Tuesday, April 1, 2008

Bilirubin made EZ

Ah good ole Bilirubin. One of those famous lab values that seems so important to so many people, but why? Understanding this simple lab concept can not only help you when it comes to NCLEX or USMLE time, but will help you as an RN, ARNP or MD to recognize certain pathologies that you will frequently encounter.


OK, lets take a look at Bilirubin in general. On most circulations through the body, RBCs have to pass through the ultimate inspection. They file through tight spaces in the spleen and are closely inspected by the watchful eye of WBCs. Any weakness is immediately noticed, and that poor RBC is bound for destruction. Their life is on average, only 40 days, and then they suffer an awful end. When they are ripped out of line, they have their core of iron ripped out to be recycled, and their skin stripped off and dumped. Talk about a bad way to go. This skin is the origin of what we see in a lab value as Bilirubin. At this point, it is simply unconjugated Bilis, often termed indirect bilirubin. It is dumped into the drainage system of the spleen, which is the bloodstream that leads to the liver, known as the Portal system. When it reaches the liver, it is then conjugated, which simply means the liver alters the structure a little bit, and we now have conjugated or direct bilirubin. This new product is now stored in the gall bladder to be used as bile salts. Bile salts are released when you eat a fatty meal, and assist the body in absorbing the fat molecules. Unabsorbed Bile salts are broken down by bacteria in your gut, and are what make your stool brown.


OK got that picture in your head? Heres how knowing this helps. If Bilirubins become elevated in the blood stream, it is usually because the liver is too congested to accept new deliveries, and they then build up in the bloodstream causing pruritis, yellow jaundice skin and sclera, and give their brown color to the urine. Meanwhile the stool is a light color with no bilis, and fat is not absorbed.


But there is more. I can use this lab value to tell what the cause of that liver congestion is. If the liver itself is the blame, such as in the case of Liver diseases like Cirrhosis, any new bilirubin is not conjugated, so I will get UNconjugated or Indirect bilirubins that are elevated. On the other hand if the Bile duct is the source of the back up congestion in the liver, the new bilis are conjugated by the liver, but can not pass on into the gall bladder or GI tract, so Conjugated or Direct bilirubins are elevated in the blood. Make sense? So don't just be satisfied to know that bilirubin is elevated, but look closer and see what type of bilirubin is elevated, and you will have a very good idea if this is a liver dysfunction or a biliary obstruction...big difference right!?

OK. One other thing you will see in the picture below. Another way you can have elevated bilis is if you are simply killing way too many RBCs, and your liver can't keep up with the delivery. This would happen in the case of Hemolysis, where RBCs are actively being destroyed in great numbers.


Check out these cheesy drawings, and hopefully they will truly be worth a 1000 words.








Wednesday, March 26, 2008

Asthma drugs made EZ

Pharmacology is often considered a dirty word in nursing and medical school, and unfortunately the NCLEX and the USMLE loves to test you on this. One subject we recently tackled in our NCLEX review course was the treatment of Asthma. Here is a summary of what we talked about...


Obstructive Pulmonary Disease (Asthma, COPD)•Medications: Site of Action
1.Adrenergic Agonists (Albuterol, etc)
2.Anticholinergics (Ipratroprium Bromide)
3.Xanthines (Theophylline)
4.Corticosteroids (Beclomethasone, etc)
5.Mast Cell Stabilizers (Cromolyn)
6.Leukotriene Antagonists (Montelukast-Singulair)


key to above figure: Allergen+IGE causes Mast cell to release histamine and leukotrienes which then seep out of blood stream and cause immune cells to inflame bronchioles. Various drugs work at different steps of this process. Some stop mast cells from releasing their products, some stop the products from leaving the blood stream, and some stop the products from causing the inflammation in the bronchioles. All three of these work directly on the immune system. On the other side of that, some drugs directly open the airway, not effecting the immunity at all. See below for the most critical details on these drugs and when we use them...

Obstructive Pulmonary Disease: Bronchodilators
1.Adrenergic Agonists (Albuterol, etc)
•Selective B2 agonists directly dilate airway; DOC for acute attack
•Albuterol: PO, inhaled via MDI; NOT for maintenance therapy
•Levalbuterol (Xopenex): Possibly less cardiac SE
•Salmeterol: Long acting (12hrs) for night s/s
•Terbutaline: Also relaxes uterus, tocolytic for premature labor

2.Anticholinergics (Ipratroprium Bromide) *technically not a dilator
•Atrovent is often combined with Adrenergics to tx COPD, as scarred airways need extra help dilating
•Slow onset, long acting best used for prevention, not acutely
•SE: Dry mouth, GI distress

3.Xanthines (Theophylline)
•Similar to Caffeine, causes bronchodilation, CNS stimulation of the respiratory center, Inotropy/chronotropy → renal perfusion → urine
•Used in cases where overuse of other bronchodilators has caused decreased effectiveness, especially used with COPD
•Slow onset, long acting best used for prevention, not acutely
•Stimulant C/I with arrhythmias, SZ, hyperthyroid, PUD
•Monitor therapeutic levels (10-20)
•Aminophylline is IV form of Theophylline

Obstructive Pulmonary Disease: Inflammation Modulators
1.Corticosteroids (Beclomethasone, etc)
•Steroids prevent further inflammation of constricted airways
•Available IV, PO or inhaled; Inhaled have benefit of being used at site of constriction without systemic effects (Rinse after!)
•DOC for asthma prevention•Beclomethasone excellent antiinflammatory with few SE
•Patients have died from not being tapered off of systemic steroids when switching to inhaled forms
•Can be used WITH albuterol for acute attacks and is given IV (Solu-Medrol)

2.Mast Cell Stabilizers (Cromolyn)
•Used to prevent the release of inflammatory mediators
•Most effective for exercise or allergen induced bronchospasm
•Also useful to control perennial allergic rhinitis
•Available PO, inhaled, and opthalmic

3.Leukotriene Antagonists (Montelukast-Singulair)
•Leukotriene receptor blockade prevents inflammatory migration into bronchiole tissue
•Used for maintenance, with effects taking up to a week
•SE: Dyspepsia, insomnia, diarrhea, and liver dysfunction
•Other ex. Zafirlukast (Accolate), Zileuton (Zyflo)

Asthma Treatment Protocol (med first introduced)
  • Step 1, Mild Intermittent S/S: Short acting B2 agonists prn
  • Step 2, Mild Persistent: Inh steroid + short B2 ag prn; Cromolyn + B2 ag prn for children; Theophylline or Montelukast alternative agents if above protocol ineffective
  • Step 3, Moderate Persistent: Med dose inh steroid + Salmeterol (long acting B2) + short B2ag prn
  • Step 4, Severe Persistent: High dose inh steroid + Salmeterol + Systemic steroid + short B2 ag prn