1. BNP 
- Things that elevate: female sex, old age, renal failure
- Things that depress: obesity
- BNP < 100 = unlikely to have acute HF
2. Coronary artery calcification score: not indicated in routine testing, but helpful to risk-stratify people with intermediate 10-year risk of CAD (10-20% risk) into less vs more aggressive medical management.
3. Cryptogenic organizing pneumonia: 
- Symptoms suggestive of lower respiratory tract infection (dyspnea, cough, fever, chills, night sweats, weight loss)
- Acute to subacute course (weeks to months) vs IPF tends to be slower
- Alveolar opacities on CXR (vs interstitial reticulnodular pattern for IPF)
- CXR findings can migrate -- involving different lung fields on different exams.
4. Asbestosis
- Clinically like IPF
- PFTs with restrictive picture (and decreased DLCO) -- sarcoid looks similar
- History with exposure lasting at least 10-15 years
- CXR with calcified pleural plaques,
5. Lung disease and eosinophilia: 
- Acute eosinophilic pneumonitis: acute course (days to 3 weeks), fever, sputum, eosinophilia, peripherally distributed infiltrate
- Drug-induced lung toxicity: subacute course (months), hypersensitivity clinical picture (low grade fever, cough, fatigue). +/- eosinophilia
6. DVT prophylaxis and renal function
- Heparin: no adjustment
- Lovenox: Dose reduction and/or interval prolongation for GFR <30
- Fonda: contraindicated if GFR<30
7. Polymyalgia rheumatica
- Get symptom control with low dose steroids (10-20mg) and then taper downwards. If you get a flare, then increase steroids to the minimum amount needed to control symptoms again, and then taper more slowly. If you fail tapering multiple times, add a steroid sparing agent (methotrexate)
- Goal is symptom control with the lowest possible steroid dose
- Infliximab has not been shown to be effective in PMR
8. Colchicine in acute gout: If given in first 24 hours, can abort an attack. Administer at first sign of attack 2-3 times a day until the patient experiences symptomatic relief, develops GI toxicity, or hits the maximum dose (6mg/attack)
9. Maintenance therapy for gout
- Indicated in people with recurrent attacks (>2), tophi or kidney stones, and decreasing time between attacks
- Goal to lower serum uric acid <6, because at that point urate crystals are reabsorbed
- Stop drugs that cause uric acid retention like salicylates and thiazides
- Low dose colchicine or NSAID (like indomethacin) prevent attacks but don't lower uric acid
- Apply low dose steroids (10mg), colchicine, or NSAID 1 week before beginnng/changing uric acid lowering therapy to prevent triggering acute attack
10. Osteoarthritis
- Diagnosed with knee pain + 3 of the following: Age > 50, morning stiffness < 30 mins (>1 hr think RA), crepitus, bony enlargement, bony tenderness, no warmth
- Osteoarthritis in someone with CPPD = pseudoosteoarthritis. Treated the same way as OA (PT/OT, pain control, joint replacement)
- First NSAIDs, then joint steroid injections.
Hand x-ray findings in various kinds of arthritis: {source in BMJ-- excellent review of literature presenting evidence-based recommendations for diagnosis of hand OA}

1. Polyradiculoneuropathies 
- Diagnose with CSF
- West nile
- Guillian Barre
- HIV
- CMV
- Carinomatous or lymphomatous nerve root invasion
2. Guillian Barre
- CSF: nl cell count, elevated protein
- Symptoms peak 4 weeks after onset
- Treat with IVIg and plasma exchange-- both equally efficacious
3. Likelihood ratios of 2, 5 and 10 increase probability of having a disease by 15, 30, and 45% respectively.
4. Indication for live influenza virus: 
- Age 5 to 49
- No chronic diseases
- Not immunosuppressed (incl chemo/rad/steroids/TNF-a drugs)
- Not living with an immunosuppressed person
- Not pregnant
- Doesn't have active, untreated TB
5. Zoster vaccine
- Indicated in anyone over 60
- Reduces incidence of zoster by 51% and of postherpetic neuralgia by 67%
- More effective in reducing disease in people aged 60-69, but reduces postherpetic neuralgia more in people age 70+
- Everyone should be vaccinated regardless of their antibody status
- However this is a live vaccine so the standard CI to live vaccines hold (see #4 on this list)
6. Tetanus vaccination and wounds
- if you have a wound and unclear/incomplete tetanus vaccination history -- complete TDaP series + tetanus immune globulin
- If no tetanus booster in the last 5 years and the wound looks bad -- TDaP booster
- If no tetanus booster in the last 10 years and the wound looks clean -- TDaP booster
7. Early stage breast cancer:
- <2cm tumor, no lymph node involvement, no sentinel node involvement
- Negative sentinel node has a high NPV, so there's no need for a full axillary dissection
- Whole body PET scan has a PPV of 1% in this population-- lots of false positives, so its not indicated.
8. Screening for colorectal cancer in high risk patients: 
- 1st degree family member with colorectal cancer: increases odds of colorectal cancer by 2-3 times. That risk doubles again if the family member was diagnosed before age 45. If two people in the family got diagnosed, the risk goes up to 20%.
- For people with a first degree relative with colon cancer, screening colonoscopy should happen at age 40 or 10 years before the family member got diagnosed, and then at 3-5 year intervals afterwards.
- For IBD patients, the annual cancer risk in people with extensive colitis is 0.5% per year. Screening should start 8 years after diagnosis and continue every 1 to 2 years afterwards.
9. Incidental small lung nodules
- For nodules <3mm, risk of cancer is 0.2%, and 4-7mm risk os 0.9%
- For an incidental nodule <4mm, no further follow up if the patient is low risk, and repeat CT in 12 months if they are higher risk for lung cancer.
10. If there is suspected advanced/metastatic lung cancer (i.e. +supraclavicular LN) you should biopsy the suspected mets, which will both diagnose and stage the cancer.

1. AIN vs ATN: 
- AIN: leukocytes and leukocyte casts, no bacteria (sterile pyuria). May be accompanied by fever, rash or eosinophilia. B-lactam antibiotics are often culpable.
- ATN: muddy brown casts (75% of the time), rarely have leukocytes or leukocyte casts.
2. Hematuria: 
- Persistent: 3 or more RBCs/hpf on 2 samples
- Suggestive of non-glomerular source: normal appearing erythrocytes, no erythrocyte casts, no proteinuria. Evaluate with cystoscopy if suspicion for malignancy is high (age >50, male, smoking hx, exposure to benzenes, cyclophosphamides, radiation)
- Suggestive of glomerular source: dysmorphic erythrocytes, no casts, proteinuria. Evaluate with kidney biospy
- You can also see hematuria in people on NSAIDs or anticoagulants
3. Rhabdo can be caused by narcotic overdose and alcohol (hypophosphatemia)
4. Haldol does not cause respiratory depression, which is one thing going for it as a treatment for delirium.
5. Causes of wernicke's-korsakoff besides alcoholism: 
- Prolonged TPN
- Hyperemesis gravidarum
- Cancer
- AIDS
- Post surgical (esp bariatric)
- Glucose loading in someone who is predisposed.
6. Neisseira meninigits vaccine covers serogroups A, C, Y and W-135, but not serogroup B
7. Rocky mountain spotted fever: 
- First systemic sx: fever, myalgias, arthralgias, headache, abdominal pain
- Rash that starts 3-4 days later, starts on wrists and ankles, moves centripetally
- Thromobcytopenia, relative leukopenia, elevated transaminases.
- Can have AKI
- Infection transmitted in spring and early summer.
8. Listeria meningitis
- Hits the immunocompromised: very young, old (>50), HIV, TNF-a inhibitor, chronic liver or kidney disease, alcoholism, cancer, diabetes, iron overload, collagen vascular diseases.
- Clinically can manifest from mild disease (fever, AMS) to coma.
9. Ischemic stroke and hypertension
- It is common to have elevated blood pressures during an ischemic stroke; for the most part, it will resolve within 24 hours.
- If someone is eligible for tPA, their BP should be kept below 185/110 (with IV labetalol or nifedipine)
- If someone is ineligible for tPA, their BP should be kept below 220/120, unless they have other indications for avoiding hypertension-- i.e aortic dissection, acute MI, heart failure, signs of end-organ damage. Otherwise just watch and wait for it to go down on its own.
10. Subarachnoid Hemorrhages 
- Early in the diagnosis of an SAH, MRI is no more sensitive than CT. Believe it or not. {BMJ}
- Risk of rebleed after SAH is 2% per day for the first 30 days

1. A beautiful explanation of the delta-delta ratio. 
- In brief:
- Delta gap/delta bicarb = absolute value (12 - measured gap) / absolute value (24 - bicarb)
- Firstoff: only some acids cause a gap-- the organic unmeasured anions. Acidemia caused by HCl (generated by diarrhea perhaps 2/2 Cl-/HCO3- transporters?) will not give you a gap because Cl is in the equation to calculate the gap.
- If you buffer every molecule of an organic acid with bicarb, you would expect to gain 1 organic acid for the loss of every bicarb (in reality because you buffer from bone and cells, you gain more organic acid than you lose bicarb... its like 1.6 acid for 1 bicarb. With ketoacidosis, you excrete the ketones pretty efficiently, while in lactic acidosis you often get a pre-renal azotemia 2/2 shock etc)
- But if you're losing way more bicarb than you would expect given the gap (caused by organic anions), that means there's another acid, that is not causing a gap, that is buffering away your bicarb-- i.e. HCl from diarrhea or renal failure. In this case, your measured bicarb is LOW. So if your measured bicarb is low, the denominator in your equation is HIGH, so your delta-delta will be LOW - <1.
- If you're losing way less bicarb than you would expect given the gap, that means something is giving you bicarb-- i.e. there's a concurrent metabolic alkalosis. In this case, you expect your bicarb to be high, which means your denominator will be LOW, which means you'll have an increased delta-delta (>2).
TL; DR: delta-delta <1 = concurrent non-gap acidosis, delta-delta > 2 = concurrent metabolic alkalosis.
2. Non-gap acidosis - is it renal or extrarenal? 
- If you're acidotic because your kidneys are retaining acid, you will expect low ammonium in your urine (ammonium is one way kidneys get rid of H+)
- If you're acidotic because an extrarenal process (say, you're losing bicarb through diarrhea) you expect your kidneys to compensate by increasing excretion of H+, ie. more ammonium in your pee.
- You can't generally measure urine NH4, but you can count it as an unmeasured cation and calculate the urine gap.
- Urine gap = Urine cations - Urine anions.
- Urine gap = Urine Na+K - Urine Cl.
- If there's tons of NH4 in your pee, there's tons of unmeasured cations, and you expect the Cl to be way high relative to Na and K, and you'll get a big, negative urine gap
- If there's little NH4 in your pee, the unmeasured cation is low, and you expect Na and K to be higher relative to Cl.
- Normal UG = 30-50
TL; DR: Urine gap high = renal, urine gap negative = extrarenal
3. Anion gap acidosis - is it alcohol or ethylene glycol? Calculate the osmolal gap.
- Osm gap = abs value (calculated osm - measured osm)
- Calculated osm= 2*Na + Glucose/18 + BUN/2.8
- Elevated osm gap = umeasured osmole in the blood, could be ethanol or ethylene glycol.
- Ethylene glycol: will see renal injury and calcium oxalate crystals in the urine.
4. Hyponatremia: 
- Can occur with decreased arterial perfusion ie. dehydration (blood vessel baroreceptors will stimulate ADH, even if Na is low-- your brain will sacrifice Na balance for perfusion volume) or CHF/cirrhosis/nephrotic syndrome-- i.e. decreased effective renal perfusion.
- Can occur with increased plasma solutes-- i.e. hyperglycemia will cause increased plasma osmolality, will cause water to leave cells and dilute plasma. {correction calculator} {data source - NEJM 1999}
- Pseudohypernatremia can occur when you have a significant amount of protein (hyperglobulinemia) or triglycerides in the blood, which will take up space and decrease the amount of plasma, leading to a falsely low measured Na.
5. Acetazolamide: blocks carbonic anhydrase IV, increases loss of urine bicarb and K => hypokalemic metabolic acidosis. Alkalinizes urine, thus increases secretion of weakly acidic drugs like salicylates and barbituates. (To acidify urine, give NH4Cl, helps excrete weak bases/tertiary amines like cocaine and amphetamines)
6. Kidneys and K: 
- Generally you don't get hypokalemic from renal disease until your GFR < 15, without the addition of aggravating factors like NSAID use.
- Thiazide diuretics are ineffective once your GFR < 30
- In the setting of hypokalemia, urine K < 20mEq/L suggests that the kidneys are adequately recovering K, implying extrarenal losses. Urine K > 20 mEq/L suggests renal losses.
7. Management of hyperkalemia: consideration of time: 
- Calcium gluconate for membrane stability - onset in 2-3 minutes
- Sodium bicarb for intracellular shift of K - onset in 10 minutes
- Albuterol - onset in 15-30 minutes
- Insulin/Glucose - onset in 30 minutes
8. Central vs nephrogenic DI: give desmopressin (selective AVP V2 receptor agonist) 1 to 2 ug subQ or IV, or give vasopressin (nonselective) 5U subQ
9. Sarcoid & Calcium
- Activated mcrophages in sarcoid granulomas secrete 1a-hydroxylase, which is the renal enzyme that converts 25-OH vitamin D to 1,25-OH vitamin D.
- Treat with steroids.
10. Phosphate
- Hypophosphatemia can develop in chronic alcoholics (decreased PO intake, vomiting, also ethanol directly stimulates kidney tubules to secrete phos)
- Often occurs 12-24 hours after admission; worsened by administration of IV glucose (stimulates insulin production, which pushes phos into cells-- also seen with refeeding syndrome)
- Sx: confusion, rhabdo, hemolysis, weakness - including weakness of respiratory muscles.
- You need phos to make ATP; without it, your ion pumps fail.

1. Small cell lung cancer: 
- So often associated with smoking that if its diagnosed in a "never smoker", recheck the history or the pathology
- Staged as either "limited" (can all fit into one radiation port) or "extensive" (can't fit into one radiation port)
- Treated with chemo (platinum agent + etoposide or irinotecan). Add radiation if the disease is limited.
- Salvage chemo after the inevitable failure of first-line chemo
2. PSA + prostate cancer 
- If you're following PSA, any rise > 0.75/year or a rise to above 4 should be investigated with a biopsy. PSA > 4 is only 25% sensitive for detecting prostate cancer.
- However the biopsy false positive rate is >75%
- Only guys aged 50-70 should be screened (start at 45 for those with family hx of prostate cancer or who are black)
3. Metastatic prostate cancer: 
- If asymptomatic, first line treatment is leupron as most prostate cancer is hormone-sensitive.
- When first starting leupron, there may be a transient increase in FSH/LH and a concomitant worsening of prostate cancer symptoms; this can be managed with an anti-androgen (nilutamide, flutamide).
- If that fails, then try docetaxel
- Samarium 153 can be used to treat painful metastatic bone cancer that hasn't responded to other treatments; however this carries significant risks including marrow failure.
4. Pap smears
- ASCUS + positivity for high risk HPV strain (16,18) buys you a colpo
- 21-30: pap smear (no HPV test) every 3 years
- 30-65: pap smear q3 or pap+HPV q5
- No screening after hysterectomy with removal of cervix unless there was a personal history of advanced disease (CIN 2, 3 or cervical cancer)
5. Bowen's disease: 
- Aka squamous cell carcinoma in situ
- Slowly growing, non pruritic, scaly lesion, well defined, erythematous
6. Nodular skin cancers: 
- Nodular melanoma: single color nodule that grows on the skin; often blue or black, 'berry like', symmetric
- Keratoacanthoma: rapidly growing from solid nodule to crater-like with a central keratotic plug. Often involutes in a few months, rarely progresses to metastatic cancer. Treat with excision or injections of 5-FU or MTX or topical imiquimod or radiation.
- Seborrheic keratosis: stuck on tan or brown lesions, benign
- Spitz nevus: elevated mole, benign, often in kids, can be pink or red or pigmented.
- Basal cell: pink, pearly, often with specks of melanin, teleangiectasias.
7. Cancer pain management: 
- Start with short acting opiates, then titrate to pain relief, and then convert to long acting opiates (with 30-50% dose reduction) + short acting for breakthrough pain.
- Try to stay with the same medicine for both short and long acting
- Treat dyspnea with morphine in end-stage cancer patients
8. COPD
- No longer use response to inhaled bronchodilators to distinguish copd from asthma or to predict response to long term bronchodilator/steroid use. Any FEV1 <80% of predicted or FEV1/FVC < 0.7 demonstrates not fully reversible disease and excludes asthma
- Dyspnea 2/2 CHF should show no PFT abnormalities except maybe lower DLCO 2/2 pulmonary edema. Same with dyspnea 2/2 PE
9. Episodic cough/chest tightness lasting weeks triggered by URI with normal PFTs in between- think asthma (cough variant asthma) even in an older person.
- Diagnose with methacholine challenge- give increasing doses of methacholine until you see 20% reduction in FEV1 from baseline (provocative concentration 20- PC20). PC20 of 4 is asthma, 4-16 is hyperreactive, 16+ is normal
10. Hepatopulmonary syndrome: increased vasodilation of lung vessels, causing V/Q mismatch; NO concentration in exhaled air is greater in people with this disease than normal. Same with NO synthetase. Dyspnea will be improved with lying down and worse with sitting upright.

1. Secondary causes of headache:
- Bleed: SAH, parenchymal  hemorrhage, sentinel bleed from aneurysm
- Vascular: aneurysm, AVM, CCM, dissection, temporal arteritis, hypertensive encephalopathy
- Intracranial non-vascular: tumor, pseudotumor cerebri, hydrocephalus
- Infection: meningitis, abscess, empyema
- Drugs/withdrawal: alcohol, cocaine, opiates, steroids, caffeine
- Metabolic: hypercapnea, hypoglycemia, anoxia, anemia
- H+N trauma: concussion, injury to the soft tissues and bones of the skull and face.
- H+N pathology: problems with sinuses, eyes (glaucoma), radiculopathy (C2 nerve compression)
- Psych
2. Cerebral aneurysms:
- Acomm most common (30%)
- Pcomm next most common (25%)
- MCA third (20%)
3. Relationship between aneurysm size and likelihood of rupture:
<10 mm: 0.05%/year
>10 mm: 1%
>25 mm: 6% (45% within the next 7.5 years)
4. MR modalities
- DWI: most sensitive for ischemia, will appear as bright. Can detect ischemia within 15-30 minutes of onset of symptoms. Pyogenic abscesses will also demonstrate restricted diffusion (bright on DWI) because of increased viscosity in their cores.
- GRE: di/paramagnetic substances (metal, most blood except hyperacute) will appear dark
- SWI (aka VENBOLD) susceptibility weighted imaging, uses GRE pulse sequence, its like GRE but higher resolution. Exquisitely sensitive for venous blood, hemorrhage, iron storage, which appear dark.
- Spect: Normal: choline and creatine about the same, NAA higher than both. Increased choline/cr ratio and decreased NAA/cr ratio seen in cancer. Lactate/lipid elevation is never normal, suggests anaerobic metabolism-- infection vs necrosis (tumor)
5. Insular ribbon sign: insula is very sensitive to ischema; loss of the grey-white matter distinction due to swelling- sign of acute MCA infarct
6. tPA during ischemic stroke:
- FDA approves use up to 3 hours after ischemic insult
- ECASS-III trial showed it is safe up to 4.5 hours.
7. Venous infarcts:
- Due to dural sinus thromboses.
- Generally cause hemorrhage not in any standard arterial distribution
- Risk factors: neonates- shock/dehydration, older children- local infection (mastoiditis) and coagulopathy, adults- hypercoagulability (70%) and infection (10%). Pregnancy, puerperium, OCP are risk factors.
- Image with GRE or SWI/VENBOLD
- Can use MR venogram (will see filling defects of the sinuses that have thrombosed)
8. Cerebral veins: 
- Labbe drains temporal lobe into transverse sinus.

9. AIDS population- ring-enhancing brain mass, think toxo vs primary CNS lymphoma
- Favors toxo: multiple lesions, involving deep structures (BG, caudate, thalami), bright center on T2 (fluid), hyperintensity on T1 (hemorrhage), tons of surrounding vasogenic edema
- Favors CNS lymphoma: single lesion, sub-ependymal, encasement of ventricles, lights up on DWI (lots of diffusion restriction - due to hypercellularity?), hypointense core on T2 (hypercellularity?)
10. Toxo becomes worrisome once CD4<100; such patients who are toxo+ should be treated even if they don't have sx, because the rate of symptomatic toxo is 30%

1. Myelophthisic (phthinein Gk. to waste away): 
- Pushing of myeloprogenitor cells from BM into peripheral blood
- Caused by replacement of red marrow with fibrosis, granulomatous disease, or malignancy (primary, mets, lymphoma). Also marrow infections.
- You will see early myeloid forms on smear-- like nucleated RBCs
2. Testing for inherited thrombophilias:
- Do not test during or right after the acute thrombotic event-- it will influence the results of the tests.
- Anticoagulate first (i.e coumadin) then test 2 weeks after completion of the course.
- Test for: APC resistance, factor V leiden, Antithrombin III deficiency, prothrombin mutation, protein C and S deficiency, antiphospholipid antibodies
3. Antiphospholipid syndrome 
- Made up of 2 antibodies: lupus anticoagulant and anticardiolipin antibody
- Transient elevation of antibodies can be present after a viral illness. Thus you want to recheck levels 12 weeks apart (because if its positive, you commit someone to lifelong anticoagulation)
- Things that cause elevations: cancer, infections (i.e HIV), lupus, drugs (hydralazine, procinamide, phenothiazines such as perphenazine, chlorpromazine) -- however the latter will often be assoc with IgMs and not cause a hypercoagulable state
- In antiphospholipid antibody + people, annual risk of new VTE is 1% per year. In women with recurrent fetal losses, its up to 10%. In people with history of VTE and who have d/c'd anticoagulation within last 6 months.
- Causes increased risk of both venous and arterial clots.
4. Genetic hypercoagulability:
- Factor V leiden: assoc with resistance to activated protein C. Among white patients with first time symptomatic DVT, 12-20% are heterozygous for factor V leiden (vs 6% in control population)
- Prothrombin mutation (G20210A): prothrombin antigen/activity increased by 30%, among white patients with first time symptomatic DVT, 6% will have heterozygous G20210A, vs 2% control
- Hyperhomocysteinemia: increases venous and arterial clots, homocysteine levels depend on levels of folate, B12, and B6 (taking vitamins will lower plasma homocysteine levels) although supplementation of these vitamins has not been shown to reduce thrombotic events in these populations.
5. MGUS criteria + management: 
- M protein <3
- BM < 10% plasma cells
- No lytic bone lesions, no anemia, no hypercalcemia, no renal insufficiency (assoc with plasma cell dyscrasia)
- More than 5% of those over 80 may have this
- No treatment, just f/u M-protein levels-- the higher it is, the more likely it is to transform into MM
6. Multiple myeloma: need 1 major criteria or 3 minor criteria 
Major criteria:
- More than 30% clonal plasma cells on BM
- High M-protein (IgG <3.5, IgA >2)
- Bence Jones protinuria (urine protein > 1g/24 h)
Minor criteria:
- 10-30% clonal plasma cell son BM
- M protein < 3.5
- Lytic bone lesions
- Low levels of non-monoclonal proteins
7. Radiation proctitis- commonly occurs after radiation to pelvis.
- Clinical presentation: frequent loose stools, tenesmus
- Workup: flex sig
- Anticipated findings: mucosal telangiectasias, bx with submucosal fibrosis, arteriole endarteritis
- Natural history: acute - occurs within 6 weeks of radiation, self resolving after radiation is discontinued. Chronic- appears months to years after radiation, worse course.
8. Rome criteria for IBS
- 6 months of abd pain and changes in bowel habits, at least 3 days/month for 3 months.
Two or more of the following:
- Pain relieved with defecation
- Onset of pain related to a change in frequency of stool
- Onset of pain is related to a change in appearance of stool
9. Indication for antibiotics for salmonella diarrhea:
- Age <2 or >50
- Immunocompromised
- Severe illness that requires inpatient care
- Atherosclerotic plaques, implanted hardware or endovascular devices --these things can all be seeded.
10. OCP can cause cholestasis (will see increased direct bili and alk phos)