I'm starting to see the light at the end of a very long tunnel - there are only 26 days and 2 exams left before I complete my second year of medical school! I'm more than excited by it!
There is an exam on Tuesday, which covers Gastrointestinal and Endocrine systems. I have so much physiology to learn (especially regarding the endocrine system, hormones have never been my thing!), and a whole lot of pathology to look over (seriously, what's up with all of these silly names for diseases?! Addison's, Cushing's, Conn's, Schmidt's, Wermer's, Sipple's, Sheehan's, Grave's, Hashimoto's, deQuervain's, Plummer Disease..can't we just have names for the diseases that relate to what they are instead of by who discovered the disease and stuck their name on it?)
Here's a little revision what each of those silly names actually mean, for those who are medically inclined:
Addison's: Primary chronic adrenocortical insufficiency, resulting from progressive destruction of the adrenal cortex. Most commonly caused by autoimmune adrenalitis due to Autoimmune Polyendocrine Syndrome Type 1 (APS1) --> characterized by chronic candidiasis and abnormalities of skin, dental enamel, and nails + hypoparathyroidism...or due to Autoimmune Polyendocrine Syndrome Type 2 (APS2) --> adrenal insufficiency + autoimmune thyroiditis + type 1 diabetes mellitus.
President John F. Kennedy had this disease.
Symptoms: Progressive weakness and easy fatigability, nausea, vomiting, weight loss, hypotension,
skin pigmentation (due to increased ACTH and MSH)
Labs show:
Low glucocorticoids (decreased glucose and then increased ACTH)
Low mineralcorticoids (hypotension due hyponatremia, Acidosis due to hyperkalemia).
*Stressors may precipitate an acute adrenal crisis, which can lead to coma and death without rapid treatment with corticosteroids.
Cushing's: hypercotisolism
#1 Cause - exogenous glucocorticoid use causes adrenal atrophy.
Endogenous causes: "Cushing's Disease" = pituitary ACTH tumor --> Increased ACTH
--> Bilateral Adrenal Hyperplasia
Endogenous: "Cushing's Syndrome" = adrenal adenoma/carcinoma or nodular hyperplasia
--> Decreased ACTH --> Contralateral gland atrophy
Endogenous: "Cushing's Syndrome" = ectopic ACTH tumor (such as small cell carcinoma of the lung)
--> Increased ACTH --> Bilateral Hyperplasia
Symptoms: Hypertension & weight gain early; then truncal obesity, moon faces, buffalo hump,
weakness, diabetes/glucose intolerance, osteoporosis, pink skin striae,
increased infections, mental disturbances.
Conn's: a solitary adrenal adenoma secretes aldosterone
Symptoms: hypertension (due to hypernatremia), with or without muscle weakness (due to hypokalemia)
Increased aldosterone = rental Na retention and K loss --> Increased blood pressure & possible hypokalemia
Schmidt's: an autoimmune polyendocrine syndrome (APS). Also known as "APS Type 2".
Addison's disease + hypothyroidism + diabetes mellitus type 1
Wermer Syndrome:AKA Multiple Endocrine Neoplasia 1 (MEN1). These are known as the "P" lesions.
Cause: Gene Mutation - MEN1 mutation (a tumor suppressor gene)
"P" Lesions:
Parathyroid - hyperparathyroidism, hypercalcemia
Pituitary - prolactinoma most common, acromegaly.
Pancreatic Islets - gastrinoma or insulinoma
Peptic Ulcers - from gastrinoma
Sipple Syndrome: AKA Multiple Endocrine Neoplasia 2a (MEN2a).
"TAP"(Thyroid, Adrenal, Parathyroid)
Diseases: Medullary Carcinoma of the Thyroid & Pheochromocytoma, plus Parathyroid Hyperplasia.
*Parathyroid Hyperplasia* is not present in MEN2b.
Cause: Mutation of RET Oncogene
Screen family of patient; suggest prophylactic thyroidectomy to those with RET mutation
Sheehan's: Post-partum anterior pituitary necrosis. Relatively common.
Various Mechanisms, including: shock, DIC (post-partum)
Hormones Affected: All anterior pituitary hormones will decrease, most notably TSH and ACTH.
Grave's:
Etiology: Usually affects women in their 20s-40s, 1-2% of entire population.
Symptoms: Triad: Hyperthyroidism, Opthalmopathy (eye proptosis), & Dermopathy (pretibial leg edema)
The cause is: Autoimmune --> antibodies to TSH receptor (TSI - "Thyroid Stimulating Immunoglobins")
Hashimoto's: lymphocytic infiltrate with germinal centers & Hurthle cell hyperplasia, maybe fibrosis. Painless.
Etiology: Women. 45-65 yrs old. Adult Down's Syndrome patients have increased risk.
Autoimmune assocation (SLE, RA, DM, etc.)
Symptoms: Painless enlargement of thyroid. Hypothyroidism
(#1 cause of hypothyroidism is Hashimoto's). Goiter.
Cause: Antimicrosomal Antibodies (antibodies to thyroid peroxidase), Anti-thyroglobulin antibodies.
Risks: Small increased risk of developing B-Cell Lymphoma (especially MALT Lymphoma)
DeQuervain's subacute granulomatous thyroiditis:
Symtpoms: Fever; Painful thyroid enlargement, Self-limited, transient hyperfunction.
Cause: Viral? (incidence peaks in summer)
Lab Findings: Giant cells/granulomas in thyroid.
Plummer Syndrome: toxic multinodular goiter (goiter is an enlarged thyroid gland). An autonomous nodule within a long-standing goiter which produces lots of T3/T4, thus producing hyperthyroidism symptoms.
Symptoms: Hyperthyroidism.
Right. Now that we have that cleared up, I think I can go ahead and continue my never-ending revisions. The GI system is easy enough for me, because the diseases are much more common, but endocrinology is more difficult. Fingers crossed for a good mark on this exam; I'm working towards getting a good final grade in organ systems!
Thursday, March 31, 2011
Monday, March 28, 2011
Step1 Revision: The Beginning
I have officially started my step 1 revision...Only a few months late! Currently, I am following the Doctors in Training 12 week study plan, which consists of: 125questions per week from the QBank (I'm actually doing 25-30questions/day, which equals 175-210 questions per week), and reading 50 pages per week of First Aid for Step 1. I purchased a pathology review book from Goljan, but I'm not finding it very helpful; its quite thorough and presented in an outline form, but it isn't very high yield in that it presents all of the details rather than the most important points. One of my professors has been giving us "partnerships" to go with pathology, which has been helpful. A partnership is making a direct connection between two ideas.
For example:
Crypt Abscesses --> Ulcerative Colitis
Osmotic Diarrhea --> Lactose Intolerance
Dermatitis Herpetiformis --> IgA Deposits in Dermal Papillae --> Celiac Sprue
Plummer Vinson Syndrome --> Cheilosis, Glossitis, Iron Deficiency anemia, Upper Esophageal Webs
Ludwig Angina --> Pancytopenia.
Chagas --> Achalasia.
Intra-Unterine Fetal Heart Blocks --> Anti-Ro Antibodies. (Sjogren's).
The partnerships are quite helpful. The difficulty with the Step1 Exam is the two-step questions. For example, the question presents a case and gives you a few clues that should allow you to determine the cause of the illness presented in the case. From there, you have to take your knowledge about that inferred disease and answer a question related to that particular disease, which can range from which tests would be abnormal, what are complications, what is the embryological origin of the main anatomic structure involved, what genetic abnormalities are associated, etc. As the years have gone by, the Step1 has become increasingly more difficult. The aim of the national boards of medical licensing is to have a 90% pass rate; when the students become smarter and more capable of excelling at the exam, the national boards make the exam more difficult to keep a 90% pass rate nationwide. My opinion is, if we've made it through 2 years of rigorous medical education, heaped on over $100,000 in debt, and do well enough to have a solid background and be able to excel in the clinical clerkships, there is no reason to fail 10% just to keep a silly quota of a 90% pass rate. But that's the way things are; when I feel like I will never be able to know everything and do as well as I deserve, I find consolation knowing that the Step1 will be harder for those medical students coming in 10 years from now! ;)
For example:
Crypt Abscesses --> Ulcerative Colitis
Osmotic Diarrhea --> Lactose Intolerance
Dermatitis Herpetiformis --> IgA Deposits in Dermal Papillae --> Celiac Sprue
Plummer Vinson Syndrome --> Cheilosis, Glossitis, Iron Deficiency anemia, Upper Esophageal Webs
Ludwig Angina --> Pancytopenia.
Chagas --> Achalasia.
Intra-Unterine Fetal Heart Blocks --> Anti-Ro Antibodies. (Sjogren's).
The partnerships are quite helpful. The difficulty with the Step1 Exam is the two-step questions. For example, the question presents a case and gives you a few clues that should allow you to determine the cause of the illness presented in the case. From there, you have to take your knowledge about that inferred disease and answer a question related to that particular disease, which can range from which tests would be abnormal, what are complications, what is the embryological origin of the main anatomic structure involved, what genetic abnormalities are associated, etc. As the years have gone by, the Step1 has become increasingly more difficult. The aim of the national boards of medical licensing is to have a 90% pass rate; when the students become smarter and more capable of excelling at the exam, the national boards make the exam more difficult to keep a 90% pass rate nationwide. My opinion is, if we've made it through 2 years of rigorous medical education, heaped on over $100,000 in debt, and do well enough to have a solid background and be able to excel in the clinical clerkships, there is no reason to fail 10% just to keep a silly quota of a 90% pass rate. But that's the way things are; when I feel like I will never be able to know everything and do as well as I deserve, I find consolation knowing that the Step1 will be harder for those medical students coming in 10 years from now! ;)
Wednesday, March 23, 2011
Medical School and Its Impact on (my) Health
Well, the season of Step1 stress is finally upon me. As I have said in a previous post, many medical students begin to study for the step1 in January...I, sad to say, am not one of those students. Don't get me wrong - I bought my package for USMLEWorld several months ago, reserved my copy of First Aid for Step 1 far before the 2011 edition was on the shelves, scheduled my testing date at a preferred testing center, and have even taken a practice step 1 (well, only a few hours of a practice test if I want to be honest!). It's just that I haven't exactly been keeping up with reviewing old material like I know I should. The problem is that we're still learning new stuff, and that takes so much time to memorize and understand completely that there just aren't enough hours in the day to study everything I'd like to study. My thought is that if I do my best to master the new material as it comes, I won't have to spend as much time reviewing that material in May, so I'm actually saving myself some trouble. But I could be totally off on this, and the idea of being off on something as important as this exam is frightening! I plan to start the revision process soon (uhm, I have literally said that since January), and I'm hoping this helps to alleviate some of my apprehensiveness about this massively important exam.
I just thought that I would share a few things about my health that have changed since I have matriculated into medical school a mere year and a half ago. (Was it only a year and a half ago??? It seems like I've been studying for a lifetime...*sigh*).
To start, last year I noticed that my heart felt funny in my chest sometimes, most often it was a fluttery feeling followed by a feeling as if someone kicked me in the chest lightly. I noticed that while the fluttering episodes occurred, my heart skipped. So I went to my family doctor and she put in an order for a 24 Holter monitor to find the cause for my symptoms. I was found to have a Type I Second Degree Heart Block, also known as "Wenckebach" or Mobitz I. A little medical info on this condition: it is almost always a disease of the AV Node; it is characterized by progressive prolongation of the PR interval (the PR Interval is the time the electrical impulse takes to travel from the sinus node through the AV node and enter the ventricles. The PR interval, therefore, is a good estimate of AV node function - hence the diagnosis of a disease of the AV Node); Prolonged PR Interval is followed by a blocked P wave and thus a dropped QRS Complex, presenting as a missed beat (QRS Complex indicates when the ventricles contract and send blood throughout your lungs and body); following the dropped QRS, the PR Interval will "reset" itself by initiating an "escape rhythm", which allows the heart to beat effectively until another prolongation of the PR interval takes place, and the cycle continues. What makes this type of rhythm Type I instead of Type II is the fact that the atrial rhythm is regular; this also can be comforting to know because it means that the heart-block is generally benign, and, in essence, won't kill me. Reassuring, for sure.
Less interestingly and more commonly, I've had several bruises on my bottom from what I like to call "excessive medical school syndrome", characterized by me sitting on my ass day-after-day trying to absorb as much material as I can, therefore producing bruises on my gluts from excessive impingement of my muscles between my hip bones and my not-so-adequately-padded chair. I think all of us med students have had this complaint before, and will probably continue to until we reach our clinical years, when it will no doubt be replaced by the complaint of "tired feet" from running around trying to keep up with the doctors all day...
Then you've got the normal things that we all get from being a med student: sleep deprivation, irritibility, caffeine overload, acne, serious anxiety, feelings of depression/worthlessness, etc.
Recently, I've found that I have a new health complaint - an annoyingly chronic eye twitch. It has to be related to the stress of the impending Step1, and I have been suffering this annoyance for a few weeks now (and I don't think it will end until after my exam).
All of these conditions, these health changes, can be attributed to stress. For me, my palpitations and irritability and bruised butt are all signs of an impending exam in the near future; which equate to stressful times, for sure.
So...Why did I sign up for this life again??? ;) Let's just get past this massively important and hugely stressing exam that's in June, and I know that I'll once again realize why I came to medical school in the first place - to compassionately and whole-heartedly help people in their most desperate hour of need.
...Now if only this darn twitch would stop...! ;)
I just thought that I would share a few things about my health that have changed since I have matriculated into medical school a mere year and a half ago. (Was it only a year and a half ago??? It seems like I've been studying for a lifetime...*sigh*).
To start, last year I noticed that my heart felt funny in my chest sometimes, most often it was a fluttery feeling followed by a feeling as if someone kicked me in the chest lightly. I noticed that while the fluttering episodes occurred, my heart skipped. So I went to my family doctor and she put in an order for a 24 Holter monitor to find the cause for my symptoms. I was found to have a Type I Second Degree Heart Block, also known as "Wenckebach" or Mobitz I. A little medical info on this condition: it is almost always a disease of the AV Node; it is characterized by progressive prolongation of the PR interval (the PR Interval is the time the electrical impulse takes to travel from the sinus node through the AV node and enter the ventricles. The PR interval, therefore, is a good estimate of AV node function - hence the diagnosis of a disease of the AV Node); Prolonged PR Interval is followed by a blocked P wave and thus a dropped QRS Complex, presenting as a missed beat (QRS Complex indicates when the ventricles contract and send blood throughout your lungs and body); following the dropped QRS, the PR Interval will "reset" itself by initiating an "escape rhythm", which allows the heart to beat effectively until another prolongation of the PR interval takes place, and the cycle continues. What makes this type of rhythm Type I instead of Type II is the fact that the atrial rhythm is regular; this also can be comforting to know because it means that the heart-block is generally benign, and, in essence, won't kill me. Reassuring, for sure.
Less interestingly and more commonly, I've had several bruises on my bottom from what I like to call "excessive medical school syndrome", characterized by me sitting on my ass day-after-day trying to absorb as much material as I can, therefore producing bruises on my gluts from excessive impingement of my muscles between my hip bones and my not-so-adequately-padded chair. I think all of us med students have had this complaint before, and will probably continue to until we reach our clinical years, when it will no doubt be replaced by the complaint of "tired feet" from running around trying to keep up with the doctors all day...
Then you've got the normal things that we all get from being a med student: sleep deprivation, irritibility, caffeine overload, acne, serious anxiety, feelings of depression/worthlessness, etc.
Recently, I've found that I have a new health complaint - an annoyingly chronic eye twitch. It has to be related to the stress of the impending Step1, and I have been suffering this annoyance for a few weeks now (and I don't think it will end until after my exam).
All of these conditions, these health changes, can be attributed to stress. For me, my palpitations and irritability and bruised butt are all signs of an impending exam in the near future; which equate to stressful times, for sure.
So...Why did I sign up for this life again??? ;) Let's just get past this massively important and hugely stressing exam that's in June, and I know that I'll once again realize why I came to medical school in the first place - to compassionately and whole-heartedly help people in their most desperate hour of need.
...Now if only this darn twitch would stop...! ;)
Subscribe to:
Posts (Atom)