(Alternative) Ways to study medicine

Today I'd like to talk about how I bring variety to my own learning by doing lots of different methods of learning.

because I am not a very patient nor hardworking person, if I were to limit myself to a single study method, (e.g. in my university, the "best" way or the most popular one was to just read from the lecture notes and MEMORIZE EVERYTHING) - I would just die. I mean, I would lose that interest and my brain would stop producing endorphin and dorpamines and all the feel-good substances that I need to sustain my healthy mental health.

I like to have variety in learning because...

1. It makes studying less boring and hence I can study longer
2. I would be able to find out what's best for me
3. I can be like hey check out my new way to study (like right now)
4. By employing other ways in which I learn, I can provide an alternative viewpoint - who needs another boring medical student who studies like everyone else?

and the list goes on. I want to study differently, so I study differently. 

Now, if you're a.... say, a third year student, you might already know those following ways to learn because you've gone through that "I would rather die than read another page of notes" and turned to other ways to study. 

So, perhaps this blog entry would benefit the more junior students more than the seniors. anyways here goes!

other ways to study!

watch youtube videos
Youtube has plenty of stuff that are both informative and fun to watch. some channels in Youtube are dedicated to provide quality information FREE OF CHARGE. Basically, there are people who want to learn medicine all over the world and we face the same pains. So might as well learn from them!
here are some youtube channels I follow!

Armando Hasudungan  - He draws a very comprehensive schematic diagram with which he describes basic medical facts. Some of his videos are really great at understanding basic concepts that you may need to straighten out before you get to the specifics in 10 minutes or less. here's an example - Overview of Immunology - great introduction to immunology and an overview of what immunology is all about. 

Geeky Medics - These guys make this blog an embarrassment because their OSCE guides and demonstrations are far easier to understand and refer to, than the text format I provide. They provide really good quality OSCE demonstrations. here's an example - Cardiovascular Examinations  - a straightforward examination of CVS. 

OnlineMedEd - This channel would be very useful for senior students OR current doctors whom (surprise surprise) are studying for exams. They are fully-fledged doctors trying to provide quality medical education to people, apparently their videos are free but with some cash, they'll teach you how to pass exams and most importantly, to be "a better doctor" - their slogan. here's an example - Antibiotic Ladder - It requires that you have some knowledge about drugs and microorganisms, but this tutorial is great for 3/4th years. 

Teach other students

You can offer to teach your friends or your juniors - the great thing about teaching is that the moment you teach, you win - teaching is one of the best ways to integrate information in your mind so that you can make it your own and answering exam questions would be a piece of cake. Teaching is hard,  but if you're able to teach so that other students can understand, that means you have really grasped the essence of the topic you're trying to cover, and this is my personal opinion but doctors should all  be teachers as well - to the peers, patients, and themselves. If there's some information to be learnt, it might as well be presented in forms that are most easily digested. Teaching will make you realize some things you needed to know, but didn't know you didn't know at that moment. 

If you're good, people would start paying you even! Which is not uncommon in medical school - some students can afford it!

Form a study group

Who does study group nowadays? Nobody! I think this is because everyone assumes that either you can manage to learn everything by yourself, or that everyone else has no time for group study. Which I beg to differ because group studying is one of the best ways to study - as evidenced by the fact that most medical schools now employ group learning sessions like PBL / TBL system. 

What is important about study group is that you're forced to output information more than you input - of course you listen to your peers, so that's an input, but when you need to present your ideas and facts to your peers, It requires that you fully understand what you're talking about.... either that or you develop a skill to beat vigorously around the bush until you bang onto something relevant - which is also a useful skill to have - but don't rely on it! Ultimately we want to be safe doctors, not politicians. 

here's me making the most out of group discussions. 

Take tests 

I like this method because it does two things - it forces me to get used to be tested, and it makes me realize what information I am missing out. Sometimes I go ahead and test myself before I read up anything about the topic so I can vaguely understand what may come out and what seems to be more important. 

It is best to take tests where the answers are properly provided on the back of the page or elsewhere. 

taking tests and checking the answers stimulate our brain more because of that pressure of answering questions, getting it wrong, and the "ahhhhhh" moment when you look at the answers. when you go  "ahhhhhh" that's when the information sticks. because memory tend to stick with emotions. 

here's me checking my answers. 15% correct...!? fffffff

Keep things at your fingertips

... and what are near your fingertips by default? YES - your smartphone.

I use apps which makes it very easy for me to readily refer to good source of medical information.

here are some example - 

Medscape  - Medscape is a website with a great deal of good quality medical information. It is also free (I think) with registration. Whenever I need to look things up, I can refer to this for a solid back-up of facts. Perhaps if i spent more time on this and less on Instagram, I could have been an A student. 

as you can see I can refer to drugs, conditions and procedures any time - even with 30% battery remaining.

but lastly....

don't study too much. get some rest. 

I personally don't need to choose where to rest. every floor is a bed. Chair is a pillow. 

Prezi Presentation

I learnt of this new presentation software called "Prezi", which can make presentations actually fun to create and watch at the same time.

I'm bored of powerpoints, so it's quite refreshing for me to be able to make some interactive-looking stuff easily with a click of a mouse.

Made an elective posting presentation using this software;

http://prezi.com/eslrmcauimux/presentation-of-jgroopmans-book-how-doctors-think/#share

its most useful for conceptual presentations, i think.

friday tutorial

just like the other day, i have summed up the tutorial done - until we were interrupted, that is.

MSK

Osteomyelitis

·         Inflammation of bone and marrow

o   Pathways of transmission

§  Posttraumatic osteomyelitis accounts for as many as 47% of cases of osteomyelitis.

§  Other major causes of osteomyelitis include vascular insufficiency (mostly occurring in persons with diabetes; 34%) and hematogenous seeding (19%).

§  Motor vehicle accidents, sports injuries, and the use of orthopedic hardware to manage trauma also contribute to the apparent increase in prevalence of posttraumatic osteomyelitis.

o   Presenting signs/symptoms - how to differentiate bet. Septic arthritis?

§  Arthritis is a joint problem, whereas OM

o   Salmonella osteomyelitis -> very common in Sickle cell trait / sufferers.

o   Bone and marrow -> limited space -> when inflammation and exudation, limited space -> cause a Necrosis around the area due to high pressure and lack of blood -> opening established (absess) to release the pus -> through a “pointing” in the skin surface, the necrotic and infective material is relaeased -> sequastrum (dead bone) ->new bone formation using the dead bone as support / buttress. New bone called involucrum

o   How to look at a microscopic bone tissue and say its dead or alive?

§  Non-viablity of bone

·         Absence of osteoblastic rimming at surface

·         Empty lacunae devoid of osteocytes

·         Learn how to describe an ulcer.

o   Malignant?

o   Ischemic?

·         Brody’s absess - subacute OM

·         Tuberculous osteomyelitis - differences from Brody’s absess

o   Cold absess

o   Usually no remodeling

o   Preferance for spine (pott’s spine)

o   Kissing sequestra

Avascular necrosis

·         Causes

o   Fracture / dislocation

o   Embolic phenemona

o    Vascular occlusion:

§  This is characterized by the interruption of the extraosseous blood supply via factors such as direct trauma (eg,fracture, dislocation), nontraumatic stress, and stress fracture.

o    Altered lipid metabolism:

§  Animal studies have led to the hypothesis that increased levels of serum lipids leads to lipid deposition in the femoral head, causing femoral hypertension and ischemia.^[2] Lipid-level–lowering drugs in animals reverse this process. Corticosteroid administration was associated with fat emboli in the femoral heads of rabbits.^[3]

o    Intravascular coagulation:

§  Disorders of the coagulation system have been implicated in the pathogenesis of AVN. Typically, it is a secondary event triggered by a familial thrombophilia, hypercholesterolemia, allograft organ rejection, other disorders (eg, infection, malignancy), or pregnancy.

o    Healing process:

§  Necrotic bone triggers a process of repair that includes osteoclasts, osteoblasts, histiocytes, and vascular elements. Osteoblasts build new bone on top of the dead bone, leading to a thick scar that prevents revascularization of the necrotic bone, with resultant abnormal joint remodeling and joint dysfunction.

o    Primary cell death:

§  Osteocyte death without other features of AVN has been seen in renal transplant patients, as well as in patients receiving steroids and those who consume significant amounts of alcohol.

o    Mechanical stress:

§  Animal studies have shown an association between increased weight bearing and an increased incidence of AVN of the femoral head.

·         White infarct / red infarct

o   Infarctions are divided into 2 types according to the amount of blood present:

o   White infarctions (anemic infarcts) affect solid organs such as the spleen and kidneys wherein the solidity of the tissue substantially limits the amount of nutrients (blood/oxygen/glucose/fuel) that can flow into the area of ischemic necrosis. Similar occlusion to blood flow and consequent necrosis can occur as a result of severe vasoconstriction as illustrated in severe Raynaud's phenomenon that can lead to irreversible gangrene.

o   Red infarctions (hemorrhagic infarcts), generally affect the lungs or other loose organs (testis, ovary, small intestines). The occlusion consists more of red blood cells and fibrin strands. Characteristics of red infarcts include: occlusion of a vein; loose tissues that allow blood to collect in the infarcted zone; tissues with a dual circulatory system (lung, small intestines); tissues previously congested from sluggish venous outflow; and reperfusion (injury)[3] of previously ischemic tissue that is associated with reperfusion-related diseases[4] such as - Myocardial infarction, stroke (cerebral infarction), shock-resuscitation, replantation surgery, frostbite, burns and organ transplantation.

Osteoarthritis

·         Consequences of OA

Osteoporosis

·         Why is it important to discuss OP?

o   Preventable

o   Common

o   Ageing population

·         Etyology of OP

·         Screening of OP

o   T-score

o   Z-score

§  Cut variables of race, sex, age

§  More reliable

·         What happens to the IVD in OP?

o   Nuclear pulposis

§  May become herniated out

o   Annulus fibrosis

§  As people age, the annulus becomes thin and slit-opening will appear, frail and break

Tumours of the bone

osteochondroma

o   most common tumour!

o   Exostoses - bony core, cartilaginous cap!

o   Can occur anywhere.

o   Lilac coloured

o   When cartilage is >1cm, may become chondrosarcoma (rare but possible)

Giant cell tumour - osteoclastoma

o   Osteoclast + spindle cells

o   Behavior of GCT is determined by ratio of osteoclast and spindle cells

o   Usually epiphyseal

o   It it benign

o   Fusiform dilatation of lower end of epiphyses

o   Eggshell crackling on palpation. (cystic spaces filled with haemorrhage)

o   Eccentric expansile tumour

Paget’s disease

·         Hats don’t fit!

·         Loss of bone -> loss+formation -> formation

·         Osteoid Osteoma

Osteoblastoma

thursday tutorial

Here’s a very brief summary of what was discussed during the tutorial we had on Thursday. I have taken the liberty to consult e-med for parts that was discussed but didn’t know what was going on (which is, MOST of the time.) enjoy.

renal

Cystic renal dysplasia

Absence of normal parenchyma of kidney

Associated with Wilm’s

Not compatible with life

horse-shoe kidney

Effects come when ureters lie behind the joined pole of kidney

Obstructive nephropathy

Most of the time it lies in front so its okay

double ureters

Can have partial hydronephrosis

Normally benign

APKD

Why is it a problem - renal cell carcinoma

The main feature of ADPKD is bilateral progressive cystic dilation of the renal tubules, which may lead to end-stage renal disease (ESRD). Hepatic cysts, cerebral aneurysms, and cardiac valvular abnormalities also may occur.

Juvenilile Cystic KD

Complication - why not compatible with life?

Hepatic fibrosis

Lung fibrosis

All patients with autosomal recessive polycystic kidney disease have congenital hepatic fibrosis (CHF), which may have more severe clinical manifestation than the renal disease.

The CHF results from malformation of the developing ductal plate.

The liver biopsy findings reveal enlarged, fibrotic portal tracts and hyperplastic, dilated, and dysgenetic biliary ducts with normal hepatocytes. The ductules can show true cystic changes, and, when the changes are macroscopic, autosomal recessive polycystic kidney disease can be indistinguishable from Caroli disease. The portal hypertension secondary to the CHF can be clinically debilitating, with splenomegaly, varices, and GI hemorrhage.

tubulointerstitial diseases

pyelonephritis acute and chronic

·         Depressed scars - chronic pyelonephritis. Granular contracted kidney of pyelonephritis

·         What are the histologic differences in chronic pyelonephritis?

o   Tubulointerstitial infiltration by chronic inflammatory cells (lymphocytes)

o   Thyroidisation of tubules

o   Glomeruli usually spared - until renal failure

o   Colloidlike material pas+

obstructive uropathy

staghorn calculus

hydronephrosis

Hydronephrosis -> pus collect ->pyelonephrosis

Hydroureter

bph

Symptoms often attributed to BPH can be caused by other disease processes, and a history and physical examination are essential in ruling out other etiologies of (lower urinary tract symptoms (LUTS) (see Diagnostic Considerations).

·         Urinary frequency - The need to urinate frequently during the day or night (nocturia), usually voiding only small amounts of urine with each episode

·         Urinary urgency - The sudden, urgent need to urinate, owing to the sensation of imminent loss of urine without control

·         Hesitancy - Difficulty initiating the urinary stream; interrupted, weak stream

·         Incomplete bladder emptying - The feeling of persistent residual urine, regardless of the frequency of urination

·         Straining - The need strain or push (Valsalva maneuver) to initiate and maintain urination in order to more fully evacuate the bladder

·         Decreased force of stream - The subjective loss of force of the urinary stream over time

·         Dribbling - The loss of small amounts of urine due to a poor urinary stream

Diagnostics

·         DRE

o   The digital rectal examination (DRE) is an integral part of the evaluation in men with presumed BPH.

·         Prostate-Specific Antigen

o   Rising levels of PSA in serum are associated with prostate cancer. The PSA level also tends to rise in men with benign prostatic hyperplasia (BPH) and is a good marker for prostate volume. PSA levels are usually elevated in men with acute bacterial prostatitis.

·         Ultrasonography

o   A more precise volumetric determination can be made using transrectal ultrasonography (TRUS) of the prostate

Gliesen’s grading of prostatic cancer

prostate cancer

prostate cancer staging

renal cell carcinoma

There is an association of renal cell carcinoma with several clinical syndromes such as Von Hippel Lindau Disease, Adult Polycystic Kidney Disease, and Acquired Renal Cystic Disease.  Renal Cell Carcinoma has also been reported to run in certain families (a familial type).

clear cell carcinoma

Smoking, obesity, and hypertension are the 3 most well-established risk factors associated with development of sporadic renal cell carcinoma (RCC).

The main inherited disorder predisposing to development CCRCC is von Hippel-Lindau (VHL) disease, which involves a germline mutation of the VHL gene at chromosome 3p25. Affected individuals are susceptible to tumors of multiple organ systems, including cysts and tumors of the kidney, which occur in 25-45% of cases with a mean age at onset of 40 years. The renal tumors are frequently multifocal and/or bilateral and are always of the clear cell renal cell carcinoma (CCRCC) histologic type

wilms tumour

·         Wilms tumors can arise…

o   sporadically

o    in association with genetic syndromes,

§  Beckwith-Wiedemann syndrome (macroglossia, gigantism, and umbilical hernia)

§  Hemihypertrophy

§  Congenital aniridia

§  Wilms tumor, aniridia, genitourinary malformations, and mental retardation (WAGR syndrome)

§  Denys-Drash syndrome (Wilms tumor, pseudohermaphroditism, and glomerulopathy)

§  Trisomy 18 mutation

o   Familial

·         Presentation

o   Wilms tumor is diagnosed at a mean age of 3.5 years. The most common feature at presentation is an abdominal mass.

§  Abdominal pain occurs in 30%-40% of cases. Other signs and symptoms of Wilms tumor includehypertension, fever caused by tumor necrosis, hematuria, and anemia.

o   Major congenital anomalies include

§  genitourinary anomalies (WAGR and Denys-Drash syndromes, 5% of cases),

§  ectopic solitary horseshoe kidney,hypospadias and cryptorchidism, hemihypertrophy and organomegaly (Beckwith-Wiedemann syndrome, 2% of cases); and

§  aniridia (1% of cases).

§  Children with such syndrome anomalies should undergo periodic testing for Wilms tumor. Ultrasonography of the kidneys (once or twice per year) is a good screening tool.

·         Dwarfing of kidney

WAGR WT related syndromes

glomerulonephritis

Know what is common in adults / children

Adults

·         Membranous - 40%

·         Minimal change disease - 15%

·         Focal glomerulo sclerosis - 15%

·         Membranoproliferative - 7%

·         Mesangioproliferative - 5%

Children

·         Minimal change - 76% of nephrotic children

·         IgA nephropathy

·         Post-streptococcal

Rapidly progressive - why important to diagnose? - because treatment for severe and acute GN, is Dialysis and Transplantation. - RPGN patients frequently recur.

Diabetic Nephropathy - Kimmestel Wilson

Kimmelstiel-Wilson disease is a kidney condition associated with long-standing diabetes. It affects the network of tiny blood vessels (the microvasculature) in the glomerulus, a key structure in the kidney that is composed of capillary blood vessels and which is critically necessary for the filtration of the blood. Features of Kimmelstiel-Wilson disease include the nephrotic syndrome with excessive filtration of protein into the urine (proteinuria), high blood pressure (hypertension), and progressively impaired kidney function. When severe, Kimmelstiel-Wilson disease leads to kidney failure, end-stage renal disease, and the need for chronic kidney dialysis or a kidney transplant. The disorder is named for Paul Kimmelstein (1900-70), a German-born pathologist in the U.S., and Clifford Wilson (1906-), an English physician. It is also known as Kimmelstiel-Wilson syndrome or intercapillary glomerulonephritis.

DGSF

endocrine

pituitary adenoma

Sheehan's syndrome - when and what does occur?

parathyroid gland adenoma /hypo

hyperthyrodism

What are hurtle cells ? askanazi cells?

Papillary carcinoma of thyroid - cellular characteristics


Cusing's Syndrome - causes, characteristics