A Year with Harrison's

Prediabetes

2009-01-19T15:34:00.003-05:00

Now that I read my cards chapter and I got a few hours of sleep in at home, it's back to endo. I'm on the diabetes chapeter and some things to point out:

- Hepatic gluconeogenesis is responsible for fasting sugars that are too high according to Harrison's. But when I was working with the endocrinologists you also have to make sure a high fasting isn't from just drifting down from a high the night before.
- When insuling resistance increases in type 2 diabetics, the free fatty acid flux from adipocytes is incrased leading to higher levels of VLDL and free fatty acids. This can lead to NASH and abnormal transaminases leading to reduced HDL and increased small density LDL.
-Two severe forms of insuline resistance have been described in adults:
+ In type A, yound women present with severe hyperinsulinemia, obesity and features of hyperandrogenism. Patients have a defect in the insulin-signaling pathway.
+ In type B, middle-aged women have severe hyperinsulinemia, features of hyperandrogenism, and autoimmune disease. It is thought to be caused by autoantibodies to the insulin receptor. It can also cause intermittent hypoglycemia as the antibodies and block or stimulate the receptor.
- In regards to prediabetes, the ADA stated that metformin could be tried in patients at hight risk which include: age < 60, BMI > 35, family history of diabetes in a first-degree relative, elevated triglcerides, reduced HDL, hypertension or A1C <6%.

Cardiac Biology

2009-01-18T23:26:00.003-05:00

So tonight is the first night in my two week stretch in our cardiac unit. It's been about 2.5 hours in and so far just one code. The code could have been a rapid response probably but we transfered her over to the MICU. Apparently there was a seizure and when I got there the sat level was in the 70s.

The census is small over in my unit so I figured I'd get some reading done. I'm going to read some about cardiology since I'm not a big fan and maybe some on seizures if there is any extra time.

The first chapter is on cardiac biology. Endothelial cells do so much more than I remembered learning in medical school. They produce all these factors for vasodilations (NO, prostacyclin, etc) and for vasoconstriction as well an anti-inflammatories, anti-oxidants, anti-thrombotics and antiproliferatives.

I never knew you could do a test to access endothelial function. Basically you can occlude blood flow with a blood pressure cuff and then measure the change in the branchial artery via ultrasound after blood flow is restored. Normal values are abour 10%. A more invasive approach would be to give acetylcholine or methacholine into the arteries to stimulate NO release.

All the rest of the good stuff reviewing the cardiac cycle. Yay.

amiodarone-induced thyrotoxicosis

2009-01-15T11:59:00.003-05:00

Amiodarone Induced Thyrotoxicosis (AIT) can occur can occur any time a patient is on amiodarone with average of about 3 years before a diagnosis is made.

There are two key terms that always come up when talking about amiodarone-induced thyroiditis.

(1) Wolff-Chaikoff effect - this is the hypothesis that excess iodine will cause hypothyroidism. Amiodarone is almost 40% iodine. There usually is mention of "escape from the Wolff-Chaikoff effect" where the thyroid function returns to normal which usually happens after about 10 days.
(2) Job-Basedow effect - hyperthyroidism that occurs after the adminstration of iodine such as via amiodarone or contrast which provide more substrate for making thyroid hormone.

There are also two types of amiodarone induces thyroiditis:
Type I - is attributed to excess iodine prividing extra substate and leading to inceased production of thyroid hormone. It is usually seen in patients who have an underlying thyroid problem such as Grave's or multinodular goiter. Color flow doppler shows increased flow. Serum IL-6 levels are normal or slighly elevated.
Type II - is from a destructive process attributed to the toxic effects of amiodarone. Color flow doppler shows decreased flow. Serum IL-6 levels are hypothesized to be an indicator of thyroid destructive processes and are markedly elevated. The increased thyroid function is secondary to leakage of hormones as cells are destroyed.

Type I is usually treated with thioamindes like methiazole 30-40 mg daily along with potassium perchlorate 1g/day for 16-40 days). Amiodarone should be discontinuted. After the thyroid and normalization of iodine in the urine, the patient should be treated with radiation or thyroidectomy.

Type II can be treated with glucocorticoids for up to 2-3 months (start prednisone 40mg/day). Stop amio. Can add thioamide and potassium perchlorate. When pt becomes euthyroid, cont to monitor for hypothyroidism.

Pterygium

2009-01-15T10:48:00.004-05:00

So I had interview #1 for fellowship yesterday. It was interesting to say the least. I think I could write a whole article on the poor planning, how I was asked about my personal life (this is actually not allowed, by the way), no lunch was planned etc. It wasn't one of my top choices for fellowship so the good thing is that I got to do a practice interview. I was pimped on amiodarone-induced thyroiditis and vit D deficiency so more on that later. The other useful thing is that now I know what parts of my resume to be prespared about and I'll be more prepared to answer questions about what I want to do in 5-10 years from now.
_______________________

But first about pterygia (the plural of pterygium) which I think is a feat in itself just to spell. Apparently they are like a joke to the opthalmology guys since they are relatively benign, but they bug patients a lot because of the cosmetic defect as well as the irritation to the conjunctiva.

They are more prevalent in African-American and pts who do outdoor work and have high exposure to UV light. They are often confused with pinguecula which arises from the limbus and stays within the cornea.

Patients don't usually present until:
(1) the growth extends onto the cornea
(2) the growth impinges onto the pupil

If surgery doesnt need to be done then the patient can be treated with drops, ointments, and gels to lubricate the eye. They can also use decongestants, NSAID and steroids, but these cause a rebound effect when stopped so they are not highly recommended.

They are also at higher risk for astigmatism and retinal detatchment.

Surgery is done when:
(1) the pterygium causes astigmatism (usually when it is >3mm)
(2) there is an opacity in the visual field
(3) either of the above is threatening to happen

The recurrence rate is 30-50%.

Ascites & GI

2009-01-10T17:50:00.004-05:00

So unfortunately, I haven't been able to update here since I've been so tired over the past week. Working the overnight shift on the weekend can certianly mess things up. Anyhow, I spent the past week on Gastroenterology which was pretty nice.

The other thing that happened this week was that I started getting interviews for fellowship. Gah! The season is starting! But we'll see how it all goes.

So my nicest and most interesting patient this week had recurrent ascites. She was getting tapped 4L for months and came in on an elective admission to try and figure out what it was. The primary team thought she had chylous ascites as she had a history of Hodgkins disease and fallopian tube cancer and "it looked like being in a milk carton" when they took a look at her. She had no liver problems, no pericarditis, and the fluid most definetly not chylous ascites with a meager triglyceride level of 9. There were no malignant cells and no signs of portal hypertension so our best guess was that there may have been some peritoneal irritation from prior intraperitoneal chemo. We started her on some lasix and spironolactone and sent her on her way.

Our noon lectures this week have been on cancer. Yesterday we covered myelosysplastic syndrome and AML. All I remember is:

-myelodysplastic syndrome can present with hypo or hypercellular marrow
-AML is defined as having >20% cells as myeloblasts on the diff
-the M3 subtype of AML is the one that is different from all the others

The other cancer lecture we had was on breast and prostate cancer.

We had a good resident report case on a patient who came in with back pain who turned out to have spinal mets from an angioma. The other one had painless hematuria. There was also a CPC case on Conn's syndrome.

Back Pain: Part Tres

2009-01-04T23:58:00.003-05:00

I worked the overnight night shift last night in the acute coronary unit and now my sleep schdule is all messed up. It wasn't too terrible of a night: two admission with one pt having pneumonia and shortness of breath and another with a retroperitoneal hematoma a couple days after a normal cath. No codes. No lines to put in. Tho I am wondering about the extremely hypokalemic pt in renal failure. Oh, and the nosebleed who had some pseudothrombocytopenia. Nothing too exciting.

So before we move on to another episode of back pain, I've probably read about 100 pages to far which means that only like 5% done with the book. Well, at least there are still 360 days left in the year. =)

More causes of back pain:

Veterbral osteomyelitis
-usually from a staph infection but can also be secondary to a UTI, PNA or cellulitis
-IVDA is a risk factor
-if it is pyogenic, check for endocarditis!!
-pain is worse with motion, tendernes usually seen over segment
-fever present, elevated ESR, increased WBC
-check CT or MRI, x-ray can take months or years to show narrowed disk spaces with erosion

Spinal epidural abcess
-back pain with movement and palpation, fever
-check MRI
-may or may not have spinal cord compression or nerve root injury

Lumbar adhesive arachnoiditis
-fibrosis s/p inflammation of subarachnoid space
-leg and back pain iwth motor, sensory, or reflex changes
-MRI shows clumped nerve roots or loculations of CSF in the thecal sac
(clumped nerve roots are also seen in demyelinating polyneuropathies and neoplasms)
-Treat with surgery, dorsal column stimulation or epidural injection, but none have been proven to work

Compression fracture
-back or leg pain worse with movement and reproducible on palpation
***compression fractures above the mid-thoracic region suggest malignancy***
check for the primary tumor!!
-tx: percutaneous vetebropasty (PVP)
-candidate for PVP if:
+ midline back pain
+ tenderness on palpation
+ <80% height loss of veterbral body
+ onset within 4 months
-PVP involves injecting polymethylacrylate into the vetrebra
-PVP may be done with kyphoplasty which inflates a balloon in the vetebral body prior to cement injection

***Sudden lumbar pain in a patient receiving anticoagulant --> Suspect retroperitoneal hemorrhage!!***

- AAA rupture presents as isolated back pain in 15% of cases
- the classic ab pain + shock + back pain happen in <20%
- pt is typically an elderly male smoker
- check for a pulsatile mass and check CT

-IBD or cancers can have a pain in a belt-like distribution

The Big List of Risk Factors in Acute Back Pain
- pain worse at rest or at night
- prior history of cancer
- history of chronic infection (esp lung, UTI, skin)
- history of trauma
- incontinence
- age >50 y/o
- IVDA
- glucocorticoid use
- h/o rapidly progressive neuro defect
- unexplained fever
- unexplained weight loss
- percussion tenderness over the spine
- abdominmal, rectal, or pelvic mass
- patrick's sign or heel percussion sign
- straight leg or reverse straight leg raising sign
- progressive focal neurologic deficit

Good Treatents for Acute Low Back Pain
- cervical collars
- heat

Questionable Treatments
- ice
- biofeedback

No proof treatments
- acupuncture
- TENS
- massage
- ultrasound
- diathermy
- magnets
- electrical stimulation

Not recommended
- facet joint injections
- trigger point injections
- ligament injections

Medical Treatment
- NSAIDS/Tylenol
- Cyclobenzaprine - start with 10mg qhs and can go up to TID, should see benefits in 4-7 days esp if sleep is affected, limited use by daytime drowsiness
- opioids should only be used short term if indolent or pt unresponsive to acet/NSAIDS
- no evidence for the use of TCAs or oral glucocorticoids
- Epidural glucocorticoids provide short term relief for ALBP with radiculopathy
- Nerve root blocks can be used for temporary pain relief

Spinal manipulation and PT are reasonable therapies for ALBP

Chronic back pain
-defined as pain >12 weeks

A study done on chronic sciatica showed that surgery hastened relief of symptoms by 2 months but at one year there was no difference

Do not exceed more than 2 weeks bed rest in treating back pain

Questionable prrof for chronic back pain
- back school, manipulation, epidural steroids, TENS, hydrotherapy

No evidence in treating chronic back pain
- acupuncture, traction

Back Pain: Part Deux

2009-01-02T23:42:00.002-05:00

So I came home after the gym today and took a nice nap and now here I am trying to stay up most of the night because I got pulled to do an overnight shift tomorrow. Today I worked with HIV and hep C patients. (separate clinics, not co-infected patients). With the hep C patients we do a lot of counseling to make sure patients are ready for treatment before actually starting since the treatment is a pain in the ass. Usually they meet with a psychiatrist, nurse, and case manager and us before the first meeting. Then we start peg-interferon which is a weekly shot and ribavirin which is a twice daily pill. Patients usually feel like they have the flu for a couple hours or a couple days every time after they get the shot. If they have an depression, it can get worse, hence the psych eval before treatment. There are also problems with neutropenia & anemia. It sounds like such a pain in the butt (being sick one day a week!), but the good news is that after 4 weeks, we get a good idea of the patient's chance for cure. But back to back pain...
_________________________________________

Causes of back pain- some can be congenital anomalies such as spondylolysis which is a defect between the pedicle and laminae, usually seen in young adults
- spondylolisthesis is anterior slippage of the vetebral body . a "step" may be palpated on spinal exam

Tethered Cord Syndrome
-presents as a progressive cauda equina syndrome or possibly myelopathy
-pt is often a young adult who c/o perianal pain some time after minor trauma
-neuroimaging reveals low-lying conus (below L1-2) and short thickened filum terminale

Trauma
-sprains and strains
-traumatic vetebral fractures - usually from ant wedging or compression

Lumbar Disk Disease
-usually at L5-S1 level and seen more in obese patients
-symptoms include back pain, abnormal posture, limitation of spine motion (esp flexion) or a radicular pain. Can have a dermatomal sensory loss or absent deep tendon reflex suggests specific nerve root. Motor sx less common and usually unilateral, but can be bilateral if herniation is big.

Indications for Surgery with Lumbar Disk Disease
1. increased weakness (on exam or on EMG)
2. sphincter abnormalities
3. incapacitating pain after more than 4 weeks of treatment
4. receurrent incapacitating pain

Cauda Equina Syndrome
-usually secondary to a msss lesion
-presents with saddle anesthesia, areflexia, weakness, loss of bowel or baldder function, low back pain
-r/o transverse myelitis & GBS
- Tx: surgery (or radiation if there is a tumor present)

Spinal stenosis
- characterized by pain worse with standing and better with sitting
- pain typically in back, butt, and leg
- Tx: NSAIDs, exercises, surgery if refractory
- check MRI for imaging

Spondylosis = arthritic spine disease
- seen later in life
- cervical and lumbar involvement
- back pain worse with movement and associated with stiffness
- no straightforward correlation with radiology

Ankylosing Spondylitis
- seen in men less than 40 years of age
- morning stiffness, no relief with rest
- nocturnal pain, better with exercise
- loss of lumbar lordosis and increase in thoracid kyphosis can be seen

Neoplasms
- usually constant dull pain, worse at night
- not better with rest

Mechanical back pain
- better with rest
- no radiation

That's all for now. I'm gonna go read and then maybe we'll get back for part 3!

Back Pain: Part 1

2009-01-01T22:50:00.004-05:00

Happy New Year!

So on to the show with back pain today. I actually took a lot of notes on this chapter and am finishing it up today so we'll talk about infectious diarrhea another time.

So back pain is a common outpatient complaint which is why I decided to read about it - not to mention the large amount of money lost each year to back pain. The unfortunate part is that back pain is often difficult to treat and a lot of spinal surgeries don't make the pain go away. I read Jerome Groupman's book "How Doctors Think" a couple months ago and he mentions touches on how spinal fusion surgeries often don't alleviate back pain.

Anyhow, some notes on the chapter:
Cervical nerve roots exit above the corresponding vertebral body, ie C6 exits at the C5-6 space
Thoracic and lumbar nerve roots exit below, ie T1 at the T1-T2 space

Serious underlying disorders to look out for when evaluating back pain are: radiculopathy, fracture, tumor, infection, and referred pain from visceral structures

Pain sensitive structures include periosteum, dura, facet joints, annulus fibrosis, epidural veins, and posterior longitudinal ligament

Types of back pain include:
1) local - secondary to pain-sensitive structures that compress or irritate nerve endings
2) Referred - abdominal and pelvic viscera pain, usually unaffected by posture
3) Spine Origin - back/butt/leg pain, upper lumbar pain leads to pain in the lumbar/groin/ant thigh while lower lumbar pain leads to pain the butt/post thigh/calves/feet. Not a dermatomal distribution but called "sclerotomal"
4) Radicular - sharp or radiating pain which follows a nerve root territory. Worse with coughing, sneezing, vasalva. Sitting stretches the sciatic nerve and can lead to pain when L5 and S1 roots are involved.
5) Muscle spasms

On physical exam:
-Pain of bony spine origin leads to reproducible pain on palpation of the spinous processes
- forward bending may be limited in muscle spasms
- lumbar spine disease - has normal hip flexion but limited lumbar flexion
- lateral bending to the opposite side stretches and irritates the nerve root
- hip pain can be elicited by
(1) Patrick's sign - flexed hip and knee with internal and external rotation
(2) tapping heel with the leg extended
-straight leg raising done with passive hip flexion (and with or without passive dorsifleciton of the foot). Normally a person can go up to eighty degrees. The test is positive if pain is reproduces on the test. Works by stretching the L5 and S1 nerve roots.
-crossed straight leg test - same as above but pain is reproduced on the opposite side. More spec and less sensitive for disc herniation than regular straight leg raise.
-reverse straigh leg raise: pt stands and test passive flexion of leg with knee extension. Stretches the L2-4 nerve roots and femoral nerve. Postive when pt's pain is reproduced.

Tests
- do routine labs for acute back pain less than 3 months - CBC, ESR, UA
- CT better for fracture, good for trauma, but usually unhelpful in acute pain
- MRI and CT myelography usually best choice for serious spine diseases with CT-myelography better for lateral recesses of spine, bony lesions and claustrophobic patients.
-EMG can test the integrity of the peripheral nervous system. Normal in sensory root injury.

You can't sue them?

2008-12-31T16:46:00.005-05:00

So yesterday I fell asleep before I got a chance to update so today should be a double entry, but I have places to be tonite. After all the patients in the morning were done, we talked a little about acute infectious diarrhea. Interestingly, there are local outbreaks of Giardia in the local area so this isn't just limited to traveling in the woods and such. Sadly, there had been one pt in the past that was being given local spring water by his mother in the thoughts that it would be healthier. Having HIV, he wasn't able to fight off Giardia and passed away. There was also an interesting case in the past where a patient was playing with the crabs in a tank and developed M. marium. More on infectious diarrhea later.

Today was a short day in clinic. There was one patient that stood out, though. He had a history or having erosions on his face because he just picked at itchy spots. He was the only patient this week that I did not shake hands with because he had dried blood on his hands. His face had an erosion that looked pretty raw, so I was a little more careful given all the exposed HIV positive blood.

Yesterday I saw a newly diagnosed HIV patient that I liked a lot. Unfortunately, it seems that he had contracted HIV from his last partner who started avoiding him since he told him about the diagnosis. What's interesting is that if a person who knows s/he is HIV positive has unprotected sex and the partner contracts HIV, they cannot be sued. It's only in cases where someone had a malignant intent to infect other people that they have ruled in favor of the case.

More about infectious diarrhea in 2009!

A cure for HIV?

2008-12-29T22:43:00.003-05:00

(The "cure" for HIV isn't Ensure, but more on that later.)

I'm back at work after a week of vacation and this week I am working in the HIV clinic. One of the first patients I saw this morning mentioned that he had seen a TV segment about a cure for HIV.

The attending that I was working with starting talking about this story. Basically, 1% of Caucasians are naturally resistant to HIV infection because of a mutation in CXCR5 which is a co-receptor for HIV infection. An HIV positive patient developed leukemia and required chemo and a bone marrow transplant. His doctor screen the marrow banck for a match that had this rare mutation, and it managed to eradicate HIV the patient's body. He was functionally cured. However, this is not applicable for the population at large with HIV. Finding a donor with the mutation who is also a match is very rare, and it would also have to be a patient who already had leukemia and was getting chemo anyways - otherwise you would be giving chemo and bone marrow transplants with HIV patients who could be treated with meds.

I talked about this with some of my coworkers and lunch and both the guys on either side of me said they would get chemo and bone marrow transplants if they ever developed an HIV infection. I was amazed. They would go through all that for a disease that we now manage so well with meds that HIV patients have a normal lifespan? I'd take the meds unless I had leukemia on top of HIV.

They also brought up the idea of giving incentives to donors who had this mutation in an effort to get more bone marrow donors. Now that's not a bad idea.

However, what the patient was actually talking about was this. It's a story about how a constant region in of HIV was discovered and how abzymes can be employed against it. However, this constant region could change once the virus mutates.

On an unrelated note, I had another patient today who came in asking for Ensure because he was too lazy to cook and he was trying to gain weight. I was then surprised to learn that "Ensure has street value" as my attending told me. It is highly popular in the Latino community and is seen as something that can be taken to make you healthy. Patients with a prescription can get it for free from Medicare and they can then sell it at a discount to a merchant who will sell it at retail value. Sneaky....

Geriatrics

2008-12-28T22:45:00.003-05:00

The results of our in-service exam came back while I was at home for the holidays and I did worse this year. Boo! I guess I should pay more attention when I am taking the test, eh? But I think last year I was half asleep and I did better! Must have been from all the studying I had done for Step 3 I took the couple months before that.

Anyhow, my results for geriatrics were by far the worst. I haven't done a geriatrics rotation yet, and I'm not really looking forward to it. The rotation in my hospital hasn't exactly gotten any rave reviews, and elderly patients are often complicated. There are only so many medication, you have to wonder how it's possible to remember to take 20 or 30 pills a day.

There is a 9 page chapter on geriatrics in Harrison's. The first weird fact that I saw was that alteration of genes involved in insulin signaling often lead to life extension. What?! I never knew this. Diabetes must be the root cause of all evil. Bwahahaha!

Altering gene expression of neurons in worms has also shown to extend lifespan. They also mention the whole calorie restriction thing and the mechanism being that is thought to be related in a family of genes called sirtuins.

The Timed Get Up and Go Test is when a patient gets up from sitting, walks 3m, turns around, walks back, and sits down again. Normally this should take less than 10 seconds. Another useful test is the Mini-Cog test which gives a patient 3 objects to remember, asks them to draw a clock, and then asks for object recall. A point is given for each object, and 2 for each clock. A score of 0-2 indicates dementia.

For dementia, Harrison's recommends using olanzapine (zyprexa) or risperidone. For depression they mention citalopram. With any anti-psychotics, watch out for extra-pyramidal side effects like bradykinesia, tremor, or rigidity. Trials of reductions in medications should be tried every 6 months.

Urinary incontinence is a risk factor for falls as these patients are often getting up to go to the bathroom in the middle of the night. Before looking into the 4 classic causes of incontinence (stress, urge, overflow, or mixed) there is a good mnemonic for reversible causes of urinary incontinence. The mnemonic is DRIIIPP which is

D - delirium
R - restricted mobility (illness, injury, gait disorder, restraint)
I - infection - acute, symptomatic, urinary tract infection
I - inflammation - atrophic vaginitis
I - Impaction - of feces
P - polyuria - diabetes, caffeine intake, volume overload
P - pharmaceuticals - diuretics, alpha adrenergic agonists or antagonists, anticholinergic agents (psychotropics, antidepressants, anti-parkinsonians)

There is some talk of pressure ulcers in this chapter. An ABI < 0.4 is a bad prognostic factor as a good blood supply is needed for good wound healing. Also, a brief summary of staging ulcers is as follows:

Stage I - skin is still intact
Stage II - partial thickness ulcer that involves epidermis and or dermis that is shallow.
Stage III - full thickness skin involvement with subcutaneous tissue involvement.
Stage IV - extensive destruction with necrosis or damage to the muscle, bone, or supporting structures.

Complimentary and Alternative Medicine

2008-12-27T14:48:00.005-05:00

In an effort to take break from the HIV chapter, I started to read about back pain, but then found that fairly dense so I read the CAM chapter so I could cross another one off the list.

CAM encompasses things like herbal remiedies, acupunture, massage, homeopathy, etc. Homeopathy sounded kinda hokey to me since it involves giving things that cause side effects in very dilute doses. It was first proposed by Samuel Hahnemann - and I wonder if he is the namesake behind my medical school. Anyhow, the whole idea is that if a substance causes side effects in a well person, it can be used to cure illness in minuscule amounts. Sounds absurd, but this formed the foundation behind immunization and allergen desensitization. When they mentioned that, I realized that I make use of it myself all the time: with lactose. If I stop drinking milk for more than a week or so, the next time I have it, I get sick. But if I have milk every day, there aren't too many problems.

Other notable facts:
- gingko bilboa prolongs bleeding times
- St. John Wort is notorious for interfering with prescription meds by altering their metabolism
- acupuncture may be able to release endogenous opiods that help with pain control
- laetrile (an extract from apricot seeds) was once though to cure solid tumors, but studies in the 1980s showed no benefit
- Linus Pauling first proposed that vit C could prevent and/or treat the common cold, but high powered studies disproved this theory. In most cases, it does no harm - you pee out excess vit C, but in patients who have iron excess, it can lead to the overproduction of free radicals. Watch out in pts with hemochromatosis or chronic transfusion patients.

Harrison's lists some good website for CAM which include:
- the Natural Medicines Comprehensive Database (www.naturaldatabase.com)
- NIH (http://ods.od.nih.gov) or (http://nccam.nih.gov/health/) or (http://www3.cancer.gov/occam.information/html)

Vitamin/Mineral Goodies:
-vit A deficiency seen in developing world and increases death rate and progression HIV/AIDS
- folic acid reduces neural tube defects in utero (knew this one!)
- folic acid, vit B6, and vit B12 combined may be able to lower homocysteine levels, but doing so has not shown to alter cardiovascular end points.
- vitamine C and E, beta cartotene and zinc combo - could reduce the progression of age-related macular degeneration.

Herbal Goodies:
- Glucosamine and/or chondroitin sulfate: good for osteoarthritis and may slow the narrowing of joint spaces
- gingko bilboa - no proof in improving cognition, but ppl still taking it for Alzheimer's
- saw palmetto - marketed for BPH but no proof it works
- St. John's wort - marketed for depression, but again, no proof
- Echinacea - used to prevent or treat respiratory infections but no clear proof although it does stimulate the immune system in vitro.

Other goodies:
-acupuncture had been shown to work for nausea and osteoarthritis
- biofeedback is helpful for incontinence, headaches, and stroke rehab
- hypnosis is good for pain from minor surgeries, chemo-related nausea, and IBS
- spinal manipulation useful for uncomplicated acute back pain, but has not been shown to be superior to conventional approaches.

I like reading about alternative therapies. Acupuncture is particularly interesting because I worked with a family doc in medical school who spent his Friday afternoons doing acupuncture. It would be kinda neat to do outpatient medicine and acupuncture. He had mentioned that there was course in LA where you could get certified, so it sounds really interesting.

C diff.

2008-12-26T19:17:00.002-05:00

I read about C.diff and pseudomembrane colitis now that I'm done with my nutrition section stint. C. diff is a common infection we see in the hospital and often follows antibiotic treatment. It is diagnosed by the presence of diarrhea along with either a positive toxin test or pseudomembrane colitis seen on endoscopy. Treatment is usually with vanc 125mg q6hx10days or metronidazole 500mg TID x 10days(preferably PO) both of which can cause C. diff themselves. Vanc is for more seriously ill patients esp ones with a white count higher than 15. Resolution of diarrhea occurs in 2-4 days but cannot be called a treatment failure until about 6 days. Unfortunately there is a high recurrence rate. One of my coworkers was questioned about this when we were on GI and that is usally a result of reinfection, recurrence of the same strain, or some effect that the treating antibiotic had on the natural flora.

So I forgot to mention some other thing about anorexia from yesterday that I thought were interesting. There are a lot of electrolyte abnormalities in anorexia and not so much in bulemia since bulemics usually get some sort of nutrition. Anorexics tend to have:
-hyppthalamic amenorrhea
-decreased leptin levels (and leptin makes you full so you think they would by hungry!)
-increased cortisol and 24hour urine free cortisol
-TFTs like a euthyroid sick pt (normal/elevated T4 and free T4, decreased T3, and increased rT3)
- increased GH but decreased IGF

They also have a tendency to develop prolonged QT intervals

Eating Disorders

2008-12-26T00:50:00.002-05:00

So I'm still working my way through the long and boring HIV chapter, but I also read the chapter on eating disorders as well. Anorexia and bulemia have been in the news enough and it seems that most of what was in Harrison's was stuff I had learned in med school. Thank goodness! Because usually I read about a bunch of stuff that is mostly new to me: usually I know the basic concept and then there's a lot more detail in Harrison's. But just a couple of quick things that I didn learn:

-You can see a transient peripheral edema in both anorexia and bulemia.
-With anorexia it can occur in the absence of hypoalbuminemia and usually happens when the pt starts to regain weight
-In bulemics the edema is usually secondary to persistent fluid and electrolyte depletion that lead to a secondary increase in aldosterone. It is transient usually happens when laxatives and diuretics are stopped.

The reason why this is so interesting to me is that I had a patient coming in with peripheral edema more so in her hands rather than legs of unknown etiology. She did not have CHF; it was not a nephrotic syndrome; there were no liver problems; her protein and albumin were normal levels. Now I wonder if she was bulemic. I think there may have been an endo consult that was placed....

Obesity Meds

2008-12-25T02:41:00.003-05:00

The chapter on HIV is like 70 pages long, but I made my way through the epidemiology section today. There are an esitmated 1.3 million ppl in North American who are HIV positive and like 22 million in Africa. Those are astounding numbers. They had this graph in the book that showed the life expectancy going from the 60s down to the 30-40s because in some countries the prevalence of HIV can reach up to 50%. I remember there was an episode of Oprah a long time ago where Lisa Ling did a story about how HIV meds are so cheap now and not readily available in Africa.

Some other interesting facts:
-For some reason there is a greater chance that a mom will pass on HIV in utero to the fetus is they are more HLA compatible. What is the reasoning behind this, I wonder?
-Also, vitamin A deficiency will lead to an increased risk of transmission via breastfeeding. Interesting, but somewhat not important since HIV infected moms shouldn't be breastfeeding anyways.

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The other piece of reading I did today (just so I could cross of a chapter on my list) was on the treatment of obesity. There was all the good stuff about the complications, (by the way, how did I not know that obesity can lead to gout?) but the more informative part talked about the meds for obesity.
-The first class was sympathomimetics and the one that Harrison's went into detail on was Meridia. Somewhat like amphethamine without the addictive quality. Can cause a small elevation in blood pressure so not good for anyone with heart problems or history of stroke.

- The next was orlistat. Seen and heard of it before and sounds gross since you get fatty poop and diarrhea. Pts will have lower levels of vit D (which is my fav vitamin), B, and beta carotene.

- The last class mentions antagonists to the cannaboid receptor - still waiting for FDA approval and not out on the market yet. But just as smoking pot can give you munchies, turning those receptors off can make you feel full.

Fat Hormones

2008-12-24T02:15:00.002-05:00

Today I did a little reading about the biology of obesity. Some key players are leptin which makes you feel full and ghrelin which makes you want to eat more. Then there were an awful lot of other hormones that I had never heard of before. It's interesting because fat cells (adipocytes) are essentially seen as endocrine cells which release all these other things I have never heard of like:

-Factor D/Adiposin which is a complement factor
- Adiponectin which is decreased in obesity and works to increase insulin sensitibity and lipid oxidation
-Resistan - which is increased in obesity
- RBP4 - which is also increased in obesity
- alpha-MSH which is what is stimulated by leptin that inhibits apetite in the hypothalmus and acts as a precursor to POMC
- AgRP (Agouti related peptide) which is overexpressed in obesity and acts to antagonize the MC4 receptor for alpha-MSH

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Dr. Oz was on Oprah today and talked about sleep terror, sleepeating, etc. The sleep expert mentioned that there are medical treatments for these disorder, but he didn't mention exactly what they are. I am curious....

HTLV

2008-12-22T22:35:00.002-05:00

Hey! It's been a long hiatus since I've been able to write in here, and I can tell you what happened in the mean time. I tried to take notes during the last entry during my noon lecture as we were talking about interesting cases when my battery died. Then I had my CPC last Wednesday so for the week prior to that I completely nerded out. Much like a college student who had finals to take before Christmas break, I spent all my free time on my presentation and I think it went well. The final diagnosis was Evans syndrome + IVIG-induced osmotic nephrosis and I learned so much while I was working on the case. It was really amazing.
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But anyways, back to my reading. So I did a little reading in Harrison's today on HTLV. I meant to start reading the HIV chapter because I am going to be working in the HIV clinic next week, but the Retrovirus introduction was the 5 pages before that. Oh, and not mention the HIV "chapter" is like 70 pages long. And there is also the fact that I have a clinic patient that is HTLV positive.

So here's what I learned. HTLV can be acquired perinatlly, from sex, or from blood. If a pt just has the virus, they should take precautions to practice safe sex and not breasfeed their kids. It's associated with T-cell lymphomas (hence the name) as well as a myelopathy that can resemble multiple sclerosis called HAM. Women are more likely to get HAM and they are also more likely to pick up HTLV from sex. There is an association between HIV and HTLV but this is usually seen in injection drug users.
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After this I started reading about HIV and so far I'm reading about how the virus infects cells.
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In other news, still no word on any interviews. I'm not sure where I am going with the whole fellowship thing and where I want to be next year, so maybe it's not even the right time to apply. But one of my co-workers did get an interview for ID so it looks like the season is starting...

calcium

2008-12-12T12:16:00.002-05:00

Booyah! I can access this website at work! I'm surprised that this website wasn't tagged as invalid content. We are talking about calicum disorders in our noon lecture right now. In particular we're talking about hyperparathyroidism now.

Mechanisms of PTH
- indirect bone resorbtion (receptor on the osteoblast)
- phosphorus wasting by kidneys
- activation of vitamin D from 25-OH to 1,25 OH
- increased calcium excretion by the kidney
- bicarb wasting causing a metabolic acidosis

MEN I presents with multiple parathyroid adeomas

Case #1 FHH
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would have had more here but computer battery died in lecture. oops!

Occam's Razor

2008-12-11T23:57:00.002-05:00

I keep forgetting that I'm trying to update this blog often with the things that I learn because I've become so wrapped up in my CPC. Today was a slow day on the GI service and I'm switching to the busier service tomorrow, but I don't know if that necessarily means more learning. Since we had some downtime the GI doc I was with pulled out some old PowerPoint presentations that he had and we went over those. The first one was on esophageal strictures and we talked about dilators. Then we went over a case of a pt with recurrent reflux that did not respond to meds who turned out to have a duodenal MALToma.
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Today's noon lecture was another CPC. It was a pt who had hemopysis intermittently every year who turned out to have bronchiectasis secondary to broncopulmonary sequestration and had a coil placed.
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We did journal club yesterday and all I remember is Spiriva can be good for COPD patients but there is the question of increased cardiac complications.
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That's all I got for now. Also Occam's razor says that the simplest explantions are the best and in medicine we take that to mean that usually there is one diagnosis to explain everything rather a bunch of different things to explain a patient's symptoms.

Capsule Endoscopy

2008-12-10T22:10:00.003-05:00

Now that I am trying to write this blog on a regular basis, I find it disturbing that there are days that I come home and think "Did I learn anything new today? Nope. No new medical knowledge." And that is bad. I felt like yesterday was one of those days, but then again we did have a good resident report that was a patient with a lower extremity rash and hand swelling. There was no final diagnosis, but cryoglobulinemia seems good. It has an association with hep C. And then I think PAN has an association with hep B.

Today I had a patient who had a metastatic cerebellar tumor with an unknown primary. After a PEG placement and tube feeds he was having tarry stools. We'll see what the scope shows tomorrow.

I also saw my first capsule endoscopy today. This a cardiac pt who had been on Plavix, developed heme+ stools and then had a clean EGD and colonoscopy. I didn't realize that between the two not the whole GI tract is covered. There was some bleeding on the capsule and there will be an eteroscope tomorrow.

I sent a copy of my CPC slides to my favorite doc. After doing some editing today, I realize that I have a lot of work to do. There was anther CPC presentation today and it was about a stroke in a pt in her 20s who had prior miscarriages. I thought it was going to be lupus and antiphospholipid antibody syndrome for sure, but it turned out to be a cerebral sinus thrombosis. Pretty neat. There should be another one tomorrow and then mine next Wednesday is the one after that. Then I will have more interesting blog entries, too.

Thrombocytopenia

2008-12-09T23:05:00.002-05:00

So I've been reading up on thrombocytopenia and acute renal failure for my CPC. I think I've got my thought process for thrombosytopenia down. Rule out pseudothrombocytopenia. Then figure out if is a production, splenic or destruction problem. I'm not so great with all the production problems except I know that myelodysplasia causes an isolated thrombosytopenia and leukemias will probably affect other cell lines. Then there are the destruction causes which can be immune or non-immune. Like prostheric cardiac valves that just shear platelets. But there are a whole host of drugs that cause thrombocytopenia - much too many to mention here.
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I worry that I don't learn too much at work sometimes. Like today. I went and saw my patients from yesterday, but there wasn't anything exciting going on. Post-transplant diarrhea. Gastroenteritis. Heme+ stools in a patient with hemoptysis. No wonder why we still have to go home and read.

Well, that's all I got today. I'll look more in renal failure and vasculitis tomorrow. Off to bed!

Ginger

2008-12-07T18:02:00.004-05:00

Last night I made myself some homemade ginger tea which was simple boiling 3 slices of ginger and adding some sugar. I have this book called "Food: Your Miracle Medicine" and looked up ginger and found that it has a structure similar to aspirin, helps with join pain, thins blood, and kills bacteria. Sounds like good stuff.

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There was an article about diabetes and hypertension in the issue American Family Physician that was in my mailbox yesterday. This is what I learned:
-Going down from 140/90 to 130/80 cuts the risk of major cardiac events in half.
-Diastolics less than 60 are not recommended in patients with CAD.
- ACE Inhibitors are good, but thiazides were surprisingly listed as second line meds leaving beta blockers and calcium channel blockers as third line. I was a little surprised that beta blockers aren't higher up on the list given their improved mortality in patients with CAD which a lot of diabetics have. Also an increase of 30% or less in GFR is okay for ACE Inhiitors.
- They also make a distinction between to dihydropiridine calcium channel blockers and the non-dihydropyridine calcium channel blockers. I had to look up which ones were in that category since the amount of pharmacology I've retained doesn't go back that far. So it looks like Dihydropyridines include norvasc, nifedipine, and nimodipine. And the non-dihydropyridine ones include verapamil and diltiazem. This is important because the non-dihydropyridenes shouldn't really be combined given the risk of bradycardia and heart block.
- The thiazide diuretic chlorthalidone is good for diabetics with isolated systolic hypertension. The ALLHAT study showed that it did just as well as lisinopril and amlodipine preventing fatal heart disease, nonfatal MI, and total mortality.
- carvediol (coreg) had alpha and beta blocking properties and is the beta blocker that is least likely to worsen insulin sensitivity.

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A high school classmate of mine posted an blog entry called "Winning the War on Cancer". It reference the Journal of the National Cancer Institute which states that for the first time since 1971 (when the war on cancer developed) the rates of cancer is declining. This is attibuted in a large part to less people smoking as lung cancer is the number one killer in the United States. Unfortunatley, there is less sucess in the Midwest and the South with quitting smoking. Also, the article mentions that the next epidemic is going to be from obesity.

Only what's relevant...

2008-12-07T00:00:00.000-05:00

Yesterday I had my semi-annual evaluation meeting with my favorite program director and mentor. He told me I was doing well, that I would make an excellent endocrinologist and offered some advice on reading: Read only what you think will change the way you practice. Taking this information back home, I looked at copy of the Annals of Internal Medicine that had been sitting by my bedside. There were articles on a doctor's perspective, a trial that showed community-acquired pneumonia was more likely within the first 30 days of starting a PPI, and the ACP guidelines on osteoporosis. Of all the articles there was only 1 that may have changed the way I practiced and lucky for me, it was endo-related. Sadly, it was the one that I haven't had to do much with other than skim.

I did do some reading about purpura yesterday. My CPC case has purpura. I thought they were palpable purpura, but that was a miscommunication which changes everything. I guess this means I can spend less time looking at the details of vasculitits and more on ITP. But one interesting fact: purpura that are irregular in shape are usually from emboli and correspond to the area that the artery or arteriole supply. Purpura that are circular are usually from a vasculitis because the blood vessels that extravasate do so in a uniform fashion around one area.

That's all I got for today. Until next time!

Palpable Purpura

2008-12-04T23:50:00.000-05:00

After turning in fellowship applications last night, I can finally focus on my CPC. One of the things that my patient has is palpable purpura so that's what I'm reading about today. Unfortunatly, my patient also had thrombocytopenia which can cause purpura itself (although it really should be nonpalpable). One interesting fact: the elderly often have purpura called senile purpura. It's also called solar purpura or actinic purpura. I think I may want to look into the origin of these names because I am thinking: senile because they are old? solar from the sun? I will go with actinic - sounds more medical.

So last night I looked up the GERD and achalasia thing, and it turns out I was right. Someone can have longstanding GERD and if they suddenly stop having reflux and start complaining of dysphagia it can be achalasia. Unfortunately, it could also be a cancer as well.

Today one of my patients had a mass in her gallbladder which was sludge v. cancer. I hope it's just sludge. We did the liver ultrasound after a sudden transaminitis in the 100s-200s, but I don't think the mass has anything to do with it. Just an incidental finding. And not a good one, either.

The noon conference today was about our clinic. I've been reading a lot of articles lately about how to run a good practice (I have a hard time deciding whether I want to do endocrinology or outpatient medicine ... or maybe even hospitalist.) It's sad that healthcare today expects us to see patients in 15 minutes and document everything as well. It made me think about how much time I spend doing things in our clinic that are inefficient or don't require an MD. I spend an inordinate amount of time sending faxes, mailing letter, calling other hospitals or practices for records, and calling pharmacies to refill prescriptions. Not to mention that I handwrite all my notes in addition to dicatating them so that we can bill for the handwritten note and others can view my notes easily in the dictation. It's no wonder that all the residents complained when they increased our clinic requirements from 105 to 150 sessions in our three years.

The other news I have is that it takes me a long time to read 7 pages in Harrisons. That stuff is dense, dude! I think tonight will be some light reading...from the beginning of the book. Heh.

Dysphagia

2008-12-03T17:25:00.000-05:00

Since the topic for today was dysphagia, I opened up the new Harrison's and there was were 2 tables that had more than 50 causes of dysphagia. The gastroenterologist discounted anxiety and thermal injury, but I swear they were in the book. Also, I seem to remember something about pts with GERD who develop a resolution of their symptoms and then dysphagia could have achalasia. However, the GI doc said that the two don't usually go together. I have to check. If I am remembering correctly, then it just underscores how much of medicine you can't learn from books because I trust the doc I am working with now.

I got to maneuver a colonoscope today which was interesting. It's a lot harder than it looks, let me tell you. There is a know to turn left and right, another to move it up and down, one for water, and another for suction. Not to mention that you are staring at the screen and trying to figure out where you are. But it was a good experience.
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Yesterday I saw that the latest NEJM had a case of endocarditis which was initially thought to be TTP. I was intrigued because my CPC is coming up and TTP was originally in my differnential. My case is someone with hemoptysis, palpable purpura, thrombocytopenia, and anemia who was thought to have ITP, refused steroids, got IVIG and then went into renal failure. At first I thought it was a pulm-renal syndrome and some sort of vasculitis, but all ANCAs are negative. Then again, there are other vasculitides that are ANCA-negative. Just not Wegener's. Or polyarteritis nodosa. And it's not Goodpasture's either. I thought about Kaposi's sarcoma, but the pt is HIV negative and then I was playing around with the idea of Sweet's syndrome but the skin biopsy was negative, too. Oh well. I guess I have to add endocarditis to my list with all the other great masqueraders.
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On a pop culture note, I just watched a Jason Mraz clip from a UK talk show. He talked about how he bought an avocado farm in San Diego and how he is a natural foodist. He also made this dessert for the hosts which was cacao mixed with avocado and agave nectar. A note on agave nectar - I heard about it earlier while reading a magazine in the gym about all the new sugar substitutes. It's being promoted as a more natural sweetener and I remembered that name because it's also a restaurant in NYC where I went on a fantastic date some time ago. Agave is a plant from Mexico that has a sweet nectar that can be tapped like maple syrup. Also, it supposedly has medicinal properties. But anyways, there's still sugar in his cacao mousse dessert, but more natural. And there's still fat - it's just avocado fat.
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Today's grand rounds was about a patient who responded well to Reiki therapy. In fact, there is apparently a hospital somewhere in the Northeast that trains its whole staff on Reiki therapy. I'm all for alternative treatments, but it difficult to find the evidence based medicine to back them. I remember working with a family doc as a student who did acupuncture every Friday afternoon. And you just need to take a course to get certified. Someone brought up offering patients red yeast rice if they refuse a statin and this makes total sense because red yeast rice is a statin, a weak one, but still a statin. It's just a marketed as an all natural product that didn't have to go through 17 years of scrutiny and 4 phases of clinical trials like prescription medications do.

Introduction

2008-12-02T18:04:00.000-05:00

The books arrived yesterday. My 2-volume 17th edition of the new Harrison's Principles of Internal Medicine was sitting outside my door when I got home from work. Normally, I would have opened them right away, but one of my coworkers was on her way over. P. had spent a month in Kenya working with a team of other doctors, and between the weeks I has spent at other hospitals and working as the critical care senior resident, I hadn't seen her in months.

So my books sat on my couch while I caught up with my friend, and it was only afterwards that I ripped the package open. The books were a more eye-catching blue with high-tech graphics rather than the seriois black 16th edition that sat on my shelf.

We have come a long way since the very boring cover of the 15th edition.

As I flipped through the book, I noticed that there was a lot more color in the text. And more diagrams. In fact, it looked almost like a children's science book. It looked like fun. But for some strange reason, it made me wonder if it had been dumbed down.

I put the books aside and got some work done. I was presenting a case for resident report the next day and I needed to go over the deatails. Resident report used to be morning report as it probably still is in many other hospitals, but we have it at 11am before our noon lecture. I had a patient who had cryptosporidum causing diarrhea who I thought was worth of mention.

Later, I looked at the books again more closely. The pictures on the front cover looked like still shots from a high tech computer animation and graphics program. It made me think of Hybrid Medical Animation in passing because I saw their demo real recently and was stunned at how they made science look so beatiful.

They also had a link to a 60-minutes segment that talked about a man with leukemia who came up with a novel treatment for cancer - using radio waves with gold nanoparticles to kill cancer cells.

I flipped through the book some more and scanned the table of contents. I noted that there was a CD that contained dozens more chapters that were not able to be published in the book. It looked exciting.

At this point I should mention that the reason I ordered the new edition was for this new project of mine. I wanted to read Harrison's Principles of Internal Medicine from cover to cover. I was inspired to do this after reading "The Know-It-All" by A.J. Jacobs where he takes a year to read the Encyclopedia Brtiannica from cover to cover.

Of course, he read through about a stack of books that reached his chest and doing the math it looks like it was about 100 pages a day, but I'm a doctor and this is my spin on the project. Of course, a lot of people have read Harrison's from cover to cover, but the majority of internists haven't. It's a whooping 2754 pages of fine print that holds essential information that could make me a better doctor. I've decided to blog about it as well because I want to record all the things I have been learning.

I'm a internal medicine resident reaching the end of my second year. With one year left to go, I am already sensing some of the anxiety of not being in training any more. After this I could be an attending physician which means that there will be no one to double check my work. There will always be colleagues to ask for advice, the decsions I make will be final. I may have learning a lot during during my medical school and training years, but there is are always new developments to read up on. By far, the best advice I got was from the man who was regarding as the brightest physician in the hospital who tells all the residents to spend an hour a day reading. I've been trying to read lately and here are some neat things I've learned.

- A recent New England Journal of Medicine (NEJM) letter to the editor recently brought up the idea of talc ingestion as a possible cause for gastric cancer. This was in response to why gastric cancer in prevalent in Japan. The link to nitrites which are found in lunch meats has been hypothesized for a long time an here is another theory. The talc is found on the surface of rice and is removed by washing the rice before cooking it. I guess I need to be a little more diligent about washing rice.

- A new study of type 1 diabetes shows that a GAD vaccine may preserve beta cell function. Will this prevent long term complications?
- Kids with speech problems can have hundreds of different problems that are genetic. I can't imagine what a speech therapist has to figure out: if they are deaf, if they can't process, if they can understand, if just can't speak.

Anyhow my goal is to read this book in year, document what I learned from it and also mention the other things I learn along the way and fear I will forget. The math works out to about 7.5 pages a day and that is very do-able even with all my hard rotations coming up.

So anyways, the project tonight is to read about dysphagia and the attending said we need 15 causes. Without opening the book, here's what I am thinking:

1. Schatski's ring
2. Plummer-Vinson's syndrom
3. Esophageal cancer
4. Esophgeal diverticula
5. Achalasia
6. Stroke
7. ALS
8. Brain tumor
9. Esophageal spasm
10. GERD

Argh - only 10!!! I need to read (and work on fellowship applications. Until tomrrow!