Term
| what are langerhans cells? |
|
Definition
|
|
Term
| what supplies the blood to the epidermis? |
|
Definition
|
|
Term
| what are the reticular portions and appendages of the dermis? |
|
Definition
reticular - elastic fibers
glands, follicles, neurovascular.
appendages - Hair - follicles, bulb, erector pili
Glands
sebaceous - sebum production
sweat (eccrine and apocrine |
|
|
Term
| arrector pili - is this a symapthetic or parasympathetic mechanism?? |
|
Definition
|
|
Term
| what is the difference between apocrine and eccrine sweat glands? |
|
Definition
Apocrine (sweat)
hair follicle associated
location/function: pheremone secretion (arms and pubic regions)
Eccrine (sweat)
ductal vs. secretory regions
myoepithelium
function: cooling |
|
|
Term
| describe how sweat glands secrete and then re-absorb sodium? |
|
Definition
| i remember him talking about this and i can't find the slide. look it up in the book. ONLY HAPPENS IN ECCRINE glands |
|
|
Term
| what are the free nerve endings in the dermis? |
|
Definition
pain receptors
mechanoreceptors
thermoreceptors |
|
|
Term
| what are the encapsulated nerve endings in the dermis? |
|
Definition
|
|
Term
| explain the thermoregulatory function of the skin |
|
Definition
Cutaneous and subpapillary plexi
arteriovenous shunts
distribution of blood during variable environments
nutritional vs. thermoregulatory conflicts |
|
|
Term
| what is a burst fracture? fatigue fractures? example? |
|
Definition
high compression forces
runners foot or a compression fracture of a vertebra |
|
|
Term
| what is an avulsion fracture? |
|
Definition
from high tensile forces.
mallet finger from baseball, or fancer's fracture. |
|
|
Term
| what is a nightstick fracture? |
|
Definition
| imagine what would happen if you held up your forearm to defend against being hit by a nightstick. thats a nightstick fracture. |
|
|
Term
| what is a toddler fracture? |
|
Definition
|
|
Term
|
Definition
| F=kx (constant x some displacement) |
|
|
Term
|
Definition
| displacement as a % of original length. |
|
|
Term
|
Definition
| force/area or change in force |
|
|
Term
| in a stres strain curve, which is the X and which is the Y axis? |
|
Definition
| strain is the x axis, stress is the y axis |
|
|
Term
| what is the slope of the line in a stress strain curve? |
|
Definition
|
|
Term
| structural vs material properties |
|
Definition
|
|
Term
| comparing like tissues (ACL vs MCL)on a stress strain curve, you can see differences in STRUCTURAL properties |
|
Definition
|
|
Term
| comparing different tissues (biceps brachii tendon vs ACL) you can see MATERIAL properties |
|
Definition
|
|
Term
| what is the toe region of the curve? |
|
Definition
| this is where we see a disproportionate stress to strain, where we are just straightening out the connective tissue |
|
|
Term
| what is the linear region? |
|
Definition
| also called the elastic region. this is where we see our linear relationship and K (stiffness) is deduced from the slope of this line |
|
|
Term
|
Definition
| load/deformation. slope of a stress/strain curve |
|
|
Term
| what is the yield? ultimate strength? |
|
Definition
| yield is where we get tissue damage, but not failure. so the tissue continues to stretch, but if you stopped pulling, it would not return to its original state. |
|
|
Term
| what is the plastic region? |
|
Definition
| the region between the yield point and the ultimate strength. |
|
|
Term
|
Definition
| is the property of being directionally dependent |
|
|
Term
|
Definition
Elasticity
Materials ability to return to original state (length or shape)
Depends on collagen and elastin content and organization
Viscosity
A fluid property dependent on the proteoglycan and water
composition
Materials resistance to flow
High viscosity = high resistance to deformation |
|
|
Term
| viscosity - the faster you pull, the more deformation you get. |
|
Definition
|
|
Term
|
Definition
| if we hold a prolonged force, eventually the tissue relaxes and you get more deformation. one cause of this is over time the force pushes water out of the tissue, causing more deformation. |
|
|
Term
| what is stress-relaxation? |
|
Definition
| a prolonged hold at a fixed length decreases the load experience by the tissue. |
|
|
Term
| what is strain-rate sensitivity? |
|
Definition
| rapidly loaded tissue can rach a higher peak force |
|
|
Term
|
Definition
Loading and unloading do
not follow the same path
on load-deformation curve
(energy is lost) |
|
|
Term
| what is a ductile material? |
|
Definition
material
undergoes considerable
plastic deformation under
tensile load prior to
failure |
|
|
Term
| what is a brittle material? |
|
Definition
| abscense of any plastic deformation prior to failure. |
|
|
Term
| what is single vs repeated loading? |
|
Definition
microfailures induces with strain into elastic and plastic regions.
repeated loading has reduced yield or ultimate strength, failure point. may elecit adaptation. |
|
|
Term
| what is the SAID principle? |
|
Definition
| specific adaptions to imposed demands. changes in relative level of physical stress cause a predictable adaptive response. |
|
|
Term
|
Definition
| for bone, but same for collagen and elastic tissues. tissues will adapt to the direction of stresses put on them. |
|
|
Term
| what are some potential mechanisms of wolff's law or remodeling of collagenous tissues? |
|
Definition
iezoelectric effect - electric potential created
when collagen fibers in bone slip relative to
one another
microtears/fractures – cause rebound healing responses to strengthen tissue |
|
|
Term
| what are the 5 factors influencing the dynamic response of tissues? |
|
Definition
| mechanical properties, geometry, loading mode, rate of loading, frequency of loading. |
|
|
Term
| How does innate immunity change with age? |
|
Definition
Exterior defenses
◦ thinning skin
◦ decreased acidity of GI tracts
Cellular responses
◦ decreased phagocyte, NK cell
function
◦ decreased basophil
degranulation
Soluble mediators
◦ Reduced interferon production
◦ Increased complement
circulation (compensation?) |
|
|
Term
| what are interferons? how do they work? |
|
Definition
| Interferons (IFNs) are proteins made and released by host cells in response to the presence of pathogens such as viruses, bacteria, parasites or tumor cells. They allow for communication between cells to trigger the protective defenses of the immune system that eradicate pathogens or tumors. |
|
|
Term
| how does acquired immunity change with age? |
|
Definition
ecreased number, function of T cells
decreased secondary antibody responses (50-80%)
regulatory gene mutations
◦ decreased IL, interferon control of T-cell activity
◦ altered apoptosis
◦ decreased nutrition |
|
|
Term
| how does exercise effect immune function? |
|
Definition
Moderate exercise
enhances function
◦ increased number/function of
neutrophils and macrophages
◦ increased lymphocytes, NK
cells (CV, endocrine triggers?)
Intense/prolonged exercise
◦ decreased lymphocyte
number/response, NK cell
function
◦ increased deleterious DNA
oxidation
◦ Cortisol
Increased risk of upper
respiratory infections |
|
|
Term
| how can altered nutritonal status alter the immune system? |
|
Definition
T- cell number/function decreased with caloric, protein
◦ T- and B- cell disruption with decreased Zn |
|
|
Term
| how can medications alter the immune system? |
|
Definition
radiation/chemotherapy
◦ immunosuppresive agents (corticosteroids)
◦ Anesthesia - T-cell depression |
|
|
Term
| how can stress alter the immune system? |
|
Definition
physical trauma/surgery
◦ neuropsychoimmunology |
|
|
Term
| what are some examples of hyperactivity of the immune system? |
|
Definition
| Widespread bacterial infection elevates cytokine production, asthma, transplant rejection |
|
|
Term
| What are some examples of antibodies which attack oneself? |
|
Definition
Occurs with streptococcal infections
◦ Loss of “tolerance” to endogenous antigens – autoimmune
Bypass of helper T-cell tolerance
Molecular mimicry (share similar epitopes)
Polyclonal lymphocyte activation (Endotoxin, EBV)
Imbalance of suppressor/helper function |
|
|
Term
| what are the types of hypersensitivity reactions? |
|
Definition
Type I (allergy/anaphylactic)
◦ Type II (antibody/cytotoxic)
◦ Type III (immune complex)
◦ Type IV (cell-mediated) |
|
|
Term
| how does a type 1 hypersensityivity reaction (allergy/anaphylaxis) work? |
|
Definition
Early phase -allergen (antigen)
interaction with
IgE on mast
cells/basophils
◦ Vasodilation
◦ Vascular leakage
◦ Smooth muscle
spasm
Late phase –
eosinophil/T-cell
recruitment
◦ Mucosal
edema/secretion
◦ Epithelial damage |
|
|
Term
| does eosinophils have IgE? |
|
Definition
|
|
Term
| what is an example of a systemic allergy/anaphylaxis? |
|
Definition
Urtricaria (“hives”), erythema
◦ Increased airway constriction –
asthmatic responses
◦ Vomiting/diarrhea
◦ Massive vasodilation –
anaphylaxis |
|
|
Term
| how does a type 2 hypersensityivity reaction (antobody dependent) work? |
|
Definition
AB formation directed
against target antigens
on cell/tissue surface
Complement dependent
◦ Direct lysis and
opsonization
◦ Transfusion reactions
(also Rh factor)
Antibody-dependent
cell mediated
cytotoxicity
Antibody-mediated
cellular dysfunction
◦ myasthenia gravis
◦ Graves disease
(antibodies similar to
TSH) |
|
|
Term
| what are some specific examples of antibody dependent type II? |
|
Definition
| myasthenia gravis (acetylcholine antagonist??), graves disease (antibodies similar to TSH) |
|
|
Term
| how do type III reactions work? immune complex mediated? |
|
Definition
Deposition of antigenantibody (immune
complexes) –
accumulation of PMNs
Antibody-Antigen
immune complexes are
deposited in organs |
|
|
Term
| what are some specific examples of type III (immune complex mediated) reactions? |
|
Definition
Vasculitis (similar to
Raynaud’s)
◦ Glomerulonephritis
◦ arthritis (akin to RA) |
|
|
Term
| how do type IV (cell mediated) hypersensitivity reactions work? |
|
Definition
Principal mechanism of
hypersensitivity
Delayed-type hypersensitivity
◦ Helper T cells – recruit
macrophages
◦ Tuberculin vaccination
◦ Poison Ivy
T-cell medicated cytotoxicity
◦ Perforin molecules
◦ Triggered apoptosis |
|
|
Term
| what are some specific examples of type IV (cell mediated) reactions? |
|
Definition
Type I Diabetes
Mellitus, Multiple Sclerosis,
Rheumatoid Arthritis,
Guilllain-Barre (maybe),
Crohn’s disease |
|
|
Term
| how does transplant rejection work? |
|
Definition
Cell and AB-mediated hypersensitivity of hostdirected against MHC of donor
Cell-mediated
◦ Helper T cells with HLA exposure by MHC II cells
◦ Cytotoxic T cells with direct exposure to foreign MHC I
AB-mediated – Helper T cells stimulate plasma
(clone) B-cell proliferation |
|
|
Term
| what are some specific forms of transplant rejection? |
|
Definition
Acute
◦ Time course: days to weeks with “normal” immune system
◦ Marked vasculitis, edema and tissue injury
T-cells – tissue and vascular injury
B-cells – vascular injury
Hyperacute
◦ Host is pre-sensitized to foreign antigens (MHC I or II)
◦ Rapid (minutes to hours) following transplantation – typically AB
mediated
Chronic - ongoing healing response with continued MHC
rejection
Graft vs. Host Disease
Treatment: MHC I and II matching, immunosuppression |
|
|
Term
|
Definition
Types II, III, IV hypersensitivity reactions
Immune responses directed against self-antigens
◦ Loss of tolerance to own tissue
◦ Self-tolerance usually developed early (clonal deletion)
Tissue, organ-specific (rheumatoid arthritis, MS) to non-specific
(fibromyalgia, SLE)
Etiology/risk factors
◦ genetic component (HLA subtypes)
◦ hormonal (increased in women, hormonal fluctuations)
◦ environmental (toxins, drugs, sunlight)
Pathogenesis
◦ class I MHC recognized by T
C
cells as non-self - Class IV hypersensitivity
◦ development of auto-antibodies |
|
|
Term
| Tell me what you know about lupus! |
|
Definition
Chronic systemic inflammatory autoimmune disease
Immune complex deposition into systemic tissues
◦ Antinuclear antibodies (ANA)
◦ DNA, histone proteins, RNA, centromeres, etc. . .
Continuum of presentation
◦ latent lupus – suggestive of SLE
◦ drug-induced lupus (hydralazine, procainamide)
◦ late-stage lupus - duration > 5 yrs
(renal, vascular, pulmonary, bone involvement) |
|
|
Term
| what is the incidence and what are some exogenous triggers of lupus? |
|
Definition
Incidence
◦ gender and age specific
females (10X greater), esp. between 15-40 yrs.
hormonal influences
◦ genetic influences
increased risk in African, Asian, Native American groups
strong familial link (25% in monozygotic twins)
Exogenous triggers
◦ streptococcal/viral infections
◦ sunlight/ultraviolet light exposure
◦ pharmacological agents (oral contraceptives) |
|
|
Term
| what are some clinical manifestations of lupus? |
|
Definition
Musculoskeletal
◦ arthralgias/arthritis = most common
symptoms
◦ symmetrical to asymmetric joint pain
mild –functionally limiting without
deformation
moderate/severe
ulnar deviation, swan-neck, subluxation
tenosynovitis, tendon rupture
Cutaneous/membranous (increased in
discoid)
◦ skin rash (butterfly) following sunlight
exposure
◦ discoid
raised red, scaling plaques
coin-like appearance
◦ vasculitis
lesions of digits, splinter hemorrhages,
digital gangrene
patchy alopecia (esp. in discoid)
europsychiatric manifestations
◦ antigen and/or cytokine-mediated CNS inflammation
◦ headache, irritability, psychosis, seizures, CVA
Cardiovascular/pulmonary
◦ vasculitis
◦ increased risk of thrombosis
◦ pericarditis, pleuritis
Renal – glomerulonephritis
Anemia
GI symptoms (diarrhea, nausea, vomiting, abdominal
pain) |
|
|
Term
| tell me what you know about rheumatoid arthritis |
|
Definition
type IV, and III. Non-suppurative proliferation
synovitis
◦ Attacks synovial joints and articular
cartilage, eventually bone
◦ IgM autoantibodies (rheumatoid
factors) against IgG receptors/ABs
form complexes
◦ Pannus – proliferating synovium |
|
|
Term
| what is the epidemiology of RA |
|
Definition
Affects about 2 million Americans
(70%+ women)
◦ No environmental link, strong
genetic link |
|
|
Term
| what are some manifestations of RA? |
|
Definition
Symmetrical polyarticular
manifestations
Pannus – proliferating synovium
◦ Fibrosis, calcification
◦ Decreased joint space,
tendon/ligament rupture |
|
|
Term
| what are some classic deformities of RA? |
|
Definition
Swan neck
◦ Ulnar deviation of phalanges
◦ Radial wrist deviation |
|
|
Term
| tuberculosis, what do you know? |
|
Definition
type IV reaction. ycobacterium tuberculosis
6% of deaths worldwide, most common cause of death
from single infectious agent
Controlled in US since 1980s, except for AIDS epidemic;
new cases typically via translocation
Increased incidence in poverty, increased population,
other pathology (diabetes, immunosuppression)
80% of individuals in African/Asian countries TB positive;
1/3 of world population |
|
|
Term
| what is the pathogenesis of tuberculosis? |
|
Definition
Type IV hypersensitivity to tuberculin antigens with
prolonged exposure in unexposed immunocompetent
individuals
Primary response
◦ M. tuberculosis gains entry into macrophage endosomes
◦ Most cases without symptoms/signs; possible flu-like illness
◦ CD4 (T-helper) cells recognize MHC II platform of TB antigen –
secretion of cytokines – 2 fates
Activated macrophages destroy bacteria
Naïve macrophages may be unable to destroy bacteria- multiplication
of infectious agents |
|
|
Term
| how do tuberculosis granulomas form? |
|
Definition
CD4 cells infiltrate an
infectious area (TB), in
delayed-type
hypersensitivity reaction
More macrophages
recruited in next 2-3
weeks
◦ Become epithelioid cells, wall
off infectious area
◦ Can fuse, become giant cells
Hypersensitivity and
increased resistance |
|
|
Term
| what is secondary tuberculosis? |
|
Definition
Reactivation of dormitory
primary lesions or reinfection
Dissemination along airways
– particularly upper lobular
areas |
|
|
Term
|
Definition
| cluster of destinate 4 (t-helper cells) |
|
|
Term
| what are primary vs secondary immunodeficiency diseases? |
|
Definition
| Genetic- vs. disease-related immune compromise |
|
|
Term
| what is Iatrogenic immunodeficiency? |
|
Definition
hospital derived.
cytoxic agents – destroy all cells (immunocompetent)
interference with lymphocyte production
bone marrow suppression
◦ corticosteriods
Anti-inflammatory, long-term immunosuppression
inhibit AB synthesis, T-cell circulation
◦ cyclosporine
Used in organ transplants
Suppresses TH cell development via IL suppression |
|
|
Term
| with is the spectrum of presentation of HIV? |
|
Definition
Asymptomatic HIV positive
◦ Early symptomatic HIV
◦ Advanced HIV (AIDS)/resultant immunosuppression
opportunistic/rare infections
malignancies (previously controlled)
autoimmune disorders (inactivation of T
S
cells?)
mortality- 80% infections |
|
|
Term
| what is the pathogensis of the initial infection of HIV? |
|
Definition
Progressive TH
cell
destruction
(B cell, macrophages)
CD4 receptors serve
as HIV receptor
viral RNA reverse
transcribed to viral
DNA
integrated into host
for replication
eventual cell death |
|
|
Term
| what is the early stage pathogenesis of aids? |
|
Definition
irus-infected cells
◦ migrate to tissue/lymph
◦ very little circulated, antibodies
in 3-6 weeks
CD4 in lymph tissue and
nodes destroyed
◦ asymptomatic
CD4 count > 500 cells/mm3
(normal: 600-1200)
positive for HIV (antibody
detection)
◦ possible virus-like syndrome
upon initial infection |
|
|
Term
| what is the later stage pathogensis of HIV |
|
Definition
Lymph tissues, attack
circulating CD4 cells
Early symptomatic stage
(CD4 = 200-500 cells/mm
3
)
◦ generalized adenopathy
◦ weight loss, fatigue, night
sweats, fever
◦ early neurological syndromes
(HIV encephalopathy)
◦ beginning opportunistic
infections, malignancy
HIV advanced disease
(CD4 < 200 cells/mm^3) |
|
|
Term
| what are some clinical presentations of AIDS? |
|
Definition
Central Nervous System
◦ toxoplasmosis, meningitis, encephalopathy
◦ HIV/AIDS encephalopathy, associated
dementia, motor control disturbances
Peripheral Nervous System
◦ inflammatory poly-, sensory neuropathies
◦ demyelinating disease (GBS?)
Musculoskeletal syndromes
◦ rheumatologic syndromes
inflammatory joint disorders
myositis, polymyositis (symmetrical proximal
weakness)
◦ muscle atrophy (HIV wasting syndrome)
◦ HIV-associated myopathy (similar to proximal
weakness without infection) |
|
|
Term
| what are some opportunistic infections common in AIDS? |
|
Definition
neumocystis pneumonia - severely
immunocompromised
Tuberculosis
◦ previously stable, rising with HIV,
multiple-drug resistant variations
◦ sub-clinical infection in check with
normal immunity
Kaposi’s sarcoma (≤40%)
◦ lesions of trunk and head (reddish,
flat or undulated)
◦ B-cell infection with KS herpes virus
Non-Hodgkin’s lymphoma (3%)
◦ lymphoid neoplasm with extranodal
sites
◦ occurs with KS and low lymphocyte
count |
|
|
Term
| what is the treatment for AIDS? |
|
Definition
Reverse Transcriptase Inhibitors
Protease Inhibitors: Inhibit the viral
proteases, prevent viral maturation
Combination therapy better than
monotherapy.
◦ HAART: Highly Active AntiRetroviral Therapy,
using multiple medications.
◦ CART: Combination AntiRetroviral Therapy.
Monotherapy no longer standard
practice |
|
|
Term
the term epitheliod granuloma accurately describes which of the following?
a. completement factor acting as an opsonin
b. macrophages surrounding an indigestible foreign body
c. multiple antibodies coating an antigen
d. the result of caseous necrosis |
|
Definition
| B. macrophages surrounding an indigestible foreign body. |
|
|
Term
agglutination would occur on the first transfusion if someone with type A- blood was given which of the following:
a. A+
b. A-
c. O+
d. None of the above |
|
Definition
d. none of the above
positve doesnt matter for 1st transfusion. O wouldn't do it because we centrifuge these antibodies out, so only the one's on the cell surface matter |
|
|
