(Hopefully) curing cancer
This anti-mitotic drug causes neuropathy as a side effect.
Bonus (100): This is the mechanism by which the drug acts as an anti-mitotic agent.
Bonus (100): This is why neuropathy is a side effect.
Bonus (100): Interactions with this drug class are a common concern during administration of the drug in question.
What is paclitaxel?
What is locking the tubulin in its polymerized state, arresting the cells in mitosis?
Neurotransmitters are carried to the cell surface via microtubules, which paclitaxel blocks.
What are cytochrome P450 modifers?
This cytokine is involved in the innate defense against viruses, and it is associated with PRR signaling pathways. It activates macrophages, dendritic cells, and NK cells.
Bonus (200): This anti-inflammatory cytokine is produced primarily by Tregs, macrophages, and chondrocytes.
What is IFN-alpha/beta (type I interferons)?
What is TGFbeta?
This is the common precursor of dendritic cells, macrophages, and mast cells.
Bonus (100): This is the common precursor of plasma cells, effector T-cells, and NK cells.
What is common myeloid progenitor?
What is common lymphoid progenitor?
PAMPs from herpes simplex virus might be recognized by this TLR.
Bonus (50): This is the PAMP recognized by the TLR.
Bonus(100): This is the adapter the previously mentioned TLR uses to initiate signaling.
Bonus (50): This is the location of the aforementioned TLR.
What is TLR3?
What is dsRNA?
What is TRIF?
What is the endosomal membrane of DCs, B cells, and phagocytes?
This is a unique genomic characteristic of the influenza virus.
Bonus (50): These are the two types of glycoprotein spikes surrounding the influenza virus.
Bonus (100): This is the function of each of the two glycoprotein spikes.
Bonus (100): This is a unique genomic characteristic of the hepatitis c virus.
What are eight ssRNA(-) segments surrounded by helical capsids?
Neuraminidase (NA): Allows hemagglutin to be hydrolyzed from the host cell surface, permitting entrance into the cell
Hemagglutin (HA): binds to sialic acid on host cell surface to trigger endocytosis
This anti-neoplastic prodrug is similar to chemical weaponry from World War I, killing dividing cells via alkylation.
Bonus (100): This is a common side effect of the drug, making it useful following organ transplantation.
Bonus (100): The drug is activated by this class of liver enzymes.
What is cyclophosphamide (aka cytoxan; aka neosar)?
What is immune suppression?
What are cytochrome P450 enzymes?
1. This is the effect of IL-1/IL-6/TNF-alpha release on the liver.
2. This is the effect of IL-1/IL-6/TNF-alpha release on the skeletal muscle and adipose tissue.
3. This is the effect of IL-1/IL-6/TNF-alpha release on the hypothalamus.
4. This is the effect of IL-1/IL-6/TNF-alpha release on the bone marrow endothelium.
1. The production of acute phase proteins (C-reactive protein and mannose-binding lectin) --> complement activation and opsonization.
2. Mobilization of proteins and energy to increase heat production --> dec. bacterial/viral replication
3. Inc. temperature --> dec. bacterial/viral replication
4. Neutrophil migration --> phagocytosis
These three cells mediate immune response to parasitic infections and allergic immune response.
What are eosinophils, basophils, and mast cells?
PAMPs from a fungal infection such as candidiasis could be recognized by this PRR class.
Bonus (100): These are two specific types of the aforementioned PRR class.
Bonus (100): These are the specific PAMPs recognized by the aforementioned PRR class.
Bonus (100): This/these TLR(s) could also recognize fungal PAMPs.
What are C-type lectin receptors?
What are dectin-1 and mannose receptor?
What are terminal fructose and mannose carbohydrate glucans from the fungal cell wall?
What are TLR2 and TLR6?
This latent viral infection of the sacral nerve ganglion can result in mucocutaneous lesions.
Bonus (100): This latent viral infection of the trigeminal nerve ganglion can result in mucocutaneous lesions.
Bonus (100): This latent viral infection of the dorsal root ganglion can result in mucocutaneous lesions.
What is HSV-2?
What is HSV-1?
What is VZV?
Your patient has HER2+ breast cancer. You are already prescribing mAbs, but are concerned about activation of a downstream proliferative pathway. You might prescribe this drug.
Bonus (100): Which pathway do these drugs inhibit?
What is rapamycin/sirolimus?
mTOR pathway
This protein that is produced by the liver in response to inflammatory cytokines is commonly determined clinically.
Bonus (150): These are two important functions of the protein.
What is C-reactive protein (CRP), an acute-phase protein?
What are the opsonization of microorganisms and binding of C1 to start the classical complement pathway?
This immune cell has a bi-lobed nucleus. Its granules contain histamine and heparin.
What are basophils?
These are the three PRR classes located in the cytosol.
Bonus (100): These are the three PRR classes that can detect bacteria.
What are NLR, RLR, and cytosolic DNA sensors?
What are TLR, NLR, and cytosolic DNA sensors?
This DNA virus is implicated in Burkin Lymphoma.
Bonus (50): This is the family the virus belongs to.
What is Epstein-Barr Virus?
Bonus: What is the herpesvirus family?
You might prescribe this treatment to a patient with HER2+ breast cancer.
Bonus (100): You might be most concerned about this side effect.
Bonus (100): Adding these two drugs to the treatment plan can suppress drug resistance caused by HER3.
Bonus (100): These are three potential treatment options for triple-negative (ER-/PR-/HER2-) breast cancer.
What is trastuzumab?
What is cardiotoxicity?
What are paclitaxel and pertuzumab?
What are paclitaxel, cyclophosphamide, and doxorubicin?
Describe the mechanism behind the swelling, warmth, and redness seen during an innate immune response.
1. Binding of DAMPs and PAMPs to PRR on macrophage surface
2. Release of TNF + IL-1
3. Vasodilation, epithelial cell contraction, leak of plasma into surrounding tissue --> swelling, warmth, redness
This strongly phagocytic immune cell presents antigens to helper T cells, thereby activating them.
Bonus: This is the precursor of the previously mentioned cell.
What is the dendritic cell?
What are monocytes?
1. NLRP3 activates ______ which cleaves ______ into ________ which is then secreted, leading to inflammation.
2. NOD recognizes ______, leading to ____ activation and inflammation.
3. RIG-like receptors recognize _____ and stimulate ____ and ____ activation, resulting in _______ production.
4. The STING pathway includes cytosolic receptors that recognize ____ and stimulate _____ resulting in ______ production.
1. What are caspase 2; pro-IL-1beta; active IL-1beta?
2. What are intracellular bacteria (bacterial wall peptidoglycans); NFKB?
3. Viral RNA; IRF-3; NFkB; type 1 IFN production
4. DNA; IRF-3; type 1 IFN production
This viral infection presents with retinitis, esophagitis, and pneumonia/pneumonitis post-stem cell/bone marrow transplant.
What is cytomegalovirus?
These are three complications of advanced regional cancer that can be treated using palliative radiation therapy. (just name any three.)
Lung Cancer
-Obstructive pneumonia/atalectasis -hemoptysis -chest pain
-esophageal infiltration -air hunger -SVC obstruction
Esophageal Cancer
-Esophageal obstruction
Hemorrhage/obstruction
-Recurrent bladder carcinoma -locally recurrent cancer of prostate
-GYN malignancies (cervix, ovary, uterus)
Pelvic Pain
-pelvic bone infiltration -lumbosacral plexus infiltration
-diffuse dural tumor infiltration involving posterior root ganglia and peripheral nerves
Describe the steps of the classical complement activation pathway from start to finish.
Bonus (100): This is the advantage of the alternative complement activation pathway.
1. binding of IgM or IgG to pathogen surface
2. C1 complex binds Fc portion of bound antibody
3. Activation of C1q --> activation of C1r + C1s4. C1q activates Ser proteases C1r and C1s
5. C1s protease cleaves of C2 and C4 into C2a/b and C4a/b (C2a and C4a leave to become anaphylatoxins)
3. Formation of C2bC4b C3 convertase
4. C2bC4b cleaves C3 --> C3a + C3b
5. Formation of C2bC4bC3b C5 convertase
6. C2bC4bC3b cleaves C5 --> C5a + C5b
7. C5b + C6 + C7 + C8 begin to form MAC
8. C9 polymerizes to form a pore
9. MAC kills microorganisms by destabilizing cell membranes
Bonus: Results in more C3b production than other pathways, allowing lots of opsonization to take place
This protein dissociates MASP-2 from the MBL.
Bonus (100): This is a serine protease that cleaves C4b and C3b.
Bonus (100): A deficiency in the two previously mentioned proteins may result in this class of chronic diseases.
Bonus (50): Deficiencies in factors B or D, C5, C6, C7, C8, or C9 can result in severe infections with these pathogens.
What is C1INH (C1 inhibitor)?
What is factor I?
What are autoimmune conditions?
What are Neisseria pathogens?
This is the pathophysiology behind leukocyte adhesion disease.
What is deficiency in CD18 adhesion molecule, trapping neutrophils and monocytes in the bloodstream and preventing them from migrating into other tissues?
This is the virus that causes Kaposi's sarcoma.
What is HHV-8?