Term
| Why do patients with Von Hippel Lindau disease often develop cancer? |
|
Definition
Mutations in VHL protein prevent it from recognizing the hydroxyproline residue of HIF1-a, thereby stabilizing the transcription factor (Recall, VHL is an E3 enzyme).
Too much HIF1-a means too much erythropoietin and too much VEGF, which means RBC and capillary growth that can cause tumor development and prominent proliferation of blood vessels. |
|
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Term
| How might mutations in TSC1/TSC2 (EGFRs) lead right heart failure? |
|
Definition
Aberrant mTOR signaling leading to abnormal hypertrophy.
Remember, these receptors inhibit mTOR, and prevent it from activating S16K, which would normally phosphorylate target proteins and up-regulate translation and growth.
Insulin inhibits TSC1/TSC2, so problems with insulin signaling would have the opposite effect (i.e. atrophy). |
|
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Term
| What does TB infection have to do with TSC1/TSC2? |
|
Definition
| These EGFRs are missing, so there is no inhibition of mTOR, and cells become GIANT (as seen in Tb). |
|
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Term
| What is Barret's esophagus? |
|
Definition
| Intestinal metaplasia of squamous epithelial lining of esophagus that occurs in response to the presence of stomach acid (you need mucus production to protect against acidification). |
|
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Term
| Which intracellular organelles are particularly sensitive to re-perfussion injury and why? |
|
Definition
Mitochondria.
Unsaturated membranes are susceptible to ROS damage. |
|
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Term
| Why are KEAP1 mutations associated with an overactive Heat Shock response? |
|
Definition
KEAP1 (cystine-rich protein in E3 complex) binds NRF2 and prevents it from acting as a transcription factor in the nucleus.
Once released, NRF2 up-regulates antioxidant genes thioredoxins, phase 2 enzymes (protective carcinogen metabolizing) and heat shock protein transcription factor (HSF1) |
|
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Term
| Why are mutations in Ataxia-Telangiectasia Mutated (ATM) associated with cancer syndrome? |
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Definition
ATM phosphorylates and activates DNA-reapir genes such as BRCA2 and genes that halt DNA synthesis and cell-cycle progression such as p53. If this fails, ATM induces apoptosis.
Without ATM, you don't have dsDNA repair, nor can you stop DNA synthesis and aberrant growth.
Say hello to TUMORS! |
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Term
| Why might mutations in HSP90 be of clinical concern? |
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Definition
It would prevent HSP90 from binding misfolded proteins and either re-folding them or passing them to the UPS for degradation.
Recall, HSP90 is bound to HSF until unfolded proteins outcompete HSF and cause it to migrate to the nucleus to up-regulate inducible heat shock proteins. |
|
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Term
| What is the major threat to the ER unfolded protein response (ERAD)? |
|
Definition
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Term
| Why might a mutation in PERK be of clinical concern? What about IRK-1? |
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Definition
These are the final two components of the ERAD system (ATF6 is the first which is important for ER chaperone transcription).
SHORT.
1) PERK- you can shut off mRNA translation (eIF2a) or turn on the oxidative response (Nrf2)
2) IRK-1- can't maintain basal state through mRNA splicing of t-factors.
2) IRK-1
1) When BiP is pre-occupied, the luminal domains of PERK normally dimerize and phosphoryates eIF2a, which turns off mRNA synthesis, as well as Nrf2, which releases it from KEAP and turns on the oxidative response.
2) Same dimerization as PERK, but it then activates RNAse domain that splices mRNA of t-factor (HAC-1/XBP-1). This usually creates an active protein which activates ER chaperone transcription, inhibits metabolic synthetic enzymes and activates itself. Without IRK-1, you can't maintain a basal state through RNA splicing. |
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Term
| Why might a lack of ATP be important in preventing misfolded protein aggregation? |
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Definition
Think about the UPS.
E1 is an ATP-dependent enzyme, so without ATP, the E1S-Ub complex could not form, proteins could not be tagged with polyubiquitin and nothing can get degraded by proteosomal complex. |
|
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Term
| How could mTOR influence the removal of damaged organelles? |
|
Definition
| mTOR activity inhibits Autophagy |
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Term
| Why might a mutation in LC3 be of clinical concern? What might you notice histologically? |
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Definition
This is a question of Autophagy-mediated organelle digestion.
ATG proteins normally link LC3 to membranes to create double membrane Autophagosomes.
Without LC3, you have no autophagosome, which means you have persistent damaged organelles that will appear as yellow brown granules of LIPOFUSCIN. |
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Term
| Why might low ATP be a problem in Apoptosis? |
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Definition
ATP released from apoptotic cells (as phosphatidylserine is exposed) binds to cell surface receptors on macrophages and activates and recruits them.
Without ATP, no clearance of apoptotic cells! |
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Term
| What does "PKK" stand for in Necrosis? |
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Definition
Pyknosis (condensed nuclei), Karyorrhexis (fragmentation) and Karyolysis (lysis).
Remember, look for acute inflammation (redness, heat, pain and swelling) and ruptured cells in necrosis, to tell apart from apoptosis. |
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Term
| How does necrosis and apoptosis occur simultaneously in brain ischemia? |
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Definition
| Infarcted area that exhibits necrosis is surrounded by apoptotic regions (delayed). |
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Term
| Why are mutations in lysosome-associated membrane protein type 2A (LAMP-2A) associated with accumulation of damaged organelles? |
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Definition
| LAMP-2A enables unfolded proteins to be directly translocated into the lysosomes by chaperone-mediated autophagy. |
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Term
| Which is more serious, a mutation in caspase 8 or caspase 10 and why? |
|
Definition
Caspase 8.
This is tricky, try to think it through.
1) Both caspase 8 and caspase 10 are initiators of apoptosis
2) Caspase 8, however, is also involved in the cleavage of regulators of mitochondrial cytochrome c release, meaning that it is important for BOTH the intrinsic and extrinsic pathways of caspase activation.
3) Therefore, by keeping caspase 8, you can keep both pathways going, but without it, you only get reduced extrinsic signaling. |
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Term
| Explain the general structure of a caspase. |
|
Definition
1) Cysteine in active site
2) pro-domain and active domain
3) cleave at tetra-peptide sequences after aspartic acid residues. |
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Term
| How might mutations in the IETD sequence of Poly (ADP ribose) Polymermase (PARP) influence DNA repair? |
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Definition
IETD is the tetrapeptide sequence that is recognized by caspase 3!
Remember, caspase 3 is an executioner caspase that cleaves and inactivates PARPs, preventing them from repairing DNA damage. |
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Term
| Why might MDM2 mutations be of clinical concern? |
|
Definition
MDM2 is a p53 regulator important for controlling cell-cycle progression. It is also a target of caspases.
Mutations might lead to cancer. |
|
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Term
| Why might MDM2 mutations be of clinical concern? |
|
Definition
MDM2 is a p53 regulator important for controlling cell-cycle progression. It is also a target of caspases.
Mutations might lead to cancer. |
|
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Term
| Why might MDM2 mutations be of clinical concern? |
|
Definition
MDM2 is a p53 regulator important for controlling cell-cycle progression. It is also a target of caspases.
Mutations might lead to cancer. |
|
|
Term
| Why might MDM2 mutations be of clinical concern? |
|
Definition
MDM2 is a p53 regulator important for controlling cell-cycle progression. It is also a target of caspases.
Mutations might lead to cancer. |
|
|
Term
| Why might MDM2 mutations be of clinical concern? |
|
Definition
MDM2 is a p53 regulator important for controlling cell-cycle progression. It is also a target of caspases.
Mutations might lead to cancer. |
|
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Term
| How does I-CAD relate to caspase-regulated apoptosis? |
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Definition
| Caspase cleavage of I-CAD releases CAD, which migrates to the nucleus and chews up DNA within inter-chromosomal regions. |
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Term
| Which pathway of caspase activation is important for killing of cytotoxic effector T cells and the deletion of self reacting T-cells? |
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Definition
The Extrinsic pathway!
1) FAS and TFN-a bind receptors and activate DDs
2) DDs act through adaptors to activate DEDs in pro-caspases
3) Caspases 8 and 10 activate 3 and 7 and lead to apoptosis. |
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Term
| Why might a mutation in Apaf-1 be associated with the development of cancer? |
|
Definition
This question is about the intrinsic pathway of caspase activation.
1) Pro-apoptotic factors cause Cyt-C release from mitochondria
2) Cyt-C associated with Apaf-1, dATP and procaspase-9
3) Caspase 9 activates caspase 3.
Without Apaf-1, caspase 9 is not activated and abnormal cells persist without regulated degradation (can cause cancer). |
|
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Term
What effect might mutations in Bax/Bak have?
What about Bid/Bim/Bad? |
|
Definition
Both prevent apoptosis!
This question requires background knowledge of how the Bcl-2 family of proteins relates to apoptosis.
1) Bcl-2 and Bcl-xL are anti-apoptotic members that interact with BH123 subfamily members (pro-apoptotic), Bax and Bak.
2) In response to stress and damage, BH3-only members (Bim/Bid/Bad) are activated and relieve the anti-apoptotic inhibition of BH123 members.
3) Death pore forms within BH123 complexes, leading to Cyt-C release.
SOOOOO...
mutations in Bax/Bak would prevent BH123-mediated Cyt-C release and prevent apoptosis.
mutations in Bid/Bim/Bad would prevent BH3-mediated inhibition of Bcl-2 and Bcl-xL |
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Term
| What type of inflammation is associated with outpouring of a thin fluid from a skin blister, blood vessels or mesothelium? |
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Definition
| Serous inflammation- outflow of transcudate. |
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Term
True or False:
Exudate is cellular and Transcudate is acellular? |
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Definition
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Term
| A patient presents with purulent inflammation, exuding thick, off-white material from localized regions of necrotic tissue. What is the first thing that you should do as a physician? |
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Definition
| The thick, off-white material is likely pus. You should send it to microbiology to determine what type of pyogenic bacteria the patient is infected with before moving forward with treatment. |
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Term
| Why might be mutations in IL-8 be of clinical concern in terms of patient's ability to generate an appropriate vascular, acute inflammatory response? |
|
Definition
IL-8 (along with IL-1, heat, cold, anaphylatoxins such as C5a and C3a and immune reactions of IG-E) activate Histamine release from Mast cells.
Without histamine release, arterioles do not become dilated and venules do not increase their permeability. You therefore will not get vasodilation or adequate luekocyte extravasation through post-capillary venules. |
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Term
| Describe one way in which Diabetes mellitus might interfere with the vascular component of acute inflammation. |
|
Definition
Diabetes mellitus raises blood sugar and increases atherosclerosis and hypertension.
Deficient NO production is common to all three of these clinical conditions, thereby preventing adequate vasodilation and platelet inhibition.
Patients are therefore more likely to develop blood clots, ischemia and acute MI. |
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|
Term
Why might P-selectin mutations be of clinical concern?
What about PECAM?
What about ICAM?
Which one is the worst? |
|
Definition
Recognize that these are all issues of LEUKOCYTE MIGRATION
1) Rolling of neutrophils, monocytes and lymphocytes
2) Diapedesis
3) Adhesion of neutrophils, monocytes and lymphocytes
Probably ICAM, because in the absence of P-selectin, E-selectin and L-selectin can still enable rolling and in the absence of PECAM, ICAM can still enable some diapedesis. Without ICAM, no neutrophils can get through venules! |
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Term
| What might the consequence of C5a mutations in the leukocyte response to inflammation? |
|
Definition
C5a is important for phagocytosis as well as Mast cel activation.
For phagocytosis, there would be a lack of opsonization and macrophages would be unable to attach to target molecules.
For Mast cells, histamine release would be suppressed, and leukocyte extravasation through venules would be prevents, because they would not be permeable enough. |
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Term
| You are concerned that a patient is experiencing acute inflammation. What systemic effects should you look for to confirm? |
|
Definition
1) Fever/Hypothermia
2) Tachypnea
3) Tachycardia
4) Leukocytosis |
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Term
| You suspect a patient is suffering from Mononucleosis. What type of Leukocyte would you expect to be elevated in the blood? |
|
Definition
Mono is a viral infection, so you should see lymphocytes!
If it was bacterial (think Tb), you would see neutrophils.
If it was allergic or parasitic, you would see eosinophils |
|
|
Term
True or False:
Steroid treatment can induce a "left shift"? |
|
Definition
False!
Realize that steroids increase WBC count, but not "band count." It is leukocytosis, but not bandemia. |
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Term
| If you suspect a case of bacterial infection, what can the ESR tell you? |
|
Definition
If the patient is experiencing an acute inflammatory response to a bacterial infection.
Increased fibrinogen (an acute phase reactant) creates sticky erythrocytes, which raises the sedimentation rate.
Infection = increased ESR |
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|
Term
| Why might a Kinin deficiency be of clinical concern for normal inflammatory responses? |
|
Definition
Without Kinin, you get to autocatalysis of factor X11a, nor do you get fibrinolytic response or subsequent complement response.
Without complement, you don't get mast cells to release histamine nor do you get macrophages to digest material (no opsonization)
This question requires knowledge of the factor XIIa clotting system that mediates the plasma protein inflammatory response.
1) Factor XIIa activates kinin (which also activates factor XIIa) and clotting cascades.
2) Kinin exhibits positive feedback to factor XIIa and also activates the fibrinolytic cascade.
3) The fibrinolytic response activates the complement system. |
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Term
| Why might you treat inflammation with NSAIDS instead of Corticosteroids? |
|
Definition
NSAIDS only block prostaglandin synthesis (inhibit cyclooxygenase) from arachidonic acid, while Corticosteroids block Arachidonic acid production in general, also preventing cells from making leukotriene and lipoxin mediators of inflammation.
Basically, you don't want to immunocompromise the patient to a point of further infection. |
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Term
| Why can you see damage to the stomach lining and gastric bleeding in patients taking NSAIDS to lower fevers? |
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Definition
| Prostaglandins are responsible for gastric mucosal protection. NSAIDS prevent their synthesis from arachidonic acid. |
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Term
1) How can NSAIDs act simultaneously as vasodilators and vasoconstrictors?
2) How does this relate to why you might treat with Aspirin instead of normal NSAIDs? |
|
Definition
1) They inhibit Cyclooxygenase.
This enzyme makes prostacyclin in endothelial cells, which is a vasodilator. So NSAIDs constrict endothelial cells.
This enzyme makes thromboxane in platelets, which is a platelet aggregation promotor. So NSAIDs dilate platelets
2) Aspirin is an irreversible inhibitor. Endothelial cells just make more prostacyclin, but Platelets cannot make more Thromboxane.
You end up with an adaptive endothelial response and vasodilation and inhibition of platelet aggregation in platelets. BLEEDING ISSUES ARE A PROBLEM |
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Term
| What do MCP-1, C5a, PDGF and TGF-a all have in common? |
|
Definition
| They all are chemoattractant signals for macrophages |
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Term
| What would you expect to see in a patient suffering from chronic inflammation in their kneed joint if they also have mutations in the gene encoding IL-12? |
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Definition
IL-12 is release by macrophages to recruit T-cells in cell-mediated immune responses.
The patient would likely be immunocompromised and might exhibit infections on top of the chronic inflammation, because the body can't fight off toxins and infections. |
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Term
| Why might you see overly-digested cell matrix in cells from a patient who has under-active macrophages? |
|
Definition
In addition to ROS, proteases and growth factors, Macrophages release TGF-b, which recruits inflammatory cells, fibroblasts and ACTIVATES TIMPs.
Without TIMP activation, MMPs will digest cell matrix. |
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Term
| You are worried that your patient is suffering from adenocarcinoma, so you take a biopsy of glandular epithelial tissue to look for tumors. Upon inspection, you discover nodules that are <1 cm in diameter. The attending scolds you and says that this is an infection. Why? |
|
Definition
These smaller nodules are most likely immune-type granulomas, that arise in response to a persistent insoluble antigen on a bacteria.
Tumors would most likely be >1cm in diameter (both metastasis and primary neoplasms). |
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Term
| How can you determine if a patient has CGD in the laboratory? |
|
Definition
CGD is a defect in NADPH oxidase, which prevents generation of superoxide and thereby prevents ROS-mediated bacterial destruction.
The lack of superoxide prevents the color reagent NBT from changing color, as it usually would in the presence of the O2- |
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Term
A patient presents with an inflamed thryoid. You order a thyroid enzyme panel and discover elevated levels of anti-thyroid peroxidase and anti-thyroidglobin in the patient's blood.
What is your diagnosis and why? |
|
Definition
Hashimotos Thyroiditis!
This is a disease of plasma cells in the thyroid, causing them to release too many antibodies that eventually lead to thyroid failure. You could also look for "germinal centers" in tissue specimens. |
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Term
| Upon examination of a tissue biopsy from the terminal illeum, you discover cryptitis (neutrophil-filled crypts), granulomas and a few ulcers. What do you think the problem is? |
|
Definition
Patient may have Crohn's Disease (CI in the terminal illeum).
You might also see fistula formation |
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Term
| A patient presents with vaginal discharge and severe ovarian inflammation. Why are you concerned? |
|
Definition
| This could be Pelvic Inflammatory Disease (PID), which is an infection that usually ascends through the fallopian tubes and can lead to peritonitis, bacteremia, meningitis and infertility. |
|
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Term
What stains would you order for your tissue biopsy if you suspected mycobacterial infection?
What about fungal infection? |
|
Definition
1) Acid-fast AFB stain
2) Grocott silver stain for fungi (if you see a necrotizing granuloma, this would tell you whether it was fungal-derived, or whether it was more likely to be Tb). |
|
|
Term
| What are the two most common Congenital causes of hypercoaguable states? |
|
Definition
1) Factor V Leiden mutation
2) Prothrombin gene mutation |
|
|
Term
| Why should you be wary of putting a patient on Heparin blood thinners if they had received the same treatment 2 months before? |
|
Definition
Heparin-induced thrombocytopenia!
Antibodies to Heparin that were generated in response to the last treatment will damage vessels and lower the platelet count! |
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|
Term
| Where might you see Libman-Sacks endocarditis? |
|
Definition
This is an autoimmune-induced case of Vegetations on the heart valves that is seen in systemic lupus erythematosus.
Usually Vegetations are non-bacterial thrombotic events, but they can also be infected, or autoimmune (such as in this case). |
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Term
| Why should you be especially careful when removing a long-dwelling catheter from a thin-walled vessel? |
|
Definition
| Thrombi may have propagated and organized (become fibrous) around the catheter. Don't rip the vessel! |
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|
Term
| What are the two most common causes of Pulmonary Emboli? |
|
Definition
1) Deep Vein Thrombosis
2) PICC lines
Medium-size ones can cause hemorrhagic infarctions
Large ones can cause acute right heart failure (cor pulmonale) |
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|
Term
What are the most common courses taken by systemic pulmonary emboli?
Fat?
Air?
Amniotic Fluid? |
|
Definition
They usually come from the heart and go to the brain or to the legs!
Fat emboli come from long bone fractures and can cause sudden onset dyspnea and thrombocytopenia within 1-3 after trauma
Air emboli occur after back surgery in a prone position (more than 100ml needed)
Amniotic fluid emboli go in pulmonary microcircuilation, causing cyanosis, shock and sever dyspnea. |
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Term
Where might you find white anemic infarcts?
Where might you find red hemorrhage infarcts? |
|
Definition
1) Artery-end organs like spleen, kidney and heart
2) Venous occlusion in ovarian torsion and dual blood supply in lungs and small intestine (there is still some supply for a hemorrhage to take place from). |
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|
Term
| Why is the liver less susceptible to infarction than the kidney? |
|
Definition
The liver has a dual blood supply!
Remember, infarction likelihood is determined by 1) vulnerability, 2) rate of vascular occlusion development, 3) blood supply and 4) oxygen content of blood. |
|
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Term
| What might histological findings might you use to determine whether tissue is granulation tissue? |
|
Definition
Look for new vascularization, fibroblasts, lymphocytes, a little collagen.
REMEMBER, THIS IS NOT A GRANULOMA |
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Term
| Why might you be concerned if a patient who suffered a severe skin laceration also suffers from diabetes mellitus, vascular disease, malnutrition, or was being treated with steroids? |
|
Definition
| These are all systemic factors that impair wound healing |
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Term
| Which is more serious, a fibrinous adhesion or a fibrous adhesion. How would you deal with each? |
|
Definition
Fibrinous is less serious and can be separated without a sharp instrument.
Fibrous adhesions require surgical lysis, which can create further adhesions! |
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Term
| A patient with severe gangrene in their right hand also presents with a defect in stromelysin-1. Why are you extremely concerned? |
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Definition
| Stromelysin-1 is a MMP (MMP-3) that is required to prevent severe wound contractures. You are worried that if you remove the digits, that there will be deformity and impaired movement. |
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Term
| Why is it important to know your patients race if you are considering a procedure that will lead to significant scarring? |
|
Definition
| African Americans are more likely to form Keloids (hypertrophic scars), consisting of collagen bundles and interspersed myofibroblasts that persist due to autocrine induction. |
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|
Term
| What would you call a malignant tumor of blood vessels? |
|
Definition
Blood vessels are composed of mesenchymal tissue (connective tissue), so it would be an angiosarcoma.
Similar examples are in bone and cartilage |
|
|
Term
| What do you call a cancer of plasma cells? |
|
Definition
| Myeloma (derived from myeloid cells) |
|
|
Term
| What features should you look for in a tumor specimen to try and determine whether it is malignant? |
|
Definition
1) Less differentiated means more malignant
2) Pleomorphism often indicates malignancy
3) Metastasis (almost always malignant).
4) Hyperplasia/Dysplasia/Anaplasia |
|
|
Term
| What are some characteristics that you should look for in a dysplastic cell population? |
|
Definition
1) Hyperchomasia
2) Clumped chromatin
3) Big nuclei
4) Pleomorphism
5) Loss of polarity
6) Abnormal mitotic figures. |
|
|
Term
| You see hard, white, fibrous tissue surrounding parenchymal cells of a neoplasm. What could this mean? |
|
Definition
| Desmoplasia of the stoma! Reactive stroma such as this can be seen in response to pre-invasive tumors. |
|
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Term
|
Definition
| A teratoma found in the ovaries |
|
|
Term
| Where do the cells arise from that end up in a Brunner gland harartoma of the duodenum submucosa? |
|
Definition
Trick Question!
The Duodenum submocosa. This is a congenital defect causing aggregation of the normal populating cells. |
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Term
| A young child presents with a tumor of primitive nerve cells. What might you call this tumor? |
|
Definition
| - Use the "blastoma" suffix for tumors composed of primitive nerve cells. In this case, it is a "Neuroblastoma." |
|
|
Term
| A patient presents with Intestinal Metaplasia of the esophageal lining (i.e. Barret's esophagus). Why are you most concerned? |
|
Definition
| This metaplasia has a tendency to develop into dysplasia and ultimately adenocarcinoma. |
|
|
Term
| A patient presents with Intestinal Metaplasia of the esophageal lining (i.e. Barret's esophagus). Why are you most concerned? |
|
Definition
| This metaplasia has a tendency to develop into dysplasia and ultimately adenocarcinoma. |
|
|
Term
| What does the pneumonic AIR DREAM have to do with tumor malignancy? |
|
Definition
In order to be considered malignant, a tumor must be
Autonomous
Invasive
Resistant
DNA repair issues
Replication without end
Evasion of apoptosis
Angiogenesis
Means to escape host response |
|
|
Term
| What are the major differences between Oncogenes and Tumor Suppressor Genes |
|
Definition
1) Oncogenes become active in response to mutations in Proto-oncogenes ("gain of function") and encourage cellular growth without external stimuli. Only one mutated copy is required.
2) Tumor Supressor Genes are growth-inhibitory genes that "put the breaks" on cell growth and division. Both copies must be eliminated in order for function to be lost. |
|
|
Term
| Explain why Nitrosamines and Alkylating agents have been described as "promotors" of carcinogenesis. |
|
Definition
After cells are "initiated" (i.e. a chemical agent has led to a genetic mutation), the changed cells must propagate this mutation for a neoplasm to develop.
Nitrosamines (used as preservatives) and Alkylating agents (chemotherapy agent) lead to cell proliferation, thereby "promoting" the initiated cells. |
|
|
Term
| Why is squamous metaplasia so dangerous in the cervix in a sub-group of women? |
|
Definition
| The HPV virus acts on squamous epithelium in the cervix leading to cervical cancer. |
|
|
Term
| How does H. Pylori infection relate to gastric adenocarcinoma and lymphoma? |
|
Definition
| Much like the case of Barret's esophagus, this infection causes stomach and duodenal ulcers, which are associated with intestinal metaplasia of the gastric mucosa. This metaplasia can lead to dysplasia and carcinoma. |
|
|
Term
| What is the "adenoma-carcinoma" sequence and how does it relate to tumor malignancy? |
|
Definition
| Loss of DNA repair gene function may lead to the inability to repair further genetic damage, leading to progressive accumulation of genetic mutations and ultimately to neoplasia. |
|
|
Term
Under the UICC system, how would you interpret the meaning of pT2 N1 M1 if the tumor is an adenocarcinoma of the lung?
How does it differ from the AJC system? |
|
Definition
Primary tumor is of the glandular epithelium of the lung and it is between 3-5cm (T2a). The pathologist found metastatic adenocarcinoma in intrapulmonary peribronchial lymph nodes (N1) and it was found in a distant site (M1).
In the AJC system, a single stage number (1-4) is given. In this case, this tumor is stage 4 if it exhibits metastasis and stage 2a if it does not. |
|
|
Term
| What is the most common tumor of the liver? |
|
Definition
| A Metastasis! Few tumors originate in the liver. |
|
|
Term
| Why do some tumors cause cachexia? |
|
Definition
Cachexia is general loss of body mass.
Some tumors increase overall body metabolism and can cause severe wasting. |
|
|
Term
| Why might you be concerned if you saw increased blood Calcium levels in a patient suffering from a mesothelioma? |
|
Definition
This could represent the paraneoplastic syndrome, "Hypercalcemia."
To remember paraneoplastic syndromes, remember "calcium" is in the name of "hypercalcemia," and both "Cushing" and "Cortisol" start with the same letter.
Other such syndromes include
Cushing syndrome (increased cortisol), which occurs when tumors produce ACTH analog and can affect metabolism.
Carcinoid syndrome (serotonin release from neuroendocrine tumors)- skin flushing, diarrhea |
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|
Term
| A patient presents to the ER and after ordering a liver panel, you discover elevated ALP levels. What is your initial diagnosis? |
|
Definition
Perhaps Intrahepatic cholestastis (Gall stones/bile duct obstruction).
However, could also be indicative of bone disease (Paget's). |
|
|
Term
| A patient presents to the ER and after ordering a liver panel, you discover elevated AST and ALT levels. What is your initial diagnosis? |
|
Definition
| Probably liver damage. These are tests of liver damage, as the enzymes are released when hepatocytes are lysed. |
|
|
Term
| A patient presents to the ER and after ordering a liver panel, you discover elevated GGT levels. What is your initial diagnosis? |
|
Definition
| Probably chronic alcohol toxicity, but cannot be sure. |
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