Another common subject on the NCLEX and USMLE examinations is the complications associated with elevated glucose. As most of you reading this blog know, glucose levels in the blood typically fluctuate only minor amounts between 80 and 110. This tight control is met through the balanced work of two pancreatic secretions named Insulin and Glucagon. Insulin picks up glucose from the blood and delivers it to cells in need of energy, or to the liver for storage. Glucagon senses when the level is low and frees stored glucose from its glycogen framework, into the bloodstream. However, for some this control malfunctions, and signs and symptoms begin to be seen. This imbalance is a life threatening emergency, and its recognition is vital to helping save our patients. What follows is a brief synopsis of a few glucose imbalance issues, and what we as practitioners must do about it.
Diabetic KetoAcidosis (DKA): (5-10% mortality)
– Almost exclusively in Type 1 diabetics
– S/S: Polyuria, dehydration, ab pain, fruity breath, AMS, ↓ Na/Mg/Phos, ↑K (↓ total body), + following:
• Hyperglycemia (above 250)
• Metabolic acidosis (pH below 7.3, HCO3 below 15, AG above 20)
• Ketonuria/Ketonemia
– TX:
• IV insulin bolus (0.1 unit/kg) then IV infusion with same amount per hr AFTER making sure pt is not ↓ K
– Continue until acidosis corrects then taper
• NS immediately upon diagnosis
– Switch to D5NS when glucose below 250; Why in the world would I give D5NS when a patient still has high glucose levels? The most important problem is the acidosis that is occurring. To reverse this we give insulin to drive glucose into the cell. Remember that K rushes into the cell along with the glucose, and wherever K can go, H+ can go. Since high levels of H+ in the blood is the cause of the acidosis, we give insulin to drive this H+ intercellularly, thereby reversing acidosis. We can't give insulin if the level of glucose is too low, so we give D5NS to keep levels around 250 so we can give insulin until the acidosis is gone.
• Add KCl to IV fluids once K below 5; replenish other electrolytes as necessary
Hyperosmolar Hyperglycemic nonketotic syndrome (HHNS):
– Severe ↑ Glucose, almost exclusively in Type 2 diabetics
– Similar to DKA but usually have much higher glucose (above 600) and NO acidosis or ketonuria/ketonemia
– Treat with fluids and low dose Insulin infusion
– An important distinction is that DKA usually occurs in Type 1 Diabetics, while HHNS most often occurs in Type 2 Diabetics. Remember this as it is a common question in the NCLEX world.
Hypoglycemia:
– Patho: When glucose drops to 80 = insulin levels ↓ ; 70 = Glucagon ↑; 50 = epinephrine ↑ along with s/s such as sweaty, ↑BP, ↑HR, tremors; Also around 50 CNS s/s (drowsy, h/a, confused) begin
– Note: S/S from epinephrine release are absent if pt is on a BB
– TX: If pt is alcoholic give Thiamine before any other treatment to prevent encephalopathy
• Can eat = ↑ sugar food;
• Can Not eat = ½ - 2 amps D50 IV push; (Glucagon alternative option if no IV access is available, however is of no use in prolonged hypoglycemia because stores of glycogen are depleted)
Points to remember:
– For high sugar (DKA, HHNS) most of the signs and symptoms are from polyuria, so look for dehydration and electrolyte imbalances...remember High and Dry
– For low sugar most of the signs and symptoms are from the release of epinephrine, so look for things that would happen when someone was high on adrenaline, such as hypertension, sweating, tachycardia and tremors.
– Imperative that you can recognize the difference between these two, as you are almost guaranteed to see a question relating to this difference!
Sunday, April 27, 2008
Saturday, April 12, 2008
Antibiotics made EZ...Part 2
If you have been studying for your NCLEX or USMLE examination for a while, you may have noticed there is some confusion about antibiotics. OK, hopefully you had a chance to read through the Antibiotics made EZ, Part 1. If you havn't, it may be better for you to jump down and read about the bugs, before we dive into the drugs. One of our worst mistakes in the vietnam war, was going into a country completely ignorant of our enemy. We took the wrong guns, and the wrong equipment, and paid for it. Same thing goes here. If you don't know the bugs, reading about the drugs listed below, will make little sense.
That being said, lets take a look at some of the most common medications used to treat Bacterial infections. NOTE that this is empiric therapy only...meaning these are the best options for treatment, BEFORE, our culture and sensitivity comes back. Once those results are ready, they should guide what we use. Also, the spectrum of resistance may be different wherever you live, so these are general recommendations on the most popular drugs. Ok that being said, lets take a look at the first and largest group...the Beta Lactams
Beta Lactams: the Penicillins
Penicillins (PCNs)
That being said, lets take a look at some of the most common medications used to treat Bacterial infections. NOTE that this is empiric therapy only...meaning these are the best options for treatment, BEFORE, our culture and sensitivity comes back. Once those results are ready, they should guide what we use. Also, the spectrum of resistance may be different wherever you live, so these are general recommendations on the most popular drugs. Ok that being said, lets take a look at the first and largest group...the Beta Lactams
Beta Lactams: the Penicillins
Penicillins (PCNs)
MOA: All Beta Lactams are Bactericidal, inhibiting cell wall synthesis; Preg Cat B
Natural Penicillins
Spectrum: G(+): Strep, Bacillus, Clostridium; G(-): Neisseria
Facts: Relatively few side effects; Allergic reactions relatively common; 98% of Staph are resistant to PCN due to enzyme able to destroy medication (PCNase)
PCN G: IV, IM (often only 1 injection need, i.e. Syphillis)
PCN V: PO, poorly absorbed so only for minor infections
Penicillinase (PCNase) Resistant PCNs
Spectrum: G(+): Staph (only indication though spectrum similar to PCN)
Facts: Original Drug was Methicillin but caused too much Interstitial Nephritis and was withdrawn; Despite this, Staph resistant to this class was termed Methicillin resistant (MRSA or MRSE)Oxacillin (PO, IV); Cloxacillin & Dicloxacillin (PO); Nafcillin (IV)
Aminopenicillins
Spectrum: G(+): Same as PCN plus Enterococcus plus G(-): Moraxella, E.Coli, Salmonella, H.influenzae, H.Pylori;Facts: NH3 group makes enhanced activity against G(-); 2nd most common cause of C.Dif Colitis Amoxicillin: PO; ENT infections, Cellulitis, Gonorrhea, C.A.Pneumonia (Strep)
Ampicillin: IV; Listeria, Enterococcus
Extended Spectrum PCNs
Spectrum: Same as AminoPCNs plus G(-): Pseudomonas, Proteus, Bacteroides
Facts: Broad Spectrum, usually reserved for serious infections with susceptible bacteria; No PCNase resistance when given alone; Often combo w/Aminoglycoside for Pseudomonas
Ticarcillin (IV); Piperacillin alone withdrawn (Combination drug Zosyn still available)
PCN/Beta Lactamase Inhibitor Combinations
Facts: PCNase inhibitor added to a Beta Lactam to extend coverage, mainly against S.aureus
Unasyn: Ampicillin + PCNase inhibitor
Augmentin: Amoxicillin + PCNase inhibitor
Zosyn: Piperacillin + PCNase inhibitor (Very Broad Spectrum)
Beta Lactams: the Cephalosporins
Class Facts:
Similar to PCN in most ways, but only 5-10% of PCN allergic will be allergic to Cephs
Generally avoided only if history of Anaphylaxis with PCN
Generally do not cover Anaerobes, Pseudomonas or cross BBB unless indicated
Do not cover MRSA (except Ceftaroline) or Enterococcus
Preg Cat B; Do not take with Alcohol; Consume at least 3 L water daily; Take w/food (avoid GI probs)
All Cephs can cause ↑PT/INR (give Vit K) and C.Dif Colitis
Similar to PCN in most ways, but only 5-10% of PCN allergic will be allergic to Cephs
Generally avoided only if history of Anaphylaxis with PCN
Generally do not cover Anaerobes, Pseudomonas or cross BBB unless indicated
Do not cover MRSA (except Ceftaroline) or Enterococcus
Preg Cat B; Do not take with Alcohol; Consume at least 3 L water daily; Take w/food (avoid GI probs)
All Cephs can cause ↑PT/INR (give Vit K) and C.Dif Colitis
1st GenerationSpectrum: Broad G (+) i/c PCNases; limited G (-): E.Coli, Proteus, Klebsiella
Cephalexin (Keflex): PO; Cellulitis, Cystitis
Cefazolin (Ancef, Kefzol): IV; Surgical prophylaxis (protect against skin bugs)
2nd GenerationSpectrum: G (+): Same as 1st Gen plus G (-): H.Influenzae, Neisseria
Cefuroxime (Zinacef): PO, IV; Limited anaerobes; Cross BBB
Cefoxitin (Mefoxin): IV; Abdominal surgery prophylaxis; Excellent against Anaerobes (i.e. DM foot infections, Peritonitis, etc)
3rd GenerationSpectrum: Excellent G (-) coverage; limited G (+)
Ceftriaxone (Rocephin): IV; qd dosing; Crosses BBB; Meningitis, Encephalitis, Gonorrhea
Ceftazidime (Fortaz): IV; Pseudomonas, Neutropenic Sepsis, Serious infx only; Cross BBB
4th GenerationSpectrum: Excellent G (+), Excellent G (-) coverage i/c Pseudomonas; Cross BBBSE: Psuedomembranous Colitis (C.Dif) most frequent in class
Cefipime: IV; Cross BBB; Complicated UTI, Severe Sepsis
Cefdinir: PO
5th Generation
Spectrum: Excellent G (+), Excellent G (-) coverage i/c MRSA
Ceftaroline: IV/IM; Pneumonia and Skin infections including MRSA
Ceftobiprole (proposed): Not yet available, but on FDA Fast-track; Claims more extensive coverage with less susceptibility though FDA states studies not conclusive
Beta Lactams: The Carbapenems
Carbapenems
Spectrum: Broadest Spectrum of any Antibiotic; Indicated for severe bone, skin, tissue infections, as well as Endocarditis, Abdominal infx, Pneumonia, UTIs, Sepsis, Acinetobacter
Used as last resort in hospitalized patientOnly obvious omission is lack of coverage against C.Difficile, Atypicals, and MRSA
Restricted use by ICU IV infusion for significant infections, to keep resistance low
SE: Nephrotoxicity and Seizures (usually with preexisting Renal or CNS disease) Preg Cat C
Imipenem (Primaxin): IV; Combined with Cilastatin to block enzyme that breaks down drug
SE: Sz in 1.5% of pts on typical dose, 10% if above 500 mg q6h (So not for Meningitis)
Meropenem: IV; May kill G (+) a bit slower than Imipenem, but less Sz, no need for Cilastatin
Beta Lactams: The Monobactams
Monobactams
Spectrum: Limited to aerobic G (-) i/c Pseudomonas; Severe systemic infections and UTIsThis powerful GNR drug is usually combo with Vanco or Clinda for Powerful Broad spectrum
Preg Cat B
Safe to administer to pt w/PCN allergy
Crosses BBB
SE: Severe nephrotoxicity if given with aminoglycosides; Monitor renal function even if given alone; Eosinophilia rarely
Aztreonam: IV, Advantage of preserving all normal G (+) and anaerobic flora
Macrolides
Class Facts:
Broad Spectrum: Similar coverage to PCN plus Atypicals (Chlamydia and Mycloplasma), plus Spirochetes (Syphillis and Lyme) plus additional G (-) i/c H.influenzae
As a rule, Clarithromycin has most and Azithromycin the least G (+) coverage
Bacteriostatic, inhibiting protein synthesis
Do NOT cross BBB, so not for meningitis
Except Azithromycin, CP450 inhibited, increasing drug levels of Theophylline, Digoxin, Coumadin, etcFood decreases absorption of Macrolides
Often used as alternative when pt is PCN allergic
Can cause QT prolongation and Rhabdomyolysis (especially with Statins)
Exhibits Enterohepatic recycling (excreted in bile, then reaborbed; cx for buildup to toxic levels)
Since excreted in bile, not kidneys, no need for adjustment in renal failure
Azithromycin: IV, PO; qd dosing; No effect on CP450 so fewer drug interactions, and no enterohepatic recycling; Atypical Pneumonia, Chlamydia
Clarithromycin: PO; H.Pylori, Pneumonia, M.Avium Complex
Erythromycin: PO, IV, Topical, Opthalmic; Acne, Skin Infx, Eye infx, Diabetic Gastroparesis
SE: Cholestatic jaundice, GI distress (overall a very safe drug)
Fluoroquinolones
Broad Spectrum: Similar coverage to PCN plus Atypicals (Chlamydia and Mycloplasma), plus Spirochetes (Syphillis and Lyme) plus additional G (-) i/c H.influenzae
As a rule, Clarithromycin has most and Azithromycin the least G (+) coverage
Bacteriostatic, inhibiting protein synthesis
Do NOT cross BBB, so not for meningitis
Except Azithromycin, CP450 inhibited, increasing drug levels of Theophylline, Digoxin, Coumadin, etcFood decreases absorption of Macrolides
Often used as alternative when pt is PCN allergic
Can cause QT prolongation and Rhabdomyolysis (especially with Statins)
Exhibits Enterohepatic recycling (excreted in bile, then reaborbed; cx for buildup to toxic levels)
Since excreted in bile, not kidneys, no need for adjustment in renal failure
Azithromycin: IV, PO; qd dosing; No effect on CP450 so fewer drug interactions, and no enterohepatic recycling; Atypical Pneumonia, Chlamydia
Clarithromycin: PO; H.Pylori, Pneumonia, M.Avium Complex
Erythromycin: PO, IV, Topical, Opthalmic; Acne, Skin Infx, Eye infx, Diabetic Gastroparesis
SE: Cholestatic jaundice, GI distress (overall a very safe drug)
Fluoroquinolones
Class Facts:
Spectrum: Broad coverage of G (-), variable G (+), broad coverage of Atypicals
As a rule, increasing Generations have better G (+) and anaerobic coverage, but less Pseudomonas
Bactericidal, inhibiting bacterial DNA production
Precautions
Cx w/arrhythmias, CI if pt on antiarrhythmic meds
As a rule, any abx that targets bacterial flora (G -), effects coagulation by inhibiting Vitamin K
Preg Cat C
Binds Ca, Al, Zn, Mg so do not administer with Milk, Vitamins, or Antacids
Electrolyte interference may cause arrhythmias (QT prolongation), Seizures, Neuropathy, and this is increased when taking with NSAIDs
May cause weakness in M.Gravis
May cause Pseudomembranous colitis, Rhabdomyolysis
Spontaneous tendon rupture can occur when taken with Corticosteroids
Do not administer with Milk, Vitamins, or AntacidsHigh % of unmetabolized drug is excreted in urine, making it excellent for UTI
1st Gen: Did not contain Fl, and were just Quinolones; Much less effective, not used today
2nd Gen: Best antipseudomonal and G (-) in class; weakest G (+) and anaerobe
Ciprofloxacin: PO, IV, Opthalmic; Nosocomial Pneumonia, UTI, Infx Diarrhea (not C.Dif); Not for children below 18
Bactrim
•PO, IV; Sulfonamide, primarily used for UTI and Pneumocystis Carinii Pneumonia (in HIV pt)
•SE: Renal stones, Stevens Johnson syndrome, Allergic reaction common; Many drug interactions; Blood Dyscrasias (report any s/s of new infx)
Vancomycin•PO, IV; Spectrum i/c all G (+); Used for MRSA and MRSE; PO is useful for C.Dificile Colitis
Metronidazole
•PO, IV; Excellent GPR/GNR Anaerobic coverage, used for intrabdominal; C.Dificile Colitis
Clindamycin
•PO, IV; Excellent Anaerobic coverage (rule is Clinda above diaphragm, Metro for below) as well as G (+)
•Often used for serious G (+) sepsis w/possible anaerobic component (i.e. postop abdomen surgery)
•Does not cross BBB; Esophagitis common if not administered with water
•SE: Pseudomembranous Colitis (C.Dif) common post treatment (10%)
Linezolid (Zyvox)
•PO, IV; Spectrum similar to Vanco plus most anaerobes; Used for VRSA, VRE
•SE: May decrease platelet count (3%); MAOI w/high risk of Serotonin Syndrome with SSRIs
Synercid
•IV; Alternative to Zyvox for VRSA, VRE
•SE: Serious arthralgia, myalgias; Central line only as thrombophlebitis in up to 75% of pts via Peripheral
Colistin
•IV; Mainly used for treatment of Acinetobacter and severe Pseudomonal infx; Spectrum i/c GNR
•Was actually first G (-) drug on market, gradually replaced by Aminoglycosides, then brought back into use by developing resistance to those drugs
•Developed so long ago, no actual recommended dosages have been studied (nightmare to prescribe)
•SE: Nephrotoxicity, Neurotoxicity (less common than with Aminoglycosides)
Spectrum: Broad coverage of G (-), variable G (+), broad coverage of Atypicals
As a rule, increasing Generations have better G (+) and anaerobic coverage, but less Pseudomonas
Bactericidal, inhibiting bacterial DNA production
Precautions
Cx w/arrhythmias, CI if pt on antiarrhythmic meds
As a rule, any abx that targets bacterial flora (G -), effects coagulation by inhibiting Vitamin K
Preg Cat C
Binds Ca, Al, Zn, Mg so do not administer with Milk, Vitamins, or Antacids
Electrolyte interference may cause arrhythmias (QT prolongation), Seizures, Neuropathy, and this is increased when taking with NSAIDs
May cause weakness in M.Gravis
May cause Pseudomembranous colitis, Rhabdomyolysis
Spontaneous tendon rupture can occur when taken with Corticosteroids
Do not administer with Milk, Vitamins, or AntacidsHigh % of unmetabolized drug is excreted in urine, making it excellent for UTI
1st Gen: Did not contain Fl, and were just Quinolones; Much less effective, not used today
2nd Gen: Best antipseudomonal and G (-) in class; weakest G (+) and anaerobe
Ciprofloxacin: PO, IV, Opthalmic; Nosocomial Pneumonia, UTI, Infx Diarrhea (not C.Dif); Not for children below 18
3rd Gen: Levofloxacin (Levaquin): IV, PO; qd dosing; UTI, Community (CAP) or Legionella Pneumonia
4th Gen: Best G (+) and anaerobe in class; weakest G (-) and antipseudomonal in class Moxifloxacin: Pneumonia (CAP); Only Quinolone not renally excreted
Aminoglycosides
•Class Facts:
–Spectrum: Primarily aerobic G (-) coverage i/c Pseudomonas, some G (+) staph
–Often used in combination with G (+) drugs for Broad Spectrum coverage; Rarely used alone
–Quinolones are often used initially instead, due to high resistance to this class, unless high suspicion of Pseudomonas
–Bactericidal, blocking protein synthesis
–Allergies are very uncommon with this class
–Precautions:•Nephrotoxicity (renal failure) and Ototoxicity (hearing loss) fairly common, so not for long term –Nephrotoxicity risk increased when taking with Vanco, Cyclosporine, or IV contrast–Ototoxicity risk increased when taking with Loop Diuretics
•Measure Trough concentrations to assure efficacy, at least every 5d (30m before next dose)
•Most Preg Cat D (exception is Streptomycin which is a B)
•Decrease intestinal Vitamin K synthesis (anticoagulant quality)
•Can bind Ca, causing neuromuscular weakness and neuropathy
–Not absorbed well, so no PO
•Streptomycin: Eye infx, Tuberculosis; Limited use due to high resistance
•Tobramycin: Best antipseudomonal in class; MRSA (w/Ampicillin)
•Gentamicin: Excellent antipseudomonal; Endocarditis (w/PCN)
•Neomycin: Hepatic Encephalopathy (kills Ammonia producing GI flora); Only drug in class given PO as it is used to clean GI tract and is not absorbed; Very toxic if given IV
•Amikacin: Synthetic derivative of Neomycin; Often still effective when bugs are resistant to all other Aminoglycosides
–Spectrum: Primarily aerobic G (-) coverage i/c Pseudomonas, some G (+) staph
–Often used in combination with G (+) drugs for Broad Spectrum coverage; Rarely used alone
–Quinolones are often used initially instead, due to high resistance to this class, unless high suspicion of Pseudomonas
–Bactericidal, blocking protein synthesis
–Allergies are very uncommon with this class
–Precautions:•Nephrotoxicity (renal failure) and Ototoxicity (hearing loss) fairly common, so not for long term –Nephrotoxicity risk increased when taking with Vanco, Cyclosporine, or IV contrast–Ototoxicity risk increased when taking with Loop Diuretics
•Measure Trough concentrations to assure efficacy, at least every 5d (30m before next dose)
•Most Preg Cat D (exception is Streptomycin which is a B)
•Decrease intestinal Vitamin K synthesis (anticoagulant quality)
•Can bind Ca, causing neuromuscular weakness and neuropathy
–Not absorbed well, so no PO
•Streptomycin: Eye infx, Tuberculosis; Limited use due to high resistance
•Tobramycin: Best antipseudomonal in class; MRSA (w/Ampicillin)
•Gentamicin: Excellent antipseudomonal; Endocarditis (w/PCN)
•Neomycin: Hepatic Encephalopathy (kills Ammonia producing GI flora); Only drug in class given PO as it is used to clean GI tract and is not absorbed; Very toxic if given IV
•Amikacin: Synthetic derivative of Neomycin; Often still effective when bugs are resistant to all other Aminoglycosides
Tetracyclines
•Class Facts:
–Spectrum: Very broad coverage of G (-), G (+), Atypicals, Protozoa; i/c Chlamydia, Mycoplasma, and Acinetobacter–Broad spectrum limited only by significant resistance, and indications now i/c: Acne, Rosacea, Anthrax, Bubonic Plague, Elephantitis, Malaria, Cholera, Syphillis, Rickettsia (Q fever)–Also inhibits ADH, and is used for SIADH–Bacteriostatic, inhibiting protein synthesis
–Precautions
•With odd strength comes odd SE; These i/c: Candida superinfections, Pseudomembranous Colitis (C.Dif), Thrombocytopenia, Coagulation irregularities, Hemolytic anemia, Lupus exacerbations, Nephrotoxicity•Bind Ca, Mg, Al, so do not give with milk, antacids, or iron salts; Also cause tooth discoloration in growing teeth (young pts); Cause weakness in M.Gravis
•Preg Cat D–Cause fibrosis in pleura, so used for direct administration to resolve pleural effusions
•Doxycycline (Vibramycin): PO, IV; You name it this will treat it, but use less harmful drugs, if effective, first
•Demeclocycline (Declomycin): PO; Reserved for the treatment of SIADH
–Spectrum: Very broad coverage of G (-), G (+), Atypicals, Protozoa; i/c Chlamydia, Mycoplasma, and Acinetobacter–Broad spectrum limited only by significant resistance, and indications now i/c: Acne, Rosacea, Anthrax, Bubonic Plague, Elephantitis, Malaria, Cholera, Syphillis, Rickettsia (Q fever)–Also inhibits ADH, and is used for SIADH–Bacteriostatic, inhibiting protein synthesis
–Precautions
•With odd strength comes odd SE; These i/c: Candida superinfections, Pseudomembranous Colitis (C.Dif), Thrombocytopenia, Coagulation irregularities, Hemolytic anemia, Lupus exacerbations, Nephrotoxicity•Bind Ca, Mg, Al, so do not give with milk, antacids, or iron salts; Also cause tooth discoloration in growing teeth (young pts); Cause weakness in M.Gravis
•Preg Cat D–Cause fibrosis in pleura, so used for direct administration to resolve pleural effusions
•Doxycycline (Vibramycin): PO, IV; You name it this will treat it, but use less harmful drugs, if effective, first
•Demeclocycline (Declomycin): PO; Reserved for the treatment of SIADH
Miscellaneous
Bactrim
•PO, IV; Sulfonamide, primarily used for UTI and Pneumocystis Carinii Pneumonia (in HIV pt)
•SE: Renal stones, Stevens Johnson syndrome, Allergic reaction common; Many drug interactions; Blood Dyscrasias (report any s/s of new infx)
Vancomycin•PO, IV; Spectrum i/c all G (+); Used for MRSA and MRSE; PO is useful for C.Dificile Colitis
•SE: Nephro/Ototoxic (Measure Peak/Trough levels); Red Man Syndrome (from rapid infusion; 60m min)
Metronidazole
•PO, IV; Excellent GPR/GNR Anaerobic coverage, used for intrabdominal; C.Dificile Colitis
•SE: Serious reaction if taken within days of Alcohol
Clindamycin
•PO, IV; Excellent Anaerobic coverage (rule is Clinda above diaphragm, Metro for below) as well as G (+)
•Often used for serious G (+) sepsis w/possible anaerobic component (i.e. postop abdomen surgery)
•Does not cross BBB; Esophagitis common if not administered with water
•SE: Pseudomembranous Colitis (C.Dif) common post treatment (10%)
Linezolid (Zyvox)
•PO, IV; Spectrum similar to Vanco plus most anaerobes; Used for VRSA, VRE
•SE: May decrease platelet count (3%); MAOI w/high risk of Serotonin Syndrome with SSRIs
Synercid
•IV; Alternative to Zyvox for VRSA, VRE
•SE: Serious arthralgia, myalgias; Central line only as thrombophlebitis in up to 75% of pts via Peripheral
Colistin
•IV; Mainly used for treatment of Acinetobacter and severe Pseudomonal infx; Spectrum i/c GNR
•Was actually first G (-) drug on market, gradually replaced by Aminoglycosides, then brought back into use by developing resistance to those drugs
•Developed so long ago, no actual recommended dosages have been studied (nightmare to prescribe)
•SE: Nephrotoxicity, Neurotoxicity (less common than with Aminoglycosides)
Antibiotics made EZ
Whether you are studying for your NCLEX or USMLE examination, or you are a practicing nurse or physician, the first step in understanding antibiotic drugs, is to know about the bugs you are trying to kill. We will take a two blog look at this subject, first by summarizing the bacteria that we frequently encounter in the hospital.
First lets take a broad look at bacteria:
•Gram Positive Cocci–STAPHYLOCOCCUS sp.
•STAPH. AUREUS
•STAPH. EPIDERMITIS
–STREPTOCOCCUS sp.
•STREP. PNEUMONIAE
•STREP. VIRIDANS
•STREP. PYOGENES (GAS)
•STREP. AGALACTIAE (GBS)
–ENTEROCOCCUS sp.
•Gram Positive Rods
–LISTERIA
–CORNYBACTERIUM DIPTHERIAE–BACILLUS ANTHRACIS (anaerobe)
–CLOSTRIDIUM (anaerobes)
•c. DIFFICILE
•c. TETANI
•c. BOTULINUM
•c. PERFRINGES
•Gram Negative Cocci
–NEISSERIA MENINGITIS
–NEISSERIA GONORRHEA
–MORAXELLA CATARRHALIS
•Gram Negative Rods–ENTERIC BUGS•ESCHERICHIA COLI
•PROTEUS sp.
•ENTEROBACTER sp.
•HELICOBACTER sp.
•SALMONELLA sp.
•SHIGELLA sp.
•KLEBSIELLA sp.
–HAEMOPHILUS INFLUENZAE
–LEGIONELLA sp.
–PSEUDOMONAS AERUGINOSA
–ACINETOBACTER sp.
–BACTEROIDES (anaerobes)
•B. FRAGILIS
•Atypical Bacteria: Think Doxy!
–CHLAMYDIA (intracellular)
–MYCOPLASMA (no cell wall)
–SPIROCHETES (curves: Syphillis)
–BORRELA (Corkscrews: Lyme)
Think INH/Rifampin/Azithro
–MYCOBACTER (Acid fast: TB, Leprosy, M.Avium Complex)
•Staphylococcus
–Staph aureus (coagulase positive)
•Most pathogenic of the staphs; toxins cause Toxic Shock, Scalded Skin, Gastroenteritis
•Cause skin infections, Pneumonia (nosocomial), Endocarditis, Osteomyelitis•Abscess formation common; Can initiate clotting (think DIC)
•Tx: Oxacillin family; (Vancomycin if MRSA; Zyvox if VRSA; Bactrim or Doxy if Community MRSA)
–Also susceptible to: 1/2/4 Gen Cephs, Carbapenems, Macrolides
•MRSA: Staph resistant to Oxacillins and most other drugs; Use Vanco, Zyvox, or Synercid
–Staph epidermidis (coagulase negative)
•Normal flora of human skin
•Causes infection in immuno-compromised or depressed patients often via Central lines
•Tx: Similar to Staph Aureus (Vanco if MRSE, Zyvox if VRSE)
•Streptococcus
–Alpha Hemolytic•Strep pneumoniae (Pneumococcus): Leading cause of Pneumonia, Otitis Media, and Meningitis
•Strep viridans: Normal flora of mouth, can cause Dental abscess and Endocarditis
–Beta Hemolytic
•Group A (Strep pyogenes): Strep throat, Rheumatic fever, Scarlet fever, Glomulerulonephritis, Necrotizing fasciitis•Group B (Strep agalactiae): Can colonize vagina and cause Meningitis or Pneumonia in newborn
–Tx: PCN G; (Quinolone if PCN resistant; Ceftriaxone if in brain)
•Also susceptible to: 1/2/4 Cephs, Macrolides, AminoPCNs, Vancomycin, Quinolones
•Enterococcus
–Facts
•Common nosocomial infection with multi-drug resistance
•Cause Sepsis, Cellulitis, Intraabdominal infx, Endocarditis, UTI
•Tx: Ampicillin (or Vancomycin) + Gentamycin; (Zyvox or Synercid if VRE)
–Only other effective drugs: Zosyn, Imipenem, and Quinolones
•Listeria
–Commonly reside in soil, sewage, and stream water but rarely cause disease; If the immune response is slow, however, they move into cells and then are missed by immune cells
–Cause of Listeriosis, a lethal food bourne illness with mortality rate of 25%; Can invade CNS
–Tx: Ampicillin (often with Gentamicin)
•Cornybacterium diptheriae
–Toxin producing (2nd most lethal toxin to humans) causes Pharyngitis w/heart/CNS damage
–Tx: Antitoxin + PCN (Erythromycin if PCN allergic)
•Bacillus anthracis
–This anaerobic bacteria is the cause of Anthrax (meaning Coal = large black lesions)
–Lives in soil, and can be ingested by grazing animals where it causes rapid death (is then possible to inhale or ingest the bacteria from dead animals)
–Tx: PCN; (Cipro or Doxycycline if PCN allergic)
•Clostridium (anaerobic species)
–C. difficile
•Overgrowth in gut after Antibiotic treatment (Clindamycin, 3/4 Gen Cephs, Amp/Amox), causes Pseudomembranous Colitis•Tx: PO Metronidazole (or PO Vancomycin if relapse after taking Metro)
–C. tetani
•Toxin producing (3rd most lethal toxin to humans) causes PNS blockade (Tetany, Seizure, Death)
•Tx: Toxin irreversible once bound, so rapid treatment with PCN or Metronidazole imperative
–C. botulinum
•Toxin producing (Most lethal toxin to humans; 500 g could kill the entire world) that causes Botulism (a nerve blockade disease that leads to rapid paralysis and death)
•Bacteria can not survive in high oxygen or acidic environment, so usually ingesting bacteria not fatal as they are killed rapidly in GI tract; Must ingest toxins to have effects
•Infants (pre solid food) have a less acidic GI tract, so things harboring this bacteria (honey) can deliver the organism, which is then allowed to grow in more basic pH GI tract
•Tx: Hardy bacteria are not killed by antibiotics; Antitoxin very hard to find so Mechanical Ventilation and removal of cause (i.e. vomiting or debridement of wound) usually only thing possible
•Neisseria meningitidis (aka Meningococcus)
–Common cause of meningitis; Also Meningococcemia (a rapidly fatal sepsis that kills over 50% of effected infants) and DIC
–Tx: PCN G (Ceftriaxone if PCN allergic) ; Best treatment is prevention with vaccine
•Neisseria gonorrhea–Cause of the STD Gonorrhea, as well as Conjunctivitis in newborn of infected mom
–Tx: Ceftriaxone (or Ciprofloxacin) and Azithromycin for possible concurrent Chlamydia
•Moraxella catarrhalis
–Causes URI and Otitis Media, as well as Pneumonia in smokers; Also COPD exacerbations
–Tx: Augmentin and Erythromycin
•Also susceptible to 2/3 Gen Cephs, Quinolones, Bactrim
A very common bug to recognize during your NCLEX or USMLE studying. It is useful to divide this class into the usual medical pathologies caused by each
•Urinary pathogens
–E. coli•Normal intestinal flora cause 90% of UTI; Also Pyelonephritis
•Pathogenic varieties are not normal flora and can cause Infectious diarrhea, Hemolytic Anemia
•Tx: Ciprofloxacin or Bactrim (Zosyn also effective)
–Proteus
•Causes UTI, in addition to renal calculi (struvite, CaCO3)
•Tx: Levaquin or Bactrim (Often treated without knowing you are treating Proteus)
•Respiratory pathogens
–Haemophilus influenzae
•Cause: Pneumonia, AOM; Also Sepsis, Meningitis, Cellulitis
•Tx: Azithromycin
–Also susceptible to po 3/4 Gen Cephs, Augmentin, Doxycycline, Quinolones, Carbapenems
–Klebsiella pneumoniae
•Usually only pathogenic in hospitalized immunocompromised causing Pneumonia and/or Sepsis
•Rapid resitance develops, especially against Cephalosporins and Quinolones
•S/S: Profuse, Jelly-like, Bloody sputum and high mortality rate
•Tx: Carbapenems or Zosyn
–Legionella•Pneumonia, derived airborn from water ducts, air conditioning units, water towers
•Tx: Macrolide (or Quinolone or Doxycycline)
–Pseudomonas aeruginosa
•Opportunistic infection causes Pneumonia, Sepsis, UTI, Right side Endocarditis, Osteomyelitis in Diabetic foot ulcers•First s/s often overwhelming Gram negative sepsis; 2nd most common cause of infection in ICU
•Extremely resistant to many drugs; All effective drugs IV, except Cipro and Levaquin so their use is severely restricted to avoid development of resistant strains
•Tx: Ceftazidime and Gentamycin (or Imipenem or Zosyn- varies widely between hospitals)
–Also susceptible to the following: Tobramycin, Cefipime, Colistin, Aztreonam
–Acinetobacter
•Pneumonia, Sepsis, Shock common, Up to 70% mortality; Can live 3 weeks on dry surface
•Tx: Imipenem
–Colistin or Doxycycline is alternative
•Gastrointestinal pathogens
–Helicobacter Pylori
•Common cause of Peptic Ulcer Disease
•Tx: (CAP) Clarithromycin, Amoxicillin, PPI (proton pump inhibitor)
–Salmonella
•Common cause of Diarrhea; Some forms also cause Typhoid or Sepsis
•Ciprofloxacin (rule out C.Dif with any infectious diarrhea)
–Shigella
•Causes bloody, purulent diarrhea in nursing homes and preschools
•Tx: Ciprofloxacin
–Vibrio Cholera
•Causes rice water diarrhea, with death from dehydration
•Tx: Doxycycline, fluids and electrolytes
–Yersenia•One form causes diarrhea; Another form causes Bubonic Plague
•Tx: Gentamicin
•GNR and Sepsis: Notes of Interest
–Many GNR have endotoxins, which are actually components of their cell wall
•When antibiotics begin their destruction, these toxins are released into the bloodstream in massive quantities, leading to Sepsis (Massive immune response) and eventually Septic Shock (Low BP and organ dysfunction)
•For this reason, Bacteremia (bugs in blood) with GNR is among the most serious of diseases, and should be treated aggresively in an ICU
•With Shock and 2 organs dysfunctioning the mortality rate is over 40%; With each additional organ dysfunction add 15%
•Sepsis is the #1 killer in the ICU, but is more preventable than you would think; The dirty source, is more often than not, indwelling catheters, so take extreme care with hygiene if you are ICU bound!!!
First lets take a broad look at bacteria:
•Gram Positive Cocci–STAPHYLOCOCCUS sp.
•STAPH. AUREUS
•STAPH. EPIDERMITIS
–STREPTOCOCCUS sp.
•STREP. PNEUMONIAE
•STREP. VIRIDANS
•STREP. PYOGENES (GAS)
•STREP. AGALACTIAE (GBS)
–ENTEROCOCCUS sp.
•Gram Positive Rods
–LISTERIA
–CORNYBACTERIUM DIPTHERIAE–BACILLUS ANTHRACIS (anaerobe)
–CLOSTRIDIUM (anaerobes)
•c. DIFFICILE
•c. TETANI
•c. BOTULINUM
•c. PERFRINGES
•Gram Negative Cocci
–NEISSERIA MENINGITIS
–NEISSERIA GONORRHEA
–MORAXELLA CATARRHALIS
•Gram Negative Rods–ENTERIC BUGS•ESCHERICHIA COLI
•PROTEUS sp.
•ENTEROBACTER sp.
•HELICOBACTER sp.
•SALMONELLA sp.
•SHIGELLA sp.
•KLEBSIELLA sp.
–HAEMOPHILUS INFLUENZAE
–LEGIONELLA sp.
–PSEUDOMONAS AERUGINOSA
–ACINETOBACTER sp.
–BACTEROIDES (anaerobes)
•B. FRAGILIS
•Atypical Bacteria: Think Doxy!
–CHLAMYDIA (intracellular)
–MYCOPLASMA (no cell wall)
–SPIROCHETES (curves: Syphillis)
–BORRELA (Corkscrews: Lyme)
Think INH/Rifampin/Azithro
–MYCOBACTER (Acid fast: TB, Leprosy, M.Avium Complex)
Gram Positive Cocci
•Staphylococcus
–Staph aureus (coagulase positive)
•Most pathogenic of the staphs; toxins cause Toxic Shock, Scalded Skin, Gastroenteritis
•Cause skin infections, Pneumonia (nosocomial), Endocarditis, Osteomyelitis•Abscess formation common; Can initiate clotting (think DIC)
•Tx: Oxacillin family; (Vancomycin if MRSA; Zyvox if VRSA; Bactrim or Doxy if Community MRSA)
–Also susceptible to: 1/2/4 Gen Cephs, Carbapenems, Macrolides
•MRSA: Staph resistant to Oxacillins and most other drugs; Use Vanco, Zyvox, or Synercid
–Staph epidermidis (coagulase negative)
•Normal flora of human skin
•Causes infection in immuno-compromised or depressed patients often via Central lines
•Tx: Similar to Staph Aureus (Vanco if MRSE, Zyvox if VRSE)
•Streptococcus
–Alpha Hemolytic•Strep pneumoniae (Pneumococcus): Leading cause of Pneumonia, Otitis Media, and Meningitis
•Strep viridans: Normal flora of mouth, can cause Dental abscess and Endocarditis
–Beta Hemolytic
•Group A (Strep pyogenes): Strep throat, Rheumatic fever, Scarlet fever, Glomulerulonephritis, Necrotizing fasciitis•Group B (Strep agalactiae): Can colonize vagina and cause Meningitis or Pneumonia in newborn
–Tx: PCN G; (Quinolone if PCN resistant; Ceftriaxone if in brain)
•Also susceptible to: 1/2/4 Cephs, Macrolides, AminoPCNs, Vancomycin, Quinolones
•Enterococcus
–Facts
•Common nosocomial infection with multi-drug resistance
•Cause Sepsis, Cellulitis, Intraabdominal infx, Endocarditis, UTI
•Tx: Ampicillin (or Vancomycin) + Gentamycin; (Zyvox or Synercid if VRE)
–Only other effective drugs: Zosyn, Imipenem, and Quinolones
Gram Positive Rods
•Listeria
–Commonly reside in soil, sewage, and stream water but rarely cause disease; If the immune response is slow, however, they move into cells and then are missed by immune cells
–Cause of Listeriosis, a lethal food bourne illness with mortality rate of 25%; Can invade CNS
–Tx: Ampicillin (often with Gentamicin)
•Cornybacterium diptheriae
–Toxin producing (2nd most lethal toxin to humans) causes Pharyngitis w/heart/CNS damage
–Tx: Antitoxin + PCN (Erythromycin if PCN allergic)
•Bacillus anthracis
–This anaerobic bacteria is the cause of Anthrax (meaning Coal = large black lesions)
–Lives in soil, and can be ingested by grazing animals where it causes rapid death (is then possible to inhale or ingest the bacteria from dead animals)
–Tx: PCN; (Cipro or Doxycycline if PCN allergic)
•Clostridium (anaerobic species)
–C. difficile
•Overgrowth in gut after Antibiotic treatment (Clindamycin, 3/4 Gen Cephs, Amp/Amox), causes Pseudomembranous Colitis•Tx: PO Metronidazole (or PO Vancomycin if relapse after taking Metro)
–C. tetani
•Toxin producing (3rd most lethal toxin to humans) causes PNS blockade (Tetany, Seizure, Death)
•Tx: Toxin irreversible once bound, so rapid treatment with PCN or Metronidazole imperative
–C. botulinum
•Toxin producing (Most lethal toxin to humans; 500 g could kill the entire world) that causes Botulism (a nerve blockade disease that leads to rapid paralysis and death)
•Bacteria can not survive in high oxygen or acidic environment, so usually ingesting bacteria not fatal as they are killed rapidly in GI tract; Must ingest toxins to have effects
•Infants (pre solid food) have a less acidic GI tract, so things harboring this bacteria (honey) can deliver the organism, which is then allowed to grow in more basic pH GI tract
•Tx: Hardy bacteria are not killed by antibiotics; Antitoxin very hard to find so Mechanical Ventilation and removal of cause (i.e. vomiting or debridement of wound) usually only thing possible
Gram Negative Cocci
•Neisseria meningitidis (aka Meningococcus)
–Common cause of meningitis; Also Meningococcemia (a rapidly fatal sepsis that kills over 50% of effected infants) and DIC
–Tx: PCN G (Ceftriaxone if PCN allergic) ; Best treatment is prevention with vaccine
•Neisseria gonorrhea–Cause of the STD Gonorrhea, as well as Conjunctivitis in newborn of infected mom
–Tx: Ceftriaxone (or Ciprofloxacin) and Azithromycin for possible concurrent Chlamydia
•Moraxella catarrhalis
–Causes URI and Otitis Media, as well as Pneumonia in smokers; Also COPD exacerbations
–Tx: Augmentin and Erythromycin
•Also susceptible to 2/3 Gen Cephs, Quinolones, Bactrim
Gram Negative Rods
A very common bug to recognize during your NCLEX or USMLE studying. It is useful to divide this class into the usual medical pathologies caused by each
•Urinary pathogens
–E. coli•Normal intestinal flora cause 90% of UTI; Also Pyelonephritis
•Pathogenic varieties are not normal flora and can cause Infectious diarrhea, Hemolytic Anemia
•Tx: Ciprofloxacin or Bactrim (Zosyn also effective)
–Proteus
•Causes UTI, in addition to renal calculi (struvite, CaCO3)
•Tx: Levaquin or Bactrim (Often treated without knowing you are treating Proteus)
•Respiratory pathogens
–Haemophilus influenzae
•Cause: Pneumonia, AOM; Also Sepsis, Meningitis, Cellulitis
•Tx: Azithromycin
–Also susceptible to po 3/4 Gen Cephs, Augmentin, Doxycycline, Quinolones, Carbapenems
–Klebsiella pneumoniae
•Usually only pathogenic in hospitalized immunocompromised causing Pneumonia and/or Sepsis
•Rapid resitance develops, especially against Cephalosporins and Quinolones
•S/S: Profuse, Jelly-like, Bloody sputum and high mortality rate
•Tx: Carbapenems or Zosyn
–Legionella•Pneumonia, derived airborn from water ducts, air conditioning units, water towers
•Tx: Macrolide (or Quinolone or Doxycycline)
–Pseudomonas aeruginosa
•Opportunistic infection causes Pneumonia, Sepsis, UTI, Right side Endocarditis, Osteomyelitis in Diabetic foot ulcers•First s/s often overwhelming Gram negative sepsis; 2nd most common cause of infection in ICU
•Extremely resistant to many drugs; All effective drugs IV, except Cipro and Levaquin so their use is severely restricted to avoid development of resistant strains
•Tx: Ceftazidime and Gentamycin (or Imipenem or Zosyn- varies widely between hospitals)
–Also susceptible to the following: Tobramycin, Cefipime, Colistin, Aztreonam
–Acinetobacter
•Pneumonia, Sepsis, Shock common, Up to 70% mortality; Can live 3 weeks on dry surface
•Tx: Imipenem
–Colistin or Doxycycline is alternative
•Gastrointestinal pathogens
–Helicobacter Pylori
•Common cause of Peptic Ulcer Disease
•Tx: (CAP) Clarithromycin, Amoxicillin, PPI (proton pump inhibitor)
–Salmonella
•Common cause of Diarrhea; Some forms also cause Typhoid or Sepsis
•Ciprofloxacin (rule out C.Dif with any infectious diarrhea)
–Shigella
•Causes bloody, purulent diarrhea in nursing homes and preschools
•Tx: Ciprofloxacin
–Vibrio Cholera
•Causes rice water diarrhea, with death from dehydration
•Tx: Doxycycline, fluids and electrolytes
–Yersenia•One form causes diarrhea; Another form causes Bubonic Plague
•Tx: Gentamicin
•GNR and Sepsis: Notes of Interest
–Many GNR have endotoxins, which are actually components of their cell wall
•When antibiotics begin their destruction, these toxins are released into the bloodstream in massive quantities, leading to Sepsis (Massive immune response) and eventually Septic Shock (Low BP and organ dysfunction)
•For this reason, Bacteremia (bugs in blood) with GNR is among the most serious of diseases, and should be treated aggresively in an ICU
•With Shock and 2 organs dysfunctioning the mortality rate is over 40%; With each additional organ dysfunction add 15%
•Sepsis is the #1 killer in the ICU, but is more preventable than you would think; The dirty source, is more often than not, indwelling catheters, so take extreme care with hygiene if you are ICU bound!!!
Sunday, April 6, 2008
The Portal System...made EZ
The Portal system? I was asked that during my NCLEX review class last week by some Jr students, and figured there may be more that are more than confused by this term. So what follows is a simple description of this system that is involved in some of the more common pathologies in the hospital.
The liver is a selfish organ. It demands first access to blood that is bringing anything new into the system, kind of like a checkpoint at the border. At this checkpoint, the liver removes anything toxic by metabolism or excretion, converts nutrients into useable or stored forms, as well as a host of other responsibilites. There are four main areas that drain their blood to the liver, before it is dumped into the system. Check out the picture below, to get an idea before we discuss this.
The easiest to picture, is blood coming from the intestines, where new food was just absorbed. The liver wants first access to this blood, and gets it via the portal system. The problem is, what if the liver is congested or scarred and little blood can get through the liver. Well anyone who has ever been on the interstate understands, that there is backup, when something is blocking the road. The blood trying to get to the liver now backs up and dilates these portal veins. In the intestines, this blood can leak out into the tissue, becoming Ascites.
The next drainage, comes from the rectum. That is a port of entry into your body, right? Well the liver wants to analyze blood coming from this area of your body (that is good when there is a medication jammed in there) and gets that blood through the portal system. If this blood backs up, you will get big dilated veins in the rectum, called Hemorrhoids.
The Spleen also drains into the Liver before its blood has access to the main system. That is good, since broken down RBCs (bilirubin) get processed there. If this part of the portal system backs up you would see Splenomegaly.
The final system that drains via the portal system, is the other port of entry into your body, the esophagus. Veins partially drain this area in case there are invaders or new toxins to metabolize. If this backs up you would see big, dilated veins in the esophagus, called Esophageal Varices (Varicose veins in the throat). This is a significant issue...imagine our patient is eating a Dorito, and an edge of that cool ranch chip nicks the dilated vein. You would get bleeding into the esophagus. Remember that the liver also makes important clotting factors, and if the liver is damaged and congested we are not going to clot well. (Remember that PT measures one of the key clotting factors? It is also the fastest lab value to change with liver damage so check that PT/INR!)
So Esophageal Varices are a very important pathology to notice in any liver patient as we must stop that bleeding. Luckily, blood is very irritating and is usually thrown at you with very violent, bloody vomiting, so you shouldn't miss that sign. One you may miss is if you forget that the Liver also makes Albumin, which, because it is so attractive to water, is what keeps volume in your blood. If you lose this albumin from a diseased liver, you are already looking at a patient that has falling blood pressure. Now take some blood away via these Esophageal varices, and you may see significant Hypotension. So make sure you are measuring those vital signs frequently!
Here is a picture that hopefully summarizes what we just covered. Now you should at least be able to recognize what the portal system is, and why we see certain signs in Liver patients, like Splenomegaly, Ascites, Hemorrhoids, Esophageal Varices, and Hypotension.
The liver is a selfish organ. It demands first access to blood that is bringing anything new into the system, kind of like a checkpoint at the border. At this checkpoint, the liver removes anything toxic by metabolism or excretion, converts nutrients into useable or stored forms, as well as a host of other responsibilites. There are four main areas that drain their blood to the liver, before it is dumped into the system. Check out the picture below, to get an idea before we discuss this.
The easiest to picture, is blood coming from the intestines, where new food was just absorbed. The liver wants first access to this blood, and gets it via the portal system. The problem is, what if the liver is congested or scarred and little blood can get through the liver. Well anyone who has ever been on the interstate understands, that there is backup, when something is blocking the road. The blood trying to get to the liver now backs up and dilates these portal veins. In the intestines, this blood can leak out into the tissue, becoming Ascites.
The next drainage, comes from the rectum. That is a port of entry into your body, right? Well the liver wants to analyze blood coming from this area of your body (that is good when there is a medication jammed in there) and gets that blood through the portal system. If this blood backs up, you will get big dilated veins in the rectum, called Hemorrhoids.
The Spleen also drains into the Liver before its blood has access to the main system. That is good, since broken down RBCs (bilirubin) get processed there. If this part of the portal system backs up you would see Splenomegaly.
The final system that drains via the portal system, is the other port of entry into your body, the esophagus. Veins partially drain this area in case there are invaders or new toxins to metabolize. If this backs up you would see big, dilated veins in the esophagus, called Esophageal Varices (Varicose veins in the throat). This is a significant issue...imagine our patient is eating a Dorito, and an edge of that cool ranch chip nicks the dilated vein. You would get bleeding into the esophagus. Remember that the liver also makes important clotting factors, and if the liver is damaged and congested we are not going to clot well. (Remember that PT measures one of the key clotting factors? It is also the fastest lab value to change with liver damage so check that PT/INR!)
So Esophageal Varices are a very important pathology to notice in any liver patient as we must stop that bleeding. Luckily, blood is very irritating and is usually thrown at you with very violent, bloody vomiting, so you shouldn't miss that sign. One you may miss is if you forget that the Liver also makes Albumin, which, because it is so attractive to water, is what keeps volume in your blood. If you lose this albumin from a diseased liver, you are already looking at a patient that has falling blood pressure. Now take some blood away via these Esophageal varices, and you may see significant Hypotension. So make sure you are measuring those vital signs frequently!
Here is a picture that hopefully summarizes what we just covered. Now you should at least be able to recognize what the portal system is, and why we see certain signs in Liver patients, like Splenomegaly, Ascites, Hemorrhoids, Esophageal Varices, and Hypotension.
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.
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.
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