Travel History - Clues to Infectious Disease Diagnosis in a Traveler
• Where did you travel? Includes layovers, intermediate stops, urban versus rural → Geographic disease association
• How long did you stay? → Risk of malaria increases with duration
• Accommodations? → Travelers' diarrhea
• Source or drinking water → Giardia
• Ingestions?
• Raw meat → Non-typhoidal salmonella
- Seafood → Hepatitis A
- Unpasteurized dairy → Brucella, Listeria
• Exposure to fresh water? → Leptospirosis
• Rafting, kayaking. swimming → Schistosomiasis
• Skin contact with soil? → Strongyloidiasis
• Animal exposure and/or bite? → Rabies, cat scratch fever (bartonella), Simian Herpesvirus B infection
• Insect exposure and/or bite?
- Mosquito → Malaria, dengue, Chikungunya, Zika
- Tick → Rickettsia, Lyme, Anaplasma
- Fleas → Murine typhus, plaque
• Tattoo's, piercings? → Hepatitis B, Hepatitis C, HIV
• Medical care while overseas? Blood transfusion → Hepatitis B, Hepatitis C, HIV
• Sexual contact?
- Unprotected sex with a new partner → HSV, HIV, Hepatitis A/B/C, syphilis
- Commercial sex worker exposure → Gonorrhea, Chlamydia, Zika
UW IM Residency @uw_IMresidency
#Travel #History #HPI #Interview #InfectiousDiseases #Infections #differential #Diagnosis #Traveler
Polycythemia - Differential Diagnosis Algorithm
Polycythemia itself isn’t a diagnosis. Like many things, it is a condition with an underlying cause.
How we define polycythemia:
- Male: Hb>16.5 g/dL, Hct>49%
- Female: Hb>16.0 g/dL, Hct>48%
Remember that a one-off value won’t cut it. Tempo and delta are key to dx. Look back in the chart. Is this new or a trend? If new, make sure you check at least one additional Hb AND make sure to account for potential hemoconcentration.
We may ask why are there so many RBCs?! Instead, pause, and try asking, “what stimulates our body to produce more RBCs?” Erythropoeitin! a.k.a EPO. Check a level.
While you’re waiting for the EPO level, check if your patient needs rx first and dx second. Too many cells in the circulation = risk of hyperviscosity. Ask some questions centered around the most frequently affected systems: neuro, heme (bleeding), CV
Hyperviscous? Better call hematology. This patient may need urgent plasmapheresis, phlebotomy, or chemo. Not hyperviscous? Sweet, we have some time, let’s see what came of that EPO level.
Most polycythemia comes in two general flavors:
- EPO-independent (primary) -> something else is driving RBC production
- EPO-dependent (secondary) -> something is ramping up EPO levels
Primary polycythemias - Typical issue: mutations, EPO levels: realllly low.
- Acquired: polycythemia vera (JAK2 V617F) and MPNs (MPL, CALR, also JAK2)
- Inherited: honestly, this list is long and obscure, and I don't know. Look it up
Secondary polycythemias - Typical issue: oxygen (delivery/sensing) vs tumor vs exogenous, EPO levels: normal/high
- Chronic hypoxia & bad oxygen sensing (at kidneys)
- Some tumors produce EPO
- Some people put things into their bodies
Note about secondary causes: Many of these conditions can be screened for with a good history! Even though you’ll do a good workup, think about common co-morbids that can drive this disease.
Finally, it’s always a good idea to call your friendly neighborhood hematologist if you’ve made a diagnosis or if you’re stuck. As with many disease processes, there can be a spectrum and overlap. Best to have an expert around to help.
Dr. Anand Jagannath @AnandJag1
#Polycythemia #Differential #Diagnosis #Algorithm #workup #hematology
The Cell Cycle
The cell cycle is the series of tightly regulated steps that controls cell growth (phase G1, G2), DNA synthesis (S phase), and the gymnastics of DNA segregation and cytokinesis (M phase). Control flux through the cell cycle arrises from interplay between the Cyclins and their Cyclin-dependent kinases (CDKs), promoting the cell cycle, and the tumor suppressors (the transcription factor (regulators) Retinoblastoma (Rb) and p53 shown here) which prevent progression through the cell cycle.
Cancer, in simplest terms, is unregulated cell proliferation. Both Rb and p53 serve as stop-gaps to unregulated cell proliferation by inhibiting the transcription factor E2F (in the case of Rb), preventing progression through the G1/S checkpoint, or directly acting as a transcription factor (in the case of p53), preventing progression through the G1/S, S/G2, G2/M checkpoints.
Did you notice how much p53 seems to be doing? Thats right, p53 regulates 3 out of 4 of the cell cycle checkpoints, including the important task of responding to and repairing damaged DNA. When the cell senses damaged DNA, p53 is activated, halting the cell cycle and upregulating enzymes that repair damaged DNA. If, however, the task is too great, p53 will initiate a programed cell death pathway to protect the organism from a potential cancer cell. It should be no surprise then that p53 is found to be mutated in over 50% of cancers.
While taking place at the cellular level, you’ve probably experienced this yourself. Ever had bad sunburn? Yes, its p53 (and a host of other proteins) that cause your top layer of skin to dye and peel off. Yuck! But it’s not just us who rely on p53. The famously long lived elephant has 40 copies of the p53 gene (TP53) to our measly 2, and researchers currently believe that may be one reason why an elephants lifetime risk of cancer is <5% compared to our +30% risk (although finding MRIs big enough for an elephant is a tad bit tricky).
#cell #cycle #p53 #Cyclins #Cyclin-dependent kinase #CDK #tumor suppressor #transcription factor #Rb #Retinoblastoma #tp53 #cell cycle #Cancer #proliferation #TF #E2F #checkpoint #DNA #cell death
