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Med Screening > Screening for Immunologic Dz > Flashcards

Screening for Immunologic Dz Flashcards

1
Q

what are the 2 categories of immunologic response and what are they each initiated by

A
  1. humoral immunity
  2. cell-mediated immunity

both initiated by lymphocytes

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2
Q

what is the location of most immunity and why

A

intestines
- main point of entry for pathogens

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3
Q

what is the intestines role in immunity

A

help to maintain immune homeostasis

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4
Q

what is the immune system composed of

A

central and peripheral lymphoid organs

peripheral = lymphoid cells circulate thru body

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5
Q

what is the general function of the immune system

A

warning against exogenous microorganisms and endogenous neoplastic cells

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6
Q

what is the risk of exogenous cells

A

can cause infection

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7
Q

what are 4 types of exogenous micro-organisms

A

viral
bacterial
parasites
fungi

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8
Q

what is humoral immunity

A

occurs in body fluids extracellularly (ie antibiotics)

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9
Q

what is cell-mediated immunity

A

occurring intracellularly
- cells are working to contain and destroy

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10
Q

as many risk factors are still unknown what are 2 main populations of people that should be screened

A
  1. previous hx of systemic or inflammatory dz
  2. familial hx of systemic or inflammatory dz (ie fibromyalgia, chronic pain, etc.)
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11
Q

what familly hx has chronic pain been associated w (5)

A

alcoholism
depression
GI disorders
panic attacks
migraines

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12
Q

what are 3 screening questions

A
  1. how long have you had this problem (acute vs chronic)
  2. has the problem gone away and then recurred
  3. have additional sx developed, or have other areas become symptomatic over time
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13
Q

what are common sx reported (7)

A
  1. new onset soft tissue/joint pain
  2. bilateral joint pain, stiffness, swelling
  3. AM stiffness >1hr
  4. weakness
  5. constitutional sx
  6. progressive neuro sx w/i 3wks of infection or vax
  7. joint pain
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14
Q

when are constitutional sx most commonly seen

A

esp w immunosuppressive meds (RA, lupus)

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15
Q

what characteristics associated w joint pain are commonly reported sx

A

w rash, eye irritation, urinary issues

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16
Q

what are general characteristics of RA

A

symmetrical
more prox joints of hands and feet

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17
Q

what are 4 categories of dysfunction in the immune system

A
  1. immunodeficiency disorders
  2. hypersensitivity disorders
  3. autoimmune disorders
  4. immunoproliferative disorders
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18
Q

what are 2 ex of immunoproliferative disorders

A

leukemia
lymphoma

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19
Q

what is the pathophys of HIV

A

direct attack on immune system
vulnerable to opportunistic infections

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20
Q

how is HIV transmitted

A

via blood contact or blood products

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21
Q

describe the onset of sx in HIV

A

delayed

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22
Q

describe the main medical management available for HIV and what the risk of it is

A

anti-viral therapy treatment
- delayed toxicity w long-term usage

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23
Q

what are s/sx of toxicity from long-term anti-viral therapy in HIV

A

rash, nausea, HA, dizziness, fatigue, ms pains/weakness, hepatotoxicity (B CTS, asterix sign)

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24
Q

what are the PT implications of someone w HIV/AIDS

A

if deconditioned, fatigued
- get back to ADLs, work/rec related

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25
Q

what does HIV inc risk of (3)

A

kaposi sarcoma
non-hodgkin’s lymphoma
tuberculosis

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26
Q

what is a kaposi sarcoma and how can one progress

A

skin lesions, initially purple/red on feet, trunk, and head

can progress to malignant tumors on inner walls of heart and vessels
- possible GI involvement

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27
Q

what inc risk of non-hodgkin’s lymphoma and what makes it difficult to treat

A

risk inc w age & further weakening of immune system

difficult to treat bc further immunosuppression not indicated since already immunocompromised

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28
Q

why is there an inc incidence of TB in HIV

A

immunocompromised, bacteria from TB become more active and leads to more pulmonary sx

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29
Q

what are early sx of AIDS (6)

A

wt loss
fevers, night sweats
changes in bowel function
- chronic diarrhea
cough, SOB, fatigue
skin changes
LBP

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30
Q

what are immunodeficiency disorders

A

HIV/AIDS

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31
Q

why can LBP be an early sx of AIDS

A

dec in activity and changes in ms mass
changes in posture
more common as Tcell count dec
- inc risk of osteopenia, osteoporosis, osteonecrosis

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32
Q

what are late sx of AIDS (5)

A

kaposi’s sarcoma
HTN (cardiac or pulm)
opportunisti dz
dementia
distal asymmetric polyneuropathy

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33
Q

how does HIV neurologic dz affect the CNS

A

space occupying lesions, encephalopathy, meningitis

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34
Q

describe AIDS dementia

A

complex
- cognitive, motor, and behavioral functioning

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35
Q

how does HIV neurologic dz affect the PNS

A

inc risk of CYTOMEGALOVIRUS - ascending polyradiculopathy
- progressive weakness from LE up to flaccid paralysis
- potential for painful sensory neuropathy
- lead dec activity levels, immobility, cardiopulm decline -> PT implication for endurance

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36
Q

what are the 4 types of hypersensitivity

A

type 1 - anaphylaxis
type 2 - cytolytic
type 3 - immune complex
type 4 - cell-mediated or delayed

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37
Q

what is anaphylaxis

A

immediate systemic allergic reaction
- vasodilation (quick drop in bp), bronchospasm (difficulty breathing), hives, anaphylactic shock

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38
Q

what are 6 clinical sx of anaphylaxis

A
  1. localized itching, edema, sneezing
  2. wheezing
  3. dyspnea
  4. cyanosis
  5. tachycardia
  6. hypotension
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39
Q

what flag is anaphylaxis

A

RED
immediate epi-pen use, call for emergency assistance (even if pen effective)
- vocal hoarseness and chest tightness

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40
Q

what is cytolytic hypersenstivity

A

destruction of RBCs w transfusion reactions
- production of auto-antibodies produced against cells of body that have any foreign proteins attached to them

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41
Q

what are 2 instances that cytolytic hypersensitivity is seen

A

hemolytic anemia
transfusion of incompatible blood

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42
Q

what are clinical sx of cytolytic hypersensitivity (6)

A

HA
back/flank pain
chest pain/angina
n/v
tachycardia/hypotension
hematuria

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43
Q

what is immune complex hypersensitivity

A

formation or deposition of antigen-antibody complexes in tissues
- depends on tissues and where, can lead to different clinical sx

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44
Q

what are clinical sx of immune complex hypersensitivity (7)

A

arthralgia
uticaria (hives/rash) - skin
nephrits - kidneys
pleuritis - lungs
pericarditis - heart
fever
lymphadenopathy

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45
Q

what is cell mediated or delayed hypersensitivity

A

occurs 24-72hrs after exposure to antigen

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46
Q

what is the role of antigens and hypersensitivity

A

antigens created on first exposure
- subsequent exposures will see hypersensitivity reactions that result in cell-mediated sx

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47
Q

what are 2 instances of cell-mediated or delayed hypersensitivity

A

graft v host dz
contact dermatitis

48
Q

what are sx of graft v host dz (3)

A

skin
GI
hepatic dysfunction

49
Q

what are sx of contact dermatitis (3)

A

itching
erythema
skin lesions

50
Q

what are autoimmune disorders

A

immune system attacks body cells/tissues
- immune system can’t distinguish self from non-self

51
Q

what are 5 risk factors for autoimmune disorders

A

genetics
sex hormones (women > men)
viruses
stress
environment

52
Q

what are 2 types of autoimmune disorders and ex

A

organ specific
- thyroiditis, ulcerative colitis, insulin dependent diabests

generalized
- see more of a systemic response than one organ

53
Q

what are ex of generalized autoimmune disorders (14 - don’t memorize just to glance at)

A

fibromyalgia
RA
PMR
SLE
scleroderma
spondyloarthropathy
AS
Reiter’s syndrome
PsA
lyme dz
MS
GBS
MG

54
Q

what is fibromyalgia

A

non-inflammatory, generalized MSK pain

55
Q

what is the etiology of fibromyalgia

A

controversy over exact cause
- thoughts ab abnormal biochemical or immunologic aspects: genetic predisposition + triggered by virus or inadequate thyroid hormone

56
Q

what are risk factors of fibromyalgia (3)

A

women > men
less common in older adults
psychosocial factors
- childhood trauma
- family issues
- physical and/or sexual abuse

57
Q

what are 5 clinical sx of fibromyalgia

A
  1. widespread tender points w generalized aching
  2. pain lasting > 3 mo
  3. swelling, ms spasms
  4. fatigue, AM stiffness, sleep disturbance
  5. inc sensitivity to sensory stim
58
Q

describe the pain experienced w fibromyalgia

A

more general and things that wouldn’t necessarily cause pain are painful
- more centrally mediated (neuropathic if you will lol)

59
Q

tender points seen in fibromyalgia vs trigger points

A

tender points:
- sx to palpation
- wide spread pain

trigger points:
- palpable difference in tissue
- myofascial pain specific to ms or region

60
Q

what scale/tool is used to assess fibromyalgia

A

sx severity scale which focuses on:
- fatigue
- cognitive function
- sleep disturbance
- other systemic clusters

61
Q

what is the PT implication of fibromyalgia sx

A

if not dx, refer out
- PT still part of treatment, but need other practitioners involved

prob a yellow flag then

62
Q

what is RA

A

chronic, systemic, inflammatory disorder affecting synovial tissues

63
Q

what is the etiology of RA

A

unknown cause
- possible genetic predisposition + environmental stim

64
Q

what are 2 risk factors for RA

A

women 2-3x men
ages 20-40yo

65
Q

what are 4 clinical sx of RA

A
  1. variable b/w and w/i pts
  2. early fatigue, malaise, diffuse ms pain
  3. 1+ swollen joints, morning stiffness >45min, MTPs/MCPs
  4. later swelling, tissue reaction, joint destruction
66
Q

what will imaging show of RA

A

80% will have significant visible joint erosions 2yr after onset

67
Q

when is a referral indicated in RA (3)

A
  1. significant discomfort w compression of MTP/MCP
  2. presence of 3+ swollen joints
  3. > 1hr morning stiffness
68
Q

what is polymyalgia rheumatica (PMR)

A

systemic, rheumatic inflammatory disorder

69
Q

etiology and risk factors of PMR

A

unknown cause
- possibly linked to autoimmune, viral and stress mechanisms

risk factors:
- >55yo (inc w age)
- women > men
- caucasian

70
Q

what path is PMR linked with

A

giant cell arteritis
- inflammation of branches of carotid artery (sx: severe HA, TMJ dysfunction, blindness if impact opthalmic arteries)

71
Q

what are 6 clinical sx of PMR

A
  1. severe aching and stiffness ms > joints
  2. AM pain
  3. HA
  4. weakness
  5. fatigue
  6. very high ESR
72
Q

where is there aching/stiffness in PMR and why is this important

A

localized to ms
- at neck, shoulder, pelvic girdle

can help to differentiate from joint disorders

73
Q

describe the course of dz for PMR

A

self limiting lasting 2-3yr
- low dose steroid tx

74
Q

what is systemic lupus erythematosus (SLE)

A

chronic systemic inflammatory dz

75
Q

discoid vs systemic lupus

A

discoid
- only affecting skin
- raised, scaly coin shaped lesions
- rarely progresses to systemic

systemic
- more severe, affects many systems/organs (ie skin, joints, kidneys, blood forming organs, mucous membranes) in body

76
Q

what is the etiology and risk factors of SLE

A

cause is unknown
- likely immunoregulatory impacted by genetics, environment, hormone, chemical factors

risk factors:
- 15-40yo
- women 10-15x > men

77
Q

what are 5 clinical sx of systemic lupus

A
  1. butterfly rash
  2. arthralgia and arthritis
    - symmetrical, usually small joints
    - can be progressive and deforming leading to osteoporosis w fx and osteomyelitis
  3. polyneuropathy
    - motor, sensory, or both
    - starting in LE and progress up
  4. neurolupus
    - neuropsychiatric manifestations of dz
    - cerebrovascular dz, sx, less commonly cog dysfunction
  5. fever/fatigue
78
Q

what is scleroderma

A

inflammation and fibrosus of body tissues (ie skin, blood vessels, synovium, skeletal ms, kidneys, heart, lungs, GI)

79
Q

etiology of scleroderma

A

unknown
- mix of genetics and environment

80
Q

what are 5 general clinical sx of scleroderma

A
  1. raynaud’s phenomenon and tightness in skin
  2. calcinosis (calcium deposits in fingertips), sclerodactyly (chronic hardening and shrinking toes and fingers), telangiectasia
  3. arthralgia, stiffness, arthritis
  4. esophageal hypomotility
  5. lung involvement (interstitial lung dz - restrictive)
81
Q

limited vs diffuse scleroderma

A

limited: just affect skin (usually hands and then esophageal dysmotility)
- better prog than diffuse

diffuse: acute onset
- constitutional sx
- widespread skin involvement and internal organ involvement

82
Q

what population is diffuse sclerodoma more common in

A

women, 20-55yo

83
Q

what is spondyloarthropathy

A

non-infectious, inflammatory, erosive rheumatic dz of spine

84
Q

what are 5 common risk factors of spondyloarthropathy

A
  1. recurring, insidious onset of backache
  2. first episode before 30yo
  3. each episode lasts months
  4. pain inc w rest, improves w movement
  5. family hx of spondyloarthropathy
85
Q

what are 3 spondolyoarthropathies

A
  1. ankylosing spondylitis
  2. reiter’s syndrome
  3. psoriatic arthritis
86
Q

what is AS

A

chronic, progressive, inflammation of fibrous tissue
- affecting ligs, tendons, capsule attachments to bones
- primarily SIJ, spine, larger peripheral joints

87
Q

what is the prevalence of AS

A

likely not a difference b/w gender
- maybe women have more milder form or more peripheral joint involvement

88
Q

what is needed for dx

A

MRI
- XR not enough

89
Q

what are 6 clinical sx of AS

A
  1. insidious onset mid-low back pain
  2. stiffness and pain >3mo
  3. AM stiffness >1hr
  4. <40yo
  5. dec lumbar AROM (esp flex) -> bamboo/fused spine
  6. extraarticular - uvitis, conjunctivitis, colitis, iritis, cardiac
90
Q

what is there an inc risk of later on in AS (5)

A
  1. spinal fx from minor trauma
  2. atlanto-axial subluxation
  3. destruction of vertebral bodies
  4. spinal stenosis
  5. cauda equina
91
Q

what is reiter’s syndrome

A

reactive arthritis after infection
- possible genetic contributions
- typically affecting knees, ankles, LE WB-ing joints

92
Q

what is the triad of sx for reiter’s syndrome

A

arthritis
conjunctivitis (redness, burning, irritation in eyes)
non-specific urethritis

93
Q

what is psoriatic arthritis (PsA)

A

chronic, recurrent, erosive, inflammtory arthritis

94
Q

what is the etiology of PsA

A

causes unknown

occurs in 1/3 of people w psoriasis

95
Q

what is key in management of PsA

A

early detection for medical intervention (using biologic agents) to prevent long-term complications (joint destruction and disability from arthritis)

96
Q

what are 5 clinical sx of PsA

A
  1. psoriatic skin lesions
  2. pitting, ridging, cracking nails
  3. arthritis
  4. diffuse swelling of fingers
  5. inflammation of soft tissue attachment sites
97
Q

what are characteristics of arthritis as a clinical sx of PsA (3)

A
  1. early and severe
  2. symmetric, distal distribution (DIP before MCP/MTP)
  3. AM stiffness >30min
98
Q

what is lyme dz and where is it most common

A

tick bite w bacterial infection

coastal NE, mid-atlantic, wis, minn, cali

99
Q

what are early sx of lyme dz (2)

A
  1. red rash (erythema migrans)
    - focal point where bite was surrounded by red ring
  2. flu-like sx (stiff neck, body ache, fatigue)
100
Q

what are 4 late sx of lyme dz

A
  1. arthritis (larger joints)
  2. neurocog sx
    - stiff neck, HAs, numbness, pain, weakness in limbs
  3. sleep disturbance
  4. peripheral neuropathy - doesn’t follow pattern
101
Q

what is key for treatment of lyme dz

A

early treatment helps w quicker and more complete recovery
- most effective

102
Q

what is MS

A

inflammatory, demyelinating dz of CNS

103
Q

what are risk factors of MS (3)

A

women>men
20-40yo
familial hx

104
Q

what are 8 clinical sx of MS (just be able to recognize)

A
  1. unilateral vision change
  2. paresthesias
  3. ataxia/unsteadiness
  4. vertigo
  5. fatigue and ms weakness
  6. tremor, spasticity, hyper reflexia
  7. bowel/bladder dysfunction
  8. lhermitte’s sign
105
Q

what is a characteristic of MS clinical sx

A

rapid onset over minutes- hours
- gradual is less common

106
Q

what is lhermitte’s sign and what dz is this seen in

A

cervical neck flexion elicits electric shock sensation down spine and thru extremities

MS

107
Q

what is GBS

A

inflammatory demyelinating dz of PNS
- abrupt onset of paralysis
- may be linked to infectious illness, vaccinations (1-3wks post)

108
Q

what are 4 clinical sx of GBS

A
  1. rapid and progressive weakness in 3-7 days
    - symmetric, LEs -> UEs -> respiratory ms
    - variable progression of paralysis
  2. hyporeflexia
  3. paresthesias
  4. fever, malaise, nausea
109
Q

what is the course of dz in GBS

A

within 6-9mo full recovery
- only ab 1/2 have lingering neuro deficits

110
Q

where is there specifically weakness and nerve related sx common in GBS

A

CN and esp facial n.

111
Q

what is MG

A

antibodies produced that block Ach receptors on ms, impairing function

112
Q

what are the risk factors for MG

A

women 20-30yo
men >50yo

113
Q

what are 4 clinical sx of MG

A
  1. ms weakness and fatigue (cranial and neck ms)
    - eyes, chewing, swallowing, facial expressions
  2. rapid fluctuating asymmetric ptosis
  3. worsens w exertion, later in day, warmer temps
  4. progressing to respiratory failure
    - impact ms of respiration and diaphragm -> breathing won’t be as efficient
114
Q

what are red flag immediate referrals for immunologic conditions (3)

A
  1. anaphylactic shock (even if epipen admin)
  2. joint pain w suspect infection
  3. blue color to skin over joint w extreme pain (septic joint)
115
Q

what are 3 yellow flag soon referrals for immunologic conditions

A
  1. joint pain w constitutional sx
  2. symmetrical joint sx (RA)
  3. neuro sx w/i 1-3wks of infection or vax (potential for GBS)

Med Screening (17 decks)

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