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Dialysis: Yes we can
The kidney is one of the few organs where modern medicine can take over the function. In other words if you lose you kidneys there is still A HOPE:
Indications for dialysis:
Acidosis (medically non-correctable)
Hyperkalemia of +6,5 mM (medically non-correctble)
Over-hydration, especially with anuria
Pericarditis due to uremia
Encephalopathy due to uremia
Diabesties II - DD: differential diabetes
Not all high BGL is simply type I, and that overweight guy might might not have type II, in fact FAT CHAPS can have some important differentials you don't wanna miss:
(one per letter in first word, two per letter in second word)
F - Pheochromocytoma
A - Acromegaly
T - Thiazides
-
C - Cushing's disease, Congenital lipodystrophy
H - HIV-meds, Hyperthyroidism
A - Antipsychotics, Acanthosis nigricans
P - Pancreas, Pregnancy
S - Steroids, Strorage disease (glycogen)
If you never find a way to keep the BGL down DIABETICS start developing complications:
D - Diabetic retinopathy
I - Ischemic heart disease
A - Autonomic
B - Blood pressure
E - Extremities
T - TCI / stroke
I - Intermittent claudication
C - Chronic kidney failure
S - Somatosensory
Unless stated otherwise all mnemonics presented on the this website are Dr. Mnemosyne originals. You are free to copy them and use them in anyway you like, but please make sure to reference by linking to this website. That way more people might enjoy the mnemonics. Thank you.
-Dr. Mnemosyne
Diabesties I - the start of a bittersweet friendship
If you were a western doctor in the 50's, chances are you'd be quite the expert on mumps, polio, rubella etc. since these were either endemic or epidemic diseases in the population and common causes of hospitalizations and death.
Luckily vaccination programs have made such en- and epidemics largely a thing of the past. Yet many diseases still thrive, and there's one epidemic that seems especially resistant to societal and medical intervention namely; obesity. And where there's obesity (and aging) there's diabetes type 2.
The modern western (and increasing non-western) world is riddled with type 2 diabetics, and the disease is perhaps the defining medical problem of our time period. In 1985 30 million people were diagnosed with diabetes type 2, but by 2010 that number was 285 million (900% increase). That is 1 in 15 of the world's population.
For this very reason - as no doctor will be able to steer clear of diabetic patients - it is a very good idea to familiarize yourself with diabetes; befriend it. Not only will you make your professional life easier; you'll also be able to help literally 100s of millions of people suffering from this usually treatable and to some extent avoidable disease.
Firstly, a few comments of incidence, prognosis and prevention:
Modifiable risk factors: Smoking, Alcohol, Food/diet and Exercise, you know, just to be SAFE
About 10% of diabetics are type 1, the rest (90%) are type 2.
Type 1 DM starts when less than 10% beta-cell function is left.
20% of type 2 diabetics will develop insulin-dependance.
Type 2 DM gives 20% diabetic nephropathy within 20 (10-30) years.
Backgound information:
p. 803 22th DPPM, p. 199 8th OHCM and wikipedia (DM)
Atherosclerosis - I would have gotten away with it too
The four modifiable risk factors for atherosclerosis is diabetes, hypercholesterolemia, high blood pressure and smoking. So it doesn't take a great detective to figure out how those plaques appeared:
SCOOBY DOO
Smoking
Cholesterol (high)
Blood pressure (high)
Diabetes
The one mnemonic to dominate them all
As you know autosomal dominant diseases are caused by tiny gene flaws initiating awesome destructive power. Hence, it is only fitting that autosomal dominant diseases get a mnemonic worthy of their dominance.
The following mnemonic provides a quite useful list of some of the most common and relevant autosomal dominant diseases. But it does more than that. As you list these 22 disease from memory it has the added beauty of listing them in chromosomal order, that is: the first is found on chromosome 1, the second is found on chromosome 2 etc. Also you might notice that most of these are structural problems, whereas autosomal recessive tend to be metabolic.
While knowing diseases for each chromosome isn't terribly relevant clinically it can yield bonuses on exams, and if nothing else, it sure is a cool party trick. Here goes:
Learn this 22-word limerick:
Hippo Ehler's fun hunting fetish
Made platypuses severely ticklish
Many asked why
Retarded hippos must pry
Nagged platypuses: My! Hippos are foolish
Recite it a few times, then get paper and list the words from memory:
Hippo - Hypokalemic periodic paralysis (type 1 on chromosome 1)
Ehler's - Ehler-Danlos Syndrome (type 3 and 4 on chromosome 2)
Fun (von) - von Hippel-Lindau disease (chromosome 3)
Hunting - Huntington's disease (chromosome 4)
Fetish - Familial adenomatous polyposis (chromosome 5)
Made - Vitelliform macular dystrophy (chromosome 6)
Platypuses - Polydactyly (multiple, yet mostly on chromosome 7)
Severely - Hereditary Spherocytosis (type 1 on chromosome 8)
Ticklish - Tuberous Sclerosis ("two hits", 1st on chromosome 9)
Many - Multiple Endocrine Neoplasia type 2 (chromosome 10)
Asked - Acute intermittent porphyria (chromosome 11)
Why - von Willibrand's disease (chromosome 12)
Retarded - Retinoblastoma (chromosome 13)
Hippos - Hypertrophic cardiomyopathy (most commonly on chromosome 14)
Must - Marfan (chromosome 15)
Pry - AD Polycystic kidney disease (chromosome 16)
Nagged - Neurofibromatosis type 1 (chromosome 17)
Platypuses - Juvenile Polyposis hemorrhagic telangiectasia (chromosome 18)
My - Myotonic dystrophy (chromosome 19)
Hippos - Albright's Hereditary osteodystrophy (chromosome 20)
Are - Amyotrophic lateral sclerosis (chromosome 21)
Foolish - NeuroFibromatosis type 2 (chromosome 22)
Background information: p. 87 2014 FA 4 USMLE(I), Wikipedia (Huntingtons, macular dystrophy, polydactyly, hereditary spherocytosis, tuberous sclerosis, Multiple endocrine neoplasia type 2, acute intermittent porphyria, von Willebrand disease, hypertrophic myopathy, hereditary hemorrhagic telangiectasia, myotonic dystrophy, Albright's hereditary osteodystrophy, Amyotrophic lateral sclerosis)
The base-ics
Nucleotides are in nearly all your cells. Are they in your memory?
PURines (A,G) are PURe As Gold
PYrimidines (C, U, T) have a midline (one ring) so you can CUT the PY (pie)
thymine (t) has methyl
uRacil (U) is in RNA
Background information:
p. 66 2014 FA 4 USMLE(I)
Early development III - The first five years
Here you'll find a mnemonic done in the style of a children's poem. It tells you at what ages certain activities should be seen in young children.
The general Early Developmental Milestones from 18 mo - 5 years of age are:
By age 18 mo the toddler should be walking, climbing stairs and able to kick a ball.
By age 2 the toddler should be able to move away from and return to the mother, use approximately 200 word and 2-word sentences and feed self with fork and spoon.
By age 3 they should be able to comfortably spend part of the day away from the mother, ride a tricycle, use about 1000 words and realize core gender identity.
By age 4 they should be able to draw by copying lines and circle and draw basic stick figures, have the dexterity to hop on one leg, form (imaginary) friends and engage in cooperative play, use complete sentences and tell detailed stories.
By age 5 the more advanced motor skills form (do buttons and zippers). Otherwise early development should be complete.
Below is the poem that encompasses nearly all of these developmental features:
1.
You're toddling around (Walking upright)
just a year and a half
you can climb up the stairs (able to climb stairs)
and kick balls with a laugh (able to kick a ball - might be later)
2.
Then soon you're two
and you eat with a spoon (can feed self with spoon and fork)
Use 200 words (use 200 words by age 2 in 2-word sentences)
and can go to the moon (Rapprochement - can leave and return to mother)
3.
And when kids are three
whether boys or birds (Core gender identity form)
They don't miss their mom (Comfortably spends part of day away from mother)
and use 1000 words (use 1000 words by age 3)
4.
You tell friends your stories (can tell detailed stories)
and can draw now you're four (can copy circles and lines and draw tick figure)
and hop around with only
one foot on the floor (has the dexterity to hop on one foot)
5.
at last you are five
and you find zippers cool (Finer motor skills)
you've mastered the basics
and you're ready for school (Early development completed)
Backgorund information:
p. 62 2014 FA 4 USMLE(I)
Early Development II - It's a rhyming development
If you think the first half of year one was fast-paced (Early Development I), just wait till the second half. This is where things really start to take off.
By the time you're 8 months you start crawling, then by 9 months you realize that objects are permanent, you can orient your attention toward someone saying your name, and you develop separation anxiety when mom or dad's not around.
By 10 months you should be standing up, using the pincer grasp and start being oratory saying "mama" or "dada".
By the time you're 1 year old you should be able to point at objects and parallel play with your peers and by now the Babinski reflex should be gone.
To remember when what happens, maybe you'll find this unusual mnemonic handy:
1.
When in months you are nine
you want mom all the time (separation anxiety)
you turn your head at your name (Orients to name and gestures)
and hate the peek-a-boo game (Early object permanence)
2.
By the time you are ten
you can stand up and then (Able to stand up)
grab things with a pinch (Can use the pincer grasp)
and make "mama" grow an inch (Oratory - says "mama" and "dada")
3.
And once you're a year
Babinski won't appear (Babinski reflex disappears)
and you can play with your peer (Parallel play)
and point to things you hold dear (Point to objects)
Background information:
p. 62 2014 FA 4 USMLE(I)
Early Development I - Half way 'round the sun
When you've only just come into this life the grown-ups in your life are already expecting you to reach certain milestones in the first half-year of your existence. What pressure!
In your first 6 months of life these milestones must be reached before a given age, or suspicions should start to form and further assessment be done:
By the times the infant's 1 month old he/she should be lifting up the head. The month after, by month 2, the infant should be smiling socially, and by month 3 the Moro reflex should disappear and by month 4 the rooting reflex should go the same way. Then in during the 5th month you finally get some time off to just be yourself, but then by month 6 there's a big test. By the times you're half a year old you should be able to roll/sit, feel stranger anxiety, pass toys from hand to hand and have lost your palmar reflex.
That's quite a curriculum for a human the size of a mutton rack, and also quite a lot to remember for the doctor, especially if you don't have kids yourself and have gone through the process.
To remember the Early Developmental Milestones of those first 6 months just think; Look, Soon Mom's Really TRAPped.
Here's how to remember which months:
1 mo - Lifts head
2 mo - Smiles socially
3 mo - Moro reflex gone
4 mo - Rooting reflex gone
(times)
6 (4 things by age 6 mo) - Toys (from hand to hand), Rolls/sits, Anxiety (with strangers), Palmar reflex gone
Alternatively you might find this limerick useful:
By 1 month they should lift their head
and by 2 months your smile should be met
at 3 Moro's so long
and by 4 rooting's gone
by 6 palms and sitting strangers are read
Background information:
p. 62 2014 FA 4 USMLE(I), wikipedia (Primitive reflexes)
Amyl-over-dosis
When Rudolf Virchow, famous for the 50's smash-hit Virchow's Triad, first saw amyloids in his microscope, he accidentally mistook them for starch. Being a hip German pathologist Rudolf fashionably gave the molecules a Latin name: amyloids, from the Latin for starch amylum.
Unfortunately amyloids are proteins not carbohydrates, but fortunately giving the protein an incorrect name was actually somewhat fitting.
Amyloids turned out to be the product of incorrect protein folding, ultimately resulting in insoluble fibrous proteins. Basically, it's like when a teenager folds the laundry and does such a terrible job that when he goes to use them he can't tell if they're clean or not, and just ends up throwing them on the floor.
Since there are a lot of different types of proteins in the body there are a lot of different types of amyloids. At least 60+, and so far 36 of these have been associated with disease.
Learning the 36 proteins by heart seems excessive and quite useless, but 7 amyloids are good for any doctor to know: AL, AA, Aβ2M, Aβ, ATTR, AIAPP and APrP or LAMB TIP (they all start with A for amyloidosis):
L - AL amyloidosis caused by amyloid light chains can affect all organ (÷CNS)
A - AA amyloidosis caused by serum amyloid A can affect abdominal organs (+kidneys)
M - hemodialysis-associated amyloidosis caused by β2 microglobulin (normal MHC protein) affecting movement (bones and joints)
B - AB amyloidosis seen in Alzheimer's disease where β amyloid builds up in brain lesions
T - TTR amyloidosis caused by transthyretin built-up as seen in familial amyloid polyneuropathies
I - IAPP (islet amyloid polypeptide) amyloidosis seen in pancreatic islets promoting apoptosis of β-cells resulting in decreased insulin in DM2
P - Prion disease caused by amyloid prions that promote protein-misfolding and are therefore contagious. As you might know prions are found in scrapie a disease of sheep where bare patches are seen at the tip of the rump , hence LAMB TIP.
Background information:
Wikipedia (Amyloidosis) and p. 364 8th OHCM
Sickly Sickle doesn't GAG
We all run around with 3.000.000.000 base pairs in our cells. In people with sickle cell disease one of these base pairs is changed in the 11th chromosome from an A to a T. So instead of the DNA encoding a glutamic acid amino acid (codon code GAG) into the beta-globin protein it encodes a valine (codon code GTG). This changes hemoglobin to a form known as HbSS. Potentially fatal disease ensues.
Read up on sickle cell disease and take the advice of the article here - learn what happens in a HBSS PAIN CRISIS:
H - Hemolysis, Hand-Foot syndrome
B - Bone Marrow Hyperplasia/Infarction
S -Stroke: Thrombotic or hemorrhagic, Subarachnoid bleeds
S - Skin ulcers (primarily leg)
P - Pain episodes, Priapism, Psychosocial problems
A - Anemia, Aplastic crisis, Avascular necrosis
I - Infections: CNS, Pulmonary, GU, Bone, Joints
N - Nocturia, urinary frequency from hyposthenuria
C - Cholelithiasis, Cardiomegaly, Congestive heart failure, Chest syndrome
R - Retinopathy, Renal failure, Renal concentrating defects
I - Infarction: Bone, Spleen, CNS, Muscle, Bowel, Renal
S - Sequestration crisis involving spleen or liver
I - Increased fetal loss during pregnancy
S - Sepsis
Bonus info:
Sickle cell disease was the first disorder ever - in any species - to be found out to be linked to a DNA mutation (1959).
Background information:
article
Do no (unanticipated) harm - When the pill makes you ill
It can be a real kick in the frank and kidney beans to forget about nephrotoxicity. There are more than 50 compounds that can cause damage to the kidneys, but luckily some of them fall into groups such as antibiotics or NSAIDs. So think about NephroToxic Compounds and Agents each time you prescribe a pill:
1 starts with N - NSAIDs
2 start with T - Tracolimus, Thiazide
3 start with C - Ciclosporin, Contrast, Cisplatin
4 start with A - ACE-inhibitors, Aminoglycosides, Antibiotics, Analgesia
The italicized compounds are considered the most important nephrotoxins due to severity/frequency of use.
Background information:
Wikipedia (nephrotoxicity), p. 307 8th OHCM
Do no (unanticipated) harm - A quick thought on AV fistulas
To accommodate hemodialysis doctors are fond of surgically creating AV-fistulas. Since it's something the doctor does to the patients it is a good idea to be extra aware of the possible complications. Remember risks related to AV-fistulas or it's THIS ASS on the line
Trombosis
Heart failure
Infection
Stenosis
Aneurism
Steal
Syndrome
Background information:
Wikipedia (AV-fistula), pp. 492-495 21th DPPM
The Hanta has become the hunted
When 3000 soldiers suddenly fell ill during the Korean War and 300 of them died, no-one knew what to make of it. After 25 years of hunting the cause, one American and one Korean virologist successfully managed to identify the villain - a tiny RNA virus found in non-symptomatic carrier rodents. They named it Hantavirus.
Today thousands of cases a year are seen in such places as Finland, Russia and China, as well as throughout Eurasia. So when the HANTAVIRUS comes 'round your way, pay heed to the outbreak of the Korean War and be thankful that at least you know what you're dealing with, because you remember:
That the virus causes:
Hemorrhagic
Acute
Nephritis
Two-Three weeks after exposure to
Animals (rodents)
And the initial sudden onset symptoms and findings are:
Vision (blurry vision, myopia and sometimes conjunctival bleeds)
Intestinal symptoms (as well as nausea and vomiting)
Renal impairment (oliguria, proteinuria (later))
Urine negative (sterile urine = UTI not likely)
Sweaty palms (fever, sweats, chills)
Obs. this mnemonic is only relevant for hantavirus hemorrhagic fever with renal syndrome (HFRS), in the Americas another syndrome caused by the hantavirus, hantavirus pulmonary syndrome (HPS), has been known for 20 years - but this syndrome is not endemic to Eurasia, just as HFRS is not endemic to the Americas. Yet...
Background information:
Wikipedia (hantavirus, HFRS), pp. 469-572 21th DPPM
Pyelonephritis and Pyonephrosis are easy as pie
Cause of confusion:
At first being introduced to nephrology the terms pyelonephritis and pyonephrosis are easily confused. The smart way to remember is to know that pyo- comes from the greek for 'pus' and pyelo- from 'trough', but just to make sure you're never among the confused, think PYO for pyonephrosis:
Pus
Yields
Obstruction
And to remember what to look out for in pyelonephiritis think PYELO:
Pain - ballottement soreness or flank-pain
Yellow - test urine, positive for leukocytes + nitrate
EPEK - Is an acronym of the most likely culprits in bladder infections, which are also found here although in different proportions - E. coli (50%), Proteus(5%)/Pseudomonas(5%), Enterococci (15%), Klebsiella (10%),
Light to heavy fever - depending on severity
Often unilateral
and just to go full circle, keep in mind that untreated pyelonephritis → pus → pyonephrosis
Background information:
Wikipedia (cystitis, pyelonephritis), p. 292 8th OHCM and pp. 469-472 21th DPPM
IgA Nephropathy - I geek, eh?
Is IgA nephropathy common? Aye. Very common? Aye! The most common? AYE!
What causes it? Eh? What's the pathogenesis? Eh!? Is there a cure? EH!?
Indeed IgA nephropathy is the most common form of glomerulonephritis accounting for approximately 20% of all GN diagnoses. There is no cure - so what do we do about it? I, I, I, A, A, A:
IgA (deposits in mesangial cells)
Infection (IgA elevation is associated with infection)
nephrItic Syndrome (micro- or macroscopic hematuria, ↑BP, proteinuria decreases likelihood of UTI as cause of symptoms)
All over (IgA can be found in the blood as p-IgA or in skin biopsies via immunoflorescence, positive results increases likelihood of IgA nephropathy)
ACE (symptomatic renoprotective and anti-proteinuremic treatment)
ARB (symptomatic renoprotective and anti-proteinuremic treatment)
If quick recovery is not achieved on symptomatic treatment, immunosuppressive is second choice.
Background info:
Wikipedia, p. 294 8th OHCM and pp. 499-504 21th DPPM
Minimal Change Disease - Mainly for minors
Minimal change disease constitutes >70% of GNs and about 80% of nephrotic syndrome in children. It commonly presents around 2-3 years of age so there are many good reasons NOT to do a biopsy. Instead the diagnosis is clinical - so keep MINORS in mind:
Minimal change (the biopsy that you shouldn't do would show no optical microscopy abnormalities, only a tendency for fusion of glomerular podocytes)
Increased proteinuria (markedly increase, 5-10g/24h)
Nephrotic syndrome (cf. the fluid overload and +3g/24h proteinuria)
Overload (fluid retention → edema)
Relapse (relapses are common but seemingly not harmful to general kidney function)
Steroids (1-2 months of symptom-free steroid treatment is the drug of choice and is usually very effective)
Background information:
Wikipedia, p. 296 8th OHCM and pp. 499-504 21th DPPM