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.

TBI

Cushing's triad, a slow heart rate with high blood pressure and respiratory depression is a classic manifestation of significantly raised ICP.

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)

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:

• 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)

Symptoms include loss of vision, pulsatile tinnitus, and CN6 palsy.

Treatment is with acetazolamide.

Vitamin A (isotretinoin is usually prescribed for acne) and OCP use can cause IIH (think obese females on isotretinoin/ OCP).

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.

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 =)

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:

• relief with defecation
• change in frequency of stool (once a week or more than 3 x a day)
• change in form of stool

no symptoms of anorexia, weight loss, malnutrition (if these exist think of malabsorbtion syndrome = celiac sprue, tropical sprue, Whipple's disease, side effect of certain drugs, pancreatic insufficiency). no progressively worsening pain (think cancer). also, rule out thyrotoxicosis by checking TSH, which can cause diarrhea/ abdominal discomfort.

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

mnemonic for Crohn's: CHRISTMAS

•  cobblestones
• high temperature (ongoing inflammation)
• reduced lumen size (thickening from sclerosis)
• intestinal fistulas
• skipped lesions
• transmural
• malabsorbtion
• abdominal pain
• submucosal fibrosis

IBDs are associated with HLA-B27 (also associated with psoaritic arthritis, reiter's, ankylosing spondylitis).

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.

smoke this

after a long absence, i'm here to write a HUGE post on a common pulmo topic: COPD. brace yourselves!

now, before we start, how good do you reckon yourselves to be reading a CXR (that's short for chest x-ray)? most vitally, before reading a CXR, do you order a CXR for every patient that comes into your practice coughing and wheezing?

going in alphabetical order, let us begin with my personal favourite: ASTHMA. patient  comes in wheezing (heeeeeeeeeeeeeee), coughing (cough here is NON productive. if there's copious sputum, think of a bacterial infection exacerbating an asthmatic patient or hop onto the next possible diagnosis: bronchitis).

oh, asthma doesn't really come under COPD (chronic obstructive pulmo dis) because it is a REVERSIBLE process. in between attacks, patients will have normal PFTs (pulmonary function tests). i'm throwing asthma in this post anyway because i want you to know how to differentiate between a person with an acute asthma attack and someone with bronchitis from having smoked for 60 years. both people will have difficulty breathing...but for very different reasons and pathogenesis.

see, in asthma, you have an allergic/ immunogenic pathogenesis. the person has either been sensitized to an ag from the environment or over-responses to something in the environment.

two main things: BRONCHOSPASM and airway INFLAMMATION which increases airway secretion ---> obstruction.


asthma attacks are usually triggered by something. such triggers can be intrinsic (non allergic), such as: a viral infection [RSV at kids and rhinovirus at adults], cold air, exercise, stress) or it could be extrinsic (atopic/ allergic), which means there's a specific ag the person is sensitized against. extrinsic triggers also cause other symptoms of allergies: urticaria, runny nose, watery eyes, itching. attacks by extrinsic triggers tend to be seasonal (e.g, at spring-pollen) or at a specific time of the day (occupational exposure-only weekdays, in the mornings).

the expiration phase is prolonged in asthma (air can't go out...hence the wheeze).

at auscultation, there will be diffused, ant and post wheezing. non productive cough (sputum is thick and there's not as much of it as there would be at bronchitis).

goal of treatment in asthma: you want to cause the bronchioles to dilate (first line: B2 agonists...then cholinoblockers-ipratropium, PDE3i-aminophylline, prevention-cromolyn [usually for exercise induced asthma]) and decrease inflammation @ immunosuppression (steroids). inhalers are usually dilators for acute attacks and steroids (+ipratropium) for prevention of future attacks. oral drugs such as monteleukast (leukotriene inhib) can also be prescribed to patients to prevent attacks.

now, after treatment, your patient should feel better, because remember, asthma is REVERSIBLE. however, if you find your patient's wheezes are diminishing, don't get too comfy just yet. it could be a sign of worse things to come, i.e RESPIRATORY FAILURE due to the respiratory apparatus fatiguing.

your patient will be using his accessory resp muscles--> bulging neck muscles, retracted internal intercostal muscles. there will be pulsus paradoxus (BP drops at inspiration...WHY? at asthma, patient takes huge breaths, which increase intrathoracic P, which increases venous return to the right side of the heart, which compromises the fillin gof the LV and therefore the systemic pressure drops. also, if you do an ABG on the patient, you will see an increase of the PCO2 (false increase, as it happens because air can't go out, and not because patient has stopped hyperventilating), no normalization of the PO2 and an acidic pH. all signs of impending respiratory failure. ahhhh!!! what to do? INTUBATE of course. just make sure your patient isn't having an increase PCO2 because of you treating him correctly, thus causing his PO2 to normalize and his peak flow to increase and him generally feeling much bettter before you stick a tube down his throat.

now, that was the easy stuff. onto the bigger thing: COPD! let's classify two main diseases under this heading, namely BRONCHITIS and EMPHYSEMA. now, they both involve chronic obstruction of the bronchioles, but are caused by very different reasons.

bronchitis's mechanism of obstruction is because the airways are filled with thich, viscous secretion. the -itis end should give you a clue about it being an inflammation of the bronchi...and what do inflammed bronchis do? they constrict, get edematous (even more obstruction) and secrete mucous (more gunk to block the already shrinking airways). so cough here, is PRODUCTIVE. to put down bronchitis as a diagnosis, the patient must have frequent, daily sputum for 3 months for 2 consecutive years.



emphysema's mechanism of obstruction is NOT due to hypersecretion, but because of the decrease elastic recoil of the lung tissue (the lung tissue must elastically shrink on itself, to push air inside out). usually, this function is lost because of the fibrosis and scarring that occurs in a constantly inflammed lung (outcome of chronic bronchitis, smoking).

the cough in emphysema is never productive, but the PFTs have an obstructive pattern because:
a) air cannot go out and
b) there's a destruction of the alveolar capillary membrane, which means that there's poorer gas exchange and therefore a decrease of the diffussion of lung carbon monoxide (DCLO). the DCLO is normal at bronchitis, because the process of gas exchange between the alveoli and capillaries isn't affected. it's getting the air exchanged to move in and out that is the problem.  

COPD is usually, more often than not a result of SMOKING. there are two non smoking causes of COPD (that i can think of now):

• cystic fibrosis. usually kids/ teens. resembles bronchitis...why?
  patient's with CF have problems with their chloride channels and make thick, viscous secretions (mucous plugs) that clog the airways.
  how to differentiate? you can confirm a patinet has CF by doing a sweat test. also CF patients are at particular risk for psuedomonas infections (rarely a causative agent for common bronchitis).
• congenital defect in alpha-anti-trypsin levels (deficient), that causes proteolytic digestion of the alveoli walls --> enlarged into blebs and then bullae.
  the danger here is, you have a huge airpocket, but the walls surrounding it are still the same thin alveoli walls, but the air pressure has increased which can cause spontaneous pneumothorax (a hole forming in the lung, without any trauma due to the rupture of the thin walls of these bullae).
  patients with a-a-t deficiencies usually have a family history of relatives with liver cirrhosis (young patients, with no history of hepatitis or alcohol abuse) or non smoking relatives with chronic bronchitis.

both CF and a-a-t deficiencies are autosomal ressesive conditions.

now, what will be your number one worry of a patient with COPD?
cor pulmonale!
but wait...how does the heart come to be involved in a problem affecting the lungs? (i hear you ask).
patients who've had COPD for a long time, usually have PHT (pulmonary hypertension).

what happens at PHT? the S2 has an increased in the P2 component. normally the A2 is louder than the P2, because of the greater pressure in the LV. however at PHT, the pressure in the RV is higher (to overcome the increased pressure in the pulmonary circulation), which causes the P2 to become louder.

you may not have the auscultation skills required to pick this up, but let's just say you got this case on an exam...what clues give you a hint about possible PHT?
a) the P2 increases at inspiration (remember the whole right side of heart has increasing pressure at inspiration, because of the increased venous return caused by the increased intrathoracic pressure).
b) patient has a right ventricular heave
c) EKG shows signs of RV hypertrophy.

but so what if the heart sounds volume increase a little bit? how does this lead to cor pulmonale?
first, what is cor pulmonale?

imagine the RV pumping against an increasing pressure in the pulmonary circulation (PHT) and it keeps working at pumping against the very high pressure, until it eventually fails. rings a bell? RHF?!! = cor pulmonale. it's akin to the LHF caused by the LV pumping against a very high systemic pressure.

*breathes* that's a lot to take in, huh?

back to CXRs.

asthmatic patients don't need a CXR, because asthma is reversible, it won't help you in the treatment of the patient and you would have just lost money for a test that didn't help with how you're going to go about treating the patient and the patient usually isn't in the condition to stand for an xray anyway,

COPD patients, do an CXR. why?

• to rule out pneumonia (a bronchitis that morphed into something more serious)
• you can see the increased lung markings (usually at chronic bronchitis)
• you can see the blebs and bullae at emphysema. also flattening of the diaphragm because of the hyperinflation of the lungs and an increase in the AP diameter if you're taking an ant-post film. the heart also appears to look smaller on the XR (although there's no direct pathology) because the borders of the hyperinflated lungs kinda mask it.

now, you know what is what...how do you go about treating COPD?

don't memorise treatment regimes. understand the goal of the treatment. what is it you set out o fix with the drugs/ instructions you want your patient to take/ follow.

treatment goals in COPD would be:

1. decrease inflammationsteroids. they won't be as affective as they were treating asthma, because COPD largely involves inflammation, scaring, as well as fibrosis.
2. increase dilation of bronchiolesipratropium will be more helpful here, as its effect is usually felt in 1/2 hour (not so great for someone having an asthma attack, hence why it's used more as a preventive measure, than an immediate treatment).
   also beta2 agonists.
3. treat any infectionpneumococcus, H. influenza, moxerella catarrhalis. rotate use antibiotics (penicillins, tet, sulfa, cephalosporins) to prevent resistance from forming.
4. improve gas exchangegive O2 to any hypoxic patient. how would you know who's hypoxic, who's not?
   if PO2 at rest is less than 55mmHg, there's obviously not enough oxygenation of tissues. give O2!
   if PO2 is 56-59mmHg and higher but patient has signs of end organ damage (ischemia) or erythrocytosis on CBC (here's a gem...COPD patients have a Hct of 50-55 because the body compensates for the hypoxia by increasing reticulocytes and its number of rbc, so don't think polycythemia rubra vera immediately when you see a high Hct...your patient could just be someone who smoked for the last 40 years). 
   
5. decrease work of breathing
   this is to prevent respiratory fatigue. best drug? PDE3 inhibitors. lousy at asthma treatment, but works like a charm here because they increase the central respiratory drive and improve diaphragm contractility. minimal bronchial dilation (hence it not being first line for asthma). also...lots of side effects (tachycardia, arryhtmias, seizures) and possible drug-drug interactions (erythromycin, cipro, cimetidine, coumadine). 

phew. i hope this helped you and i got the topic covered proper =)
until the next huge mind dump...over and out and back to the books!