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
Q

complement system?

A

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
Q

epitope?

A

the part of an antigen molecule to which an antibody attaches itself. light chain?

27
Q

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
A

failure to produce enough oxygen so killing power reduced NADPH absense - deficient respiratory burst

Children with these diseases - recurrent infections.

28
Q

Oxygen burst mechanism

Oxygen Burst
H2O2-MPO-halide system

A

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
Q

oxygen independent killing not as strong - various methods

A

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
Q

Myeloperoxidase (MPO) deficiency?

MOST common inherited defect of phagocytes

A

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
Q

Chediak -Higashi 
Syndrome
?

albinism,
can’t form phagolysosomes

DEFECT - in MICROTUBULE polymerization

A

Autosomal Recessive Disease:

Recurrent Infections, Neutropenia,

32
Q

What can call in eoisinophils?

A

Interleukin 5 - secreted by Th2 cells -

Allergen reacts with IgA receptors.

33
Q

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

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
Q

NK cells - HALL MONITOR MHC1 check

A

can kill in two instances

  1. MCH 1 not present on a cell
  2. MHC 1 is showing a virus
35
Q

cd 8 - can also kill same cells

ARMY

A

look for MHC1 - and what presenting

ARMy

not activated at all times - they get activated - day 3 - 5

36
Q

IL 7

A

hematopoietic growth factor

37
Q

IL 10

A

suppresses cell mediated immunity

38
Q

il 12

A

promotes cell mediated immunity

39
Q

IL 1 - Pyrogen - FIRST - pyromaniac

A

creates fever

40
Q

IL 2 - strongest

A

recruits everyone

IL3 - bone marrow - b cell proliferation
IL 4 IgM to IgE
IL 5 IgM to IgA
IL 6

41
Q

INF gamma

IL 8 - recruits NEUTROPHILS

IL 2 / 12 activates NK cells

A

increases macrophages and NK cells

IL8 -

42
Q

what stimulates production of neutrophils? GM- CSR glycoprotein

G-CSF is produced by endothelium, macrophages, and a number of other immune cells.

A

producted by endothelial cells, T cells, fibroblasts, monocytes -

stims neutro, eosino, baso, monocytes, dendritic cells

LESS potent that G-CSF

43
Q

eiosinophils contain what to kill things?

Costocosteriods? reduce eosinophils

A

Major basic protein,, cathepsin

44
Q

medulla of lymph nodes?

A

HEV and memory cells

45
Q

interfurons?

A

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
Q

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

A

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
Q

blood transfusion problem?

A

type 2 hypersenstivity

48
Q

IgD and IgM

A

b cell receptor

49
Q

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

A

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
Q

Other types of complement system? opsonization?

A

if stops at C3B - macrophage eats because macrophage has C3b receptors -