Immunology Flashcards
Systemic AutoIM
Scleroderma, RA, SLE
Organ specific AUTOIM with organ
CNS-2
mm
Heart
GI-2
Endo
Kidneys-2
CNS Gullian-Barre, MS
MM-Myasthenia Gravis
Heart-RF
GI- Celiac, Ulcerative Colitis
Endocrine- type 1 DM
Kidneys glomnepth, goodpasture
Corticosteroids 2 MA
Inhibits cytokine production, Inhibits T Cell
Calcineurin Inhibitors
four things
two drugs
One thing about one drug
Two more things
Foundation of Immunosuppression and most aeffective
Decreases t and B cell activity-prevent cell mediated attack
Do not Cause bone marrow suppression or change normal inflam response
Tacrolimus (prograft)
Cyclosporine-Nephrotoxic
Grapefruit can increase tox we need to monitor drug level closely
Cytotoxic drugs
MA
2 drugs
One thing about second drug
Supress T and B cell Synthesis and inhibits purine synthesis
Methotrexate
Mycophenolate Mofetil-GI Toxic
Monoclonal Antibodies
6 things
Targets specific cell/receptor
Treats acute rejection
MAB drugs
Attack t-cells
Developed from mice- Antibodies
may cause flu-like symptoms
Polyclonal Antibodies
5
side effects-3 and tx
Mix of different antibodies
tx acute rejection
Attacks t cells
From horses and rabbits
Can cause leukopenia and thrombocytopenia
SE-fever jointpain, tachy-can reduce by giving slower
Why do we use IV immunosup drugs
At first for rejection and reverse acute rejection
Triple therapy for organ transplant
often use three drugs to help stop rejection calcineuurine inhibitor, corticosteroid, mycophenolate mofetil are common
goal is to reduce
What are the opportunistic cancers for AIDS 5
Burkitts lymphoma
immunoblastic Lymphoma
Invasive Cervical Cancer
Kaposi Sarcoma
Primary lymphoma of the brain
Opportunistic infections HIV 4
Pneumocysitis Jiroveci pneumonia-Really only HIV
cytomegalo virus
Toxoplasmosis of the brain
Mycobacterim tuberculosis
One thing about Kaposi Sarcoma
Can invade organs
Criteria For wasting syndrome 5
Greater than 10% weight loss
chronic Diarrhea greater than 30 days
Chronic weakness/fever
GI malabsorption
Not helped by increased prots or calories
Other medical issues with HIV 5
Pancytopenia, Anemia, Altered liver functions, Hep B or C
Cognitive issues
In 2-3 sentences, explain how multiple sclerosis is diagnosed
There is no definitive diagnostic test however in the process of being diagnosed, it’s imperative to obtain a complete health history and examination of all clinical manifestations. An MRI will show plaque formation in the CNS- must have at least 2 inflammatory demyelinating lesions in 2 different locations in the CNS. All other possible causes must be ruled out.
What is MS
Multiple sclerosis is an autoimmune disease that occurs due to chronic inflammation, antigen-antibody reaction, and scarring of the CNS that leads to demyelination of the brain and spinal cord.
Teaching for MS
If C.A. is confirmed to have MS, it would be important to explain that the course of the illness is chronic and progressive-onset can be gradual with few initial symptoms. There are periods of exacerbations and remissions that can occur. This disease can be very individualistic in pattern and progression.
What assessment findings would you expect to see in this acute exacerbation of MS?
Every patient is different but acute exacerbations of the disease can cause fatigue, various types of paresthesia’s, vision problems, muscle spasms, and motor impairment and bladder dysfunction.
What will you as the nurse teach the patient to do to help avoid exacerbations of the illness of MS
It is important to teach patients to avoid triggers that might cause an exacerbation to occur along with preventing complications related to immobility (exercise, PT), and resistance to illness by promoting vaccines and decreasing exposure to infection. We also want to promote healthy eating and staying active as much as possible.
- Corticosteroids -
- Cholinergics -
- Anticholinergics -
- Muscle relaxers
- Electrical brain stimulation -
- Corticosteroids - b. Used during acute exacerbations in order to reduce inflammation and provide symptom relief.
- Cholinergics - e. (Bethanechol) Used if the patient is experiencing a flaccid bladder to stimulate the muscle and help treat urinary retention.
- Anticholinergics - c. (Oxybutynin) Used if the patient is experiencing a spastic bladder to help prevent abnormal bladder contractions and incontinence.
- Muscle relaxers - d. (Baclofen) Used to help with muscle spasms associated with MS
- Electrical brain stimulation - a. Used to treat severe tremors unmanageable with medication.
What similarities are there between myasthenia gravis and multiple sclerosis? Are treatments the same for both disorders?
Both are autoimmune disorders that lead to muscle weakness. Both disorders have a variable course that are described with periods of exacerbation and remission that progress over time. They are exacerbated by similar triggers such as stress, temperature extremes, pregnancy and illness. Both disorders are more likely to effect women.
Both MS and MG are treated with immunosuppressants and corticosteroids to stop the antibody formation and attack on the tissues. MS is treated with other meds for symptoms present in addition to immunosuppressing meds. MG is mainly treated with pyridostigmine an anticholinesterase med to help muscle contraction and to decrease muscle fatigue.
Below list 5 complications of MG as a result of the muscle weakness in specific muscle groups.
What crisis and what are the s/s?
- ptosis/facial drooping
- difficulty with speech
- issues with chewing food
- problems with swallowing
- difficulty breathing (increased risk for aspiration and infections).
Other complications: fatigue, risk of falls/injury
These complications are associated with the lack of Ach and subsequent progressive muscle weakness. Muscle weakness in the face, neck and chest are especially concerning because they are vital for eating/swallowing/breathing.
Myasthenic Crisis-Exacerbation, worsening of mm weak like swallowing and breathing
6) Explain why patients with suspected MG are given the drug edrophonium chloride (Tensilon).
Tensilon is an anticholinesterase drug that is used to help diagnose MG. If muscle contraction improves after Tensilon is given, this is a positive indicator that the patient has MG. The drug increases the amount of Ach present in the synapses.
OA
Osteoarthritis is a slowly progressive noninflammatory disorder of the diarthroidal (synovial) joints. It is characterized by a gradual loss of cartilage with boney outgrowths. It is caused by direct cartilage destruction from a known event or gradual wear and tear of the joint. Deformity of the joint is asymmetrical meaning it affects one side of the body typically.
RA
Rheumatoid arthritis is a systemic autoimmune disease that is characterized by inflammation of connective tissue in diarthrodial (synovial) joints. The person will have fever, fatigue and potentially organ involvement. Joint stiffness is a common symptom and can last several hours. There is a genetic predisposition associated with RA. Unlike osteoarthritis, those with RA experience periods of remission and exacerbation.
Explain what extraarticular symptoms are. Give 3 examples from your book.
Extraarticular manifestations are specific to rheumatoid arthritis and indicate systemic manifestations affecting almost all body systems. These manifestations are likely to occur with increased levels of rheumatoid factor. There is no systemic component with osteoarthritis and no RF levels found as it is not an autoimmune disorder.
Some examples from the book: FIG 64.5- Sjogren’s syndrome, Felty syndrome, Raynaud’s phenomenon.
You are doing patient teaching on the treatments used in RA. Explain in layman’s terms to the patient the types of drug therapy used in RA, how they work and any side effects of the drug therapy.
DMARDs (Disease Modifying Antirheumatic Drugs) are the main treatment for slowing the disease progression and decreasing the risk for joint erosion or deformity. Methotrexate is the preferred DMARD. Methotrexate side effects include bone marrow suppression and hepatoxicity. Lab monitoring must take place -therapeutic levels can be reached in 4-6 weeks.
BRMs (Biologic Response Modifiers)- are a form of immunotherapy that slow disease progression and help manage inflammation. They may be used as a standalone or in conjunction with DMARDs. Depending on the BRM- fatigue, flu like illness, risk for infections
Corticosteroids may be used during flareups along with antibiotics and immunosuppressants. Many side effects-hyperglycemia, osteoporosis, impaired wound healing, weight gain
Aspirin and NSAIDs are used for pain management and anti-inflammatories. Side effects include increased risk of bleeding.
We want to encourage use of nonpharmacological means such as adequate resting time, alternating hot and cold compresses, ROM exercises and weight control. Surgery is an option for severe disfigurement and pain of the joints.
Your patient has systemic lupus erythematosus (SLE) and would like to get pregnant in the next year or so. What information would you give to the patient about having this disease and being pregnant?
I understand you would like to start a family in the near future. Although it is possible, I want to be sure you know the risks involved. SLE is an autoimmune disease that can affect various parts of the body, although not everyone will be affected the same/have the same progression. It can attack the kidneys, heart, joints, skin and brain. This disease impacts women of childbearing age more commonly. Certain treatment options such as steroids or immunosuppressants will potentially cause infertility so these treatment options need to be discussed with the HCP. Women with considerable organ damage already should consider not becoming pregnant due to the risk to the fetus and woman. Immune complexes can occur in the placenta or the arteries which can lead to miscarriage. If possible, the woman should attempt to become pregnant during a remission period of SLE.
Does every individual with SLE experience the same course of the disease? Explain why or why not.
Severity and progression is highly individualized due to variation in the antibodies produced against nucleic acids and the potential for the deposition and inflammation to occur in so many body systems. Some individuals may experience mild symptoms whilst other can have a rapidly progressive disease effecting multiple body symptoms.
Why is fibromyalgia so difficult to diagnose?
This disease is difficult to diagnose because its presentation can be vague and mimic other diseases. Other diseases are ruled out and this can delay treatment. Lack of knowledge or acknowledgement of symptoms can also complicate the diagnosis process.
There is no singular well-known cause of the disease. The patient will report widespread burning pain that worsens and improves over the course of a day with an average of 11-18 focal points. These points generally don’t respond to pressure or stimulus and are also highly variable and apt to change on a day to day basis. It also manifests with fatigue and muscle stiffness/aches without clear etiology.
Fibromyalgia diagnosis can be confirmed by muscle biopsy and the presence of muscle fiber atrophy. Diagnosis is also based on two criteria; pain is experienced in 11 of the 18 tender points on palpation and history of widespread pain (pain that occurs on both sides of the body and above and below the waist) for at least 3 months. Also; fatigue, cognitive symptoms, and extensive somatic symptoms are considered.
Specific tender points are the knee, greater trochanter, second rib, trapezius, low cervical, occiput, supraspinatus, gluteal, and at the lateral epicondyle.
Pharmacology of fibromyalgia: How do tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs) work in the treatment of fibromyalgia? How do muscle relaxers work to treat fibromyalgia?
Two common drug tx
One last thing
TCAs and SSRIs are used to relieve pain and helping with depression and treat insomnia that comes with the debilitating nature of extreme pain. Muscle relaxers also help reduce pain/spasms and treat sleeping difficulties. Non-pharmacological treatments include massage and stretching to help with muscle pain.
Lyrica, symbolta
NO OPIOIDS
) Chronic fatigue syndrome AKA systemic exertion intolerance disease (SEID) is another disorder that is similar to fibromyalgia. What are the commonalities of both of these diseases?
CFS/SEID is a serious, complex, multisystem disease in which exertion of any kind (physical, emotional, cognitive) can adversely affect multiple organs. Is characterized by debilitating fatigue for greater than 6 months without relief. Fatigue is also a debilitating symptom for fibromyalgia. Both can significantly interrupt ADL’s and can often impact ability to be productive/have a job. Both are many time misdiagnosed and poorly understood diseases. Both affect women more commonly than men.
How is CFS/SEID treated? What sort of challenges will D.L. have to face with this illness?
Treatment involves supportive management including NSAIDS for any symptoms such as headaches, aches and pains or fever, antihistamines may be given for allergy type symptoms if any, TCAs/SSRIs can be helpful for anxiety, sleep problems, Clonazepam can also treat anxiety.
Challenges D.L. will face include how to manage this disease that is not well understood by the healthcare community and making sure her voice is heard regarding her patient experience. She may struggle with normal daily tasks from the exhaustion that can occur. She may struggle with working a job and making a living. She may become socially isolated because of these challenges.
You are educating your patient who is newly HIV positive on ART therapy. What important points will you teach the patient?
Drug therapy, although not curative, has resulted in huge improvements in HIV infected patients by helping to maintain immune function and by decreasing viral load. It is critical to take the drug combination specifically as prescribed to prevent the resistance of the virus. If the drugs can’t be taken for any reason, the HCP should be notified. There are many side effects of the drugs, some of which can be controlled and some which can prevent the use of the drugs. OTC drugs should not be taken without checking with the HCP or pharmacist about drug interactions.
ART will decrease the viral load to undetectable levels if used correctly and compliance is maintained. The risk of transmission is virtually zero.
ART is started as soon as possible
Explain the difference between PrEP and PEP antiretroviral prophylaxis therapy. Give an example of who would receive each type of this ART.
PrEP= PreExposure Prophylaxis- HIV prevention strategy given to reduce risk of sexually acquired HIV or in other risky behaviors in individuals who are NOT infected
(ie partner of HIV + person)
Truvada ART is one example of med given
PEP-Post Exposure prophylaxis=Incident of exposure to HIV infected fluids (ie high risk event occurred -needle sharing with HIV+ person)
Truvada & another ART added in for combo effect
What are the long-term effects of people living with HIV (PLWH)?
People who are living long term with HIV are susceptible to the same diseases as other people of similar age. Long term use of ART does have side effects including metabolic disorders of increased lipids, insulin resistance, increased blood sugar, and fat deposits.
Also, there is risk of malignancies, CKD, and neurological problems many times related to ART therapy.
There is also the stigma associated with HIV that these people have to live with-attitudes and beliefs towards PLWH. This can affect their social, mental, and emotional well-being. Discrimination can be experienced throughout their life.
- Corticosteroids
- Calcineurin inhibitors
- Cytotoxic drugs
- Monoclonal antibodies
a. Decrease activity of t-cells and b-cells (ie- Tacrolimus)
b. Suppress t-cell and b-cell activity (ie- Methotrexate)
c. Target specific cell or receptor type
d. Long term use related to many side effects
Corticosteroids- Long term use related to many side effects
Calcineurin inhibitors- Decrease activity of t-cells and b-cells (ie- Tacrolimus)
Cytotoxic drugs-Suppress t-cell and b-cell activity (ie- Methotrexate)
Monoclonal antibodies-Target specific cell or receptor type
Apheresis
separates components of the blood followed by removal of one or more componants
plasmapheresis
removes antigen/antibody complexes replaced by NS, LR, Frozen plasma, albumin
What is human leukocyte antigen system
which are associated with transplantation
HLA cells are highly variable and are on the sixth chromosome we use this to match chromosomes.
A B DR
Matches for transplant criteria 4
ABO (Not Rh), urgency, time on list, location
transplantation matching and antigens
THere are six possible we want 4 or greater
What is PRA
Panel of reactive Antibodies shows the recipient’s sensitivity to HLA before transplant. r serum is mixed with d lymphocytes. It is calculated in percentages high=Cytotoxic antibodies not good low is good
Cross Match and what do results mean
Used to determine existence of antibodies agains donor mix r serum with d lymphocytes
negative is safe
positive is not safe and means cytotoxic antibodies to the donor
Transplantation rejection
Huge problem use testing to decrease three stages
HyperAcute, Acute, Chronic
Hyperacute transplant rejection 5
With in 24 hours
blood vessels are rapidly destroyed from antibodies
Person had preexisting antibodies to transplant
no tx have to remove
Rare
Acute Transplant Rejection 5
Cell mediated response by recipients Lymphocytes,
Common especially with cadaver
Usually reversible with Imunodepressant therapy=Increase corticosteroids or monoclonal or polyclonal antibodies
Happens in first 6 months
Chronic transplant rejection
Occurs over months to years and is irreversible
t and b cells infiltrate and cause inflammation and damage scaring and fibrosis
eventually will lead to organ failure
Graft vs host disease
How?
What transplant?
What?
can cause?
When?
Affects?
Tx
Occurs when immunoINCOMPITENT person gets Immunocompetent Organ
most common in hematopoietic stem cells
The graft rejects the host
can cause granulocytopenia
7-30 days after transplant
Skin, Liver, GI
immunosuppressants
How long will a babe test positive for HIV
12-18 months
CD4 levels
Normal
Healthy
AIDS
800-1200
>500
<200
When do we get antibodies from HIV
3w-3m
kaposi sarcoma
HIV lesions all over and very different
Oral Hairy leukopenia
epstine bar painless white raised lesions on lateral tongue
4 opportunistic infections with HIV
PCP pnemonia, mycobacterium TB, Cytomegalovirus, toxoplasmosis
What can we use to test for HIV
Blood, Saliva, Urine
Goal for tx for HIV
To decrease numbers to undetectable
two important thing about HIV drug therapy
Lots of interactions
Resistance is a problem
What is ART
Antiretroviral therapy drugs work together to stop replication at different steps
START ASAP- regardless of CDC
Drug interactions with ART
St johns wort, PPI, antacids, other herbs
What is PrEP 3
Used for adults that are at risk for HIV
TRUVADA
test q 3 months
What is PEP
For high risk exposure non occupational have three days to take
take 1-2 x a day for a month
Truvada and raltegravir
What can long term HIV patients develop?
Lactic acidosis, fat deposits, hyperlip, hyperglycemia, insulin resistance, Cardiac disease, bone disease, renal disease, lipsostrophy- change to body shape
What is MS
Death?
One way to remember
Three things that happen
Slow chronic progression of demylenation of brain and Spinal cord AUTOIMMUNE
Death usually from immobility issues- pnemnonia
m for myelin
antigen-antibody reaction, chronic inflam, scarring the CNS
Manifestations of MS
4 to know
Extra 4
remission and excacerbations, can vary
Blurred double vision, fatigue, pain-low t to ab, Numb/ting
Breathing problems, bladder/bowel, nystagmus, issues walking
How do we diagnose MS?
#1
and Criteria
Health and clinical history #1
Criteria- 2 demy spots in CNS in 2 different spots
MRI plaques have attack on two different area at 2 different times
Drugs for MS
6 and why
immunomodulators-decrease inflam, and nerve damage
Immunosupressants- no antibodies
corticosteroids for excacerbations
cholinergics-for flaccid bladder anticholinergics for spastic
mm relax
nerver conduction Enhancers
Discharge teaching for MS 3
Keep moving! -water
electrical stimulation
teach triggers
about Myasthenia gravis
AUTOIMMUNE disorder of neuromuscular junction marked by fluctuating weakness that increases with mm use.
Etiology of MG 3
Antibodies attach ACh receptors and stimulate mm contraction
can cause thymus hyperplasia
increase in day and some relief at night
Clinical manifestations of MG
effects 6 areas
3 s/s
2 other things
one test
Weakness that effects eyes, eyelids, chew, swallow, speak and breathe,
Pitosis, double vision, fading voice,
NO SENSORY LOSS, normal reflex,
EYE test
Triggers for MG
All the usuals
hypo k, drugs-beta blockers, starting new steroids
What is MG crisis?
What are we most concerned about?
Acute exacerbation of mm weakness triggeref by triggers most importantly- Respiratory infection/steroids
Breathing issues and aspiration
How do we diagnose MG?
3 and about
EMG-stimulate decrease response=MG
Tensilon test-Give anticholineresterase Pryidostgmine blocks enzyme that breaksdown ACH if there is an improvement it =MG have atropine available
CT to look at thymus
Drugs for MG3
Pyridostigmine, corticosteroids every 2 days, imminosup
Other tx for MG 3
Surgery for thymus, plasmapherisis, IV-G
Nursing for MG 3
Watch lung function, mm strength, swallowing,
What is RA?
Chronic Autoimmune disorder characterized by inflam of the connective tissue of diarthridal (synovial) joints Periods of exacerbation and remission
EARLY TX is IMPORTANT
Etiology of RA
An antigen triggers abnormal formation of IgGAntibodies known as RF combine with IgG complexes that line the synovial membranes=Inflam
Manifestations of RA
6 big
4 others
Fatigue, anorexia, weight loss, general stiffness, fever, BL joints,
Dislocation, nodules, deformity, felty syndrome, raynauds
Labs for RA 4
RF, CRP, ESR, ANA
Other diagnosis for RA 4
Hx and exam, labs, x-ray, cloudy synovial fluid- straw colored with freakles, increased WBCc
Drugs for RA and what they do
4
steroids for exacerbation
DMARDS-aggressivly methotrexate (takes time)
BRM-Slows progression
NSAIDS
OA about
Slowly progressive NONIMMUNO and NONinflam disorder of diarthrodial joints. most common joint disease in NA Not normal aging,
Loss of soft cart with formation of boney outgrowths.
OA manifestations 3
Pain/stiff pain is worse with mo but better with rest
pain worse when pressure drops
asymetrical
diagnosis of OA
CT/MRI, xray, fluid in joints looks good
drugs for OA
ACE, NSAIDS, Cortico
what is joint protection for?
OA
what is lupus?
systems? 8
multisystem inflammatory disease that effects skin, joints, serusmembranes, pleura, pericardium, renal and Heme, neuro
antibodies attack cells neuclous and makes complexes that settle in basement membranes of the capillaries
triggers for lupus 7
hormones, ultraviolet light, stress, chemicals, toxins, virus, drugs
Progression of lupus
Variable!
Manifestations of lupus 6
Kidney function, arthritis, butterfly rash, seizures, alopecia
diagnosis for lupus
No test but ANA are usually present
drugs for Lupus 4
NSAIDS, Antimalarials, immune suppress, cortico steroids
Tx for lupus
Find and tx early, pain control, save organs
About fibromyalgia
Chronic pain with widespread nonarth mmsk pain, fatigue with many points,
Diagnosis with finromyalgia
Process of elimination, Mm biopsy-moth eaten, 11 out of 18 spots hurt with palpation, hx of widepread pain for 3 months .
treatment for fibrom
Non pharm2
pharm 4
One thing to remember
Involve patient and alturnative care
Lyricam cymboltia, TCA, SSRI,
No opioids-They don’t work
About Chronic Fatigue syndrome
Immune dysfunction characterized by debilitating fatigue
Chronic fitigue syndrome diagnosis
and one thing
Profound fatigue longer than 6 moths
Post exertional malase- crashing
unrefreshing sleep
and one
Cognitive impairment-brain fog
Orthostatic intolerance
no labs or tx plan
