Thursday, 8 December 2011
bats
Desmoteplase-vampire bat saliva, that could maybe help stroke victims. catalyses plasminogen to plasmin. 3-9 hour window period makes it ideal for 'wake-up' stroke patients or those who presented late (outside the 3-4.5 hour window). currently in phase III.
Wednesday, 21 September 2011
TBI
Cushing's triad, a slow heart rate with high blood pressure and respiratory depression is a classic manifestation of significantly raised ICP.
Saturday, 18 June 2011
Endocrine Myopathies
Thyroid dysfunction:
- Hypothyroid myopathy: Characterized by slowed muscle contraction and relaxation. This may be caused by a shift in the distribution of muscle fiber types from fast-twitch fibers to slow-twitch fibers and diminished energetic consumption, causing muscle weakness, fatigue, and exertional pain.
- Thyrotoxic myopathy: due to over stimulation of muscle fibers causing fatigue, weakness, and finally degradation, as a result of increased mitochondrial respiration and enhanced beta-adrenergic sensitivity. could also be due to accelerated protein degradation and lipid oxidation.
Adrenal dysfunction:
- Adrenal insufficiency: Contributing factors to muscle weakness include circulatory insufficiency, fluid and electrolyte imbalance, impaired carbohydrate metabolism, and starvation. However, myopathy is not likely to be a presenting finding.
Parathyroid dysfunction:
- Hyperparathyroidism: muscle weakness is due to reduced neuronal excitability. High plasma calcium decreases the permeability of neuronal membranes to sodium ions, decreases the ease with which action potentials can be initiated.
(in contrast with hypoparathyroidism, in which low plasma calcium increases neuronal excitability hence tapping nerves, not muscles, will further exaggerates neuronal excitability, eliciting Chvostek's and Trousseau's signs)
- Hypothyroid myopathy: Characterized by slowed muscle contraction and relaxation. This may be caused by a shift in the distribution of muscle fiber types from fast-twitch fibers to slow-twitch fibers and diminished energetic consumption, causing muscle weakness, fatigue, and exertional pain.
- Thyrotoxic myopathy: due to over stimulation of muscle fibers causing fatigue, weakness, and finally degradation, as a result of increased mitochondrial respiration and enhanced beta-adrenergic sensitivity. could also be due to accelerated protein degradation and lipid oxidation.
Adrenal dysfunction:
- Adrenal insufficiency: Contributing factors to muscle weakness include circulatory insufficiency, fluid and electrolyte imbalance, impaired carbohydrate metabolism, and starvation. However, myopathy is not likely to be a presenting finding.
Parathyroid dysfunction:
- Hyperparathyroidism: muscle weakness is due to reduced neuronal excitability. High plasma calcium decreases the permeability of neuronal membranes to sodium ions, decreases the ease with which action potentials can be initiated.
(in contrast with hypoparathyroidism, in which low plasma calcium increases neuronal excitability hence tapping nerves, not muscles, will further exaggerates neuronal excitability, eliciting Chvostek's and Trousseau's signs)
Sunday, 29 May 2011
psuedomotor cerebri
Also referred to as idiopathic intracranial hypertension (IIH), is a form of communicating hydrocephalus. the pressure at the ventricles and subarachnoid space is equilibrated with the lumbar cistern.
It's safe to do a lumbar puncture in there patients and the results will yield a high opening pressure (>20mm H2O).
Criteria for Dx includes:
Treatment is with acetazolamide.
Vitamin A (isotretinoin is usually prescribed for acne) and OCP use can cause IIH (think obese females on isotretinoin/ OCP).
It's safe to do a lumbar puncture in there patients and the results will yield a high opening pressure (>20mm H2O).
Criteria for Dx includes:
- increased ICP at an alert patient
- absence of neuro signs except for CN6 abnormality
- normal CSF findings, except for increased opening pressure
- absence of ventricular abnormality (MRI will show an empty sella and slit like ventricles)
Treatment is with acetazolamide.
Vitamin A (isotretinoin is usually prescribed for acne) and OCP use can cause IIH (think obese females on isotretinoin/ OCP).
Friday, 22 April 2011
associations
hypokalemia predisposes to digoxin toxicity and digoxin use causes hyperkalemia.
hyponatremia (and dehydration) predisposes to lithium toxicity and lithium (polyuria) causes hypernatremia.
hypercalcemia predisposes to pancreatitis and pancreatitis causes hypocalcemia.
severe hypokalemia causes rhabdomyolysis and rhabdomyolysis causes hyperkalemia.
hyponatremia (and dehydration) predisposes to lithium toxicity and lithium (polyuria) causes hypernatremia.
hypercalcemia predisposes to pancreatitis and pancreatitis causes hypocalcemia.
severe hypokalemia causes rhabdomyolysis and rhabdomyolysis causes hyperkalemia.
Sunday, 17 April 2011
the heart sings
abnormal heart sounds. the way textbooks describe them, just doesn't help me form a lasting memory of what they are.
S3, rapid ventricular filling.
S4, at atrial systole, blood hits stiff LV.
so you memorise these factoids, but really, without understanding the mechanism of how these sounds come about, you can't say you know your S3s and S4s.
let's start with S4. blood hitting stiff LV. what makes the LV stiff? what makes the LV lose it's normal flexibility?
hypertrophy! increased mass. STIFF. atrial systole, blood goes from LA to LV...it cannot stretch, so the blood SMACKS on its stiff walls =S4.
so someone who has had HT for years and years. the LV has been contracting against an increased systemic pressure. it hypertrophies. it grows stiff. you hear the S4.
what else would mess with the normal structure of the LV and therefor mess with its flexibility?
infarctions. think: new onset S4. infarcted tissue will fibrose. fibrous tissue is inflexible. it cannot stretch as well as cardiac muscles. blood sent from the LA at atrial systole will smack into the fibrous walls that won't stretch to accommodate its arrival.
incidentally, you can apply this theory to real life as well. it's pathological to be stiff/ inflexible.
it's intelligent to be accommodating and flexible.
=)
now S3, is the evil heart sound. with S4, you treat the underlying HT (there's nothing much you can do about the infarcted tissue) and try to decrease systemic resistance, so that the heart doesn't have to pump against high pressures and grow stiffer.
you hear an S3, think splish splash. the patient is having a fluid overload. normally, there shouldn't be splishy splashy sounds of blood filling into the ventricle. when there's too much fluid, it RAPIDLY FILLS THE VENTRICLE. before the ventricles have had a chance to pump out what was already there, more comes in and splashes against the blood already in the ventricle. more. more. more. splish. splash. slosh. too much fluid. it starts to back up? you get where this is going? congestive heart failure? congestion. what are you congested with? excess fluid!
how to you fix this? you decrease the fluid levels. how do you do that? DIURETICS. ACEi. Bb.
ACEi decrease fluid levels (affects renin, therefore inhibits aldosterone) AND is cardioprotective.
Bb...why would you give someone with a failing heart something that would slow his heart rate? aren't Bb a contraindication? NO! Bb lower mortality! they decrease the sympathetic affect on the heart. they increase diastolic time, allowing the coronary arteries time to profuse the heart muscles.
and diuretics, they make you pee out all that excess fluid.
so, S4, have a Bb...relax. don't be so stiff.
S3...time to get rid of fluid before you get congested. pee it out (diuretics), stop holding it in (ACEi blocking aldosterone, whose main function is to retain Na+, which in turn holds onto water), and have Bb. block that sympathetic system from activating the juxtoglomerular apparatus and increasing renin output. don't let angiotensin stress you out (constrict your vessels and increase your BP) and have its friend aldosterone keep sodium around, because we know that where there's sodium, there's water (best of buds) and when there's too much water, there's splishy splashy S3 sound because the heart can only handle so much at a time, dammit.
=)
see, cardio isn't that hard. think of it as a plumbing system: a pump connected to lots of pipes. don't overload the system. don't let the system leak. don't clog the pipes. don't let in bugs that can mess up the pump.
don't just read the text. picture it happening. it helps retain the information and all this information will help you help someone one day.
happy studying folks =)
S3, rapid ventricular filling.
S4, at atrial systole, blood hits stiff LV.
so you memorise these factoids, but really, without understanding the mechanism of how these sounds come about, you can't say you know your S3s and S4s.
let's start with S4. blood hitting stiff LV. what makes the LV stiff? what makes the LV lose it's normal flexibility?
hypertrophy! increased mass. STIFF. atrial systole, blood goes from LA to LV...it cannot stretch, so the blood SMACKS on its stiff walls =S4.
so someone who has had HT for years and years. the LV has been contracting against an increased systemic pressure. it hypertrophies. it grows stiff. you hear the S4.
what else would mess with the normal structure of the LV and therefor mess with its flexibility?
infarctions. think: new onset S4. infarcted tissue will fibrose. fibrous tissue is inflexible. it cannot stretch as well as cardiac muscles. blood sent from the LA at atrial systole will smack into the fibrous walls that won't stretch to accommodate its arrival.
incidentally, you can apply this theory to real life as well. it's pathological to be stiff/ inflexible.
it's intelligent to be accommodating and flexible.
=)
now S3, is the evil heart sound. with S4, you treat the underlying HT (there's nothing much you can do about the infarcted tissue) and try to decrease systemic resistance, so that the heart doesn't have to pump against high pressures and grow stiffer.
you hear an S3, think splish splash. the patient is having a fluid overload. normally, there shouldn't be splishy splashy sounds of blood filling into the ventricle. when there's too much fluid, it RAPIDLY FILLS THE VENTRICLE. before the ventricles have had a chance to pump out what was already there, more comes in and splashes against the blood already in the ventricle. more. more. more. splish. splash. slosh. too much fluid. it starts to back up? you get where this is going? congestive heart failure? congestion. what are you congested with? excess fluid!
how to you fix this? you decrease the fluid levels. how do you do that? DIURETICS. ACEi. Bb.
ACEi decrease fluid levels (affects renin, therefore inhibits aldosterone) AND is cardioprotective.
Bb...why would you give someone with a failing heart something that would slow his heart rate? aren't Bb a contraindication? NO! Bb lower mortality! they decrease the sympathetic affect on the heart. they increase diastolic time, allowing the coronary arteries time to profuse the heart muscles.
and diuretics, they make you pee out all that excess fluid.
so, S4, have a Bb...relax. don't be so stiff.
S3...time to get rid of fluid before you get congested. pee it out (diuretics), stop holding it in (ACEi blocking aldosterone, whose main function is to retain Na+, which in turn holds onto water), and have Bb. block that sympathetic system from activating the juxtoglomerular apparatus and increasing renin output. don't let angiotensin stress you out (constrict your vessels and increase your BP) and have its friend aldosterone keep sodium around, because we know that where there's sodium, there's water (best of buds) and when there's too much water, there's splishy splashy S3 sound because the heart can only handle so much at a time, dammit.
=)
see, cardio isn't that hard. think of it as a plumbing system: a pump connected to lots of pipes. don't overload the system. don't let the system leak. don't clog the pipes. don't let in bugs that can mess up the pump.
don't just read the text. picture it happening. it helps retain the information and all this information will help you help someone one day.
happy studying folks =)
Tuesday, 1 March 2011
gut wrenching diseases
today we are gonna talk about IBS and IBDs.
IBS (irritable bowel syndrome) is common amongst young people, females more often than males, and usually presents with coexisting psych disorders, chronic fatigue syndrome or fibromyalgia (you'd think it's a factitious disorder, but something is indeed causing your patient to have the runs, but it's just not something you can prove with any diagnostic tests).
there's NO inflammation/ abnormalities histologically.
symptoms include: crampy abdominal pain, along with alteration of bowel habit (constipation, diarrhea, alteration between both), brought on by irritants/ precipitating factors such as certain foods/ stress.
it's not an organic problem, so:
no mucus or pus in stool.
not guiaic positive (no inflammation, so no cause for bleeding).
no nocturnal diarrhea.
ROME diagnostic guidelines for IBS = 12 weeks of abdominal discomfort and pain with:
really, IBS is a diagnosis of exlusion, having ruled out the main etiologies such as infectious, neoplastic, organic causes for diarrhea etc.
treatment for IBS includes TCA/ SSRIs for diarrheal form of IBS (remember the coexisting psych disorder) and imodium for severe cases (presenting with fecal incontinence etc); fiber bulking agents and adequate hydration for constipation forms of IBS.
now, IBDs are a bit of an opposite to IBS. IBDs are all about inflammation!
the two main stars of IBDs are Ulcerative Colitis (UC) and Crohn's disease. these two diseases differ a lot though, and once you've read the table below, you'll learn how not to mistake one for the other =)
mnemonic for U.C:
CECAL PLUMB
extra intestinal manifesations of IBDs are erythema nodosum, abcess at mouth ulcers (crohn's), pyoderma gangrenosum, arthritis, uveitis, iritis, primary sclerosing cholangitis (fibrosis and sclerosis of bile duct). these extra intestinal disorders do not follow activity of bowel disease and are treated by treating the underlying IBD + according to presenting symptoms.
IBS (irritable bowel syndrome) is common amongst young people, females more often than males, and usually presents with coexisting psych disorders, chronic fatigue syndrome or fibromyalgia (you'd think it's a factitious disorder, but something is indeed causing your patient to have the runs, but it's just not something you can prove with any diagnostic tests).
there's NO inflammation/ abnormalities histologically.
symptoms include: crampy abdominal pain, along with alteration of bowel habit (constipation, diarrhea, alteration between both), brought on by irritants/ precipitating factors such as certain foods/ stress.
it's not an organic problem, so:
no mucus or pus in stool.
not guiaic positive (no inflammation, so no cause for bleeding).
no nocturnal diarrhea.
ROME diagnostic guidelines for IBS = 12 weeks of abdominal discomfort and pain with:
- relief with defecation
- change in frequency of stool (once a week or more than 3 x a day)
- change in form of stool
really, IBS is a diagnosis of exlusion, having ruled out the main etiologies such as infectious, neoplastic, organic causes for diarrhea etc.
treatment for IBS includes TCA/ SSRIs for diarrheal form of IBS (remember the coexisting psych disorder) and imodium for severe cases (presenting with fecal incontinence etc); fiber bulking agents and adequate hydration for constipation forms of IBS.
now, IBDs are a bit of an opposite to IBS. IBDs are all about inflammation!
the two main stars of IBDs are Ulcerative Colitis (UC) and Crohn's disease. these two diseases differ a lot though, and once you've read the table below, you'll learn how not to mistake one for the other =)
| Ulcerative Colitis | Crohn's |
| distal most rectum (anus not involved) | terminal ileum involvement mostly, |
| | but affects anus --> mouth. |
| | gum to bum |
| columnar mucosa | transmural |
| symmetric, continous disease | skip lesions / cobblestone appearance |
| ~proctitis | |
| ~proctosigmoiditis | |
| ~pancolitis | |
| bloody diarrhea | watery diarrhea (can be bloody) |
| < colon function so < H2O reabsorption | presence of undigested food because |
| > ulceration so blood | of small bowel involvement. |
| chronic process | |
| if accute, think of infectious colitis or | if accute think of yersenia |
| ischemic colitis | |
| pANCA positive | ASCA positive |
| (perinuclear antineutrophil cytoplasmic ab) | (antiyeast saccharomyces ceverisiae ab) |
| flexible sigmoidscopy and biopsy | upp. GI small bowel series (term. Ileum) |
| | and biopsy |
| Rx | |
| sulfasalazine, mesalamine | sulfasalazine * |
| steroids | works @ colon, not small intest coz 5ASA |
| total proctocolectomy (curative) | cleaved at distal ileum by colonic bacteria |
| | so use MESALAMINE *directly 5ASA* |
| | broad spectrum antibiotic |
| | steroids |
| | TNF-alfa for severe crohn's. |
| | anti inflammatory: azathioprine/ mercaptopurine |
| | if meds fail --> surgical resection (non curative) |
| complications | |
| high risk colonic cancer | abcess formation |
| haemorrhage | fistulas |
| toxic megacolon | fissures |
| bowel obstruction | malabsorbtion coz small intest. Invovled |
| | toxic megacolon |
mnemonic for U.C:
CECAL PLUMB
- continuous
- extraintestinal symptoms at eyes, joints, skin and liver
- cancer risk
- abcess in crypts
- large bowel only
- psuedopolyps
- lead pipe (loss of haustra)
- ulceration
- mucosa/ submucosa involvement
- bloody diarrhea
- cobblestones
- high temperature (ongoing inflammation)
- reduced lumen size (thickening from sclerosis)
- intestinal fistulas
- skipped lesions
- transmural
- malabsorbtion
- abdominal pain
- submucosal fibrosis
extra intestinal manifesations of IBDs are erythema nodosum, abcess at mouth ulcers (crohn's), pyoderma gangrenosum, arthritis, uveitis, iritis, primary sclerosing cholangitis (fibrosis and sclerosis of bile duct). these extra intestinal disorders do not follow activity of bowel disease and are treated by treating the underlying IBD + according to presenting symptoms.
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