Practice Questions Flashcards
A 65 year old female patient comes into the ER with classic anemic symptoms. What would be a smart next step if the basic physical and history is unremarkable for cause of anemia?
GI Consult to find occult bleed
- You are working with a teenage patient who has Hodgkin’s Lymphoma. What is the best explanation for the molecular mechanism underlying this patient’s anemia?
. Anemia of chronic disease likely has to do with hepcidin production. An increased production of hepcidin in causing the enterocytes to retain iron and not let it into the bloodstream. Iron is being lost when these cells are eventually sloughed off.
- What is the classic triad of symptoms you would see in a 45 year old patient that has had underlying hereditary hemachromatosis for decades?
. Diabetes myelitis, hepatomegaly, and hyperpigmentation
i. Labs will show increased serum iron, serum ferritin, and transferrin
- Why is it that type 1 hemachromatosis labs will show increased serum iron, serum ferritin, and transferrin??
. This disease causes a decrease in hepcidin production. Genetic mutation in HFE interacts with TfR1/2 to decrease hepcidin production. Without hemocidin the enterocytes will not retain Fe.
- It is easier to be iron deficient human as a herbivore or carnivore?
. Not sure, but probably as a herbivore.
. Heme iron is absorbed better than non heme iron! You get heme iron from animal meats and non-heme iron from other food sources like vegetables.
- A teenage patient is admitted to the hospital. He attempted to get high by taking a bunch of his grandma’s medication. He is now looking sort of blue(like the color) and you find out that he took sulfonamides rather than the opiates he was going for. How can you treat this condition?
a. Acquired methemoglobinemia. Can happen if you ingest oxidants such as nitrites, quinones, aniline, and sulfonamides. Treat with administration of reducing agents like METHYLENE BLUE or ascorbic acid.
- A 30 year old, black male is admitted to the hospital because he is found to have active tuberculosis. Curiously he also presented with dark urine, jaundice, and hepatomegaly. What do you think could be an underlying metabolic problem leading to these hepatic symptoms?
. It could definitely be a G6PD deficiency! Why you ask? This deficiency makes it much more likely to lyse under oxidative stress (like in Tb).
i. You need G6PD to make NADPH, and you need NADPH to keep glutathione reduced
ii. Reduced glutathione is used to get rid of reactive oxygen species that are going to destroy your erythrocytes
- How does a congenital genetic mutation causing ankyrin deficiency lead to the anemia, jaundice, and splenomegaly seen in hereditary spherocytosis?
. Ankyrin is one of the proteins involved in holding together the RBC membrane that forms the biconcave disc shape. Without enough of it, RBC’s will begin to lose this shape, forming spherocytes. Spherocytes are not deformable like normal RBC’s and are trapped in the spleen and destroyed by macrophages. Now you have anemia because you are losing RBC’s fast, jaundice with all that extra bilirubin, and splenomegaly with all that work it’s doing.
- A 40 year old diabetic patient is currently being treated for Tb with Isoniazid. The patient begins to complain of worsening neuropathy and shows signs of anemia. You realize, “Oh Dang! I forget to supplement her with ________.” What is the mechanism behind the need to supplement?
. Isoniazid can cause b6 deficiency. Vitamin b6 (pyridoxine) is required as part of the heme synthesis pathway. Without enough heme synthesis, the symptoms are pretty self-explanatory. B6 supplementation is particularly important in patients that have diseases where neuropathy is common, pregnancy, and seizure disorder patients.
- You are seeing a 60 year old female patient in clinic. She is a chronic alcoholic and you notice that lab findings and history reveal anemia. She also has a yellowing of the sclera of the eyes. Is her liver cirrhosis going to cause lab findings to show indirect or direct bilirubinemia?
. It’s going to be indirect bilirubinemia. Why? Because it is indirect until the bilirubin is conjugated in the liver. In this case there is probs a lot of heme being broken down, but the liver capacity is shot with cirrhosis and so a lot of it is remaining unconjugated. If you have lot of conjugated bilirubin, this would be considered direct. Direct bilirubinemia happens in cases where you have an obstruction of bilirubin excretion into the bile. (biliary obstruction or hepatitis)
- The whole innate immune response is based on one principle. Certain leukocytes have innate immune receptors called __________________ . These must recognize ______________________, which are common on foreign invaders, but not the host cell.
a. (PRR’s : Pattern Recognition Receptors)
b. (PAMP’s : Pathogen-Associated Molecular Patterns)
- If the complement system is activated directly by a polysaccharide on the surface of a Strep Pneumo bacterium, is this an example of the classical or alternative activation pathway?
. Alternative Pathway!
i. Microorganisms spontaneously activate the complement system = “alternative pathway”
ii. Complement system activated by antibodies or lectin bound to the pathogen surface = “classical pathway”
- One of the infected cells in your body sends out a last ditch distress signal before a gruesome death to help the surrounding cells. Very heroic. How did it send this signal?
. IFN-alpha or IFN -beta (interferons)
. remember T cells will use IFN-gamma
i. Basically interferons, as part of innate immunity, create a state of viral resistance that can buy time for the adaptive immune response to kick in. Like the bat signal?
- TLR3 is an example of a PRR, what kind of PAMP is it looking for?
. dsRNA - which would signal that the cell is infected by a virus
- You have a patient with a rare mutation in their IRF3, which does not allow IRF3 to homodimerize (not a real thing…). Explain how this would affect IFN-beta production when dsRNA binds TLR3.
. IRF3 still activates TRIF and TAK1 which activate the kinases TBK and IKK. These kinases then phosphorylate IRF3, but now IRF3 cannot come together to be a good transcription factor. TRIF could still free up the dimerized NF-kappa-B’s to be transcription factors though. So it looks like you will still get increase of IFN-beta production, but it’s just not going to be the full effect.
