Pathologies Related to the Immune System: Test 2 Flashcards
What are the 3 broad groups of cells
innate
adaptive
macrophages
describe innate cells. Examples?
non specifics from birth
i.e. monocytes, neutrophils, eosinophils, basophils, mast cells, natural killer cells
describe adaptive cells
acquired following exposure
remember foreign invaders
i.e. B and T cells or lymphocytes
how MOST vaccines work
describe macrophages and dendritic cells
innate AND adaptive
where do stem cells occur? What do they do?
in bone marrow and blood
they generate immune cells
what are neutrophils
predominately leukocyte or white blood cells
1st cells to arrive
take part in phagocytosis
describe the process of phagocytosis
ingest and kill pathogens and debris
short lived; when they die it forms pus along with the bacteria
a decrease in phagocytosis is the principal cause of susceptibility to infection
describe monocytes and macrophages
long lived cells
monocytes mature into macrophages
filter the pus/bacteria from neutrophils and kill larger pathogens
what are eosinophils
next cells to participate after neutrophils and monocytes/macrophages
handle even larger invading pathogens
release histamines (vasodilator; cause of Redening); basophils and mast cells also release histamines
describe lymphocytes
B lymphocytes- produce antibodies in reaction to antigens or foreign substances
T lymphocytes- stimulate B lymphocytes that directly kill infected host cells
describe natural killer cells
large lymphocytes (distinct from B and T cells)
function is to directly kill cells infected with pathogens (avoiding any prior steps)
NK cells can also activate macrophages
describe the key components of the first line of defense in terms of innate cells (x5)
natural and preventative
they are capable of resolving most threats
have pattern recognition of some pathogens
limited specificity so they may not remember all future invaders
both external and internal defenses
describe the external defenses of innate cells
physical, chemical, and mechanical barriers that limit host penetration- non specific
i.e. skin, mucus, peristalsis, coughing, sneezing, stomach acid, ear wax, tears, saliva
describe internal defenses of innate cells
soluble factors- modify cell behavior and enhance inflammatory response
innate cells and components from birth mentioned earlier
what is the second line of defense
the inflammatory response
describe the vascular response of the second line of defense or “inflammatory response”
activated at time of injury or exposure
series of vascular and cellular activities
possibly start a fever
natural killer cells are released
describe the plasma protein systems of the second line of defense or “inflammatory phase”
clotting to control bleeding
kinin that:
-produces bradykinin for vasodilation and vascular permeability
-activates fibrinolytic system, producing plasmin to lyse clots
-makes debris/pathogen vulnerable to phagocytosis
what is the third line of defense
specific immune system
adaptive immunity
describe the adaptive immunity of the specific immune system
acquired and relative (memory of immune system)
characterized by specificity and memory of a pathogen, B and T cells
days to weeks for a full response
develops throughout the life
responds more efficiently on subsequent exposure (reps/recognition)
describe active immunity
concept of mist vaccinations using a harmless virus to produce a secondary immune response with antibodies and memory cells
describe passive immunity
passing of antibodies through birth/breast feeding but is only temporary due to lack of memory cells
describe cell mediated immunity
not involving antibodies but instead cells like WBCs, B, and T cells that can kill antigens
what are the phases of the immune response
1- recognition phase: pathogen marking
2- amplification phase: producing of army of cells
3- effector phase: antigen removal
4- termination phase: “pull troops” as pathogen is cleared; important to avoid excessive/prolonged immune response
5- memory: generation of long lived B and T lymphocytes that involve both innate and adaptive immune responses
what factors affect immunity
aging
hormonal imbalance
environmental pollution
trauma/illness
inadequate sleep
lack of exercise
stress (excess cortisol)
diet
describe key characteristics that make gut health important for the immune system
all categories of immune cells in the gut (70-80% of all immune cells)
good bacteria/immune response is diminished by SAD, medications (analgesics, antihistamines, and antibiotics), and infections
leaky and porous gut from these factors contributes to many physical/mental conditions (i.e. good things leak out and bad things leak in)
describe how exercise affects age immune system
immune system = enhanced/supressed by ex. depending on intensity
moderate = beneficial
overtraining without adequate recovery can impair immunity (proper diet and sleep are other conclusive factors)
describe what happens with immunodeficiency diseases
absent/depressed immune response due to primary or secondary immunodeficiency
primary = genetic DEFECT involving T cells, B cells or lymphatic tissue
secondary = results from underlying disease or factor that depresses or blocks the immune response (MOST COMMON)
what is AIDS
secondary immunodeficiency
“acquired immunodeficiency syndrome”
massive destruction of the immune system by Human Immunodeficiency Virus (HIV)
incidence/prevalence of AIDS
nearly 40 million worldwide with HIV/AIDS
greatest impact in US with male to male sex and IV drug use
pathogenesis of aids
HIV depletes T lymphocytes along with other immunity cells
HIV has a very high mutation rate
clinical manifestations of AIDS
constitutional S&S
NeuroMSK conditions
-distal peripheral neuropathy
-balance and gain deficits
-myalgia and arthralgia
-bone degradation
-weakness
integumentary breakdown
cardiopulmonary conditions
lipodystrophic syndrome (central fat accumulation in neck and trunk but decrease in extremities)
PT implications for AIDS
exercise unrestricted with usual benefits for initial asymptomatic HIV
more limited with symptomatic and advanced HIV and less beneficial
what is chronic fatigue syndrome
immune dysfunction characterized by unexplained fatigue of more than 4 months that significantly limits ADLs
incidence/risk factors of chronic fatigue syndrome
most common in minority females with lower socioeconomic status
etiology and pathogenesis of chronic fatigue syndrome
immune deficits and or traumatic event may be a trigger
poorly managed stress
abnormal neuroendocrine function
inward focused and introversion personalities
inactivity
clinical signs and symptoms fo chronic fatigue syndrome
varied and often cyclical
constitutional signs and symptoms
overwhelming fatigue
muscle pain/weakness
forgetfulness
hypotension that worsens throughout the day
chronic fatigue syndrome PT implications
lifestyle management for stress, sleep, diet, and activity levels
gentle/graded exercise but gauge physiological distress by vital sign monitoring to mitigate fatigue
what are hypersensitivity disorders
no response on 1st exposure
hypersensitivity occurs on 2nd exposure to antigens formed from 1st exposure
type I or Type II, or type III, or type IV
describe type I hypersensitivity
immediate type
seasonal or food allergy; i.e. bee sting
possible anaphylactic or severe potentially life threatening response that requires immediate action associated with bronchoconstriction
describe type II hypersensitivity
tissue or organ specific
autoimmune condition; tissue and its cell function are diminished
antibody binds to antigen on tissue or cell surface
describe type III hypersensitivity
immune complex mediated
named because antibody binds to antigen and then released into circulation to reach the tissue
systemic lupus erythematosus (SLE) attacks immune tissue throighout the body
tissue but not organ specific so there are potentially wider spread affects
describe type IV hypersensitivity
cell mediated immunity
only hypersensitivity not involving antibodies
T lymphocytes are present and kill target cells it does not recognize
examples:
-graft rejection
-contact allergen like latex
-also includes diseases and cells like Rheumatoid arthritis with all connective tissue, MS with myelin, and diabetes with pancreas cells
overview of autoimmune diseases
body fails to distinguish self from non self
over 60 identified
etiology and risk factors of autoimmune diseases
genetic (single gene not identified; clusters present; gene expression caused by epigenetic)
hormonal (women affected more than men)
environmental (physical or mental)
infections
pathogenesis of autoimmune diseases
immune mechanism attacks self antigens systemically
common signs/symptoms of autoimmune diseases
GI S&S
consittutional S&S
gradual onset
inflammation (persistent with possible acute bouts; local or systemic)
myalgia/arthalgia
swollen lymph nodes
typically affects more than 1 part of body
emotional changes
general PT implications for autoimmune conditions
infection control
exercise prescription
nutritional guidance
sleep health
what implications might be present for PT if a pt is using corticosteroid medications for an autoimmune condition
usually used over prolonged time to suppress immune system response
side effects include:
-sleep/mood changes
-GI irritation
-hyperglycemia
-BONE LOSS
-Fluid retention: can contribute to electrolyte imbalance
-decreased healing potential: can’t expect normal results/timeline
-MOST SERIOUS = increase susceptibility to infection
what are the PT implications of the bone loss symptom of using a corticosteroid
more susceptible to fx, osteoporosis, avascular necrosis, etc
offset ideally with weight bearing and resistance exercise
avoid joint mobilizations
10 most observed autoimmune diseases observed in the US and the area of the body they most affect
1-type I diabetes- foot/ankle
2-Rheumatoid arthritis-hand
3- chrons disease-lumbopelvic
4-systemic lupus erythematosus (SLE)
5-multiple sclerosis- head and neck
6- ulcerative colitis- lumbopelvic
7- Addison’s disease- lumbopelvic
8- celiac disease- lumbopelvic
9- immune thrombocytopenia purport- head and neck
10- sjogre’s syndrome
incidence of lupus and clinical manifestation
primarily young women
more common in minorities
all systems may be involved
possible skin/joint symptoms of lupus
skin lesions = particularly butterfly rash across nose
arthralgia = most common S&S; typically targets the hand, wrist, and knee
other possible signs and symptoms aside form skin/joint symptoms
cardiopulmonary abnormalities
neurological symptoms including headache, irritability and depression as well as cognitive deficits, seizures, neuropathies, and even strokes
urinary with renal disease
circulatory with anemia and amenorrhea
hepatistis may develop
what are the PT implications with lupus
don’t want to add anymore inflammation on top of whats already there
protect w/ bracing or assistive devices
monitor symptoms to maximize movement
gentle/regular exercise (land and aquatic based)
identify triggers and allow self monitoring to watch for exacerbations
** follow fibromyalgia interventions
what is sjogre syndrome
type of spondyloarthropathy or spindyloarthritide
what are spondyloarthropathies or spondyloarthritides
group of diverse auto inflammatory conditions that affect the spine more than the extremity joints
types of spondyloarthropathies and spondyloarthritides
ankylosing spondylitis
reactive arthritis
inflammatory bowel disease (Crohns)
psoriatic arthritis
sjogrens syndrome
common features/S&S of spondyloarthropathies and spondyloarthritides
gradual onset
constitutional S&S
multi joint inflammation and pain
familial predisposition
extraarticular involvement of eyes, skin, GI tract, and renal and cardiac systems
how might the multi joint inflammation and pain of spondyloarthropathies and spondyloarthritides present
over 30 minutes of pain after prolonged positions (doesn’t go away after a few steps/seconds)
improved pain with easy/regular movement
chronic inflammation/P! of axial skeleton most often
asymmetric or unilateral extremity involvement to a lesser degree (typically smaller joints)
why might those with spondyloarthropathies and spondyloarthritides have a predisposition to tendinitis
inflammation is often localized to enthuses (insertion points of connective tissue) so lots of -itises
preferential tissue
how might some describe spondyloarthropathies and spondyloarthritides
“hurts to see, pee, and bend my knees”
incidence/risk factors of sjogren syndrome
2nd most common rheumatic disease but no Rh factor present in blood
most often in postmenopausal women
etiology and pathogenesis of sjogre syndrome
gland destruction of exocrine glands (mainly lacrimal and salivary)
additional pituitary and adrenal gland dysfunction
functions of the pituitary and adrenal glands
pituitary helps regular growth, BP, and reproduction
adrenal helps regulate metabolism, immune system, BP, and stress response
unique clinical manifestations of sjogre syndrome
spondyloarthritide S&S
peripheral neuropathy due to vasculitis
hallmark symptoms = dry eyes/mouth but potential effect on all systems
fatigue is dominating and disabling
sleep disturbances
what is fibromyalgia syndrome
similar to other conditions but there are distinct differences
systemic and NOT the same as a more localized myofascial pain syndrome
not the fatigue level of chronic fatigue syndrome
chronic/widespread myalgia
incidence/prevalence of fibromyalgia syndrome
most common MSK disorder in US
more common in women than men
20-55 years of age
minimal fitness level
risk factors for fibromyalgia (also pain triggers)
prolonged anxiety/emotional stress
trauma
rapid steroid withdrawal
thyroid disorders
infections
etiology of fibromyalgia
often unknown but risk factors are possibilities
genetic possibility
may be triggered by inflammatory conditions
psychological and cognitive behavioral factors occur
pathogenesis of fibromyalgia
not entirely understood
misprocessing of pain with sensitization and nociplastic pain
micro spasms of muscles contribute to hypo vascularity and fatigue
hypothalamic pituitary adrenal (HPA) axis dysfunction
functions of the hypothalamic-pituitary-adrenal gland axis dysfunction
interactive neuroendocrine unit
plays large role in body’s response to stress
pituitary helps regulate growth, BP, and reproduction
adrenal helps regulate metabolism, immune system, BP, and stress response
how does the ANS contribute to the pathogenesis of fibromyalgia
ANS is hyperactive sympathetic (flight or fight) branch and underachieve parasympathetic (rest) branch
how does the ANS contribute to the pathogenesis of fibromyalgia
ANS is hyperactive sympathetic (flight or fight) branch and underachieve parasympathetic (rest) branch
how does the immune system play a role in the pathogenesis of fibromyalgia
increased pain activated glial cells in spinal cord to release pain facilitating cells
also releases pain neurotransmitters
top 6 signs and symptoms of fibromyalgia
visual problems
mental and physical fatigue
sleep disturbances/morning fatigue
morning stiffness that persists >30 min
global anxiety
cognitive problems
describe what might be found in tests/measures for fibromyalgia dx
all imaging/blood tests are neg
dx by exclusion partly
greater than or equal to 11/18 points tender to palpation found by pressure until your nail bed blanches
PT implications for the initial approach to treating fibromyalgia
initial = strong support
pt education
exercise prescription = low/mod global exercises with aerobic/resistance activity
1-1.5 hr sessions, 2-3x/wk, for more than 13 wks
*monitor vital signs to avoid hyperactive sympathetic response
hat options for fibromyalgia treatments are weakly supported
cognitive behavioral therapy
pharmacological for pain, anxiety, and sleep disturbances
sleep study
general PT implications for fibromyalgia syndrome
nutritional guidance
stress management
often minimal benefits over long term management
