1. Human nasopharynx is a reservoir for neisseria meningitis; use droplet precautions.
2. PPD skin test cutoffs for TB
- 5: HIV, transplant, immunosuppressed (ie. lupus, >15mg/day of prednisone for >1mo). Close contact with TB+ person. Suspicious CXR (c/w prior TB)
- 10: Recent immigrants (<5 yrs) from high prevalence countries, IV drug users, people close to jails, homeless shelters, hospitals, kids < 4 years old, kids exposed to high risk adults, some chronic diseases (DM, renal failure, some cancers like leuk, lymph, head+neck, lung, silicosis, gastrectomy, some GI bypass procedures)
3. TB:
- BCG vaccine induced false-positive PPDs should fade after 10 years, so anyone >10 years out should be treated like anyone else and the tests interpreted accordingly.
- Exposure in the distant past may lead to a false neg PPD; repeat testing in 1-3 weeks may reveal a positive test. Indicated in older people, people who may have had a distant exposure
- B6: 2% of people develop peripheral neuropathy on isoniazid without B6. People at esp high risk for neuropathy: diabetes, uremia, alcoholism, malnutrition, pregnancy, HIV, seizure disorders.
- Screen for latent TB before getting solid organ transplant, starting chemo, or starting TNF-a inhibitor (infliximab, adalimumab, etanercept). Any PPD >5 qualifies as + in these people (regardless of their other risk factors) and should get 6-9 months of INH + B6. You can probably start the TNF-a inh 2 months into INH therapy but this is a matter of debate.
4. Severe CAP
- Pseudomonas risk factors: bronchiectasis, recent (<1 month) steroid/broad spectrum antibiotic use, malnutrition.
- MRSA risk factors: severe, rapidly progressive course, infection during flu season, cavitary infiltrates on CXR, history of MRSA
5. Legionella
- Risk factors: smoking, DM, HIV, CKD, liquid and solid tumors.
- Often presents with high fevers, hyponatremia, GI sx,
- Urine legionella test: 70-90% sens and 99% spec for L. pneumophila serogroup 1-- doesn't detect other serogroups. Neg test does not r/o. Test will be pos day 1 of infection and remain + for weeks.
- Blood and thora cx will not grow + cultures so don't bother
6. CKD + immunity
- Uremia causes an immunocompromised state
- CKD associated with dysfunction in innate and adaptive immunity, TLR, etc
7. Erythromycin does not cover h.flu.
8. Criteria for antibiotic prophylaxis before dental procedures:
- Prosthetic valve
- History of infective endocarditis
- Congenital heart disease that is unrepaired/not fully repaired or has been repaired within last 6 mos
- S/p heart transplant with valve disease
9. Antibiotic prophylaxis before dental procedure:
- Cover for strep viridians
- PO amox
- IV amp, cefazolin, ceftriaxone for people who can't take PO
- Clinda, azithro, clarithro for people who are pen allergic
- Take 30-60 mins before procedure
10. Injection drug user, multifocal pneumonia, heart murmur:
- Think septic emboli from tricuspid valve endocarditis
- Usually s.aureus, cover MRSA, pseudomonas until cx come back proving they're not present.
Saturday, May 31, 2014
Friday, May 30, 2014
1. Cold agglutinins are usually due to infections or lymphoproliferative disorders
- Lymphoproliferative disorders: anything involving increased production of antibodies (i.e B-cell cancers), so waldenstrom's macroglobulinemia, lymphoma, CLL, multiple myeloma.
- Viral infections: CMV, EBV (60% of mono pts will have cold agglutinins, but hemolytic anemia is rare), VZV, Mumps, rubella, HIV, influenza
- Bacterial infections: legionella, e.coli, syphilis, listeria
- Parasitic infections: trypanosomes, malaria
- CANOMAD syndrome (chronic ataxic neuropathy ophthalmoplegia M-protein agglutination disialosyl antibodies): gait and upper-limb ataxia, external ophthalmoplegia, cold agglutinins, IgM paraprotein, and anti-disialosyl antibodies. Neurologic and hematologic symptoms respond to rituximab.
2. Warm agglutinins:
- 80% of all autoimmune hemolytic anemia (AIHA).
- Always polyclonal. IgG1 and IgG3 are the most destructive, and the people with AIHA with a significant component of one or either will have a more advanced, aggressive course. The composition of Ig subtypes is unique and does not always reflect serum composition.
- Usually caused by drugs
- Drugs: cephalosporins (cefotetan most commonly, ceftriaxone next), penicillins (esp piperacillin), NSAIDs,
- Systemic autoimmune diseases: Lupus, RA
- S/p URI
- CLL
3. Acute chest
- Infarctions may lead to secondary infections, so pneumonia in a homozygous sickle cell patient may represent ACS
- Multiple infarctions -> pulmonary congestion, shunting of blood, hypoxia -> more sickling
- Treat with exchange transfusion to goal of HbA > 50% to decrease sickling.
- Hydroxyurea is good to prevent sickle crises (increases Hb F production), but is not an effective treatment in the acute setting.
4. Osteonecrosis (aka avascular necrosis) of the femoral head:
- Common in sickle cell, hypercoagulability (i.e. antiphospholipid), steroid use, gout, alcohol use, lupus, s/p trauma, gout.
- Unclear why alcohol use causes this... but there is a clear relationship. Compared to demographically matched controls, RRs of osteonecrosis of the femoral head were 3.3, 9.8, and 17.9 for current consumers of less than 400, 400-1000, and greater than or equal to 1000 ml/week of alcohol {source}
- CXR: initially will show nothing, later on may show increased density (marrow infarction -> calcification). MRI is >90% sensitive, good for detection in the early phases.
- Can use radionuclide bone scan in people who can't get MRI- although this is not as sensitive.
5. Complex regional pain syndrome/reflex sympathetic dystrophy
- pain in the extremities, swelling, local vasomotor instability (hot flashes), limited range of motion,
- local osteoporosis (bone densitometry scan)
6. Septic arthritis:
- Always should suspect in acute onset monoarticular arthritis, but is uncommon in the absence of prosthetic hip, recent trauma/surgery, previous hip disease
7. Platelet transfusion should be avoided in consumptive processes unless there is life-threatening bleeding.
8. TTP
- ADAMTS13 normal levels: 65-133%, in fulminant TTP expect to be very low.
- More importantly, ADAMTS13 inhibitor should be positive. No inhibitor = No TTP
9. Evans syndrome:
- Coombs+ warm AIHA + ITP
- Smear: spherocytes/microspherocytes + decreased platelets + elevated retics
- Tx like TTP: steroids and IVIg. children have a good response to steroids.
10. Thrombocytopenias:
- Pseudothrombocytopenia: where platelets agglutinate in large clumps, occasionally to neutrophils but sometimes to other cell types. These large platelet clumps are not read by the cell counter and you get a falsely low platelet count. Repeat the test with heparin or sodium citrate (instead of EDTA).
- Gestational: occurs in 5% of pregnancies, appears in late gestation. Platelets are 70-150K. Generally no treatment.
- ITP: no findings other than low platelets. No large spleen, no adenopathy, no abnormal white or red cell morphology. Sometimes you will see giant (i.e. immature) platelets on smear.
- Lymphoproliferative disorders: anything involving increased production of antibodies (i.e B-cell cancers), so waldenstrom's macroglobulinemia, lymphoma, CLL, multiple myeloma.
- Viral infections: CMV, EBV (60% of mono pts will have cold agglutinins, but hemolytic anemia is rare), VZV, Mumps, rubella, HIV, influenza
- Bacterial infections: legionella, e.coli, syphilis, listeria
- Parasitic infections: trypanosomes, malaria
- CANOMAD syndrome (chronic ataxic neuropathy ophthalmoplegia M-protein agglutination disialosyl antibodies): gait and upper-limb ataxia, external ophthalmoplegia, cold agglutinins, IgM paraprotein, and anti-disialosyl antibodies. Neurologic and hematologic symptoms respond to rituximab.
2. Warm agglutinins:
- 80% of all autoimmune hemolytic anemia (AIHA).
- Always polyclonal. IgG1 and IgG3 are the most destructive, and the people with AIHA with a significant component of one or either will have a more advanced, aggressive course. The composition of Ig subtypes is unique and does not always reflect serum composition.
- Usually caused by drugs
- Drugs: cephalosporins (cefotetan most commonly, ceftriaxone next), penicillins (esp piperacillin), NSAIDs,
- Systemic autoimmune diseases: Lupus, RA
- S/p URI
- CLL
3. Acute chest
- Infarctions may lead to secondary infections, so pneumonia in a homozygous sickle cell patient may represent ACS
- Multiple infarctions -> pulmonary congestion, shunting of blood, hypoxia -> more sickling
- Treat with exchange transfusion to goal of HbA > 50% to decrease sickling.
- Hydroxyurea is good to prevent sickle crises (increases Hb F production), but is not an effective treatment in the acute setting.
4. Osteonecrosis (aka avascular necrosis) of the femoral head:
- Common in sickle cell, hypercoagulability (i.e. antiphospholipid), steroid use, gout, alcohol use, lupus, s/p trauma, gout.
- Unclear why alcohol use causes this... but there is a clear relationship. Compared to demographically matched controls, RRs of osteonecrosis of the femoral head were 3.3, 9.8, and 17.9 for current consumers of less than 400, 400-1000, and greater than or equal to 1000 ml/week of alcohol {source}
- CXR: initially will show nothing, later on may show increased density (marrow infarction -> calcification). MRI is >90% sensitive, good for detection in the early phases.
- Can use radionuclide bone scan in people who can't get MRI- although this is not as sensitive.
5. Complex regional pain syndrome/reflex sympathetic dystrophy
- pain in the extremities, swelling, local vasomotor instability (hot flashes), limited range of motion,
- local osteoporosis (bone densitometry scan)
6. Septic arthritis:
- Always should suspect in acute onset monoarticular arthritis, but is uncommon in the absence of prosthetic hip, recent trauma/surgery, previous hip disease
7. Platelet transfusion should be avoided in consumptive processes unless there is life-threatening bleeding.
8. TTP
- ADAMTS13 normal levels: 65-133%, in fulminant TTP expect to be very low.
- More importantly, ADAMTS13 inhibitor should be positive. No inhibitor = No TTP
9. Evans syndrome:
- Coombs+ warm AIHA + ITP
- Smear: spherocytes/microspherocytes + decreased platelets + elevated retics
- Tx like TTP: steroids and IVIg. children have a good response to steroids.
10. Thrombocytopenias:
- Pseudothrombocytopenia: where platelets agglutinate in large clumps, occasionally to neutrophils but sometimes to other cell types. These large platelet clumps are not read by the cell counter and you get a falsely low platelet count. Repeat the test with heparin or sodium citrate (instead of EDTA).
- Gestational: occurs in 5% of pregnancies, appears in late gestation. Platelets are 70-150K. Generally no treatment.
- ITP: no findings other than low platelets. No large spleen, no adenopathy, no abnormal white or red cell morphology. Sometimes you will see giant (i.e. immature) platelets on smear.
Thursday, May 29, 2014
1. DKA: most common cause of death is the thing that precipitated the DKA.
- If someone has abdominal pain, look for the source, don't just chalk it up to DKA. People typically only get abdominal pain from DKA if their bicarb is <10. Even if it's less than that, there's still other things that can cause it.
- Get lactate - if its high look for the source.
2. Symptom approach to dyspnea:
- Dyspnea + fever : pna, pna, pna, PE, COPD/Asthma with infection, endocarditis,
- Dyspnea and pleuritic chest pain: pna, PE (Ultrasound for UE DVT is not as sensitive because the large UE veins go behind the clavicle bones)
- Dyspnea + nonpleuritic chest pain: Angina,
- Dyspnea with nothing else: look for highest yield diseases: heart failure, pna, asthma, copd, PE
3. Meds that directly cause edema:
- Direct vasodilators, like hydralazine.
- Dihydropuridine Ca channel blockers (peripherally acting)
- Glitazones: 1/3 of patients who use get significant edema (now only pyoglitazone is used)
- Steroids
- Estrogen.
- Don't forget that anemia is always on the differential for edema!
5. Primary Nephrotic syndrome (i.e. idiopathic)
- FSGS (33%)
- Membranous (33%) 5-20% of adults with this have cancer
- Minimal change (15%) - can occur in adults.
6. Secondary causes of nephrotic
- DM
- lupus
- infections (hep b, c, hiv, syphillis, malaria)
- amyloid
- MM
- CAncer
- Meds - NSAIDs, ACE, tamoxifen, lithium, heroin.
7. Types of nephropathy
- Hypertensive nephropathy- modest proteinuria,
- DM nephropathy- more significant proteinuria (Nephrotic- pr/cr ratio > 3-3.5)
8. Types of pulmonary hypertension
- PAH (3%) idiopathic, genetic, drug/toxin, 2/2 - connective tissue dx, HIV, portal hypertension, congenital heart dx, chronic hemolytic anemia, schistosomiasis
- PVH (66%): heart failure. 83% of ppl with diastolic HF have PH.
- PH 2/2 hypoxia: COPD (50% hae PH), ILD (1/3 have PH), OSA, high altitude.
- Chronic PE (<2%)
- Misc causes of PH: myeloproliferative, sarcoid,
9. Diagnosing Cirrhosis
- Plt <110 LR+ 9.8
- Plt > 160 LR 0.29
- Alb <3.5 or elevated INR: LR+ 5
- MRI - LR ~5
10. SBP
- 10-30% in hospitalized patients
- Usu GN, and s.pneumo
- 25-75% abdominal pain
- Indication for paracentesis: active GI bleed, labs suggestive of infection, new renal problems, change in clinical status,
- Paracentesis with single organism, >250 polys = diagnostic of SBP
- Paracentesis with polymicrobial - secondary BP (i.e. perforated viscous)
- If someone has abdominal pain, look for the source, don't just chalk it up to DKA. People typically only get abdominal pain from DKA if their bicarb is <10. Even if it's less than that, there's still other things that can cause it.
- Get lactate - if its high look for the source.
2. Symptom approach to dyspnea:
- Dyspnea + fever : pna, pna, pna, PE, COPD/Asthma with infection, endocarditis,
- Dyspnea and pleuritic chest pain: pna, PE (Ultrasound for UE DVT is not as sensitive because the large UE veins go behind the clavicle bones)
- Dyspnea + nonpleuritic chest pain: Angina,
- Dyspnea with nothing else: look for highest yield diseases: heart failure, pna, asthma, copd, PE
3. Meds that directly cause edema:
- Direct vasodilators, like hydralazine.
- Dihydropuridine Ca channel blockers (peripherally acting)
- Glitazones: 1/3 of patients who use get significant edema (now only pyoglitazone is used)
- Steroids
- Estrogen.
- Don't forget that anemia is always on the differential for edema!
5. Primary Nephrotic syndrome (i.e. idiopathic)
- FSGS (33%)
- Membranous (33%) 5-20% of adults with this have cancer
- Minimal change (15%) - can occur in adults.
6. Secondary causes of nephrotic
- DM
- lupus
- infections (hep b, c, hiv, syphillis, malaria)
- amyloid
- MM
- CAncer
- Meds - NSAIDs, ACE, tamoxifen, lithium, heroin.
7. Types of nephropathy
- Hypertensive nephropathy- modest proteinuria,
- DM nephropathy- more significant proteinuria (Nephrotic- pr/cr ratio > 3-3.5)
8. Types of pulmonary hypertension
- PAH (3%) idiopathic, genetic, drug/toxin, 2/2 - connective tissue dx, HIV, portal hypertension, congenital heart dx, chronic hemolytic anemia, schistosomiasis
- PVH (66%): heart failure. 83% of ppl with diastolic HF have PH.
- PH 2/2 hypoxia: COPD (50% hae PH), ILD (1/3 have PH), OSA, high altitude.
- Chronic PE (<2%)
- Misc causes of PH: myeloproliferative, sarcoid,
9. Diagnosing Cirrhosis
- Plt <110 LR+ 9.8
- Plt > 160 LR 0.29
- Alb <3.5 or elevated INR: LR+ 5
- MRI - LR ~5
10. SBP
- 10-30% in hospitalized patients
- Usu GN, and s.pneumo
- 25-75% abdominal pain
- Indication for paracentesis: active GI bleed, labs suggestive of infection, new renal problems, change in clinical status,
- Paracentesis with single organism, >250 polys = diagnostic of SBP
- Paracentesis with polymicrobial - secondary BP (i.e. perforated viscous)
Wednesday, May 28, 2014
1. "dizziness" means one of 4 things
- Vertigo : world is spinning
- Pre syncope: feeling like you're gonna pass out
- Dysequilibrium: feeling like you're gonna fall down
- Ill defined lightheadedness
2. When people can't describe it, look for clues that its neurological or cardiac- ie.. look for other neurological or cardiac symptoms.
3. Vertigo:
- Peripheral: BPPV, labyrinthitis
- Central: posterior fossa. Cranial nerves, gait, cerebellar coordination
4. History for vertigo:
- BPPV is often positional, but just b/c its positional doesn't mean its BPPV-- central can be too
- Length of vertigo: BPPV (minutes), menieres (hours), vestibular neuritis (days), cerebellar stroke/central lesions (days). If they have a lot of risk factors for stroke and vertigo and no other neuro sx or findings,
5. Tests for central vs peripheral:
- skewed deviation: have them follow your finger up, if their eyes become disconjugate = think brainstem lesion
- head thrust test: distinguish vestibular neuritis from cerebellar stroke in someone who has had vertigo for days.
- If those are both negative, pretty good sensitivity for r/o central lesion.
6. History: rule out central lesion
- CN: diplopia, weakness, slurred speech
- Cb: ataxia, coordination
- Headache: r/o posterior fossa bleed
- History of cancer, anticoagulation
7. Nystagmus:
- Benign (i.e. peripheral, labyrinthitis): unidirectional, a few beats, fatigues with repeated exam, only happens on one side (i.e. to the left, nystagmus in one direction, to the R, nothing)
- Malignant: bidirectional, vertical,
8. Symptom approach to abdominal pain:
- Abdominal pain + peritonitis: call surgery
- Abdominal pain + jaunidce: biliary or hepatic
- Abdominal pain + significant distention: air or fluid.
- Abdominal pain + unexplained hypotension (i.e. no n/v/d, no sepsis, no GI bleed): intra-abdominal hemorrhage.
9. Any exertional pain from mouth to belly-- think angina. Even if its in a weird place like uvula.
10. Bowel perfusion:
Ischemic colitis: splenic flexure, hypoperfusion. Typically spares the rectum because of the dual blood supply.
Chronic mesenteric ischemia - usually 2 vessel dx (celiac and sma)
- Vertigo : world is spinning
- Pre syncope: feeling like you're gonna pass out
- Dysequilibrium: feeling like you're gonna fall down
- Ill defined lightheadedness
2. When people can't describe it, look for clues that its neurological or cardiac- ie.. look for other neurological or cardiac symptoms.
3. Vertigo:
- Peripheral: BPPV, labyrinthitis
- Central: posterior fossa. Cranial nerves, gait, cerebellar coordination
4. History for vertigo:
- BPPV is often positional, but just b/c its positional doesn't mean its BPPV-- central can be too
- Length of vertigo: BPPV (minutes), menieres (hours), vestibular neuritis (days), cerebellar stroke/central lesions (days). If they have a lot of risk factors for stroke and vertigo and no other neuro sx or findings,
5. Tests for central vs peripheral:
- skewed deviation: have them follow your finger up, if their eyes become disconjugate = think brainstem lesion
- head thrust test: distinguish vestibular neuritis from cerebellar stroke in someone who has had vertigo for days.
- If those are both negative, pretty good sensitivity for r/o central lesion.
6. History: rule out central lesion
- CN: diplopia, weakness, slurred speech
- Cb: ataxia, coordination
- Headache: r/o posterior fossa bleed
- History of cancer, anticoagulation
7. Nystagmus:
- Benign (i.e. peripheral, labyrinthitis): unidirectional, a few beats, fatigues with repeated exam, only happens on one side (i.e. to the left, nystagmus in one direction, to the R, nothing)
- Malignant: bidirectional, vertical,
8. Symptom approach to abdominal pain:
- Abdominal pain + peritonitis: call surgery
- Abdominal pain + jaunidce: biliary or hepatic
- Abdominal pain + significant distention: air or fluid.
- Abdominal pain + unexplained hypotension (i.e. no n/v/d, no sepsis, no GI bleed): intra-abdominal hemorrhage.
9. Any exertional pain from mouth to belly-- think angina. Even if its in a weird place like uvula.
10. Bowel perfusion:
Ischemic colitis: splenic flexure, hypoperfusion. Typically spares the rectum because of the dual blood supply.
Chronic mesenteric ischemia - usually 2 vessel dx (celiac and sma)
Tuesday, May 27, 2014
1. Transient loss of consciousness - seizure vs trauma vs hypoglycemia vs drugs/alcohol vs stroke/TIA vs syncope
2. Syncope: vasovagal/reflex vs orthostatics vs cardiac
- Vasovagal: ask about pain, anxiety. Pathogenesis: Heart squeezes down until there's no volume left, brain sees that they need to slow down to fill better, tells vagus nerve to brady and peripheral vessels to vasodilate
- Orthostatics: orthostatic BP. Pathogenesis: dehydration, autonomic instability (old people-- can't mount tachycardic response), diabetes (peripheral neuropathy)
- Cardiac: ask about cardiac dx, risk factors for cardiac dx. In someone with a history of heart disease, you have to rule out NSVT as the cause. In someone young and healthy, still get an EKG because if they have a congenital QT prolongation or if they are on a drug that can prolong QT (macrolide, quinolone) they can go into torsades.
3. When to not blow it off as just vasovagal/orthostatic:
- Occurs lying down (by definition you can't be orthostatic)
- Occurs during exercise
- Supine HR > 100 (12% sens, 96% spec, LR+ 3, LR - 0.9)
- Supine hypotension <95 (33% sens, 97% spec, LR+ 11.0, LR- 0.7)
6. EP techinques to work up arrhythmia
- Measure H-V interval (see how long a signal takes to get thru his-purkinje to check for AV node block)
- Overdrive pace SA node, then stop, see how long it takes the node to recover (longer in sick sinus syndrome).
7. WPW: afib is dangerous, because there's no block through the AV node-- you conduct thru your accessory pathway, and you can pace the ventricle to a rate of 200s-300s.
8. Hypothyroidism:
- Diagnosis: TSH- LR- <0.01, LR +99
- Elevated TSH + low T4 is overt hypothyroid
- Elevated TSH + normal/high T4 is subclinical hypothyroidism.
- Indications for synthroid: symptoms, TSH > 10 (high risk of progression from subclinical to overt hypoT),
9. Bactrim does not cover strep
10. Skin infections
- Cellulitis: systemic symptoms (ie. fever) are rare except in bacteremia or nec fasc, so when you see them, get worried. Without abscess, usu strep, with abscess, think staph
- Erysipelas - usually strep, clear demarcated border, usually superficial, often with fever (i.e. not a worrisome sign)
2. Syncope: vasovagal/reflex vs orthostatics vs cardiac
- Vasovagal: ask about pain, anxiety. Pathogenesis: Heart squeezes down until there's no volume left, brain sees that they need to slow down to fill better, tells vagus nerve to brady and peripheral vessels to vasodilate
- Orthostatics: orthostatic BP. Pathogenesis: dehydration, autonomic instability (old people-- can't mount tachycardic response), diabetes (peripheral neuropathy)
- Cardiac: ask about cardiac dx, risk factors for cardiac dx. In someone with a history of heart disease, you have to rule out NSVT as the cause. In someone young and healthy, still get an EKG because if they have a congenital QT prolongation or if they are on a drug that can prolong QT (macrolide, quinolone) they can go into torsades.
3. When to not blow it off as just vasovagal/orthostatic:
- Occurs lying down (by definition you can't be orthostatic)
- Occurs during exercise
- Any history of heart disease
4. Syncopal convulsions: couple of twitches after syncope is common-- no postictal phase tells you its not a true seizure.
5. Orthostatics:
- Postural increase in pulse > 30 (97% sens, 98% spec, LR+ 48, LR- 0.03)- Supine HR > 100 (12% sens, 96% spec, LR+ 3, LR - 0.9)
- Supine hypotension <95 (33% sens, 97% spec, LR+ 11.0, LR- 0.7)
6. EP techinques to work up arrhythmia
- Measure H-V interval (see how long a signal takes to get thru his-purkinje to check for AV node block)
- Overdrive pace SA node, then stop, see how long it takes the node to recover (longer in sick sinus syndrome).
7. WPW: afib is dangerous, because there's no block through the AV node-- you conduct thru your accessory pathway, and you can pace the ventricle to a rate of 200s-300s.
8. Hypothyroidism:
- Diagnosis: TSH- LR- <0.01, LR +99
- Elevated TSH + low T4 is overt hypothyroid
- Elevated TSH + normal/high T4 is subclinical hypothyroidism.
- Indications for synthroid: symptoms, TSH > 10 (high risk of progression from subclinical to overt hypoT),
9. Bactrim does not cover strep
10. Skin infections
- Cellulitis: systemic symptoms (ie. fever) are rare except in bacteremia or nec fasc, so when you see them, get worried. Without abscess, usu strep, with abscess, think staph
- Erysipelas - usually strep, clear demarcated border, usually superficial, often with fever (i.e. not a worrisome sign)
Monday, May 26, 2014
1. Drugs that amplify warfarin:
- Tylenol, NSAIDs
- Phenytoin
- The standard CYP inhibitors
- Omeprazole
- Antibiotics
- Amiodarone
- Synthroid
- Foods: cranberry juice, ginkgo, vitamin E.
2. Drugs that dampen warfarin:
- The standard CYP inducers (st.johns wort, rifampin, carbamazepine etc)
- Foods rich in vitamin K (leafy greens)
- Ginseng
- OCPs
3. Lupus
- Cyclophosphamide is indicated in the management of lupus when there are significant renal or CNS symptoms
- For lupus nephritis, this small trial (n=80s) found that cyclophosphamide was superior to azathioprine in terms of measured Cr at 5 year f/u and incidence of HZV infection.
4. Miscellaneous drug side effects:
- Cochlear dysfunction: platinum chemo agents, aminoglycosides, lasix
- Optic neuritis: ethambutol, hydroxychloroquine/plaquenil (tx malaria, lupus, RA, sjogrens)
- Peripheral neuropathy: vincristine, isoniazid, phenytoin, heavy metals, chronic alcoholism
- Digital vasospasm/raynauds: beta-blockers, ergot
- Thyroid dysfunction: lithium (also causes tremor, nephro DI, teratogen), amiodarone (also makes you blue)
- Crystal arthritis/gout: cyclosporine
- Acute pancreatitis: steroids
5. Bronchiectasis
- Signs: COPD sx + copious sputum (>100ml/day), hemoptysis, cough + sputum most days of the week, rhinosinusitis, fevers, sx resolve with antibiotics
- Causes: post-infectious (aspergillus, viral, TB), congenital (CF, a1-antitrypsin), immunodeficiency (hypogammaglobulinemia), obstruction (ie. cancer), toxins, systemic rheum (RA, sjogrens)
- Dx with high-res CT; bronch them if its focal to look for tumor, genetic/immune/autoimmune testing if its diffuse.
6. Guillain-Barre
- Assoc with respiratory and GI infection (often campy)
- Sx: symmetric ascending muscle weakness with absent/low deep tendon reflexes, bulbar sx (dysarthria/dysphasia), facial nerve palsy, mild sensory symptoms, autonomic dysfunction. 2/3 c/o severe back or LE pain.
- Dx: LP with elevated protein, normal white count
- Treat with plasmapharesis, IvIg (steroids do not help)
7. Nephrotic syndrome
- Abnormal lipid metabolism (elevated LDL, low HDL)
- Hypercoagulability (affects vv>aa, esp renal vv)
- Increased risk of MI/stroke (because of the above 2)
- Can cause hyperparathyroidism 2/2 loss of vitamin D in the urine
8. Giant cell/temporal arteritis:
- Affects branches of the aorta-- aortic aneurysm is a possible complication. Patients should be followed with serial chest x-rays
9. Toxic shock syndrome
- High fevers T > 38.9 (102)
- Overlapping macular erythematous rash (looks like sunburn)
- Shock vitals
- Multiorgan involvement:
GI (v/d)
Renal (Cr>1-2x upper limit of normal)
Heme (platelets <100K)
MSK (severe myalgias, CK up)
Liver (ast/alt/t-bili >2x ULN)
Mucous membrane hyperemia
CNS (AMS without focal signs)
- +/- leukocytosis: bands usually up, platelets usually down.
- Toxic shock toxin = superantigen, T-cell activation
- Tx with antistaph antibiotics
10. Post infectious glomerulonephritis
- IgA nephropathy: few days (<5) after URI. Nl complement.
- Post strep: GN occurs 10 days after strep pharyngitis, 21 days for strep impetigo. Complement low.
- Tylenol, NSAIDs
- Phenytoin
- The standard CYP inhibitors
- Omeprazole
- Antibiotics
- Amiodarone
- Synthroid
- Foods: cranberry juice, ginkgo, vitamin E.
2. Drugs that dampen warfarin:
- The standard CYP inducers (st.johns wort, rifampin, carbamazepine etc)
- Foods rich in vitamin K (leafy greens)
- Ginseng
- OCPs
3. Lupus
- Cyclophosphamide is indicated in the management of lupus when there are significant renal or CNS symptoms
- For lupus nephritis, this small trial (n=80s) found that cyclophosphamide was superior to azathioprine in terms of measured Cr at 5 year f/u and incidence of HZV infection.
4. Miscellaneous drug side effects:
- Cochlear dysfunction: platinum chemo agents, aminoglycosides, lasix
- Optic neuritis: ethambutol, hydroxychloroquine/plaquenil (tx malaria, lupus, RA, sjogrens)
- Peripheral neuropathy: vincristine, isoniazid, phenytoin, heavy metals, chronic alcoholism
- Digital vasospasm/raynauds: beta-blockers, ergot
- Thyroid dysfunction: lithium (also causes tremor, nephro DI, teratogen), amiodarone (also makes you blue)
- Crystal arthritis/gout: cyclosporine
- Acute pancreatitis: steroids
5. Bronchiectasis
- Signs: COPD sx + copious sputum (>100ml/day), hemoptysis, cough + sputum most days of the week, rhinosinusitis, fevers, sx resolve with antibiotics
- Causes: post-infectious (aspergillus, viral, TB), congenital (CF, a1-antitrypsin), immunodeficiency (hypogammaglobulinemia), obstruction (ie. cancer), toxins, systemic rheum (RA, sjogrens)
- Dx with high-res CT; bronch them if its focal to look for tumor, genetic/immune/autoimmune testing if its diffuse.
6. Guillain-Barre
- Assoc with respiratory and GI infection (often campy)
- Sx: symmetric ascending muscle weakness with absent/low deep tendon reflexes, bulbar sx (dysarthria/dysphasia), facial nerve palsy, mild sensory symptoms, autonomic dysfunction. 2/3 c/o severe back or LE pain.
- Dx: LP with elevated protein, normal white count
- Treat with plasmapharesis, IvIg (steroids do not help)
7. Nephrotic syndrome
- Abnormal lipid metabolism (elevated LDL, low HDL)
- Hypercoagulability (affects vv>aa, esp renal vv)
- Increased risk of MI/stroke (because of the above 2)
- Can cause hyperparathyroidism 2/2 loss of vitamin D in the urine
8. Giant cell/temporal arteritis:
- Affects branches of the aorta-- aortic aneurysm is a possible complication. Patients should be followed with serial chest x-rays
9. Toxic shock syndrome
- High fevers T > 38.9 (102)
- Overlapping macular erythematous rash (looks like sunburn)
- Shock vitals
- Multiorgan involvement:
GI (v/d)
Renal (Cr>1-2x upper limit of normal)
Heme (platelets <100K)
MSK (severe myalgias, CK up)
Liver (ast/alt/t-bili >2x ULN)
Mucous membrane hyperemia
CNS (AMS without focal signs)
- +/- leukocytosis: bands usually up, platelets usually down.
- Toxic shock toxin = superantigen, T-cell activation
- Tx with antistaph antibiotics
10. Post infectious glomerulonephritis
- IgA nephropathy: few days (<5) after URI. Nl complement.
- Post strep: GN occurs 10 days after strep pharyngitis, 21 days for strep impetigo. Complement low.
Sunday, May 25, 2014
1. Management of acute decompensated heart failure
- If BP is high (i.e. hypertension induced HF), give afterload reducers (i.e. hydralazine) and diurese if they're fluid overloaded. The etiology of this is assumed to be excessive afterload.
- If BP is normal, diuresis is the cornerstone of treatment. The etiology is assumed to be fluid overload.
- If BP is low, then give dobutamine with lasix. The etiology is assumed to be insufficient contractility. If you just give lasix, it may or may not work depending on how bad the cardiac output is. If cardiac output is really low, there will be both insufficient forward flow to the kidneys (people can be up 12 liters with a BNP over 100K and edema up the wazoo and still have pre-renal azotemia) and decreased venous return, leading to back pressure in the kidneys that further worsens forward filtration rate. The addition of dobutamine gtt (start low dose 2.5mcg/kg/min, titrate up to max dose 20mc/kg/min as needed) augments contractility, allowing the lasix to actually work. If you titrate up dobutamine all the way and you're still not diuresing, add dopamine.
2. Wide complex tachycardia: SVT +aberrant conduction vs VT.
- SVT + aberrant conduction. Essentially sinus tach + bundle branch block.
- To distinguish between the two, give adenosine. Adenosine blocks conduction through the AV node and if it's SVT, the rhythm will break and it will slow down to a more normal rate so that you are able to see the P waves (although they may be oddly placed). If it's VT, adenosine won't do anything, because it's ventricularly paced. You can also distinguish with history-- a history of ischemic heart disease = its almost certainly VTach.
- Adenosine 6mg IV push, wait 2 minutes, if it doesn't change then 12mg IV push, wait another 2 minutes, then another 12mg. If after all 3 the rhythm didn't break, it's VT.
- If the rhythm does break and you get p-waves, it was SVT with aberrancy; this can be treated with a low-dose beta blocker. However, make sure its not VT before you beta-block because you can push someone into asystole doing that.
3. Management of VT
- If the patient is unstable, call a code and go down the ACLS pathway.
- If the patient is clinically stable, give Amiodarone 150mg at once, then 1mg/minute for 6 hours, and then 0.5mg/min for 18 hours. Max dose 2.2 g/day.
- DO NOT GIVE BETA BLOCKERS TO SOMEONE IN VT. Don't give any drugs that block conduction. The ventricles are the last source of pacing-- the SA/AV nodes are no longer pacing, and so if you give a drug that could potentially block the ventricular pacers you will end up with asystole.
4. Diagnosing narrow-complex tachycardia:
- Differential: sinus tach, SVTs including AVNRT, a-flutter with 2:1 block
- 100-140, think sinus tach. Upper limit of sinus tach is 220-age.
- 140-160, think aflutter with 2:1 block. Look for p-waves going at a rate of 300.
- 160 + think SVT (AVNRT, atrial tachycardia)
5. Management of regular, narrow-complex tachycardia:
- For sinus tach, fix the underlying problem-- most commonly dehydration, pain, infection, anxiety. Less common thyroid storm, etc. Don't just beta-block people, there's always a hypothetical risk of taking down all the pacers.
- For AVNRT, treat with adenosine. Warn people that they're gonna feel like crap.
- For a-flutter, see 'management of a-fib' below, its the same treatment.
- Don't give adenosine in any narrow-complex tachycardia if there is any suspicion of wolff-parkinson-white syndrome; if you take down the AV node, then all the conduction will go through the accessory pathway, which conducts fast, and you will end up with a circular conduction in the opposite direction of normal conduction that may be even faster than the original rhythm. Luckily the effects of adenosine wear off quickly so the person should hypothetically return to normal, but you don't want to go there. Definitely don't give these people any class II or IV antiarrhythmics; since they have such long half lives, they'll be in this horrible re-entrant tachycardia for a while.
6. Irregular narrow-complex tachycardia:
- A-fib with RVR (most common cause of narrow complex tachycardia that you will get paged about) a-flutter with variable conduction and MAT
- MAT is usually caused by electrolyte abnormalities (specifically K, Mg, Ca). If you think someone has MAT, send a BMP and replenish whatever is low. If nothing is low, empirically give Mg 2g over 15 minutes and 4g over the next 6 hours. At these doses, the mag will not accumulate in the blood and cause toxicity; it's a heavily intracellular ion (DNA polymerase cofactor) and it will get sucked into cells. It's only at the really high doses used by ob/gyns that you have to worry about mag toxicity
7. Management of a-fib with RVR (and also of a-flutter with variable/constant block)
- Rate control first (then anticoagulation and eventually cardioversion once they have been fully anticoagulated for 4 weeks)
- Metoprolol 5mg IV push. Can be given up to 3 times with a 5 minute wait between each one. The benefit of metop is that it's fast, but the problem is there is no drip metop so if it fails then you have to switch to dilt. If you think there's high chance of success that a few IV pushes of beta-blockade will make them better (i.e. you know the patient, metop has worked in the past, etc) then this is fine. Otherwise start with dilt. Of note, the patient will need to go home on PO metoprolol and may need to remain on it indefinitely.
- Diltiazem: Bolus 0.25mg/kg. Wait 15 minutes. If it didn't work, bolus 0.35 mg/kg. Wait 15 minutes. If that still doesn't work, start drip at 5-15mg/hr. Preferred drug for patients you don't know (may have atrial thrombus) and for people with tough to break a-fib who you think may need a drip.
- Amiodarone: 150mg IV push, then 1mg/min for 6 hours. The dangerous thing about amio is that it's a class III antiarrhythmic, and you can inadvertently cardiovert the patient, and if they have a mural thrombus you may have just given them an embolic stroke. So if you know the patient well and you're sure that they don't have a mural thrombus, or their a-fib is less than 48 hours old, or they are properly anticoagulated (4 weeks on warfarin), choose diltiazem instead, even in patients with heart failure.
- Digoxin: crappy drug for this purpose; 1 hour onset time. At 6 hours, a significant number of people will still be tachycardic. Only use this as an addon drug in heart failure patients who are unable to be rate controlled with amio alone.
- Esmolol: great drug, works really well for this purpose, but has to be given as a drip with constant careful titration (half life 9-12 minutes) and thus requires ICU admission.
8. Contraindications to direct thrombin inhibitors (xarelto aka rivaroxaban, pradaxa aka dabigatran)
- CYP3A4 interactions
- GFR <15. These drugs are all cleared renally. At GFR 15-30, recommend halving the dose. But really, the best thing to do is just to avoid these in people with any amount of significant renal disease.
9. Statins can help treat fatty liver disease, but it should be avoided in people who have elevated LFTs. Pravastatin is the cleanest one with the fewest LFT perturbances. Simvastatin has bad interactions and is not used much anymore.
10. The bigger the stent, the less difference there is in outcomes between bare metal and drug eluting.
- For larger vessels taking larger stents (3.5mm), there is probably no difference in restenosis rates between the bare metal and drug eluting ones. The old studies showing the superiority of drug eluting stents were done with an older technique that was less aggressive about opening the plaque with the balloon. New data with better technique shows a restenosis rate of bare metal stents that is <1%.
- For smaller stents (2.5mm) drug eluting is probably better.
2. Wide complex tachycardia: SVT +aberrant conduction vs VT.
- SVT + aberrant conduction. Essentially sinus tach + bundle branch block.
- To distinguish between the two, give adenosine. Adenosine blocks conduction through the AV node and if it's SVT, the rhythm will break and it will slow down to a more normal rate so that you are able to see the P waves (although they may be oddly placed). If it's VT, adenosine won't do anything, because it's ventricularly paced. You can also distinguish with history-- a history of ischemic heart disease = its almost certainly VTach.
- Adenosine 6mg IV push, wait 2 minutes, if it doesn't change then 12mg IV push, wait another 2 minutes, then another 12mg. If after all 3 the rhythm didn't break, it's VT.
- If the rhythm does break and you get p-waves, it was SVT with aberrancy; this can be treated with a low-dose beta blocker. However, make sure its not VT before you beta-block because you can push someone into asystole doing that.
3. Management of VT
- If the patient is unstable, call a code and go down the ACLS pathway.
- If the patient is clinically stable, give Amiodarone 150mg at once, then 1mg/minute for 6 hours, and then 0.5mg/min for 18 hours. Max dose 2.2 g/day.
- DO NOT GIVE BETA BLOCKERS TO SOMEONE IN VT. Don't give any drugs that block conduction. The ventricles are the last source of pacing-- the SA/AV nodes are no longer pacing, and so if you give a drug that could potentially block the ventricular pacers you will end up with asystole.
4. Diagnosing narrow-complex tachycardia:
- Differential: sinus tach, SVTs including AVNRT, a-flutter with 2:1 block
- 100-140, think sinus tach. Upper limit of sinus tach is 220-age.
- 140-160, think aflutter with 2:1 block. Look for p-waves going at a rate of 300.
- 160 + think SVT (AVNRT, atrial tachycardia)
5. Management of regular, narrow-complex tachycardia:
- For sinus tach, fix the underlying problem-- most commonly dehydration, pain, infection, anxiety. Less common thyroid storm, etc. Don't just beta-block people, there's always a hypothetical risk of taking down all the pacers.
- For AVNRT, treat with adenosine. Warn people that they're gonna feel like crap.
- For a-flutter, see 'management of a-fib' below, its the same treatment.
- Don't give adenosine in any narrow-complex tachycardia if there is any suspicion of wolff-parkinson-white syndrome; if you take down the AV node, then all the conduction will go through the accessory pathway, which conducts fast, and you will end up with a circular conduction in the opposite direction of normal conduction that may be even faster than the original rhythm. Luckily the effects of adenosine wear off quickly so the person should hypothetically return to normal, but you don't want to go there. Definitely don't give these people any class II or IV antiarrhythmics; since they have such long half lives, they'll be in this horrible re-entrant tachycardia for a while.
6. Irregular narrow-complex tachycardia:
- A-fib with RVR (most common cause of narrow complex tachycardia that you will get paged about) a-flutter with variable conduction and MAT
- MAT is usually caused by electrolyte abnormalities (specifically K, Mg, Ca). If you think someone has MAT, send a BMP and replenish whatever is low. If nothing is low, empirically give Mg 2g over 15 minutes and 4g over the next 6 hours. At these doses, the mag will not accumulate in the blood and cause toxicity; it's a heavily intracellular ion (DNA polymerase cofactor) and it will get sucked into cells. It's only at the really high doses used by ob/gyns that you have to worry about mag toxicity
7. Management of a-fib with RVR (and also of a-flutter with variable/constant block)
- Rate control first (then anticoagulation and eventually cardioversion once they have been fully anticoagulated for 4 weeks)
- Metoprolol 5mg IV push. Can be given up to 3 times with a 5 minute wait between each one. The benefit of metop is that it's fast, but the problem is there is no drip metop so if it fails then you have to switch to dilt. If you think there's high chance of success that a few IV pushes of beta-blockade will make them better (i.e. you know the patient, metop has worked in the past, etc) then this is fine. Otherwise start with dilt. Of note, the patient will need to go home on PO metoprolol and may need to remain on it indefinitely.
- Diltiazem: Bolus 0.25mg/kg. Wait 15 minutes. If it didn't work, bolus 0.35 mg/kg. Wait 15 minutes. If that still doesn't work, start drip at 5-15mg/hr. Preferred drug for patients you don't know (may have atrial thrombus) and for people with tough to break a-fib who you think may need a drip.
- Amiodarone: 150mg IV push, then 1mg/min for 6 hours. The dangerous thing about amio is that it's a class III antiarrhythmic, and you can inadvertently cardiovert the patient, and if they have a mural thrombus you may have just given them an embolic stroke. So if you know the patient well and you're sure that they don't have a mural thrombus, or their a-fib is less than 48 hours old, or they are properly anticoagulated (4 weeks on warfarin), choose diltiazem instead, even in patients with heart failure.
- Digoxin: crappy drug for this purpose; 1 hour onset time. At 6 hours, a significant number of people will still be tachycardic. Only use this as an addon drug in heart failure patients who are unable to be rate controlled with amio alone.
- Esmolol: great drug, works really well for this purpose, but has to be given as a drip with constant careful titration (half life 9-12 minutes) and thus requires ICU admission.
8. Contraindications to direct thrombin inhibitors (xarelto aka rivaroxaban, pradaxa aka dabigatran)
- CYP3A4 interactions
- GFR <15. These drugs are all cleared renally. At GFR 15-30, recommend halving the dose. But really, the best thing to do is just to avoid these in people with any amount of significant renal disease.
9. Statins can help treat fatty liver disease, but it should be avoided in people who have elevated LFTs. Pravastatin is the cleanest one with the fewest LFT perturbances. Simvastatin has bad interactions and is not used much anymore.
10. The bigger the stent, the less difference there is in outcomes between bare metal and drug eluting.
- For larger vessels taking larger stents (3.5mm), there is probably no difference in restenosis rates between the bare metal and drug eluting ones. The old studies showing the superiority of drug eluting stents were done with an older technique that was less aggressive about opening the plaque with the balloon. New data with better technique shows a restenosis rate of bare metal stents that is <1%.
- For smaller stents (2.5mm) drug eluting is probably better.
Saturday, May 24, 2014
1. Complicated pleural effusion:
- pH < 7.2
- LDH > 1000
- Glucose < 60
- Gross pus visible
- Loculations (may need VATS to break it up for adequate drainage)
- Gram stain or cultures of fluid +
- Need to be drained
2. Tactile fremitus:
- Feeling vibration on the chest when the patient is vocalizes low frequency sounds (toy boat, blue balloons)
- Increased with consolidated lung (solid/liquid is better at transmitting vibrations than aerated lung)
- Decreased with pleural effusions- decreased transmission/increased space between lung and body wall.
3. Tuberculous pleural effusion
- Exudative (ie. pleural/plasma LDH > 0.6, pleural/plasma protein > 0.5)
- Predominantly lymphocytic in nature (although can be neutrophilic in first 2 weeks)
- Subacute course of illness (weeks to months)
- Fluid cx positive in 1/3 of cases
- Diagnose with pleural biopsy and fluid cx (combo will be positive in 2/3 of cases)
4. Chylothorax
- Most commonly due to malignancy, but can also be caused by trauma, TB, chronic mediastinal infections, sarcoid, radiation fibrosis, lymphangioleiomyomatosis (proliferation of smooth muscle cells in bronchioles, alveolar septa, vessels, lymphatics throughout lung)
- Will see high pleural fluid triglycerides (>110, if its less than 50 it's probably not chylothorax) and low pleural fluid cholesterol
- Usually milky, but can be serous or serosanguinous in someone who is chronically malnourished and has low fat intake.
5. Pathogenesis of respiratory failure in asthma:
- Narrowed airway diameter (airway edema, bronchospasm, collapse) lead to prolonged expiratory phase. Breathing fast leads to incomplete expiration, leading to air retention. This causes flattening of the diaphragm, reducing its function, forcing reliance on accessory airway muscles which are less efficient (i.e. more lactate/CO2 generated and O2 required per unit work)
- Significant air trapping can lead to ruptured blebs (pneumothorax) or decreased venous return (hypotension)
- Signs of impending respiratory failure: PCO2 that is normal or high, tachypnea > 30, tachycardia >120.
6. Asthma control
- Steroid burst for asthma: 0.5mg/kg of prednisone for 5 to 7 days.
- Inhaled steroids are, as far we we know, safe during pregnancy (budesonide is the best studied), and certainly less dangerous than poorly controlled asthma.
- Other drugs that are also probably safe in pregnancy: theophylline, LABAs, cromolyn
- Start with low to moderate dose inhaled steroid; when that fails, adding LABA is better than doubling the steroid dose.
- Third line drugs: leukotriene-modifying drugs (although montelukast is first-line for allergic type asthma) and theophylline
- Inhaled anticholinergics have an unclear role in asthma (although they are beneficial in COPD)
7. COPD exacerbation treatment
- Mainstay: oxygen, albuterol, systemic steroids
- Addition of antibiotics has been shown to speed up resolution (and reduce hospital stay and mortality) in moderate to severe COPD exacerbations or people who are on ventilators. Either ceftriaxone + azithro or levoquine. Amoxicillin no longer first line given resistance in H.flu and moraxella.
- Theophylline not recommended for acute symptom management as it adds no benefit over standard treatment and has significant side effects (n/v/heartburn/palpitations/arrhythmias). Also methylxanthines have significant drug interactions.
- Inhaled steroid adds no benefit when someone is already on systemic steroids.
8. Home O2 for COPD
- Has been shown to improve survival (vs inhaled steroids/LABA which improve symptoms and decrease hospitalizations but have not been shown to increase survival)
- Indication: Sats <88% on RA or PO2 <55
- Indication: Sats <89 or PO2 <59 if there is concomitant sequelae of COPD: R heart failure, pulmonary HTN, hematocrit > 56
9. COPD management
- GOLD score: grading based on FEV1: >80 is GOLD I, 50-80 is GOLD II, 30-50 is GOLD III, <30 is GOLD IV. FEV1<50 + severe chronic symptoms also makes you GOLD IV. In all cases, FEV1/FVC must be <70%
- First line is PRN short acting bronchodialtor (either albuterol or ipratropium/atrovent). If that fails, you add long acting bronchodilator, either LABA or long acting anticholinergic (tiotropium/spiriva). If that fails, you add inhaled steroids.
- Lung reduction surgery benefits those with upper lung disease and limited exercise tolerance after pulmonary rehab. Ideal candidate: FEV1 20-35% predicted, DLCO > 20% predicted, hyperinflation, limited comorbidities
- Indication for transplant: hypercapnea pCO2>5, FEV1<20; either homogenous disease on high-res CT or DLCO<20, unlikely to survive after lung reduction surgery
- In patients <45 who have bibasilar emphysematous disease, r/o a1-antitrypsin
10. COPD and supplemental oxygen
- You want to give oxygen for hypoxic COPD exacerbation, however, O2 supplementation can exacerbate hypercapnea (both by worsening VQ mismatch from blunting of the hypoxic vasoconstriction reaction and from decreasing respiratory drive)
- Titrate oxygen to keep sats > 90 or PaO2 > 60-70.
- Indication for NPPV: tachypnea > 25, pH < 7.5, pCO2 > 45
- pH < 7.2
- LDH > 1000
- Glucose < 60
- Gross pus visible
- Loculations (may need VATS to break it up for adequate drainage)
- Gram stain or cultures of fluid +
- Need to be drained
2. Tactile fremitus:
- Feeling vibration on the chest when the patient is vocalizes low frequency sounds (toy boat, blue balloons)
- Increased with consolidated lung (solid/liquid is better at transmitting vibrations than aerated lung)
- Decreased with pleural effusions- decreased transmission/increased space between lung and body wall.
3. Tuberculous pleural effusion
- Exudative (ie. pleural/plasma LDH > 0.6, pleural/plasma protein > 0.5)
- Predominantly lymphocytic in nature (although can be neutrophilic in first 2 weeks)
- Subacute course of illness (weeks to months)
- Fluid cx positive in 1/3 of cases
- Diagnose with pleural biopsy and fluid cx (combo will be positive in 2/3 of cases)
4. Chylothorax
- Most commonly due to malignancy, but can also be caused by trauma, TB, chronic mediastinal infections, sarcoid, radiation fibrosis, lymphangioleiomyomatosis (proliferation of smooth muscle cells in bronchioles, alveolar septa, vessels, lymphatics throughout lung)
- Will see high pleural fluid triglycerides (>110, if its less than 50 it's probably not chylothorax) and low pleural fluid cholesterol
- Usually milky, but can be serous or serosanguinous in someone who is chronically malnourished and has low fat intake.
5. Pathogenesis of respiratory failure in asthma:
- Narrowed airway diameter (airway edema, bronchospasm, collapse) lead to prolonged expiratory phase. Breathing fast leads to incomplete expiration, leading to air retention. This causes flattening of the diaphragm, reducing its function, forcing reliance on accessory airway muscles which are less efficient (i.e. more lactate/CO2 generated and O2 required per unit work)
- Significant air trapping can lead to ruptured blebs (pneumothorax) or decreased venous return (hypotension)
- Signs of impending respiratory failure: PCO2 that is normal or high, tachypnea > 30, tachycardia >120.
6. Asthma control
- Steroid burst for asthma: 0.5mg/kg of prednisone for 5 to 7 days.
- Inhaled steroids are, as far we we know, safe during pregnancy (budesonide is the best studied), and certainly less dangerous than poorly controlled asthma.
- Other drugs that are also probably safe in pregnancy: theophylline, LABAs, cromolyn
- Start with low to moderate dose inhaled steroid; when that fails, adding LABA is better than doubling the steroid dose.
- Third line drugs: leukotriene-modifying drugs (although montelukast is first-line for allergic type asthma) and theophylline
- Inhaled anticholinergics have an unclear role in asthma (although they are beneficial in COPD)
7. COPD exacerbation treatment
- Mainstay: oxygen, albuterol, systemic steroids
- Addition of antibiotics has been shown to speed up resolution (and reduce hospital stay and mortality) in moderate to severe COPD exacerbations or people who are on ventilators. Either ceftriaxone + azithro or levoquine. Amoxicillin no longer first line given resistance in H.flu and moraxella.
- Theophylline not recommended for acute symptom management as it adds no benefit over standard treatment and has significant side effects (n/v/heartburn/palpitations/arrhythmias). Also methylxanthines have significant drug interactions.
- Inhaled steroid adds no benefit when someone is already on systemic steroids.
8. Home O2 for COPD
- Has been shown to improve survival (vs inhaled steroids/LABA which improve symptoms and decrease hospitalizations but have not been shown to increase survival)
- Indication: Sats <88% on RA or PO2 <55
- Indication: Sats <89 or PO2 <59 if there is concomitant sequelae of COPD: R heart failure, pulmonary HTN, hematocrit > 56
9. COPD management
- GOLD score: grading based on FEV1: >80 is GOLD I, 50-80 is GOLD II, 30-50 is GOLD III, <30 is GOLD IV. FEV1<50 + severe chronic symptoms also makes you GOLD IV. In all cases, FEV1/FVC must be <70%
- First line is PRN short acting bronchodialtor (either albuterol or ipratropium/atrovent). If that fails, you add long acting bronchodilator, either LABA or long acting anticholinergic (tiotropium/spiriva). If that fails, you add inhaled steroids.
- Lung reduction surgery benefits those with upper lung disease and limited exercise tolerance after pulmonary rehab. Ideal candidate: FEV1 20-35% predicted, DLCO > 20% predicted, hyperinflation, limited comorbidities
- Indication for transplant: hypercapnea pCO2>5, FEV1<20; either homogenous disease on high-res CT or DLCO<20, unlikely to survive after lung reduction surgery
- In patients <45 who have bibasilar emphysematous disease, r/o a1-antitrypsin
10. COPD and supplemental oxygen
- You want to give oxygen for hypoxic COPD exacerbation, however, O2 supplementation can exacerbate hypercapnea (both by worsening VQ mismatch from blunting of the hypoxic vasoconstriction reaction and from decreasing respiratory drive)
- Titrate oxygen to keep sats > 90 or PaO2 > 60-70.
- Indication for NPPV: tachypnea > 25, pH < 7.5, pCO2 > 45
Friday, May 23, 2014
1. SMART trial: RCT, n=5000, comparing taking antiretrovirals all the time despite CD4 counts ("viral suppression") vs only taking them when CD4 counts are below 250, and stopping when they are above. Found that people on continuous HAART had decreased risk of mortality from all causes, AIDS-defining and non-AIDS-defining (like MI, renal or hepatic disease) - HR ~1.7.
N Engl J Med. 2006 Nov 30;355(22):2283-96.
CD4+ count-guided interruption of antiretroviral treatment.
4.First line HAART therapies as of today:
Truvada = emtricitabine (NRTI) and tenofovir (NRTI)
- Truvada + Efavirenz (NNRTI) = Atripla. (One pill qD, but contains efavirenz and so can make you crazy)
- Truvada + Raltegravir (II) (BID dosing)
- Truvada + Boosted Atazanavir (PI) (i.e. Atazanavir/Ritonavir) (Ataz needs acidic environment, CI in people on PPIs)
- Truvada + Boosted Darunavir (PI) (i.e. Darunavir/Ritonavir) (Daru can set off sulfa allergies)
5. Side effects of anti-retrovirals: NRTI
- All can cause lactic acidosis, nausea/vomiting, Hep B flare if the drug is stopped
- AZT/zidovudine: black-box warning for BM suppression: aplastic anemia/neutropenia
- d4t/ddI (ddI = don't do it): pancreatitis, neuropathy, lactic acidosis, lipodystrophy
- Tenofovir: increased creatinine, proteinuria. Incidence of renal insufficiency ~0.5%. Can cause fanconi's syndrome.
- Abacavir: can cause abacavir hypersensitivity syndrome, which starts as flu-like symptoms, with GI symptoms, and then a sepsis-like picture with shock vitals. One can screen for likelihood of this happening with HLA B*5701 testing (people with a certain SNP there are much more likely to get this).
6. Side effects of anti-retrovirals: NNRTI
- Efavirenz: nightmares, hallucinations, feeling hung over, dissociative symptoms. 23% have CNS side effects, usually goes away. This drug is teratogenic.
- Nevirapine: hepatic necrosis, increased risk with increased CD4 counts.
7. Side effects of anti-retrovirals: Protease inhibitors
- All cause nausea, vomiting, diarrhea, dyslipidemia
- Mostly metabolized through CYP 3A4 so mad drug interactions
- Darunavir: has sulfa moiety, avoid in people with sulfa allergy. Well tolerated.
- Ritonavir: bad nausea/vomiting/diarrhea
- Atazanavir: indirect hyperbilirubinemia, like Gilbert's syndrome (conjugation enzyme defect). Benign. Resolves if you stop the drug.
8. Drug interactions:
- Significant interactions with statins, which are also CYP3A4 metabolized.
- 24-hour area under the curve for simvastatin increased by more than 3,000% when it was coadministered with saquinavir/ritonavir. {source}
- 24-hour area under the curve for atorvastatin increased more than 800% and the maximum concentration (Cmax) increased more than 760% when coadministered with tipranavir/ritonavir {source}
- Other interactions: benzodiazepines (also CYP 3A4), ergot-derived agents, and agents known to be CYP affectors (rifampin, st.John's wort, etc)
9. New HAART agents:
- Rilpivirine = NNRTI, replaces efavirenz in atripla to make a new combo pill called Complera. Hopefully just as good as atripla but doesn't make you as crazy. Not for people with high viral loads
- Stribild, which is a quad pill. Truvada + Elvitegravir and cobicistat (booster). Lots of GI side effects.
- Dolutegravir, which is a nice integrase inhibitor with qD dosing (better than raltegravir's BID dosing), and while raltegravir has a low barrier to resistance, Dolu is highly potent and seems mutation resistant.
10. Pre-exposure prophylaxis: it works!
N Engl J Med. 2006 Nov 30;355(22):2283-96.
CD4+ count-guided interruption of antiretroviral treatment.
METHODS:
We randomly assigned persons infected with HIV who had a CD4+ cell count of more than 350 per cubic millimeter to the continuous use of antiretroviral therapy (the viral suppression group) or the episodic use of antiretroviral therapy (the drug conservation group). Episodic use involved the deferral of therapy until the CD4+ count decreased to less than 250 per cubic millimeter and then the use of therapy until the CD4+ count increased to more than 350 per cubic millimeter. The primary end point was the development of an opportunistic disease or death from any cause. An important secondary end point was major cardiovascular, renal, or hepatic disease.
RESULTS:
A total of 5472 participants (2720 assigned to drug conservation and 2752 to viral suppression) were followed for an average of 16 months before the protocol was modified for the drug conservation group. At baseline, the median and nadir CD4+ counts were 597 per cubic millimeter and 250 per cubic millimeter, respectively, and 71.7% of participants had plasma HIV RNA levels of 400 copies or less per milliliter. Opportunistic disease or death from any cause occurred in 120 participants (3.3 events per 100 person-years) in the drug conservation group and 47 participants (1.3 per 100 person-years) in the viral suppression group (hazard ratio for the drug conservation group vs. the viral suppression group, 2.6; 95% confidence interval [CI], 1.9 to 3.7; P<0.001). Hazard ratios for death from any cause and for major cardiovascular, renal, and hepatic disease were 1.8 (95% CI, 1.2 to 2.9; P=0.007) and 1.7 (95% CI, 1.1 to 2.5; P=0.009), respectively. Adjustment for the latest CD4+ count and HIV RNA level (as time-updated covariates) reduced the hazard ratio for the primary end point from 2.6 to 1.5 (95% CI, 1.0 to 2.1).
CONCLUSIONS:
Episodic antiretroviral therapy guided by the CD4+ count, as used in our study, significantly increased the risk of opportunistic disease or death from any cause, as compared with continuous antiretroviral therapy, largely as a consequence of lowering the CD4+ cell count and increasing the viral load. Episodic antiretroviral therapy does not reduce the risk of adverse events that have been associated with antiretroviral therapy.
2. NA-ACCORD study: Observational cohort study, n=17,000; the lower you let your CD4 drop before you started therapy, the higher your risk of death.
N Engl J Med. 2009 Apr 30;360(18):1815-26.
Effect of early versus deferred antiretroviral therapy for HIV on survival.
METHODS:
We conducted two parallel analyses involving a total of 17,517 asymptomatic patients with HIV infection in the United States and Canada who received medical care during the period from 1996 through 2005. None of the patients had undergone previous antiretroviral therapy. In each group, we stratified the patients according to the CD4+ count (351 to 500 cells per cubic millimeter or >500 cells per cubic millimeter) at the initiation of antiretroviral therapy. In each group, we compared the relative risk of death for patients who initiated therapy when the CD4+ count was above each of the two thresholds of interest (early-therapy group) with that of patients who deferred therapy until the CD4+ count fell below these thresholds (deferred-therapy group).
RESULTS:
In the first analysis, which involved 8362 patients, 2084 (25%) initiated therapy at a CD4+ count of 351 to 500 cells per cubic millimeter, and 6278 (75%) deferred therapy. After adjustment for calendar year, cohort of patients, and demographic and clinical characteristics, among patients in the deferred-therapy group there was an increase in the risk of death of 69%, as compared with that in the early-therapy group (relative risk in the deferred-therapy group, 1.69; 95% confidence interval [CI], 1.26 to 2.26; P<0.001). In the second analysis involving 9155 patients, 2220 (24%) initiated therapy at a CD4+ count of more than 500 cells per cubic millimeter and 6935 (76%) deferred therapy. Among patients in the deferred-therapy group, there was an increase in the risk of death of 94% (relative risk, 1.94; 95% CI, 1.37 to 2.79; P<0.001).
CONCLUSIONS:
The early initiation of antiretroviral therapy before the CD4+ count fell below two prespecified thresholds significantly improved survival, as compared with deferred therapy.
3. HPTN-052 trial: multicountry RCT, n=1700, studying the effect of antiretrovirals on transmission of HIV between serodiscordant couples. Couples who were randomized to the group where the infected partner was treated with antiretrovirals had a 95% reduction in HIV transmission. Out of the 800 or 900 people in couples randomized to treatment, there was only one case of HIV transmission, and that was early on before the person was virally suppressed, meaning that the incidence of HIV transmission from a virally suppressed person was 0%. Let me re-iterate: 0%.
N Engl J Med. 2011 Aug 11;365(6):493-505.
Prevention of HIV-1 infection with early antiretroviral therapy.
METHODS:
In nine countries, we enrolled 1763 couples in which one partner was HIV-1-positive and the other was HIV-1-negative; 54% of the subjects were from Africa, and 50% of infected partners were men. HIV-1-infected subjects with CD4 counts between 350 and 550 cells per cubic millimeter were randomly assigned in a 1:1 ratio to receive antiretroviral therapy either immediately (early therapy) or after a decline in the CD4 count or the onset of HIV-1-related symptoms (delayed therapy). The primary prevention end point was linked HIV-1 transmission in HIV-1-negative partners. The primary clinical end point was the earliest occurrence of pulmonary tuberculosis, severe bacterial infection, a World Health Organization stage 4 event, or death.
RESULTS:
As of February 21, 2011, a total of 39 HIV-1 transmissions were observed (incidence rate, 1.2 per 100 person-years; 95% confidence interval [CI], 0.9 to 1.7); of these, 28 were virologically linked to the infected partner (incidence rate, 0.9 per 100 person-years, 95% CI, 0.6 to 1.3). Of the 28 linked transmissions, only 1 occurred in the early-therapy group (hazard ratio, 0.04; 95% CI, 0.01 to 0.27; P<0.001). Subjects receiving early therapy had fewer treatment end points (hazard ratio, 0.59; 95% CI, 0.40 to 0.88; P=0.01).
CONCLUSIONS:
The early initiation of antiretroviral therapy reduced rates of sexual transmission of HIV-1 and clinical events, indicating both personal and public health benefits from such therapy. (Funded by the National Institute of Allergy and Infectious Diseases and others; HPTN 052 ClinicalTrials.gov number, NCT00074581.).
Truvada = emtricitabine (NRTI) and tenofovir (NRTI)
- Truvada + Efavirenz (NNRTI) = Atripla. (One pill qD, but contains efavirenz and so can make you crazy)
- Truvada + Raltegravir (II) (BID dosing)
- Truvada + Boosted Atazanavir (PI) (i.e. Atazanavir/Ritonavir) (Ataz needs acidic environment, CI in people on PPIs)
- Truvada + Boosted Darunavir (PI) (i.e. Darunavir/Ritonavir) (Daru can set off sulfa allergies)
5. Side effects of anti-retrovirals: NRTI
- All can cause lactic acidosis, nausea/vomiting, Hep B flare if the drug is stopped
- AZT/zidovudine: black-box warning for BM suppression: aplastic anemia/neutropenia
- d4t/ddI (ddI = don't do it): pancreatitis, neuropathy, lactic acidosis, lipodystrophy
- Tenofovir: increased creatinine, proteinuria. Incidence of renal insufficiency ~0.5%. Can cause fanconi's syndrome.
- Abacavir: can cause abacavir hypersensitivity syndrome, which starts as flu-like symptoms, with GI symptoms, and then a sepsis-like picture with shock vitals. One can screen for likelihood of this happening with HLA B*5701 testing (people with a certain SNP there are much more likely to get this).
6. Side effects of anti-retrovirals: NNRTI
- Efavirenz: nightmares, hallucinations, feeling hung over, dissociative symptoms. 23% have CNS side effects, usually goes away. This drug is teratogenic.
- Nevirapine: hepatic necrosis, increased risk with increased CD4 counts.
7. Side effects of anti-retrovirals: Protease inhibitors
- All cause nausea, vomiting, diarrhea, dyslipidemia
- Mostly metabolized through CYP 3A4 so mad drug interactions
- Darunavir: has sulfa moiety, avoid in people with sulfa allergy. Well tolerated.
- Ritonavir: bad nausea/vomiting/diarrhea
- Atazanavir: indirect hyperbilirubinemia, like Gilbert's syndrome (conjugation enzyme defect). Benign. Resolves if you stop the drug.
8. Drug interactions:
- Significant interactions with statins, which are also CYP3A4 metabolized.
- 24-hour area under the curve for simvastatin increased by more than 3,000% when it was coadministered with saquinavir/ritonavir. {source}
- 24-hour area under the curve for atorvastatin increased more than 800% and the maximum concentration (Cmax) increased more than 760% when coadministered with tipranavir/ritonavir {source}
- Other interactions: benzodiazepines (also CYP 3A4), ergot-derived agents, and agents known to be CYP affectors (rifampin, st.John's wort, etc)
9. New HAART agents:
- Rilpivirine = NNRTI, replaces efavirenz in atripla to make a new combo pill called Complera. Hopefully just as good as atripla but doesn't make you as crazy. Not for people with high viral loads
- Stribild, which is a quad pill. Truvada + Elvitegravir and cobicistat (booster). Lots of GI side effects.
- Dolutegravir, which is a nice integrase inhibitor with qD dosing (better than raltegravir's BID dosing), and while raltegravir has a low barrier to resistance, Dolu is highly potent and seems mutation resistant.
10. Pre-exposure prophylaxis: it works!
N Engl J Med. 2012 Aug 2;367(5):399-410. doi: 10.1056/NEJMoa1108524. Epub 2012 Jul 11.
Antiretroviral prophylaxis for HIV prevention in heterosexual men and women.
METHODS:
We conducted a randomized trial of oral antiretroviral therapy for use as preexposure prophylaxis among HIV-1-serodiscordant heterosexual couples from Kenya and Uganda. The HIV-1-seronegative partner in each couple was randomly assigned to one of three study regimens--once-daily tenofovir (TDF), combination tenofovir-emtricitabine (TDF-FTC), or matching placebo--and followed monthly for up to 36 months. At enrollment, the HIV-1-seropositive partners were not eligible for antiretroviral therapy, according to national guidelines. All couples received standard HIV-1 treatment and prevention services.
RESULTS:
We enrolled 4758 couples, of whom 4747 were followed: 1584 randomly assigned to TDF, 1579 to TDF-FTC, and 1584 to placebo. For 62% of the couples followed, the HIV-1-seronegative partner was male. Among HIV-1-seropositive participants, the median CD4 count was 495 cells per cubic millimeter (interquartile range, 375 to 662). A total of 82 HIV-1 infections occurred in seronegative participants during the study, 17 in the TDF group (incidence, 0.65 per 100 person-years), 13 in the TDF-FTC group (incidence, 0.50 per 100 person-years), and 52 in the placebo group(incidence, 1.99 per 100 person-years), indicating a relative reduction of 67% in the incidence of HIV-1 with TDF (95% confidence interval [CI], 44 to 81; P<0.001) and of 75% with TDF-FTC (95% CI, 55 to 87; P<0.001). Protective effects of TDF-FTC and TDF alone against HIV-1 were not significantly different (P=0.23), and both study medications significantly reduced the HIV-1 incidence among both men and women. The rate of serious adverse events was similar across the study groups. Eight participants receiving active treatment were found to have been infected with HIV-1 at baseline, and among these eight, antiretroviral resistance developed in two during the study.
CONCLUSIONS:
Oral TDF and TDF-FTC both protect against HIV-1 infection in heterosexual men and women.
Thursday, May 22, 2014
1. Is it dangerous to perform PCI at institutions without cardiac surgery capabilities? No. No it's not. The CPORT-E trial randomized 18,000 to PCI at hospitals with and without on-site cards surg.
- 6-week mortality rate was 0.9% vs 1.0% (P=0.004 for noninferiority).
- 9-month rates of major adverse cardiac events were 12.1% and 11.2% (P=0.05 for noninferiority).
- rate of target-vessel revascularization was higher in hospitals without on-site surgery (6.5% vs. 5.4%, P=0.01).
{NEJM, 2012)
2. Predicting in-hospital mortality after PCI: the NCDI CathPCI risk score system, developed on a dataset with N of 180,000, and validated on 2 different sets of data (n=120,000 and n=280,000). Not only is this data highly powered, it's also reflects modern practice (2004 to 2006 data), is nationally representative, and reflects a good proportion of acute and stable cases. {JACC, 2010)
- Presents clinically as an acute MI, +/- STEMI
- Can also accur subacute (within 30 days) or chronically (years)
4. Periprocedural complications of PCI: contrast nephropathy
- A good percent of people undergoing PCI will get renal damage from the contrast load, particularly if they have underlying disease
- The good news is that the POSEIDON trial showed that hydration (titrating to LVEDP) can significantly reduce the renal injury
5. Periprocedural complications of PCI: stroke
- Pushing a guide wire around the aorta (full of atherosclerotic plaques in many) is unsurprisingly a risk factor for stroke.
- Study examining incidence of stroke after PCI {Circulation, n=46,000, 2005-2008 data, published 2013}
- Stroke was observed in 0.4% of the procedures in the total population, in 0.3% of PCIs in elective patients, and in 0.6% in PCIs performed for ACS.
- Overall in-hospital mortality was 19.2% for patients who developed stroke (elective PCIs, 10.0%; PCI for ACS, 23.2%) compared with 1.3% for those without stroke (elective PCIs, 0.2%; PCI for ACS, 2.3%).
- In multivariate analysis hemodynamic instability, age ≥75 years, history of stroke, and congestive heart failure were found to be independent predictors for periprocedural stroke in ACS, whereas only PCI of a bypass graft and renal failure could be identified as independent predictors for stroke in elective patients.
6. Periprocedural complications of PCI: Coronary artery dissection
10. Periprocedural complications of PCI: Anticoagulation-associated bleeding
- Generally, people are anticoagulated right before and during the procedure (to reduce clotting from balloon-mediated damage to the plaque, prevent immediate/acute rethrombosis)
- People are also anticoagulated after-- aspirin forever, plavix 30 days (BM stent in a stable patient) or 3-6 months (new drug eluting stents), or 12 months (old drug eluting stents, any stent in a patient experiencing acute MI)
- Such anticoagulation will cause all the typical anticoagulation bleeds (GI, access site, etc)
- 6-week mortality rate was 0.9% vs 1.0% (P=0.004 for noninferiority).
- 9-month rates of major adverse cardiac events were 12.1% and 11.2% (P=0.05 for noninferiority).
- rate of target-vessel revascularization was higher in hospitals without on-site surgery (6.5% vs. 5.4%, P=0.01).
{NEJM, 2012)
2. Predicting in-hospital mortality after PCI: the NCDI CathPCI risk score system, developed on a dataset with N of 180,000, and validated on 2 different sets of data (n=120,000 and n=280,000). Not only is this data highly powered, it's also reflects modern practice (2004 to 2006 data), is nationally representative, and reflects a good proportion of acute and stable cases. {JACC, 2010)
3. Periprocedural complications of PCI: stent thrombosis
- Incidence of intraprocedural stent thrombosis - 0.8% (per post hoc data analysis on CHAMPION-PHONENIX trial n=10,000)- Presents clinically as an acute MI, +/- STEMI
- Can also accur subacute (within 30 days) or chronically (years)
4. Periprocedural complications of PCI: contrast nephropathy
- A good percent of people undergoing PCI will get renal damage from the contrast load, particularly if they have underlying disease
- The good news is that the POSEIDON trial showed that hydration (titrating to LVEDP) can significantly reduce the renal injury
5. Periprocedural complications of PCI: stroke
- Pushing a guide wire around the aorta (full of atherosclerotic plaques in many) is unsurprisingly a risk factor for stroke.
- Study examining incidence of stroke after PCI {Circulation, n=46,000, 2005-2008 data, published 2013}
- Stroke was observed in 0.4% of the procedures in the total population, in 0.3% of PCIs in elective patients, and in 0.6% in PCIs performed for ACS.
- Overall in-hospital mortality was 19.2% for patients who developed stroke (elective PCIs, 10.0%; PCI for ACS, 23.2%) compared with 1.3% for those without stroke (elective PCIs, 0.2%; PCI for ACS, 2.3%).
- In multivariate analysis hemodynamic instability, age ≥75 years, history of stroke, and congestive heart failure were found to be independent predictors for periprocedural stroke in ACS, whereas only PCI of a bypass graft and renal failure could be identified as independent predictors for stroke in elective patients.
6. Periprocedural complications of PCI: Coronary artery dissection
- Given that you're opening a balloon within a stenotic vessel aiming to expand it, it's no surprised that the plaques crack, and sometimes lead to vessel dissections
- A and B dissections are considered benign, while the others could be more dangerous
7. Periprocedural complications of PCI: Perforation
- In a study {Am J Cardiol, n=10,000, data from years 1993 to 2001}, reported incidence of perforation was 0.84%.
- The worse the perforation, the worse the complications/outcomes
- Management: emergent pericardiocentesis if tamponade results
- Typically, tamponade will occur 6-8 hours after the procedure
8. Periprocedural complications of PCI: Retroperitoneal hemorrhage
- If you hit the back wall of the femoral artery above the inguinal ligament, you can get a retropertioneal hemorrhage that is not amenable to compression
- Will manifest clinically as hypotension and tachycardia after a procedure
- One of the most common causes of mortality after PCI
- Don't trust the groin-- just because it looks clean and perfect does NOT mean there is not a giant retroperitoneal hematoma.
9. Periprocedural complications of PCI: vascular site bleeding
- Now the new trend is to use radial rather than femoral access, as it is compressible.
Lancet. 2011 Apr 23;377(9775):1409-20. doi: 10.1016/S0140-6736(11)60404-2. Epub 2011 Apr 4.
Radial versus femoral access for coronary angiography and intervention in patients with acute coronary syndromes (RIVAL): a randomised, parallel group, multicentre trial.
METHODS:
The RadIal Vs femorAL access for coronary intervention (RIVAL) trial was a randomised, parallel group, multicentre trial. Patients with ACS were randomly assigned (1:1) by a 24 h computerised central automated voice response system to radial or femoral artery access. The primary outcome was a composite of death, myocardial infarction, stroke, or non-coronary artery bypass graft (non-CABG)-related major bleeding at 30 days. Key secondary outcomes were death, myocardial infarction, or stroke; and non-CABG-related major bleeding at 30 days. A masked central committee adjudicated the primary outcome, components of the primary outcome, and stent thrombosis. All other outcomes were as reported by the investigators. Patients and investigators were not masked to treatment allocation. Analyses were by intention to treat. This trial is registered with ClinicalTrials.gov, NCT01014273.
FINDINGS:
Between June 6, 2006, and Nov 3, 2010, 7021 patients were enrolled from 158 hospitals in 32 countries. 3507 patients were randomly assigned to radial access and 3514 to femoral access. The primary outcome occurred in 128 (3·7%) of 3507 patients in the radial access groupcompared with 139 (4·0%) of 3514 in the femoral access group (hazard ratio [HR] 0·92, 95% CI 0·72-1·17; p=0·50). Of the six prespecified subgroups, there was a significant interaction for the primary outcome with benefit for radial access in highest tertile volume radial centres (HR 0·49, 95% CI 0·28-0·87; p=0·015) and in patients with ST-segment elevation myocardial infarction (0·60, 0·38-0·94; p=0·026). The rate of death, myocardial infarction, or stroke at 30 days was 112 (3·2%) of 3507 patients in the radial group compared with 114 (3·2%) of 3514 in the femoral group (HR 0·98, 95% CI 0·76-1·28; p=0·90). The rate of non-CABG-related major bleeding at 30 days was 24 (0·7%) of 3507 patients in the radial group compared with 33 (0·9%) of 3514 patients in the femoral group (HR 0·73, 95% CI 0·43-1·23; p=0·23). At 30 days, 42 of 3507 patients in the radial group had large haematoma compared with 106 of 3514 in the femoral group (HR 0·40, 95% CI 0·28-0·57; p<0·0001). Pseudoaneurysm needing closure occurred in seven of 3507 patients in the radial group compared with 23 of 3514 in the femoral group (HR 0·30, 95% CI 0·13-0·71; p=0·006).
INTERPRETATION:
Radial and femoral approaches are both safe and effective for PCI. However, the lower rate of local vascular complications may be a reason to use the radial approach.
- Generally, people are anticoagulated right before and during the procedure (to reduce clotting from balloon-mediated damage to the plaque, prevent immediate/acute rethrombosis)
- People are also anticoagulated after-- aspirin forever, plavix 30 days (BM stent in a stable patient) or 3-6 months (new drug eluting stents), or 12 months (old drug eluting stents, any stent in a patient experiencing acute MI)
- Such anticoagulation will cause all the typical anticoagulation bleeds (GI, access site, etc)
Wednesday, May 21, 2014
1. Dermatomyositis
- Proximal muscle weakness
- Heliotrope rash
- Gottron papules: red-purplish plaques on the dorsal hands, more prominent over the joints
- Anti-Jo-1 antibodies associated with increased risk of ILD
- ILD: can present with the onset of myopathy or develop over time; interstitial opacities on CXR, interstitial pneumonia on high-res CT. Don't need a lung bx for diagnosis, but may need to bronch to r/o infection
- Dermato and polymyositis have a slightly higher risk than other rheumatic diseases (1-2% risk) of developing PCP on combo immunosuppression (incl steroids). Presentation: acute onset of fever and respiratory failure.
- Polymyositis unlikely without proximal muscle weakness and elevated CK
2. Fibromyalgia:
- Diffuse pain on both sides of the body, above and below the waist, +/- tender points
- Often have fatigue and sleep disturbance, high rates of comorbid chronic fatigue syndrome, migraine, IBS, TMJ pain, pelvic pain.
3. ANA
- Can be elevated in general population, especially people with autoimmune thyroid disease or first-degree relatives of people with lupus.
- High titers do not necessarily indicate autoimmune disease.
4. Sjogen's
- Lymphocytic inflammation of lacrimal glands => no tears, keratoconjunctivitis sicca
- Lymphocytic inflammation of major/minor salivaary glands => xerostomia/salivary gland enlargement
- Can have many autoantibodies, including SSA/Ro or SSB/La but also ANA, RF, and hypergammaglobulinemia.
- Schirmer's test- stick a piece of filter paper in both eyes (after topical anaesthetic to prevent paper-irritation-induced tears) rely on capillary action to draw fluid into paper chromatography style. >15 mm in 5 minutes is normal, although in older adults (like the age group of sjogren's, 40-60s) about 1/3 may only be able to wet up to 10mm.
5. Polyarteritis nodosa
- Necrotizing inflammation of medium or small arteries
- Fever, msk symptoms, vasculitis
- Heart: affects coronaries, can cause HF 2/2 ischemia or HTN from renal effects
- Renal failure with proteinuria or hematuria. Kidneys are most common organ affected. Aneurysms in kidney can rupture spontaneously leading to perinephric hematomas, or they can be ruptured during attempted renal biopsy (so try to avoid biopsying the kidney). Generally you will see sub-nephrotic proteinuria and hematuria, but no red cell casts as there is no glomerular inflammation (only ischemia). If you see red cell casts, consider a different diagnosis like an ANCA+ GN or lupus.
- Nerves- mononeuritis multiplex-- affects up to 70% of people with PAN, polyneuropathy affecting named nerves like radial, ulnar, peroneal that starts asymmetric and expands to a confluent distal polyneuropathy
- GI: mesenteric angina picture, can worsen to the point of infarct and perforation
- Diagnose with sural nerve biopsy or kidney angiography
6. Wegener's - necrotizing vasculitis of upper/lower respiratory tract (alveolar hemorrhage, otitis media) and kidneys. Can cause arthritis and joint effusions of large and small joints. C-ANCA/antiproteinase 3 = 90% specific.
7. GCA- should initiate high dose steroids (1g/day or 100mg TID for 3 days) if suspected. Does not compromise results of temporal artery biopsy, recommend bx within 2 weeks (although positive results have been seen after 6 weeks). Bx yield higher when performed sooner.
8. ACS
- Stable angina: angina that occurs predictably with a certain degree of exertion, relieved by nitroglycerin or rest
- Unstable angina; angina at rest, no biomarkers
- NSTEMI: significant angina at rest (or acutely worsening/different angina), with biomarkers but no ST elevation on EKG
- STEMI: clinical presentation for acute MI + ST elevation on EKG
- Typically, to be concerned enough to send someone for cath, you want at least 2/3 warning signs: either convincing clinical history, biomarkers, or significant EKG changes
- PCI + stent has better 30-day mortality vs tPA, and is preferred in cardiogenic shock and those with a CI to tPA (ischemic stroke w/in 3 mos, hx of intracerebral hemorrhage, suspected aortic dissection, bleed). PCI/stent within 12 hours, <90 minutes best.
9. Pericarditis
- Diagnose with 2/3 of the following: pleuritic chest pain (worse with supination or inspiration), friction rub (triphasic: heard during atrial contraction, ventricular contraction, and rapid ventricular filling), diffuse ST-segment elevation and PR depression
- May radiate to shoulder
10. Angina without coronary disease: what is the cause?
- Proximal muscle weakness
- Heliotrope rash
- Gottron papules: red-purplish plaques on the dorsal hands, more prominent over the joints
- Anti-Jo-1 antibodies associated with increased risk of ILD
- ILD: can present with the onset of myopathy or develop over time; interstitial opacities on CXR, interstitial pneumonia on high-res CT. Don't need a lung bx for diagnosis, but may need to bronch to r/o infection
- Dermato and polymyositis have a slightly higher risk than other rheumatic diseases (1-2% risk) of developing PCP on combo immunosuppression (incl steroids). Presentation: acute onset of fever and respiratory failure.
- Polymyositis unlikely without proximal muscle weakness and elevated CK
2. Fibromyalgia:
- Diffuse pain on both sides of the body, above and below the waist, +/- tender points
- Often have fatigue and sleep disturbance, high rates of comorbid chronic fatigue syndrome, migraine, IBS, TMJ pain, pelvic pain.
3. ANA
- Can be elevated in general population, especially people with autoimmune thyroid disease or first-degree relatives of people with lupus.
- High titers do not necessarily indicate autoimmune disease.
4. Sjogen's
- Lymphocytic inflammation of lacrimal glands => no tears, keratoconjunctivitis sicca
- Lymphocytic inflammation of major/minor salivaary glands => xerostomia/salivary gland enlargement
- Can have many autoantibodies, including SSA/Ro or SSB/La but also ANA, RF, and hypergammaglobulinemia.
- Schirmer's test- stick a piece of filter paper in both eyes (after topical anaesthetic to prevent paper-irritation-induced tears) rely on capillary action to draw fluid into paper chromatography style. >15 mm in 5 minutes is normal, although in older adults (like the age group of sjogren's, 40-60s) about 1/3 may only be able to wet up to 10mm.
5. Polyarteritis nodosa
- Necrotizing inflammation of medium or small arteries
- Fever, msk symptoms, vasculitis
- Heart: affects coronaries, can cause HF 2/2 ischemia or HTN from renal effects
- Renal failure with proteinuria or hematuria. Kidneys are most common organ affected. Aneurysms in kidney can rupture spontaneously leading to perinephric hematomas, or they can be ruptured during attempted renal biopsy (so try to avoid biopsying the kidney). Generally you will see sub-nephrotic proteinuria and hematuria, but no red cell casts as there is no glomerular inflammation (only ischemia). If you see red cell casts, consider a different diagnosis like an ANCA+ GN or lupus.
- Nerves- mononeuritis multiplex-- affects up to 70% of people with PAN, polyneuropathy affecting named nerves like radial, ulnar, peroneal that starts asymmetric and expands to a confluent distal polyneuropathy
- GI: mesenteric angina picture, can worsen to the point of infarct and perforation
- Diagnose with sural nerve biopsy or kidney angiography
6. Wegener's - necrotizing vasculitis of upper/lower respiratory tract (alveolar hemorrhage, otitis media) and kidneys. Can cause arthritis and joint effusions of large and small joints. C-ANCA/antiproteinase 3 = 90% specific.
7. GCA- should initiate high dose steroids (1g/day or 100mg TID for 3 days) if suspected. Does not compromise results of temporal artery biopsy, recommend bx within 2 weeks (although positive results have been seen after 6 weeks). Bx yield higher when performed sooner.
8. ACS
- Stable angina: angina that occurs predictably with a certain degree of exertion, relieved by nitroglycerin or rest
- Unstable angina; angina at rest, no biomarkers
- NSTEMI: significant angina at rest (or acutely worsening/different angina), with biomarkers but no ST elevation on EKG
- STEMI: clinical presentation for acute MI + ST elevation on EKG
- Typically, to be concerned enough to send someone for cath, you want at least 2/3 warning signs: either convincing clinical history, biomarkers, or significant EKG changes
- PCI + stent has better 30-day mortality vs tPA, and is preferred in cardiogenic shock and those with a CI to tPA (ischemic stroke w/in 3 mos, hx of intracerebral hemorrhage, suspected aortic dissection, bleed). PCI/stent within 12 hours, <90 minutes best.
9. Pericarditis
- Diagnose with 2/3 of the following: pleuritic chest pain (worse with supination or inspiration), friction rub (triphasic: heard during atrial contraction, ventricular contraction, and rapid ventricular filling), diffuse ST-segment elevation and PR depression
- May radiate to shoulder
10. Angina without coronary disease: what is the cause?
Int J Cardiol. 2013 Jul 15;167(1):168-73. doi: 10.1016/j.ijcard.2011.12.053. Epub 2012 Jan 10.
Invasive findings in patients with angina equivalent symptoms but no coronary artery disease; results from the heart quest cohort study.
BACKGROUND:
The cause of angina in patients presenting at coronary angiography without significant coronary artery disease (CAD) has not been systematically assessed in a large prospective cohort. This study is aimed to identify the cause of angina in these patients.
METHODS:
This prospective cohort comprised 718 consecutive patients with angina equivalent symptoms and no CAD (defined as no coronary stenosis ≥ 50%) between January 1st 1997 and July 31st 2008. All patients underwent additional invasive testing (intracoronary acetylcholine administration, fast atrial pacing). Small vessel and vasospastic diseases were diagnosed according to symptoms and vessel reaction during testing.
RESULTS:
Mean age was 56.3 ± 11.0 years (range 15 to 81 years). A majority of 431 patients (60.0%) had small vessel and/or vasospastic disease (233 patients had small vessel disease, 145 vasospastic disease and 53 a combination of both). Additional 87 patients (12.1%) had another cardiac disease. Only in a minority of 200 study participants (27.9%) that the symptoms were attributed to an extracardiac problem. Patients with small vessel disease were more likely to be female, to have hypertension, to have a family history of CAD and to have effort-related symptoms. Patients with vasospastic disease were more likely to be current smokers, to have angina at rest or to present as myocardial infarction, and to have coronary sclerosis and/or endothelial dysfunction.
CONCLUSIONS:
In a majority of patients with angina but no significant CAD, a cardiac cause of their symptoms can be found. Systematical invasive testing may help optimizing the medical management of these patients.
Tuesday, May 20, 2014
1. Diagnosis of RA:
- Cardinal - marginal erosions/joint space narrowing. Seen within 2-3 months of onset, often present by 6 months.
(source)
- Cardinal - marginal erosions/joint space narrowing. Seen within 2-3 months of onset, often present by 6 months.
(source)
- CBC may show mild leukocytosis, thrmobocytosis, mild anemia (i.e. chronic disease type)
- ESR or CRP may be elevated
- RF is positive in 75% of people with RA, can be as low as 50% early in the disease. Can also be elevated in chronic active Hep C and with Parvo B19
- RA is more common in the first 3 months postpartum
- Severe long standing RA may lead to interstitial pneumonitis (esp in men), often appears 5+ years after diagnosis.
2. Steroids interfere with TSH release and can decrease secretion of thyroid binding globulin.
3. Treatment of RA
- Start DMARDs as soon as possible (early DMARD has better outcomes than starting with NSAID +/- steroids and then initiating DMARDs later)
- Mildly active RA: start either hydroxychloroquine or sulfasalazine
- Moderate to severely active RA: start methotrexate plus either NSAID or steroid.
- Can add TNF-a inhibitor if DMARD is not enough, however there is not currently evidence that a TNF-a inhibitor alone is an effective management strategy for RA.
- Methotrexate is contraindicated in people who regularly drink as it alcohol increases the risk of mtx-induced hepatotoxicity
4. HIV associated psoriatic arthritis:
- CD4<200 can predispose to psoriasis and other skin conditions-- photodermatitis, prurigo nodularis, mollsucum, drug reactions
- 20-40% of those with psoriasis will develop arthritis
- Suspect in someone with explosive onset, widespread psoriasis with dactylitis, significant DIP joint involvement, asymmetric joint involvement, enthesitis, joint ankylosis.
5. Whipple disease:
- Trophyeryma whippelii
- Arthritis, diarrhea, malabsorption, CNS and constitutional symptoms (i.e. skin findings)
- Arthritis is migratory and chronic
6. Uveitis
- Anterior: seronegative spondyloarthropathies (esp unilateral presentation that fluctuates between the 2 eyes over time), lupus, sarcoid, vasculidities, whipple disease
- Posterior: sarcoid, vasculidites
7. Diagnose ankylosing spondylitis with MRI (need radiographic evidence of sacroilitis to make the diagnosis)
8. Scleroderma
- Anti topoisomerase I aka anti scl-70 is seen in ~50% of people with diffuse systemic sclerosis and predicts development of ILD. Diffuse systemic sclerosis tends to have skin thickening proximal to the elbows and knees. Can affect face.
- Anti centromere antibody is associated with limited cutaneous systemic sclerosis aka CREST syndrome (calcinosis, raynaud's, esophageal dysmotility, scelerodactyly, teleangiectasias), skin thickening distal to the elbows and knees, can affect face.
9. Infliximab
- Often causes development of antibodies: ANA, anti-sm, anti-dsDNA
- Rarely causes drug-induced lupus. If it does, stop it and start prednisone. Consider adding hydroxychloroquine as well
- Drug induced lupus has mostly cutaenous and pleuropericardial involvement-- rarely CNS or renal.
10. Lupus
- ACE inhibitors are first-line for control of hypertension in lupus nephritis patients as it helps reduce proteinuria.
- Rash triggered by UV-A and UV-B (so rash that appears after outdoors trip etc), erythematous plaques with fine scale that spares the nasolabial folds (vs rosacea, which involves nasolabial folds and has more of a pustular acneiform appearance and doesn't have any systemic symptoms)
- Usually have anemia, leukopenia or lymphopenia
- Can cause elevated ANA in first degree family members (!)
Monday, May 19, 2014
1. Pleural effusions
- Need 150 cc to see on CXR, need 5-10 cc to see on chest CT
- Pleural fluid pseudotumors more common in pleural effusion assoc with CHF
2. Factors that make an incidentally found solitary pulmonary nodule more likely to be malignant
- Size (>1 cm more likely to be malignant)
- Edge (spiculated/stellate more likely malignant)
- Presence and pattern of calcification
- Growth/change from prior images
- Clinical factors (history of lung fibrosis, asbestosis, etc.)
- Age (> 40 more likely malignant)
- Smoking hx
- Travel history and history of living in areas where granulomatous disease is endemic (over 40% of people have nodules in some endemic histoplasmosis regions)
- History of other malignant diseases (mets?)
3. PET scans
- Pt must be fasting for 6 hours beforehand, and no glucose-- no dextrose in saline, no dextrose-saline in riders, no steroids, diabetics must be carefully titrated with insulin to the correct levels
- Some tumors can produce false negatives (esp benign lesions like hamartomas and carcinoids)
- Some tissue can produce false positives-- like moving muscle, so patients must be very still
- 95% sensitive, 85% specific for evaluating solitary lung nodules
4. Pneumonectomy
- Post op, the entire hemithorax with the removed lung will gradually fill with fluid
- Decrease in the fluid is usually bad, as it means that the fluid is either leaking out through the surgical wound in the chest or leaking into the airway through the residual bronchial stump
5. FOBT
- Screening test
- False positives can be caused by recent ingestion of red meat (Hb in meat will light up the test), trauma during rectal exam. Thus patient should not be eating red meat before the test
- If someone is going to be admitted for GI bleed, it should be significant-- ie visible on the glove as either red or black. If blood is not grossly visible, the bleed is not serious enough to require admission. Thus don't do an FOBT in the ER
6. Melena
- Is midnight black, tarry/sticky, and has a strange/bad odor different from typical stool
- Not just dark, otherwise normal appearing stool.
- Things that can cause dark-appearing stool: pepto bismol, milk of magnesia, iron supplements
7. Phosphodiesterase inhibitors
- Nonselective: caffeine, theophylline, IBMX
- PDE 3 inhibitors: milrinone, cilastazol, imarinone, enoximone. These guys are used as vasodilators (milrinone in pHTN and s/p cardiac surgery to lower afterload and increase contractility, cilastazol in PAD and SAH vasospasm)
- PDE 4 inhibitors: rolipram, ibudilast, roflumilast
*PDE4 is in immune cells, so PDE4-I are often used as anti-inflammatories esp in people with inflammatory lung diseases (asthma, copd)
- PDE 5 inhibitors: dipyridamole aka persantine, all the viagra-type drugs (sildenafil, tardalafil, etc)
- PDE 10 inhibitors: papaverine (opium alkaloid antispasmotic). Treats GI/ureter spasm, can induce vasospasm in coronary and cerebral vessels (use in SAH, angina). Can be directly applied to blood vessels in microsurgery
- Also, forskolin is an Adenylyl cyclase activator.
8. Prinzmetal's angina
- Tends to occur at the same time every day
- Diagnosed clinically but can also be diagnosed with ergonovine infusion in cath lab
- Tx with calcium channel blockers
9. Cardiology Potpourri:
- ACE inhibitors increase serum K (via decreased aldosterone secretion). {Detailed explanation of mechanism}
- In older adults with sinus bradycardia, it's better to do atrial pacing only rather than AV pacing; there is much less risk of a-fib.
- In the US, people who need ventricular pacing will usually get AV pacing, because people who just get V pacing get pacemaker syndrome (loss of A-V synchrony, loss of atrial kick contribution to ventricular filling, decreased cardiac output). {more on pacemaker syndrome}
- Indications for inpatient admission for CABG: unstable acute coronary syndrome, cardiogenic shock requiring balloon bump bridge to CABG. If someone is stable, they can just come in the AM of the procedure and go to the CT surg service, no need to be admitted the night before to cards.
- Causes of PVCs: electrolyte abnormalities, ischemia, ventricular ectopy -- treat this when people are symptomatic (i.e. syncopizing) with b-blockers, ca-channel blockers, ablation.
10. Bradycardia
- If it's regular, and you don't see p-waves: junctional rhythm, Afib + complete block, dig toxicity
- If you don't see P-waves, it's not a cut-and-dry AV nodal block, which will always present with p-waves (without a-fib)
- Sinus brady can be caused by beta-blocker or ca-channel blocker toxicity; treat with glucagon 1mg which is a chronotrope that acts directly on the cardiac myocardium, bypassing the entire sympathetic pathway.
- Other common causes: hypothyroidism, increased vagal tone, anorexia, sick sinus syndrome, hypothermia.
- Extensive differential
- Need 150 cc to see on CXR, need 5-10 cc to see on chest CT
- Pleural fluid pseudotumors more common in pleural effusion assoc with CHF
2. Factors that make an incidentally found solitary pulmonary nodule more likely to be malignant
- Size (>1 cm more likely to be malignant)
- Edge (spiculated/stellate more likely malignant)
- Presence and pattern of calcification
- Growth/change from prior images
- Clinical factors (history of lung fibrosis, asbestosis, etc.)
- Age (> 40 more likely malignant)
- Smoking hx
- Travel history and history of living in areas where granulomatous disease is endemic (over 40% of people have nodules in some endemic histoplasmosis regions)
- History of other malignant diseases (mets?)
3. PET scans
- Pt must be fasting for 6 hours beforehand, and no glucose-- no dextrose in saline, no dextrose-saline in riders, no steroids, diabetics must be carefully titrated with insulin to the correct levels
- Some tumors can produce false negatives (esp benign lesions like hamartomas and carcinoids)
- Some tissue can produce false positives-- like moving muscle, so patients must be very still
- 95% sensitive, 85% specific for evaluating solitary lung nodules
4. Pneumonectomy
- Post op, the entire hemithorax with the removed lung will gradually fill with fluid
- Decrease in the fluid is usually bad, as it means that the fluid is either leaking out through the surgical wound in the chest or leaking into the airway through the residual bronchial stump
5. FOBT
- Screening test
- False positives can be caused by recent ingestion of red meat (Hb in meat will light up the test), trauma during rectal exam. Thus patient should not be eating red meat before the test
- If someone is going to be admitted for GI bleed, it should be significant-- ie visible on the glove as either red or black. If blood is not grossly visible, the bleed is not serious enough to require admission. Thus don't do an FOBT in the ER
6. Melena
- Is midnight black, tarry/sticky, and has a strange/bad odor different from typical stool
- Not just dark, otherwise normal appearing stool.
- Things that can cause dark-appearing stool: pepto bismol, milk of magnesia, iron supplements
7. Phosphodiesterase inhibitors
- Nonselective: caffeine, theophylline, IBMX
- PDE 3 inhibitors: milrinone, cilastazol, imarinone, enoximone. These guys are used as vasodilators (milrinone in pHTN and s/p cardiac surgery to lower afterload and increase contractility, cilastazol in PAD and SAH vasospasm)
- PDE 4 inhibitors: rolipram, ibudilast, roflumilast
*PDE4 is in immune cells, so PDE4-I are often used as anti-inflammatories esp in people with inflammatory lung diseases (asthma, copd)
- PDE 5 inhibitors: dipyridamole aka persantine, all the viagra-type drugs (sildenafil, tardalafil, etc)
- PDE 10 inhibitors: papaverine (opium alkaloid antispasmotic). Treats GI/ureter spasm, can induce vasospasm in coronary and cerebral vessels (use in SAH, angina). Can be directly applied to blood vessels in microsurgery
- Also, forskolin is an Adenylyl cyclase activator.
8. Prinzmetal's angina
- Tends to occur at the same time every day
- Diagnosed clinically but can also be diagnosed with ergonovine infusion in cath lab
- Tx with calcium channel blockers
9. Cardiology Potpourri:
- ACE inhibitors increase serum K (via decreased aldosterone secretion). {Detailed explanation of mechanism}
- In older adults with sinus bradycardia, it's better to do atrial pacing only rather than AV pacing; there is much less risk of a-fib.
- In the US, people who need ventricular pacing will usually get AV pacing, because people who just get V pacing get pacemaker syndrome (loss of A-V synchrony, loss of atrial kick contribution to ventricular filling, decreased cardiac output). {more on pacemaker syndrome}
- Indications for inpatient admission for CABG: unstable acute coronary syndrome, cardiogenic shock requiring balloon bump bridge to CABG. If someone is stable, they can just come in the AM of the procedure and go to the CT surg service, no need to be admitted the night before to cards.
- Causes of PVCs: electrolyte abnormalities, ischemia, ventricular ectopy -- treat this when people are symptomatic (i.e. syncopizing) with b-blockers, ca-channel blockers, ablation.
10. Bradycardia
- If it's regular, and you don't see p-waves: junctional rhythm, Afib + complete block, dig toxicity
- If you don't see P-waves, it's not a cut-and-dry AV nodal block, which will always present with p-waves (without a-fib)
- Sinus brady can be caused by beta-blocker or ca-channel blocker toxicity; treat with glucagon 1mg which is a chronotrope that acts directly on the cardiac myocardium, bypassing the entire sympathetic pathway.
- Other common causes: hypothyroidism, increased vagal tone, anorexia, sick sinus syndrome, hypothermia.
- Extensive differential
Sunday, May 18, 2014
1. Gilbert's- Tbili will often be <3, with direct bili <0.3
Acute cholecystitis- Tbili usually <2 (cholangitis may be higher)
2. Pancreatitis:
- Parental nutrition (esp PPN) has super high infection rate. Enteral feeding if at all possible.
- Antibiotics only indicated with necrotic pancreatitis (IV contrast CT-- pancreatic tissue that doesn't enhance is necrotic)
3. Manage erosive esophagitis (thought to be 2/2 GERD) with PPI
4. Indications for endoscopy in someone with dyspepsia (i.e. "alarm signs")
- Weight loss
- Dysphagia
- Odynophagia
- Unexplained iron deficiency anemia
- Jaundice
- Age over 55 (because incidence of gastric cancer is higher)
5. Differential for multiple nodular opacities concentrated in the upper lobes on CXR
- Granulomatous infection (TB, histo, blasto)
- Localized bronchiectasis with mucous plugging (tubes can look like nodules if shot at obliquely) - ABPA, which occurs in asthmatics. CF tends to produce more distributed bronchiectasis and is an unlikely diagnosis in an older person
- Much less likely - cancer. Metastatic disease tends to be more evenly distributed and if anything concentrates in the lower lobes as there is more blood flow, and it would be unusual to have dozens of primaries.
6. Critical care learning:
http://www.aic.cuhk.edu.hk/web8/Renal.htm
7. Screening for hepatocellular carcinoma
- Abdominal u/s + aFP > 500 is diagnostic without a biopsy
- You can develop HCC in hep B without cirrhosis.
8. Primary Biliary Cirrhosis
- Occurs predominantly in women (80-90%), typically aged 40-60
- Diagnostic triad: cholestatic liver profile, +Antimitochondria antibody, liver bx
- Alk phos is often 10x normal
- Normal alk phos and negative antimitochondria ab => look for a different disease.
9. Microscopic colitis:
- Older people
- Nonbloody diarrhea
- Macroscopically normal
- Histology shows either increased intraepithelial lymphocytes (lymphocytic colitis) or increased submucosal collagen layer (collagenous colitis)
- Typical onset is 60s for collagenous, 70s for lymphocytic. Affects women more than men
10. Crohn's disease in the small bowel can present as non-bloody diarrhea.
Acute cholecystitis- Tbili usually <2 (cholangitis may be higher)
2. Pancreatitis:
- Parental nutrition (esp PPN) has super high infection rate. Enteral feeding if at all possible.
- Antibiotics only indicated with necrotic pancreatitis (IV contrast CT-- pancreatic tissue that doesn't enhance is necrotic)
3. Manage erosive esophagitis (thought to be 2/2 GERD) with PPI
4. Indications for endoscopy in someone with dyspepsia (i.e. "alarm signs")
- Weight loss
- Dysphagia
- Odynophagia
- Unexplained iron deficiency anemia
- Jaundice
- Age over 55 (because incidence of gastric cancer is higher)
5. Differential for multiple nodular opacities concentrated in the upper lobes on CXR
- Granulomatous infection (TB, histo, blasto)
- Localized bronchiectasis with mucous plugging (tubes can look like nodules if shot at obliquely) - ABPA, which occurs in asthmatics. CF tends to produce more distributed bronchiectasis and is an unlikely diagnosis in an older person
- Much less likely - cancer. Metastatic disease tends to be more evenly distributed and if anything concentrates in the lower lobes as there is more blood flow, and it would be unusual to have dozens of primaries.
6. Critical care learning:
http://www.aic.cuhk.edu.hk/web8/Renal.htm
7. Screening for hepatocellular carcinoma
- Abdominal u/s + aFP > 500 is diagnostic without a biopsy
- You can develop HCC in hep B without cirrhosis.
8. Primary Biliary Cirrhosis
- Occurs predominantly in women (80-90%), typically aged 40-60
- Diagnostic triad: cholestatic liver profile, +Antimitochondria antibody, liver bx
- Alk phos is often 10x normal
- Normal alk phos and negative antimitochondria ab => look for a different disease.
9. Microscopic colitis:
- Older people
- Nonbloody diarrhea
- Macroscopically normal
- Histology shows either increased intraepithelial lymphocytes (lymphocytic colitis) or increased submucosal collagen layer (collagenous colitis)
- Typical onset is 60s for collagenous, 70s for lymphocytic. Affects women more than men
10. Crohn's disease in the small bowel can present as non-bloody diarrhea.
Friday, May 16, 2014
1. Adult Heparin gtt protocol: Initiation
- DO NOT START heparin for 24 hours after a patient gets tPA for an ischemic stroke.
- Baseline labs: PT, PTT, CBC, BMP (within 24 h of initiating therapy)
- Discontinue: other anticoagulants, aspirin > 162 mg, IM injections
2. Adult heparin gtt protocol: exclusion criteria
- Epidural catheter
- Platelets <50, PTT higher than whatever your goal PTT would be
- TTP, HIT (Not DIC - you can treat thrombotic DIC with heparin actually)
- High bleeding risk or current bleed
3. Dosing of heparin depends on body weight and indication. See chart:
4. Titration and monitoring of Heparin depends on goal PTT. Below is a sample titration algorithm:
- DO NOT START heparin for 24 hours after a patient gets tPA for an ischemic stroke.
- Baseline labs: PT, PTT, CBC, BMP (within 24 h of initiating therapy)
- Discontinue: other anticoagulants, aspirin > 162 mg, IM injections
2. Adult heparin gtt protocol: exclusion criteria
- Epidural catheter
- Platelets <50, PTT higher than whatever your goal PTT would be
- TTP, HIT (Not DIC - you can treat thrombotic DIC with heparin actually)
- High bleeding risk or current bleed
3. Dosing of heparin depends on body weight and indication. See chart:
5. Heparin titration patterns for other goal PTTs, depending on bleed risk:
6. Bridging to warfarin:
- Need to overlap 5 days AND have INR to goal
- Can start warfarin the same time you start heparin for most people
7. Goal INR and duration of anticoagulation depending on indication:
- A-fib, stroke, antiphospholipid syndrome, mechanical aortic valve: INR 2-3, FOREVER
- Antiphospholipid syndrome with multiple clots through anticoagulation, mechanical mitral valve: INR 2.5-3.5 forever
- Bioprosthetic heart valve: INR 2-3, 3 months.
- First time DVT or PE provoked by time-limited risk factors (surgery, temporary immobilization, trauma, estrogen use) - INR 2-3 for 3 months, then stop.
- First time DVT/PE that is unprovoked, INR 2-3 for 3 months, then reassess bleed risk-- if their bleed risk is high, stop; if their bleed risk is low, continue forever.
- Multiple DVT/PE: INR 2-3 for the rest of their life.
- All the above refer to proximal DVTs-- distal DVTs just get 3 months of therapy then stop.
8. Lovenox & heparin & antithrombin
- Both lovenox and heparin are able to bind Antithrombin, and antithrombin is capable of inhibiting thrombin (factor II) AND factor Xa. Heparin binding will accelerate activity of antithrombin against factor II/Xa by a factor of 1000.
- However lovenox, because of its shorter tail, is only able to accelerate the activity antithrombin against factor Xa. So it's much more of a Xa inhibitor than a factor II inhibitor.
- So you can check levels of both heparin and lovenox with anti-Xa levels.
9. Pharmacokinetics:
- Lovenox: Half life 3-6 hours after subQ injection.
- Lovenox: Anti-Xa levels peak 3-5 hours after dosing.
- Lovenox renally cleared, standard dose 40 for GFR>60, 30 for GFR 30-60, <30, pick a different anticoagulant, or be careful.
- Heparin: half life depends on dose! Clearance is a combination of a fast (saturable) non-linear mechanism and a slow, first-order (non-saturable) mechanism. The fast phase -- binding to endothelial cells and macrophages, where it is depolymerized. The slow phase is renal. At IV doses of <25 U/kg (i.e. when we'll almost always be using it) it's mostly degraded through the fast mechanism, and the apparent half life is 30 minutes. At IV doses of 100 U/kg, the apparent half life is 60 minutes, and at IV doses of 400 U/kg, the apparent half life increases to 150 minutes. {source: Circulation}
10. More data for heparin dosing depending on indication: {source}
- DVT/PE prophy: 5000 U sq TID
- DVT/PE tx: 80 u/kg bolus, 18 u/kg/hr drip
- Catheter patency aka Heparin lock IV: 100units/mL, enough fluid to fill lumen
- STEMI: 60 u/kg bolus (max 4000), 12 u/kg/hr drip (max 1000). goal PTT 50-70
- NSTEMI/unstable angina: 60-70 u/kg bolus (max 5000), 12-15 u/kg/hr (max 1000), goal PTT 50-70.
Thursday, May 15, 2014
1. DNA synthesis inhibitors
- Fluroquinolones: No matter what the lab susceptibility says, these drugs have NO clinically significant MRSA coverage. In fact, they make it worse-- they increase MRSA colonization because they kill off everything that isn't staph, and encourage the development of resistant strains. Cipro and levo typically cover pseudomonas, while moxi does not.
- Metronidazole: lead to DNA fragmentation
- Rifampin: has terrible, awful, horrendous drug-drug interaction. Ridiculous CYP inducer. On warfarin 7.5? Add rifampin, and you'll need 25. Outside of TB, used as a supplement/combination antibiotic with an anti-staph agent for MRSA to improve penetration -- useful in cases like osteomyelitis with hardware. Also turns all your bodily fluids orange.
2. Antibiotics that target the cell membrane:
- Colistin aka Polymyxin E. Super, super toxic as the difference between prokaryotic and eukaryotic cell membranes are not that different. Very nephrotoxic. Generally used as an inhaled neb against pseudomonas; it shouldn't have much systemic absorption (just like inhaled steroids don't have much systemic absorption) unless your lungs are really crappy.
- Polymyxin B: Useful against MDR gram negs, very similar to colistin
3. PO anti-MRSA agents:
- Doxy
- Clinda (sorta bad)
- Bactrim
- Linezolid
4. Agents that cover atypicals
- Macrolides
- Tetracycline
- Flouroquinolones
- Chloramphenicol
5. Major risk factors for pancreatic cancer:
- First degree relative with panc cancer
- Hereditary pancreatitis
- Germline mutations (BRCA1, BRCA2, Peutz-Jeghers)
- Cigarettes - most significant environmental risk factor. Dose-dependent; heavy smokers have 2-3x the risk of nonsmokers.
- Obesity, inactivity
- Nonhereditary chronic pancreatitis
- AdenoCA most common histology; overall pancreatic cancer typically occurs after 45, more common in men and AA pateints.
6. Inferior MI
- After an inferior MI, you expect hypotension. There should be compensatory tachycardia; if not, suspect concomitant SA node ischemia.
- After a R sided MI, people need tons of fluids to maintain the preload to the LV. Do not give diuretics or nitroglycerin, as you need all the pre-load you can get (LV infarct its a good idea, it pulls fluid off the R side and lungs)
- Expect +JVD and +Kussmaul's sign: increase in JVD with inspiration.
7. Stevens-Johnson syndrome:
- Aka erythema multiforme major.
- Immune complex mediated hypersensitivity
- Drugs that commonly trigger: NSAIDs, sulfonamides, phenytoin.
- Presentation: sudden onset mucocutaneous target-shaped lesions on 2 sites (usually oral/conjunctival).
- Associated symptoms: fever, tachycardia, hypotension, altered mental status, conjunctivitis, seizures, coma.
- Supportive treatment--fluids, pain control.
- VS erythema multiforme minor, which is part of the same spectrum as SJS: sudden onset erythematous rash, target lesions, occurs after herpes simplex infection. Generally doesn't involve mucosal surfaces, systemic sx less severe.
8. DI
- Central: causes- idopathic, trauma, pituitary surgery, ischemia. If the thirst mechanism is impaired, serum Na can be > 150
- Nephrogenic causes: chronic Li use, hypercalcemia, AVPR2 mutations. Serum Na usu <150 due to intact thirst mechanism.
9. Acute acalculous cholecystitis: acute inflammation of GB without gallstones. Common in hospitalized patients with the following:
- Extensive burns
- Severe trauma
- Prolonged TPN
- Prolonged fasting
- Mechanical ventilation
Pathophys: local/general ischemia, biliary stasis, infection, external compression.
10. Someone who presents with new a-fib, think PE, not MI. Afib is commonly associated with PE but rarely with MI.
- Fluroquinolones: No matter what the lab susceptibility says, these drugs have NO clinically significant MRSA coverage. In fact, they make it worse-- they increase MRSA colonization because they kill off everything that isn't staph, and encourage the development of resistant strains. Cipro and levo typically cover pseudomonas, while moxi does not.
- Metronidazole: lead to DNA fragmentation
- Rifampin: has terrible, awful, horrendous drug-drug interaction. Ridiculous CYP inducer. On warfarin 7.5? Add rifampin, and you'll need 25. Outside of TB, used as a supplement/combination antibiotic with an anti-staph agent for MRSA to improve penetration -- useful in cases like osteomyelitis with hardware. Also turns all your bodily fluids orange.
2. Antibiotics that target the cell membrane:
- Colistin aka Polymyxin E. Super, super toxic as the difference between prokaryotic and eukaryotic cell membranes are not that different. Very nephrotoxic. Generally used as an inhaled neb against pseudomonas; it shouldn't have much systemic absorption (just like inhaled steroids don't have much systemic absorption) unless your lungs are really crappy.
- Polymyxin B: Useful against MDR gram negs, very similar to colistin
3. PO anti-MRSA agents:
- Doxy
- Clinda (sorta bad)
- Bactrim
- Linezolid
4. Agents that cover atypicals
- Macrolides
- Tetracycline
- Flouroquinolones
- Chloramphenicol
5. Major risk factors for pancreatic cancer:
- First degree relative with panc cancer
- Hereditary pancreatitis
- Germline mutations (BRCA1, BRCA2, Peutz-Jeghers)
- Cigarettes - most significant environmental risk factor. Dose-dependent; heavy smokers have 2-3x the risk of nonsmokers.
- Obesity, inactivity
- Nonhereditary chronic pancreatitis
- AdenoCA most common histology; overall pancreatic cancer typically occurs after 45, more common in men and AA pateints.
6. Inferior MI
- After an inferior MI, you expect hypotension. There should be compensatory tachycardia; if not, suspect concomitant SA node ischemia.
- After a R sided MI, people need tons of fluids to maintain the preload to the LV. Do not give diuretics or nitroglycerin, as you need all the pre-load you can get (LV infarct its a good idea, it pulls fluid off the R side and lungs)
- Expect +JVD and +Kussmaul's sign: increase in JVD with inspiration.
7. Stevens-Johnson syndrome:
- Aka erythema multiforme major.
- Immune complex mediated hypersensitivity
- Drugs that commonly trigger: NSAIDs, sulfonamides, phenytoin.
- Presentation: sudden onset mucocutaneous target-shaped lesions on 2 sites (usually oral/conjunctival).
- Associated symptoms: fever, tachycardia, hypotension, altered mental status, conjunctivitis, seizures, coma.
- Supportive treatment--fluids, pain control.
- VS erythema multiforme minor, which is part of the same spectrum as SJS: sudden onset erythematous rash, target lesions, occurs after herpes simplex infection. Generally doesn't involve mucosal surfaces, systemic sx less severe.
8. DI
- Central: causes- idopathic, trauma, pituitary surgery, ischemia. If the thirst mechanism is impaired, serum Na can be > 150
- Nephrogenic causes: chronic Li use, hypercalcemia, AVPR2 mutations. Serum Na usu <150 due to intact thirst mechanism.
9. Acute acalculous cholecystitis: acute inflammation of GB without gallstones. Common in hospitalized patients with the following:
- Extensive burns
- Severe trauma
- Prolonged TPN
- Prolonged fasting
- Mechanical ventilation
Pathophys: local/general ischemia, biliary stasis, infection, external compression.
10. Someone who presents with new a-fib, think PE, not MI. Afib is commonly associated with PE but rarely with MI.
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