Pathology Test 2 Lecture 2

Front 1

natural protective mechanisms:
_ macrophages and NK cells
_ mucus, cilia, alveolar macrophages
_ kuppfers cells
gastric acid, bile, enzymes, mucus, normal flora
_ barrier
_ flushing or urine and acidity or urine
_ tears
_ leukocytes
_ macrophages & NK cells
_ macrophages

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Lymph nodes
respiratory
liver
GI system
skin
GU tract
eyes
blood
spleen
connective tissue

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Immune system recognizes __ & distinguishes from __-> develops a specific response to non-self & stores that response in __ for future reference. Responses to that non-self invader in the future are faster & more intense.

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foreign (non-self)
self
memory cells

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First line of defense: __ acts to prevent the entry of pathogens. Born with this immunity

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Innate immunity

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__—reacts the same every time. No memory of type of invader

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Nonspecific

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First line of defense is the __ and its __
Second line of defense is (_) __ !! (same extent no matter how many times the infectious agent is encountered)

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SKIN and its mucosal barrier.
(nonspecific) INFLAMMATION

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__ immunity: Specific and involves memory. Its job is to recognize & destroy foreign invaders. (Bacteria, fungi, parasites)

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acquired

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This type of immunity results when a pathogen gains entry into the body and the body produces a specific response to the invader. __means the next time that pathogen tries to invade, the body remembers it and reacts w/a stronger reaction.

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Acquired immunity x's 2

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2 types of acquired immunity:

1. __ —protection by natural or artificial (vaccine) introduction of an antigen into a responsive host.

2. __ —antibodies or sensitized lymphocytes produced by 1 person are transferred to another. Ex—mom transfers antibodies to infant through breast milk.

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Active
Passive

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Type of acquired immunity: __ Environmental exposure. Usually permanent but may be temporary

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active-natural

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Type of acquired immunity: __Vaccination. Usually permanent but may be temporary

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active - artificial

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Type of acquired immunity: __ Natural contact w/antibody transplacentally OR through colostrum & breast milk Temporary

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passive- natural

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Type of acquired immunity: __ Inoculation of antibody or antitoxin; immune serum globulin. Temporary

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passive - artificial

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Bacteria, viruses, parasites, foreign tissue cells, & large unrecognized proteins are all __

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antigens

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An __ is any foreign substance that does not have the characteristic cell surface marker of THAT individual. (self vs non-self) If non-self, then quick IMMUNE response is initiated.

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Antigen

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__- Subunits of an antigen that elicit an immune response.
These areas protrude from the surface of an antigen & combine with an antibody. Each antigen may display hundreds of __. The more __ displayed, the greater the antigenicity of a substance & the greater the immune response

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epitopes x's 3

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__= bad
__- produced by the body to fight infection
-If they match it is self, if they don’t match it is non-self

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Antigen
Antibody

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factors affecting immune response: 1. Amount of _ introduced
2. _ of introduction
Ex-skin gives a local response
3. Type of __ introduced
(Some are deadly, some are not)
4. __

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antigen
Site
antigen
Host

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_ determine type & strength of response. They allow immune cells to recognize & communicate w/each other

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cell markers

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_ (_) —membrane proteins on the surface of ALL cells that tell if SELF or NON-SELF. These are projections on __. Projections on __ are epitopes.

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Major Histocompatibility Complex (MHC or HLA)
antibodies
antigens

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__are inherited & can predispose or increase susceptibility to certain diseases.
(Such as diseases that affect the joints, endocrine glands, & skin such as RA, Graves disease, & psoriasis.)

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HLA’s

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innate immunity:
__ defenses:
Skin
Eyes
Ears
Nose
Stomach acid
Vagina
Acidic urine
Gastro-duodenal junction (rapid pH change)

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Exterior

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The two principal phagocytes are:
1.
2.
All are part of __ or __

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Neutrophils
Monocytes
WBC’s or leukocytes.

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types of leukocytes:
_ _ _ (all are _)
_ _ (are _)

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Neutrophils
Eosinophils
Basophils
Granulpcytes
Monocytes
Lymphocytes
a granulocytes

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__ Aka polymorphonuclear cells (_)
Derived from _
Increase in response to _ and _
May damage host tissues during _
Dead PMN’s =‘s _

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neutrophils
PMN
bone marrow
infection & inflammation
destruction
pus

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high count of __ you have an infection or inflammation

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neutrophils

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__ Circulate in the blood
When they migrate into tissues, their name changes to __ (large eaters)
After neutrophils kill the invading organism, __ clear up the debris.
Both neutrophils & _ have receptors for antibodies & complement so coating of bugs occurs (mark the invader-code it (called opsinin)). Ex-PB&J

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monocytes
macrophages
macrophages
macrophages

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after phagocytosis: __ serve as antigen-presenting cells to introduce the pathogen to lymphocytes. The _ processes the pathogen and presents the epitope. (projections of the antigen) to HELPER lymphocytes. They recognize the coded invader
This is the immune response

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macrophages x's 2

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These T lymphocytes or HELPER lymphocytes carry microscopic markers located on their surface that identifies them specifically.
_ are the helper cells
_ are cytotoxic T cells (_ T cells)

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t4
t8
killer

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_ T cells turn on Killer cells & B cells
_ T cells kill non-self by insertion of a protein channel
_ T cells limit immune response
_ T cells are activated during initial exposure, can be activated quickly w/re-exposure.

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Helper
Killer
Suppresor
Memory

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The Macrophages help the T cells by secreting a chemical messenger w/many roles known as _.
_ are a type of cytokine; protein released by macrophages, to trigger the immune response.

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Interleukin-1
Interleukins

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interleukins function to:
Increase the _ set point in the hypothalamus- (_,_)
Increase _ in bstem & duodenum to cause_ and _
Stimulate production of _ thus leading to decrease in _ (_-muscle pain & _- joint pain)
Increase synthesis of _ results in destruction of _
KICKS THE _ cells into ACTION

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temperature (fever, pyrexia)
serontonin sleep & nausea
prostaglandins pain threshold
myalgia , arthalgia
collagenases cartilage
T4

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_: Derived from bone marrow
Multiply in both allergic disorders & parasite infestations.
When bugs are too big, _ get into close contact & release their contents of granules to kill the bugs

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eosinophils x's 2

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High content of _- allergic disorder and parasite infestation

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eosinophils

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_- Leukocytes that circulate in the blood & function similarly to mast cells in allergic disorders.

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Basophils

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_ release histamine that dilates blood vessels when released.
Example: bee sting the anaphalactic shock

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Mast cells

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__: Large granular lymphocytes
Function is to KILL viruses, other intracellular microbe-infected cells & tumor cells.
Kill w/o prior sensitization or activation

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NK cells

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high level of __- there is a virus

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NK cells

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(_) _ migrate throughout the body to increase interaction w/antigens.
Think of _ as an antibody churning machine that pumps out antibodies (MADGE).

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b lymphocytes B cells B cells

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_—defends external body surfaces, mucus membrane. Found in saliva, colostrum, urine, seminal fluid, tears, nasal fluids, respiratory, GI & GU secretions.

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IgA

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_—predominates in initial immune response. Found mostly in intravascular compartment.

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IgM

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_—serves mainly as an antigen receptor & may fx in controlling lymphocyte activation or suppression

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IgD

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_—is the major antibacterial & antiviral antibody & is the predominant antibody in the blood.

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IgG

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_—primary for parasitic infections. Also fxs by activating mast cells & releasing histamine in allergic rxns, anaphylaxis, asthma & urticaria-skin condition temperature.

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IgE

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hypersensitivity rxns:
1. _—(immediate) allergies, asthma, analphylaxis. IgE sits on outside of mast cell or basophil, allergen comes into contact & causes IgE to react. If throughout the body, then analphalaxis.
2. _ —cytotoxic. (autoimmune dx). IgM or IgG formed against SELF, specifically on SURFACE of own body. Examples: 1. myasthenia gravis 2. graves disease
3. _—immune complex dzs. Forms antibodies on something floating IN the body, NOT on surface. Antibody attaches to another ANTIBODY, leads to inflammation. Examples: 1. RA 2. Lupus 3. vasculitis (inflimation of the vessels) 4. glomeular nephritis
4. _—NOTHING to do w/B cells, related to T cells & macrophages. The body overreacts to antigen. Example: Allergis reaction to latex

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Type 1
Type II
Type III
Type IV

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twp types of type 4 hypersensitivity:_—antigen processed in macrophage, antigen recognition & T cell activation. Amplification & recruitment of MAC’s & T cells. Damage to area where antigen is present. Ex: poison ivy
_—Target antigens recognition of antigen by T cells, activation of T helper & killer cells. Destruction of target cells & adjacent tissue. Ex: TB

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Delayed
Cell mediated Cytotoxicity

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_ rxns:
Host against graft
Graph against host

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transplant

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Types of Grafts
_- self
_- of the same type of cell tissue from the self
__- from the same species
_- from a different species

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Autograft
Isograft
Allograft
Xenograft

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autoimmune dz
-__
- _-_ —mast cells release histamine all over

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anaphylaxis
Pathogenesis—IgE

Front 49

disease _:
Pathogenesis: considered a Type II hypersensitivity in which Ach receptors on muscle are eliminated by antibodies
s&s: Muscle fatigue, proximal weakness, worse w/exertion
*Respiratory failure w/Progressive resp use (really bad)
Ptosis
Dysarthria
Diploplia
Severe quadriparesis
Bulbar involvement
Alteration in voice quality, dysphagia, nasal regurgitation, choking, difficulty w/mastication

Back 49

myasthenia gravis

Front 50

disease _: or Acute idiopathic Polyneuritis
Incidence: young adults 5-8th decade
Trigger mechanism: infection
Pathogenesis— type II hypersensitivity. Antibody attacks PNS myelin on motor neurons
S&S: Muscular weakness (B progressing from LE to UE to chest & neck)
Diminshed DTR’s
Paresthesias (w/o loss of sensation, with light touch sensation)
Fever, malaise
Nausea
Resp failure
Quadriparesis- some motor loss in all four limbs, then it comes back

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guillian barre syndrome

Front 51

_- loss of motor and sensation
_- loss of sensation and a motor loss but it is not complete
_- some motor loss

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Peralysis
Plesia
paresis

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disease _:

Incidence—dz of young women in childbearing years
Pathogenesis—specific to the organ; inflammation, cellular proliferation, basement membrane abnormalities & Igm, IgG & IgA complexs

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systemic lupus erythematosus

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disease _: Progressive autoimmune dz affecting synovial tissue & joints. has extrarticular manifestations (outside of the joint) involving bone, muscle, eyes, lung, heart, and skin.
Most frequent skin sign is the _, large deposit of collagen, usually found on extensor surfaces such as back of the hand or forearm.
Incidence is 1-2% of adults. Etiology is unknown.
_ factor present in 80%; B cell antibody formed to destroy antibodies.
S & S:
Morning stiffness, anorexia, weight loss, fatigue/malaise, joint involvement (one or more joints), immobility & inflammation (dolor, calor, rubor), muscle atrophy, & subcutaneous nodules.

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RA
rheumatoid nodule
Rheumatoid

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_—neutrophil phagocytises RF complex & eventually DIES in the joint space

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PMN

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with _ there is a thickened synovial memb, hyperplasia of the synovial memb leads to a growth formation

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RA

Front 56

disease _: Incidence—30-65 y/o, men
Are 2-3X more likely than women
Pathogenesis—chronic inflammation @ sites of attachment of cartilage, tendons, & ligaments. HLAB27 test to identify. Low Back Pain!!

Back 56

ankylosing spondylitis

Front 57

_ means the joints fuse. (through chest, ribs, SI joint… anywhere where there is cartilage)

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Ankylosing

Front 58

_ s&s:

Early stages
Low grade fever
Fatigue
Anorexia, wt loss
Anemia
Sacroilitis
Spasm of paravertebral muscles
Intermittent LBP
Advanced stages
Constant LBP
Ankylosis
Muscle wasting in shoulder & pelvis
Loss of lumbar lordosis
Marked kyphosis
Decreased chest expansion
Arthritis
Iritis
Carditis
Pericarditis
Fatigue & wt loss
Low grade fever

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ankylosing spondylitis

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good treatment for ankylosing spondylitis- __ so they have a lot farther to drop down to get worse

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endurance training

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disease _: Incidence—11.9% adults, 7-9% child
Etiology—extrinsic vs intrinsic. Extrinsic—mast cells & IgE react to antigen. Intrinsic—no trigger, over 40 y/o
Pathogenesis—more later in resp system
Prognosis: depends
S&S: Episodes of dyspnea
Prolonged expiration w/increased FEV/FVC
Cough w/w/o sputum production, 5-10 minutes post exercise
Skin retraction (clavicles, rib, sternum)
Tickle in throat & occ. Back of neck
Wheezing
Nostril flaring (advanced)

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asthma

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hypersensitivity rxns:
_—(immediate) allergies, asthma, analphylaxis. IgE sits on outside of mast cell or basophil, allergen comes into contact & causes IgE to react. If throughout the body, then analphalaxis.

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type 1

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hypersensitivity rxns: _ —cytotoxic. (autoimmune dx). IgM or IgG formed against SELF, specifically on SURFACE of own body. Examples: 1. myasthenia gravis 2. graves disease

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type 2

Front 63

hypersensitivity rxns:_—immune complex dzs. Forms antibodies on something floating IN the body, NOT on surface. Antibody attaches to another ANTIBODY, leads to inflammation. Examples: 1. RA 2. Lupus 3. vasculitis (inflimation of the vessels) 4. glomeular nephritis

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type 3

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hypersensitivity rxns: _—NOTHING to do w/B cells, related to T cells & macrophages. The body overreacts to antigen. Example: Allergis reaction to latex

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type 4