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.