1. Contraindications to stress testing: 
- Dobutamine - hypertension
- Exercise EKG - beta blocker (need to be able to get to 80% of max HR - max HR = 220 - age), not able to exercise ie claudication
- Dipyridimole/adenosine - bronchospasm
2. Secondary prevention of stroke - antiplatelet > anticoagulation. Best evidence aspirin alone, also good evidence for aspirin + dipyridamole, OK evidence for plavix, do not give aspirin+plavix (MATCH trial - increased risk of bleed)
3. For people with a-fib on anticoagulation with a high risk of stroke (stroke/TIA within 3 mos or CHADS2 4-5) who need to temporarily stop anticoagulation (ie for surgery), should bridge with coumadin
4. Tod's paralysis - post ictal, typically focal peripheral weakness (paresis in limbs), but can also present with aphasia, ophthalmoplegia.
5. Never do exercise stress test in asymptomatic patient. 
6. Goal INR
- Aortic mechanical valve - 2 to 3, +Afib - 2.5 to 3.5
- Mitral mechanical valve - 2.5 to 3.5,
- If systemic emoboli at therapeutic INR, then add aspirin
7. Causes of pulmonary HTN
- Heart (valve, intrinsic heart)
- Lungs - chronic hypoxia
- Weight loss drugs (phen fen, serotonin)
- HIV
- Chronic liver disease (hepato-pulm)
- Collagen vascular disease
- Idiopathic/Primary
8. Maternal mortality in severe pulmonary hypertension - 30-50%, even if she is asymptomatic. Pt should be counseled to avoid pregnancy, and if it happens, counseled to terminate.
9. Pulmonary artery pressures: 
- Exercise-induced rise in pulmonary systolic pressure abnormal if > 25 change or it total systolic pressure > 60
- Pulm artery HTN defined as mean pulm artery pressure > 25 or systolic > 40
10. CVVH vs hemodialysis: 
- CVVH uses convection while hemodialysis uses diffusion - both use semipermeable membrane
- CVVH can take off larger molecules like cytokines, thus theoretically works better in sepsis but has not been shown to pan out in clinical trials

1. Urine pH and kidney stones: 
- <5 : uric acid (treat with alkalinizing agents) - pure uric acid stones radiolucent
- 5-7 : ca-oxalate - radio-opaque
- 7-8 : struvite - radio-opaque
2. B-OH butyrate not detected in dipstick 
3. Mechanism of thromobcytopenia in chronic hep C infection: If cirrhotic - splenic sequestration
If no cirrhosis (and these mechanisms probably have a role in cirrhotic hep C thrombocytopenia as well)
- Thrombopoetin decreased
- Direct HCV virus infection of megakaryocytes
- Autoimmune (HCV falls onto platelet, you make antibodies against HCV-platelet epitope, platelets get tagged and taken up by spleen)
- Interferon therapy can cause thrombocytopenia
4. "Corkscrew esopahgus" = diffuse esophageal spasm
5. Rule out acute upper GI bleed  
- NG tube placement NOT sensitive test. Will miss up to 20% of acute GI bleed. Especially true if you don't see bile in the aspirate.
- Endoscopy is the gold standard, can be performed so long as INR < 3
6. Treatment for IBD
- 5-ASA aka mesalamine for UC and mild crohn's
- For new onset moderate to severe crohn's, use anti-TNFa +/- immunomodulator like azathioprine (imuron) or 6-MP
7. Low threshold for starting SSRI in chronic illness patients who meet MDD criteria
8. Malingering = secondary gain, vs factitious disorder = sick role.
9. Management of pulmonary hemorrhage
- Bronch (can intervene with balloon tamponade or electrocautery)
- If bronch cannot locate the source, pulmonary arteriography for embolization
- If the above two fail to control bleed and bleeding is unilateral, can go to OR for thoracotomy
10. Rotavirus vaccine has small risk of intussusception - contraindicated in patients with history. Live attenuated vaccine - contraindicated in pregnant women but not their household members, CI in severe illness but not mild.

1. Dengue vs malaria: 
- Dengue transmitted by aedes mosquito (bites during the day), malaria by anopheles mosquito (bites at night)
- Dengue much more likely to have a maculopapular rash (50% of time), malaria much less likely (5-10%)
- Dengue can present with red eyes
- 98% of the time, dengue is a self-limiting illness that resolves on its own. Treatment is supportive.
- In people who have had prior exposure to a different strain of dengue, re-infection can cause dengue shock or dengue hemorrhagic fever -- this is why it is so hard to develop a vaccine.
2. Typhoid 
- Fecal-oral transmission
- 1-3 week latency period
- Fevers, constitutional symptoms, leukopenia, mildly elevated liver enzymes
- "Rose spots" rash on trunk 2 weeks out
- treat with 3gen cephalosporin (preferred), azithro, fluroquinolone (resistance)
3. Eschar at site of tick bite - rickettsial disease
4. GLP-1 agonists: 
- I.e exenatide (byetta) which is qD injection, there's also a once-weekly injection (bydurion)
- Liraglutide
- Increase insulin secretion
- Decrease glucagon secretion
- Decrease gastric emptying - through this, causes weight loss
- Works in glucose-dependent manner, so they don't cause hyperglycemia
- Cons: Injectable only, $$$$
5. DPP-IV inhibitors: 
- inhibit DPP-IV which breaks down GLP-1
- Sitagliptin (Januvia)
- pros: PO formulation
- cons: do not cause weight loss like GLP-1 agonists do
6. DDx Hyperthyroidism: 
- Grave's disease
- Functional nodule
- Toxic multinodular goiter
- Thyroditis
- Early stage hashimoto's
- Iodine-induced (jod-basedow effect): from amiodarone or contrast! This does NOT happen with large quantities of iodine ingestion in a normal person, but rather in modest iodine ingestion from someone with a thryoid gland who is no longer under negative feedback control from the pituitary - i.e. grave's disease, toxic multnodular goiter, thyroid adenoma, endemic goiter. Many people with Jod-basedow will have anti-TPO antibodies or TTA antibodies. The wolff-chaikoff effect is the opposite - hypothyroidism from ingestion of large quantity of iodine, can happen in normal people as well.
- Struma ovarii
7. Grave's disease - can just present with isolated eye complaints without exopthalmos
8. Sulfonylureas
- Glyburide interferes with ischemic preconditioning and is associated with a increased risk of CV disease - affects K/ATP channels in the heart as well as in beta cells
- Glipizide or glimeperide doesn't have the same effect
9. Secretory diarrhea causes: 
- Bile salt induced (s/p chole)
- Eosinophilic gastroenteritis
- Microscopic colitis
- Cholera
10. Stool osmotic gap: 
290 - 2 (stool Na + Stool K)
If >100, implies osmotic

1. Vein of galen malformation
- Not really vein of galen, actually median prosencephalic vein of markowski, which is an embryonic precursor of the vein of galen that doesn't regress to be replaced as it should
- Occurs in 16th to 18th week of embryogenesis-- sinuses that later regress are visible (Falcine sinus? although this can also be patent in patients with thrombosed straight sinuses)
- Presents with high-output heart failure; can even present as antenatal heart failure
- If cases of massive shunt, the first task should be to evaluate the extent of brain damage to evaluate likelihood of meaningful recovery to guide care options, especially in light of the fact that these kids also suffer from liver failure and renal failure (presumably from lack of perfusion) and consumptive coagulopathy
- Can get parinaud's because the malformation is sitting on tectum
- They are hard sticks because their peripheral vessels are all collapsed (all blood shunted)
2. Types of malformations (Lasjaunia's classification) 
- Choroidal type: presents earlier in infancy, more severe shunt; multiple feeder vessels (choroidal, thalamoperforating, callosal)
- Mural type: presents later in childhood, less severe shunt, single fistula between median prosencephalic vein of markowski and feeder vessels.
3. Vein of galen malformations and hydrocephalus: 
- causes hydrocephalus from increased pressure in sinuses, lack of forward drainage.
- placing VP shunt can cause upward herniation
- placing VP shunts are also a high risk for bleeding because of the altered venous drainage pattern in the brain- blood is shunted to medullary veins, exactly where the catheter goes.
4. Aneurysms
- Form where there is shear stress -- in the direction of the net vector of flow. i.e., when at a bifurcation, it forms distal to the branch.
- Plaques form where there is low shear stress.
5. Ascending pharyngeal artery (APA) has anastomoses to many intracranial vessels
- Anastomosis to ICA via meningiohypophyseal trunk-- ACA sends branches up clivus, MHT sends branches down clivus
- The neuromeningeal trunk supplies the cranial nerves; as one would logically expect, the branch that goes through the jugular foramen (jugular division) supplies IX, X, and XI, while the one that goes through the hypoglossal canal (hypoglossal division) supplies XII.
- IF YOU EMBOLIZE EITHER OF THE ABOVE BRANCHES YOU WILL CAUSE CN IX, X, XI, or XII PALSIES. 
- Often, posterior fossa dural fistulas or dural-vascular lesions or mengiomas will have blood supply from the APA so it's useful to angio

{source}

{source}

"Intracranial Branches of the AP: {source}

A: Neuromeningeal Trunk

B: Hypoglossal Division of the Neuromeningeal Trunk (medial to Jugular divion on the AP view), which typically supplies: 

      C: Ascending clival branches which anastomose with each other and with inferior clival branch of MHT (L)

      D: Descending branch exiting thru foramen magnum and anastomosing at C3 with vertebral branches (odontoid arcade)

 E: Jugular Division of the Neuromeningeal Trunk, which typically supplies:

           F: Anterior branches anastomosing with lateral clival branches of the inferolateral trunk (ILT) near Dorello’s canal

           G: Sigmoid Sinus branch along Sigmoid Sinus wall, anastomosing with petrosquamosal branches of the MMA (J), Lateral Tentorial Artery of the MHT, and Occipital Artery transosseous branches (N)

 H: Inferior tympanic branch, supplying middle ear and anastomosing with carotidotympanic branch (N) of the ICA  (see aberrant carotid artery below)

 I: Foramen Lacerum branch of the pharyngeal division of AP, anastomosing with recurrent lacerum branch of the ILT (M)" 

6. Nervous tissue testing before embolization or other procedures: 

- Brain: amytal

- Peripheral: lidocaine

- Spine: both, but with a saline flush in between; amital is an acid and lido is a base, if they are in the blood together at the same time they will crystallize. 

- Eye: amytal 

7. Embolization of meningomas

- Some people wait a week after embolization to operate, with the logic being that you increase necrosis and thus make it easier to suck out

- Some people will go right after embolization, with the logic that you avoid postprocedural swelling 

8. Cartoid dissections

- Classically, a low, smoothly stenotic segment in a young person. 

- Stops at the skull base, because the way the layers of the vessel is tacked to the dura. 

- If someone has acute neck pain during angio, suspect iatrogenic dissection; you'll want to immediately give heparin and then aspirin if you caught it early; if you catch it late, aspirin only. Most will heal. Some will embolize and stroke. 

9. Intracranial dissections

- Vessels in the brain have a thinner adventitia than vessels outside; dissections often go through all 3 layers

- Higher bleed rate than aneurysms 

- Intracranial vert dissection - most common intracranial dissection, can sacrifice if non-dominant 

- Supraclinoid dissection ( = blister aneurysm) - second most common.  Impossible to clip. Difficult to coil. Can attempt coil + pipeline or coil + bracing stent. Generally speaking, carotid blister aneurysms are associated with horrible outcomes, especially if you have to sacrifice the carotid. The goal in management is to prevent carotid sac at all costs. 

10. Traumatic carotid cavernous fistula

- If someone has vision loss, if it's immediate - it was due to the trauma and will not recover, if the onset is gradual, it's due to the fistula and will improve when  you fix the fistula. 

- Delayed hemorrhage after trauma: c-c fistula with dissection 

- Delayed epidural hemorrhage after trauma: skull base fracture with middle meningeal artery fistula formation 

1. GVHD: 
- Skin is most commonly affected organ - next GI tract, liver
- Causes itchy maculopapular rash that often starts on palms and soles
- Skin may blister and even ulcerate
- Most commonly occurs after hematopoetic stem cell transplant (can even occur after blood transfusion in people who don't have T-cells or getting transfusions from close relatives - see June 15 2014 blog post about transfusion related GVHD and for a detailed description of all transfusion reactions) can rarely occur after solid organ transplant
- Treat with IV steroids to suppress engrafted T-cells
2. Dermatitis herpetiformis responds so quickly to dapsone (2-3 days) that a response is considered diagnostic
3. Erythema nodosum: 
- Inflammatory reaction of fat cells
- causes tender, inflamed nodules of shins
- Most common causes - idiopathic (50%), infectious (25%) (strep throat, mycobacteria, mycoplasma, the systemic fungal infections we learn about (histo, coccidioides) chlamydia, yersenia, rickettsia), sarcoid 25%, drugs (rare <5% OCPs, sulfa drugs, amoxicillin), IBD (<5%), pregnancy (<5%)
- Mnemonic for causes: "sore shins"
Sarcoid
OCPs
Rickettsia
Eponyms - like behcets
Sulfa drugs
Hansen's disease (leprosy)
IBD
NHL - non hodgkin's lymphoma
Strep
- Treat underlying cause. manage symptoms (bedrest, leg elevation, compressive bandages, wet dressings). NSAIDs work best in early phase, K-iodide in late phases.
4. Pyoderma gangrenosum: 
- Altered neutrophil chemotaxis
- Deep, nonhealing ulcers of legs (can affect hands - atypical pyoderma gangrenosum) with rolled violet edges
- Display pathergy- worse with debridement
- Associated with IBD, RA, seronegative spondyloarthritis, AML
- Treat with nsaids, steroids, biologics, antibiotics
- Good prognosis, frequent recurrence.
5. Acute promyelocytic leukemia - aka M3 subtype of AML. Responds well to all-trans retinoic acid. Can cause rapid death via DIC. Can also use retinoic acid with 5-FU to treat actinic keratosis.
6. Timing of repeat colonoscopy:
- At 3 years = high risk colon polyps: >1cm, high grade dysplasia, villous features, >3 adenomas
- At 5 years = low risk colon polyps: <1cm, low grade dysplasia, tubular adenomas, 1-2 polyps
- At 10 years = everyone else. Small hyperplastic polyps, esp in rectum.
7. Dieulafoy's lesion - large tortuous arteriole in stomach that can rupture and cause massive gastric hemorrhage - these are thought to be a congenital vascular malformation rather than degenerative.
8. Benzos safe in hepatic insufficiency: oxazepam, lorazepam
9. Steroids convey a survival benefit in severe alcoholic hepatitis 
- Contraindications: acute infection (SBP/sepsis), GI bleed, renal failure - this one I don't understand. The reasoning is not clear to me... steroids are primarily hepatically metabolized, although there is a renal metabolism component - 11-OH BSD converts cortisol to inactive cortisone, and prevents it from hitting mineralcorticoid receptors too hard. Perhaps that is the rationale... in acute hepatitis perhaps the renal metabolism becomes more important. Although it is unclear to me how much synthetic or metabolic function is lost in acute hepatitis.
This little ditty in the AJG suggests that there was some thought that steroids are not effective in the management of acute hepatitis when there is concomitant hepato-renal syndrome, but at least in this short case it seemed to help....
10. Dietary causes of osmotic diarrhea: 
- Lactose/fructose intolerance
- Excessive ingestion of magnesium, vitamin C

1. Neprilysin inhibitors-- block neprilysin, an endopetidase that degrades bradykinin, natriuretic peptides, and adrenomedullin. Increase endogenous vasodilation, diuresis, and inhibition of adrenomedullary activity.
2. PARADIGM-HF trial {double-blind RCT, n=8442, NEJM} shows neprilysin inhibitors effective in reducing mortality (20% reduction) and hospitalization for heart failure (20%) in patients with NYHA class II, III, or IV heart failure and EF < 40.
3. DEGRA trial in australia of bifrontal decompressive craniectomy for TBI {RCT, n=150, NEJM} found no benefit (long term death/disability) from the surgical procedure, and in fact more harm than for standard medical care. Importantly, there was a significantly (12% vs 27%) higher rate of people with non-reactive pupils that were randomized to surgery. Post-hoc analysis adjusting for that rendered the difference between surgical and medical care insignificant -- ie surgery was no longer harmful.

4. Prevention of venous thromboembolism in neurosurgery: a metaanalysis, {Chest 2008}

METHODS: We searched the medical literature to identify prospective trials reporting on VTE prevention (either mechanical or pharmacologic). The rates of VTE and bleeding were our primary end points and were pooled using a random-effects model.

RESULTS: We identified 30 studies reporting on 7,779 patients. There were 18 randomized controlled trials and 12 cohort studies. The results of pooled relative risks (RRs) showed LMWH and intermittent compression devices (ICDs) to be effective in reducing the rate of deep vein thrombosis (LMWH: RR, 0.60; 95% confidence interval [CI], 0.44 to 0.81; ICD: RR, 0.41; 95% CI, 0.21 to 0.78). Similar results were seen when pooled rates from all 30 trials were analyzed. In head-to-head trials, there was no statistical difference in the rate of intracranial hemorrhage (ICH) between therapy with LMWH and nonpharmacologic methods (RR, 1.97; 95% CI, 0.64 to 6.09). The pooled rates of ICH and minor bleeding were generally higher with heparin therapy than with non-heparin-based prophylactic modalities.
5. DVT rate overall {from same paper: Chest 2008} lower with chemoprophylaxis than mechanical prophylaxis 

6. ICH rate overall {from same paper: Chest 2008} higher with chemoprophylaxis than mechanical prophylaxis; most of the studies with lovenox are newer than the ones with heparin, I wonder if that impacts the findings at all. 

7. Death rate overall {from same paper: Chest 2008} is actually the same.... interesting. I wonder how robust this data is. It would also be interesting to see neurological morbidity as an outcome. 

(Major and minor referring to bleeds) 

8.  Venous thromboembolism prophylaxis in patients undergoing cranial neurosurgery: a systematic review and meta-analysis {Neurosurgery 2011}

METHODS: We selected RCTs that evaluated LDUH or LMWH prophylaxis of VTE in patients undergoing elective cranial neurosurgery. A meta-analysis assessing heparins vs no heparin (either with or without mechanical methods) was performed.

RESULTS:Eight RCTs were identified. Six RCTs involving 1170 patients evaluated LDUH or LMWH vs a control group. Five of 6 trials found a significant reduction in the risk of symptomatic and asymptomatic VTE with heparin prophylaxis. The pooled risk ratio was 0.58 (95% confidence interval, 0.45-0.75). ICH was more common in those receiving heparin, but not statistically significantly. For every 1000 patients who receive heparin prophylaxis, 91 VTE events will be prevented (approximately 35 of which are proximal deep vein thrombosis or pulmonary embolism and 9 to 18 of which are symptomatic), whereas 7 ICHs and 28 more minor bleeds will occur.

9. Patchell surgery for spinal cord mets study (methods) 
- Inclusion criteria: Age > 18, compressive lesion of spinal cord (not only cauda), at least one neuro deficit (incl pain), only one compressive lesion, no chronic paraplegia (>48 hrs), no radiosensitive tumors (germ cell tumors, lymphoma, multiple myeloma), no neuro-deficit-causing comorbidity (ie brain cancer), no previous radiotherapy such that would preclude further radiation of the dose requrired by the study
-  Cohort: N approx 100, half in control group (radiation only- 30 gy to spine incl 1 level above and below), half in surgery group (immediate circumferential decompression - specific technique was surgeon's choice + radiation)
10. Patchell surgery for spinal cord mets study (results)

Post treatment outcomes All-comers:
- 57% that could walk in rad only group, 84% could walk in surgery + rad group.
- Patients retained ability to walk for 13 (rad only) vs 122 days (surgery + rad), p<0.003
Excluding people who were paraplegic at baseline:
- 74% vs 94% could walk in rad only vs surgery + rad (p=0.02)

1. Trachoma

- Major cause of blindness worldwide

- Due to chlamydia trachomatis types A, B, and C

- Cause follicular conjunctivitis and pannus (neovascularization) formation in cornea. 

- Concurrent infection in nasopharynx can cause nasal discharge

- Diagnose with giemsa stain of conjunctival scrapings

- Tx with topical tetracycline or PO azithromycin, as repeated infections can lead to corneal scarring 

2. Neonatal chlamydial conjunctivitis
- Chlamydial conjunctivitis presents later (around 5-14 days after birth) than gonococcal
- Infants infected with chlamydia have a 30-50% chance of developing conjunctivitis and a 5-30% risk of getting pnemonia.
- Presents with chemosis, eyelid swelling, watery/mucopurulent discharge
- Cannot be prevented with topical eye drops
- Mange by testing mom - standard is testing at first prenatal visit for all women, and then repeat testing in 3rd trimester for all "higher risk" women - anyone under 25, women with new or multiple partners, inconsistent condom use.
- These kids can also get chlamydial pneumonia at around 1-3 months.
- Treat both conjunctivitis and pneumonia with 14 day course of PO erythromycin (note: there is a risk of hypertrophic pyloric stenosis with systemic erythromycin but in this case the cost clearly outweighs the benefit)
3. Gonococcal conjunctivitis
- Aka ophthalmia neonatorum
- Presents at 2-5 days after birth
- Eyelid swelling and copious purulent discharge
- Prevent with erythromycin ointment in eyes within 1 hour of birth
4. Paget's disease 
- hearing loss
- elevated alk phos may be the only aberrant lab (Ca, Phos, PTH all normal)
5. Transdermal patches take 8-12 hours to take full effect
6. Severe hypomagnesemia may mimic hypocalcemia as it causes decreased PTH secretion and decreased peripheral responsiveness to PTH
{some guidelines for electrolyte replacement dosing}
7. DDx for renal transplant dysfunction: 
- Calcineurin inhibitor toxicity (most studies have been with cyclosporine/sandimmune but tacrolimus/prograf is believed to have similar toxicity) - mechanism is believed to be vasoconstriction of afferent and efferent arterioles
- Acute rejection (tx with IV steroids)
- Ureteral obstruction
- Vascular obstruction
- ATN
8. HGSIL on pap smear in pregnant women: 
- Nearly 50% of HGSIL (pap) and CIN 2/3 (bx) will regress spontaneously during pregnancy; progression to invasive carcinoma is rare (<0.5%)
- If HGSIL is found, pt should get coloposcopy to exclude invasive cervical cancer. Neg colpo- repeat pap and colpo 6 weeks after delivery. Abnormal colpo - biopsy suspicious lesions. If CIN 2 or 3, then repeat cytology biopsy at 12+ week intervals
- Invasive procedures on the cervix (i.e. biopsy, LEEP) should be avoided on pregnant women unless there is a lesion present that suggests invasive cancer
9. Brain death
- Vagal control of the heart is lost - heart rate becomes invariant, and does not respond to atropine.
- Apnea test - no spontaneous respiration at PCO2 of 50+
- No reactive pupils, no oculovestibular reaction
10. Vectors 
- Rabies - Generally reservoirs are carnivores and bats - Raccoons are most prevalent rabid animal in US, esp east coast (caues Hydrophobia and aerophobia - the feeling of water or air triggers involuntary pharyngeal muscle spasms)
- West nile - mosquitos - culex species in the US
- Malaria - mosquitos - anopheles
- Dengue - mosquitos - aedes aegypti - bites during the DAY so if question stem says "patient was sleeping under mosquito net" they can still have dengue! This one way you distinguish from malaria.
- Lyme - tick - ixodes (deer) tick
- RMSF - tick - dermacentor (dog) tick 

1. Susceptibility bias: when treatment regimen selected depends on the severity of the patient's illness (i.e. crossover effect). Type of selection bias.
2. Conjunctivitis: 

- Bacterial: manage with erythromycin ointment, polymyxin-trimethroprim drops, azithro drops or fluoroquinolone drops (preferred in contact lens wearers) 

- Viral (usually adenovirus in summer/fall): warm/cold compresses, antihistamine or decongestant drops. Steroid drops are contraindicated. 

- Allergic (sx similar to viral but shorter duration): OTC antihistamine/decongestant drops, mast cell stabilizer/antihistamine drops for frequent episodes. 

- Mast cell stabilizing agents  - olopatadine, azelastine

3. HSV keratitis: 

- painful red eye

- impaired vision

- corneal ulceration 

- corneal opacification 

4. ACTH secreting tumors: 

- Tumors that secrete lots of ACTH and raise levels quickly (malignant tumors like small cell) cause more of the Aldosterone/mineralcorticoid effects - hypertension, hypokalemia, metabolic alkalosis, hyperpigmentation without the classical "cushingoid" effects. Cortisol has high affinity for mineralcorticoid receptors, but is generally converted to cortisone (inactive) by 11-B-hydroxyl dehydrogenase (11-beta-HSD) in kidneys; but when ACTH secretion is rapid and high the enzyme is saturated, leading more cortisol available to activate mineralcorticoid receptors 

- Tumors that secrete ACTH slowly and raise levels slowly (benign tumors like carcinoids) cause more of the cushingoid symptoms - moon facies, buffalo hump, striae 

- Ectopic ACTH causes worse HTN and hypoK than endogenous. Perhaps because it doesn't respond to the natural negative feedback patterns? 

5. Adrenal insufficiency: 

- Most common cause in developing countries is TB (calcifications in bilateral adrenal glands is pretty typical of TB). Adrenal function usually does not return after treatment of TB, and people need to be on lifelong glucocorticoids and mineralcorticoids 

- Most common cause in developed countries is autoimmune - responsible for 80% of patients with primary adrenal cortical insufficiency. You will not see calcifications on CT 

- In HIV+ patients, CMV, atypical mycobacteria, fungi, and TB are common causes of adrenal insufficiency; antifungals (like ketoconazole) can precipitate AI by inhibiting adrenal steroid synthesis 

- AI due to adrenoleukodystrophy - accumulation of very long chain fatty acids in adrenal glands - will show enlarged adrenal glands with no calcifications 

6. Eye infections: 

- Dacryocystitis: lacrimal sac infection, usually infants and adults > 40, sudden onset of pain and redness in medial canthus, usually s.aureus and beta hemolytic strep. Treat with systemic antibiotics 

- Episcleritis: infection of episcleral tissue between conjunctiva and sclera. Conjunctiva - thin layer of stratified squamous epithelium that lines inside of eyelids and covers "whites of eyes" (sclera) 

- Hordoleum: abscess on upper or lower eyelid, usually s.aureus - localized red, tender swelling

- Chalazion - chronic granulomatous inflammation of meibomian gland - hard, painless lid nodule. 

- Orbital cellulits: behind orbital septum (ie. orbital rim to eyelids) - proptosis, ophthalmoplegia, fever. 

7. Veiscoureteral reflux (VUR) is estimated to be present in 30-45% of children with UTI. 

- American academy of peds recommends all kids 2-24 mos with first UTI should undergo renal u/s to eval for anatomic abnormalities that may predispose to VUR

- VCUG should be done in any kids with recurrent UTI, but not after the first. 

8. Steroid mediated adrenal insufficiency: 

- Leads to decreased ACTH and cortisol, but aldosterone levels are generally normal since that's more regulated by renin-angiotensin and K levels

- May be associated with hyponatremia, as cortisol normally suppresses ADH secretion; in the absence of cortisol, an SIADH picture may occur 

9. Diagnosing cause of renal failure 

- <10 mEq/liter is considered low, and consistent with pre-renal 

- Hepatorenal syndrome has prerenal component as splanchnic vasoconstriction robs perfusion pressure 

- Clean dipstick suggests against intrinsic renal pathology 

- Cr does not rise with obstructive uropathy unless both ureters are obstructed 

10. Bipolar with psychotic features vs schizoaffective: 

- In bipolar with psychotic features, the psychotic episodes occur only when the mood symptoms occur. 

- The diagnosis of schizoaffective disorder is only applicable if the patient has psychotic symptoms in the absence of mood symptoms for at least 2 weeks. 

- Vs schizophrenia: in schizophrenia, the mood symptoms are a minor component of the disease and occur rarely. In the above 2 diagnoses, the mood components are a significant component of the disease and occur more often than not. 

1. Whipple's disease: 
- Malabsorption diarrhea
- PAS+ lamina propia
- Migratory polyarthropathy
- Chronic cough
- Myocardial or valve disease - may get CHF or valve regurg
- May get low grade fever, skin pigmentation
- Late stage disease may get CNS involvement - dementia, supranuclear ophthalmoplegia, myoclonus
2. Hypochloremic hypokalemic metabolic alkalosis 
- Vomiting -> Lose HCl -> excess HCO3- generated in serum as you try to make more HCl to replace losses -> loss of gastric acidity means less HCO3- secreted by pancreas into GI tract meaning more HCO3- is retained in blood -> volume depletion activates renin-angiotensin system -> aldosterone causes losses of H+ and K+ in urine in an attempt to retain fluid and Na.
- Manage with fluid resuscitation
- In very severe cases, can consider infusion of ammonium chloride but this can be toxic esp in people with impaired hepatic function
- HCl is used very rarely because it can cause hemolysis- saved for very severe metabolic alkalosis
3. Isolated systolic hypertension: 
- Should be treated because of association with risk for cardiovascular events
- Treat with thiazide, ACE, CCB
4. Macular degeneration
- Earliest signs are difficulty reading or driving, as they require fine visual acuity
- One of the earliest findings is that straight lines appear wavy
- Can now be treated with stem cells! Who needs magic when you have science
5. Basophilic stippling 
- Can be seen in lead poisoning, which typically causes a microcytic anemia
- Can also be seen in alocholism - ribosomal precipitates form blue granules in RBC cytoplasm.
- Can also be due to thalassemias.
6. Acute management of STEMI:
- Reperfusion (either with balloon angioplasty or tPA; angioplasty preferred within 90 mins of hospital arrival, 12h of onset of symptoms; tPA associated with higher risk of ICH and recurrent MI, only use if angioplasty CI or unavailable in the window of time)
- Antiplatelet: full dose aspirin (chew tab for fast release) + P2Y12 receptor blocker (ie clopidogrel, ticagrelor)
- Heparin gtt
- Oxygen
- Beta blocker, unless patient is bradycardic, has CHF, or is in cardiogenic shock... (which is hopefully obvious)
- Nitrates - contraindicated if patient is preload dependent, like aortic stenosis, RV infarct (which happens in 30% of people with inferior wall MIs i.e. STEMI in II, III, aVF). Also contraindicated if patient has had recent phosphodiesterase inhibitor use.
- Morphine for pain control if nitrates are not enough
7. Placental hormones: 
- Placental estrogens inhibit GnRH secretion during pregnancy; levels drop quickly with evacuation of placenta
- Human placental lactogen (hPL) is produced while placenta is in body-- has insulin antagonist effect; causes maternal lipolysis and insulin resistance which increases nutrition for fetus.
8. Stepwise approach to the treatment of asthma: 
- mild intermittent: albuterol PRN
- next step up: low dose inhaled steroid + albuterol PRN
- next step up: med dose inhaled steroid + albuterol PRN
- next step up: med dose inhaled steroid + LABA + albuterol PRN
- next step up: high dose inhaled steroid + LABA + albuterol PRN
- next step up: oral steroids + high dose inhaled steroid + LABA + albuterol PRN
{source}

9.  Asthma severity: 

{source}
Essentially for older kids (>5)
- < 2x/week attacks, <2x/month nighttime attacks = intermittent
- 2x/week to almost daily attacks, 3-4x/month nighttime = mild persistent
- Daily attacks, weekly nightttime awakenings = mod persistent
- Multiple times a day attacks, multiple times a week awakenings = severe persistent
10. Dermatology cancer terms 
- Marjolin ulcer = SCC that arose in a wound. Tend to have more aggressive behavior than SCC that didn't
- Dysplastic nevi = melanocytic nevi with odd characteristics (size > 6mm, irregular borders/coloration, cytologic atypia and disorder). I imagine they are precursor/precancerous lesions? These are usually monitored clinically

1. Defense mechanisms: Disassociation vs Repression 
- Disassociation: disruptions in memory, identity, consciousness, or perception to retain illusion of control; ie amnesia following a cancer diagnosis, being unable to remember such appointment despite others' reminding her.
- Repression: blocking upsetting ideas from entering consciousness - blockage of inner states (vs denial, blocks external sensory data). I.e. repressing memory of personal cancer diagnosis, and then not understanding why one is anxious when their child reaches the age that the patient was diagnosed with cancer.
- Psychiatrists tend to think of disassociation as a clinical, measurable phenomenon while repression is more of a  Freudian psychoanalytic concept that may be dated; I guess for the purposes of USMLE it sounds like disassociation may be used for discrete events while repression is a broader suppressive concept..?
2. CSF studies: 
- Albumino-cytologic disassociation (elevated protein with normal cell count) - Guillian Barre
- Oligoclonal bands - 85-90% of MS cases. However can be elevated in other neurological conditions as well.
- IgG index, the other test used for MS, seems to have less value than Oligoclonal bands.
3. ADPCKD: 
- Increased incidence of abdominal wall/inguinal hernias and colonic diverticula.
- Cysts in kidney, liver, pancreas
- Increased incidence of berry aneurysms in circle of willis
- Mitral valve prolapse
4. Henoch Schonlein purpura:
- Immune-mediated vasculitis: deposition of IgA in various tissues
- Most common in kids < 15
- Palpable purpura - normal platelet and coagulation studies
- IgA nephropathy - UA shows red cell casts, hematuria, mild proteinuria, Cr can be normal or elevated
- Abdominal pain - increased risk for intussusception - occurs in up to 4% of cases, and is frequently small bowel or ileo-ileal (rather than the usual ileo-colic of non HSP kids which can be reduced with air enemas); usually requires surgical management
- GI bleeding
- Arthralgias
- Scrotal swelling
5. DVT management
- First time DVT with clear reversible inciting incident: 3 months of coumadin (bridge with heparin)
- If post surgical, OK to start heparin in someone who is hemodynamically stable 48-72 hours after surgery UNLESS IT'S NEUROSURGERY then consult neurosurgical team for when its OK to restart anticoagulation
- Clot-lysing agents like streptokinase - not shown to improve survival with DVTs; may decrease post-phlebitic syndrome. Not commonly used.
- First time DVT in someone with no clear inciting incident - indefinite anticoagulation if bleeding risk low; 3-6 months then re-evaluate if bleeding risk high.
6. Turner syndrome: 
- Increased risk of osteoporosis: low estrogen from gonadal dysgenesis. These patients get estrogen supplementation for development reasons which also helps with osteoporosis prevention.
- Coarctation of aortic valve, aortic valve abnormalities
7. Lysosomal storage diseases: 
- Niemann-Pick: sphingomelinase deficiency, sphingomyelin accumulates in reticuloendothelial system and brain - hypotonia, hepatosplenomegaly, cervical lymphadenopathy, protuding abdomen, cherry-red macula
- Tay Sachs: hexosaminidase A deficiency - hyperacusis, mental retardation, seizures, cherry red spot, NO accumulation in reticuloendothelial system
- Gaucher's: glucocerebrosidase deficiency - hepatosplenomegaly, pancytopenia
- Krabbe's: galactocerebrosidase deficiency - hyperacusis, irritability, seizures
- Mucopolysaccharidosis I (Hurler's) - a-L-iduronase coarse facial features, HSM, corneal clouding/retinal degeneration
- Mucopolysaccharidosis II (Hunter's) - iduronate sulfatase deficiency - dermatan and heparan sulfate accumulation, HSM, frequent infections
8. Side effects of clozapine:
- See post from January 10, 2014 for thorough description of side effects.
- Briefly: agranulocytosis (need weekly CBC for 1st 6 mos then titrate down, 3% incidence in caucasians), myocarditis, seizures (give c depakote), metabolic syndrome
9. Postpericardotomy syndrome: 
- After pericardotomy, can develop reactive pericarditis (post op inflammatory reaction), pericardial effusion, even tamponade
- In small children can present with vomiting, decreased appetite, abdominal pain
- In older children presents as adults - pleuritic chest pain exacerbated by lying supine or inspiration,
10. Diabetic nephropathy
- Glomerular hyperfiltration -> Basement membrane thickening -> Mesangial expasnion -> nodular sclerosis
- Glomerular hyperfiltration can be seen within days of DM diagnosis; the ability of ACE-I to decrease this is believed to be the mechanism of their effectiveness in the treatment of diabetic nephropathy.

1. Before surgery
- Foley if case > 2 hrs
- Anesthesia on the side of the bed facing the face, for access to ET tube
2. Positioning
- Supine (+/- turning of head/neck, +/- shoulder roll) for frontal, temporal, and parietal approaches
- 3/4 prone (lateral oblique or park bench) for posterior parietal, occipital, sub-occipital
- Sitting: some prefer for sub-occipital approach; pros: increased venous/csf drainage. Cons: increased risk of air emboli, muscle fatigue from having to operate with your arms outreached the whole case
3. Incision
- Base should be broad in flap; flaps with narrow base are more likely to go ischemic.
- Try to avoid superior temporalis artery in case patient needs future EC-IC bypass (especially try to avoid cutting through main trunk of parietal STA.. that one's the really good one for this procedure) and try to avoid hacking up the facial nerve at the root (in front of tragus). Basically don't cut right in front of tragus.

4. Skin + Bone Flap elevation 

- Use periosteal rather than bovie to elevate temporalis as the vessels and nerves that supply it run in that fascial attachment layer and electrocautery will destroy it  

- The more burr holes you drill (i.e. the smaller the distance between burr holes) the lower the risk of tearing the dura in between. This is why you put them close together if you're going across a sinus. 

5. Moya moya disease
- Progressive intimal thickening affecting arteries coming off COW
- Usually b/l, can be u/l
- Cause unknown; may be genetic (thought to be AD with variable penetrance). Some have a higher level of thyroid antibodies; may have autoimmune component as well
- Higher incidence in asians, especially Japan
- Death (~5% in children, 10% in adults) is usually from hemorrhage. Deterioration from progressive strokes.
- Adults have more hemorrhage, children more ischemia
- Medical treatment: antiplatelet/anticoagulation, control BP if there is hemorrhage
6. Surgical management of moya moya: 
- EC-IC bypass - STA to MCA (M4) graft. Very difficult in children <2 years 2/2 small diameter of STA
- EDAS - dissect out STA, lay directly on arachoid (or on pia) and wait for smaller blood vessels to come in. Some theorize that its' not so much the direct revascularization process as the pro-angiogenic factors released by extracranial vessels that is of benefit.
7. Posterior fossa Tumors - ependymoma vs medulloblastoma
- both most common posterior fossa tumors in kids - each about 1/4-1/3, but medulloblastomas more common
- can appear very similar on imaging - somewhat heterogenous, T2 bright, enhancing.
- ependymomas tend to arise from floor of 4th, and medulloblastoma from roof ("medulloblast" thought to be granular cell layer precursors, hence cerebellar)
- if it extends through the foramina of lushka or magendie, it's more likely an ependymoma
- medulloblastomas tend to light up hot on dynamic perfusion MR (dsc-t2) since they are higher grade, while ependymomas (and jpa) are colder.
- maybe ependymomas are a little brighter on dwi/adc... They are hypercellular and so tend to restrict
- other possibly helpful tips that may or may not help - ependymomas sometimes are calcified, some say ependymomas conform to the shape of the 4th while medulloblastomas are rounder.
8 Cystic posterior fossa lesions with mural nodule
- Kid - jpa
- Adult - hemangioblastoma. (Also should make you think of von hipple lindau)
- In the above, the capsule usually doesn't enhance but if it does you need to take it surgically (along w mural nodule).
- enhancing capsule should make you expand differential to include higher grade lesions (mets, gbm)
9. Posterior fossa lesions in adults:
- most common tumor: met
- most common primary: hemangioblastoma
10. CPA Tumors
- 7/9 vestibular Schwannoma aka acoustic neuroma
- 1/9 meningioma
- 1/18 epidermoid cyst (diffusion restricts)

1. Hunt Hess grades for SAH: 
- 0: unruptured aneurysm
- 1: asymptomatic, or mild headache, and slight nuchal rigidity
- 1a: any neurological deficit, but no acute meningeal/brain reaction
- 2: CN palsy, mod-severe headache, nuchal rigidity
- 3: Mild focal neuro deficit, lethargy, confusion
- 4: Stupor, moderate-severe hemiparesis, early decerebrate posturing
- 5: Rigidity, deep coma, decerebrate rigidity, moribund appearance
2. Risk of vasospasm based on Hunt Hess grade 
- 1: 22%
- 2: 33%
- 3: 52%
- 4: 53%
- 5: 74%
3. Modified Fisher grade for SAH {source} 
- 0: No SAH, no IVH on CT
- 1: Thin focal/diffuse SAH, no IVH
- 2: Thin focal/diffuse SAH, + IVH
- 3: Thick focal/diffuse SAH, no IVH
- 4: Thick focal/diffuse SAH, + IVH
4. Risk of vasospasm based on modified fisher scale {source} 
- 0-1: 24%
- 2: 33%
- 3: 33%
- 4: 40%
5. More on the modified Fisher grade; from the {original study} "Explicit criteria for classifying blood as thick or thin, or focal or diffuse, were not applied."

1, 2, 3, and 4 correlate to modified fisher grades 1, 2, 3, and 4.
6. Modified fisher scale vs original fisher scale: 

7. Segments of MCA

There are a few different classification systems for the segments of the MCA; the surgical approach names the following: 

- M1 (sphenoidal): the straight part of the MCA, shown above in blue

- M2 (insular): the rising part of the MCA, inside the insula

- M3 (opercular): where the MCA once again turns straight as it runs along the parietal and temporal operculae.

- M4 (cortical/terminal): where the MCA turns out into the cortex. 

Some systems lump the insular and opercular segments together as M2, and call the cortical branches M3. 

The radiographic system names M1 as the MCA before bifurcation, and M2 as the MCA after bifurcation (seen below): 

8. Branches of the internal carotid: from a paper in {neurosurgical focus} 

9. Branches of ICA:

C1: cervical: no branches

C2: Petrous: has 3 parts (see below for best image - source)

- vertical segment 

- posterior loop (antero-interior to cochlea)

- horizontal segment (deep and medial to greater/lesser superficial petrosal nerves) 

C3: lacerum: passes over foramen lacerum, passes petrolingual ligament 

C4: cavernous: passes anteriorly, then supero-medially, then bends anteriorly to anterior clinoid. Ends at proximal dural ring (see below for best image- source) 

Branches in C4: 

- MHT (meningiohypophyseal trunk) - prominent MHT may indicate petroclival meningioma or dural AVM

- Tentorial artery (prominent may indicate petroclival/tentorial meningoma) 

- Inferior hypophyseal artery (supplies posterior lobe of pituitary) 

C5: clinoid: labelled as "C" in above image, between proximal and distal dural rings; distal dural ring completely encircles carotid-- it is at this point that the carotid becomes intradural. 

C6: Opthalmic: distal dural ring to just proximal to p-comm origin. 

- Opthalmic artery - origin distal to cavernous sinus in 89%, in cav sinus in 8%, absent in 3%. 

- Superior hypophyseal artery: supplies anterior lobe of pituitary and the stalk! 

C7: communicating: from just before p-comm origin to just below anterior perforated substance (where it bifurcates into ACA/MCA) 

- p-comm: gives off few anterior thalamoperforators (supplies optic tract, chiasm, posterior hypothalamus)

- anterior choroidal: supplies optic tract, medial globus pallidus, genu of internal capsule, inferior half of posterior limb of internal capsule, uncus, optic radiation, lateral geniculate body. 

10. Branches of the ICA (angiographic) {source} 

1. Lillequist membrane separates:
- the interpeduncular from prepontine cisterns (mesencephlalic part here shown by m)
- supracellar from interpeduncular cisterns (diencephalic shown here by d).
- Diencephalic is thicker and more often competent, which isolates the chiasmatic/supracellar cistern, while the mesecephalic is less likely competent
- Blood in interpeduncular cistern = low pressure pre-truncal source of bleed.
- Blood in supracellar/chiasmatic cistern = raises concern about aneurysmal bleed

2. Ruptured A-Comm aneurysm pattern of SAH

{image source}
Data on 81 patients from {a paper in AJNR} from the 1980s correlating pattern of hemohrrage with location of aneurysm

3. A-comm aneurysms (from greenberg)
-  Interhemispheric blood in almost all cases, and intraparenchyma hemorrhage in ~2/3 of cases, IVH in ~80%, acute hydrocephalus in about 25%.
- Frontal lobe infarcts happen in ~20%, usually within several days
- Bilateral ACA territory infarcts (causing prefrontal lobotomy like symptoms of abulia, apathy) are rare, but one cause is vasospasm after A-comm rupture.
4. Angiograph of a-comm aneurysms: 
- Check via angio if the aneurysm fills from both sides of the carotid vs one; if you think it's only one side, make sure by holding pressure on that side and injecting the other side again just to see if there's any collateral filling. Essentially, are you going to be able to get proximal control by clamping one ICA?
- Also check via angio if each ACA fills from its own side - this tells you whether or not you can trap the aneurysm. If both ACAs are supplied by one ICA and you trap the aneurysm, you'll give the person a unilateral ACA stroke.
5. Pterional approach to A-comm aneurysms:
- The classic approach. dissect down sylvian fissure as you retract frontal lobe, find ICA, follow anterior to find A1 and acomm. {Great article from WFNS} on surgical approaches to a-comm aneurysms. Same article is source of below image.

- If aneurysm is too high and would require excessive retraction on frontal lobe, you can either extend craniotomy to OZ, or do a cortisectomy into gyrus rectus (may cause neuropsych deficits)

"Illustration showing the difference in working angle obtained when the pterional approach (light blue) is converted to an orbitozygomatic approach (dark blue). The net difference is 10°, which provides a more shallow and wider exposure when the lateral wall and orbital roof are removed" {source for image and text}
6. When to do a L-sided pterional craniotomy: 
- For a-comm aneurysms you generally want to do a R crani, except:
- When dome of the aneurysm is pointing R, such that you would encounter dome before neck in a R crani
- When aneurysm is only supplied by L side; better proximal control with L crani
- There are multiple aneurysms, some on the L.
7. Other approaches to a-comm aneurysms
- Subfrontal: good for aneurysms that are pointing superiorly accompanied by significant frontal clot that you can evacuate at same time.
- Anterior interhemispheric: pros: less brain retraction; cons: suboptimal proximal control, low-forehead incision. Contraindicated in anteriorly pointing aneurysms.
8. Recurrent artery of Heubner 
- Often encountered in Acomm aneurysm surgery. Don't cut this.
- Most often comes off A2

From a {Rhoton} paper in JNS in the 70s: 

 More variant anatomy:

 photo from same rhoton paper:

More photo from internet: 

What happens when you cut Heubner: stroke of ipsilateral caudate, anterior internal capsule, and putamen. May cause hemiparesis of face and UE. 

9. A1 perforators
- As you can see from the above rhoton images, there are many perforators off A1 and the A-comm itself that go to the optic tract/chiasm and anterior perforated substance.
10. Anterior perforated substance:
- Posterior to trigone of olfactory nerve, anaterior to optic tract
- Important because the Anterior choroidal and many of the lenticulostriate perforators off M1 and A1 that supply the internal capsule and caduate, putamen, globus pallidus go through it

The following image is from {this paper} 

1. Giardia: 
- Adhesive disks allow adherence to bowel mucosa
- Cause malabsorption, leading to foul-smelling diarrhea, fatty stools, boating, flatulence, nausea, malaise, cramps
2. Osteogenesis imperfecta: 
- Blue sclerae
- Often associated with dentinogenesis imperfecta - bluish gray to yellow brown discoloration of teeth from dentin showing through translucent/weak enamel
- Hypotonia
- Osteopenia/recurrent fractures
- Easy bruisability
- Hearing loss
3. Nephrotic syndrome causes:
- FSGS: african american/hispanic, heroin, HIV, obesity
- Membranous: adenocarcinoma, NSAIDs, Hep B, lupus
- Membranoproliferative: Hep B/C, lipodystrophy
- Minimal change: idiopathic (kids), NSAIDs/lymphoma (hodgkins) in adults
- Amyloidosis: multiple myeloma, chronic inflammation (RA, bronchiectasis)
- IgA nephropathy (presents with nephrotic syndrome in <10%, more commonly presents as nephritic syndrome after URI)
4. Bladder trauma
- Dome of bladder has developmental hiatus where urachus originates during embryonic life and is most susceptible to rupture with sudden increases n pressure
- Dome is also only part of bladder with peritoneal border- rupture here can cause spillage of contents into peritoneum, resulting in chemical peritonitis
- Most common site of extraperitoneal rupture is bladder neck
5. Baker's cyst: 
- Inflamed synovium produces excess fluid, expanding popliteal bursa beyond normal size and causing a tender mass in popliteal fossa
- Caused by RA, OA, cartilage tears
- May occasionally rupture and cause DVT-like picture of whole calf swelling
6. Bronchiectasis 
- Presents with copious sputum production, hemoptysis, cough, dyspnea, weight loss, fatigue, fevers, pseudomonas infections
- Vs chronic bronchitis which is more of a dry cough
- Work up: high res chest CT, if focal bronch to look for a mass/biopsy, if diffuse test for systemic disease (autoimmune titers, antibody levels for immune deficiency)
- Management: antibiotics, steroids to reduce airway inflammation, chest PT, decongestants/mucolytics
7. Bronchiectasis DDx
- Post infectious: viral, TB
- Immunodeficiency: hypogammaglobulinemia:
- Congenital: a1-antitrypsin, CF
- Obstructive: lung cancer
- Rheumatic/systemic diseases: RA, Sjogrens
- Toxin
8. Histoplasmosis
- Soil, bird, bat droppings; no person-to-person transmission

- Mild pulm disease in immunocompetent, disseminated disease in immunocompromised (pancytopenia, HSM, adenopathy, diffuse reticulonodular/cavitary pneumonia, mucocutaneous lesions). Mortality > 90% in untreated disseminated disease from shock. 

- Diagnose with urine or serum antigen (sens >95%). Other lab abnormalities: cytopenias, elevated LFTs, elevated LDH & ferritin, culture, microscopy. 

- Serum antibody testing is of questionable sensitivity in immunocompromised patients given impaired antibody response; skin testing is also of lower sensitivity, as is culture (60-70% sensitive) 

- Treat mild disease with nothing or PO itraconazole. 

- Treat severe disease (T>39.5/103, lab abnormalities, fungemia) with IV amphotericin B for 2 weeks, switch to oral itraconazole for 1 year once documented response. 

9. Foot pains

- Morton neuroma: pain between 3rd and 4th toes on plantar surface, with clicking sensation when palpating the space and squeezing metatarsal joints (Mulder sign)

- Stress fracture: pain over bony surface (2nd, 3rd, or 4th metatarsals most commonly) can be dorsal or plantar surface. Young female athelete with oligomenorrhea, poor nutrition, osteoporosis) 

- Plantar fasciitis: burning pain in plantar distribution, worse in AM, improves with activity, worsens at end of the day

- Tarsal tunnel syndrome: compression of tibial nerve as it goes through ankle; often s/p fracture. Burning pain in distal plantar surface of foot that can radiate up calf

- Tenosynovitis: usually in hands, following bite or puncture. pain and tenderness along tendon sheath esp with flexion/extension 

10. Premature ovarian failure:
- Symptoms: amenorrhea, hypoestrogenism, elevated FSH for 3 months
- May be due to accelerated follicle atresia or low number of primoridal follicles
- May be due to mumps, oophoritis, radiation, chemo
- May be associated with autoimmune diseases - hashimotos', type I DM, addisons', pernicious anemia.
- Implies lack of viable oocytes-- so the only treatment if the patient desires fertility is donor eggs/IVF.
- If patients have some ovarian reserve (PCOS for example) can induce ovulation with clomiphene citrate or pulsed GnRH agonists (continuous GnRH agonists suppress ovulation)

1. Acute monocular vision loss:
- Central retinal artery occlusion: acute onset, retinal pallor, cherry red fovea, boxcar segmentation of retinal veins
- Central retinal vein occlusion: painless, subacute onset, "blood and thunder" retinal exam - swollen tortuous veins, retinal hemorrhages, optic disk edema, cotton wool spots. Risk factors: coagulopathy, artherosclerosis, chronic glaucoma.
- Amarugosis fugax: temporary, carotid emboli
- Uveitis: painful, red sclera
- Acute angle closure glaucoma: painful, hard eye, halos around lights.
- Optic neuritis: severe pain, swollen optic disk, central scotoma visual defficit
2. Side effects of antithyroid treatments: 
- PTU: black box for hepatic damage. Also causes vasculitis, which methimazole does not cause. Both can cause rash and arthralgias. Safer than methimazole in first trimester of pregnancy though, so indicated in that circumstance. Allergic reaction in 2% (most common), agranulocytosis in 0.3% - monitor cbc if pt has symptoms of sickness, however routine cbc is not indicated.
- Methimazole: teratogenic towards fetus in first trimester. Can also cause hepatitis, arthralgias, rash, agranulocytosis.
- People are typically treated for 1 year, and then the drugs are stopped to see if someone has gone into permanent remission (30-40% of people will); if so, they can stop; if not, they have to go back on the drugs for life.
- Radioiodine ablation: can cause permanent hypothyroidism, worsening of exopthalmos.
3. Subcortical strokes: 
- Pure motor - subcortical white matter, brainstem
- Pure sensory - thalamus
- Ataxia-hemiparesis: pons
4. Cortical strokes: 
- ACA: lower body weakness/sensory deficit, dyspraxia, abulia (lack of will/initiative), emotional disturbances, urinary incontinence
- MCA: weakness, aphasia (dominant), hemineglect (nondominant), eye deviation towards infarct
5. Posterior circulation strokes: 
- Midbrain: ipsilateral CN III palsy, contralateral weakness/ataxia
6. Menorrhea: 
- Primary: normal exam, pain concomitant with onset of menses
- Adenomyosis (ectopic endometrium in the myometrium) uterine enlargement & tenderness
- Endometriosis: adenexal lumpiness and tenderness; pain typically precedes menses
- Infection: cervical motion tenderness, purulent discharge
- Fibroids: lumpy uterus
7. Anti-TPO antibodies: 
- Present in 10% of general population, 30% of older females, 90% of those with hashimotos
- May herald thyroid disease if pt is asymptomatic
- Titers higher earlier in disease course, fall with time.
8. Graves disease: the lesser known symptoms
- A-fib
- Proximal muscle weakness/wasting (up to 60-80% of untreated people will develop acute/chronic myopathy)
- Acute thyrotoxic myopathy: distal or proximal muscles, but spares bulbar/respiratory
- Chronic: proximal muscle weakness weeks to months after onset of hyperthyroidism
- Hyperreflexia
9. DDx proximal muscle weakness (can't comb hair, drops into chair)
- Connective tissue disease: polymyositis, dermatomyositis
- Endocrine: hyperthyroidism, hypothyroidism, cushings
- Neuromuscular junction: lambert eaton, myasthenia gravis
- Drugs: steroids
10. Inherited immune deficiencies: 
- SCID: recurrent sinopulm, diarrhea, candidiasis from birth. No tonsils, lymph nodes, thymus. Severely reduced levels of B/T/NK cells
- CVID: presents like Bruton's, but with less severe symptoms at a later age (15-35). Decreased IgA, IgG, IgM, IgE, but NORMAL B-cell counts
- Bruton's/x-linked: recurrent onset of pyogenic infections (S.pneumo and H. flu) at 6-9 months of age, with decreased IgG, IgA, IgM (dx criteria: 2 SD below mean), and DECREASED B-cell counts (dx criteria: <2% CD19+ B cells in circulation). Absent isohemagglutinins, poor response to vaccines
- Wiskott Aldrich: x-linked. Eczema, thrombocytopenia, recurrent infections with encapsulated organisms. May present with bleeding early on (bleeding c circumcision, petechiae, bloody stools). Low IgM, high IgA and IgE, poor antibody responses to polysaccharide antigens, moderately reduced T cells and platelets
- Chronic Granulomatous Disease: recurrent infections with catalase-positive organisms - lymphadenitis, abscesses of skin and viscera (liver). Defect in NADPH oxidase complex. Nitro blue tetrazolium test.

1. Eplerenone is a selective mineralocorticoid antagonist with low affinity for progesterone/androgen receptors, so it'll block aldosterone excess without causing libido effects or gyencomastia or menstural irregularities, like spironolactone can. useful for medical management of aldosterone secreting tumor or adrenal hyperplasia.
2. Androgen insensitivity: 
- Androgen receptors insensitive to testosterone
- Elevated T (within normal male ranges 300-1100 but over normal female ranges 20-80)
- Normal testes develop, secrete mullerian inhibiting factor leading to agenesis of upper vagina, uterus, fallopian tubes
- Normal breasts as testosterone is converted to estrogen peripherally
- VS mullerian agenesis, which have absence of same internal organs but XX karyotype and normal female levels of T
- Random fact: Wolffian ducts become seminal vesicles, epididymis, ejaculatory ducts, and ductus deferens
3. DDx of primary hypoparathyroidism: 
- Post surgical (most common - after thyroid or parathyroid resection)
- Autoimmune hypoparathyroidism (most common after surgical)
- Congenital absence of parathyroids (ie DiGeorge)
- Infiltrative replacement of parathryoids (ie. Wilson's, hemochromotosis, neck radiation)
- Defective calcium sensing receptor (I guess it would be the opposite of familial hypocalciuric hypercalcemia)
4. Hyperparathyroidism:
- Primary: parathyroid hyperplasia, adenoma, (rare) carcinoma
- Secondary: vitamin D deficiency or renal failure (cannot convert 25-OH vitamin D to 1,25-OH vitamin D). Leads to low serum Ca, thus serum PTH elevates to compensate, which leads to Phos losses in urine. {source}
5. Congenital diseases:
- Toxo: chorioretinitis, intracranial calcifications, hydrocephalus, hepatosplenomegaly, lymphadenopathy, microcephaly, micropthalmia
- Rubella: Cardiac anomalies (PDA, ASD), congenital deafness, cataracts, congenital glaucoma
- Syphillis: fever, osteitis, osteochrondritis, mucocutaenous lesions, persistent rhinitis
- HSV: encephalitis, chorioretinitis, but no structural congenital malformations (ie microcephaly)
6. management of acute limb ischemia from embolus: 
- IV heparin
- IA tPA or embolectomy with either vascular surgery or IR
7. Pancreatic pseudocyst:
- Not a true cyst as lacks epithelial layer; actually surrounded by fibrous capsule
- Diagnose with ultrasound
- Indication for draining: not resolved after 6 weeks, >5cm, superinfected
- May erode into blood vessel causing hemorrhage
- Can complicate acute or chronic pancreatitis
8. Other bad things that can happen to pancreas:
- Hemorrhagic pancreatitis (presents like hemorrhagic shock + necrotic pancreas)
- Infected pancreatitic necrosis - occurs 1-2 weeks after acute pancreatitis with infection picture then septic shock picture. Manage with surgery
- Pancreatic ascities: rupture of pancreatic duct or cyst into peritoneal cavity - abd distention + shifting dullness
- pancreatic abscess: tender epigrastic mass, fever, leukocytosis
9. Blastomycosis
- Can cause ulcerating skin lesions, lytic bone lesions, lung lesions that resemble TB, "B symptoms" (weight loss, night sweats, etc)
- Highest infection rate is wisconsin, affects great lakes, ohio, mississippi river basins
- Broad based budding yeast
- Tx with itraconazole, amphotericin B
10. Bone conditions:
- Avascular necrosis: steroid use, lupus, sickle cell, alcoholism
- Osteitis deformans = paget's disease, increased osteoclast activity
- Osteitis fibrosa cystica = von recklinghausen disease. Occurs with severe hyperparathyroidism- primary (carcinoma), secondary, or tertiary.