Prediabetes

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

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

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

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.
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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

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

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

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...
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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!