1. A 32-year-old woman had a firm nodule palpable on her uterus three years ago noted on a routine physical examination. The nodule has slowly increased in size and is now about twice the size it was when first discovered. She is asymptomatic. Which of the following does this patient most likely have?
A. Adenocarcinoma
B. Leiomyosarcoma
C. Rhabdomyosarcoma
D. Leiomyoma
2. A 36-year-old woman finds a lump in her right breast. Her physician notes a 4 cm firm, irregular, fixed mass in the upper outer quadrant of her right breast. A fine needle aspiration is performed, and the findings are consistent with infiltrating ductal carcinoma. The mass is removed, and a sentinel lymph node dissection is performed. Which of the following findings will best predict a better prognosis for the patient?
A. The patient has concurrent ductal carcinoma in situ in the same breast
B. The sentinel node is negative for tumor
C. The patient has a sister who had a similar type of breast cancer
D. The tumor has a high grade
3. Which of the following neoplasms is derived from all three germ layers?
A. Carcinoma
B. Teratoma
C. Sarcoma
D. Apudoma
4. An 82 year old, otherwise healthy male is found to have a firm prostate nodule on rectal examination. His serum PSA is 20 ng/mL. The microscopic appearance seen on the prostate biopsy will most likely show which of the following?
A. Chronic prostatitis
B. Adenocarcinoma
C. Leiomyoma
D. Rhabdomyosarcoma
5. Gonorrhea:
A. Is commonly seen as a testicular infection in men
B. Can be prevented by immunization
C. Is usually asymptomatic in women
D. Is usually asymptomatic in men
6. A skin rash is characteristic of which stage of syphilis?
A. Primary
B. Secondary
C. Tertiary
Boards review presentation: STDs
11.25.09
Here's a little info on STDs that might help as you prepare for boards. There are a few board review questions here and there in Dental Stax and Dental Decks on STDs - so you should probably know a little bit.
Mammograms: wait until 50?
11.26.09
That be crazy talk. Here's a New York Times article from last week with opinions on the recent pronouncement by the United States Preventive Services Task Force.
Happy Thanksgiving!
11.26.09
I hope you have a wonderful day. Safe travels, if you're going somewhere; if you're staying home, I hope you can think of a long list of things to be grateful for. My list includes having a job I love. Thank you for being such a nice class: attentive, curious, kind, and just all around pleasant...I look forward to coming to "work". I wish for the same for you when you finally finish!
Here's a post on the New York Times Well blog about prostate cancer screening using the PSA. We talked about this a bit on Friday. The PSA may not be as good at screening as was originally thought. It seems it may save few (if any) lives, while causing lots of unnecessary and debilitating treatment. Something to ponder.
Help!
11.30.09
I received an email today from someone who felt that despite trying to write as many notes as possible, it was still hard to catch names of illnesses and just the overall plan - and the notes seem to provide little guidance as to how to approach the material. I realize there are a lot of images in the powerpoint from today - and a lot of information in the notes (which are posted in our notes section but were not passed out in class today). I put together a summary of the main diseases and a few important points about each one. There may be a test question or two on material not in the summary (we don't have the test questions yet) - but I think if you focus on the summary, that should be a good study plan.
More help!
12.1.09
More emails today regarding the nervous system lectures. Here is a summary of what I think you should take away from the lectures. I would focus on this summary when studying, using Dr. Santa Cruz's powerpoint and notes to fill in meaning when necessary.
Epidural/subdural hematoma diagram
12.2.09
Here's the diagram from Robbins that I showed in class today. I think it shows nicely the difference between epidural and subdural hematoma. It even has the middle meningeal artery ruptured on the epidural hematoma side.
Melanoma warning signs
12.2.09
I talked briefly about some of the warning signs for melanoma. There are a few different ways to evaluate moles. One common mnemonic is "ABCDE," which stands for asymmetry, border, color, diameter, and evolving. Another more recently-described way to evaluate moles is the "ugly duckling" method, in which you look for moles that stand out from all the patient's other moles. This may be easier than trying to evaluate each mole for each of the ABCDE signs. It has been shown to be a sensitive and effective way to screen for melanoma, even among lay people. Whatever method you choose, the important thing is that you do it, on yourself and your loved ones - and frequently. The incidence of melanoma is rising alarmingly; prevention and early detection are critical.
Quiz 7 scores are now posted. I also posted your total score so far, your total score minus your two lowest quizzes, and your current grade.
I'm bored
12.2.09
If you haven't checked out our "More" page, you should do so immediately. There are two new sites (an ASCII art generator that really works and a totally addictive snake thingy) and one sort of new site (lethal penguin). Don't miss the Wu-name generator. Mine is New Fast Automatic F-REEK. Not listed, but also fun, is the pimp name generator. My favorite was Professor Truth Krafts Dogg. Either that or Suede Krafts Shizzle. I'm not sure.
Some of you asked yesterday if there was going to be a summary of developmental pathology. Here it is. I would focus on the summary, and then go to the powerpoint currently posted on our website for explanations.
Marfan syndrome
12.8.09
Speaking of Marfan syndrome, one of my uncles has the disease, and he let me take some pictures of his hands (one of which is at left). You might want to take a look at the photos - and read a bit about some famous people who had Marfan syndrome (or something resembling Marfan) in case you encounter a patient with the disorder some day. Patients with Marfan have an increased risk of cardiovascular disease - mostly aortic valve lesions and aortic dissection - so you would be doing someone with undiagnosed Marfan syndrome a great service by recognizing their signs and symptoms.
4. Which lipid storage disease results from lack of sphingomyelinase and can lead to severe neurologic impairment in children?
A. Gaucher's disease
B. Fabry's disease
C. Tay-Sachs disease
D. Niemann-Pick disease
Patient voices: rheumatoid arthritis
12.9.09
The New York Times has a very interesting feature called Patient Voices, in which you can listen to patients talking about how their disease has affected their lives. Here is an installment with patients talking about their rheumatoid arthritis.
Boards review questions: Endocrine pathology
12.14.09
Please check these questions out...there is some good info in the answers that both highlights and supplements the material we will be covering in class today!
1. Acromegaly is a chronic metabolic disorder of adults caused by an overabundance of:
A. Parathyroid hormone
B. Growth hormone
C. Epinephrine
D. Thyroid hormone
2. A 58-year-old female has had a 20-pound weight gain over the past two years. She has noticed increasing cold intolerance and sluggishness. On physical exam her heart rate is decreased, and her reflexes are delayed. Her serum TSH is 11.8 mU/L (normal = 0.3 - 3.0), and her T4 is 2.3 micrograms/dL (normal = 4.5 - 12.5). A year ago, anti-TSH-receptor antibodies were detected at high titer. Which of the following diseases does she most likely have?
A. Papillary thyroid carcinoma
B. Hashimoto's thyroiditis
C. Goiter
D. Graves disease
3. Extreme hypothyroidism in adults is called:
A. Addison's disease
B. Myxedema
C. Graves disease
D. Rickets
4. All of the following are true regarding type I diabetes EXCEPT:
A. It accounts for 90% of all cases of diabetes
B. The body makes little or no insulin
C. Daily injections of insulin are required to sustain life
D. Likely long-term complications of poorly-controlled type 1 diabetes include: hyaline arteriolosclerosis, proliferative retinopathy, nodular glomerulosclerosis, and peripheral neuropathy
E. It is usually diagnosed in childhood
5. Addison's disease is caused by damage to the:
A. Pancreatic islets
B. Thyroid gland
C. Parathyroid glands
D. Adrenal cortex
6. The most characteristic symptom of pheochromocytoma is:
A. A bleeding tendency
B. Persistent or paroxysmal hypertension
C. Hypoglycemia
D. Persistent diarrhea
7. Chvostek's sign and Trousseau's sign indicate:
A. Botulism
B. Rickets
C. Tetany
D. Bell's palsy
8. A 55-year-old patient presents with recently diagnosed diabetes. He also has front teeth that are more widely spaced than normal and have recently begun to flare. Which undiagnosed disease does this patient most likely have?
A. Gigantism
B. Hyperparathyroidism
C. Paget's disease of bone
D. Di George syndrome
E. Acromegaly
9. A patient presents with osteomalacia, loss of the lamina dura around the teeth, brown tumors in bone, and duodenal ulcers. His family reports his personality has changed. Which of the following disorders should you suspect him of having?
A. Hyperparathyroidism
B. Hypoparathyroidism
10. All of the following statements regarding multiple endocrine neoplasia II are true EXCEPT:
A. Patients have increased incidence of thyroid carcinoma
B. Patients have increased incidence of pheochromocytoma
C. Patients have increased incidence of mucosal neuromas
D. It is autosomal recessive
E. Differential diagnosis includes von Recklinghausen's disease
11. Which of the following statements regarding pheochromocytoma are true?
A. Patients may present with torso pain
B. Norepinephrine production is decreased
C. It is a tumor of the adrenal cortex
D. It causes jitters and hypertension
E. Patients may have severe headaches
12. Cushing Syndrome may be caused by all of the following EXCEPT:
A. An adrenal cortex tumor
B. A posterior pituitary tumor
C. A paraneoplastic syndrome
D. Iatrogenic factors
E. All of the above may cause Cushing Syndrome
13. Patients with Graves' Disease may show all of the following EXCEPT:
A. Decreased appetite
B. Exophthalmos
C. Heat intolerance
D. Tachycardia
E. Irritability
14. Which of the following is associated with Addison's disease?
A. Hypotension
B. Diabetes
C. Osteoporosis
D. Central obesity
E. Increased appetite
15. Patients with hypothyroidism may show all of the following symptoms EXCEPT:
A. Short stature
B. Retention of deciduous teeth
C. Stunted skeletal growth
D. Hair in the oral cavity
E. Mental slowness
16. Which of the following is a function of the parathyroid glands:
A. Secrete calcitonin
B. Decrease serum calcium
C. Stimulate osteoclasts
D. Aid in the absorption of calcium from the gut
World's tallest man
12.14.09
Here is a video showing a bit about the life of Leonid Stadnyk, the world's tallest man at 8 feet 5 inches. We talked about him a bit in class today; do you remember the disease responsible for his abnormal growth? He is not happy about either his height or his notoriety; he has been quoted as saying that his height is "God's greatest punishment for him." Although his life is difficult in many ways, his fame has brought help from people all over the world, and he says he feels better as a result.
Stress in women
12.14.09
We talked about oxytocin in class - it's a hormone that appears to be linked to everything from trust, to cuddling, to monogamy. Here's a cool study on stress in women. The study says that when women are stressed, they tend to turn to their families and friends for support, whereas men tend to hole up alone. The hormone oxytocin - which we'll talk about tomorrow - has a calming effect, and may play a role in this behavior. Estrogen appears to enhance the effects of oxytocin, but testosterone reduces its effects. Interesting.
Iodine deficiency
12.14.09
We also talked today about hypothyroidism. Here is a short story about how this disease affected one child's life. Congenital hypothyroidism is the biggest cause of preventable mental retardation in the world, and it is most prevalent in disadvantaged areas of the world. In most cases, it is simply due to a lack of iodine in the diet. Unicef is working to eliminate iodine deficiency in all parts of the world. Iodine is cheap; even a small donation will make a big difference in many children's lives.
Things that increase estrogen
12.18.09
When we did female reproductive pathology a few weeks ago, we talked about risk factors quite a bit. One big-time risk factor for lesions in the female reproductive tract is estrogen. Increased estrogen exposure is a risk factor for endometrial hyperplasia, endometrial carcinoma, ovarian carcinoma, and breast carcinoma. Several things can increase a woman's exposure to estrogen, including: obesity (estrogen is increased in adipose tissue), post-menopausal estrogen replacement therapy, late age at first pregnancy, nulliparity (no pregnancies), a long duration between menarche and menopause, and anovulatory cycles (if you don't ovulate, you don't get that nice progesterone phase that comes after ovulation; in effect, you don't get a break from estrogen). Oral contraceptives appear not to be related to an increase in estrogen exposure. At least, they do not appear to increase the risk of these tumors. In fact, they are related to a decrease in ovarian carcinoma! I wanted to clarify those risk factors in case they did not make sense in class. Let me know if you have any questions.
Questions that came up while studying
12.19.09
Here are some good questions that came in today and yesterday - thought everyone might benefit from them.
Q. How does uniparental disomy work?
A. This is kind of complicated; I'll try to summarize it and then give you a website with more info.
Uniparental disomy means that you inherit two copies of a particular chromosome from one of your parents, and no copy from the other parent. It can happen in three ways, all of which involve two consecutive mistakes in cell division.
1. Trisomic rescue. This happens when you get a trisomy (as happens when the chromosomes don't split up the way they should during meiosis, and you end up with two copies of some chromosome from mom and one from dad - or vice versa), and then you lose one of those three chromosomes (the "odd one out", the lone one from one of the parents). You're left with two chromosomes from one parent, and none from the other.
2. Monosomic rescue. This happens when you have a monosomic zygote (only one copy of a particular chromosome - the other parent's dropped out), and that chromosome duplicates itself.
3. Gamete complementation. This is when you have a gamete with two copies of a chromosome (should have only one), and it gets fertilized with a gamete that happens to have no copies of that chromosome.
Here's a good reference with diagrams. When I read about this stuff, it's amazing to me that things usually go right.
Q. I have been trying to figure out the thyroid lab tests. If you have a high TSH and a low T4 does that mean that the pituitary gland is going crazy to reach homeostasis but the thyroid is not responding? And inversely if the T4 is high and the TSH is low does that mean for some reason the thyroid is goin workin overtime due to an outside influence such as graves disease and the Pituitary is trying to compensate by not producing TSH?
A. That's exactly right! When the two (TSH and T4) are opposite of each other - high T4/low TSH or low T4/high TSH - that means that the problem is intrinsic to the thyroid gland (Graves disease or Hashimoto thyroiditis, for example) and the pituitary is trying to control the thyroid by producing more or less TSH. Those are the most common types of thyroid disease - those that are intrinsic, or primary to the thyroid gland itself.
On the other hand, if both TSH and T4 are either low or high - high T4/high TSH or low T4/low TSH - that means that the process is being driven by TSH. Either there's a pituitary adenoma making a ton of TSH, or the pituitary is not working well for whatever reason (it's been radiated, or has undergone necrosis) and it's not making enough TSH.
Q. With regards to Array CGH, I do not understand why balanced rearrangements could not be detected...Why can they not make a probe for an inversion of a few genes or an insertion of a gene? I guess I do not see how these would be any different from making a probe for a deletion or duplication. I am sure I am missing something though...
On that same note, what would a translocation be considered?? Similar to an inversion, I am assuming (balanced).
A. (From Dr. Dolan) Array-based CGH is a DNA based test that, in a much-simplified nutshell, looks at the quantity of DNA in a patient vs the quantity of DNA in a specimen derived from a pool of normal controls. Thousands of different probes from loci spanning the genome are present on a chip. If there is LESS DNA in the patient than the control for a particular probe, the a-CGH will show a DELETION of material from the patient for that particular locus; if there is MORE DNA in the patient than the control for a particular probe, the a-CGH will show a GAIN of material from the patient for that locus. In a balanced translocation, there is NO gain or loss of material, so the probes will show that the patient and the control have equal amounts of DNA in those translocated regions.
To detect a translocation, then, one would need to do a G-banded chromosomal analysis (i.e, look at the chromosomes under the microscope, the "old-fashioned" way). In that way, the material exchanged between the chromosomes involved in the translocation could be identified because they would LOOK different than their normal homologs -- but because the translocation is balanced, there is NO gain or loss of DNA in this exchange, so array-CGH would not detect any genetic imbalance. In cancer cases, in which the genetic abnormalities involved in certain translocations have been well characterized (e.g., the 9;22 translocation in chronic myeloid leukemia involves breakage and rejoining of the ABL gene on chromosome 9q34 and the BCR gene on chromosome 22q11.2), FISH probes can be developed because we know the gene sequences of ABL and BCR. In contrast, however, for a constitutional balanced translocation that is passed on through a family or develops de novo in a patient, we don't know what those genes are -- so we don't know the base-pair sequences that would enable us to develop a FISH probe. For these cases, then, we are limited to characterizing the abnormality as best we can by means of a G-banded chromosomal analysis.
At the risk of complicating this picture, I will add one further little scenario. Not all translocations that LOOK balanced in a G-banded chromosomal analysis really ARE balanced at the level of the DNA sequences. That is, in the process of formation of the translocation, sometimes very small amounts of DNA can be gained or duplicated at the breakpoints of the translocation. These amounts of DNA are way too small to be detected under the microscope in a G-banded chromosomal analysis (remember, the limit of detection for our eyes at the microscope is about 3 megabases of DNA (i.e. 3 million base pairs)). Gains or losses of DNA at the breakpoint of these apparently balanced translocations that are SMALLER than about 3 MB would NOT be detected in a G-banded chromosomal analysis. For this reason, if a patient is diagnosed with a de novo (not inherited from the parents) translocation that LOOKS balanced under the microscope (via a G-banded chromosomal analysis), we would still recommend that a-CGH be performed -- because a-CGH would be able to detect any such small imbalances at the breakpoints of the translocation.
Q. What should we focus on for the alcohol/drug lecture in terms of the exam? I am assuming we won't be tested on the testimonial portion but was hoping you might be willing to give some direction beyond that assumption.
A. I would focus on the powerpoint - perhaps take a look at it in our lecture video. There are only a few slides so I don't think it would take long to read through (you don't even need to listen to the audio) and get the gist of what he's saying. You don't need to remember specific numbers, but you might want to remember general trends (e.g., the number one drug of abuse for adults is alcohol). You're right - the testimonial was just illustrative, to give you a feel for how addiction develops.
Q. Are goiters developed in the thyroid mainly with an increased level of TSH?
A. Goiters are produced when the thyroid gland is stimulated to grow - either by TSH, or by autoantibodies that bind to/turn on TSH receptors. So you can get a goiter with Graves disease, with a thyroid-producing adenoma, or with lack of iodine/inability to make thyroid hormone for whatever reason (these patients have an increased TSH). So you can have a goiter in the setting of increased TSH (like in iodine deficiency) or in the setting of decreased TSH (like in Graves disease).
Q. So does that mean that a primary hyperthyroidism wouldn't cause a goiter?
A. You can get a goiter with a problem that is primary, or intrinsic to the thyroid gland. Graves disease is considered a form of primary hyperthyroidism - because the problem is in the gland itself; in effect, the gland is stimulating itself to grow (with the help of the autoantibodies).
Q. Would Graves disease cause a goiter because of the anti-TSH receptor antibodies?
A. Yes. Those antibodies stimulate the TSH receptors and cause T4 release and thyroid growth.
More questions that came up while studying
12.20.09
Q. Would nulliparity also be a risk factor in endometrial hyperplasia?
A. Yes, actually, it is, although our textbook doesn't mention it. It falls into the category of things-that-increase-estrogen-exposure, so it's a risk factor for any of the tumors related to estrogen excess.
Q. When it comes to prostate cancer, you mentioned that PSA detection isn't always indicative of a malignancy, would palpation be a better way to detect prostate cancer?
A. PSA is a problematic test for exactly the reason you stated: a positive result is not always indicative of malignancy. So a lot of men are being subjected to further tests and perhaps even treated unnecessarily. The problem I see with just abandoning the PSA is that there really isn't a better, more specific way to detect prostate cancer. Many prostate cancers are detectable by palpation (because they tend to occur in the peripheral zones of the prostate), but if that was your only detection method, you'd only detect cancers that were 1) in that area (and many are not) and 2) big enough to palpate. SO...although they've abolished the PSA as a routine screening test in many other countries, we haven't quite crossed over yet, and we're still using both PSA and rectal exams as our screening methods.
Q. Do we have to focus on the histology portions of the lesions that were given to us in the skin pathology section, i.e. do we have to know what's going on histologically?
A. For the skin section, I would focus on the summary sheet, and fill in whatever you don't understand from the ppt/notes. I would not focus on the histology portions of the lesions, beyond knowing that melanoma comes from melanocytes, basal cell comes from basal cells, etc. You aren't going to be getting specific questions on skin histology on the boards, if the past is any indication.
Q. Should we focus on the various parts of the brain affected by the neurological lesions, such as those that are affected in a stroke?
A. No. I would focus on the summary sheet, and there is little or no mention of specific brain regions in the summary - except in just a few places (like Parkinson's disease involves the substantia nigra).
Q. Is the back pain associated with ovarian cancer localized or general, and if localized, could you please enumerate?
A. To my knowledge it is pretty generalized; it is often more lower-back, probably associated with pelvic pain. It’s not something that’s described in great detail; most sources just say “back pain”
Q. In endometriosis, is the glandular tiss found outside of the uterus & not assoc. w/it at all other than being of similar cellular make up? In other words, is this essentially extra-uterine menses?
A. It is extra-uterine endometrial tissue, not associated with the stuff inside the uterus at all – other than it is under the same hormonal control, so when the endometrial tissue inside the uterus undergoes cyclic changes, so will the endometrial tissue (endometriosis) outside the uterus.
Q. In the risk factors for endometrial hyperplasia is exogenous hormone equivalent to the use of estrogen replacement therapies?
A. I think you’re asking whether the terms “exogenous hormone” and “estrogen replacement therapy” are the same thing – if not, let me know. In this setting, yes, they are the same thing. If you want to be complete about it, there are other kinds of exogenous hormones – like birth control pills – but when we’re talking about endometrial hyperplasia, the exogenous hormomes referred to are estrogen replacement therapy (birth control pills don’t have that effect on the endometrium).
Q. There are 3 categories of EH: simple, complex & atypical. Do "we" need to be be able to differentiate between the three & if so, how shall "we" do so?
A. No, you don’t need to for purposes of the exam. I showed them so that you would know somewhere, in the back of your mind, that there are different types of endometrial hyperplasia (with the “atypical” type being most risky for development of carcinoma) in case you run into it some time.
Q. It seems like too much estrogen causes a bunch of issues. Do many of said pathologies present simultaneously in the presence of XS estrogen?
A. No, not usually, if you’re talking about estrogen-related tumors. The chances of any one tumor arising are relatively small (even though the risk is increased compared to the setting of normal estrogen), so the chances of two developing at the same time
Q. Is there a stress/cortisol/obesity/estrogen connection in any way?
A. Hmmm – I’m not sure. I know there is a connection between obesity and estrogen (obese women = more estrogen) and obesity and cortisol (obese patients = less glucose-tolerant). And there is a connection between stress and cortisol (more stress = more cortisol, at least in the short term). But as for the linkage between these connections, I’m not sure about that.
Q. Can you give an example of what/where etc. Metrorrhagia would be or take place?
A. Metrorrhagia = bleeding outside the normal period time. That could be breakthrough bleeding at ovulation, or abnormally-timed bleeding around the time of menopause, or bleeding from an intra-uterine tumor (which would not follow normal hormonal stimuli).
Q. Could a/an/the teratoma be a/an extopic/tubal pregnancy?
A. No – a teratoma is a neoplasm; it is monoclonal. It arises from a germ cell that has gone bad, and has decided to develop into all three germ cell layers. The cells may grow to look like normal tissues, but they’re not under any embryologic organization or control (they just grow haphazardly). A pregnancy, whether it is intrauterine or extrauterine, is not monoclonal; the tissues are growing in response to embryologic signals, and if left alone, will organize into a human.
Q. In peau d'orange, there is mention of "glandular tissue appearance" in my notes. Does this mean *new* glandular tissue appears or that *existing* tissue changes to appear as though it is now glandular in its type/origin?
A. Peau d’orange (“skin of the orange”) happens when you have a breast cancer that has infiltrated the lymphatics of the breast skin, making the skin edematous and orange-peel-looking. This change often happens in inflammatory breast cancer (so-named because the skin can look inflamed), in which the tumor preferentially involves lymphatics. I’m not sure where the “glandular tissue appearance” came from in your notes…I can’t think of how that could be related to peau d’orange.
Q. Is the TNM staging chart worth committing to memory?
A. No. It is different for every tumor anyway. I wanted you to know what it is (a staging system used for almost all tumors, in which you look at Tumor size (T), number of Nodes positive for tumor (N), and whether or not there are Metastases (M).
Q. In neoplasms, when looking for fluid accumulation, is it in the scrotum or somewhere else?
A. When you’re looking for testicular tumors, one of the things you look for is fluid accumulation in the scrotum – not other places.
Q. In Prostate carcinoma, are the osteolytic lesions a form of METS or something or what?!?
A. The osteolytic lesions are metastases from the primary prostatic tumor.
Q. Other than the review you placed in our hands do you have any insight on what/how this will be addressed in the exam?
A. My advice would be to stick with the review, make sure you know that, and if you need to go to her notes/ppt that is fine, but if you know what’s in the review you should be good.
Q. I penned in the word "sporocytosis" on my packet on the page related to scabies. Would you be willing/able to help me out with that one in terms of meaning (google = no good on this one) & relevance to the discussion that this packet covered?
A. I don’t know what “sporocytosis” means – maybe you were writing down “sporotrichosis” which is a fungal infection (caused by Sporothrix shenckii, a fungus that likes to live on trees/plants/decaying vegetation). It’s often called the “rose gardener’s disease” because you can get it from pricking yourself with a rose thorn. It’s not related to scabies – maybe it just got written there by accident.
In case you need a laugh
12.20.09
Here is a PowerPoint depicting a day in the life of Clucky, my little gumball-pooping chicken. This is back in the day when they used to put us up at Fitgers, a nice hotel in Duluth, because I was a guest lecturer. Ah, those were the days.
Also: two funny youtube videos involving cats. No, these are really funny.
Just a reminder that our exam rooms are Mayo 3-100 and 3-125. We'll be dividing up alphabetically - there are signs on each door saying which letters of the alphabet go to which room.
Thank you!
12.20.09
Hi everyone...I hope you all had a restful and safe Holiday break. Thank you for a wonderful semester! I really enjoyed getting to know you all, and I had a great time in class with you. Thanks for being so receptive, and for giving me feedback throughout the course. I wish you all the very best in your remaining time here. If you ever have pathology questions, drop me an email! On another note: if you haven't done your course evaluation, please do so as soon as possible so we can issue grades. I'll post them as soon as the evaluation is complete.
