1. Digoxin Toxicity
– Most common symptoms are GI: nausea, anorexia, vomiting
– EKG: bidirectional ventricular tachycardia and accelerated junctional rhythm (AV node outpaces SA node due to stimulation and suppression respectively). You also may see scooping T-wave depressions (pretty characteristic of digoxin toxicity)
– Visual symptoms - "yellow halos" around objects
– May be 2/2 verapamil which decreases renal clearance of dig
– Anything that affects renal function/GFR will affect dig levels
– Target levels 0.8-2.2
– Treat with digitoxin Fab (Digibind is >$10,000 per vial). Mag and lidocaine may help. Check and replenish lytes.
2. Vaccinations in HIV
– Generally should not be given live vaccines, except MMR, varicella, zoster and yellow fever if the CD4 count is > 200 & the patient has never had an AIDS defining illness
– Should get TDaP q10, pneumococcus, hep A (MSM only), hep b, HPV
– Meningococcus: same indications as not HIV- college student, military, no spleen, travel to endemic areas
– HiB if not given in infancy
3. Endocrine: 
- Metabolic derangements in hypothyroidism: hyperlipidemia, hyponatremia (from increased water retention), increasing creatinine kinase, transaminitis
- Thyroid disease can affect deep tendon reflexes and muscle tone .
- Low T with low FSH and LH suggest central cause. Should check prolactin levels = if they are high then MRI
- Cushing's can cause shift neutrophilia
- Management of SIADH - fluid restriction and salt tablets -/+ loop diuretics. Hypertonic saline in resistant cases. Demeclocycline is an anti-ADH but It can be nephrotoxic and is rarely used
- Hyperparathyroidism can cause elevated calcium levels in the blood which leads to chondrocalcinosis and pseudogout
- Familial hypocalciuric hypercalcemia has mutated calcium sensing receptors in both kidney tubules and parathyroid gland leading to inappropriately high-normal PTH.
- Calcium to creatinine ratio greater than .02 suggests calcium losing process such as primary hyperparathyroidism; Ca-to-Cr ratio less than 0.01 suggests calcium retaining process such as FHH
- Low Ca AND low phos: think vitamin D deficiency (chronic pancreatitis, decreased absorption of fat soluble vitamins) or acute pancreatitis
- Low C and high phos: primary hypoparathyroidism or pseudohypoparthyroidism (body can't respond to PTH)
- Immobility can cause hypercalcemia: possibly due to increased osteoclastic bone resorption. Usually occurs about 1 month in, but people with renal insufficiency can see it in days. Treat with bisphosphonates.
4. Ectopic ACTH production
– Can occur in small cell and carcinoid
– If ACTH production is slow you will get a cushingoid symptomatology
– If ACTH production is high then You get a hyperaldosteronism picture along with hyperpigmentation. Cortisol has high affinity for mineralocorticoid receptors, however it is normally rapidly converted to inactive cortisone by 11 beta HSD in kidney tubule cells, However the acute and high ACTH production saturates the enzyme.
5. Vitamins: 
- Serotonin syndrome can lead to niacin deficiency; the increased synthesis of serotonin shunts tryptophan away from niacin synthesis. Diarrhea dermatitis dementia and death.
- Vitamin A overdose can cause pseudotumor cerebri. Headaches and blurry vision. Dry skin. Abdominal pain
- B12 deficiency - think pernicious anemia - think gastric cancer
- Give B6 and folate supplements to reduce levels of homocystine in homocystinemia. Homocystine is highly reactive and predisposes to venous clots and atherosclerosis. Homocysteine can be broken down into methionine (requires B12 and folate) or into cysteine (requires B6).
Vitamin K: onset of action 8 to 12 hours when given iatrogenically. Most people have a 30 day supply In the liver but those with underlying liver disease can become deficient in 7 to 10 days
6. Going back to the Pharm: 
- Aspirin hypersensitivity reaction: Shunting of arachidonate acid to leukotrienes by cox inhibitors in susceptible individuals leads to nasal polyps and bronchoconstriction. Treat with leukotriene inhibitors
- Aspirin can cause idiopathic thrombocytopenia
- Primodone is an anticonvulsant that breaks down into phenobarbital. This can precipitate acute intermittent Porphyria. It is used to treat essential tremor.
- Sildenafil should not be combined with nitrates, or any other vasodilators as it can worsen hypotension. If you're administering with alpha blockers like doxazosin, wait 4 hrs in between to prevent hypotension.
- Trihexiphenydil - Anticholinergic like benztropine. Used to treat Parkinson's and dystonia from anti-dopaminergics
- Drugs that can cause pseudotumor cerebri: vitamin a derivatives (all trans retinoic acid, accutane), tetracyclines, growth hormone
- Side effects of epo:  Worsening hypertension, headaches, flu like symptoms, rarely red cell aplasia
- Fluphenazine: high potency typical antipsychotic. Injectable, long lasting. Can inhibit shivering response and lead to significant hypothermia in cold environments.
7. Management of anemia
– Defuroxime to manage iron overload in patients with frequent transfusions (B thal major or sickle cell)
– Folate supplementation in patients with high red cell turnover ie hemolysis (PNH, HS, sickle cell) or B thal
– No treatment for b thal minor
– Prednisone for AIHA
– Indications for epo: CKD anemia, anemia of chronic disease, anemia after bone marrow transplant or chemo
8. More heme: 
- Lupus anticoagulant causes falsely elevated PTT by binding to phospholipids in the test. Mechanism of thrombosis unknown: possibly concentration of antibodies on cell surfaces causing activation of coagulation cascade
- Polycythemia vera causes gout in up to 40% of people. Characteristic pruritus after a hot bath due to increased histamine released from increased basophils. This increased histamine secretion can also lead to gastric ulcer. Splenomegaly.
- Isolated thrombocytopenia: test for hep C and HIV (can cause isolated cytopenias). Other causes: EBV, myelodysplastic (age>60), alcohol, B12 or folate deficiency.
9. Neuro 
- Diplopia after prolonged eye use, dysarthria after prolonged speaking, or jaw fatigue after prolonged chewing = Think myasthenia gravis. CPK will be normal which distinguishes it from primary muscle pathology. Reflexes will be normal which distinguishes it from ALS.  Approximately 15% of those with MG have a thymoma. MG tends to affect bulbar muscles first.
- Alcoholic cerebellar degeneration causes typical cerebellar signs such as dysmetria and dysdiadochokinesia as well as ataxia and truncal ataxia. You can also see muscle hypotonia leading to pendulum swing (striking of patellar tendon leads to slow pendulum like swinging of the leg - more than four swings is considered pathologic)
- Clasp knife rigidity and clonus are pyramidal signs
- Hemineglect: parietal lesion.
- Achilles tendon reflexes often fade With age
- Distinguishing dementia from typical aging. Dementia is:impairment of normal functioning, loss of insight about memory loss and declining functioning (anosognosia), not only expressive but some receptive aphasia, getting lost in familiar environments, losing the ability to remember recent important memories
- After sub-arachnoid or intraparenchymal bleed, you can see cerebral salt-wasting 2/2 SIADH and secretion of BNP (which wastes salt)
10. ID in HIV 
- Causes of dysphagia in HIV patients: Candida most common overall. Causes mild to moderate esophagitis and is usually associated with thrush. Severe pain + no thrush think CMV or HSV
- Candida: empirically treat with 3-5 days fluconazole. If it's resistant you can go to voriconazole, caspofungin or amphotericin
- If there is no thrush or does not respond to treatment you should scope to look for CMV (linear ulcers) or HSV
- Treat apthous ulcers with topical steroids, and if that fails, systemic steroids
- Treat CMV with ganciclovir: CMV does not include the viral thymidine kinase needed for acyclovir to be effective
- Pentamidine is the treatment for PCP pneumonia in AIDS patients who cannot tolerate bactrim

1. Upper lobe lesions in the lungs
– Aspiration while supine: rapid onset, very sick patients
– TB: chronic course
– Primary cancer: usually one lesion
– Mets: uncommon, these tend to occur more in the lower lobes where there is better more blood
– Histo, blasto.
– Aspergillus fungal ball.
2. Rheum to grow: 
– Ankylosing spondylitis: primarily involves the apophyseal (= facet) joints.
– Arthritis pain that occurs in a young person, symptoms occur at night, and improve with exercise => think inflammatory arthritis. (most injury or degenerative arthritis is worse with exercise, improve with rest and doesn't have nighttime symptoms)
– Manage lupus with limited skin and joint involvement with hydroxychloroquine. Do eye exams q6 months as this drug may cause retinopathy or corneal damage.
– Dermatomyositis is associated with an increased risk of internal malignancy. Up to 10% of people with adult onset DM will develop malignancy. DM is six times more common in women than men. The most common cancers are ovarian, breast, lung, uro-gyn malignancies
– Treat inflammatory polymyopathies with high dose steroids
– Treat reactive arthritis with NSAIDs

- Stills disease: maculopapular rash that occurs on the trunk and extremities that coincides with fever and joint pain

3. Complications of rheumatologic disease 
– Aortic aneurysm: behcets, Takayasu, giant cell, the seronegative spondyloarthropathies notably AS, RA
– Renal failure: Wegener's, lupus, Goodpasture's, HSP, PAN, Scleroderma
– Alveolar hemorrhage: churg Strauss, Goodpasture's, wegners, behcet
– Pulmonary fibrosis: dermatomyositis, scleroderma
– Carpal tunnel: sarcoid, amyloidosis, RA (can also happen in hypothyrodism)
– Mononeuritis multiplex: Churg Straus, PAN, Wegener's, lupus, amyloid,sarcoid,  cryoglobulinemia, RA
4. Amyloidosis
– Primary AL, secondary AA - Chronic Inflammatory state like RA, IBD, chronic infections (Bronchiectasis, osteomyelitis, TB), Cancer, vasculitis
Manifestations:
– Cardiac - hypertrophy without change in chamber diameter
– Renal: nephrotic syndrome
– Neuropathy : Autonomic (orthostatic hypotension), peripheral neuropathy (carpal tunnel syndrome)
– Hepatomegaly
– Other organ enlargement like macroglossia
– Waxy skin
– Easy bruising/bleeding diathesis
– Colchicine is used in the prophylaxis and treatment of AA amyloidosis
5. Stuff that crystallizes in your kidney tubules 
- Acyclovir
- Protease inhibitors (indinavir)
- Ethylene glycol (ca-oxylate crystals - envelope shaped crystals)
- Sulfa drugs
- Methotrexate
- Stuff that gives you AIN - B lactams, PPIs, usually takes 7-10 days
6. More renal stuff 
– Nephrotic GN: Membranous, diabetes, IgA, Amyloidosis, minimal change, FSGS
– Mild Nephritic GN: thin basement membrane syndrome, IgA, lupus
– Moderate/severe Nephritic GN: Post strep/infectious, membranoproliferative, lupus, vasculitis,  RPGN
– If a patient with pyelo does not respond after 48-72 hours of appropriate antibiotics, urologic imaging (CT or ultrasound) is indicated to look for complicating pathology like an obstruction or abscess
– Hypertensive nephropathy: characterized by increased pressures, leading to nephrosclerosis, that is, fibrosis of the renal arterioles, progressing to sclerosis of the glomerular capillaries
– Diabetic nephropathy: characterized by increased filtering, leading to increased extracellular matrix, thickening of the glomerular basement membrane, and mesangial proliferation
– Analgesic abuse nephropathy: characterized by focal glomerulosclerosis. Its a tubulointerstitial disease. Additionally analgesia mediated vasospasm of the vasa recta => papillary necrosis resulting in painless hematuria. On UA the red cells appear normal, in contrast with glomerular sources of bleeding where the red cells appear dysmorphic. The bleed can be significant to where the blood clots will cause renal colic.

- Acetylcysteine has been shown to decrease IV contrast nephropathy, perhaps because of its antioxidant and vasodilatory properties 

- Goodpasture's disease: you make anti-glomerular basement membrane antibodies. Treat with immediate plasmapheresis to prevent renal injury. 

- Treat Wegener's with cyclophosphamide and steroids

- Prednisone can cause fluid retention in people with renal failure 

7. Everybody loves ID 
- Treat bartonella henselae with five days of Azithro
- Influenza can cause proteinuria and leukopenia - there's data that h5n1 virus destroys lung epithelial cells and leukocytes in replication.
- Viruses that cause myocarditis: Coxsackie B, adeno, entero, parvo, HHV-6
- Colitis and pneumonia one month post bone marrow transplant: think CMV. Diarrhea and other GI symptoms caused by ulcers.
- Hepatitis B initially goes through an immune tolerant phase where the virus replicates; AST and ALT are low, HBV DNA and E Antigen are high. Then there is an immune clearance phase where the body starts to attack infected hepatocytes. ALT rises, biopsy shows inflammation in the liver, and markers of Hep B Infection ( E antigen and viral load) fall during this. Follow ALT and HBeAg q3-6 months to ensure total clearance.
Palm and sole rash:
- syphillis secondary and congenital (copper)
- RMSF (outside in) and typhus
- Kawasaki, TSST, measles (peeling)
- coxsackie A / hand foot mouth
Others: contact dermatitis, lupus, erythema multiforme
8. Measles (rubeola) vs rubella  
- both have same prodrome - cough, conjunctivitis, coryza, lymphadenopathy
- measles has higher fever > 40
- rash moves from head down, fast in rubella, slow in measles
- rubella associated with arthritis in women older than adolescent age (not men or children)
9. CML versus leukemoid reaction
– Both = leukocytosis with marked left shift
– Leukemoid reaction is a response to severe infection / Inflammation
– Leukocyte alkaline phosphatase is the critical distinguishing factor. It will be elevated in leukomoid but decreased in CML
– CML blast crisis is where CML behaves like AML: > 20% blasts on peripheral smear
10. GI stuff 
– Melanosis coli: Brown Stained colon with white patches representing Lymphoid tissue, 2/2 Dulcolax/Bisacodyl (ab)use
– GI angiodysplasias are often diagnosed in the setting of acquired coagulopathy, such as acquired von Willebrand disease (aortic stenosis => shearing of large VWF multimers) or uremic platelet dysfunction 2/2 ESRD
– Hemolytic anemia + acute onset transaminitis and ascites: think PNH. PNH predisposes to venous clots, particularly in hepatic veins.

- Chronic portal vein thrombus can present as varices

1. Glucagonoma

- Derm: erythematous plaques that can coalesce and blister around perineal area, extremities, face

- Neuro: ataxia, dementia, proximal muscle weakness

- Can cause increased DVT

- Serum glucagon > 500.
- Other conditions that cause elevated glucagon: cushing's, pancreatitis, sepsis and hypoglycemia, although in these cases serum glucagon is generally < 500 

2. Theophylline toxicity 

– CNS stimulation – Headaches, insomnia, seizures

– G.I. disturbances: nausea and vomiting

– Arrhythmias: Atrial tachycardias, SVT, v-tach

– Narrow therapeutic window, levels can be increased by CYP inhibitors (macrolides, Verapamil, cimetidine, cipro), by acute illness and by cirrhosis.

3. DDx SVC Syndrome

– Malignancy: lung cancer, non-Hodgkin's lymphoma

– Fibrosing mediastinitis: 2/2 Histo, TB 

– Giant clot from an indwelling line 

4. Hep C cryoglobulinemia: 

– Think of it like lupus with elevated transaminases: vasculitis of skin, kidneys, nerves, joints.
– Renal: proteinurea and hematuria 

– Skin: Palpable Purpura. 

– Joints: Arthralgias
– Systemic inflammatory symptoms: malaise, fatigue

– Nerves: peripheral neuropathy

– Hepatosplenomegaly

– Labs: Decreased complement (low C3, C4), elevated RF. 

5. DDx Pulsus paradoxus

– cardiac tamponade

– Severe asthma or COPD 2/2 significantly increased intrathoracic pressure on inspiration - sucks blood out of the heart into the pulmonary venous system, reducing preload 

6. Dermatology 

– Tinea versicolor: flat white pink or brown macules that do not tan, scale on scraping. Treat with ketoconazole or selenium sulfide. 

– Seborrheic keratosis: brownish stuck on lesions
– Seborrehic dermatitis: rash that affects anywhere with sebaceous glands (face, intertriginous, parasternal, scalp). Greasy yellow scale over erythematous base. Often associated with underlying Parkinson's or HIV.

– Tinea corporis: erythematous rings with scaly edges 

– Pityriasis rosacea: flat fawn colored macules up to 2 cm, christmas tree, herald patch

– Sudden onset seborrheic dermatitis or severe psoriasis - think HIV or GI malignancy 

– Photo allergic contact dermatitis can occur with certain kinds of sunscreen. Prior exposure is needed

7. Optho 

- Tarsal conjunctiva = conjunctivae lining the inside of the eyelid. Granular appearance suggests viral conjunctivitis (among other things). Treat viral conjunctivitis with cool moist compresses

- Macular degeneration causes central vision loss - can be atrophic with sores or proliferative with increased blood vessels.

- Open angle glaucoma causes loss of peripheral vision and is more common among diabetics. On exam you will see increased cupping. 

- Acute closed angle glaucoma: hard eye, dilated/fixed pupil, blurred vision, halo, pain, conjunctivitis, headache, nausea. Treat with pilocarpine to open canals of schlemm and timolol to reduce synthesis of aqueous humor. 

- Anterior uveitis: inflammation of uvea, especially iris. May have conjunctival inflammation next to cornea is usually spared. 

- Conjunctivitis vs keratitis: keratitis implies involvement of cornea. 

- Fungal keratitis is often found in agricultural workers and immunocompromised patients; you'll see multiple stromal abscesses

- Bacterial keratitis is common in contact lens wearers (particularly gram negatives like pseudomonas and serratia). The cornea will appear hazy with a central Ulcer and surrounding stromal abscess-  you may see hypopyon. 

- Herpes simplex keratitis: recurrent infections triggered by sun exposure (outdoor work) fever or immunodeficiency and are characterized by dendritic ulcers & corneal ulcers

- Episceritis: mild pain and discharge. RA, IBD. Does not affect vision or cornea. 

- Standard diabetic retinopathy includes micro hemorrhages and cottonwood spots

- Central Retinal vein thrombosis causes sudden loss of vision often in the morning; you will see dilated and torturous veins on exam, and disc swelling

8. Indications for aortic valve repair in aortic stenosis

– Any symptoms: Syncope, dizziness or lightheadedness, dyspnea

– Significant stenosis in a patient getting a CABG or other valve surgery

– Significant AS + plus poor LV function, poor exercise tolerance, or significant LV hypertrophy

9. Liquid cancer treatment

– Hairy cell: cladribine (purine analog) 

– CLL: prednisone plus chlorambucil

– Non-Hodgkin's: CHOP
- Hodgkins: ABVD (adriamycin, bleomycin, vincristine, dacarbazine)
- APML: All-trans retinoic acid
- AML: induction (cytarabine + anthracycline like daunorubicin) + consolidation (more chemo drugs or stem cell transplant depending on cancer genetics) 

10. NAFLD

– Due to insulin resistance => increased peripheral lipolysis, which is taken up by the liver 

1. Medical management after MI: 
- ACE inhibitors prevent ventricular remodeling (i.e. aneurysm information after MI)
- Carvedilol may actually be able to to reverse remodeling 

2. Oral leukoplakia is a precancerous lesion. It will resolve with cessation of tobacco or alcohol. Transformation into a more nodular or ulcerated or indurated appearance suggests transformation into squamous cell carcinoma 

3. Vaccinations 

- HiB: Asplenia 

- Pneumococcus: everyone >65. If given to an HIV-positive person with a CD4 < 200 you should repeat when CD4 is higher.  Repeat at five years. 

- Indication for early pneumococcus: No spleen, chronic heart lung liver kidney disease, diabetes, alcoholics, smokers, cochlear implant, CSF leak, immunocompromised 

- Meningococcus: college students, military recruits, no spleen, travel to endemic areas. Can repeat At five years if still at risk. Indications for meningiococcus vaccine in HIV+ is same as in HIV-

- Hepatitis A – travel to endemic areas, MSM, IV drug use, concomitant hep B or hep C or liver disease that would amplify the consequences of hep a infection 

- Tetanus – TD q10, replace one of these with TDaP before 65 

4. Fibromuscular dysplasia in unilateral renal artery should be treated with stenting if the hypertension was recent onset or the hypertension cannot be managed with meds due to intolerance or ineffectiveness. The goal of stenting is to treat the hypertension. 

5. Dementias: 
- Alzheimer's disease: memory is first, then visual spatial, then later on possibly executive function, urinary incontinence, gait abnormalities

- NPH: marked gait abnormalities are the first presenting symptom. Later on, you get dementia and incontinence

- Lewy body dementia: visual spatial is affected first, and then memory later on. + Parkinsonian features. 

- Vascular dementia: In the early stages has significantly more executive function impairment than memory impairment 

6. PTU or methimazole
- If someone develops a fever and sore throat while taking these drugs, discontinue and check CBC. White count < 1000 = likely agranulocytosis (immune mediated destruction of granulocytes). If WBC > 1500, it's unlikely to be agranulocytosis.
- Treat PTU or methimazole induced agranulocytosis with IV broad-spectrum antibiotics - cover for Pseudomonas 

7. Acute Pancreatitis: 

- Viruses that cause: Mumps, HIV, coxsackie, CMV, HSV, Hep B

- Can present with ileus, lung pathology (including pleural effusions, atelectasis, ARDS due to release of enzymes and cytokines and pancreas -> systemic inflammation). 

- Clinical presentation ranges from very mild epigastric tenderness on palpation or severe abdominal pain with rebound/guarding. Occasionally the pain is made better with sitting up or leaning forward.

- Vs: Intra-abdominal abscess has a more indolent Course

8. AIDS CNS pathology 

- EBV DNA in the CSF is very specific for primary CNS lymphoma

- PML presents with unilateral weakness, changes in vision and hearing, and ataxia

- CNS toxoplasmosis infection is unlikely in someone taking bactrim 

9. Cystinuria 

- Decreased renal reabsorption of dibasic amino acids such as cysteine, arginine, ornithine, lysine

- Hexagonal crystals in the urine.

- Urine cyanide nitroprusside test + (test for urine Cysteine)

10. Drugs That cause hyperkalemia

- Bactrim inhibits ENaC transporter. It also causes an elevation in creatinine that is not associated with renal injury. And causes pseduo-type 4 RTA. 

- Beta blockers (notably B2 receptor, hence why you use albuterol to treat hyperkalemia) 

- Digoxin-  from blocking Na/K ATPase

- Heparin inhibits aldosterone synthesis

- Cyclosporine inhibits aldosterone activity

- NSAIDs - harm kidneys, reduce aldosterone

- ACE, ARB - Reduce aldosterone

- K Sparing diuretics 

1. Transfusion reactions 

- seconds to minutes -anaphylaxis. Anti IgA. Use washed RBC next time 

- minutes in someone on ACEI - transfusion hypotension from bradykinin in the blood, which is usually broken down by ace 

- within the first hour - hemolysis from ABO incompatibility. F/c, Flank pain, hemoglobinuria => renal failure, DIC

- minutes to hours - bacterial sepsis from contamination (pseudomonas can grow in the cold) - sepsis, shock, DIC

- within the first six hours it's either TRALI (donor anti-leukocyte reaction => pulmonary edema and interstitial infiltrates on CXR) or febrile Non-hemolytic Transfusion reaction (from stored cytokines in the blood). Prevent both with leukoreduced pRBC. 

- 24 hours to two weeks - delayed hemolysis due to minor antigens

- Occurs after two weeks - transfusion associated GVHD. Donor leukocytes engraft and replicate, and then attack the skin causing rashes, the liver causing hepatitis, the G.I. tract causing mucositis and diarrhea, and the bone marrow causing pancytopenia. Death rate is nearly 100% without a bone marrow transplant. Prevent with irradiated RBC. 

2. Preparations for pRBC

- Leukoreduction: reduce white cell component of packed RBC. Prevents non-hemolytic transfusion febrile reactions because it stops the accumulation of cytokines from remnant white cells. It also stops the transmission of CMV so it's good for patients who are CMV negative who you really don't want to get CMV, such as AIDS patients, people awaiting transplant or status post transplant. Leukoreduction is also good for preventing HLA sensitization and thus is good for people who are going to need chronic transfusions. 

- Washing the cells will remove any plasma antibodies. This is especially good for people are IgA deficient and will have anaphylactic reaction to IgA in transfused blood. 

- Irradiating blood causes cross-linking of DNA which prevents replication of transfused leukocytes.  This is to prevent TA-GVHD. Someone with a a normal number of functional T-cells will be able to destroy the transfused white cells. But people with congenital T cell immune deficiencies (such as Wiskott-Aldrich, SCID), bone marrow transplant recipients, premature infants and fetuses, can't. Also people receiving transfusions from close relatives - because the HLA is similar enough that the recipient T cells will not recognize the donor cells as foreign.  

3. Microangiopathic Hemolytic Anemia (MAHA): In all causes, the mechanism is the formation of a fibrin mesh due to increased activation of coagulation. The red blood cells are physically cut by these protein networks => schistocytes.
- Valves: Rapid acceleration, fragmentation, and collision jets were associated with high shear stress and hemolysis whereas slow deceleration and free jets were not.
- Malignant HTN: The characteristic vascular lesion is fibrinoid necrosis of arterioles and small arteries, which causes the clinical manifestations of end-organ damage. Red blood cells are damaged as they flow through vessels obstructed by fibrin deposition, resulting in MAHA.
- TTP: <5% ADAMTS-13 activity + presence of ADAMTS13 inhibitor + clinical symptoms of an acute thrombocytopenia and evidence of MAHA, appropriately defines a diagnosis of TTP. Because the sensitivity of ADAMTS-13 deficiency it is not well established, a deficiency of the protein alone does not constitute a diagnosis of TTP.
- TTP + pregnancy: The association of pregnancy with TTP may account for some of the hypercoagulable risk in women near term and postpartum. In a large study of TTP cases, 10% of all cases were diagnosed during pregnancy or postpartum, with the majority of episodes occurring near delivery.
- HUS: kids < 4-5 years, prodrome of bloody diarrhea caused by shiga-toxin producing EHEC (0157:H7). 5-10% with  0157:H7 present with acute HUS. Thrombocytopenia, MAHA, and renal failue. The toxin binds glycolipid surface receptor on endothelial cells under the influence of inflammatory cytokines => platelet clumping.
- HELLP: preeclampsia + MAHA + thrombocytopenia. Usually resolves within days following delivery. The risk of TTP in subsequent pregnancies is hard to determine.
4. TTP & Drugs: quinine (common), mitomycin, penicillin, oral contraceptives, and anti-platelet agents (ticlopidine and clopidogrel)
- Mechanism: either antibody vs drug => immune destruction or direct side effect.
- Make quinine-dependent platelet antibodies => make antibodies to multiple target tissues, which result in the systemic involvement seen in TTP.
- Mitomycin: dose-related effect, causes MAHA and thrombocytopenia. Onset may be sudden due to the initial toxicity or may appear gradually due to the cumulative toxicity of the drug. Most patients in this category responded well to plasma exchange.
- Ticlopidine and clopidogrel: deficiency of ADAMTS-13 and an inhibitor of ADAMTS-13 activity has been noted. Most respond to plasma exchange.
5. Lesser known hemoglobinopathies: 
- Hb S-B-thal: When you make all Hb S and no Hb B-thal (called sickle cell-beta zero thalassemia), it's almost identical to sickle cell disease. When you make some B-thal (called sickle cell-beta plus thalassemia), the condition is less severe.
- HB lepore: similar to beta-thalassemia (electrophoresis and smear); decreased hemoglobin synthesis. Homozygous Hb Lepore is rare. Patients of Balkan descent have the most severe presentation of - severe anemia during the first five years of life + significant splenomegaly, hepatomegaly, and skeletal abnormalities similar to homozygous beta-thalassemia. The amount of Hb Lepore in the patients blood ranged from 8 to 30%, the remainder being fetal hemoglobin (Hb F). Homozygous Hb Lepore is similar to beta-thalassemia major, however the clinical course is variable. Patients with this condition typically present with severe anemia during the first two years of life. The heterozygote form is mildly anemic (Hb 11-13 g/dl) but presents with a significant hypochromia and microcytosis.
6. Electrophoresis vs HPLC : 
- Electrophoresis allows the simultaneous study of about 90 samples on a single plate, using a central cathode and two anodes. At a glance, any band with abnormal mobility is detected as well as the absence of the normal Hb A band. This method is considered as a first line test and requires a confirmation by a second one, usually CE-HPLC.
- HPLC allows quantitative detection of Hb S and of the most common Hb variants
7. Fluid where there shouldn't be fluid: 

- Lymphocytic pleural effusion - think granulomatous disease such as TB or sarcoid, lymphomas or RA
- Hepatic hydrothorax: typically R sided, manage first with diuretics and salt restricted diet, if that fails consider TIPS if the synthetic function is holding, and there are no contraindications. If TIPS is contraindicated consider pleurodesis.
- Pathophysiology of Baker's cyst: Inflamed synovium produces excess synovial fluid which overflows into the popliteal burs => cyst. If the cyst bursts it can release it's fluid contents into the calf causing an appearance like a DVT; sometimes with crescent-shaped bruise over malleolus. These cysts are associated with RA, OA, and cartilage tears 

8. Transplant & Rheum drugs: 

- Methotrexate: Inhibits Folic acid usage and thus will affect rapidly dividing cells. It will cause G.I. disturbances like nausea/mucositis, alopecia, toxicities of the liver, macrocytic anemia and sometimes pancytopenia, interstitial lung disease, rash

- Hydroxychloroquine can cause visual disturbances, trigger G6PD, and cause G.I. disturbances

- Cyclosporine : Calcinurin inhibitor = will take down T cells - increases viral infections and lymphoma and can cause kidney damage. Also causes hyperplasia of gingiva + hirsuitism, hyperkalemia, hypertension (2/2 kidney effects), GI effects, increases risk of squamous cell carcinoma. 

- Azathioprine: toxic to the pancreas, liver, and bone marrow
- Prograf/Tacrolimus: hits your kidneys hard, narrow therapeutic window. Doesn't cause gingival hyperplasia or hirsuitism, like cyclosporine. Can also hit liver, heart. Also causes hyperkalemia and hypertension. 

9. Trousseau syndrome: migratory thrombophlebitis, seen in pancreatic, lung, prostate, colon, stomach cancer and acute leukemias. The tumors release mucins that react with platelets to form microthrombi. 

10. Infectious endocarditis

- Vascular manifestations: systemic thrombi to brain, spleen, or kidney, septic emboli to lungs, spleen. conjunctival hemorrhages, mycotic aneurysms, Janeway lesions (erythematous macules on palms and soles)

- Immune manifestations: arthritis, positive RF, glomerulonephritis (dark and cloudy urine 2/2 hematuria and proteinurea, Osler's notes (painful violaceous lesions on the fingers and toes), Roth spots (retinal hemorrhages)

- Specialized bacteria and their sources: Eikenella from oral cavity, strep bovis from occult colon cancer, enterococcus from complicated UTI, staph aureus from contaminated needles

1. Spontaneous bacterial peritonitis. 

- People with cirrhosis are often hypothermic so any temp > 100/37.8 warrants investigation 

- Ascites fluid with more than 250 Polys and a + culture are diagnostic 

- SAAG greater than 1.1 suggests portal hypertension as the source of the Ascites fluids and makes SBP more likely. 

- Treat empirically with third-generation Cephalosporin to cover enteric Gram negatives

- Other ascites facts: in pancreatic ascites, Amylase in the fluid is usually over 1000

- Secondary bacterial peritonitis occurs when there's a rupture of viscous organ into the ascites fluid. because the ascites separates the parietal and visceral peritoneum, the patient will not develop a rigid abdomen even with a raging infection. 

2. The most common cause of bloody diarrhea in the absence of a fever is EHEC.

- Test with stool Shiga toxin. 

- Treat supportively. 

- Do not give antibiotics as it increases the risk of HUS

3. Contraction alkalosis is mediated by Aldosterone. When intravascular volume drops, aldosterone secretion is increased, leading to renal excretion of protons and potassium

4. Rinne test 

- Put the tuning fork on the mastoid and then when the patient can't hear anymore you move it to the air in front of the ear. Air conduction should be twice as long as bone conduction. If this is not the case, thats considered abnormal and suggestive of conductive hearing loss

- Causes of conductive hearing loss: cerumen impaction, chronic otitis media or effusion, otosclerosis, bony tumors within the ear

- Otosclerosis causes conductive hearing loss in adults particularly in their 20s and 30s. It's thought to be potentially autoimmune. Stapes footplate becomes fixed to the oval window. There may be low frequency hearing loss. Treat with hearing aid or stapedectomy. 

5. The hepatojugular reflex is positive when the right ventricle is unable to handle the increased preload that comes from increased intra-abdominal pressure. 

- Causes include right heart failure, constrictive pericarditis (Such as TB), restrictive cardiomyopathy

6. General surgery smorgasbord: 

- No colonoscopy, sigmoidoscopy, or barium enema during acute inflammatory bowel process as the risk of perforation is high. 

- Diverticulitis that does not improve on antibiotics:: suspect intra-abdominal process/publication 

- Causes of toxic megacolon: IBD (UC that erodes through smooth muscle), c.diff, diverticulitis. Mange with bowel rest, pain control, antibiotics. Go to surgery if it doesn't resolve. 

7. Guillain-barre 

- Goes from legs up to arms and cranial nerves. 

- Progresses in hours to days. 

- Affects motor primarily, but can have distal paraesthesias. Can involve autonomic system and respiratory muscles, which can be life threatening. 20-30% of people will end up needing a vent.

- Track development of respiratory weakness and failure by serial measurements of vital capacity: <15mg/kg indicates significantly increased risk of respiratory failure. Other things like chest wall movements, or anything measured on spiro or peak flows or ABG or CXR are not as predictive as VC. 

- Treat with IVIg and plasmapharesis - steroids not indicated. 

8. Hepatic adenoma
- Common in young women with a long history of OCP use. Can also be seen with anabolic steroid use, pregnancy, diabetes glycogen storage diseases. Thought to be hormonal potentially but with unknown pathogenesis

- Path shows enlarged hepatocytes with cytoplasmic inclusions of lipids and glycogen. Nuclei are small and regular but hepatic architecture is distorted (no bile ducts etc)

- Can be found incidentally with imaging or labs (incidentally found LFTs). Elevated alk phos and GGT often indicate multiple adenomas or intratumoral bleed.
- Can present as collapse from rupture and intraabdominal bleed. Risk of bleed in symptomatic adenoma (ie abdominal pain) is 40%. 

- Do not biopsy as the risk of bleed is high.

- Manage symptomatic adenoma with resection. With asymptomatic, treatment is controversial, some resect b/c there is a risk of rupture or malignant transformation (8-13% of adenomas transform), others treat conservatively by d/cing OCPs, serial imaging and following AFPs. Many will spontaneously regress with this.  

9. Focal nodular hyperplasia is a benign tumor in the liver that arises from atypical blood vessels That cause hyperperfusion and local fibrosis. Biopsy shows Kupffer cells and sinusoids 

10. EBV mononucleosis typically will cause cervical lymphadenopathy and pharyngitis. While CMV mono generally does not.
Speaking of pharyngitis, EBV and group A strep are the most common causes; EBV tends to cause posterior LAD and splenomegaly, while GAS tends to cause anterior LAD and doesn't mess with your spleen. 

1. Empiric management of endocarditis: 

- Native valve: pen + gent. 

- Native valve, IVDU: nafcillin + gent to cover MSSA. vanc + gent if suspicion for MRSA

- Mechanical valve: cover MRSA, add rifampin for biofilm penetration 

- Replace vanc with linezolid if there is renal failure (issues with vanc levels) 

- Viridians strep endocarditis - IV penicillin continuous or q4-6 or once daily ceftriaxone for 4 weeks 

2. Don't treat HIT with Coumadin-- the rapid drop in protein c can aggravate the procoagulant state. Manage with argatroban or bivalrudin until platelets are > 150K, then you can start warfarin 

3. Some words on some drugs: 

- Bactrim covers s pneumo but not other strep species 

- Sodium bicarb blocks the effect of TCA on fast Na channels in cardiac tissue, hence the protective effect in overdose. 

- NSAIDs potentiate ADH and can lead to SIADH.

- Statins decrease  coenzyme q10 synthesis which is important for muscle energy - thought to be a possible etiology of the myositis. 

- Aspirin can trigger bronchoconstriction

- Alcohol sensitizies you to hypomagnesemia, increasing risk of torsades. 

- Drugs that prolong the QT: quinolones, macrolides, TCAs, class III antiarrhythmics 

4. Hemochromatosis 

- bronze DM

- hepatomegaly or cirrhosis (this disease is often diagnosed initially as incidentally raised LFTs on routine labs) 

- small testicle/decreased libido

- cardiac disease (dilated or restrictive myocarditis, conduction problems)

- Increased vulnerability to infections with listeria and vibrio vulnificus 

5. Splenic abscess

- Occurs in the setting of infective endocarditis (10-20% incidence?), immunosuppression (HIV), trauma, hemoglobin disease like sickle cell, IVDU. 

- Staph, strep, salmonella

- With antibiotics alone, there is a  50% mortality. Need splenectomy or percutaneous drain if they are too sick to go through surgery. 

6. Retropharyngeal abscess 

- Symptoms: trismus (pain w opening mouth), pain on neck extension, fever 

- Often history of local trauma (fishbone in throat) 

- Can dissect down into anterior or posterior upper mediastinum or all the way down the posterior mediastinum and cause necrotizing mediastinitis (requires urgent surgical debridement) 

- Vs: Meningitis, which has pain with neck flexion 

7. Back pain red flags

- Pain at night, not relieved by rest, not worsened with movement. 

- Bone that is tender to palpation, symptoms lasting > 1 month, age>50, 

- Get X-ray to r/o lytic lesion vs fracture, MRI if not diagnostic 

- Manage acute back pain with NSAIDs- acutely its better than PT. 

8. Acanthosis nigricans- DM or GI cancer

- More likely benign - young, obese person

- More likely malignant - older age. atypical locations such as mucous membranes, palms, soles

9. O2 supplementation in COPD: 

- In chronic COPD, people develop chronic hypercapnia and increased levels of deoxyhemoglobin, which has a higher CO2 affinity and increases carbon dioxide clearance. Adding oxygen blunts the amount of deoxyhemoglobin, decreasing clearance of CO2. 

- Acute hypercapnia: less myocardial contractility, lower seizure threshold, global loss of consciousness 

- Goal saturation for treatment of acute on chronic COPD with oxygen is 90-94% 

10. Polycythemia vera 

- causes gout in up to 40% of people 

- characteristic pruritus after a hot bath due to increased histamine released from increased basophils-  - - increased histamine secretion can also lead to gastric ulcer

1. Osteomalacia
- Vitamin D deficiency-- thus often seen in malabsorptive states (celiac's, bariatric surgery, bacterial overgrowth, etc)
- Initially, Ca and Phos will be low - stimulate PTH, which will bring Ca levels back up by leeching from bone and increasing reabsorption in kidneys
- Final labs: normal ca, low phos, high PTH, high alk phos.
- Sx: weakness, bone pain, pseudofractures (line of increased lucency on bone with surrounding thickened periostium/callouses), real fractures (in wt bearing lower extremities).
2. PCP pneumonia:
- LDH often up
- Treat with bactrim; if unable to tolerate bactrim then pentamidine
- Add steroids if PaO2 < 70 or A-a gradient > 35
3. PORT score (figure out whether to admit for pneumonia)
- Things that get you +30 points: cancer, arterial pH < 7.35
- Things that get you +20 points (end-organ damage): liver disease, AMS, tachypnea (>30), hypotension (SBP < 90), impaired renal function (BUN > 30), Na < 130
- Fever buys you +15 (Temp <35 or >40).
- Things that get you +10 points (comorbidities, labs that imply decreased reserve): nursing home, CHF, CAD, CVD, CKD, tachycardia (>125), glucose > 250, crit <30, PaO2 <60, pleural effusion
- You get 1 point for every year of age.
- Subtract 10 points for women.
- Risk class I if: age <50, no vital sign perturbations, not altered, doesn't have cancer, no major-organ comorbidities (brain, kidney, liver, heart)
- Class II if score is <70
- Class III 71-90
- Class IV 91-130
- Class V >130
- Send I home, use your judgement on II, III and IV need admission, V needs ICU admission

4. ESRD calciphylaxis
- Vessel calcifications and ulcerations on extremities (hand) - dx with skin bx.
- Tertiary hyperparathyroism.
5. Abortive treatments for migraine
- Tryptans
- NSAIDs / tylenol
- Caffeine
- Fioricet/fiorinal (butalbital + caffeine + aspirin/tylenol)
6. Calcifications around heart - chronic pericarditis
- autoimmune
- viral
- malignancy
- drugs
- uremia
- s/p radiation
7. Diagnose this: 
- RA on steroids + back pain + cauda equina sx: compression fracture vs infection/abscess
- Fever, LAD, lung nodules on CXR: HIV vs lymphoma vs disseminated fungal
- DM + diarrhea: metformin side effect (lasts weeks) vs autonomic enteropathy (gastroparesis in colon) vs c.diff
- Hemolytic anemia + bullous myringitis: mycoplasma
- Muscle pain + heavy menses + weight gain: hypothyroid
- Fever + alopecia + palmar rash: secondary syphilis
- History of surgery + vomiting: SBO
8. DVT prophylaxis
- low risk: mechanical prophylaxis, or nothing (make them walk)
- medium: heparin/lovenox,
- high (ortho, neuro): therapeutic anticoagulation (ortho: coumadin,
9. Incidentally found adrenal mass: 
- Likelihood to be cancer increases if the mass is big (2% if <4cm, 25% if >6cm), hypervascular, necrotic, irregular borders. Mets are likely to be b/l.
- Most common are tumors that secrete cortisol (sub-clinical levels) so screen with dex suppression test. Also screen for pheo as they can have intermittent symptoms.
- Don't screen for aldosterone secreting tumor unless you have clinical signs, same with androgens.
10. Cosyntropin = synthetic ACTH. Good to evaluate adrenal function in adrenal insufficiency states.

1. Solitary pulmonary nodule:
- Calcifications that favor benign pathology: popcorn (hamartoma), bulls-eye (granuloma)
- In low risk (age <40), if there is evidence of no radiographic change in last 12 months its considered benign. CXR q3 months for next 12 months, if there is no growth you're done.
- If high risk (ie smokers), need more w/u - CT then FNA. If that fails open lung bx.
2. Dermatitis herpetiformis 
- Intensely pruritic papules over knees, elbows, buttocks, posterior neck, scalp.
- IF: granular IgA along dermal papillae. +anti-endomysial ab.
- Treat with dapsone and a gluten free diet. Unclear why dapsone works-- antiinflammatory/immunemodulating effects?
3. Erythemas
- Multiforme: often acral distribution + mucous membranes, target shaped, associated with many diseases incl recent HSV infection
- Nodosum: nodular, associated with sarcoid
- Marginatum: ring shaped lesions on extensor surfaces, one of the JONES criteria
- Migrans: lyme disease; target shaped
4. Bullous derm: 
- Bullous pemphigoid: benign, pruritic. Tense blisters - IgG and C3 in dermal-epidermal junction. Rarely affects mouth.
- Pemphigus vulgaris: flaccid bullae, +nikolsky sign, IgG in the epidermis - autoantibodies against desmoglein (adhesion molecule). Treat with steroids, DMARDs like azathioprine or mtx.
- Bullous impetigo: s.aureus
5. Skin cancer: 
- On the lips: squamous cell
- Basal cell almost never appears on the lip, and when it does its the upper lip. Histo: spindle cells + palisaded basal cells.
6. Adrenal insufficiency 
- AI from TB is permanent- even after you treat the TB they will need lifelong mineralcorticoid and glucocorticoid supplementation.
- In developed countries 80% is from autoimmune
- Often occurs in HIV+ patients (CMV, mycobacteria, fungi, TB). Antifungals (keto) can precipitate AI by inhibiting steroid synthesis.
- Rare from mets.
7. ADPKD: 
- Incidence 1:500
- Positive family history in 75% of cases
- 50% + have hypertension at presentation
8. PBC
- Insidious, affects middle aged women
- Exam: hepatosplenomegaly,. xanthomas => jaundice, steatorrhea, portal HTN, osteopenia
- +antimitochondrial antibodies
- Assoc with sjogrens, raynaud's scleroderma, autoimmune thyroid, hypothyroid,. celiac.
- Treat with ursodeoxycholic acid - slows progression, relieves symptoms. MTX and colchicine have shown moderate benefit. NO role for steroids.
- Without liver transplant, survival 7-10 years after onset of symptoms.
- Can manage symptoms with cholestyramine.
9. MIBG scans are more specific but less sensitive than CT for detecting pheo.
- Use it when the CT is equivocal, when there is extra-adrenal pheo, or if you suspect cancer.
10. Steroids for AI
- Stress dose is 10x the normal daily dose-- for most people this will mean 100 mg hydrocortisone IV. Give divided in 3-4 doses.
- Hydrocortisone is a glucocorticoid, but once the dose is 60mg/day, it has mineralcorticoid activity and you no longer need fludrocortisone.

1. Erysipeloid:
- E.rhusiopathiae.
- Comes from handling fish and meat- bacteria gain access into hands, causes finger cellulitis
- Treat with penicillin, erythro or doxy if pen allergic. Inherently vanc resistant.
2. Ruptured baker's cyst
- Can present like DVT with posterior calf swelling. Fluid will sometimes leak down leg and cause crescent shaped bruise over medial malleolus.
3. BUN/Cr ratio most sensitive predictor of dehydration 
4. Intestinal lymphoma: 
- Diarrhea, nausea, vomiting, weight loss. Distention, occult blood.
- Typically don't see malabsorption
- Bx will show atypical lymphocytes.
5. Criteria for home O2 in COPD: 
- RA sat < 88, PaO2 < 55
- RA sat < 89, PaO2 < 59 + evidence of R HF
- Hypoxia during exercise or sleep
Titrate O2 to >90%. Survival benefits of home O2 are when it is used for >15 hours a day.
6. Knee pain
- Patellofemoral pain syndrome (women > men, typically young, perhaps due to the shape of the hips - knees, less stability of patella). Constant pain, worse with stairs or squatting. Test by pressing down on patella
- Patellar tendinitis: jumper's knee, typically affects athletes. Episodic pain. Pain at lower border of patella.
- Osgood schlatter: doesn't affect adults. children/adolescents during growth spurt, pain at tibial tubercle.
7. Management of heat stroke
- Exertional: immerse in cold water
- Non-exertional: evaporative (spray with leukwarm water, use fans to blow air). Cold water immersion associated with increased mortality in this group.
8. Indication for valve replacement in aortic regurg
- Severe regurg + cardiopulmonary symptoms
- Severe regurg + signs of heart failure/enlargement/adverse hemodynamics
- Severe regurg + LV EF < 50-55%
9. Hypothyroidism and pregnancy: 
- Follow TSH and total (not free) T4.
- Keep T4 1.5x normal and keep TSH on the low side of normal.
- May need 30-50% increased dose of synthroid as early as first trimester
- Do not give iodine supplements to pregnant women with normal iodine levels-- pharmacologic levels of iodine can cause fetal goiter and wolff-chaikoff, preventing release of iodine in the fetus.
- Postpartum thyroiditis- can present with hyperT, hypoT, or like hashimotos'- thyrotoxicosis phase (decreased iodine uptake) followed by hyperthyroid phase (increased iodine uptake as the thyroid attempts to recover). People generally make a full recovery.
- For treatment of hyperthyroidism in pregnancy, do PTU in first trimester, then methimazole later on. Methimazole is a first trimester teratogen.
10. Euthyroid sick syndrome
-  Lowered levels of TSH, T3 and or T4 after severe illness (starvation, ICU stay, sepsis, pneumonia, etc)
- Repeat tests in 4-8 weeks- they will often return to normal
- Mechanism- may be false negative tests (2/2 perturbations in homeostasis, the tests may not function normally), may be that cytokines are inhibiting the pituitary, may be decreased peripheral de-iodination of T4 to T3. More details on mechanism here

1. Angina equivalent or atypical angina: dyspnea, dizziness, syncope, fatigue, diaphoresis, nausea, epigastric pain
2. Right sided MI
- ST elevation in V4-R is the most predictive finding
- Treat hypotension with fluid first (to increase preload). If that fails, go to inotropes-- inotropes will increase myocardial O2 demand and possibly extend the infarction so it's not first-line
3. Second degree AV block
- Mobitz I: can occur in the absence of structural heart disease- in athletes or old people. It can also occur in conjunction with ischemic heart disease, and with AV nodal blocking agents (b-blockers, ca-channel blockers, digoxin). Only treat if you get symptomatic bradycardia resulting in decreased cerebral or cardiac perfusion. Start treatment by stopping things that slow conduction through AV node (the drugs), fix any increased vagal tone (i.e. 2/2 vomiting or pain), fix ischemia.
- Mobitz II: often occurs in conjunction with other conduction disease (bundle, fasicular block). Needs a pacemaker, because this suddenly and unpredictably progresses to complete heart block.
-Second degree AV block in conjunction with any other conduction disease (bundle or fascicular block) buys you a pacemaker, even asymptomatic wenckebach's.
4. Management of chronic stable angina:
- Anti-anginal agents: PRN nitrate (can increase to long acting if frequently using PRN), beta-blocker (20% decrease mortality), calcium channel blocker
- Vasculoprotecive agents: ACE (17-23% reduction in cardiovascular mortality), statin (25-30% reduction cardiovascular events), aspirin (33% decrease MI/stroke/sudden death). Plavix has no role in management of chronic stable angina- increases bleed risk.
- If someone is hypertensive or tachycardic, increase B-blocker - should titrate to resting HR of 55-60 and 75% of the heart rate that produces angina on exertion.
- Ranolazine new antianginal agent (affects Na-dependent Ca channels? prevents Ca overload? Shifts to carbohydrate-focused metabolism rather than less efficient fatty acid metabolism?). Add on when optimal medical therapy, including long-acting nitrate and max-dose b-blocker and ca-channel blocker, have failed.
- If still have angina despite max medical therapy, PCI is warranted.
5. Stress test: 
- Indication: CHD risk score 10-90% based on symptoms age and gender (see below), complete RBBB or <1mm ST depression at rest

- Exercise stress test is preferred to chemical, as it tells you how much work is possible before you get angina, hemodynamic response and exercise tolerance are both predictive of outcomes (if you're not healthy enough to do the treadmill test, that's a really bad sign). Exercise to goal of 85% of ideal HR = 0.85 (220-age)
- Limitations of exercise stress- it's EKG based, so abnormal EKG @ baseline = should pick a different test.
6. Adenosine nuclear perfusion 
- Contraindicated in patients with significant bronchospastic disease (since adenosine may stimulate A2B receptors, which lead to bronchospasm), significant hypotension, sick sinus or high degree block as it may worsen block.
- Theophylline and caffeine should be avoided for 48 & 12 hours beforehand as they may blunt the response to vasodilation
7. Dobutamine stress echo 
- Used when patients have a contraindication to vasodilators, have taken theophylline within last 48 hrs or caffeine within last 12.
- Contraindications: hypertension (systolic at rest >180), hemodynamically significant LV outflow obstruction, aortic disseection, sustained ventricular arrhythmias
8. CAD workup
- Framingham risk score <10: nothing, go home
- Risk 10-20: coronary calcium scoring
- When to go to coronary angiography? Lifestyle limiting angina despite optimal medical therapy, markedly positive stress test, resuscitation from sudden cardiac death, documented vtach, complete r/o of CAD in someone with chest pain
- When to place a stent? Angina despite medical therapy, large area of at-risk myocardium on stress test, high-risk obstructions like left main disease or 3-vessel disease, significant CAD with decreased LV systolic function.
9. Tachycardias
- Idioventricular tachycardia/slow ventricular tachycardia: wide QRS, HR 60-100
- MAT: 3+ p-wave morphologies, often occurs in chronic lung disease.
10. Complications of acute MI:
- Acute mitral regurg from papillary muscle rupture -- occurs several days after the MI, more common after inferior MI -- treat with balloon pump as a bridge to surgery
- Ventricular free wall rupture- occurs 1-4 days after MI, presents as tamponade, PEA, sudden death
- LV aneurysm: late complication. presents as intractable v-tach, systemic emboli, heart failure
- Ventricular septal defect: 2-7 days after MI, presents as sudden onset dyspnea, hypotension, new systolic murmur

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)

1. Modified Duke criteria for infective endocarditis: Need 2 major criteria, or 1 major and 3 minor, or 5 minor.
Major criteria: 
- 2+ blood cx drawn 12 hrs apart, or 3 cx (2 of which are drawn 1 hr apart) of organisms that classically cause endocarditis (strep viridians, strep bovis, HACEK, enterococcus and s.aureus without other source)
- Echo findings: oscillating mass on valve, abscess, new valve regurg, dehiscence of part of prosthetic valve.
Minor criteria: 
- Fever > 38
- Heart valve dx, IVDU
- Vascular phenomena: arterial emboli, intracranial hemorrhages, pulmonary emboli, conjunctival hemorrhages, janeway lesions
- Immune phenomena: glomerulonephritis (immune complex deposition), rheumatoid factor (IgM against IgG), olser nodes, roth spot (immune complex mediated vasculitis leading to hemorrhages in retina)
- Blood cx findings that don't quite meet major criteria
2. Staph endocarditis: 
- Penicillins and b-lactams are the best drugs.
- In the rare incidence when it's susceptible to penicillin, use pencillin
- MSSA: use nafcillin, oxacillin, or cefazolin. Adding gent for the first 3-5 days may speed up clearance of bacteremia. Vanc is slower than these drugs, and clinda has a high failure rate in vivo (maybe because its bacteriostatic against many strains of s.aureus). Linezolid is +/- in efficacy.
- Use vanc for pen allergic people.
3. Endocarditis of prosthetic valve:
- Treat with rifampin, gent, and something to cover staph-- Naf/ox/cefazolin for MSSA or vanc for MRSA.
4. Anti-pseduomonals:
- Third gen cephalosporins: ceftazidime (no MRSA coverage), cefoperazone (has a side chain which can inhibit vitamin-K activity and cause a disulfram like reaction)
- Ag: tobra, gent, amikacin
5. Diabetic foot ulcers
- If a metal probe hits bone, 90% PPV for osteomyelitis
- Need bone bx to find the deep organisms that are responsible for the infection-- superficial ulcer organisms often do not correlate with the deep organisms.
6. Spine osteomyelitis
- If blood cx are negative, will need CT-guided needle biopsy.
7. Aplastic anemia
- Cell lines down but cell maturation normal, BM <20% cellularity
- 50% of the time no identifiable cause, 50%: drugs, chemicals, viral, collagen vascular, thymoma
- Workup: withdraw all potential causative agents, CT chest to r/o thymoma
- Interferon-activated T-cells targeting hematopoietic stem cells implicated in pathogenesis, immunosuppressives sometimes effective
8. ITP
- Platelets low, but white count normal
- May have associated hemolytic anemia, or iron-deficiency anemia from bleeding.
9. B12 deficiency:
- Serum homocysteine and MMA levels will elevate before B12 levels drop
- In folate deficiency, only homocysteine will be high.
10. Indications to screen for coagulopathy before surgery: 
- Personal or family history of bleeding
- Heavy alcoholism: alcohol partially inhibits platelets, reduces fibrinogen/factor VII/wWF levels, activates tPA -- this is perhaps responsible for the decreased risk of cardiovascular disease seen with mild or significant alcohol consumption. {source} The truth is that raging alcoholics don't get heart disease-- they die young of liver disease, or cancer, or accidents, or any of the other comorbidities of alcoholism, but they don't die of cardiovascular disease.
- Liver disease
- Malnutrition
- Anticoagulation
- For the purposes of exams, people without the above risk factors do not need a PT/PTT/INR before surgery.