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HEHI Adult Week 4 Immunity
Terms in this set (71)
What is an older term for a "substance" that generates disease?
What is an allergen?
something that does not present a threat to the body (like pet dander) that still provokes an immune response.
What has antigenic sites?
pathogen or allergen
pathogen! many sites on its surface, T and B cells read them
What is e.coli?
What is ragweed?
When does an autoimmune disease occur?
3. your immune system interprets your own tissue as antigenic
What is the bodies innate immunity?
1. physical/chemical barrier
2. inflammatory response
How does innate and adaptive immunity overlap?
The inflammatory response. Innate releases cytokines (both pro and anti inflammatory). The adaptive immunity has T & B cells- which also release cytokines.
How is inflammation is characterized?
o Dilation of vessels
o Increasing capillary permeability (this allows all those white blood cells to get into the tissue where they can fight off pathogens)
3. Increased leukocyte migration to the area of injury
4. Fever (may help inhibit viral and bacterial function)
True/False: Inflammation will only occur in the case of an infection.
False! Tissue damage causes release of molecules that will lead to inflammation!
What are the cells of the innate immune system?
5. Dendritic Cells
How do the cells of the innate immune system work?
Mostly work by phagocytizing and degranulating
What is agranulocytosis characterized by?
loss of neutrophils, basophils, eosinophils
What is the main way that adaptive immunity differs from innate immunity?
The adaptive immune system MUST be activated and cannot respond to nonspecific threats.
How does sensitization occur?
occurs when antigen presenting cells (usually a dendritic cell) digests and display antigens to T and B cells
How does adaptive immunity work?
1. sensitization occurs allowing for activation.
2. once activated, a "memory" is developed which lets it respond to pathogens it has seen before.
What is the fundamental problem of autoimmunity?
T and B cells are activated and respond to "self" antigens. We are unable to delete the T and B cells that are sensitized that way.
What is CAR-T therapy?
harvest T-Cells and genetically engineer them with receptors that are more effective at identifying/killing cancer cells.
What organ plays a big role in the adaptive immunity?
1. thymus is where T cells go to mature/undergo "deletion" to prevent autoimmunity
2. lymph nodes "meeting place" for T/B cells and antigen-presenting cells
3. spleen-removal increases risk of infection
After a splenectomy what vaccinations are required again?
HIB, Meningococcal (both types), Pneumococcal
What are the cells of adaptive immunity?
T-Cells: effective at recognizing "compromised" cells (e.g., virus-infected or cancerous cells) and destroying them.
B-Cells: antibody release
What occurs to T-cells in the thymus?
1. negative selection: If a T cell matches too strongly against a "self" protein in the thymus, it's killed
2. Differentiation (1. Cytotoxic CD-8, attack cells; 2. Helper T Cells CD4, activate T&B cells, release cytokines; 3. suppressor T-cells, modulate the immune system)
What form of T-Cells are implicated in autoimmunity?
Suppressor T-Cells which modulate the immune system response
What are the only cells that release antibodies?
What are the 2 main methods of attack for B cells?
1. Phagocytosis 2. Production of antibodies: ALL EXTERNAL
(· "Gum up the works" (agglutination)
· Promote phagocytosis
· Antibody-dependent cellular cytotoxicity - antibodies "tee up" pathogens for destruction by other immune cells (IgE - eosinophils)
· Activate complement system
· Block ability of viruses and bacteria to adhere to mucosa)
What are Antibody-producing B cells called?
What are the 5 differen types of antibodies?
1. IgA - Found in breast milk (esp. colostrum), responsible for conferring passive immunity from mother to child. Found in other body secretions as well.
2. IgG - Most powerful antibody, but B cells must be activated in order to produce them
3. IgM - produced by naïve B cells
4. IgD - bound to the surface of the B-cells, not released into the plasma like other antibodies.
5. IgE - Responsible for allergic reactions. Promotes Eosinophil production
What would elevated IgG and low IgM would indicate?
previous exposure (this can be measured as an antibody titer to determine whether a person is still protected from pathogens)
What would elevated IgG and IgM indicate?
What would elevated IgM and low IgG indicate?
How do vaccines work?
based on the ability of the adaptive immune system to maintain a memory of antigens it's been previously exposed to. This is done via memory B and T cells, which live for a long time
When are these vaccines recommended?
1. pt starting at age 50
2. every 10 years
4. beginning at age 65
When will Polyclonal Antibodies can be given to confer immediate passive immunity?
1. After exposure to toxins: antivenoms
2. After needle-stick or other pathogen exposure: e.g., anti Hep-A
3. IVIg can be used either as replacement for people who are immunocompromised, OR given in autoimmune conditions where it acts to modulate the immune response
What are Monoclonal Antibodies (-mab drugs)?
Plasma b-cells that release the specific antibody you want
ie. induce B-cell death
What occurs in HIV?
retrovirus destroys CD4 cells
-inters with the function of the entire immune system
Who are increased risk of HIV?
-Men who have sex with men - 27x increased
-People who use IV drugs
What should CD4 counts be? What count indicates worsening disease and increased risk of developing opportunistic infection?
When is AIDS diagnosed?
1. above 500
2. below 500
3. below 200
What are the main opportunistic infections associated with HIV?
1. Pneumocystis Jirovecii Pneumonia - fungal pneumonia
2. Thrush - fungal infection in the mouth
3. Kaposi's Sarcoma - endothelial cancer which causes characteristic blood-filled lesions
Do you need to guess the viral load of a patient with HIV?
nope it can be measured directly
What is the Tx for HIV?
1. antiretroviral drugs (dependent on CD4 counts)
2. neutropenic precautions for necessary
What Patient Education/Prevention is needed for HIV?
1. Safe sex practices
2. Regular testing
3. PrEP (pre-exposure prophylaxis)
What is Shingles?
Reactivation of the varcella virus that has been dormant in ganglionic satellite cells.
-painful blister filled rash
What is post-herpatic neuralgia? What causes it?
-Shingles tends to appear along a single "dermatome" (nerve pathway) - most commonly thoracic
-It tends to cause severe neuropathic pain, and the neuropathic pain can persist even after the rash has resolved.
What is the treatment for Shingles?
Ideally adults over the age of 50 will receive a shingles vaccine!!
antiviral drugs (e.g., acyclovir, valacyclovir). Anti-shingles immunoglobulin can also be used 😊
What is important if there is a bacterial infection? How do you get it?
Classifying the bacteria!!
-"process of elimination"
-gram pos/neg, shape (bacillus, rods, spirochets), even more tests
-blood or wound culture
What is important to remember for Clostridium Difficile?
What is the treatment?
1. Develops spores that are not killed by alcohol (handsanitizer), so you must wash your hands
2. Contact precautions required/wear appropriate PPE
3. Causes a diffuse, watery diarrhea
4. can cause toxic megacolon requiring surgery/colectomy
TREATMENT: metronidazole (systemically) or vanc (PO)
What does Staph Aureus cause? Why is MRSA special?
-toxic shock syndrome
MRSA is resistant to penicillin-class drugs
What are 4 reasons the immune system over-activates?
2. Solid-Organ Transplant
3. Bone Marrow Transplant
4. Blood Transfusion Testing
What occurs in allergies?
IgE causes eosinophil activation. Basophils and mast cells are also activated.
o Hay Fever/Allergies
What occurs with Solid-Organ Transplant? What drugs must they be on?
HLA crossmatching ensures that the donor organ is as close to "self" as possible, but the patient must still take immunosuppressive drugs for the rest of their life.
Mycophenolate and tacrolimus are two very common anti-rejection drugs.
What is graft vs host disease?
Bone marrow transplants reject (TK, MP)!
The donor tissue is rejecting the host!
What is important to remember for blood transfusions?
ABO and Rh
What do these autoimmune disorders affect?
1. Type 1 Diabetes
2. Rheumatoid Arthritis
3. Guillain Barre
4. Idiopathic Thrombocytopenic Purpurae
5. Myasthenia Gravis
7. Grave's Disease
1. beta cells of the pancreas
2. synovial capsule (DMARDS)
3. myelin sheath of peripheral nerves
4. your immune system attacks your own thrombocytes
5. acetylcholine receptors
What is Systemic Lupus Erythematosus?
chronic progressive, systemic inflammatory with many systemic manifestations
Who is affected most by SLE?
What are s/sx of SLE?
2. Skin Symptoms
3. Systemic Issues
4. Kidney Disease
What are skin symptoms of SLE?
1. Malar Rash (butterfly face rash)
2. Discoid Lesions (thick and disk-shaped. They often appear on the scalp or face and can cause permanent scarring. They may be red and scaly, but they do not cause pain or itching)
What are systemic issues with SLE?
1. Arthritis - joint pain
2. Sjrogen's Syndrome
4. Hemotologic manifestation (Thrombocytopenia, Leukopenia, Hemolytic Anemia)
5. Cardiac involvement (Thickening of leaflets, Pleuritis)
What will occur if lupus is not managed properly?
What is lupus nephritis? What would the UA show?
A form of glomerulonephritis. You will see elevated creatinine!
o White blood cells WITHOUT bacteria
o Blood in the urine (+RBCs)
o Some protein (but less than 3.5g/day
How can you differentiate between lupus nephritis and a UTI? or DM1?
both WBC, but lupus without bacteria!!
only some protein, but less than 3.5 (DM have lots of proteinuria)
What are tests to determine SLE?
none are foolproof! ANA (looking for antibodies that are attacking)
-monitor kidney function!!
What is treatment for SLE?
1. DMARDs can help prevent flareups. 2. Corticosteroids may be required during active flareups
3. Analgesics for pain control, up to and including opioids
Why is it important for a patient with SLE to be on DMARDS?
-prevent flare up
-prevent systemic manifestations
What is important education for SLE?
-Fatigue management/planning the day
-Help people navigate difficult psychosocial sequelae
What is Sjorgren's Syndrome?
autoimmune destruction of moisture-producing glands
1. Salivary Gland destruction causes xerostomia
2. Issues with lachrymal glands causes dry eyes (Keratoconjunctivitis sicca)
3. Issues with Bartholin's glands causes vaginal dryness
What are you at an increased risk of with Sjogren's Syndrome?
Education for it
Salivary: Increased risk of cavities/gum disease. (Educate patient on using sugar-free gum or saliva substitutes. Patient can also sip water.)
Lachrymal: Increased risk of corneal abrasion (Treat by punctal plugs or eye drops/ointment)
Vaginal: Risk of dyspareunia (pain during sex) (Educate patient on using lubricants)
What are the 2 main kinds of inflammatory bowel disease?
Autoimmune-mediated inflammation of the GI system.
2. Ulcerative Colitis
What are the similarities and differences between Crohn's
and Ulcerative Colitis?
-increased risk of cancer.
-malabsorption -weight loss
Crohns: can occur anywhere in GI tract, occurs in discontinuous tracts/scattered or patchy manifestations, Ulcerations tend to be deeper, increasing the risk for fistula formation and bowel perforation. cobble stones polyps
UC: · Found only in the colon, tends to be continuous, Ulcerations tend to be more superficial. Can be treated with removal of the affected part of the colon
What are general approaches for inflammatory bowel diseases?
· Assess for malnutrition
· Ensure medication compliance/assess for barriers
· Keep a bowel diary
· Stool culture (to distinguish from c. diff or other issues)
· May need endoscopy for diagnosis
· Will likely require immunosuppressive medications
What is celiac disease? What is the treatment?
-autoimmune inflammation in the digestive tract,
-abdominal cramping, pain, diarrhea, or constipation
-Can also cause malabsorption of nutrients
treatment is to avoid gluten-containing foods
What is irritable bowel syndrome?
most common GI disorder!
-abdominal pain, plus constipation and/or diarrhea
What are causes of IBS?
no inflammation or tissue damage!
-visceral hypersensitivity (feel like more full or needing to go than for reals)
-intolerances of foods
-elevated cytokines in the GI flora
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