Teaching Resident Session: Cirrhosis
Dr. Saji Abraham
Cirrhosis is classically categorized as micro or macronodular, though there is no clinical correlation, and micro becomes macronodular; alcohol is classically macronodular. Etiologies include alcoholism, the #1 cause in the U.S. EtOH is a mitochondrial poison and initiates a fibrotic process involving the peroxidase system. Hepatitis B and C, sclerosing cholangitis, Wilson‟s disease, in which patients have chorea, psychiatric disorders, Kaiser-Fleischer rings in
the limbus of the cornea, low ceruloplasmin (though that isn‟t pathognomonic); treatment is penicillamine; alpha-1 antitrypsin deficiency, primary biliary cirrhosis, cardiac cirrhosis, CREST syndrome, hemochromatosis- hereditary or acquired- for which phlebotomy is the first line of treatment; SB; prolonged use of TPN; and Budd-Chiari syndrome, which is associated with HRT, causing portal vein thrombosis leading to cirrhosis. Hypervitaminosis A can give jaundice without scleral icterus.
Presenting features include palmar erythema, ascites, asterixis, mental status change, fatigue, anemia; acute alcoholic hepatitis advances to cirrhosis, and presents with pain and jaundice, and a 2:1 AST to ALT ratio, since alcohol inhibits ALT and promotes AST release. Cirrhosis becomes the diagnosis when coagulation factors, testosterone drop and asterixis setts in. Usually, in cirrhosis, the PT is the first to change, then albumin, then later, testicular atrophy, gynecomastia, asterixis, ascites, etc.
Complications include ascites, esophageal and gastic varices, caput medusae, retroperitoneal bleeds, leg swelling, hepatic encephalopathy, generalized constitutional symptoms, hepatoma, jaundice, low libido, heart failure, splenomegaly, hepatorenal syndrome- whose etiology is not clearly defined but involves Na retention and intravascular depletion; treatment requires liver transplant, and it commonly sets in after use of NSAID, diuretic, vasoconstrictive agent; the patient has prerenal azotemia though he looks overloaded.
Ascites is due to portal hypertension- high pressure and low oncotic pressure leads to fluid buildup in the peritoneum that exceeds lymphatic ability to resorb it. The serum:ascites albumin gradient, if >1.1, indicates portal hypertension as the etiology of the ascites; if less, leads us to suspect another cause such as TB or carcinomatosis. Spontaneous bacterial peritonitis is usually caused by e. coli and can be prophylaxed for with nitrofurantoin.
Varices, encephalopathy- a patient may develop encephalopathy despite a relatively low ammonia level due to medications or a GI bleed and the concomitant hemolysis and protein release. Treatment is lactulose, which traps ammonia in the gut, and neomycin, which kills protein-digesting bacteria in the gut without being absorbed by gut mucosa.
Ascites can be treated with beta blockers, which lower portal hypertension, and spironolactone is maintenance therapy; only 900 cc is handled by the liver, so care should be taken not to diurese more, since the patient is already in a state of reduced effective blood
volume, and he may get dehydrated and prerenal. If ascites continues to worsen, options include paracentesis; albumin is a temporizing measure; lasix, but no more than 1L of diuresis per day; also, watch urine lytes. Paracentesis of 4-6 L 2-3x a week, send labs on the fluid- WBC, chemistry, albumin, cytology (if there is carcinomatosis- e.g. hepatoma, ovarian carcinoma), ADA (adenosine deaminase, which helps in TB diagnosis; gram stain and culture. Next step- TIPS, which relieves portal pressure, helping ascites and varices but accelerating encephalopathy.
Varices treatment- a Blakemore balloon can be used to stabilize the patient if no gastroenterologist is available to do immediate banding; complication rates are high in the wrong hands. Banding is better than sclerotherapy for acutely bleeding varices.
Misconceptions in Opioid Management
Dr. Robert R. Duarte
Top ten list- “I left my bottle upstate at the ski lodge (in chronic pain, yet can go to ski
lodge?)”, “my sister stole my bottle (she is the addict)”, “The drug store computer broke down and...”; “someone stole my Percocet from my car (they left everything else, even the radio)”, “My dog ate it,” “my husband needs the prescription”, “the pills fell into the toilet”, “the druggist dropped nail polish remover on the prescription”, “I‟ve been throwing up and my pills...”, “my girlfriend put a gun to my head, said „I will only have sex with you if...‟”.
Pain is the most common reason individuals seek medial attention. 75% of all advanced stage cancer patients, 85% of AIDS patients have moderate to severe pain, 50% of post-op patients undermedicated, women, minorities, substance abusers undertreated for pain.
Pain is all in your head- true; to feel pain, you need a cortex; all pain has a psychological component, so there is a need for a multidisciplinary approach; includes psychiatrists, physiatrists, neurologists, and nurses. Acute pain- hurt arm, leg- comes and goes, is over, nothing left. Chronic pain- “affective and sensory component”- IASP- numbness, tingling, burning- but
also frustration, anger, etc. McCaffrey- pain is “whatever the patient states hurts”- if you don‟t
believe the patient, transfer to someone who willing to treat it. “Pain that has outlived its
Pain diagnosis- acute vs. chronic, intensity, pathophysiology- neuropathic syndrome; i.e., Reflex Sympathetic Dystrophy (CRPS), diabetic neuropathy, trigeminal neuralgia, shingles then- nociceptive- non-neuropathic- achy- arthritis, bone cancer; then- kvetch- don‟t know what‟s
going on. Neuropathic agents- pain modulators- antidepressants, anticonvulsants- gabapentin, and even anti-arrhythmics- mexilitine; but rare, usually former two. Analgesic agents- for nociceptive pain- NSAIDs; which is the most effective? All are about the same; combination analgesics- Vicodin, Percocet, etc. Then- opioids- short-acting vs. long-acting; morphine, hydromorphone is short-acting, while oxycontin, duragesic, etc. are long-acting. Opioids- some evidence to show that IV fentanyl is effective in some neuropathic pain; TD fentanyl- peripheral neuropathic pain; oxycodone- PHN, tramadol- diabetic neuropathy.
1970- Controlled substances act- regulates controlled substances; before approval of any
drug, must be approved by FDA and DDA; classified opioids, drugs into five schedules
according to relative potential for abuse. Class I- high potential for abuse, no currently accepted
medical use- heroin; class II- is high abuse potential but accepted medical use; class III-V- less
abuse potential. Yet lower-end drugs are likelier to be abused, probably because easier to access
them. Brand vs. generic- brand of vicodin makes more money on the street, should be no
difference in effect, so why asking for it? Looking for quick onset, short duration of action-
quick rush, intensity, whether a product can be injected or snorted successfully- has high street
value if can be injected.
Back in 1970‟s, drug abuse warning network to monitor what happened with these drugs. Drug-related deaths #1- cocaine; then heroin/morphine, then alcohol-in-combination, then
codeine. Methadone was number 8; Propoxyphene- Darvocet- #11 drug cause of death; we
consider it very mild- Tylenol with side effects! Meperidine was #32- oral form doesn‟t give
quick rush. Fentanyl was lower down, as was hydromorphone, but latter has risen on the list.
Joint commission- administer analgesics “around the clock” rather than PRN; administer
drugs orally whenever possible; avoid intramuscular injections. Avoid using meperidine (for no
more than 48 hours- metabolite- normeperidine- toxicity), never for chronic pain state. Addiction
occurs very rarely in patient who receives opioids for pain control.
Barriers to effective pain management- pain is under-recogized; health care providers
lack knowledge about what is addiction, dependency, tolerance; fear of legal consequences, that
DEA coming after you; patient, family, societal beliefs- „I don‟t want to get addicted.‟
Dependence simply means that if take drug, then decide to stop it, will go through withdrawal
process, and are dependent upon the drug; if stop taking it, will have a problem; same with
opioids. Tolerance- if tend to need more to get the same effect; in cancer patients- Kathleen
Foley showed- if cancer worsens, tend to need more. In non-malignant pain, see it less often- if
pathology doesn‟t change, tolerance doesn‟t change. Addiction- chronic problem- if taking on
chronic basis- craving to get a high, altered sensation, use it despite harm- had patient taking 100
tramadol pills a day, had seizures and renal failure but still took them. “I feel like a king”
syndrome- that‟s not what drug is supposed to do for you.
Addiction is common- false; 0.034% in hospitalized patients. Behaviors more suggestive
of addiction disorder- selling prescription drugs, prescription forgery, injection of
oral/transdermal formulatons, multiple dose escalations despite harm, multiple episodes of
prescription loss, seeking prescriptions from multiple doctors, stealing prescription pads, missing
multiple appointments, the “out of towners.”
Moderate to severe pain, put on occasional Darvocet or codeine, still complain of pain-
may be pseudo-addicted- may really be undertreated. Drug hoarding at times of reduced pain-
very common- patient may actually keep e.g. a 3-week extra supply that they keep when they
don‟t need it as much; this doesn‟t mean they‟re addicted, just that using it as needed.
If they come in, ask for specific drug- I want methadone, I want codeine, etc.- they allow you to evaluate record, etc., then they tell you “this is what works for me”- maybe that is the best
thing to do, follow closely, be sure no other signs of aberrant behavior. If demand up front- show them the door. Obtaining strong analgesics for minor procedures- Ok. Unsanctioned dose escalations- if uncommon, episodic- 1-2 occasions- Ok. Resistance to change to another medicine- Ok. Call on weekends or after hours for prescription- I consider that aberrant behavior. Call from an anonymous informant- really can‟t go on that; can bring it up with patient the next
time, but sometimes these are just trying to get the patient in trouble.
Tolerance- to nausea, respiratory depression; sedation- usually goes away in 3-7 days. They never get tolerant to constipation, so give them prophylaxis. Opioids have no end organ toxicity- no effect on kidney or hepatic function, but does have constipation, decreased libido. We do recommend repeat LFT, renal function panels every few months. The DEA, State medical boards are watching- goal is to protect patients and society; exchanging prescriptions for sex, running a cash business, etc. DEA isn‟t out to get you- recognize legitimate use of these agents
in treating pain for legitimate use of these agents in treating pain for legitimate medical purposes. Is the practice consistent with acceptable medical standards? They understand that all docs can be duped; as long as are documenting it, is Ok. In 1992 survey- 40% agreed that their prescribing of opioids for chronic pain was influenced by legal concerns. Total sanctions imposed- 4467, controlled-substance related- 337, 40 license revocations- so not very common. Just document.
Ask self- is pain expected to be opioid responsive? Neuropathic, nociceptive, mixed? If neuropathic- try on anticonvulsants, etc. first; has patient tried other viable therapies? For severe pain, must start on opioid, but sometimes can try NSAIDs, etc. for more minor pain. Assess risk for addiction- ask about behaviors suggestive of abuse, prior history of addiction, records of prior docs, treatments; include pharmacists- but need to have understanding with patient that are allowed to speak with pharmacist- otherwise privacy violation. Contract- clarify expectations and goals, set limits, use drug screen, stress importance of using this drug appropriately. One and no- one doctor, pharmacist, monthly visit, monthly prescription, report of my dog ate it; no weekend calls, etc.
Follow-up visit- analgesia, ADL‟s, an adverse effects, aberrant behavior? Must get in any
chronic pain patient. If no H&P- unlawful prescribing.
Pharmacist is legally allowed to change directions on prescriptions if they call you; maximum daily dose, strength of dose if less, can be changed by pharmacist on phone; they can write in DAW; they can decrease quantity of drug only. Forged prescriptions- felony; telephone prescription is still a felony. Tell patients this. Also, write out „ten‟, because they can change number to 40, 70, etc.
Rinsing prescriptions- can simply take nail polish remover, lift all the writing on a script if it‟s a simple white pad, except for your imprint, they can write whatever they want there, can take your penicillin prescription, write vicodin. Designate number of refills, even if non; consider duplicate prescriptions, consider tamper-resistant pads, don‟t pre-print your DEA number on
prescription. Can by law give 3 month supply if write code D- relief of chronic pain. Post-dated prescription- illegal. Need to date it today, write „to be filled by‟ because can‟t write prescription
if not see patient- is fraudulent. Emergency prescription- 3-day supply, document- for emergency
dispensing; can give over phone.
If you know patient is addicted, can‟t prescribe to maintain the addicted state. Want a
written treatment objective and plan. In contract- can get in trouble- abide by contract, because
patient can sue you for maintaining him in addicted state. Must document that saw patient at
least every three months- on a regular basis. Should send him to someone else for second opinion
if you have problems with it. Document.
[Soma- red flag- I try to use other muscle relaxants.] [Don‟t put patient on anti-
inflammatory and acetaminophen on regular basis- hurts kidney function.] [Ultram-
acetaminophen and tramadol combination that is synergistic.] [How treat these patients when say
no? Evaluate the patients, be up front with them from day one, set rules, parameters, that‟s it- if
don‟t abide by it, are out the door; if want to go further, can send you to someone else. Once enter into relationship, are stuck, so set parameters from day one.]
Dr. Tu Tu Aung
Case- 35-y/o lady who came in with pulmonary emboli while on oral contraceptives,
completed 3-6 months of coumadin, now see she‟s heterozygous for prothrombin gene mutation-
what to do? Not need long-term therapy, but d/c oral contraceptives. Homozygote- would treat
with coumadin for life.
PE 1 week after 16-hour airplane trip in 40-y/o Chinese woman- in Caucasian woman,
would look for Factor V Leiden and prothrobin G20210A mutation; in Asian women, this is
extremely low, so no testing required. Protein C assessment- is consumed at time of acute
presentation, may produce false positive result. Once have started warfarin, can‟t assess, so wait 6 months, stop it, test. Lupus anticoagulant also isn‟t measured because patient is placed on
heparin now. Screening for cancer- in older people, more malignancies can be suspected; this is
relatively young person after flight, don‟t need whole body scan for one DVT.
67-y.o. with peripheral vascular surgery 2 months ago, now with myocardial ischemia,
two days later- pain persists, platelet count drops- patient has heparin-induced thrombocytopenia,
usually takes 5 days but he was exposed previously in his surgery; so stop the heparin
immediately, use hirudin or argatroban, whichever thrombin-inhibitor you use. Platelets- if
falling precipitously, even if not at 50,000, still assume HIT; also, anti-platelet antibodies.
Lovenox also cannot be used if HIT.
50-y/o woman wants HRT for hot flashes, her daughter had DVT with OCP,
heterozygous for factor V Leiden mutation- what do you do? Recommend against use of HRT;
initiate anticoagulant prophylaxis at times of increased thrombotic risk- long flights, etc. 30 mg
of Lovenox for prophylaxis. Even if get up and walk- low-pressure cabins, can still happen. If
must give her HRT, don‟t give coumadin unless prior clot- risk/benefit ratio.
25-y/o at end of first trimester, had DVT on oral contraceptives three years ago- what to do? This patient did have one episode of thrombosis; although wasn‟t pregnant at that time, had one previous episode so still has risk; so- continue to monitor, after delivery, give enoxaparin for 6 weeks- usually get thrombi soon post-delivery.
65-y/o man with three-day history of swelling, warmth, erythema in left calf, DVT on ultrasound, heavy smoker. DRE, stool specimen- normal, CBC, PT, PTT, chemistry, PSA, SLE panel, CXR normal. Next best step- nothing- not cost effective to do full-body CT for every 65-y/o with DVT. Upper, lower GI- if patient never had colonoscopy done, is recommended but not relates to DVT.
50-y/o with 3-day hx of low-grade fever, confusion, physical- pallor, ecchymoses, low Hb, WBC, platelets at 12K, peripheral smear- schistocytes, decreased platelets- TTP; add up clinical suspicion.
Heparin-induced thrombocytopenia- platelets dropping after bypass surgery; no schistocytes in peripheral smear, PT/PTT normal so not DIC or TTP. HIT- serotonin-release assay for heparin-platelet factor 4; HIT causes arterial thrombosis.
DVT treatment- lovenox 1 mg/kg, and warfarin 5 mg/d, adjusted to INR of 2 to 3.
40-y/o woman with DVT, PE 1 month post-partum, warfarin started, brother, father, she too- protein S deficiency; after 6-month coumadin for DVT- how treat? She developed DVT post-partum, had pre-eclampsia- want to consider giving her a chance- thrombosis risk is higher than others but DVT attack wasn‟t unprovoked- considerable risk factors- so give nothing,
counsel about prophylactic anticoagulation in high-risk situation. Start with heparin, move to coumadin.
Switching over from argatroban to warfarin- initate warfarin at 5 mg/d, and discontinue argatroban when INR is greater than 4; if INR is just 2, may be sole warfarin effect; need effects of both, so wait until INR is greater than 4.
Low-molecular weight heparin post-DVT- 3-6 months. Unprovoked DVT, heterozygote for G20210A- test her whole family. Higher risk of recurrence is true of everyone who has had one DVT- always at risk for another DVT, prophylax for high-risk situations with lovenox.
Coagulation pathway- natural anticoagulant- antithrombin III- to prevent clotting, protein C and S act on IX to X. Natural anticoagulant system- Protein C, S, ATIII, fibrinolytic system. All hereditary disorders associated with venous clots except for homocysteinemia; both arterial and venous- homocysteinemia, antiphospholipid antibody syndrome, HIT, myeloproliferative disorder- need phlebotomy, malignancy. Cost of transfusion- each bag is $500. Test informative in presence of anticoagulation agents- factor V Leiden, protrombin gene mutation, hexagonal phospholipids neutralization test, homocysteine levels. Thromboembolism association with OCP, HRT, pregnancy, puerperium but should still be tested for hereditary thrombotic disorders if one develops.
Vena cava filters- higher recurrent DVT levels though sustained PE smaller, so place filter when anticoagulant therapy is contraindicated. Order D-dimer, if negative, clinical suspicion very low- can say „It‟s nor a DVT.” If D-dimer is positive, not necessarily PE or DVT.
Negative does rule it out though.
Pt with high blood pressure, one second of sharp pain, bingeing for four days, drinking 4 glasses of scotch a day, works as cab driver. Denies nausea, vomiting, diarrhea, any prior angina. Came to ER- 180/90. No caput medusae, asterixis, liver span normal, no spider angiomas, no scleral icterus or jaundice. Palmar erythema, dupuytren‟s contracture. Alcohol 41- probably
drank 2-6 hours earlier. AST, ALT look normal- liver Ok.
Alcohol syndrome- 8 million people in US are alcohol dependent. Some get more severe withdrawal syndromes than others. 7 to 34 days of drinking- minor withdrawal syndrome; 48-87 days- major withdrawal symptoms, but usually no withdrawal because drinking episodically.
Gamma-aminobutyric acid, epinephrine, serotonin involved. Minor withdrawal
symptoms- tremulousness, mild anxiety, headaches, diaphoresis, palpitations, anorexia, GI upsetetc. Withdrawal seizures- generalized tonic-clonic convulsions usually occurring within 48 hours after the last drink; alcoholic hallucinosis- 12-24 hours- usually visual, resolve in 24-48; global clouding of sensorium- no- specific hallucinations. Delirium tremens- delirium, tachycardia, hypertension, agitation, fever, diaphoresis; last 1 to 5 days; are associated with 5% death rate from arrhythmias, etc. Is diagnosis of exclusion. Risk factors- sustained drinking, previous DT‟s, etc. DT‟s- three days after abstinence, so must follow up patients. Ativan- use as
maintenance- short-acting, can be used in cirrhotics, unlike valium. Librium not used as much because require conjugation in liver. Valium- has active metabolite.
Fixed-dose, front-loading therapy, or symptom-trigger therapy- total amount needed is 5x less. Is option of lorazepam or oxezapam IV; surgical floors- like to give atenolol. Treatment- frequent reevaluatiion- rule out infection ltrauma, metabolics, drug overdose, hepatic failure, etc. Fetal position- so if vomit, won‟t aspirate, and good for psancreatitis. Is situation in whch can get
very hyponatremic very quickly- usually not. but must monitor, fix metabolic derangements. Give vitamins. May need LP, CT to rule out other causes.
Now- JCAHO- mandated to offer alcohol counseling, rehabilitation, must be documented. How much drinking- suspect alcoholism? Screen with CAGE, if suspect risk, must offer some counseling, help.
Dr. Slava Fuzaylov
55-y/o female who immigrated from Jamaica 12 years ago, nurse‟s aide at Elmhurst; one
episode of hemoptysis, abnormal CXR but PPD negative. No recent travel. Pulmonologist sent
after abnormal CXR. Right upper lobe- asymmetric density in right apex- fuzzy, nodular pleural thickening, doesn‟t completely go to apex; asymmetric infiltrate in right upper lobe. No obvious areas of cavitation, no obvious mediastinal, hilar lymphadenopathy. Apical lordotic view- tilt the ribcage, shows lung apex better. Patchy infiltrate again seen in right upper lobe. Makes us think about tuberculosis; really no lymphadenopathy, though, to indicate it. Intraparenchymal lesion could be present in mesothelioma, but usually marked pleural thickening throughout the chest. CT- densities we saw are much better characterized- is cavity in lung apex, little ball of soft tissue in the cavity; also see adjacent scarring, fibrosis. No adenopathy in chest; not typical for tuberculosis- no pleural effusion, no infiltrate, etc. Scarring, fibrosis, cavity- can get superimposed fungal infection; also must consider neoplastic process- cancer arising from scar. Mesothelioma would be very unlikely given this CT finding. We do thin slices with hemoptysis to look for bronchiectasis, none seen.
Bronchoscopy was done, fungal, AFB, gram stain, etc.- all negative. Antibody tests- not particularly useful in fungal infection except urinary histoplasma antigen. Coccidiomycosis- never send for culture because is dangerous.
Based on CT- admitted in 3/2004 for right thoracotomy with en block wedge resection of right upper lobe. due to possibility of malignancy. Physical exam- some wheezes. Differential diagnosis of hemoptysis with cavitary lesions- mycetoma in a cavitary lesion caused by TB, histoplasmosis, coccidiomycosis, sarcoidosis, bullous emphysema, and malignancy.
Pathology- hyphae, majority detached from wall of cavity, sitting like foreign material. Some round because seeing them on cross-section, have septae- differentiates from mucor- no septae. Granulation tissue forms the wall of the cavity; plasma, lymphoid cells, then fibrotic wall of cavity- caused dense fibrous tissue; then- lung tissue which is approximately normal. Is it angioinvasive or not? I.e., does it just sit there or can it travel to other organs? No angioinvasion seen. Rest of the lung- bloody; if have invasive aspergillosis- can infarct lung tissue in wedge shape; here- lung parenchyma fine, not infarcted. Treatment algorithm is completely different. Fungus ball in cavity- resect for symptoms, not to treat; is no fungal therapy given to people with fungus in cavity. If is invasive, do need to provide antifungal therapy. If is angioinvasion, treat, duration depends upon underlying host risk factors.
Frozen pathology specimen showed some aspergillus invading the tissue, since frozen section isn‟t as reliable, so patient was given Amphotericin B for one day, then continued on Cancidas for 5 days; discharged on Voriconazole 200 mg PO BID on the 5th day, for 2 weeks. In tissue, but not angioinvasive so 2 weeks, not 6-9 months.
Aspergillus- genus of 200 fungi found worldwide; appear as round single cells like yeast, or chains- hyphae; filamentous fungus, can be easily made airborne. First known case- 1842; catalogued in 1729; caused allergic lung disease in wig combers. Some aspergillus makes mycotoxins, poisons in food; some are pathogenic, some make useful products. We normally breathe in 100-200 spores daily. Most common cause of invasive disease- aspergillus fumigatus, flavus; former and clavatus causes allergic disease most commonly.
Fever, cough, chest pain, breathlessness, usually in immunocompromised or suffer other lung conditions. Three forms- Allergic bronchopulmonary aspergillosis, aspergilloma, or acute invasive aspergillosis- former to latter up with immune malfunction; other risk factors- diabetes; need tissue biopsy for diagnosis since it‟s an environmental pathogen- is all over.
ABPA- hypersensitivity, often in asthmatics or cystic fibrosis patient; can show fleeting pulmonary infiltrates or impacted bronchial atelectasis. Aspergilloma- mycetoma fungus ball which develops in a preexisting cavity in lung; less commonly- can arise de novo in bronchi with subsequent erosion. Crescent of air partially outlining solid mass; may be free floating or attached to wall with stalk. Invasive aspergillosis- rapidly proghressive infection in patients with prolonged neutropenia or immunosuppression; interestingly, not seen very commonly in AIDS patients, but bone marrow or solid organ transplants, chemo, neutrophil dysfunction. Characterized by invasion of blood vessels and dissemination to other organs. Typically manifest with fever, dyspnea, pleuritic chest pain, hemoptysis. Variable CXR; CT may show Halo sign- ground-glass area around cavitation. Allergic bronchopulmonary aspergillosis diagnosis- history of asthma/cystic fibrosis, fleeting pulmonary infiltrates, mucoid impaction, aspergillus in sputum, eosinophilia, etc. Definitive diagnosis- needle or open-lung biopsy.
ABPA- mainstay of treatment- corticosteroids, and antifungal treatment decreases symptomatology, though unclear why since aspergillus isn‟t invasive. Aspergilloma- treatment is
surgery; antifungal therapy is not required unless patient not fit for surgery or concurrent tissue invasion. Amphotericin B for IPA; but toxicity is high, so recent studies show that sequential treatment with caspofungin and the azoles comparable to Ampho B. Amphotericin- cidal, as is caspofungin, while azoles are static; in immunocompromised patients, is just your therapy, no immune system to help you out, so use combination therapy; animal studies- sequential therapy bad idea, if want to do it- ampho first, then azoles because latter decreases sterol production. Can give Ampho or cancidas with azoles. Diflucan- doesn‟t work for aspergillus, so use itraconazole
or voriconazole- latter is better absorbed. Problem- significant CYP450 drug-drug interactions, must adjust for that, except with diflucan. So if choose azole, voriconazole with either amphotericin or cancidas. Why used latter- less nephrotoxic, and dose of amphotericin for aspergillus is highest possible, so give alternatives if they‟re as efficacious. If had been angioinvasive, would have given cancidas with voriconazole for one month, then latter alone for 6-9 months.
We decided- she had TB cavity that became infected with minimal tissue invasion. Surgeon was concerned because was aspergillus at stump, feared stump would dehisce; otherwise, needs no treatment once resected.
Resident Family Feud
Three clinical/serological differences of drug-induced SLE and idiopathic SLE: Anti-DNA or anti-Histone antibodies; idiopathic can cause nephritis, cerebritis; drug-induced is reversible.
Four top symptoms of Lyme disease- myalgias, arthralgias, headache, fatigue, erythema migrans. Four top causes of lower GI hemorrhage- hemorrhoids, arteriovenous malformation, diverticuli, carcinoma. Glucose > 200, LDH >350, Age > 55, AST > 250, WBC > 16,000. Four tumors that spread to bone- Prostate, Lung, Breast, Thyroid, Kidney. 3 common types of strokes- hemorrhagic, ischemic, embolic. 5 common causes of CK elevation- MI, rhabdomyolysis, brain injury, myositis, renal injury, myocarditis, muscular dystrophy.
Major modifiable CAD risk factors- tobacco, cholesterol, diabetes, hypertension. LDH elevation- 4 common causes- hemolysis, MI, hepatic injury, large PE, renal infarction, prosthetic heart valve. PCP, leukemia/lymphomas- less common. 5 diagnostic criteria for schizophrenia- hallucinations, delusions, disorganized speech, negative symptoms greater than 6 months. 3 top causes of community-acquired pneumonia- Pneumococcus, H. Influenza, M. Catarrhalis. Four kinds of thyroid cancer- Papillary, Follicular, Medullary, Anaplastic. Three hyperkalemia with metabolic acidosis- RTA 4, Addison‟s, hyperalimentation. Lab analysis of transudative pleural
effusion vs. exudative- 10% of transudates are malignant.
Primary Care Internal Medicine
Dr. Cruz M. Fana
46-y/o little league coach pitched batting practice over the course of a 6 week season and his right shoulder became sore. Symptoms persisted for several weeks after the end of the little league season despite Ibuprofen self-treatment. Loss of PROM in external rotation and abduction, pain with elevation of his arm above horizontal, pain and weakness are present when his right shoulder is positioned at 90 degrees of abduction, elbow flexed and forearm pronated. Relief of symptoms with lidocaine. What would be appropriate management at this time? Subacromial injection of a long-acting anesthetic-corticosteroid followed by physical therapy- not surgical candidate until goes for physical therapy, physical exam alone reveals rotator cuff tear. If not get better in six months, MRI- think rupture, not tear.
38-y/o man got inversion sprain of ankle, iced on and off, now can‟t bear weight, left
ankle ecchymotic and swollen, tenderness on anterior, lateral aspects, painful inversion; ligamentous testing reveals third-degree (complete) tear of lateral ankle ligaments; no fractures. How treat him? Inversion sprain- most common type of ankle injury. Think of RICE- rest, ice, compression, elevation within 24-72 hours; use compression bandage to reduce swelling- need full leg cast but aircast, ice them down for 2-3 days, send to rehabilitation ASAP.
20-y/o woman dislocated glenohumeral joint of throwing arm for first time, anteriorly; dislocation reduced; no fractures, no neurologic impairment of axillary nerve. These- first-time- 80% chance of recurrence, can reduce rate with arthroscopy by orthopedic surgeon.
42-y/o man in-line skating fell on outstretched hand, treated for a comminuted fracture of his clavicle, abrasions, lacerations, mild concussion; gets better, but getting worsening wrist pain with active wrist flexion, extension and ulnar deviation. Pain localized to anatomical snuffbox. Problem with scaphoid fractures- often overlooked on X-ray, can get avascular necrosis, loss of