Superoxide Superoxide is then converted by spontaneous Dismutation into Hydrogen Peroxide Myeloperoxidase converts hydrogen peroxide to HYPOCHLOROUS acid in the presence of a halide such as Cl¯ HOCl¯ is a powerful Oxidant and antimicrobial agent
29
oxygen independent killing not as strong - various methods
Less Effective than oxygen dependent killing Mediators in Leukocyte Granules: Lysozyme: attacks oligosaccharides in cell membrane Lactoferrin: keeps iron away from bacteria Major Basic Proteins: deal with parasites … Neutrophils, Basophils, Eosinophils Bacterial Permeability Increasing Protein (BPI): activate phospholipase and degrade cell membrane phospholipids Defensins: punch holes in cell membrane
30
Myeloperoxidase (MPO) deficiency? MOST common inherited defect of phagocytes
Common 1:2,000 Autosomal Recessive Absence of MPO in Neutrophils and Monocytes Susceptible to Infections with Candida albicans, Diabetics Can develop Candidiasis Acquired MPO Deficiency May be Seen in Acute Myeloid Leukemia, Myelodysplastic Syndromes, and Lead Poisoning All Bacteria Survive (Catalase +ve and Catalase –ve) An enzyme in leukocytes (white blood cells) that is linked to inflammation and cardiovascular disease. An elevated blood level of the enzyme predicts the early risk of myocardial infarction (heart attack). Abbreviated MPO.
31
Chediak -Higashi 
Syndrome
? albinism, can't form phagolysosomes DEFECT - in MICROTUBULE polymerization
Autosomal Recessive Disease: | Recurrent Infections, Neutropenia,
32
What can call in eoisinophils?
Interleukin 5 - secreted by Th2 cells - Allergen reacts with IgA receptors.
33
IL 12 creates different kind of t helper cells - 4 different kind of helper cells th1 th2 th17 th reg IL1 - ONLY creates Th2 ``` Th 2 - 4 5 6 ```
a Th1 or Th2 helper cell Hot T Bone stEAK TH1 IL2 - t cells IL 3 - bone marrow IF gamma - calls out macrophages, NK, and neutrophils - this cytokine ONLY createed by Th 1 IL2 and 3 - can be produced by all T cells IL 1 - (fever) creates Th2 - 4 ILE - allows CLONAL expansion of B cells into IGE class created from IGM 5 - IGA class created from IGM - clonal expansion to make IGA 6
34
NK cells - HALL MONITOR MHC1 check
can kill in two instances 1. MCH 1 not present on a cell 2. MHC 1 is showing a virus
35
cd 8 - can also kill same cells ARMY
look for MHC1 - and what presenting ARMy not activated at all times - they get activated - day 3 - 5
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IL 7
hematopoietic growth factor
37
IL 10
suppresses cell mediated immunity
38
il 12
promotes cell mediated immunity
39
IL 1 - Pyrogen - FIRST - pyromaniac
creates fever
40
IL 2 - strongest
recruits everyone IL3 - bone marrow - b cell proliferation IL 4 IgM to IgE IL 5 IgM to IgA IL 6
41
INF gamma IL 8 - recruits NEUTROPHILS IL 2 / 12 activates NK cells
increases macrophages and NK cells IL8 -
42
what stimulates production of neutrophils? GM- CSR glycoprotein G-CSF is produced by endothelium, macrophages, and a number of other immune cells.
producted by endothelial cells, T cells, fibroblasts, monocytes - stims neutro, eosino, baso, monocytes, dendritic cells LESS potent that G-CSF
43
eiosinophils contain what to kill things? Costocosteriods? reduce eosinophils
Major basic protein,, cathepsin
44
medulla of lymph nodes?
HEV and memory cells
45
interfurons?
if virus infects a cell or macrophage - interfurons alpha, beta, gamma can be generated via IFR in a cell sent to nearby cells telling them to create KINASE that kills virus of the 2nd cell - Gamma - deal w/ macrophages - macrophage creates gamma signaling to other macrophages to proliferate fast, which they do - and can also cause NKs to come kill original cell that has the virus -
46
IgE - lamina propria, lymphatic tissue, RESPIRATORY Fc epsilon weird binding - stem of antigen goes right into other stem parasitic worm (calls in eoisinophils, Major basic protein - kills it) allergies
type 1 hypersensitivity whe IgE binds - causes histamines, proteglandins, leukotrines Ige - alaphylaxis - affects ? leaky blood vessels near bronchi - liquid comes out, swelling (choking bronchi) muscle contractions near bronchi (squeezing bronchi) HARD TO breath for these reasons
47
blood transfusion problem?
type 2 hypersenstivity
48
IgD and IgM
b cell receptor
49
IL 12 - TH1 cells - OKs IL 2, 3, and IF gamma (macrophages) DOESN"T OK B cells IL 1 - Th2 cells - 4/5/6 OKS B cell developement
Interleukin 12 (IL-12) is produced by activated antigen-presenting cells (dendritic cells, macrophages). It promotes the development of Th1 responses and is a powerful inducer of IFNγ production by T and NK cells.
50
Other types of complement system? opsonization?
if stops at C3B - macrophage eats because macrophage has C3b receptors -