USMLE  

Step 1 Notes   
(from first pass to midway through second pass) 
 
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Countries and associations: 2 
Differential diagnoses: 2 
Common/key presentations: 3 
Fruit associations: 4 
Important tidbits: 4 
“MOST COMMON” of each tumor type: 5 
Strange wording/phrasing in UW: 5 
PREGNANCY and LABOR: 11 
POST-PARTUM: 12 
PART 2 of UWorld pg22: 22 
>> End of general UW 40 
UWSA1: Dec 13th -- please please don’t read if you haven’t done it yet! 41 
PHYSIO: 46 
MECHANICAL VENTILATION: 48 
ANAT: 51 
BIOCHEM: 55 
FASTING: 56 
ETHICS: 58 
BIOSTATS: 58 
BEHAV SCI: 60 
 EXERCISE: 62 
AGING: 63 
EYE/ophthalmology: 65 

NBME 24: please do not read if you haven’t done this yet 68 
 

1
Countries and associations:
By ethnicity:
● Ashkenazi Jews: Tay-Sachs, Niemann-Pick, some forms of Gaucher
● Japanese, West African or Carribean: HTLV/adult T-cell lymphoma/leukemia
● Caucasian:
○ Middle aged men: T. Whipplei disease

In Asia:
● Kawasaki: Asian child <4
● Takayasu: Asian woman
● IgA nephropathy: Asian
● Buerger thromboangiitis obliterans: most prevalent in Asian men
● Lactose intolerance: Asian
● Brugada syndrome: Asian man
●

In Europe:
● Pernicious anemia, MS: older women from Northern Europe
● Kaposi sarcoma: older Eastern European males (and organ transplant and HIV patients)
● Hereditary spherocytosis: northern Europe
● Behcet: Turkish, Eastern Mediterranean
● G6PD deficiency: Mediterranean, Persian
● PKU: Scandinavian

In Africa/African Americans:
● SCD (most common autosomal recessive disease)
● Familial amyloid cardiomyopathy (ATTR, 5% of AA patients have mutant allele)

Differential diagnoses:
● Night sweats: Takayasu, Mycobacterium (avium, TB., Pott disease), nHL and HL (B symptoms),
Brucella, Nocardia (-PPD), sarcoidosis
● Rash on palms and soles: Coxsackie A, secondary syphilis, Rocky Mountain spotted fever
● Laron vs achondroplasia? Laron has proportionally smaller head, while in achondroplasia the head
is a normal size
● Urine black on exposure to air? AIP or alkaptonuria
● Photophobia? Rabies, leptospirosis, N. fowleri, migraines, acute anterior uveitis, chronic GVHD
(Osmosis), Q fever (Coxiella)
● Fibrinoid necrosis? PAN, serum sickness, hypertensive emergency, preeclampsia, rheumatoid
nodules
● Chorioretinitis? Toxo or CMV
● NEW murmur? Infective endocarditis (acute TR), papillary muscle rupture post-MI
● Dry tap on BM aspiration? Hairy cell leukemia or myelofibrosis or aplastic anemia
● Splenomegaly without LAD? Hairy cell leukemia
● Oral ulcers? Behcet, pemphigus vulgaris, initial HIV infection, Crohn’s, SLE… others as well
● Pancytopenia without splenomegaly? Aplastic anemia (!) or megaloblastic anemia (B12 or folic),
acute leukemias, some MDS → to ddx, you’d need a bone marrow biopsy
● Decreased red reflex? Cataracts or retinoblastoma

2
● Purple/red-blue neoplasm underneath the fingernail? Glomus tumor (thermoregulatory body) or
melanoma
● Cystic hygroma? Main association is with Turner Syndrome, but can also appear in neos with Down
● Sudden onset constipation? Cauda equina syndrome

Common/key presentations:
● Male with dark urine? XR G6PD deficiency (esp. after previous infection)
● Dead birds? West Nile Virus
● Previously undiagnosed HIV patient with pneumonia? Pneumocystis (methenamine silver stain)
● Loss of pubic hair? Sheehan syndrome - Pathoma
● Deepening of voice? Myxedema in hypothyroidism - Pathoma
● Hair loss in the lateral ⅓ rd of the eyebrow? Hypothyroidism
● Tender thyroid? De Quervain subacute granulomatous thyroiditis - Pathoma
● Perioral numbness and tingling? Hypoparathyroidism
○ aka perioral paresthesias, due to hypocalcemia
● Sigmoid-shaped interventricular septum? Normal aging heart
● Vesicles on hard palate? HSV1 / vesicles on soft palate? Coxsackie’s “hand foot and mouth”
disease
○ If adult has ulcer on hard palate: might be SLE
● Coffee ground emesis? Gastric ulcer bleeding → vomiting (brown b/c heme iron is oxidized upon
encountering gastric acid)
● Murmur loudest at left infraclavicular area? PDA
● E Coli sepsis in neos? Classic galactosemia
● Glycogen storage disease with lactic acidosis? Only Von Gierke (type 1)
● Shoulder and pelvic girdle pain? Polymyalgia rheumatica
● Sandpaper-like rash? Scarlet fever
● Perioral pallor? Scarlet fever (along with tonsillar exudates (help ddx it from Kawasaki’s strawberry
tongue) and sandpaper-like rash)
● Brain lesion “angiomatous cerebellar lesion” + kidney mass? Von Hippel-Lindau syndrome
● Patient has no pain sensation? Syringomyelia (in the upper extremities)
● Infectious itching that’s worse at night? Scabies
● Blue toes? Atheroembolic event (post-intravascular procedure)
● Thyroid problem with elevated ESR? De Quervain thyroiditis (subacute - follows viral illness)
● Vitamin deficiency with heart failure? Wet beriberi (thiamine)
● Differential cyanosis/clubbing (only in LL, not UL) without significant pulse or BP changes?
Pathognomonic for severe PDA complicated by Eisenmenger syndrome
● Early satiety? Gastric adenocarcinoma (acc. to FA, but I think gallstone disease could also present
similarly?)
● Asthma diagnosed at a late age? Churgg-Strauss
● Microbe with “mouse-like” odor? Pasteurella multocida
● Inguinal lymphadenopathy in New Mexico? Bubonic plague, Y. pestis is endemic in NM, USA (!)
● Severe polyarthritis and lymphopenia? Chikungunya virus
● Bilateral vas deferens agenesis? Pathognomonic for CF
● Painful hand/feed swelling in child (esp. if African American)? SCD
● Asymmetrical flaccid paralysis with concurrent parkinsonian tremor? West Nile Virus
● Common presentations from UW itself:
○ Homeless man with jaundice, fever, abdo pain: acute viral hepatitis
○ Fatigue, high ALK in patient with long history of UC: primary sclerosing cholangitis
○ Weight loss, epigastric mass, jaundice, abdo discomfort in older woman: pancreatic cancer
● Anemia with low reticulocytes and normal MCV? Aplastic anemia
● Adult (that hangs around with children) afflicted with acute symmetric arthritis? Parvovirus B19
(immune complex-mediated, not due to viremia)

3
● Hoarseness, loss of P/T sensation, with neck pain, vertebra fracture? Wallenberg (lateral
medullary) syndrome, secondary to PICA lesion due to vertebral artery
○ Hiccups are also unique to this
● Postauricular lymphadenopathy? Rubella (togavirus)
● Child presenting with daily spiking fevers, macular rash and arthritis? Systemic juvenile
idiopathic arthritis

Fruit associations:
● Cherry hemangioma - adults, doesn’t regress
● Strawberry hemangioma - children, grows then regresses
● Strawberry cervix - trichomonas
● Grape-like mass emerging from vagina - sarcoma botryoides
● Strawberry tongue - Kawasaki, scarlet fever
● Onion-skin - arteriolosclerosis (hyperplastic type), Ewing sarcoma (periosteal), Tay Sachs
(lysosomes with onion skin), primary sclerosing cholangitis (concentric bile duct fibrosis)
● Mulberry-like appearance - hemangiomas (purple vascular clusters)
● Coffee (cafe-au-lait spots) - McCune-Albright syndrome, NF1, Fanconi anemia

Important tidbits:
● Types of Carcinomas that metastasize hematogenously: renal cell carcinoma, hepatocellular
carcinoma, follicular carcinoma and choriocarcinoma
○ (these are unique since carcinomas usually spread via lymph node)
● GAIN of function mutations:
○ FGFR3 (achondroplasia)
○ RET (MEN 2A/2B)
○ Liddle syndrome (increased eNAC —> treat with amiloride)

4
“MOST COMMON” of each tumor type:
● Salivary gland tumor: pleomorphic adenoma
● Neoplasm in fetuses: sacrococcygeal teratoma
●
●
●
●
●
●

Strange wording/phrasing in UW:

● Suprabasilar cells with perinuclear vacuolization: koilocytes
● Capillary angiomas of face and choroid: facial port-wine stain and leptomeningeal capillary-venous
malformation
● Cystic collections of MPS in artery: cystic medial degeneration (Marfan)
● Myelin protein gene mutations: Charcot-Marie-Tooth
● Pt has frequent involuntary jaw, neck, trunk muscle contractions, triggered by sensory stimuli; he has
a h/o injection drug use, and has had multiple site infections: tetanus
● Small cuboidal cells in sheets with gland-like structures containing acidophilic material; cells are
arranged in microfollicular pattern around an eosinophilic center: Call Exner bodies
● Excessive production of mineralized bone: which tumor? Osteosarcoma
● 1 week h/o progressive confusion, lethargy, with moist mucous membranes: sx-atic hyponatremia
● No past medical history, and she does not use tobacco/alcohol as they made her feel sick in the past:
AIP (b/c alcohol/cigs trigger attack by inhibiting ALAS)
● Decreased erythroid precursors and giant pronormoblasts containing inclusions: aplastic crisis
● Early morning emesis and papilledema: obstructive hydrocephalus (along with headaches)
● Scattered bilateral wheezes: bronchospasm
● 25 y.o. man experiences severe intolerance to certain drugs; twice he had to be hospitalized: G6PD
deficiency
● Anemia and episodes of food chunks getting stuck in throat: Plummer Vinson
● Poop is small pellets: constipation
● Between cerebellum and lateral pons: cerebellopontine angle

5
UWorld notes from 2nd pass:
● Field defect vs association: field defect is due to an initial disturbance that causes many other
issues, whereas association is multiple seemingly unrelated anomalies occurring together (VACTERL)
● Biochem enzyme locations → BAcK TO our MIGHTy origins // HUGs take BOTH NEW people:
mnemonic in booklet
○ Mito: B-ox, Acetyl Coa production, Ketogenesis, Tca cycle, Oxidative phosph
○ Both: Heme shunt, Urea, GlucoNEOgenesis (PC is in mito)
● Cannonball metastasis: choriocarcinoma, which gives hematogenous mx to the lungs
○ Also RCC!
● Two things to consider when treating bipolar dsr:
○ Avoid SSRIs monotx bc may precipitate mania
○ Give valproate if pt has a history of associated seizures
● Pt with absence and TC seizures should also be started on valproate — ethosuximide won’t do it
● Chlamydia and K. granulomatosis are VERY similar, but chlamydia has LAD, and K. granulomatosis
does not (lymphogranuloma venereum has lymph in it)
● HPV prefers stratified squamous epithelium (thus cancer of vagina, cervix, anal canal and true
vocal cords)
● CD14 is the cell surface marker of MPH/monocyte cell line
● A high Ki-67 is a sign of increased proliferation; Burkitt stereotypically has a very high Ki
● Gynecomastia treatment: aim is to keep androgen/estrogen ratio “normal,” so if patient is on
anti-androgens (ie for prostate cancer), then best to give ER blockers (tamoxifen)
○ Danazol (synthetic androgen) may improve gynecomastia but increases risk of prostate cxc
● Lisdexamfetamine is the treatment of binge eating disorder
● Substance-induced psychotic disorder cannot be ruled out just because no drug is mentioned in
the vignette; if the patient has somatic symptoms (mydriasis, tachy, HTN, diaphoresis), it could be due
to something like a stimulant (suggested by the fact that the patient was “staying up late to study”)
● Arsenic poisoning: think vampire (pigmentary skin changes and cancer, vomiting and having
diarrhea, running away from a QT (long QT) with garlic breath)
○ Due to lipoic acid inhibition; treat with dimercaprol (cute vampires are a dime a dozen)
● HIV: the only glycosylated HIV polyprotein is gp160 (product of the env gene) → this is then
cleaved into the two envelope glycoprotein -- gp120 (viral attachment) and gp41 (viral fusion with host
cell)
○ Glycosylation is important for immune evasion, bc it acts a shield/mask, host cell binding and
proper protein folding
● Membranous nephropathy (primary) is due to anti-podocyte antigen antibodies, like anti-PLA2R Abs
● Memorizing the neural crest cell derivatives: p 599 - mnemonic
○ SOME SALT: schwann, odonto, melano, enterochromaffin, spinal membranes (pia,
arachnoid), adrenal medulla, laryngeal and tracheal cartilage
● Hemolytic disease of the newborn with ABO issues occurs ONLY in moms with Type O blood,
because in this case the mom makes IgG (if mom is A or B, she makes anti-B or anti-A antibodies that
are IgM!)
● PRPP synthetase mutation: strange question, in which pts had increased enzyme activity → what
would that cause? GOUT. Because if you have increased purine synth, you’d have increased purine
breakdown → hyperuricemia
● In a kidney transplant, the proximal donor ureter’s blood supply (the renal artery) is KEPT, and it’s
attached to the external iliac artery; thus proximal ureter is safe, but the distal can become ischemic
● Infection (esp ParvoB19) might trigger hemolysis in hereditary spherocytosis patients -- look for a
history of infection
● Pt taking drugs for seasonal allergies has flushed cheeks and dilated pupils? It’s the antimuscarinic
SE of first generation histamine blockers
● Do not give htCMP patients diuretics or vasodilators, including ACEis and DHP CCBs
● Hyaline vs hyperplastic arteriolosclerosis: both can be@ seen in hypertension, but:

6
 ○ hyaline : HTN and DM
○ hyperplastic : severe HTN -- onion-skinning and proliferation of smooth muscle cells,
reduplicated BM
● Prinzmetal angina: smoking is a RF, but normal CAD RFs like HTN and hypercholesterolemia are
not
● First-dose hypotension seen with ACEi in patients that have volume depletion (diuretic use) or HF,
because sudden initiation of this new drug decreases ATII, which normally vasoconstricts; therefore
huge drop in BP due to decreases peripheral vascular tone
● Malignant otitis externa: extremely painful, seen esp. in elderly DM patients, due to pseudomonas;
granulation tissue in ear canal and intact tympanic membrane (tx: ciprofloxacin)
● Liver infarcts are very rare except in the case of transplanted liver
● Gout vs. septic arthritis: might seem similar, but septic would have a much higher WBC count
(>100,000)
● TCA toxicity can be treated with sodium bicarb b/c 1. it increases serum pH, which favors the
non-ionized form of the TCA drug, making it less accessible to bind to sodium channels; also, 2. it
increases EC sodium concentration, which helps overcome the competitive rapid Na ch.blockade
induced by the TCA
● 2-week washout period between MAOis and other serotonergic drugs is to allow MAO to be resynth.
● The ‘synchronous’ production of two enzymes in response to lactose by E.Coli is due to the fact
that a single mRNA codes for both enzymes -- known as polycistronic (aka a single mRNA molecule
that codes for more than one protein, rare in eukaryotes)
● Of the three anaphylatoxins, only C5a is a neutrophil chemotactic agent; another one is LB4 (before
everything else)
● In primary osteoporosis, labs (calcium, phosphorous, PTH) are NORMAL
● Hearing loss: high frequency hearing loss, due to chronic noise-exposure, is due to damage to the
stereo ciliated hair cells of the Organ of Corti (increased shearing forces against the tectorial
membrane)
● OTC vs orotic aciduria: OTC has hyperammonemia, OA does not - also, OTC is the most common
urea cycle disorder
● Vernet aka Jugular Foramen Syndrome: lesion here causes damage to CN 9, 10, 11 and a
constellation of symptoms (loss of taste, gag reflex, dysphagia, hoarseness, uvula deviation,
SCM/trapezius paresis)
● Buspirone is important b/c it treats anxiety (GAD), without causing dependence (like BZDs) - it’s a
5HT1A R partial agonist
● Parietal lobe has the association cortex that integrates multisensory info, to comprehend events and
generate responses → lesions (nondominant): contralateral neglect, anosognosia (unaware of illness)
and apraxia (inability to draw objects) - ask pt to draw a clock/bisect horizontal line
● The CLEARANCE of PAH is equivalent to the RPF, so you have to use the equation CL =
Upah*V/Ppah , where urine and plasma concentrations of PAH, and urine flow (V) have to be given
● Pt with sarcoidosis could have asx hepatomegaly, due to scattered non-caseating granuloma
formation; mildly elevated LFTs, but also
○ Also elevated CD4/8 ratio in BAL
● Huntington pathomech: acetylation is good (ACE it, yay), whereas deacetylation, as seen in
Huntington, is bad
● ParvoB19 binds to erythrocyte precursors via the group P antigen (aka globoside); on histo, you’d
see giant pronormoblasts with glassy viral inclusions
● Do NOT confuse Goodpasture and Wegener’s (GPA): Goodpasture = hemoptysis, Wegener’s =
ENT issues (nasal ulcerations), and pulmo
● Malaria (P. falciparum) tx must be continued for a month after return from affected areas, to
eradicate the liver schizonts that are released 8-30 days after infection (note that they’re not dormant;
that would be P. vivax, ovale)
● Patients with HF can avoid peripheral edema for a while because lymphatic drainage increases to
compensate for the raised interstitial hydrostatic pressure; but this only lasts for a bit before the
lymphatic return capacity is overwhelmed

7
● Murmur maneuvers: LEARN
○ Ddx between VSD and HOCM might rely on the fact that in handgrip, VSD increases but
HOCM decreases, bc you have increased volume (also, VSD is holosystolic)
● pol gene encodes for RIP (reverse transcriptase, integrase, protease) - inconsistent antiretroviral
therapy can result in increased pol mutations
● Anorexia patients do have low estrogen, FSH and LH, but it’s due to a decrease in leptin, which
inhibits pulsatile GnRH → thus functional hypothalamic amenorrhea
● Elevated FFA is a major contributing factor to insulin resistance; it impairs insulin-dependent glucose
uptake and hepatic gluconeogenesis --
○ Note that DM2 is described as a combo of insulin resistance and relative insulin deficiency
(especially low in later levels)
● Decreased bile acid is actually a risk factor for gallstones → bile acids and phospholipids solubilize
the cholesterol to prevent stone formation, and if you have decreased bile acids, then the bile
becomes supersaturated with cholesterol → crystallizes
○ Thus administering bile acids can be an alternative treatment for gall stones in patients not
wanting surgery
● TWINNING: if fraternal (aka dizygotic) - most common is dichorionic-diamniotic (two kids, two
chorions, two amnions, two everything)
○ If identical (aka monozygotic) - most common is monochorionic, diamniotic
● Thiazides cause hyperGLUC but also hypokalemia and hyponatremia -- they are the only diuretics to
decrease the sodium level
● Pt with decreased peripheral vision, dry skin and itching has vit A deficiency secondary to PBC →
obstruction of the bile ducts results in fat soluble vitamin malabsorption
● Warfarin and INR: normal INR is 1.0, so an INR of 2.0 means that it takes the blood twice as long to
clot as it normally would; the blood is “thinner”
○ If pt is on warfarin and their INR is 1.2, it is subtherapeutic and you need to increase the dose
○ If pt is on warfarin and their INR is 4, dose is too high → decrease dose, b/c high risk of
bleeding (blood too “thin”)
● Autism spectrum disorder ASD becomes apparent at age 2 (!): look for lack of social engagement,
speech delay, repetitive play
● Normal method of copper removal is hepatic excretion into bile
● Chlamydia infection can lead to recurrent genital ulcers, not vulvar carcinoma
○ Note that HPV can cause both vulvar and cervical cxc
● PT is the best indicator of liver function (along with hypoalbuminemia), because it indicates
impaired biosynthetic capacity → while thrombocytopenia may be seen (due to sequestration and
direct fx), the increased bleeding time is not a poor prognostic factor in cirrhosis
● Ectopic pregnancy is possible after a tubal ligation; endometrium will be decidualized, with
dilated, coiled glands and vascularized edematous stroma, in preparation of implantation (driven by
progesterone), but no villi
● Celiac disease: you CAN develop it as early as 10-14 months of age - do not be thrown off by the
youth of the child if the symptoms are fitting
● Polymyositis is CD8+, dermatomyositis is CD4+ (counterintuitive mnemonic - longer word, smaller
number); dermatomyositis is associated with a rash and perimysial, perifascular, perivascular
inflammation (Perry has a rash!)
○ Ddx dermatomyositis and scleroderma: dermato affects the upper esophagus mainly
(striated muscle), whereas scleroderma affects the lower
● Why are aluminium hydroxide and magnesium salts given together in GERD? Aluminum causes
constipation (forms insoluble salts), while magnesium causes osmotic diarrhea, so by combining
them, we decrease the SE of either as monotherapy (Mg = Must Go [to to the toilet]
○ How do they work? As alkali mineral salts, they increase the stomach pH by neutralizing HCl
→ symptom relief
● [An unaffected individual with unaffected parents, who has a sibling affected by an AR condition has a
⅔ chance of being a carrier for that condition (AA, Aa or aA genotype, and two out of those
possibilities would result in carrier status).

8
 ○ The chance of passing this onto the offspring is ½, and given a father with AR dz, ½*⅔ = ⅓ is
the chance that the offspring will be affected]
● LAD type 1 is due to absence of CD18 (integrin subunit) -- you would have delayed umbilical cord
separation and recurrent skin infections without pus, because leukocytes cannot bind tightly and
extravasate (LADs, she was so TIGHT I-CAMe (CD54) right int-egrin her, and she was LFAing too).
● Mouse-odor infectious wound represents Pasteurella multocida
● In trinucleotide repeat, anticipation is more severe when repeats are inherited from dad (b/c during
spermatogenesis, more duplicates are made) so earlier onset
● Parietal cells are located in the upper glandular layer of the stomach mucosa → they are also called
oxyntic cells
● VHL encodes a protein that normally inhibits HIF (hypoxia-inducible factors), thus a mutation in VHL
leads to constitutive activation of these proteins → overexpression of multiple angiogenic GF (VEGF,
PDGF, etc)
○ Tx of RCC that has VHL mutation: angiogenesis inhibitors
○ RCC originates from the PROXIMAL TUBULE
● Dyspnea is often the main/only sign of a pulmonary embolism (in this patient’s case, he had a swollen
calf post-op/car accident, which was a dead giveaway)
● Sporothrix schenckii has granulomas on histology; also a/w cigar-shaped budding yeast that grows in
branching hyphae with rosettes of conidia (which are spores produced asexually)
● Detrusor underactivity, which may cause overflow incontinence (i.e. problem with emptying, can be
caused by injury to the pelvic nerves, as well as DM neuropathy, MS and BPH (which is due to outlet
obstruction, rather than nerve damage)
○ Urethral hypermobility causes stress incontinence; urethra might be hypermobile in cases of
weakened female urogenital diaphragm → urine leaks when patience coughs, etc.; treat with
pessaries, weight loss or Kegels (levator ani)
● Asthamic reaction employs BOTH IL-4 (for stimulating IgE formation by plasma cells) and IL-5 (for
activating/recruiting eosinophils)
● Connection b/w GOUT and polycythemia vera: increased RBC production → increased RBC turnover,
thus more uric acid production (note that ALL myeloproliferative disorders may lead to gouty arthritis)
● Flushing due to niacin access is caused by prostaglandin (prostitute-induced flushing) and can be
prevented with aspirin (spear)
○ Vanco’s red man syndrome is histamine-mediated (non-IgE mast cell degranulation)
● Collagen type ONE in bONE is also the collagen we see in tendons, ligaments, dentin, cornea,
blood vessels and scar tissue
● Sensitivity: the ability of a test to correctly identify individuals with the disease, thus it is the TP divided
by the total number of people with the disease (did the test pick up on all the afflicted patients?
○ Whereas PPV: is the TP/total positive, aka what percentage of positive tests actually had the
disease
● LN regions:
○ Paracortex - T cells
○ Outer cortex - B cells; follicles are where isotope switching takes place
○ Medulla - macrophages
● Pyruvate kinase deficiency results in a lack of ATP production, so that ATP can’t be used to transport
cations against their concentration grade in the RBC membrane → echinocyte formation, hemolysis
○ Red pulp hyperplasia because the RES cells there are responsible for the removal of the
damaged RBCs → splenomegaly
● Acute phase of Chagas disease may be asx or have nonspecific symptoms (fever, malaise, anorexia),
but more importantly: inflammation, swelling at inoculation site (i.e. in this question, the pt had
conjunctival swelling; the major complication is Chagas cardiomyopathy → arrhythmias
● Germinal matrix fragility and bleeding cause to that would not be seen in babies born at full-term; it
starts involuting at age 28weeks and is fully gone by full term
● Hepcidin is an acute phase reactant (synthesized by the hepatocytes)
● Decreased cholesterol 7-alpha hydroxylase activity results in bile stone because 7alpha-OHase is
responsible for bile salt formation

9
● Histo vs. coccioides: histo is smaller than surrounding RBCs, whereas cocci are larger than the RBCs
● CSF findings:
○ Low hypocretin 1 and 2 are associated with narcoLepsy with catapLexy (the two
neuropeptides are produced in the Lateral hypothalamus)
○ Low 5HIAA are a/w impulsive, destructive behaviors like aggression, suicide, violence
○ High 14-3-3 protein is seen in CJD
○ Melatonin seems to decrease with progression of Alzheimer
● To prevent neonatal tetanus, you would vaccinate the mother with tetanus toxoid → this is because
the mom can pass the IgG to the baby, since we cannot vaccinate the child before the age of 2m
● Child with worsening fever and lethargy (h/o of recurrent URTI) was vomiting, eating poorly and
pulling at her ears → CT shows ring-enhancing lesion in the left lateral temporal lobe; dx: single brain
abscess, due to spread from mastoid air cells
○ Frontal lobe abscess → from ethmoid or frontal sinusitis
○ Note that multiple brain abscesses are usually a sign of hematogenous dissemination of a
distant infection (usually endocarditis, or sometimes lung abscess/empyema)
● Keratoderma blennorrhagicum (keratinized-mucosy-discharge of the skin), a symptom a/w reactive
arthritis; it is lesions usually found on the palms and soles, may resemble psoriasis (Wiki)
● AML vs CML on ddx: this 45-year old patient with 1% blast cells had CML -- AML’s mean age of dx is
65, and although it’s the most common acute leukemia in adults, it would have a blast cell count >
20% (CML would not)
○ Also note that they mentioned that the LAP score was low, to help you distinguish between
CML and leukemoid reaction.
○ CML has a ‘myelocytic bulge’ (meaning that there’s more myelocytes compared to more
mature forms, such as metamyelocytes) when compared to a leukemoid reaction
○ CML is also associated with absolute eosinophilia, basophilia
● Pt comes to clinic with breast tenderness and amenorrhea; she’s taking risperidone, and she lost a lot
of weight recently. Which causes her amenorrhea? RISPERIDONE → b/c weight loss might cause
amenorrhea (like in AN, but would not cause the breast tenderness)
● Bone marrow biopsy findings:
○ Hypercellular marrow with numerous blasts → primary myelofibrosis (splenomegaly, fatigue)
or CML (leukocytosis), or in MDS (in elder patients) or AML (blasts on periphery though)
○ Hypercellular marrow with megaloblastic hematopoiesis → MDS (in elder) or megaloblastic
anemia (macrocytosis)
○ Hypergranular promyelocytes with Auer rods → AML (note that you’d have blast cells in
periphery)
○ Hypocellular marrow with fat cells, marrow stroma → aplastic anemia
● Antiemetic therapy is best based on its source:
○ → emetogenic substance in the chemoreceptor trigger zone: D2 receptor ATG
■ I.e. in acute migraines; not great for nausea though, b/c causes GI upset
○ → vestibular system (motion sickness, vertigo): H1, M1 receptor
○ → GI (due to mechanical and chemical irritants): CNIX and 5HT3 R ATG
■ I.e. traveller’s diarrhea (note that lopearmide can worse nausea/vomiting due to
colonic retention, even if it does reduce the diarrhea)
● Hartnup disease often presents with cerebellar ataxia (not mentioned in Pixorize); the ataxia and
attacks of pellara-like skin eruptions become less severe with increasing age
● Only T cells undergo selection in the thymus; first positive “do you at least bind? Good, you can live”
→ then negative “do you bind too well? Die!”
● Digoxin can actually cause QT shortening (!)
● Portal vein thrombosis can result in splenomegaly and esophageal varices (→ hematemesis), without
changes in liver parenchyma or causing ascites
● Confounding vs effect modification: EM is not a bias, but rather a natural phenomenon that should be
described; confounding is a bias and when you stratify the results, the significance disappears (p
value increases to >.05)

10
● Pt has right leg pain, fever, confusion → operating watercraft; has small laceration: caused by vibrio
vulnificus (condition causing iron overload), NOT to do with infected rodent urine
○ V. vulnificus needs iron to grow, so any patient with a condition causing iron overload
(hemochromatosis) is at increased risk
● If a patient is overtreated for hypothyroidism, there is an increased risk of atrial fibrillation →
hyperthyroidism causes CV disorders (indication that the dose is too high is if TSH is significantly
suppressed) → causes hyperadrenergic state via increased beta R expression
○ Diff q: hyperthyroidism due to exogenous sources results in atrophy of the thyroid and
decreased colloid
● Mycobacteria is contained in granulomas, NOT eliminated completely; finding a patient with a Ghon
complex (in the lower lobe and ipsilateral hilar LN) signifies a primary infection of TB
● Homocystinuria (cystathionine synthase deficiency) can actually be made better by supplementing
patient with B6; also, restricting methionine helps (homocystinuria is the most common inborn error of
methionine)
● Metalloproteinases in lipid plaques can result in plaque rupture; usually the enzymes are secreted by
macrophages
● Women with Mullerian duct defects (septate uterus, etc) should undergo renal US b/c about half of
these patients have unilateral renal agenesis
● PBC and GVHD actually appear similarly on histology of the liver: both have lymphocytic infiltrates
and destruction of small and mid-sized intrahepatic bile ducts and slight increase of LFTs
● The increased 1-alpha-hydroxylase activity seen in sarcoidosis is due to increased enzyme
expression in activated macrophages
● Giving penicillins (pen G, ampicillin) too early in a pregnancy too early would serve to eliminate the
bacteria at the time, but 4 weeks later the baby would again be vulnerable; that is why the optimal
intrapartum Abx are given at 35-37 weeks
● 3 main pathogens causing COPD exacerbation: H.flu, Moraxella, S. pneumo, maybe Pseudomonas
(severe COPD); leading viral cause is rhinovirus
○ Exacerbation cau also be due to allergen or environmental pollution exposure
○ Note that most COPD exacerbations are due to UPPER respiratory tract pathogens, so you
wouldn’t see any opacities on X-ray; ie pathogens causing pneumonia (Klebsiella, S. aureus
(post-influenza) are less common than those mentioned above
● Fast fermenters: Klebsiella, E.coli, Enterobacter -- thus indole can be used to distinguish E.coli and
Enterobacter
● PREGNANCY and LABOR:
○ hCG levels: 8 days after fert in blood, 14 days in urine
○ Stress urinary incontinence, due to increased intraabdominal pressure, and also because
pregnancy hormones decrease urethral tone and relax pelvic floor muscles, which would be
needed to maintain closure of the valve
○ Immediately prior to delivery, estrogen —> upregulates oxytocin R and gap junctions (via
increased formation of more connexins), to allow the individual myometrial SMCs to
communicate for coordination and synchronization
○ Increased risk of gallstones: Beginning in the third trimester of pregnancy, increased
circulating estrogen levels result in an increased hepatic cholesterol synthesis and the
formation of cholesterol-supersaturated bile. Moreover, higher progesterone levels cause
smooth muscle relaxation, decreased and incomplete emptying of the gallbladder, and
subsequent bile stasis. Together, cholesterol-rich lithogenic bile and gallbladder stasis
predispose to gallstone formation. Similarly, hormone replacement therapy and oral
contraceptive use also predispose to cholelithiasis. (Amboss)
■ Note: states of increased estrogen (obesity, HRT, OCPs, etc) predispose to gallstones
● POST-PARTUM:
○ Increased risk of developing MyGravis, which may present as muscle fatigue even when
patient is asleep
○ Breastfeeding: OCPs are an absolute contraindication in the first 30 days post-partum, b/c
estrogen may decrease milk production and may enter milk itself (Amboss)

11
● In TB infection, the first thing that happens is that the phagolysosome cannot mature and thus there is
increased TB proliferation; as a result, the infected alveolar MPHs migrate to the LN, where they
present their antigens to the TH cells and those release IFNgamma
● NK cells (CD 16 or 56) are large, with cytoplasmic granules containing perforins and granzymes
(which gain access to the target cell via perforin, and can then induce target cell apoptosis); note that
NK cells do not directly lyse cells; they are found in athymic patients bc no thymus is needed for
maturation
○ Are activated by interferon-gamma and IL-12 (same cytokines that induce differentiation of T
cells into Th1 cells)
● Patient complaining of lower back pain and has no anal wink reflex (w/o h/o trauma) likely has cauda
equina syndrome
● CF: it’s important to supplement salt in patients who are exclusively bre ast or formula fed, or those
who are exposed to high temperature or exercise; pts with CF can’t reabsorb chloride and sodium,
and thus they secrete sweat with high sodium and chloride —> hyponatremia (vomiting, sleepiness,
dehydration, etc)
● Hyperglycemia - caused by infection, pain, sleep deprivation and/or severe mental/emotional distress,
b/c increased production of counterregulatory hormones like catecholamines, cortisol; hypoglycemia
is caused by skipped meals or intense exercise, because glucose is taken up by muscle cells, but
insulin levels are not physiologically decreased, so you have impaired endogenous glucose
production —> hypoglycemia
● In which diseases can the primary infection be self-limited or asx? Dengue fever, and second infection
with a different serotype can cause a much more severe illness
● Gastroparesis can be seen in diabetes mellitus, uremia, hypothyroidism and some other metabolic
disorders; causes constipation, early satiety, food stasis with vomiting
● Systemic mastocytosis —> can cause gastric hypersecretion, why? Because mast cells are
overproduced —> serotonin increases, and can stimulate the histamine receptors (H2R) on parietal
cells, which causes increased HCl production KIT CD117
● 15 yo with 3m h/o sudden, brief jerking movements involving both arms; usually upon awakening and
aggravated by sleep deprivation is most likely JME (juvenile myoclonic epilepsy), which affects BOTH
cerebral hemispheres at onset; consciousness is usually preserved
○ TOC is valproic acid (broad-spectrum that covers generalized and focal seizures; whereas
narrow-spectrum ones could actually worsen seizure sx in myoclonic)
● A SULFUR donor is used to treat cyanide poisoning; thiosulfate promotes conversion of cyanide to
thiocyanate, which is easily excreted in the urine
● 15yo can get MCD; do not be put off by the age (median age is 2-3); can be precipitated by NSAID
use, along with recent infection, immunization, or other immune stimulus (bee sting, etc)
● Both causes of aphasia (Wernicke, Broca’s) are due to MCA ischemia (so you don’t even have to
know which one is which, if the q wants to know which vessel caused the lesion)
● Why does low citrate in the urine predispose patient to calcium-oxalate stones? Because the citrate
excreted by kidneys usually binds to ionized calcium in the urine, so that insoluble Ca-ox complexes
can’t form; but when citrate is low (hypocitraturia), the stones can form
○ Causes of hypocitraturia: as in enhanced citrate reabsorption, like in metabolic acidosis
(chronic, as seen in distal RTA and chronic diarrhea)
○ Tx: oral potassium-citrate can be given to prevent Ca-ox stones
● When an RNA molecule is purified from a virus, it means that the viral capsid and envelope are
removed, so in order for that virus to be infectious, it has to be single stranded and positive sense
(SS+), because only then can it enter a host cell and act as an mRNA within the host’s own
machinery, without having its own machinery/enzymes
● Pt presents with fever and rash, with SEVERE polyarthritis —> possible chikungunya virus, an alpha
virus in the tropics; virus also causes lymphopenia and thrombocytopenia; it’s transmitted by the
Aedes mosquito so co-infexn with Zika, dengue
○ Note that the word chik means “stooped walk aka incredibly severe join sx

12
● A trick question: pt is having a COPD exacerbation, and you do a sputum sample, which grows
round-to-oval budding yeast that forms germ tubes at 37C; what is it? Contamination by normal oral
flora: candida!
● Woman with heavy menstrual bleeding might have adenomyosis; may develop even in middle-age,
and the uterus is uniformly enlarged; menstrual bleeding is worse b/c there is a higher endometrial
surface area. Note that on endometrial biopsy, normal endometrium would be seen (secretory or
proliferative, depending on the phase), b/c the glands infiltrate the myometrium (hysterectomy
specimen needed to dx)
○ Endometrial hyperplasia also causes heavy bleeding (and irregular), but it is not painful
● GVHD vs chronic rejection: if the pt has a skin rash or GI manifestations, most likely GVHD; chronic
would have organ-specific manifestation
● Oogenesis arrest: pro1, meta2 (P1M2AT)
● Salmonella - typhoidal vs non: the typhoid Vi capsule inhibits the PMN/MPH response that deals with
the non-typhoidal one, so typhoid fever develops (high fever, bradycardia, rose spots, etc); unchecked
intracellular proliferation of the pathogen makes this disease more severe than the non-typhoidal one
(1-5 day gastroenteritis only)
● E. histolytica actually inserts an amebic channel-forming protein into the host cell membrane that
causes cell death —> considered “contact-dependent host cytotoxicity”
● MRSA is usually resistant to most beta lactam Abx, including cephalosporins, due to acquisition of a
mobile genetic element that contains the mecA gene, which encodes for a different PBP (2a)
● Risk of myopathy is higher when statins are given with gemfibrozil b/c the fibrate impairs hepatic
clearance of the statin —> excessive blood levels of statins
● Descending aortic dissection originates near the left subclavian artery
● Pseudocyst wall is made up of granulation tissue and no epithelial lining
● In patients with SEVERE aortic stenosis, sudden onset AF can actually precipitate HF, due to the
sudden loss of normal atrial contraction (which leads to sudden decrease in LV preload, and thus
hypotension)
○ In patients with concentric LV hypertrophy (aka reduced compliance), atrial contraction is
really important to maintain adequate LV filling
● S3 sound would be heard over apex (aortic stenosis would not, and it’s not really considered “dynamic
LVOT” b/c it’s not dynamic
● Treating a patient with MTX for abortion would result in dihydrofolate polyglutamate accumulation in
the embryonic tissues; it’s good for early txt of ectopic pregnancy
● Motile trophozoites on wet mount is very helpful in dx Naegleria fowleri
● In patients with a history of irregular menses, accurate gestational age might be difficult to figure out
— AFP levels might be unusually low (other causes of low AFP is aneuploidies)
● Direct thrombin inhibitors increase thrombin time (duh), so if pt is on a medication that prolongs his
APTT and PT, but not thrombin, it’s likely that its an Xa inhibitor (direct = apixaban, rivaroxaban;
indirect = fondaparinux)
○ Unfractionated heparin also binds thrombin, along with Xa, so it would increase TT (and not
increase PT significantly, b/c heparin neutralizers usually minimize that effect in the lab)
● H. pylori colonization:
○ Antrum: causes depletion of SST-producing delta cells, which are mostly in the antrum; SST
normally inhibits gastrin release, so without SST, you have elevated gastrin —> increased
acid secretion, that travels to duodenum, which is lacking protection
■ Also H pylori cytotoxins inhibit duodenal bicarb production —> DUODENAL ulcer
○ Body: chronic inflammation, which causes atrophic gastritis and decreases HCl-producing
parietal cells, but delta cells are untouched do acid secretion is normal (or sometimes low);
the ulcer formation is due to direct mucosal damage from bacterial productions like ammonia,
cytotoxins and subsequent inflammation
● False negative syphilis tests are common in the first/early stage of the disease, especially if it's the
rapid reagent test
● 12 yo caucasian male with h/o seizure dsr experiences several stroke-like episodes with residual
neuro deficit, and suffers from muscle weakness —> labs show elevated lactate post exercise and at

13
 rest: describing MELAS - mitochondrial encephalomyopathy with lactic acidosis and stroke-like
episodes
● Brain herniations:
○ Central = abducens palsy b/c along clivus — locked in syndrome
○ Uncal aka temporal lobe = oculomotor palsy — blown pupil
● How does a blood transfusion cause hypocalcemia? Very high transfusion rate —> lots of citrate
(which is used as an anticoagulant in stored donated blood) is transferred into the body, and the liver
cannot convert it all to bicarb fast enough, and citrate is a calcium-chelator (note: rate would have to
be very fast, >9 units/hour) but if pt has underlying hepatic insufficiency, like alcoholism, it can occur
before that)
○ Note that post-trauma, rhabdomyolysis can also cause hypocalcemia (release of IC
phosphate can precipitate calcium salts, but this is a delayed finding)
● Acute hemolytic transfusion reaction:
○ Onset is FAST, within an hour, due to ABO incompatibility; sx = flank pain, fever,
hemoglobinuria, jaundice, etc.
○ HS II - complement mediated: anaphylatoxins mediate shock, and MAC leads to
complement-mediated cell lysis
● PK deficiency can cause iron overload due to impaired erythrocyte survival (no ATP, so RBCs are
rigid and broken down by spleen)
● Leuprolide is a GnRH analog; it’s an agonist when given pulsatile, so at the initiation of the treatment,
it might cause transient increase of LH and therefore testosterone (and therefore DHT too); it has no
5alpha reductase properties so testosterone and DHT fall and rise together
○ This is known as the startup flare; to treat prostate cancer, it is often given with flutamide, an
antiandrogen at androgen receptors)
● Methylphenidate causes anorexia and weight loss! —> they are sympatho-imitators, so they increase
heart rate, BP, cause nervousness/agitation/anxiety, tics and insomnia
● Measles vs mumps: measles (weasel butler, baby weasel and weasel gf in ruby dress) comes with the
“C” symptoms, whereas mumps (mummy) only has a few classical associations - orchitis, parotitis
and aseptic meningitis
○ Measles has HA and fusion protein (baby weasel) virulence factor, whereas mumps has both
NA, HA and fusion protein (baby mummy)
● Recent travel + transient pulm sx + subsequent GI sx —> parasitic infection
● HIGHEST risk factors of aortic dissection: male gender + smoking (and age > 65)
○ Note that the risk of AAA in DM pts is actually lower, perhaps due to the effects of in the
aortic wall
● Floppy, puffy-faced baby who has constipation, hypotonia, large tongue, large fontanelle and
reducible umbilical hernia: likely hypothyroidism causing cretinism; initially normal, b/c maternal T4
helps; likely caused by Ab-mediated maternal hypothyroidism
● 6 mo boy: delayed motor devo, weak and cannot lift his head or roll over, hypotonia and decreased
DTRs —> spinal muscular atrophy, due to mutation in SMN1 (survival motor neuron), which encodes
for protein involved in assembly of snRNPs in lower motor neuron —> impaired snRNP results in
impaired spliceosome function and degen of anterior horn cells in SC
● DDx between CO and MetHb and CN: see back of book; what’s key is that the PaO2 does not change
for ANY of them; also that CN doesn’t affect hemoglobin at all - it's just toxic to the mitochondria
● Ddx between PSC and PBC: the key is that the sclerosing one affects intra and extrahepatic ducts
(fibrosis everywhere), whereas the PBC is only intrahepatic (lymphocytic infiltrate with granulomas)
● Oropharyngeal ulcers and maculopapular rash are two key early signs of HIV infection; others might
be non-specific (flu-like sx, night sweats)
○ Humoral response devo’s 6-8 weeks after initial infection
● The ONLY lung patho in which breath sounds/tactile fremitus are increased is consolidation —> why?
b/c sound vibrations travel faster through liquid than through air/gas
○ Two key examples of consolidation are pulmonary edema and lobar pneumonia
● Nitrate-free interval is really important in long-term nitrate therapy; pts often take the drug morning,
afternoon, but not at night (works out, b/c cardiac activity is lowest at night time anyway)

14
● BOTH raloxifene and tamoxifen can reduce the risk of osteoporosis; tamoxifen is a STRONG
estrogen ATG, so it’s better for active breast cancer, but also has risk of endometrial cancer
○ Thus for a patient with osteoporosis who has a family history of breast cancer, raloxifen is the
better drug choice
● the reason S. viridans affects damaged heart valves is because the dextrans adhere to fibrin, and
fibrin and platelets are deposited at sites of endothelial trauma, i.e. valve lesions
● Pericarditis may be heard as a triphasic friction rub: three phases b/c occurs during atrial systole,
ventricular systole, and early ventricular systole
● Opiates open potassium channels (K+ efflux — open banana baskets poolside) and closes
voltage-gated Ca channels
● Adjunctive GC therapy in treatment of bacterial meningitis is beneficial because it decreases the
inflammatory response in the CSF —> fewer neuro sequelae, lower risk of death
○ This is mainly the case in GP meningitis, such as S. pneumo; those due to H flu or Neisseria
don’t seem to benefit, maybe because these GN organisms have thinner cell walls (less
release of cytokine)
● Tetracyclines will stain the teeth of even fetuses, thus CI in utero
○ Use amoxicillin for children with LYME disease
● 2ndary achalasia aka pseudoachalasia can be caused by T. cruzi —> megaesophagus; it can also be
seen in extra-esophageal malignancies, due to mass effect or paraneoplastic
● Pt with postprandial epigastric pain with food aversion, that does not radiate and doesn’t respond to
antacids (endoscopy shows no abnormalities) likely has chronic mesenteric angina
● Pleural plaques are not only a/w mesothelioma: think of asbestosis (ferruginous bodies)
● Toxo is OBLIGATE intracellular
● DDx HBV and HCV:
○ HBV has initial acute sx —> rash/urticarial vasculitis, joint pain, LAD, RUQ pain (tender
liver), usually non-icteric but can have jaundice; transmitted through B’s - blood, baby-making
(sex), birthing (perinatal)
■ HBsAg accumulates in infected hepatocytes 00> pale, eosinophilic ground-glass
appearance on histo
■ HBV is the MOST COMMON CAUSE of HCC worldwide (85% of cases) —> usually
due to vertical transmission during birth, thereby vaccination would help reduce the
incidence of HCC
○ HCV does not have initial sx; also, primarily through blood (transfusion, IVDU)

● pHTN is due to endothelial dysfunction, that in turn leads to increased VC mediators (endothelin,
TXA2) and decreased VD mediators (PGI2, NO)

15
 ○ Tx relies on these as targets: PGI2 (prostacyclin) analogues like epoprostenol, and
NO-enhancing agents such as sildenafil promote VD, whereas bosentan inhibits endothelin
● HUS and TTP are NOT associated with DIC
● Enhancing vs non-enhancing
○ Non-enhancing: neurocysticercosis
○ Ring-enhancing
■ (multiple): toxo
■ (solitary): CNS lymphoma in HIV
● T. solium in pt from Guatemala (b/c it’s endemic in central, south America, especially in rural areas)
● Carcinomas metastasize via lymph, that is true, but LIVER mx are usually via the portal circulation
from colon >> stomach > pancreas (“cancer sometimes penetrates liver”)
● Pilocytic astrocytoma may have both solid and cystic components, so don’t expect it to be perfectly
cyst-shaped (spherical)
● Promoter MUST be close to the coding site; it binds the DNA polymerase and TFs; enhancer (made
up of ‘response elements’ can be upstream, downstream, far away from the promoter, and strand can
BEND to bring the promoter and enhancer close to each other
● Menses IS apoptosis
● FEBRILE NEUTROPENIA:
○ Leukemic patient undergoing CTX —> fever with absolute neutrophil <500
■ Calculating ANC: x% neutrophils * total leukocyte count
○ Most common infection is GP organisms, but prolonged neutropenia (days) is a/w viral and
fungal infections
■ Aspergillus (invasive pulmonary type): dense focal infiltrates (ex. upper lobe), Abx
are ineffective ← UW question had this one
■ Pneumocystis: would be diffuse, bilateral (seems to be less associated with febrile
neutropenia)
● Men CAN get sarcoidosis: do not be put off by the fact that the patient presenting with non-caseating
granulomas on a supraclavicular LN biopsy is male!
● TNFalpha does the following:
○ Cachexia —> leads to appetite suppression in the hypothalamus and increases BMR
○ Fever (along with IL-1)
○ Septic shock mediator
○ APR release (CRP and fibrinogen from liver)
● Smoking is the #1 cause of chronic bronchitis
● Diverticulum: main sx can be constipation
○ Diverticulosis: may lead to bleeding or diverticulitis, abdominal pain, microperforation, fever,
nausea, vomiting, alteration in bowel habits
○ Risk factors: HIGH red meat, HIGH fat, low residue (i.e fiber)
● D-penicillamine works as a copper chelator via its free sulfhydryl group, b/c excess copper (as in
Wilson) causes injury by binding to the sulfhydryl groups of cellular proteins
● Theophylline: adenosine receptor ATG, causes increased cAMP by inhibiting phosphodiesterase,
causes cardiotoxicity (tachyarrhythmias) and neurotoxicity (seizures) in OD; can treat with B1 blockers
(to decrease cAMP)
● Aplastic ANEMIA vs CRISIS:
○ Anemia — usually idiopathic, decrease in ALL cell lines, NO splenomegaly, because there is
a decrease in hematopoietic precursor cells so there is no chance to do extramedullary
hematopoiesis
○ Crisis — secondary usually to ParvoB19, results only in anemia aka red cell aplasia, only in
patients with pre-existing hematological disorders (SCA, hereditary spherocytosis)
● Tumor that has sx of deafness, left-sided facial numbness, asymmetric smile, diminished corneal
reflex: think of vestibulopontine angle tumors
● Trigeminal nerve is the landmark for the middle cerebellar peduncle —> infarct at the anterior pons
can affect:
○ Corticospinal tract —> contralateral hemiparesis, + Babinski

16
 ○ Corticobulbar tract —> contralateral lower facial palsy, dysarthria
○ Corticopontine fiber —> contralateral dysdiadochokinesia, dysmetria
● In neutropenic fever, the most dangerous source of infection is the endogenous bacterial flora b/c the
mucositis (damage to rapidly dividing epi cells of GI) allows the commensal organisms to penetrate to
the bloodstream
● Glioblastoma multiforme is associated with overexpression of EGFR!! ← very important, not in FA
● NF2: merlin tumor suppressor gene lack
● Insulin CANNOT cross the placenta, but glucose can —> thus the baby’s beta cells undergo
hyperplasia because they are secreting so so much insulin in response to the hyperglycemia from
mom: causes neonatal hypoglycemia postpartum
● STRANGE DRUG NAMES:
○ Chlordiazepoxide: benzo
○ Bumetanide: loop
○ Indapamide: thiazide
● Drug metabolism:
○ Acetylation: procainamide, hydralazine, isoniazid
○ Plasma esterase: some drugs, such as the ones for anesthesia, are metabolised by plasma
hydrolysis: the esterases rapidly cleave the ester linkages after the drug enters the circulation
—> makes for a short duration of action
● C.Diff you don’t NEED sterile gloves: contact precautions include proper hand hygiene, nonsterile
gloves and a gown
● Exogenous GC use results in decreased CRH, ACTH, cortisol → this is especially important for
post-surgical patients who continue taking their dose of
GCs even perioperatively, because the exogenous
glucocorticoids inhibit the ‘stress’ response, thus pt
has relative GC deficiency → acute adrenal
insufficiency (adrenal crisis)
● Ewing sarcoma tends to metastasize to the lungs if the
primary tumor isn’t treated with both radiation and
CTX; EWSR1 and FLI1 translocation -- histo shows
fibrous septae and patches of necrosis amongst
uniform, small round cells with scant cytoplasm
● SAH: major (most common) complication is arterial
vasospasm → new focal neuro deficits 3-12 days after
SAH, causing delayed cerebral ischemia; treatment is nimodipine (to promote VD and prevent
excitotoxicity)
● Retroperitoneal hematomas are
commonly a/w abdominal, pelvic trauma
→ frequently can be pancreatic injury
(contusion) from a seat belt or steering
wheel
● Dialysis: can speed up rate by
increasing the surface of the membrane
● Oropharyngeal vs nasopharyngeal
carcinoma:
○ Oro: HPV, traditionally
non-smokers, non-drinkers,
earlier onset, presented with
persistent sore throat,
swallowing discomfort right ear
pain, no nasal congestion,
enlarged right tonsil with small
ulcer

17
 ○ Naso: EBV, present with headache, diplopia, facial numbness (due to CN invasion or neck
mass due to cervical LN spread)
● Congenital pulmonic stenosis, which is usually asx, may be unmasked by pregnancy )due to
increased plasma volume); heard as a pulmonic ejection click with a crescendo,decrescendo systolic
murmur and widened splitting
● Silent GERD: when pts have no heartburn, but extra-eso sx such as nocturnal cough, hoarseness
○ Note that histo may show eosinophils; this does not mean its eosinophilic esophagitis; esp if
pt’s sx improve with PPIs
● Primary hyperparathyroidism will lead to subperiosteal thinning (cortical bone of appendicular
skeleton)
● Major ddx for NMS vs SS: rigidity! SS has hyperreflexia, whereas NMS has rigidity (lead-pipe, think of
parkinsonism due to increased DA AGism
● MyG and muscle relaxants:
○ Nondepolarizing agents like vecuronium are competitive ATGs of nAchRs, thus they are very
dangerous to MyG patients (who have very few functioning receptors, so they are extremely
sensitive → can induce paralysis
○ Depolarizing agents like succinylcholine are competitive AGs of nAchRs → persistent depol
→ desensitization of motor end plate, but b/c MyG patients have so few functioning Rs, they
are resistant to these agents (large doses are required to induce muscle relaxation)
● Actinomyces has two non-Sketchy manifestations:
○ Pulmonary action, 2ndary to aspiration (air bronchograms)
○ PID with IUDs (seen as cotton candy on Pap smear)
● Eosinophils contribute to defense against parasites via ADCC → antibody-dependent cell-mediated
cytotoxicity, in which eosinophils bind via their Fc R to the IgG antibody
● Young (23 yo) male presents with acute pancreatitis that resolves rapidly on fasting; likely
underlying cause is hypertriglyceridemia: pathomech = lots of TGs → increased production of FFAs
within pancreatic capillaries by pancreatic lipase, which would normally be bound to albumin, but if the
TG level is very high, then albumin gets saturated and TGs cause direct tissue toxicity
● Prolactin actually inhibits GnRH, thus decreases LH/FSH -- especially important in patient with
prolactinoma
● IMMUNO:
○ Experiment prevents acidification of lysosomes within APC; the affected cells show impaired
interaction with T cell upon Ag exposure, this is due to low surface expression of which
molecule? MHC II, which is charged with presenting exogenous antigens after the proteins
are degraded in lysosomes -- no lysosomes, no APC presentation via MHC II
● Bacteroides fragilis (GN anaerobe) can be treated by clindamycin, metronidazole or
piperacillin-tazobactam, b/c it often produces beta lactamase enzyme
● Turner patients with mosaicism will have somatic mosaicism (recall that germline mosaicism would
not manifest in the patient, but only their offspring)
● Staph’s Protein A works by binding to the Fc portion of IgG, thereby inhibiting complement activation
● Target cells are seen post-splenectomy b/c the spleen is charged with ‘pruning’ the extra RBC
membrane (high surface area to volume ratio); eventually though, extra-splenic MPHs take over
pruning, so these target cells are only really seen early post-splenectomy (in qstem, pt was 6 months
post-op and she still had target cells)
● Diabetic gastroparesis is a failure of the ENTERIC plexus, not the vagus
● Pseudomonas treatments of choice: cefepime or ceftazidime, fluoro (cipro, levofloxacin), aztreonam,
carbapenems (imipenem, meropenem)
● Tricky q: bilateral LL swelling in the presence of a ballotable left flank mass → RCC that invaded the
IVC and thus edema; note that prominent abdominal collateral veins might form (this suggests that
obstruction is high up in the IVC)
● PV vs paraneoplastic EPO production ddx: in PV you would have increased in all cell lines, whereas
with RCC for ex., you’d just see increased hemoglobin
● IBD with bowel wall thickening is ALWAYS Crohn -- bloody stool or not

18
● Collagenous colitis: chronic watery diarrhea, middle aged women, not a/w bleeding, ulcers,
inflammation or abdo pain
● Reninomas are rare, but suspect in pt with no clear signs of renovascular disease (i.e. young male
without atherosclerosis and marked hyperreninemia); it’s a juxtaglomerular cell tumor
● Hyperoxaluria is a less common cause of stones than hypercalciuria; you’d get hyperoxaluria from a
diet high in chocolates, nuts, spinach; or low-calcium+malabsorption disease
● Familial hypercholesterolemia is due to defective LDL receptors, resulting in low LDL uptake by the
liver → hepatocytes clear approx 70% of the plasma LDL
● C.diff diagnosis: single best test for dx-ing C Diff with strong clinical suspicion is a nucleic acid
amplification test (NAAT) aka “PCR for bacterial gene encoding a toxin” (in FA too; PCR or antigen
detection of toxin A and/or B in stool)
○ You can add in an enzyme immunoassay for bacterial antigens, but it’s less sensitive (high
amount of Ag needed)
● Costochondritis aka costosternal syndrome
aka anterior chest wall syndrome: after
repetitive activity (like moving boxes), hurts
with movement, reproducible with palpation
-- no swelling, erythema, warmth
● Alcohol withdrawal sx: mild (tremors) →
seizures → hallucinosis → delirium tremens
○ mnemonic : My School’s Hallway
Demon
● Atrial flutter is usually due to a large
reentrant circuit that traverses the
cavotricuspid isthmus of the RA, so RFA
would block conduction through the area b/w
the tricuspid valve and IVC
● Succinylcholine is contraindicated in pt with
risk of hyperkalemia b/c it results in even more potassium release → this includes burn, crush,
myopathy, denervation (i.e. GBS or quadriplegia) pts, bc they have either increased upregulated
muscle nAchRs and/or rhabdomyolysis; use vecuronium instead
● Sarcoidosis treatment is ONLY steroids, and only if symptomatic
● Kallmann syndrome patients might have some pubic hair b/c adrenarche is normal (b/c adrenals can
still produce androgens in response to CRH), but they would have central hypogonadism and
anosmia, and maybe some midline defects (cleft things) → delayed puberty
● Hyperdynamic precordium could be due to any number of pathologies; in this question (QID 188) it
was b/c of Down’s syndrome → complete AV canal defect
● Brainstem injury/trauma:
○ Fixed, dilated pupil -- upper midbrain (contains optic nerve, pretectal nuclei, EdWestphal
nuclei, CN III) and mediates the direct and consensual pupillary light reflex
○ Pinpoint pupils -- pons (bilateral injury), because it deals with the oculocephalic reflex
(horizontal gay center aka doll’s eye), and contains CNV and
● West Nile virus: can be seen in Texas (southern US, Latin Am, Africa); pt presents with rash, fever,
HA; motor sx are asymmetric flaccid paralysis, especially diagnostic if pt has concurrent parkinsonian
features
○ Neuroinvasion is RARE, but fatal in 10% of cases; elderly, and those with h/o cxc or organ
transplant are especially susceptible to encephalitis/meningitis
○ CSF would show anti-WNV Abs (but PCR test is often not needed)
○ Pt without duodenum is most likely to develop microcytic anemia (IDA)
○ M. furfur and M. leprae (tuberculoid Th1 type) both cause hypopigmented macules, but furfur
is pruritic whereas leprosy is hypoesthetic (decreased sensation to pinprick)
● Clubbing is a/w prolonged hypoxia, as in: large-cell lung cancer, TB, CF, suppurative lung diseases
like empyema, bronchiectasis, chronic lung abscesses, congenital heart disease (Eisenmenger,
ToF), bacterial endocarditis, pHTN, and other: IBD, hyperthyroidism, malabsorption.

19
● Ddx: lacunar infarct vs Charcot-Bouchard aneurysm rupture: both are caused by chronic
hypertension, both involve the same small penetrating arteries (such as lenticulostriate), but the key
difference is that lacunar infarct is so small that it is not seen initially on CT; it may be seen weeks
later as a cavitary space (CSF fluid-filled lesion)
● Buprenorphine and methadone are both used for withdrawal, via different mechanisms:
○ Buprenorphine (given with naloxone) acts as a partial agonist
○ Methadone has a long half life (used to suppress cravings and withdrawal symptoms)
● Hepatic abscess can be caused by staph aureus via HEMATOGENOUS spread → this is a much
more common cause of hepatic abscess in the US than the “classic” Entamoeba, echinococcus;
pyogenic bacteria can get to liver from biliary tract infection, portal vein pyemia, penetrating trauma,
peritonitis, cholecystitis, etc.
● Ddx fibromyalgia vs polymyalgia rheumatica: age (fibro in 20-50, PR in >50 yo), both in women more;
fibro is due to central pain processing issues (normal CRP, ESR, etc), whereas PR is an inflammatory
disorder; also note that fibro has neurosx as well (fibro fog) and pain that worsens with exercise (but
regular, consistent exercise long term actually helps)
● Tocolytics are aka as inhibitors of uterine contraction; can be achieved by “it’s not my time” drugs aka
indomethacin, nifedipine, mg-sulfate and terbutaline (beta 2 agonist)
● Amiodarone is the LEAST likely to cause torsade, although it does also elongate the QT
(prolongation)
● Renal infarct presenting sx: hematuria, flank pain, nausea, vomiting, low-grade fever; hypertension
b/c of renin release from hypoxic tissue
○ Ddx from pyelonephritis (according to UW) b/c that would have pyuria, dysuria
● HDV is considered replication defective bc it requires the HBsAg coating in order to penetrate the
hepatocyte
● Thoracic aortic aneurysm presents with hoarseness, dysphagia (due to compression), and can cause
hemiparesis of diaphragm (due to phrenic nerve compression); rupture leads to shock/cardiac arrest
→ seen on CXR as widened mediastinum, enlarged aortic knob, tracheal deviation
● VEGF and FGF are involved in angiogenesis and wound healing; laminin in BM may pose a physical
barrier to the sprouting of new vessels
● Essential tremor: MOST common movement disorder; AD inheritance (!), worsens with
movement/anxiety; bilateral, usually in ULs; often self-medicated with alcohol, otherwise,
propranolol (DOC), primidone!
● HOCM has “patchy interstitial fibrosis,” abnormally shaped cardiomyocytes
● Myocardial hibernation: a state of chronic myocardial ischemia, in which both myocardial metabolism
and function are reduced to match the reduction of blood flow -- new equilibrium, which prevents
necrosis; coronary revasc can “revive” this myocardium via restoration of blood flow

20
PART 2 of UWorld pg22:
● Prolonged PT in the setting of NORMAL aPTT shows that it’s a defect in the extrinsic coagulation
system that is not shared by the intrinsic system (aka cannot be in common pathway) → factor VII
deficiency
○ Note that factor VIII deficiency would show prolonged aPTT and normal PT
● Lateral pterygoid is the only muscle that opens the jaw (inn. by CNV3 just like the masseter, medial
pterygoid and temporalis -- all close the mouth)
● Acne vulgaris can be caused by mechanical trauma, friction (tight workout clothing, rough scrubbing)
○ OCPs can actually decrease acne because they inhibit androgen synthesis usually
● Female with gestational diabetes and family hx of gestational/DM2 diabetes likely has a
glucokinase mutation that causes MODY (unmasked by pregnancy); disease is non-progressive even
without treatment
● The GRANULOSA cells convert androgens into estrogens (contain aromatase)
○ Theca interna makes androgens from cholesterol (via desmolase)
○ Think of layers and their locations: externa protects; interna does first step, then granulosa
(most internal) does final step of conversion)
● Adult that works around children and develops coughing and post-cough vomiting -- consider
pertussis; if they haven’t had their vaccination boosters, very possible that they got disease from the
children (xray shows no consolidation - helps ddx from S.pneumo, mycoplasma)
● Histoplasma capsulatum proliferates unchecked in MPHs and forms granulomas; in health pt,
cell-mediated immune system can eventually fight off organism, but in IC → disseminated disease
○ qstem pt was on adalimumab (TNF-alpha inhibitor → increased risk of infection with
pathogens that are controlled by cell-mediated IR such as TB, granulomatous fungi)
● Mycelial form = mold form (mold in the cold, yeast in the heat, so in normal human body, the fungi
are in yeast form (infectious form))
○ Exception: M. furfur in its mycelial form is pathogenic → tinea versicolor
● Sick sinus syndrome: bradycardia on ECG with dropped P waves; sx: lightheadedness,
near-syncope; usually due to age-related
degeneration of the sinoatrial node (right
atrial wall)
● Class 1 antiarrhythmics:
○ Use dependence: faster HR → more
time the Na channels spend in
open/inactivated state → more that
become blocked
○ Weak binding means that
dissociation occurs SO rapidly that
there is minimal cumulative effect
over mult.cardiac cycles → minimal
use dependence
○ Strong binding: slow dissociation →
greater blockade at higher heart
rates → best for terminating
tachyarrhythmias
● Aortic stenosis can cause angina (even without CAD); angina is directly related to the increased
LV wall stress (as a result of outflow obstruction → higher chamber pressures and increased
myocardial oxygen demand → angina)
○ AS also causes a decrease in LV compliance, but that doesn’t directly cause angina (which is
what the question asked)
○ QID 14966 (this is a bit simplified)
● BB helps treat htCMP in two ways that both increase EDV; 1) decreased HR thus more filling time
and 2) decrease contractility so less volume is ejected out

21
● Lumen obstruction is the #1 inciting cause of acute appendicitis → in adults: fecalith, in children:
lymphoid hyperplasia
● Pt presents with ARF, confusion and oxalate crystals on renal biopsy: ethylene glycol poisoning! →
causes ATN (PT cell ballooning and vacuolar degeneration)
● In drug dosing → the higher the peak or average plasma levels, the more chance of side effects
○ Trough: the lowest concentration level before next dose
● Pt has AGMA caused by lactic acidosis: many things can cause lactic acidosis, including end-organ
hypoperfusion as seen in septic shock (which is what this pt had, judging by his hypotension, fever,
leukocytosis, tachy) → thus LA is due to decreased oxidative phosphorylation: buildup of NADH and
shunting of pyruvate to lactate
● Pancreas embryo:
○ Failure to FUSE: pancreas divisum
○ Failure to migrate/rotate: annular pancreas
○ NOTE: ventral pancreatic bud forms the main pancreatic duct → it flips around the duodenum
and joins with the dorsal bud (that gives rise to the ‘accessory pancreatic duct, tail, most of
the head, body)
● Churg-Strauss can cause wrist drop due to mononeuritis multiplex (vasculitis of epineural vessels) --
asthma patient may present with what seems like radial nerve injury (w/o history of trauma)
● Cat exposure is not necessary for toxoplasmosis; especially in HIV patients (pt presents with
headache, seizures, ring-enhancing lesions and oral thrush)
○ Diff q: can be from undercooked meat of farm animals
● QT prolongation can be acquired (seen in chronic heavy alcoholics)
● Bupropion is CI in patients with eating disorders because EDs often come with electrolyte
imbalances (higher risk of seizure)
● Information from the retina is processed by the primary visual cortex aka the striate: cuneus gyrus
gets info from upper retina // Lingual gyrus from Lower retina
● Reid Index of COPD is equal to the (mucous glands/(submucosa+LP)), without taking into
consideration the epithelium or the cartilage
○ Normal: 0.4 (the higher the value, the more severe/longer the chronic bronchitis)
● Glycogen storage disease with “abnormally short outer chains” refers to limit dextrins (as seen in
Cori aka debranching enzyme deficiency)
● PCOS pts have increased LH and often increased LH receptor expression; TOC is estrogen receptor
modulation - ie clomiphene
○ can also give androgen receptor antagonists (tx hirsutism, etc.), but not good for those
wishing to be pregnant because of risk of fetal abnormalities
● Pay attention to whether or not child can be comforted post-nightmare/terror → helps with the ddx;
nightmares may be associated with ‘voluntary muscle atonia’ aka muscle paralysis
● Beta thalassemia is initially caused by ‘mRNA formation” problem; can be transcription, processing
or translation problem of the beta-globin mRNA (commonly = aberrant splicing or premature chain
termination)
● FNH is thought to be due to vascular abnormality that causes localized hyperperfusion (seen in young
women); you would see a central stellate scar with fibrous septae that surround these abnormally
large hepatic arterial branches (that is found within the ‘scar’)
● Goljan mnemonic: membranous nephro = Hep B, and membranoproliferative = Hep C (sequential)
● Certain solid tumors (lung, breast, prostate) are a/w membranous glomerulonephritis
● DVT therapy can be tPA, but usually it’s reserved for really severe cases (aka risk of limb ischemia or
PE), because it can cause massive bleeding; instead, use ENOXAPARIN in hemodynamically stable
patients (such as this pregnant woman - note that heparin is safe in pregnancy, and LMWH is good
because doesn’t require monitoring)
● Trauma patient was treated in ER, was stabilized, then suddenly had low urine output, pulmonary
edema, and died: why? -- at first he was likely given mannitol to decrease his ICP and manage his
cerebral edema; but aggressive osmotic diuresis can cause volume depletion, (dilutional)
hyponatremia and pulmonary edema (lung spots on shirt and spilled peanuts next to patient)
● M protein: prevents phagocytosis in strep (group A)

22
● Campylobacter is another very important source of pet-infections (puppy from kennel); esp. seen in
children
○ Note: couldn’t have been norovirus, bc norovirus is non-inflammatory so you wouldn’t seen
any blood/leukocytes in the child’s stool
● Drug OD with violent behavior: seen in both PCP and meth (PCP - nystagmus, hallucinations, meth
- choreiform movements)
● Berry aneurysm locations:
○ anterior communicating artery/ACA → most common location of saccular aneurysm,
compresses central optic chiasm causing bitemporal hemianopia
○ posterior communicating artery → CN III (IPSILATERAL diplopia, mydriasis, down and out
eye)
● MCC of encephalitis in the US is the arbovirus family (esp. seen in the summer months); flu-like
illness with meningitis and/or encephalitis (focal neuro deficits, tremor, seizure, confusion)
● Viruses can cross the species barrier via antigenic SHIFT that occurs thanks to genetic
reassortment
○ Hemagglutinin vs neuraminidase: ddx?
■ HA: antibodies against HA protects pt from disease when exposed to that same
strain; it’s a glycoprotein on the surface of influenza virions that binds to sialic acid
residues on the respiratory epithelium of human cells. Following endocytosis,
hemagglutinin causes fusion of the viral envelope with the host endosomal
membrane. This protein is also the target of neutralizing antibodies against influenza -
it can undergo lots of antigenic variation
● Changes in HA alter the tropism of the virus
■ NA: promotes progeny virion release (scalpel) → we have inhibitors of NA
(olsetamivir)
■ Changes in either of HA/NA can result in antigenic drift, but shift requires
reassortment (so has nothing to do with HA/NA)
● Which is worse, ‘shift’ or ‘drift’? Think ‘oh sh*t, we’ve got genetic shift!’
● Chronic pancreatitis pt who has pancreatectomy will develop exocrine insufficiency, thus all the
digestive enzymes may become deficient (lipase, trypsin, trypsinogen); but D-xylose absorption
would be normal, because this monosaccharide can be absorbed directly without the action of
pancreatic enzymes
○ Used to test brush border absorptive function (independent of pancreatic function), b/c unlike
polysaccharides that have to be broken down by pancreatic enzymes, xylose is absorbed w/o
pancreatic help
○ D-xylose absorption can decrease with SIBO
●
● Treatment of TIA: antiplatelet agents and statins (and lifestyle mods)
● Treatment of achalasia: botox (botulinum toxin) because it inhibits Ach release, thus less contraction
of the LES (allows relaxation)
● DDx between selective albuminuria vs non-selective proteinuria in nephrotic syndromes:
selective is seen specifically in MCD, because there is a loss of podocytes → therefore, loss of
anionic properties of GBM (allows albumin to pass through); all other forms of nephrotic syndrome
result in non-selective proteinuria, incl. albumin
● Membranous nephropathy is best visualized with methenamine silver stain (shows irregular spikes
protruding from GBM); a/w HBV, SLE, syphilis
● “Foreign Ag recognition at the cell surface by CTL stimulates a response that leads to rapid cell
death → what is the effector of this response? Caspase”
● Radiation therapy (external beam radiation) is ionizing radiation (gamma, x-rays) that causes dsDNA
breakage and free radical formation
● Child with ‘bright red tongue’ could have Group A strep or Kawasaki -- ddx via pharyngeal exudate
(seen mainly in strep throat, not in Kawasaki (where you would also see other sx like conjunctiva
injection))

23
● T-cell ALL is more likely to present with mediastinal symptoms (causing SVC syndrome, etc.); note
that B-cell ALL is much more common (70-80%)
● Genital herpes treatment (prevention of recurrence) requires continuous daily valacyclovir
● Opioids (via mu R) can cause biliary colic via contraction of the SMC of the sphincter of Oddi
(causes spasms, increased bile duct pressures, cramping, RUQ pain)
● Frontal eye field vs. Broca area: frontal eye field is higher than Broca (part of the inferior frontal
gyrus)
○ Broca aphasia may be a/w right upper limb and face wakness (if the lesion extends into the
primary motor cortex)
○ Note that Broca is frontal lobe, while Wernicke is temporal lobe, but both are supplied by
MCA
● Celiac disease may lead to malabsorption → Vit D deficiency (hypocalcemia, etc.)
● Pt with microcytic anemia who eats out a lot and drinks casually is unlikely to have the severe
malnutrition you’d see in alcoholics; her anemia is likely due to occult blood loss
● Cephalosporin resistant organisms: Listeria, MRSA, enterococci, atypicals (with no cell wall, like
Mycoplasma, CHlamydia)
○ Listeria is resistant because it has a special PBP that have a low affinity for cephalosporins;
therefore to treat Listeria, you have to add ampicillin (it has a specialized side-group that
allows it to bind to and inactive the PBPs of Listeria)
● H.pylori causing duodenal ulcer is found in the gastric antrum (NOT duodenum); biopsy from there
● Unilateral renal artery stenosis would result in the atrophy of the affected kidney (cortical
thinning,interstitial fibrosis, small crowded nuclei) and the contralateral kidney would undergo
‘thickening of the arteriolar wall’ due to both hyaline and hyperplastic arteriolosclerosis
○ Hyaline - due to extravasation of plasma proteins
○ Hyperplastic - due to concentric smooth muscle cell proliferation in response to pressure
● Tricky micro q: GP bacterium is treated with Abx and then placed into isotonic solution (--> swells),
and then into hypotonic solution (--> disintegrates); what kind of Abx was given? It has to be
something that affects the strong peptidoglycan cell wall of the GP bacterium (i.e. a cephalosporin,
vanco, penicillins - as a result of any of these, the bacterium cannot survive osmotic stress)
● Mallory-Weiss tears develop due to rapid increase of intraabdominal/intraluminal gastric pressure
(i.e. retching, vomiting); a/w alcoholism -- not usually life-threatening
● Acute epididymitis in youth is due to STDs (urine culture usually negative so requires NAAT), and in
elderly due to ‘coliform’ bacteria like E.coli
● Ladd’s fibrous bands that connect the retroperitoneum to the right colon/cecum is seen in midgut
malrotation
● Bupropion is not associated with sexual dysfunction (it’s a NE/DA reuptake inhibitor); this is in contrast
to the SSRIs)
● Phosphatidylcholine is required for cholesterol solubility (along with bile salts); with low levels of
these two and high cholesterol levels, the pt will likely develop cholesterol gallstones - the bile is the
detergent, and the phosphatidylcholine is a phospholipid
● Synovial pannuses in RA release proteinases (matrix metallopeptidase 13) → destruction of
articular cartilaginous matrix → erosion
● Pseudomonas produces an enzyme “located on the cytoplasmic surface of the cell membrane, which
catalyzes transfer of acetyl groups to exogenous substances” -- this is pseudomonas’s main method
of antibiotic resistance; with this, it confers resistance to aminoglycosides
○ This is called an “antibiotic-modifying enzyme” and it adds chemical groups (acetyl, adenyl,
phosphate) to the drugs,
so the antibiotic has
reduced ability to bind to
the 30S ribosomal RNA
(increased minimum
inhibitory concentration)
○ Enzymes are usually arise
via plasmid/transposon

24
 transfer (not chromosomal mutation)
● Beers criteria: drugs to avoid in elderly -- some ‘unusual’ ones: BB, CCBs, diuretics (low dose OK),
many anti-arrhythmics (UW), anti-histamines, antidepressants like SSRIs and TCAs), antihistamines,
PPIs (FA: increased risk of Cdiff); UW QID 11567 was really unclear (bad question)
● Elimination of INTRACELLULAR bacteria relies generally on cell-mediated immunity (because
immunoglobulins can’t reach them… obviously)
● In tetanus, clinical diagnosis is enough to start treatment!
● Heme is synthesized primarily in RBCs and hepatocytes, but only erythrocyte precursors can make
heme (after they mature, they lose their mitochondria -- necessary for heme synthesis)
● Finasteride (treating BPH for ex.) can cause gynecomastia because it blocks the conversion of
testosterone to DHT; therefore excess testosterone is then made into estrogens in the peripheral
tissues → breasts enlarge
● Beta thalassemia minor patient with diabetes may have a misleadingly low HbA1c level (pt has
increased HbA2, which are prone to hemolysis → increased RBC turnover); clever clinicians can use
glycated serum proteins (like fructosamine) to estimate glycemic control
● Pt with some sort of nephritic syndrome and normal complement likely has IgA nephropathy (IgA
can’t fix complement as well as IgG, IgM) - IgA nephropathy can occur totally spontaneously
● BB can mask symptoms of hypoglycemia
● Conversion of non-pathogenic corynebacterium to pathogenic one requires phage conversion via
lysogenic bacteriophage → this permits exotoxin production (diphtheria AB toxin)
● Leukocyte adhesion deficiency (LAD) is due to decreased expression of beta-2 integrin molecules,
which are neutrophil cell-surface receptor proteins; as a result, you have delayed separation of
umbilical cord that’s considered >1 month, omphalitis, leukocytosis
○ Note that a neo’s differential of 50% neutrophils and 45% lymphocytes is totally normal
● SHOX gene is missing in Turner syndrome → this gene, found on the X chromosome, normally
promotes long bone growth therefore Turner patients have short stature (meiotic nondisjunction,
usually in the paternal gamete)
● S. epidermidis can cause meningitis (for ex if patient has ventriculoperitoneal shunt)
● K+ regulation in the renal tubules: K+ is freely filtered so at BS, the concentration is 100% (ie that
of the serum); then, most of the K+ is reabsorbed in the PCT (2/3rd, so you’re left with 35% in the PT)
and TAL (so you’re left with 10%) -- these processes are relatively fixed (you’d have the same
happening even in hyperkalemic states)
○ The region of the tubule that regulates K+ is mainly the DCT and CD -- in hypokalemia,
reabsorption of K+ can result in 1% of the filtered load remaining; and in states of increased
K+ (i.e. high dietary K+ intake), the amount of K+ in collecting tubules can actually exceed
that of the filtered load (110%!)
○ QID 1554
● Exertional heat stroke can trigger DIC!! → increased fibrinolysis, increased thrombin and plasmin
generation
● WPW triad: shortened PR interval, widened QRS, delta wave
● Heparin is the most important cause of thrombocytopenia in hospitalized patients
○ Direct thrombin inhibitors bind to the thrombin active site without needing antithrombinIII for
their action (note: they are DOC in heparin-induced thrombocytopenia)
● Virtually all infants born to HBeAg+ mothers will be infected perinatally; you would see a rapid
appearance of HBsAg and HBeAg within a few days; however, they are ‘immune-tolerant’ for a time,
meaning that they have maybeee mildly elevated LFTs but really no symptoms (because their T-cell
responses are immature)
○ Treatment: Neo hepatitis B vaccination and immunoglobulin within 12 hours (most cases of
infection occur during delivery)
● Textured breast tissue with dimpling, redness and warmth, itchiness, swelling, no discrete masses
and enlarged, hard LN in the axilla all point toward inflammatory breast cancer, which is due to
invasion of the lymphatic spaces (ie obstruction); this is the one associated with peau-d’orange

25
● To prevent intravascular catheter infections: use sterile drapes (and other barrier precautions),
alcohol-based hand scrub, chlorhexidine antiseptic at the preparation site, and prompt removal when
you’re done
○ Preferred choice is subclavian and IJV (femoral has highest risk of infection! - it’s the largest,
maybe that’s why?)
○ Do not replace catheters are timed intervals; only change if it’s infected
● CCB that is effective for lowering a patient’s blood pressure without worsening his ECG
(bradycardia, PR elongation) would be nifedipine or any of the dihydropyridines, because they do not
act on the cardiac muscle and therefore have no effect on cardiac conduction/contractility
○ Additionally, DHPs can cause reflex tachycardia (due to peripheral VD), so may actually
benefit a hypertensive patient with resting bradycardia
● CNS lymphomas, as seen in HIV patients, are usually a/w EBV
● Erythropoiesis-stimulating agents have two made adverse effects: worsening hypertension (maybe
due to activation of EPO receptors on vasc endothelial and SMCs), and increased thromboembolic
events (inc. viscosity)
● Main ddx between opportunistic diarrhea in HIV:
○ CMV → multiple ulcers and mucosal erosions; histo = large cells with basophilic
intranuclear and intracytoplasmic inclusions
■ CMV is the most common viral opportunistic infection of GI in advanced AIDS; it’s
usually a reactivation (initial infection may be asymptomatic or similar to EBV-mono
● Side note: CMV retinitis is the most common reactivation syndrome in HIV
patients; 2nd most common is CMV colitis
○ Cryptosporidium → nonulcerative inflammation; basophilic clusters seen on the surface of
intestinal mucosal cells (acid-fast, basophilic parasites attach to mucosal brush border)
■ Crypto can cause disease in IC and immunocompetent, and usually in small
intestine (not colon)
● HIV-treatment: protease inhibitors block viral protease from cleaving gag-pol polyproteins → formation
of immature virions that are non-infectious
● AML has myeloperoxidase, whereas ALL has TdT positivity
○ PDGF is seen in GIST
● Spermatocele vs. hydrocele: spermatocele is also known as an epididymis cyst; hydrocele is around
the testicle, located in the scrotum

● Patients on ampho B: monitor their renal function (causes renal VC and decreased GFR;
hypokalemia and hypomagnesemia); patients on conazoles should have their liver function tests
monitored
● Tap1 gene → TAP protein, used in MHC 1 antigen processing (it’s required to move peptide
fragments that are generated by the cytosolic proteasome into the RER); this is for INTRACELLULAR
○ Recall that MHCII has the invariant chain (processes endocytosed extracellular pathogen)
● Patients with Apoliprotein E4 are at a greater risk of old-age onset Alzheimer’s, but patient with
Down syndrome is not affected by this (rather, they have increased amyloid precursor protein, which
is found on chromosome 21
● Chloroquine-sensitive malaria is treated with chloroquine, with additional primaquine (added to
prevent disease relapse caused by hypnozoites)

26
 ○ Recall that this patient had fevers every 48 hours aka tertian malaria → may be vivax, ovale
or falciparum; the first two are unique
because they establish a latent hepatic
infection (exo-erythrocytic)
● Blocking voltage-gated calcium channels
inhibits the fusion/release of NT vesicles
● Ddx between compound and junctional nevi:
○ Junctional do not penetrate into the
dermis (stay at the basement
membrane levels, neighbors to the
melanocytes)
○ Compound are BOTH in the BM and
also in the dermis
● Ddx of Babesia vs. Ehrlichia:
○ Ehrlichia spreads to mononuclear cells (mulberry-shaped, intraleukocytic inclusions aka
morulae), associated with a rash (maculopapular); labs = lymphopenia, thrombocytopenia,
elevated LFTs
○ Babesia is found in red blood cells, seen as ring-shaped parasite within RBC (like malaria)
● Long-term effects of untreated prolactinoma is actually decreased BMD, as well as hot flashes,
infertility (in premenopausal women) → why? High levels of PRL suppress GnRh → decreased LH,
estrogen
● S4 heart sound (right before S1, at end of diastole) is especially loud in LV hypertrophy and
restrictive CMP; due to rush of blood against stiff ventricle wall when the atria contract
● Asymptomatic patient with IgG antibodies against HAV likely had HAV as a child; under age of 6,
HAV is usually anicteric aka clinically silent (pt had negative anti-hep A IgM and positive anti-Hep A
IgG)
○ +IgM would signify reactivation of HAV, but in general, people with persistent anti-HAV IgG
antibodies are usually immune to repeat infection
○ Note that only HBV has ‘window period’ - don’t let that confuse you
● Neprilysin causes the breakdown of natriuretic peptides and angiotensin; thus inhibition of neprilysin
by sacubitril → overactivity of these enzymes; however, we combine neprilysin inhibition with
valsartan, so we can block the negative effects of angiotensin II (VC, fluid retention) but maximize the
positive effects of the natriuretic peptides (vasodilation, diuresis); the overall effect is increased
urinary sodium excretion
● Answer option ‘impaired cleavage of vWF’ is not referring to vWD; rather, it’s seen in thrombotic
thrombocytopenic purpura, due to low ADAMTS13 level, which doesn’t cleave vWF multimers and so
the platelets are trapped together
○ Patient presented (with a lot of symptoms and, uniquely) decreased light touch sensation in
left upper extremity and lower left face → may be due to microvascular thrombosis (methinks,
UW didn’t specify)
● Prolonged hypoglycemia due to DM2 medication (i.e. patient is hypoglycemic, given sugar, feels
okay, then glucose drops again a few hours later): most likely a SU, because none of the rest would
cause such repeat episodes of low BG
○ Meglitinides do cause hypoglycemia, but they have a very short half-life (1hr)
○ Sitagliptin increases glucose-dependent insulin release (so doesn’t cause hypoglycemia)
● Young male presents with SAD symptoms of aortic stenosis? Consider bicuspid aortic valve
(common cause of AS in USA) → auscultation: harsh, crescendo-decrescendo systolic ejection at
RIGHT sternal border
● Damage to the parotid gland causes facial DROOP, because the facial nerve innervates the facial
muscles (peripheral facial palsy - T/Z/B/M/C); facial numbness would be caused by damage to the
CNV nerve
○ Ten zebras buggered my car - temporal, zygomatic, buccal, mandibular, cervical are MOTOR
● Spleen in sickle cell disease will be fibrotic and atrophic; pt may develop megaloblastic anemia bc
there’s an increased folic acid requirement due to the constant hemolysis

27
● Intense pruritis is a hallmark of atopic dermatitis; AD can be a/w mutations affecting epidermal
barrier proteins (filaggrin) → imapired barrier function of skin, thus immune hypersensitivity
● C.diff: single biggest RF is antibiotic therapy (consider even if there was no mention of prior Abx
use)
● COPD exacerbations: most common = infections (vitral (rhinovirus) > bacterial (MuSH)); air
pollution and pulmonary embolism can also cause but less common; allergic responses are very
uncommon triggers
● Hemoglobin in alveoli (such as in Goodpasture) can lead to increased alveolar O2 absorption and
high DLCO (note that it’s due to alpha 3 chain of type IV collagen)
● Trypsin is unique because it can activate itself (i.e. trypsin cleaves more trypsinogen into trypsin
within the duodenum), but it can also inactivate itself (within the pancreas, it can cleave active trypsin
molecules to prevent digestion of the pancreas); this is VIP because despite the body’s best efforts, a
small amount of trypsinogen always ends up getting activated in the pancreatic acini
○ In rare cases, patient has a mutation of the SPINK1 gene → leads to production of
abnormal trypsin that is not susceptible to inactivating cleavage by trypsin → hereditary
pancreatitis
● Duchenne’s is usually due to a frameshift mutation, but it can also (less commonly) be caused by a
nonsense mutation → premature stop codon (UAA, UAG, UGA); when given a question with lots of
codons, start by identifying ALL the start and stop codons (got this right because of a lucky guess)
● Major cells causing emphysema (via parenchyma destruction): PMNs, MPHs, CTLs): release elastase
● Cilia remove particles until the terminal bronchioles; after that, from the respiratory bronchioles
down, macrophages remove particles
● Orbitofrontal cortex damage → personality change, disinhibition, irritability (strongly tied to limbic
system)
○ Lateral prefrontal cortex: executive functioning
○ Recall from Anki: left-sided frontal lobe lesions lead to disinhibition, whereas right-sided cause
apathy
○ Temporal cortex injury can cause Kluver-Bucy syndrome
● Researchers found an increasing number of nosocomial bloodstream infections due to staph: it’s
NOT due to the increased use of Abx, but rather, more intravascular catheters
○ Note that increased Abx use causes MRSA (drug resistant), but MRS causes skin abscesses,
pneumonia, etc., not bloodstream infections
● Two types of urinary incontinence are associated with MS: early on -- a spastic bladder
(overactive, due to presence of UMN lesion in spinal cord); then, later, they may develop a neurogenic
bladder (overflow incontience, due to detrusor underactivity)
● Atropine can induce acute closure glaucoma, because the mydriasis side effect causes narrowing
of the anterior chamber angle → decreased outflow of humor (thus it’s CI in glaucoma patients)
● Acute parotitis is a possible complication inb or post-op patients, especially in elderly or those taking
anticholinergics (which decreases salivary outflow); caused by staph
● Hydralazine and procainamide are the most likely to cause DILE; you would not see anti-dsDNA
antibodies, but rather anti-histone
● Two autoantibodies associated with systemic sclerosis/CREST: systemic (aka diffuse) sclerosis -
anti-DNA topoisomerase I (Scl-70), anti-RNA polymerase III; CREST (limited sclerosis) -
anti-centromere
● Vasopressin acts on the collecting ducts to, yes, increase water permeability; but it also activates
urea transporters in the medullary collecting duct → increases urea absorption (this increases the
medullary osmotic gradient, allowing production of maximally concentrated urea)
● PCR amplification requires primers that are complementary to the DNA regions flanking the
segment of interest → without these primers, you cannot start PCR
○ Note that the exact sequence of the target region does not need to be known
● Sarcoidosis is due to Th1 → IL2, INFgamma production; Th1 cells are central to cell-mediated
immunity, which is important for the formation of granulomas; these cells secrete IL2 (which stims
further Th1 cell activation/recruitment) and IFNgamma (the latter of which stimulates MPHs, inducing
granuloma formation)

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● Noro and rotavirus present similarly, but norovirus is the #1 cause of viral gastroenteritis in
developed countries (b/c we vaccinate against rotavirus)
● Omphalomesenteric duct normally obliterates during 7th week of development
● Pt with atopic dermatitis is predisposed to 2ndary skin infections like impetigo, cellulitis
● E.coli sample is seen to produce pink colonies on MacConkey; then, a few days later, the same
bacteria form white colonies on the same agar - genetics show that there’s a single nucleotide
deletion within lac operon DNA sequence → likely a frameshift mutation, which results in a premature
stop codon (so protein necessary to metabolize lactose was likely not produced)
○ NOTE: the other options given (missense, nonsense, silent, etc) are all point mutations aka
single base substitutions, and question said deletion
● Dubin Johnson liver is black due to impaired excretion of polymers of
epinephrine metabolites that accumulate within lysosomes!
○ Gilbert/Crigler-Najjar are both conjugation
issues; DJ/Rotor are both excretion issues
● Although we think of candida as causing vulvovaginal,
oral or cutaneous infections, in IC patients, it can cause
disseminated disease including pneumonia,
esophagitis, endocarditis, abscess, candidemia, etc.
○ VIP to ddx from cryptococcus neoformans
(pic on right), which has no hyphae or
pseudohyphae (or germ tubes)
○ Neon green is CANDIDA (note germ tubes,
which are growing hyphae)
● DKA’s metabolic acidosis is usually accompanied with a
compensatory respiratory alkalosis, therefore you’d see a
low PaCO2 (along with the low pH, low bicarbonate)
● Blue-black deposits in sclerae, ear cartilage: alkaptonuria
● Pt in his 20s with acne -- unusual, consider anabolic
steroids (methyltestosterone)
○ Note that severe perspiration does not cause acne,
but can exacerbate it
● Retained sutures can cause a foreign body
granuloma -- tender, erythematous brown or purple
papule/nodule
○ Scars CAN undergo malignant transformation;
very rare, seen 10+ years after initial scar
(called Marjolin’s ulcer -- aggressive, ulcerating
SCC)
● Intestinal cryptosporidiosis would actually be seen
with little cryptos lining the intestinal epithelium
● Humoral hypercalcemia of malignancy: most
common cause of hypercalcemia in patients with malignancy, due to secretion of PTHrP
○ Key diff between PTH and this is that PTHrP doesn’t increase vitamin D production
● Rebound rhinitis is due to tachyphylaxis (alpha-adrenergic receptor internalization)
● Granuloma inguinale (donovanosis) does NOT have LAD; chancroid does (inguinal LAD); syphilis
would be painless
○ In granuloma inguinale, you would see Donovan bodies (deeply staining gram negative
intracytoplasmic cysts)
● Main immune defense against Giardia: CD4 helper T cells and secretory IgA (clears infection by
binding trophozoites, impairing their adherence)
● Reduced cortisol can lead to: normocytic anemia, eosinophilia and hypoglycemia!
● Primary adrenal insufficiency described as: worsening generalized weakness, myalgias,
unintentional weight loss, orthostatic hypotension, emaciated
○ Dx of PAI requires low aldo and low cortisol, unlike dx of adrenal insufficiency (low cortisol)

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● Quick guide to treating heart problems acutely:
○ Atropine: for bradycardia (post inferior MI)
○ Adenosine: for PSVT
○ Amiodarone: for ventricular tachyarrhythmias in acute MI (not good for bradyarrhythmia bc of
negative chronotropic fx)
● Psoas abscess: due to hematogenous seeding from distal site or contiguous spread from adjacent
structures (vertebra, for ex.); primary is esp. seen in HIV, DM or IVDU
● Splenomegaly in alcoholic liver disease is due to congestive hypersplenism → expansion of red pulp
○ Treatment of varices in ALD: lowering of portal pressure; so why does SST and it’s
long-acting analog octreotide work? They inhibit the release of glucagon, VIP, etc., so they
cannot induce splanchnic vasodilation, so they indirectly reduce portal blood flow
● Cells undergoing ischemia increase in size (i.e. myocardial cells): why? accumulation of intracellular
calcium -- when there’s no ATP, not only do the sodium-potassium pumps stop working, but the
Ca2+-ATPase in the sarcoplasmic reticulum also stops working; therefore, increased
intra-mitochondrial calcium concentrations (and intracellular Na+ concentrations), which attract free
water → cellular and mitochondrial swelling
○ Also, since we can’t sequester calcium, we can’t contract our muscles
● Patient with positive leukocyte alkaline phosphatase test had “basophilic oval inclusions in
mature neutrophils” aka Dohle bodies; they are blue because of the ribosomes bound to the RER;
seen in toxic systemic illnesses (leukemoid reaction), burns, myelodysplasia
● Fanconi anemia vs Diamond Blackfan: ddx
○ Fanconi anemia: AR, impaired repair of interstrand DNA crosslinks → most common cause of
aplastic anemia (short stature, no thumbs, increased malignancy risk)
● MOA of GLP-1 agonists (and DPP4 inhibitors): increase glucose-dependent insulin secretion (thus
no hypoglycemia risk), decrease glucagon secretion; GLP-1 is usually secreted by L cells in GI
● When Down syndrome is caused by a Robertsonian translocation, the genotype is written as
46,XX, t(14;21), so it may not seem like a trisomy (oh, but it is, bc we have 3 effective copies of 21)
○ Recall that upslanting palpebral folds refers to Down, and startle reflex (aka Moro reflex) is
weak in these babies
● Serum sickness: very very important diagnosis - constellation of fibrinoid necrosis, neutropenia,
arthralgias, fever, pruritic skin rash, hypocomplementemia; HS rxn type III
○ Neutropenia bc C5a is a PMN chemoattractant that causes marginalization, and
hypocomplementemia bc the deposition of IgG and/or IgM complement-fixing Abs
● Cellular compartment contents: intracellular = Na, Cl, Ca2+ // extracellular = ONLY K+
● ACEi, diuretics and ARBs would all cause increased renin (thus pt who was prescribed any of these
drugs but shows no increase in renin levels is likely non-compliant)
● Angina pectoris pt who can’t tolerate low dose aspirin should be given clopidogrel (alternative
anti-plx therapy, just as effective)
● Two drugs to treat male pattern baldness: finasteride and minoxidil (direct arteriolar VD)
○ Finasteride works because DHT is thought to be the primary pathogenic factor; if used
early in the progression of the disease, finasteride can minimize progression (pathomech of
androgenetic alopecia = shortened anagen aka hair follicle growth phase, thus follicular
miniaturization (this is thought to be caused by DHT)
○ Androgenetic alopecia pts have higher levels of 5 alpha reductase, and more androgen
receptors → that’s why using finasteride can be useful!
● HSP can present with joint pain (self-limited migratory arthralgias, esp in the ankle and knee joints),
along with GI symptoms (hematemesis, bloody diarrhea, bowel wall edema, increased risk of
intussusception)
● ATM presents with (besides ataxia and telangiectasias) IgA deficiency and increased AFP; it’s due to
a mutation of the ATM gene, which is charged with DNA break repair, therefore pt is hypersensitive to
X-ray radiation
● Weightlifter drops massive weight bc his arm suddenly/involuntarily relaxes → due to GTO
(sensory receptor located at the junction between muscle and tendon); innervated by group 1b
sensory axons; they’re in contact with inhibitor interneurons within the SC, which synapses with the

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 alpha motor neuron of that same muscle; if the muscle exerts too much force, GTO can inhibit
contraction → prevents damage
● Pt with severe abdominal pain, nausea, vomiting (CT shows distal ileal wall thickening/lack of
enhancement with IV contrast) likely has acute mesenteric ischemia → tissue ischemia can lead to
accumulation of NADH, which inhibits PDH → lactic acidosis
● METABOLIC ACIDOSIS leads to compensatory respiratory alkalosis in most cases, as patient will
likely hyperventilate to eliminate CO2
● Rice-water diarrhea is so called because there are no leukocytes or erythrocytes but there is some
mucus (due to the activation of goblet cells)
● DRESS syndrome symptoms: symmetrical face swelling, morbilliform rash, fever, generalized LAD;
may seen hepatomegaly, elevates ALT, acute interstitial nephritis, cough, etc.
● Pt waiting to undergo hemodialysis develops sudden catheter exit site bleeding = common
presentation of a patient with significant renal dysfunction → he has accumulated uremic toxins
○ Leads to qualitative platelet disorder, which only affects the bleeding time (rest are normal)
● CAH treatment: low doses of exogenous corticosteroids, to suppress the excessive ACTH secretion
→ subsequent reduction of adrenal cortex stimulation
○ Why does this work? Because the key issue in 21-hydroxylase deficiency is that there is no
cortisol synthesized, which feeds back on the pituitary and increases ACTH secretion →
androgen overproduction
● Valsartan overdose: hyperkalemia, hypotension, renal failure
● Ichthyosis vulgaris: mutation of filaggrin that results in
epidermal hyperplasia and defective keratinocyte
desquamation → dry, scaly skin with loss of normal barrier
function; it’s worse with age and in the winter (less humidity)
and has a + family history; seen on trunk and extensor
surfaces
○ Note that atopic eczema is also due to a filaggrin
mutation
● Reticulocytes appear blue because they have a basophilic,
reticular network of residual ribosomal RNA → when they mature, this disappears
● Myotonic dystrophy: classically can’t release things (handshake, jar lid, doorknob), a/w testicular
atrophy and hair loss (toupee); CTG repeats, CATARACTS
○ Ddx: ion channel myopathy, which is rare (never seen in questions); sx are myotonia and
hypotonic paralysis that’s a/w exercise; histo shows PAS+ intracytoplasmic vacuoles; no
muscle atrophy is seen
● Erythroid precursor cells in liver/spleen → indicates extramedullary hematopoiesis, which can
cause ‘bone deformities’
○ EMH is most often caused by severe chronic hemolytic anemias (beta thalassemia, etc.)
● Cerebral inflammatory vasculitis can resemble MS, and may even have oligoclonal bands, but
usually patients have severe headache and systemic sx, incl. night sweats
● Osteoclasts in Pagets are very large (can have up to 100 nuclei!)
○ 2 key factors for osteoclastic differentiation: M-CSF and RANK-L (produced by osteoblasts
and BM stromal cells)
○ OPG: decoy receptor that decreases binding of RANKL to RANK (so decreased survival of
osteoclasts → less bone resorption → increased bone density)
● Elastin is strengthened by interchain cross-links with lysine (aka desmosine cross-links) between
neighboring polypeptides (hold the elastin molecules together); these account for its rubbery property
● TM portion of a GPCR contains hydrophobic amino acids (ala, val, leu, ile, phe, trp, met, pro, gly)
● Hemeproteins (intracellular iron-containing proteins) include Hb, Mb, cytochrome oxidase
● Normal A-a gradient: 5-15mmHg (can be due to hypoventilation or high altitude)
● Pembrolizumab blocks PD-1 in cancers that overexpress PD-L1 (melanoma, RCC) → promotes
tumor cell apoptosis; how? PD-1 Rs are found on CTLs, and when the cancer produces this ligand, it
binds the R, and the CTLs are suppressed (T-cell exhaustion) - so with this mAb, we disinhibit the
T-cells, leading to renewed apoptosis by CD8+ lymphocytes

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 ○ BACKGROUND QID 14956: cancer cells avoid immune recognition by overexpressing
PD-L1, which binds to the PD-1 R on CTLs and inhibits their response by causing T-cell
exhaustion
■ anti-PD-L1/PD-1 mAbs are effective against cancers that express high lvls of
neoantigens on their surface (bc these tumors are particularly susceptible to immune
recog by cytotoxic T cells)
○ NEOANTIGENS: unique proteins that are produced during oncogenesis and not found in
healthy cells; cancers with defects in MMR proteins and those with high microsatellite
instability create lots of mutations (they have 20x more neoantigens than tumor cells with
normal MMR), therefore they are more susceptible to immune recognition → (my thoughts =
more likely to lead to T-cell exhaustion, so we can use pembrolizumab to treat these cxc)
● Bone pain that is worse at night, progressive and not helped by analgesics, in the elderly: most
suspicious for malignancy
● Cysts that form following ischemic stroke are called glial scars, and post-brain infarction they form a
cystic cavity with walls composed of astrocytic processes (dense fibers)
● Painful ulcers on tongue and gingiva, swollen gums and cervical LAD: gingivostomatitis,
diagnosed by Tzanck (but PCR is better, bc Tzanck can also be positive in VZV)
● Ubiquitin ligase (enzyme) is key in initiating the ubiquitin-dependent proteasome pathway (tags
proteins for breakdown)
● Note that no matter how high the PTH is, phosphate will be high in CKD!
● Cleft lip: fusion of intermaxillary segment and maxillary prominence
● Woman post-partum comes with fecal incontinence; cause is pudendal nerve injury (symptoms
include decreased anal sphincter tone and loss of anal wink reflex) - injury happens during labor,
due to stretching somewhere along its curved course around the ischial spine
○ How can we know its not cauda equina syndrome? That’s an emergency, has bilateral
radicular pain, saddle anesthesia, hyporeflexia; of note, bowel incontinence = late sx
● Crohn’s patient presents with fatigue, poor appetite, joint pain at night and several large
ecchymoses on LLs: likely has vit K deficiency, secondary to loss of bile acids (fat malabsorption)
○ The joint pain is due to hematoma formation in deep tissues/joints
● Exudate vs transudate: one giveaway could be that exudate (likely due to bacterial pneumonia) may
be unilateral, whereas transudate (probably due to HF) is bilateral (also, check for fever)
● Pulsus paradoxus (decreased of SBP by more than 10mmHg on inspiration): cardiac tamponade,
severe asthma, COPD, constrictive pericarditis
● Tx COPD: beta adrenergic agonists → increase cAMP in bronchial smooth muscle cells
● Lipid-lowering drug that increases TG levels if used as monotherapy? Cholestyramine (the bile
acid binding resins)
● PREGNANCY
○ In utero infection: toxoplasmosis (only happens if mom is infected within first 6 months)
○ Intrapartum infection: HSV, neonatal conjunctivitis (Chlamydia, Neisseria, various viruses,
GBS)
○ NOTE: ddx between toxo and CMV - toxo has diffuse intracranial calcifications, whereas
CMV has periventricular
● Atenolol (and other beta1 antagonists) result in ↓ cAMP in the cardiomyocytes and the JG cells, but
no effect in the VSM cells
○ note that non-selective BBs, like propranolol, are also effective in vascular and bronchial
SMCs!
● MIGRAINE Therapy:
○ Acute treatment aka abortive medications: NSAIDs, triptans, antiemetics, ergotamines
○ Preventative treatment: topiramate (reduces frequency of migraines, BBs (meto or
propranolol), TCAs and other anti-epileptics like valproate
● B vs. T-cell ALL: B-cell is usually in early childhood, while T-cell (CD3+) is in teenage years/early
adulthood and is associated with mediastinal mass → compresses airway (cough, dyspnea, SVC
syndrome)
○ mnemonic: T-cells mature in the thymus, which is in the mediastinum

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● Urothelial carcinoma prognosis is determined by depth of invasion into the bladder wall/muscle
● HBV vaccination will look like (+) Anti-HBs but (-) HBsAg (infected patient will have other Ags too,
like anti-HBc)
● Sertoli-Leydig cell ovarian neoplasm produces testosterone!
● GLUT receptors are transmembrane carrier proteins that work by facilitated diffusion (ie follow their
concentration gradient): doesn’t require energy, but does require a transport protein (they are
stereoselective and prefer D-glucose)
○ Note that it’s not active transport, which moves it against its concentration gradient (i.e. the
sodium-glucose symporter)
● Complete AV block: the ventricle is paced BY the AV! - that’s why you have narrow QRSes;
otherwise, if the ventricle was paced by anything below the AV, it would be <20bpm and wide
○ SA → gives impulse for atrial contraction / AV → impulse for ventricle
● In Lesch-Nyan syndrome, purine salvage pathway is impaired, so the body has to work hard to
make enough purines via the de novo pathway → therefore, PRPP amidotransferase (the first
committed step of de novo purine synthesis) must be upregulated
● BZD withdrawal: rebound anxiety, tremor, insomnia, sympathetic hyperactivity, even psychosis,
seizures, death
○ Note that withdrawal from lamotrigine and valproate would not provoke seizures in a patient
without an underlying seizure disorder (i.e. when used to treat bipolar)
● New onset SOB, confusion in a trauma patient (bilateral femur, pelvic fractures); he has a petechial
rash on his chest → “fat embolism syndrome,” which occurs 1-3 days after a long bone or pelvic
fracture); rash is due to RBC extravasation in the dermal capillaries
● Entcapone increases the bioavailability of levodopa specifically by inhibiting its peripheral
methylation (it’s a COMT inhibitor, since levodopa is metabolized to 3-OMD via COMT enzyme)
● Echinococcus hydatid cyst has eggshell calcifications
● Dermatofibroma: benign proliferation of fibroblasts (lower extremities, solitary); it’s
aka a superficial benign fibrous histiocytoma (UWorld pic was more white)
● Liver is the second most common site of metastatic spread (#1 = LN)
○ Note that mets can elevate the enzymes (i.e. isolated ↑ alk phosphatase)
● Paget disease of the bone can cause bone bowing; labs: normal everything with
elevated alkaline phosphatase; you would see cortical and
trabecular thickening (increased formation of new bone, which
also explains the high alkphosph → “picture frame” look,
increased blood flow (creating local warmth without erythema)
○ Bowing therefore is NOT only seen in osteomalacia,
rickets
● Mature B-cell leukemia is also known as CLL (!) has
neoplastic cells with CD 19 and can coexpress CD5 (T-cell
marker)
● UNCAL herniation (of the medial temporal lobe) causes CNIII
oculomotor palsy
○ central/downward herniation is CNVI (abducens →
sunset eyes): look at where the abducens nerve exits
the brainstem
● C.diff toxin results in ↓ cytoskeletal integrity (actin
polymerization - licorice factory!), whereas C. perfringens toxin
results in ↓ cell membrane integrity
● Bone biopsy in MM would reveal mature plasma cells and plasmablast cells (>10%)
● Outcomes of HBV is one of 3 things:
○ 1) acute hepatitis with complete resolution (95% of cases!)
○ 2) chronic hepatitis ± cirrhosis
○ 3) fulminant hepatitis with massive liver necrosis
● Ddx Kaposi sarcoma and Bacillary angiomatosis requires HHV8 testing; clinically they appear similar
● Histoplasma is a filamentous mold in the environment

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 ○ DISSEMINATED histoplasmosis: affects the RES system, so you would seen HSM, LAD,
pancytopenia and,
characteristically,
ulcerated lesions on
the tongue; histo would
show oval/round yeasts
within macrophages
● Role of OPG in bone
metabolism: activation of
osteoclasts requires the binding
of RANK by RANK-L; OPG is a
decoy receptor for RANK-L,
therefore it reduces the
differentiation/survival of
osteoclasts → increased BMD;
loss of OPG at menopause
leads to increased osteoclasts:
osteoporosis
● DM1 is associated with HLA class 2; DM2 has a stronger genetic association, but not with HLA
● NO and prostacyclin (PGI2) together inhibit platelet aggregation and cause vasodilation; this limits
thrombus propagation; in atherosclerosis, endothelial cells are damaged and cannot secrete these
two, which creates a localized predisposition to increased platelet thrombus formation
○ Recall that they oppose TXA2 (also a PG)
● In some cases, NSCLC can be caused by a tyrosine kinase fusion protein, between EML4
(echinoderm microtubule-associated protein-like 4) and ALK (anaplastic lymphoma kinase)
○ Rx: crizotinib (protein kinase inhibitor ‘nib’)
● Rare case: healthy, non-smoker middle aged man has sharp left-sided flank pain → kidney stone; but
when docs are working up his stone, they incidentally find foci of calcification in the left lower lung,
spleen and mediastinal lymph nodes, patient is symptomless and there are no changes seen on
repeat imaging (note, he lives in Ohio): YES, fungal infection (H. capsulatum), which in healthy people
does NOT produce symptoms
○ Granulomas in the lungs and RES fibrose and calcify over time
● Primary polydipsia patients have mild hyponatremia, while primary ADH def patients (DI) have
hypernatremia
● Down syndrome: maternal meiosis I (anaphase, acc to Amboss)
● Selective arteriolar vasodilators like hydralazine/minoxidil do lower
BP (decrease SVR), but they also result in reflex symp activation,
sodium/fluid retention; therefore they’re not used for chronic tx
○ When given acutely (in HTN crisis), they are given with
sympatholytics and diuretics to mitigate the SE
● Cryptococcus neoformans is visualized on mucicarmine (in which
the capsule stains RED); the capsule is clear with India ink
● RBC mass measurement: needed to differentiate between relative
and absolute erythrocytosis - in relative, the RBC mass does not change (i.e in aggressive
diuretics)
○ Hypoxic erythrocytosis would be when O2 saturation is under 92% - usually when PaO2 falls
below 65 mmHg
● Headache that’s worse in the mornings: space-occupying brain lesions
● In pernicious anemia, there is a decreased parietal cell mass (CD4+-mediated immune response
against parietal cells themselves) → causes decreased IF, etc.
○ This results in decreased secretion of HCl (achlorhydria) → intraluminal pH rises, and that
stimulates gastrin secretion by G cells

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● Antimicrobial agent that inhibits bacterial glycosyltransferase will mainly affect bacteria that have
cell walls (peptidoglycan is a major component of both GP and GN bacteria, and it’s partly
synthesized by glycosyltransferase)
○ However, bacteria without a cell wall are resistant to these Abx (penicillins, etc.): mycoplasma
● Blasto: Great Lakes, described as “doubly refractile wall” and “single broad-based bud”; in its mold
form, it has branching, tubular cells
● Fungal rhinosinusitis: caused by Aspergillus; pt in qstem was undergoing treatment for CML, and
he complained for headaches, scant nasal discharge, and left orbital swelling and cellulitis, along
with proptosis and ptosis; histo shows thin septate hyphae
● Most COMMON cause of unilateral fetal hydronephrosis: ureteroplevic junction (due to inadequate
canalization, since its the last segment to canalize)
○ NOTE: issues at the vesicoureteral junction can also cause hydronephrosis, but it’s a
non-obstructive
○ Posterior urethral valves = most common cause of bilateral hydronephrosis
● TB’s Pott disease frequently forms abscess behind the anterior ligament (result of hematogenous
seeding of vertebrae from primary pulm infection, months to years after; likes to seed highly vascular
organs like the spleen, liver, bones (L1-L3 vertebral bodies))
○ Ddx from Staph aureus? It’s the most common cause of spinal epidural abscess, yes, so it
may present the same as Pott disease; the key is risk factors (for ex., in Nepal, TB is
endemic, whereas staph aureus is associated with IVDU, direct spinal procedure or
endocarditis)
● Cyclin-dependent kinase inhibitors result in bone marrow suppression
● Pt had 2ndary syphilis: what might have given it away? He had gonorrhea 3 months ago
(co-infection with gono is frequent), but tested negative for other STDs (early syphilis often yields
FN tests); he presents with fatigue, arthralgia, faint macpap rash involving trunk, extremities, palms,
soles; he has enlarged, nontender inguinal LN and multiple wart-like lesions (condyloma latum) on
the scrotum/perineum)
○ Histo: plasma cell rich infiltrate with proliferative endarteritis
● Choriocarcinoma has no hydropic villi! - its muo cyto and syncytiotrophoblastic cells
● Atypical lymphocytes (aka Downey cells) in mono are CTLs, not helper T cells (Sketchy: killer
knight with giant T-cross on his outfit, to the left of the EBV bar)
● MCCOD (most common cause of death) in Friedrich ataxia: htCMP
● Colorectal cancer associated with colitis (IBD) is unique because it tends to originate multifocally
○ Early p53, late APC gene mutation
○ (whereas sporadic follows the ‘AK-53’ mnemonic)
● CLL vs Hodgkin lymphoma ddx: HL would present with B symptoms and anemia,
thrombocytopenia, leukocytosis would be very unusual; CLL, you would see accumulating mature B
cells in the BM (impairs normal hematopoiesis, leading to anemia, thrombocytopenia, neutropenia)
● Primary biliary cholangitis (female-disease) → ONLY intrahepatic
○ PSC (male-disease) is both intra and extrahep
● Melanoma has unique feature of color variegation: red = ectasia, brown/black = advancing
neoplastic cells, white = regression
○ Parts of a melanocytic lesion can regress bc CTLs recognize tumor antigens (like melan-A)
and induce apoptosis (clear patches)
○ Tx: pembrolizumab (PD-1 inhibitor)
● Point mutations in neurophysin II could actually cause hereditary central DI (bc neurophysins
transport and package ADH via ER and Golgi into the neurosecretory granules)
● Neprilysin is a metalloprotease! - breaks down ANP, BNP
● Intussusception before age of 2 is likely due to a structural cause or viral infection; after age of 2,
some sort of lead point (Meckel diverticulum, foreign body, tumor) should be sought
● Tamoxifen is a prodrug that needs to be metabolized by CYP450, thus patients that are poor
metabolizers (polymorphism) may have decreased levels of the active metabolite and thus higher
risk of disease relapse

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● FASTEST symptomatic relief for rheumatoid arthritis: prednisone (or NSAIDs) - surprisingly,
because I thought GCs were slow
○ Methotrexate is first line as a DMARD (disease-modifying anti-rheumatic drug) but
apparently it takes weeks
● MM is unique in that it not only stimulates osteoclasts, but it also inhibits osteoblasts (one of very
few tumors to do that) → leads to purely osteolytic aka radiolucent bone lesions
○ MM cells produce RANKL which stimulates osteoclast maturation; they also destroy OPG
● Pulmonary edema: engorged pulmonary capillaries (due to increased pulmonary venous pressure),
intraalveolar, acellular, pink material (transudation) mostly at the lung bases
● Centriacinar emphysema (smoking) would have macrophage-predominant infiltrates
● Tropheryma whippelii is treated with antibiotics (it’s a gram-positive actinomycete!)
● Best initial way to diagnose DM: HbA1c or fasting glucose test (note that urinalysis is not sensitive
enough)
● Treating DM in a non-medical setting (given that there’s a first aid kit): ideal is glucagon (IM or
SC) - should work in 15 minutes (glycogenolysis and gluconeogenesis); if there is no glucagon
available, buccal or sublingual glucose/sucrose (slow, may be ineffective)
○ In medical setting: IV 50% dextrose
○ ORAL glucose is not recommended in unconscious patients (risk of aspiration!!)
● Cortical blindness: due to injury of bilateral occipital lobes - patient may confabulate/deny
blindness
● Partial vs complete nephrogenic DI: in partial, patients have a slow but steady rise after water
deprivation; there is no further increase when given AVP, and the osmolality will stay <500mOsm/L
● If you give a patient carbidopa, most of the SE of levodopa will decrease except the anxiety/
agitation (bc those are the central effects of dopamine, and we’re increasing DA penetration to the
brain) - the only thing that can decrease the CNS SE is reducing the dose
● Primary lactase deficiency has NORMAL intestinal mucosa on histology
○ The ONLY time you would have injury to the villi if the lactose intolerance was 2* to a viral
enteritis or something
● 17yo boy: skin rash that he’s had for 1 day; a week ago he was treated for a sore throat with oral
penicillin: dx = leukocytoclastic vasculitis aka cutaneous small vessel vasculitis, can be caused by
Rx (beta lactams, sulfonamides, phenytoin, allopurinol); you’d see non-blanching palpable purpura
with fibrinoid necrosis → early would be dominated by neutrophils and fragmented neutrophilic nuclei
(leukocytoclastic vasculitis), and later with mononuclear cells
● Pituitary adenoma, just like a craniopharyngioma, is derived from ADENOHYPOPHYSIS aka surface
ectoderm!
● Cellulitis is most commonly caused by strep or staph; beta-hemolytic streptococci, specifically group
A, is the most common of all (S.pyogenes); edges are indistinct
○ Note that pseudomonas usually only causes folliculitis (hot tub)
● Alcoholism also affects the periaqueductal gray area as well as mammillary bodies, and thiamine
def is diagnosed if baseline RBC transketolase activity is initially low and increases after TPP infusion
● MVP classically described: midsystolic CLICK, followed by systolic murmur, that disappears with
squatting; it’s due to damage of connective tissue
○ Primary MVP: myxomatous degeneration -- deterioration of CT
○ Secondary MVP: inherited CT disorders (OI, ED, Marfan)
● BRCA is a tumor suppressor gene involved in DNA
repair, specifically dsDNA breaks
● Diphtheria vaccination generates neutralizing IgG
antibodies against the B-subunit of the diphtheria
exotoxin, thereby inhibiting toxin-mediated cell damage
(DPT vaxx)
● In HSV Tzanck smear, we see lots of little round ‘ground
glass opacities’ in a multinucleated giant cell - think of
an armored truck carrying many little bombs

36
● Gamma-hemolytic microbes: we should know TWO - enterococci and streptococcus gallolyticus
(associated with colon cancer)
● Mesna’s sulfhydryl group is what binds and inactivates acrolein, the toxic metabolite of
cyclophosphamide
● Neurophysins are actually involved in the post-translational processing and stabilization of
oxytocin/AVP within the neurosecretory vesicles during transport
● Phenytoin causes gingival hyperplasia by increasing PDGF → gingival MPHs respond by
stimulating the proliferation of gingival cells and alveolar bone
● ATN stages: initiation 1-1.5 days → actual damage; maintenance 1-3 weeks → oliguric RF, thus
decreased urine output, increased potassium, metabolic acidosis; recovery months → high volume
diuresis, so you have electrolyte wasting
● New onset headache that’s worse when pt bends over? Often seen in GM; associated sx are
nausea, vomiting, focal neuro defects and/or seizures
○ Ddx from pleomorphic xanthoastrocytomas (in qstem): usually seen in children, young
adults; has reticulin deposits and chronic inflammatory infiltrates; it’s benign and may rarely
transform to GM
● Pt with anemia will likely have high EPO, but always check to see if the kidney function is normal
before answering the question
● Occipital or parietal hemorrhage: consider cerebral amyloid angiopathy → most common cause of
lobar hemorrhage, esp in the elderly!; due to deposition of beta amyloid in small/med-sized cerebral
arteries, causing vessel wall weakening; hemorrhages tend to be RECURRENT
○ Ddx from hypertensive encephalopathy: it is usually a progressive headache with
nausea/vomiting, and non-focal neuro symptoms, like confusion
● Neurodegenerative disorders like Alzheimer and Parkinson are associated with impaired
ubiquitin-proteasome → imapired degradation of abnormal proteins so they aggregate, obstruct cell
traffic, cause cell death, etc
● Acute hypertensive intracerebral hemorrhage of the thalamus → due to hypertension, specifically
the formation of a Charcot-Bouchard aneurysm (commonly causes intracerebral bleed in the basal
ganglia, cerebellum, thalamus, pons); PROGRESSIVE neuro deficits, maybe headache
● RCA perfuses BOTH LV (inferior surface) and RV; specifically, proximal RCA occlusion can
cause RV MI, which presents as hypotension (reduced CO) and distended jugular veins → elevated
central venous pressure); note that the lungs are clear and xray shows no pulmonary edema unless
there’s a concomitant LV MI
○ Note that elevated central venous pressures are seen in right sided heart failure, which can
occur as a result of persistently high LV pressures
● In X-linked recessive disorder, only females are carriers (if male has the affected X, he would have
the disease); subsequently, males cannot pass the gene onto their offspring (only women can)
● Pyloric stenosis is caused by smooth muscle hypertrophy; more common in male infants
(multifactorial inheritance!)
● Obesity comes into play with HYDROPHILIC drugs, such as aminoglycosides (which are large and
charged, so cannot cross cell membranes → their VD is limited to EC space), because they do not
distribute into adipose tissue, so you have to use an adjusted dose (based on lean body weight, for
ex.)
○ Drugs that have high plasma protein binding (like warfarin) are kept in the intravascular
space → their VD is also limited, but its less affected by body weight
○ Ags have minimal plasma protein binding so can distribute extensively into the interstitial
compartment
● Deficiency of Vit A is actually associated with higher risk of complications in measles -- this is
because acute measles infection depletes Vit A stores, leading to a risk of keratitis/corneal ulceration
○ That’s why we treat with Vit A (decreases ocular complications, and reduces the risk of other
comorbidities such as pneumonia, encephalitis, recovery time, length of hospital stay)
● DM neuropathy is caused by endoneurial arteriole hyalinization - NEG of nerve, vasa vasorum
● Tinea corporis: only infects stratum corneum, aka the keratinized structures; doesn’t invade dermis

37
● On-off phenomenon of levodopa can be explained to the patient as “drug response is
unpredictable” - great answer, doc
○ Drug holidays are not helpful, and stopping it abruptly can induced NMS
● Formation of atheroma requires PLATELET derived GFs, from platelets (shocker)
● Independently, simvastatin decreases hepatic cholesterol synthesis, while cholestyramine
INCREASES it (by sequestering the bile acids, therefore the liver has to make more bile acids →
consumes liver cholesterol stores)
○ Therefore, we don’t give cholestyramine alone (we add statins so that we block this effect =
synergistic action)
● Bullous pemphigoid → hemidesmosomes; TENSE bullae; rare oral/mucosa involvement, mainly in
elderly
○ Pemphigus vulgaris → much more severe; flaccid bullae in all various stages of
healing/popping; has tombstone cells along basal layer (desmosomes, desmoglein 1, 3) and
EOSINOPHILIC infiltrate (see pic below)

● “Large, waxy, eosinophilic casts in tubular lumen” are referring to Bence Jones protein (MM)
○ You’d also see an elevated gamma gap (aka the diff between total protein and albumin)
● Candida CAN be scraped off easily - in young, healthy people with thrush, do 4thgen HIV Ag/Ab test
○ Leukoplakia cannot be scraped off
● “Late onset neonatal jaundice” aka jaundice in a 4-8 week old child is indicative of biliary atresia
(aka extrahepatic obstruction of bile ducts); biliary tree is normal at birth and then subsequently
undergoes destruction → immune or viral induced, we don’t know; increased direct bilirubin and GGT
● Hypertensive emergency leads to FIBRINOID
NECROSIS and hyperplastic (onion-skin)
arteriolosclerosis; note that you might seen
schistocytes due to MAHA
○ Look for signs of insanely high BP and
end-organ-damage (such as elevated
seCr/BUN)
○ Chronic hypertension would show
interstitial fibrosis, tubular atrophy, and
homogenous acellular thickening of
arteriolar wall (aka hyaline)
● Congestive hepatopathy (due to RS HF) affects
the centrilobular regions (zone 3), while periportal

38
 region (zone 1) stays normal ⇒ nutmeg liver; you see the hemorrhage around the central veins
● Stool osmotic gap (Amboss): total stool osmolality relies on the electrolytes - the ‘gap’ is the
non-electrolyte substances; i.e. lactose (in lactose intolerance, you would have an increased gap bc
lactose contribute to stool osmolality)
○ You’d have elevated stool osmotic gap in all forms of osmotic diarrhea, such as laxatives
● Cold agglutinin disease (Amboss) is also a/w CLL (along with mycoplasma and hepatitis C!)
● Liver cells cannot use KBs (Amboss) because they lack thiophorase (aka succinyl-CoA
acetoacetyl-CoA transferase), which would convert acetoacetate to acetyl CoA ( → KB)
● If hepatic gluconeogenesis is impaired (ie alcoholic cirrhosis) (Amboss), intestinal
gluconeogenesis is the primary extra-hep site; kidney is another important site
● HIV affects the microglial cells to cause meningoencephalitis (Amboss)
● Cancer-related muscle wasting (Amboss) is due to proteasomal degradation of ubiquitinated
proteins; note that atrophy in general is due to apoptosis (be it intrinsic or extrinsic path), but in
cancer, it’s due to proteasomes (via TNF alpha, and also appetite suppression)
● Aldesleukin (IL-2 AGONIST) that activates T cells and NK cells, which is thought to be helpful in
treating malignant melanoma and RCC (also activates B cells and monocytes, but doesn’t seem
important)
● CF’s delta508 causes abnormal protein folding and failure of glycosylation → thus its targeted for
degradation by proteasome before reaching the cell surface (since its a TM protein)
○ This is the purpose of lumacaftor/ivacaftor: it’s meant to restore CFTR to the membrane
● 12 year old boy who has chest pain and seems to have MI/CAD -- might have homocystinuria (in
which case cysteine is essential, bc you can’t make cysteine)
● In DKA, the urine is going to be acidotic (because you attempt to reabsorb all the bicarb, to offset the
metabolic acidosis of the body), and so bicarb in the urine is also low, while H2PO4 is high (bc kidney
uses acid buffers like hydrogen phosphate and ammonia (NH3) to buffer the acid in the urine)
○ In states of metabolic acidosis, bicarb is completely reabsorbed from tubule!
● Inhibiting COX-2 can decrease risk of reoccuring adenoma in pt with hx of polyps; adenoma to
carcinoma sequence: APC → [hyperproliferative epi] methylation abnormalities → COX2 →
[adenoma] KRAS → DCC → P53)
● Medullary thyroid carcinoma (RET mutation) has spindle-shaped cells; pt in qstem had HIGH
calcitonin (that’s a dead giveaway); usually has amyloid stroma (Congo red)
○ Anaplastic is described as pleomorphic cells with irregular giant cells and also
spindle-shaped (so the calcitonin helps differentiate)
● “Genetic analysis reveals inactivating mutation affecting a structural component of a neutrophil
oxidase enzyme” → describing NADPH oxidase; this enzyme is usually responsible for transferring
an electron from NADPH to oxygen to make superoxide → ROS (deadly, both directly and also by
activating the granule proteases like elastase, cathepsin G)
○ Microbes produce hydrogen peroxide normally (a byproduct of their own metabolism), and
catalase negative organisms cannot prevent the accumulation of this hydrogen peroxide
within the phagosomes, but so they can still be destroyed even if the NADPH pathway for
ROS is dysfunctional
○ But catalase +, including Burkholderia cepacia, Serratia, Nocardia, Aspergillus, can destroy
their own hydrogen peroxide
● GC use leads to dermal atrophy, specifically due to dermal collagen loss (Amboss)
● Hyaline arteriolosclerosis is seen in both HTN and DM, but malignant HTN leads to onion-skinning
aka hyperplastic arteriolosclerosis
● Fat embolism syndrome (FES): respiratory distress, neuro sx, petechial rash (i.e. on trunk) within
24-72 hours of long bone/pelvic fracture
● Xanthoma ddx: they are composed of lipid-laden histiocytes in the dermis
○ Eruptive: appear abruptly with high TG, lipids
○ Tuberous and tendinous: Achilles tendons and extensor tendons of the fingers
○ Plane: linear lesions in skin folds -- strong associated with PBC
○ Xanthelasma: eyelid, usually -- no lipid abnormalities in 50%

39
● Psoas abscess: fever, flank pain that’s worse with extension of the hip; a/w DM, HIV, IVDU and
retrocecal appendicitis
● NCC migrate caudally through GIT, so in Hirschsprung, rectum is ALWAYS affected
● Eosinophilic esophagitis was described as ‘stacked, circular ringlike indentations, linear furrowing
and small, whitish papules” - the papules are small eosino microabscess
○ Main sx: feeling of solid food getting stuck (and in severe cases, food impaction; req.
urgent endoscopy)
● MS has acute demyelination → the decreased saltatory conduction is due to the increased
distance between Na channels → conduction block; note that over time, the sodium channels can
redistribute across the naked axon and some oligodendrocytes can partially remyelinate neurons:
some signal transmission can be restored
● Oral polio vaccine results in duodenal luminal IgA; note that BOTH polio vaccines (Salk and Sabin)
are oral; it’s just that one is alive (Sabin’ alive, Sabin’ alive), and the other is killed (sulky Salk skull)
○ Note that serum IgA (monomeric), IgG and IgM also increase with polio vaccine (even if given
IM), and help protect against viral dissemination
● Adenomatous villous polyps are villainous → more likely to become malignant
● CML diagnosis via rtPCR would show a messenger RNA transcript containing both BCR and ABL
exons; RT-PCR is used to detect/quantify levels of mRNA: mRNA gets converted to cDNA, which is
then amplified (it’s muo exons of the gene, along with the 5’ and 3’ UTRs) - QID 12278
● SVC is derived from the common cardinal veins of the developing embryo → drain into sinus
venosus
● Tamoxifen has a good effect on lipid profile: decreases LDL
● DM1 pt with CKD is having recurrent hypoglycemic episodes; this is bc GFR decreases in CKD, thus
less insulin is cleared from the body
● Pt with macular rash, GI symptoms (esp if first constipation then diarrhea) and progressive fever:
suspect S. typhi; you might see mild hepatomegaly, normocytic anemia and leukopenia with left shift
○ Suspect if patient has traveled, if he has pulse-temperature dissociation (aka fever with
bradycardia)
● DIFFERENTIAL culture means that there’s an indicator; selective is when you kill off other potential
pathogens (reducing is when you remove oxygen; used to culture anaerobes)
● Actually have to know which parts of the world has chloroquine-resistant malaria (bc then you
would use atovaquone-proguanil)
○ Chloroquine-sensitive: Mexico, Argentina, Turkey/Iraq, few other countries; most of Africa is
RESISTANT
● DOC for psoriasis: vit D analogs (calcipotriene, calcitriol) and steroids
○ Diclofenac can be used for actinic keratosis
● PKU (seizures, devo delay, mousy odor) may also cause pallor of brain nuclei (substantia nigra,
locus ceruleus and vagal nucleus dorsalis), since that dark pigment is called neuromelanin; excess
Phe inhibits melanin synthesis
● SCLC has neural cell adhesion molecule (along with chromogranin, neuron specific enolase, and
synaptophysin positivity)
○ Note that EGFR is only seen in some NSCLC, mainly Adc (ALK, EGFR+ - non smokers,
and KRAS+ - smokers)
● CYP450 metabolizes metronidazole and OCPs but they do not induce nor inhibit it
● Rosenthal fibers are seen in pilocytic (pilocystic) astrocytoma, NOT ependymoma (the roses in the
Pixorize image are the pseudorosettes!); recall that astrocytomas can have eosinophilic bodies,
hair-like glial processes and both cystic and non-cystic regions
● NE infusion can result in induration/pallor of the IV site (due to NE extravasation); to counteract the
alpha1 VC that NE causes (which could lead to local tissue necrosis), infuse phentolamine (alpha
blocker → causes vasodilation!; must be given within 12 hours of extravasation to help)
○ If the pt had a thrombus (cold, pulseless, painful limb), then you would give heparin
● CTS in CKD patient: how can you explain median nerve compression in CKD patients? → history of
hemodialysis can cause deposition of beta-2 microglobulin, which is aka dialysis-associated
amyloidosis

40
● GANcyclovir is for CMV (stop forgetting that!) - Sketchy: green can recycling bin at the front door of
the CMV market
● Y. pestis: abrupt high fever, chills, headache, weakness while hiking in New Mexico; intensely painful
swellings in groin
● Pretibial myxedema is aka thyroid dermopathy → due to stimulation of fibroblasts by TRAb and
activated T cells (cause production of GAGs and adipogenesis)
● Viable sperm hangs out in ejaculate for 3months and/or 20 ejaculations post-vasectomy
● PPI tx is a RF for vibrio cholera bc the microbe is very acid-sensitive
● Factor V Leiden mutation (pts have normal aPTT): when testing a patient with it, labs add activated
protein C to the sample plasma, and aPPT remains the same → this shows that the sample is
resistant to the normal antithrombotic fx of activated protein C (this is bc the mutated Factor Va cannot
be inactivated by protein C as it should be)
○ In APS, aPTT is usually elevated
○ Folic acid def can cause hyperhomocysteinemia → can be prothrombotic but aProtC
resistance would be seen
● AFib: the ventricular rate depends entirely on the transmission through the AVN (due to its long
refractory period, not ever SA impulse is sent to the ventricles, so AFib results in 90-170 bpm usually)
● McCune-Albright syndrome: due to GNAS mutation (think of the mechanic - McCune, and the gas
- GNAS); polyostotic fibrous dysplasia with lytic lesions (broken fibers and windshield, coffee in her
ONE hand - one sided lesions, and horny teenagers leering at her - precocious puberty/endocrine dz)
● Osteonecrosis causes can be: sickle cell disease, vasculitis
(impaired blood supply, like in SLE), high dose steroid therapy,
alcoholism (mechanism of last two is unknown)
● Fibroadenoma: myxoid stroma with glandular and cystic spaces
● Thyroglossal duct cyst is due to incomplete obliteration of a
duct
○ Branchial cleft cyst is lateral, and found on the SCM
● When they give the CK level...check to see if it’s in the normal
range -_- just because they give it doesn’t mean it’s high.
● Centriacinar emphysema is mediated by neutrophils! - this
qstem gave symptoms of emphysema and showed a CT; the key
is that macrophages and PMNs release proteases that degrade the ECM → destroy acinar wall
○ I answered type 1 pneumocytes bc that’s what makes up the wall and thus gets destroyed
● ICA aneurysm can compress the uncrossed temporal retinal fibers, causing ipsilateral nasal
hemianopia
● Child ate poison mushroom that ‘stimulates muscarinic receptors’ - the direct effect of the toxin is
NO synthesis; muscarine was the agent, which stimulates M2/M3 mainly → M3 stimulation
promotes synthesis of NO which results in vasodilation and hypotension (somnolence)
● Most common cause of skin/soft-tissue abscess is staph aureus; case - pt comes in with recurrent
papules on back that become enlarged, red, and painful - need to be drained and treated with Abx;
note that oral Abx does not clear the body of the nasal/skin colonies of staph!
● Dermatomyositis may be a paraneoplastic syndrome for ovarian (or lung/pancreas) adenocarcinoma
● Fibrates → promote GB formation bc they inhibit 7 alpha hydroxylase → reduce the formation of bile
acids and thus decrease cholesterol solubility → higher chance of GB stone precipitation
○ NOTE: fish oils actually do the opposite: increase bile acid synthesis and increase GB motility
● Sterile platelet-rich thrombi: NBTE - marantic, associated with malignancy or SLE; first
manifestation is commonly systemic embolization
● Pituitary apoplexy symptoms: severe headache, bitemporal hemianopsia, ophthalmoplegia (due
to CNIII compression); note that it usually occurs in the background of a PREEXISTING pituitary
adenoma, so pt might have sx of prolactinoma, etc.
○ Beware that pt might devo CV collapse bc of ACTH deficiency → adrenal insufficiency; treat
with GCs (emergently! - pt in qstem died)
○ VIP to ddx from pituitary ischemic necrosis (Sheehan), which is chronic, and you do not have
severe headaches or visual field defects

41
● Motilin receptors are located on the muscularis externa; stim by erythromycin (agonist!)
● “Fine” inspiratory crackles (soft, high-pitch) is for PULMONARY FIBROSIS! - pt in qstem had
pleural effusion, which has decreased breath sounds, tactile fremitus and dullness
● HIV-associated dementia is bc the virus infects the microglia → forms microglial nodules, which can
combine into multi-nucleated giant cells
● Hypocalcemic pt is hyperventilating: what is the connection? Hyperventilation → decreased CO2,
which the brain responds to by VC the cerebral vessels (hypocapnic response), which causes
lightheadedness; the body tries to compensate for this alkalosis by releasing the H+ bound to
albumin in the blood, and as a result, the ionized calcium floating around in the bloodstream bind to
the albumin, thus ↓ ionized calcium (note that total serum calcium stays the same) (Amboss)
● Pt needing acute tx for painful RA should be started in steroids; DMARDs take 6+ weeks (Amboss)
● DLCO differential diagnosis:
○ Can be high in things like polycythemia (i.e. pt had hemoptysis), asthma (but may be normal)
○ Can be low in emphysema (decrease surface area for diffusion)
● Hepatic ADENOMAS may regress with cessation of OCPs
● Holosystolic murmur that increases with inspiration: MR
● Omeprazole → osteoporosis bc it decreases calcium absorption
● SE of digoxin/digoxin toxicity: life threatening arrhythmia; my logic was that we use it to treat
arrhythmias so surely it doesn’t induce arrhythmia, but it’s NOT class 5 antiarrhythmic (duh), it’s a HF
drug and arrhythmia is one of its SE (various dances/arrhythmias on dance floor)
○ Note that hypotension isn’t really a common SE (bc its an inotrope), although it can occur due
to bradyarrhythmias and severe vomiting → hypovolemia
○ NEW QUESTION: Digoxin can slow ventricular firing rate during afib due to increased PSY
tone (Las Vagus) → inhibits AV nodal conduction in pt who developed afib with rapid
ventricular response (RVR) - so it IS used for ventricular rate control in afib (kind of like an
anti-arrhytmic drug)
● Primary myelofibrosis is mediated by TGF-beta (the neoplastic megakaryocytes secrete TGF-beta
which stimulates fibroblasts to secrete collagen)
● JVP can have a more rapid/deeper y-descent if the pt has constrictive pericarditis (causes:
radiation tx, cardiac surgery, TB-as in this patient, an immigrant from Russia, where it is endemic)
● Hyperphosphatemia as seen in CKD can bind to free calcium and precipitate in soft tissues / it can
also trigger FGF23 release from bone, which attempts to lower phosphate by inhibiting 1-alpha
hydroxylase; these both can lead to reduced calcium absorption
● Pt who comes in a few days after abortion with fever, chills, pelvic pain is probably suffering from
retained products of conception → septic abortion, usually due to staph aureus (don’t let ‘foul
smelling discharge’ mislead you!) (E.Coli and strep are two other common causes, but Staph is #1)
● Septic pt is intubated, and on 3rd day his Hb drops; NG suction shows bright red blood → likely due
to a stress-related mucosal injury, specifically a Cushing ulcer (lots of small circular lesions of
stomach that can bleed or perforate)
● Hydrocele transilluminates (varicocele does not, bc that’s a bag of worms)
● Pt experiences right arm tingling/numbness → this later develops into right-sided convulsions, then
bilateral TC seizure; the site of ORIGIN of this seizure was likely in the postcentral gyrus, ie the
somatosensory cortex (it was a focal onset seizure that cause the numbness)
● Lightning related death: arrhythmia is most common cause (death withinfirst hour of injury is most
likely due to arrhythmia or respiratory failure (but not barotrauma))
● H. pylori-associated atrophic gastritis vs pernicious anemia-associated gastric damage: H.pylori
has patchy, multifocal atrophy, with sparing of some parietal cells, so you still have normal IF/B12
absorption // autoimmune gastritis results in diffuse destruction of parietal cells (spares antrum,
though, which is where this pt had H.pylori); mediated by lymphocytes and MPHs (no PMNs like in H
pylori)
○ Acute H pylori → duodenal ulcers
○ Chronic H pylori → gastric
● Fatty liver 2ndary to alcohol occurs bc of TG accumulation (increased TG synthesis): alcohol
metabolism produces excess NADH, which decreases FFA oxidation (!)

42
● Copper reduction test is used to detect reducing sugars (fructose, glucose, galactose)
● NF1 neurofibromas are derived from NCC (nerve-sheath neoplasms muo Schwann cells)
● Reassortment can ONLY occur in segmented viruses; easy to differentiate from recombination in that
sense → passed onto progeny; recombination can occur with nonsegmented genomes and it
involves crossing over → passed onto progeny)
○ Viral changes that are not passed on to progeny: transformation (uptake of naked DNA),
phenotypic mixing (genome remains unchanged), interference (when one virus inhibits
replication or release of a 2nd virus)
● Congenital hydrocephalus (macrocephaly, poor feeding) can cause upper motor neuron injury →
muscle hypertonicity, hyperreflexia; this is due to the stretching of the periventricular pyramidal
tracts
● Tryptophan ALSO uses BH4 (not just phenylalanine), thus a decrease in BH4 would cause low
serotonin too (tryptophan hydroxylase requires it); note that in PKU, Phe is HIGH
● Clindamycin is good ‘above the diaphragm’ for things like aspiration bc it has both aerobe and
anaerobe coverage, and lung abscesses are usually polymicrobial with some anaerobes
● Pt with apparent MRSA infection and a vancomycin-allergy was treated with an Abx, and devo’s
muscle pain and increased CK levels; I thought it was probably linezolid (she was on SSRIs → SS),
but actually she was given daptomycin → myopathy is a common side effect
○ Daptomycin affects the microbe’s membrane potential: it depolarizes the cell membrane
by creating TM channels → IC ion leakage and thus cell death); recall that it can’t be used
in GN bc it cannot permeate the outer membrane of GN microbes; it’s also inactivated by
pulmonary surfactant; it also inhibits macromolecular synthesis (DNA, RNA, protein)
● Lipofuscin is due to lipid peroxidation (it’s an insoluble pigment, muo lipid polymers and
protein-complexed phospholipids)
○ LIPID PEROXIDATION: “the oxidative degradation of lipids. It is the process in which free 
radicals "steal" electrons from the lipids in cell membranes, resulting in cell damage. This 
process proceeds by a free radical chain reaction mechanism.” 
● Immediate COD after an MI of the mid-RCA is most likely VFib 
○ death due to “regional contractile dysfunction” occurs when a large portion of the LV dies (like 
in a LAD occlusion), and is uncommon in mid-RCA occlusion. 
● Hypertensive nephrosclerosis would have intimal thickening and luminal narrowing of renal
arterioles, with glomerular sclerosis (renal atrophy, finely granular surface)
○ Ddx from analgesic nephropathy: papillary necrosis (hematuria, proteinuria),
tubulointerstitial nephritis (acutely: pyuria, eosinophilia, fever, rash) (not sure about the two
crossed out ones, see below for Amboss on this)
● Woman 8 months post-delivery presents with hypothyroidism (labs = low TSH, low T4, and
symptoms); how to know if it’s secondary hypothyroidism or postpartum thyroiditis? Postpartum
is a variant of Hashimoto, which means it’s a PRIMARY hypothyroidism (so you would have elevated
TSH, not low); postpartum is considered anything within the first year of delivery
● PCP works on NMDA receptor; it’s an ANTAGONIST
● Pt with heartburn that’s gotten worse recently (w/o symptoms of choking, coughing, food getting
stuck) likely developed esophageal ulcers (due to erosive esophagitis) → classically “worsening of
baseline GERD sx and odynophagia
○ Note that development of Barrett esophagus is usually asymptomatic (baseline GERD
won’t change), but if pt develops and adc, he will likely have dysphagia/weight loss
○ Note also that a stricture would cause the sensation of food getting stuck; strictures occur in
the setting of a healing ulcer (collagen fibers contract)
● Dengue fever: look for retro-orbital pain, hemorrhage, and of course, joint pain
○ Aedes mosquito, which transmits Dengue, also transmits chikungunya (febrile illness with
flu-like sx, polyarthralgias and diffuse macular rash); bc of this, many areas have
simultaneous outbreaks of both
● Dapsone is another drug that can cause hemolysis in G6PD deficient patients (so always check);
other SE of dapsone are fever, rash, metHb-emia

43
● Bacterial vaginosis can be treated by metronidazole, yes, but also clindamycin (also a preferred
treatment option acc. to UW)
● WHY does Vit E deficiency cause neuro and hemolysis sx? vitE acts as an antioxidant, so it protects
fatty acids from oxidation → cells susceptible to injury are neurons with long axons (large surface
area) and RBCs (lots of O2 exposure)
● Pt with night sweats, diarrhea, weight loss, LAD and HSM, weakness and a hx of HIV (CD count is
16) has an acid-fast bug that’s not TB: is it nocardia or MAC? The reason it’s not nocardia is bc
nocardia usually causes just pneumonia and/or brain abscess (the GI, LAD and BM sx would be very
very rare)
● Tumor cells increase laminin expression to help them adhere to the BM (once they’ve detached
from their own cells by decreasing E-cadherin) and traveled to their site of implantation); they then
produce proteolytic enzymes like metalloproteinases, cathepsin D protease to invade the BM
● ALS = most common motor neuron disease; thin anterior roots, mild precentral gyrus atrophy;
demyelination (involves both UMN and LMN)
● Pt with an apparent infection has a high ESR, which mediator causes it? IL-6 (stims liver to generate
APRs, one of which is fibrinogen, and it causes RBCs to overcome the negative charge that
separates them → they stack)
● Nitrate affects LARGE veins
● HCV drugs like sofosbuvir and ledipasvir inhibit viral replication/assembly; sofosbuvir specifically
targets RNA-dependent RNAP, while ledipasvir inhibits inhibits NS5a (a protein important for viral
replication and assembly)
● Fibromuscular dysplasia can have cerebrovascular involvement (HA, stroke, aneurysm rupture;
young female patient died after severe, sudden headache) → you would see tortuous vessels (“both
carotids seem tortuous distally”) and alternating bits with fibrotic webs or dilation
○ LACKS INTERNAL ELASTIC LAMINA
● Osteoarthritis vs RA: osteoarthritis is DIP (mnemonic: “no morning sickness so I can go for my
morning ‘dip’ in the pool!”) - proximal = Bouchard, distal = Heberden
○ Note that this patient had <30 mins of morning stiffness as well, buuuut that’s within normal
for OA (brief is ok)
● Brain TB → ventriculomegaly (symmetrically, thus likely communicating hydrocephalus); this usually
occurs due to 2ary dysfunction of subarachnoid villi (can be secondary to meningeal infection like
TB meningitis, or hemorrhage (subarachnoid or interventricular)
● Senile amyloidosis: on HE stain, it would look like normal myocardial cells with some areas of
amorphous/acellular pink material; Congo red is a much better stain though
○ Pt had a rapid ‘y’ descent, prominent S4: signs of diastolic HF (esp bc he had LA
enlargement and LV h.t., with normal EF) → this is all likely due to the restrictive
cardiomyopathy caused by senile or ‘wild-type’ transthyretin amyloidosis
● Pseudomonas is a common cause of neutropenic infection; specifically causes ecthyma
gangrenosum (when the ANC < 500/mm3)
○ BUT important that it’s usually the commensal bacteria that invade and cause infection in
neutropenia; it’s important to differentiate between
those and pseudomonas (which has these
necrotic/ulcerative skin lesions)
● Gestational DM occurs when body can’t overcome the
pregnancy-caused insulin resistance (due to hPL); screening in
3rd trimester
● Cystic medial degeneration happens in ALL aortic
dissections; it’s bc with age, collagen/elastin/SMC of the aortic
media (which is usually the strongest portion) are broken down
→ mucoid ECM replaces it (mucopolysaccharides);
characteristic basket weave pattern
○ Seen in ANEURYSMS as well - in Marfan, who are at an increased risk; characteristic
fragmentation of elastic tissue and separation of the tunic media layers → filled with
amorphous ECM like MPS

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 ○ Experimentally, sweet peas can induce this type of “myxomatous degeneration” in animals
● Up to 90% of duodenal ulcers are caused by H.pylori!!
○ Also, PG analogs are only good against NSAID-caused ulcers; sucralfate (cytoprotectant) is
good for healing duodenal ulcers, but not for preventing them
● Flasked-shaped ulcers were described as ‘ulcers with undermining edges that contain trophozoites’
● Gallbladder dysmotility makes it more likely that the GI/GB symptoms are due to biliary sludge and
not a stone (neither brown or black)
○ BLACK is due to chronic hemolysis → radiopaque
○ BROWN is due to bacteria → radiolucent
○ Mnemonic: black is the darkest color so we know it’s definitely opaque; once you go black
(you hemolyse), you never go back (those RBCs are goners)
● Induction therapy for cryptococcus is ampho B and flucytosine (flute) → then you can give
fluconazole later
● RF does not usually occur from PSGN (it’s often self-limited)
● Hand hygiene is the #1 most important part of not spreading methicillin-sensitive staph
○ Note that contact precautions (such as non-sterile gloves, gowns) is required for people with
MDR bugs such as MRSA, VRE, etc.
● NPH stretches cortical fibers → leads to impaired cortical and subcortical function
○ Note that the ‘normal pressure’ means that you have increased CSF (due to decreased
absorption at granulations, for ex.), but the ventricles enlarge so the pressure isn’t really
increased
○ Micturition happens bc the cortex usually inhibits detrusor hyperactivity → without cortical
inhibition, you get URGE incontinence
● IL-4 is required for HS type 1, bc it induces IG class switching to IgE
● Tricky q: pt with pancreatitis who has AST/ALT ratio over 2 → what additional findings would you
see? MCV above 100 (you assume s/he is a chronic alcoholic, and malnourished)
● Tricky q: pt comes with mesenteric vein thrombosis due to NPH; what would you see in the
kidney? hemosiderosis! - this is because the chronic hemolysis we see in NPH causes iron
deposition in the kidney (can interfere with PT function → cause interstitial scarring and cortical
infarcts)
○ Note that you can also have microvascular thrombosis of the kidney; these two together can
cause cKD
● EARLIEST finding in the development of rheumatoid arthritis → synovial neovascularization:
activated T cells against rheumatoid antigens (like type 2 collagen, citrullinated peptides) cause
synovial hyperplasia → accelerated metabolic rate of this inflamed synovial tissue leads to local
hypoxia, increased production of HIF1 and VEGF by local MPHs, fibroblasts: ANGIOGENESIS → this
later becomes a pannus (muo granulation tissue, inflammatory cells, synovial cells)
● Granulation tissue (Wiki): new
connective tissue and microscopic blood vessels that
form on the surfaces of a wound during the healing process; typically grows from the
base of a wound and is able to fill wounds of almost any size
● MS vs LV h.t.: in mitral stenosis, only the LA is enlarged → the LV is actually normal or even small,
because very little blood can get through. In LV hypertrophy, LA and LV are both enlarged
● Hb mutation can cause Hb to have HIGHER oxygen affinity (Chesapeake, Kempsey); that’s a left
shift → this leads to erythrocytosis
○ Note: HbS results in hypoxia-induced hemolysis, meaning that low oxygen levels causes Hb
to polymerize → cell damage, hemolysis (right shift)
● HBV virus has no direct cytotoxic effects: it causes damage bc the CTLs destroy infected hepatocytes
● Familial disease leading to ‘enlarged heart with a ventricular mural thrombus’? Likely familial dCMP
(truncating gene mutation of titin, autosomal dominant)
● Fragile X: macroorchidism, typical long face/everted (donkey) ears, hyperlaxity of joints in the hand,
devo delay (no turtle in Pixorize though) and neuropsychiatric features like ADHD, anxiety, ASD,
etc), MVP (according to Pix!)
● Smoking in household → increased risk of SIDS (and also of middle ear disease…)

45
● Asthma treatment: although albuterol is used so frequently, it’s really just for symptomatic control (it
causes bronchodilation); to prevent inflammation-induced airway remodeling and/or alter chronic
disease course, you NEED a corticosteroid (fluticasone) -- it’s used short-course for acute
exacerbations, but can be used for long-term asthma control if sx persist
○ Mg-sulfate (inhibits calcium influx into airway SMC → bronchodil) can be used for acute
asthma flare-up and also to reduce inflammation (Mg stabilizes T cells and inhibits mast
degranulation
● SGLT2 inhibitors cause orthostatic hypoTN bc they cause osmotic diuresis
● “Sclerotic” bone lesion = blastic (mnemonic: Blast it, I have to go back to the SHoP - SCLC, HL,
prostate)
● MVP is the MOST COMMON valve disease predisposing to IE in developed countries
● IGRA is an IFN-gamma release assay that tests for latent TB (measures the response of T cells when
exposed to antigens unique to M.tb; both this and the PPD measure cell-mediated immunity (they
have equal sensitivity/spec, and note that neither can distinguish active from latent)
○ Advantage over PPD: no x-reactivity with BCG and doesn’t require follow-up
● B. pertussis exerts its effects via: tracheal cytotoxin which actually destroys the ciliated epi cells,
and pertussis toxin (AB toxin that increases AC and) inhibits phagocyte activity → lymphocytosis
● SLE has decreased complement consumption bc the ICs that deposit in various tissues cause
complement activation
● PNMT enzyme (converts NE to epi) is upregulated by cortisol, and note that since the veins of the
adrenal cortex drain THROUGH the medulla, cortisol concentrations in the medulla can be very high
○ Pituitary resection: no ACT, no cortisol, less PNMT activity thus less epi
● Candida: superficial is due to T-lymphocyte problem (i.e in HIV, esophageal candidiasis is an
AIDS-defining illness CD<100); dissemiNated is due to Neutrophil problem (candidemia, endocarditis)
● Familial hypocalciuric hypercalcemia is due to a mutation in calcium-sensing receptors (Gq coupled):
autosomal dominant → high to normal PTH, normal vit D, low urinary calcium and mild hypercalcemia
● Mitral leaflet commissures fuse together in mitral stenosis
● Brain and kidneys are more commonly affected by embolic infarcts bc they are perfused at higher rate
● Parietal inflammation is p-p-p-painful!
● Asthma diagnosis: methacholine testing is HIGHLY sensitive, high NPV, so it’s great for dx
● KEY CONCEPT: estrogen increases thyroxine-binding globulin!! → therefore in states with high
E, like HRT or pregnancy, we get increased total T4 (total means that it’s bound plus free T4) and total
T3, but bc the level of free hormones is normal, the pt remains euthyroid
○ Note that there’s a TRANSIENT decrease in free T3/T4 levels when we make all that new
TBG, to which the body responds by increasing TSH → more thyroid hormone production,
until all the new TBG is saturated, and eventually TSH decreases again
● Recognizing acute PE: sudden-onset SOB, chest pain, nearly fainted; patient is in alkalosis with JVD
and clear lungs
● Cavernous hemangiomas: seen in brain and liver; this pt had epilepsy and histology showed
engorged purple clusters with dilated capillaries
○ Capillaries have no elastic fibers or SMC → weak walls, so recurrent hemorrhage
○ Ddx from Kaposi: usually on the skin or GI/respiratory → highly vascular tissue with
elongated spindle cells
● Strongyloides dx: rhabditiform larvae in stool (note that the eggs and adults are seen only in
intestinal biopsies)
○ Trophozoites are seen in giardia and entamoeba; proglottids in taeniae and diphyllobothrium
● GCs result in gluconeogenesis and increased glycogen synthase (so glycogen storage increases):
these require more metabolic enzymes, so that leads to an overall increase in liver protein synthesis
(i.e. increased expression of liver enzymes)
● Lithium toxicity: induced by hydrochlorothiazides (pasty white thighs on high dive!!); this is bc TZDs
decrease sodium reabsorption at the distal tubule → mild volume depletion and stimulates PT
sodium/lithium reabsorption
○ ACEi and NSAIDs can have similar fx of lithium toxicity

46
● Regional wall motion abnormality of the heart usually refers to IHD, such as MI → only the
damaged portion of the myocardium has impaired contractile function
● Triamcinolone is a corticosteroid!
● Pt who has anemia (labs and sx) and low reticulocytes, but normal thrombo/granulopoiesis might be
suffering from pure red cell aplasia (rare form of marrow failure); associated with immune diseases
such as THYMOMAS and LYMPHOCYTIC leukemias
○ Note that parvo b19 can also cause PRCA bc the virus attacks proerythroblasts
● Fluid treatment in septic shock: bolus isotonic crystalloid in the form of 0.9% (normal) saline or
lactated Ringer solution through large-bore peripheral IV; these are good for volume resuscitation bc
their osmolarity is v close to the normal 290mOsm/kg water, and the NaCl ions help retain the fluid in
the EC space
● PV is actually due to an increased sensitivity of hematopoietic stem cells in BM to growth factors,
due to the JAK2 mutation; note that EPO levels are actually LOW (due to negative feedback)
○ The aquagenic pruritis can be attributed to histamine release from basophils
● Atherosclerosis risk in order: aorta > coronary > popliteal > carotid
○ Mnemonic: “a coroner popped his cherry”
● Inhibitor of fungal protein synthesis: flucytosine, bc it replaces uracil with 5-FU in fungal mRNA
● HBV virus replication: first, binds to bile salt transporter on surface of liver cells and enters; it’s
uncoated in cytoplasm → it currently exists as single-stranded DNA aka partial dsDNA → this is
repaired by HOST DNA polymerases → creates dsDNA, which is then transcribed by HOST RNA
polymerase into a positive, single-stranded RNA pregenome
○ + ssRNA template is translated into proteins the compose the virus, and it’s converted by
DNA polymerase/reverse transcriptase into partially dsDNA progeny

● Pt with clasp-knife spasticity likely has an internal capsule stroke (right arm, leg, and right lower
face involved); this is an UMN lesion, which can occur when any part of the pyramidal motor system
is affected (such as the IC)
○ Note that IC strokes can have BOTH sensory and motor deficits, but pure motor is more
common
● Spontaneous retroperitoneal hematoma is common in patients receiving anticoag therapy like
warfarin (acute, severe pain in groin, lower abdo, back; can injury the femoral nerve)
○ Femoral nerve mononeuropathy: quad weakness (can’t climb stairs, knees buckling),
decreased patellar reflex, sensory loss over anterior/medial thigh/leg
● Ddx of parasites causing anemia:
○ Hookworm (necator, ancylostoma): hooked appearance on microscopy, transient rash,
causes microcytic anemia due to IDA
○ Tapeworm (diphillobothrium): operculum on microscopy, no rash, causes megaloblastic due to
VitB12 deficiency
● INH inhibits pyridoxine phosphokinase → B6 deficiency; required for d-ALA synthase
● HIV patient gets a lung infection: s. pneumo or PCP?

47
 ○ S.pneumo is the MOST COMMON cause of CAP in both HIV and non-HIV patients → causes
LOBAR pneumonia (this pt had left-sided chest pain)
○ PCP affects pts when their CD <200; takes weeks of worsening dyspnea and fever to
develop; affects both lungs, as bilateral reticulonodular infiltrates
● Myoclonic epilepsy and blotchy red muscle fibers on Gomori trichrome: MERRF - mito inheritance
● In AMI, pt might present with a new onset mitral regurgitation; this can be due to ischemia to the
papillary muscle, which becomes tense and prevents appropriate closure of the cusp; if the pt is
reperfused in time, the papillary muscle survives and the MR can disappear
● Osteoporosis on histology: affects primarily the trabecular bone → trabecular bone THINS, fewer
connections (interconnecting bridges) are seen; later can affect the cortical bone of the appendicular
skeleton as well
○ BONE HISTOLOGY
○ Paget → defective osteoid formation (haphazard collagen, so mosaic pattern of irregular
sections of lamellar bone
■ Enlarged vertebral bodies with cortical THICKENING leading to picture frame look
○ Osteomalacia → unmineralized osteoid deposits on trabecular surfaces
■ Vit D deficiency: defective mineralization of bone matrix; osteoblasts need calcium for
its calcium-binding proteins/phosphatases that promote bone mineralization
○ Osteopetrosis → impaired osteoclast function aka impaired remodeling; primary spongiosa
remains in the medullary cavity (a/w cytopenias due to BM crowding)
○ HyperPTHism (osteitis fibrosa cystica): increased resorption in cortical bone with
subperiosteal thinning and cystic degeneration; otherwise, bone spaces are filled with brown
fibrous tissue muo osteoclasts and hemosiderin from hemorrhages
○ Osteogenesis imperfecta: due to impaired osteoid production by osteoblasts, bc type 1
collagen is the predominant collage in osteoid (organic portion of bone matrix, allows bone to
be strong but flexible) → leads to brittle bones
● Psoriasis in rare cases can cause destructive arthritis mutilans (esp in B27 + people)
● Euthyroid sick syndrome: often seen in pts with severe systemic illnesses like sepsis → excess
cortisol, inflamm.cytokines, starvation, some drugs can cause decreased T4→T3 conversion,
leading to low serum T3; T4 and TSH are usually normal, and rT3 is typically high
● Differential clubbing: when either JUST the toes or just the fingers are involved; ie ‘toe
cyanosis/clubbing but no finger abnormalities’ → this is characteristic for PDA, bc the patent duct
delivers unoxygenated blood DISTAL to the left subclavian artery!
○ Any uncorrected left-to-right shunt can cause Eisenmenger syndrome (i.e. VSD, ASD, PDA),
but PDA is the only one with differential cyanosis!
● HSV encephalitis has red blood cells AND lymphocytes on LP (-_-)
○ Note that there’s increased cell count and increased protein in the CSF in all infectious
etiologies; GBS is the only one that has normal everything except increased protein
● Risk of IMA injury (and sigmoid ischemia) in AAA repair surgery (Rx)
● Ulcers and mucosal erosions (i.e. esophagus or in Crohn’s) leads to healing by granulation tissue
→ fibrosis → narrowing of lumen and strictures! (pathoma)
● Microsatellite instability simply means that: microsatellites are repeating sequences of noncoding
DNA; the integrity (stability) of these is maintained during cell division; an instability means that you
have defective DNA copy mechanisms, such as DNA MMR enzymes (Pathoma)
● Fragile X is so called bc when you have the trinucleotide repeats on the X-chromosome and you stain
it, the repeats don’t stain and appear ‘broken’; “cytogenetic studies showed a small gap near the tip of
the long arm of the X-chromosome”
● Psoriasis histo: epidermal hyperplasia aka acanthosis, hyperkeratosis (thickening of str.corneum),
parakeratosis (retention of nuclei in str.corneum)
○ Epidermal thinning would be seen in scleroderma
● Aortic calcifications develop in the bkg of cell necrosis (dystrophic calc)
● Renal angiomyolipoma: benign tumor, a/w TUBEROUS SCLEROSIS (not anything else)
○ Bilateral RCC is associated with cerebellar hemangioblastomas, retinal hemangiomas, liver
cysts

48
 ○ Sturge-Weber: with leptomeningeal capillary venous malformation and port-wine stain
(described as capillary angiomas of face and choroid)
● EHEC O157:H7 is unique because it does not ferment sorbitol, unlike other E.coli strains (!); it doesn’t
produce glucuronidase (recall it has a Shiga-like toxin that inactivates the 60S ribosomal subunit)
○ Recall: ETEC (traveller’s diarrhea aka toxigenic Ecoli) is the one with the two toxins: LT is
heat-labile and is coupled to cAMP, whereas ST is heat-stabile and coupled to cGMP
■ eL Agua de San Gabriel
● PYR test has replaced bacitracin bc the bacitracin one isn’t that sensitive; S.pyogenes is PYR+
● Legionella can’t be gram stained because its unique LPS chains inhibit it
● BPH can cause microscopic OR gross hematuria bc new, friable blood vessels can arise in the area of
the prostatic hyperplasia → cystoscopy shows detrusor trabeculations due to muscle h.t.
● Certolizumab is a pegylated humanized mAb that targets TNF-alpha; since it lacks the Fc region, it
helps minimize complement activation and cell-mediated cytotoxicity
● Although kidney eliminates MOST drugs, the liver is the site of biotransformation; drugs that are
more lipophilic (thus high volume of distribution, good CNS penetration) are preferentially processed
by the liver into more polar compounds for easier elimination in the bile/urine
○ Anything with a low Vd would be stuck in the bloodstream, so can’t pass into the hepatocytes’
bile: aka high plasma-protein-bound and hydrophilic
○ Low rate of redistribution implies low lipid solubility/high hydrophilicity, thus stuck in intravasc
● Trastuzumab causes cardiotoxicity that results in worsened myocardial contractility (stunning)
WITHOUT cardiomyocyte destruction or fibrosis
● ESBL is transmitted via plasmid / passed to each other via conjugation
○ Porin mutations: penicillin or Ag resistance
● Weight loss and hyperpigmentation together suggest chronic primary adrenal insufficiency, esp. if
pt has history of other autoimmune endocrinopathies (hypothyroidism in this case); tx = dexameth
● TB cavities are due to aggregations of activated leukocytes: the cavities are made up of caseating
granulomas, which require digestive enzymes from the MPHs to cause necrosis
● Short bowel syndrome: malabsorption due to massive small bowel resection//Crohn’s (decreased
absorptive area) → leads to Vit B12 deficiency bc loss of functional distal ileum
● Focal seizures of temporal lobe can cause transient gustatory or olfactory disturbances; more
permanent anosmia might suggest tear of the olfactory nerve rootlets

49
● Myxoma histology: mucopolysaccharide background, with stellate myxoma cells (purple); most likely
from LEFT atrial myxoma, may present with constitutional sx bc it produces IL-6
○ Presentation: acute limb ischemia with the 6P’s of paresthesia, paralysis, pulse absence,
poikilothermia (coolness), pain, pallor → 30s woman, sudden

● Bone lesion with “increased focal radiotracer uptake”:

hematogenous osteomyelitis (affects mainly male
children) → affects the METAPHYSIS (slower blood flow
and capillary fenestrae there)
● Two drugs: one’s CTX fx can be overcome by adding
N5-formyl-THF supplementation, but the second is not;
what are the drugs?
○ MTX and fluorouracil; that’s the compound for
folinic acid; but 5-FU requires reduced folate in
order to form complexes with thymidylate
synthetase, so it’s cytotoxic effects are reduced in
cells that are deficient in THF
● Abrupt onset gross hematuria in healthy patient with
family hx of SCD is probably due to renal papillary
necrosis due to SCT
○ other things that can cause RPN: analgesic
nephropathy, DM, pyelonephritis/UTI
● Post-hysterectomy pt has fever and right-sided back
pain; urine output is normal → likely due to injury of the
ureter during uterine vessel ligation
● Copper-requiring enzymes: cytochrome C oxidase,
superoxide dismutase, dopamine B OH-ase tyrosinase,
lysyl oxidase, ceruloplasmin
●
●

50
 ● ↓↑

>> End of general UW

51
Calculations (basic ones, the rest are in Word doc)
● Mom and dad have baby with AR disease; what are the chances that 2nd child will inherit one or
more mutant alleles? 75%
● Cumulative incidence: total number of new cases over a period / people at risk at the BEGINNING
of the period; ie if 20 people of 100 are sick at the start of 2016, and 10 more develop the disease,
then the incidence rate is 10/80 (QID 1270)
● Risk of developing Alzheimer’s disease if pt is in the low carotene group? = ppl-who-devo’d-Alz /
total people who had low carotene
○ The calculation I did (how many with low carotene developed Alz / total with Alz) showed the
prevalence of low carotene exposure in Alzheimer patients
●

52
Questions to go back to:
● 1314: immune response to leprosy
● 1619: PAH filtration

53
 UWSA1: Dec 13th -- please please don’t read if you haven’t done it yet!
● Osteosarcoma is a potential complication of long-term Paget!
● DNA laddering: when certain interleukins are withdrawn, cell may undergo apoptosis; you would see
180 bp sequences (fragments) on gel electrophoresis -- very sensitive indicator of apoptosis
● BZD use in elderly causes confusion b/c the drug is usually metabolized by the hepatic oxidative
reduction, but in elderly the mechanism is impaired, so more adverse effects are seen
● Two parents without achondroplasia can have children with the disease given that they have
germline mosaicism (note that only one parent needs to be mosaic)
● DM patients should inspect their feet DAILY for signs of trauma, infection
● IL-2 is a cytokine that’s produced exclusively by lymphocytes
● Injury to the popliteal artery is a serious consequence of both an anterior AND posterior knee
dislocation, because it’s rigidly fixed by the adductor magnus/soleus muscles
● Postpartum endometritis -- usually polymicrobial, especially common post-cesarean section; sx are
foul-smelling vaginal discharge and lower abdomen tenderness
○ Ddx from cervicitis: in endometritis, the cervix can be the portal of entry for bacteria, but it is
not infected (unlike in PID, in which case the cervix is infected and can ascend to the uterus,
causing non-obstetric endometritis)
● Repeating a patient’s complaints back to them is reflection (interview technique)
● Cocaine use (intranasally) can cause: chronic nasal discharge, atrophic nasal mucosa, thinning of
septum → perforation, oro ulcers, osteolytic sinusitis; may present similarly as Wegegener’s and may
even have + antineutrophil cytoplasmic antibody (!)
● Erectile dysfunction drugs (PDE-5 inhibitor like sildenafil) act on the SMC of the corpora cavernosa
(deep artery)
● Bitemporal hemianopia is commonly tested (craniopharyngioma,adenoma, etc.), but binasal
hemianopia is much less commonly tested → it occurs when there is bilateral, lateral pressure on the
optic chiasm such as due to calcification of both ICAs
● Long thoracic nerve injury such as during tube thoracostomy, axillary LN dissection, trauma, causes
winging of the scapula due to damage of serratus anterior
● Pancreas vs. eccrine (sweat glands) in healthy: pancreatic secretions vary with flow rate -- bicarb
increases with faster flow rates, while chloride decreases; flow rate increases in response to secretin
hormone; inverse relationship of chloride and bicarb is maintained by the Cl-HCO3-exchanger at
apical surface of duct cells
○ Sweat glands regulate temperature by secreting sweat; they secrete hypotonic solution that
has very very minimal bicarbonate (mostly water, NaCl, some K+)
● CALCULATIONS (see word doc): all three were wrong -_-
BLOCK 2 ~
● Don’t confuse acute cerebellar degeneration (which is due to damage of the Purkinje cells in the
cerebellar cortex -- seen in extensive alcohol abuse, and manifests as tremors and gait ataxia) and
subacute combined degeneration (due to VitB12/cobalamin deficiency)
● Don’t be put off by a man presenting with MyG symptoms: it can happen; it’s associated with thymic
abnormalities that can be thymoma or simply thymic hyperplasia

54
● Joint infection vs. gout: the monosodium urate crystal are visible on regular H&E staining (!)
○ Septic arthritis is a/w trauma (bumping knee into table apparently qualifies?) and usually due
to S. aureus or N. gono; look for the cocci on the image because it may be visible
● DiGeorge can be dx via flow cytometry, which would show low CD3+ (aka T-cells) but normal CD20+
(because B cells are unaffected)
● In DKA, you have hyperkalemia (because no insulin to shift K+ into cells) and hyponatremia (due to
hyperglycemia-induced osmotic diuresis → lose Na+ in the urine
● Androgen insensitivity syndrome is a pt with female phenotype but 46XY karyotype and high levels
of testosterone likely has “x-linked defect of androgen R,” which results in breasts being normal but
vagina ends in blind pouch; testosterone and LH levels are high but FSH is normal
● SCC in white male with associated painless neck mass and submandibular LAD likely has a TONGUE
origin (or anything else in the oral cavity -- most head/neck cancers are SCC) - all other options could
not cause SCC
● Nitroglycerin dilates the veins → decrease of EDV
(thus decreased wall stress) and compensatory
increase in HR is seen (reflex tachy)
● RNA vs DNA splicing: which one is it? It’s easy to
know, because DNA splicing does not occur under
normal condition (in the pic given, the DNA and its
complementary mRNA were aligned, with DNA
looping in certain places → the loops are explained
by RNA splicing)
● Epistasis in genetics is the interactions between multiple genes that combine to create new
phenotypes or mask/modify the phenotype of one of the genes (ex. pt with sickle cell anemia who has
a mutation that increases their fetal Hb might have less severe clinical signs)
● Allelic heterogeneity vs. genetic vs. phenotypic: allelic = different mutations at same genetic locus
→ similar phenotypes // genetics = different mutations at different genes → similar phenotype
○ VS phenotypic = mutations in the same gene → different phenotypes
● Cysteinyl-containing leukotrienes are C4, D4, E4; they’re released from mast cells and eosinophils
● An indirect ELISA uses an anti-human immunoglobulin Ab that is coupled to a ‘substrate-modifying
enzyme,’ such as a peroxidase (and then when you add the substrate, the color change can be
detected)
● IMPETIGO - can be seen on wounds, including burn wounds, and can be caused not only by GAS,
but also by staph aureus ← the yellow crusting is very specific for these two (burn ≠ pseudomonas
by default)
● Some bacteria rely on efflux pumps to eject antibiotics and if you change the agar (by increasing
the pH for example, which neutralizes the proton gradients), then the antibiotic can become more
effective again
● Space between third and fourth digit → achondroplasia (not fetal alcohol syndrome!); SPOCK
hand; also enormous head (90th percentile) and midface hypoplasia
● In a BM transplant, the donor karyotype can be different than the host (i.e. if a male donor is inserted
into a female host)
● Where does the peptide accumulate if you mutate the signal sequence at the N-terminus (i.e. of
insulin)? In the cytosol; because translation by the ribosome starts in the cytosol, and if the peptide
doesn’t have the N-terminal signal sequence, it cannot be bound by the SRP (signal recognition
particle) to help insert it into the RER pore (so the usual co-translational processing cannot happen, in
which the peptide is fed through the RER membrane’s pore)
● Sertoli cells synthesize androgen-binding protein (ABP) → these have to maintain high local
concentration of testosterone in the seminiferous epithelium needed for spermatogenesis; ABP is
synth in response to FSH and binds to testosterone and DHT (making them less lipophilic, so they
cannot diffuse out of the lumen)
○ Note that a patient with normal serum testosterone but low testosterone in the testis likely has
Sertoli cell dysfunction → low ABP

55
 ● Severe sweating can be treated by surgically interrupting the thoracic sympathetic trunk → since
sweating is mediated by cholinergic postganglionic fibers, ablating the symp trunk at T2 can disrupt
innervation of eccrine and apocrine sweat glands (not sebaceous)
○ Stellate ganglion disruption is used to treat hyperhidrosis of the hands/Raynaud
phenomenon
● Acid-base profile of pulmonary embolism: low pH (respiratory alkalosis), low pCO2
(hyperventilation), low pO2 (blood is flowing past the accessible alveoli too fast)
● Pulmonary hypertension is caused primarily by endothelial cell dysfunction
Block 3:
● Young female with heavy menses (lasting 10 days) and pelvic heaviness has leiomyoma (not
cancer, which is rare in pre-menopausal pt without risk factors); pt may need blood transfusion (!) --
heavy menstrual bleeding is the most common symptom of fibroids
○ Endometriosis doesn’t have incredibly heavy menstrual bleeding because usually the ectopic
tissue is extrauterine
● Ischemic colitis → mucosal hemorrhage and patchy areas of necrosis
● Osteogenesis imperfecta might just manifest
as premature osteoporosis (age 20)
● MCAD can be triggered by viral illness
because usually sick people eat less food →
fasting
● Lineweaver-Burke plot of warfarin + CYP
inducer (rifampin): rifampin increases CYP
concentration in hepatocytes → increased
enzyme concentration leads to increase in
hepatic warfarin metabolism → rise in Vmax
● Microbe genome = haploid; a gram negative
organism has both inner and outer
membrane, and prokaryotes have no nucleus (so no nuclear membrane) - if the organism is
susceptible to penicillins, might be E.coli
○ Note that chlamydiae (cysteine-rich outer membrane with S-S bridges) and mycoplasma (no
cell wall) are insensitive to penicillins
○ Fungi are diploid, viruses are haploid
● Apoptosis: in rare cases, when a cell is undergoing apoptosis, internal ribosome entry is an
alternative method they can use (to allow translation of the proteins needed for apoptosis) to begin in
the middle of the mRNA (this is done at a distinct nucleotide sequence, usually at the 5’UTR, because
the 5’cap with the AUG/Kozal consensus sequence isn’t accessible) → brand new concept
○ Recall: Kozak consensus is for translation in eukaryotes, Shine-Dalgarno is for translation
initiation in prokaryotes
● Biopsy the ILEUM in suspected Crohn’s (duodenum and proximal jejunum are mainly affected in
celiac)
● Hepatic encephalopathy can be treated by acidifying the intestinal contents → lactulose actually
does this because it is degraded by gut bacteria to form lactic acid and acetic acid → NH3 is thus
converted to NH4+
● In osteomalacia, patient has impaired mineralization of osteoid
○ Compact and trabecular bone are both affected in osteoporosis - but it’s an issue of excessive
resorption, not impaired mineralization
○ Lamellar bone is affected in Paget disease of the bone (abnormal formation of lamellar bone,
which is the second phase of osteogenesis)
● Behav science: patient is suffering from insomnia (post divorce, after a move, being a single parent,
fighting with daughter): proper answer is, “You’re really trying to take care of your family; how have
you been handling all of this?” -- avoid close-ended questions like, “do you think this is related to your
insomnia?”

56
 ● Virus that replicate in the nucleus using host enzymes: all DNA viruses except poxvirus replicate
in the nucleus; they rely on cellular molecular mimicry -- they use host cell DNA and RNA
polymerases
○ RNA viruses replicate in cytosol (except orthomyxo and retrovirus); + sense can be directly
translated, while negative sense have to bring their own RNA-dependent RNA polymerase
● In X-linked recessive, when doing calculations keep in mind that only half of the offspring will be male
● Cutting unmyelinated nerve fibers will most likely affect autonomic postganglionic nerve → they are
unmyelinated (the other ones given, such as motor nerve to skeletal muscle, sensory nerve from
tendon, from pacinian corpuscle or autonomic preganglionic nerve) → they’re all myelinated
○ Examples of unmyelinated nerves: heat sensation, dull/burning/visceral pain/olfactory (first
order neurons)
● Invariant chain component of MHC II is digested by MPHs during antigen presentation to CD4 T cells
● High baseline insulin level in the setting of normoglycemia is a sign of DM due specifically to
increased peripheral insulin resistance

Block 4:
● Reactive arthritis is caused by immune complexes involving bacterial antigens; common in men
20-40 (HLA B27)
● Dermatitis herpetiformis does not only present with vesicular rash; it can be papules and even
urticaria on extensor surfaces (elbows, knees, sacrum, butt) and it is pruritic!
○ Ddx from Whipple disease, which has a non-pruritic rash
● Cardiac hypertrophy is associated with increased rate of protein synthesis → more (myosin) proteins,
more sarcomeres and more mitochondria within each cardiomyocyte
○ Fetal cardiac development genes are upregulated
● Callus results in thickening of the epidermis, specifically the stratum corneum (callus, corn)
● In PCOS, ‘elevated ovarian androgen levels stimulate development of small ovarian follicles and
prevent the formation of a single dominant follicle’
● Puromycin (despite sounding like an aminoglycoside) does not bind to the 30S subunit; they block the
aminoacyl-tRNA directly (they are structurally analogous)
○ Whereas tetracyclines DO bind the 30S subunit (and are bacteriostatic, although question did
say ‘cell death…’)
● Cell differentiation and dedifferentiation (to become pluripotent) is dependent on transcription
factors → recall that all enucleated cells possess the entire genome, but tissue-specific transcription
factors allow for only the expression of genes that are relevant for a particular cell type
○ In experiment with mature fibroblasts, retrovirus transferred genes encoding specific TFs that
likely promoted the dedifferentiation of the mature fibroblasts back into pluripotent SCs
● In a denervated eye, physostigmine (indirect cholinergic agonist) would have no affect (b/c it
requires Ach release from PSY neurons); therefore, pilocarpine (direct muscarinic agonist) would
be the only drug that could cause the eye to constrict
● Pernicious anemia (autoimmune, therefore a/w other autoimmune disorders) will eventually cause
atrophic gastritis, thus decreased production of gastric acid and hypochlorhydria → compensatory
increase in serum gastrin levels
● Varicocele vs hydrocele (ddx): varicocele does not transilluminate (‘bag of worms’ are not
see-through), whereas hydrocele does
○ Both* can improve when patient is lying down; venous return increases so it diminishes in
size (*only if it’s a communicating hydrocele)
● Sudden appearance of acanthosis nigricans (or involving the palms/soles/mucus membranes) can
be a sign of adenocarcinoma of the GI or lungs; if it’s slow → insulin resistance, obesity
● TOC in patients with mechanical valves: WARFARIN
● DiGeorge syndrome is associated specifically with what kind of heart defect? Conotruncal (outflow)
tract defect, such as Truncus arteriosus and Tetralogy of Fallot (also, interrupted aortic arch)
● CD40L and CD40 immunodeficiency defect: hyperIgM syndrome, so you’d have low IgA, IgG
○ QID: 6500

57
● 18 y.o. male with right groin pain and right lower extremity pain; nontender HSM, osteopenia with
cortical collapse -- what enzyme is deficient?
○ Gaucher → pancytopenia, HSM; bone pain crises and avascular necrosis can be due to
compromised blood supply of the bone (because the lipid accumulation triggers release of
lysosomal proteolytic enzymes and inflammatory mediators that are destructive to bone i.e.
osteopenia)
● You can have ‘brisk’ upper GI bleeding due to excessive ibuprofen use → in response to this
bleeding, sympathetic system is activated and therefore you have VC (activation of alpha-1 receptor
→ Ip3 → SMC contraction) - note: was a convoluted question
● FGGS: HIV and heroin!!

● Broom-like structure on silver staining: ASPERGILLUS;

do not be fooled into thinking its pneumocystis just because
it’s silver stain! (the conidiospores give the broom-like
appearance)
○ Look for a history of TBC -- aspergillomas love the
cavitary lesions
○ Ddx: pneumocystis is described as ‘cup’ or
‘disc-shaped’ organism, that’s seen in HIV+ pt (not
TBC)
● Transduction vs transformation: transformation is the
taking up of naked bacteria
● Hand-foot-genital disease = HOX gene defect; you’d see finger, toe hypoplasia and uterine
didelphys
○ Recall: HOX codes for TFs and deals with craniocaudal direction
○ PAX6: deals with eye, CNS, so defect would cause aniridia (not limb hypoplasia)
● Skeletal muscle: afterload = the force against which the muscle fiber must contract; thus, the
greatest velocity of shortening is seen when there is 0 afterload
○ Increasing preload → increases
contractile velocity (up to a
maximum)
○ Decreasing passive tension (aka
its resting length) correlates to a
decrease in maximal contraction
● Osmolar gap calculation:
2*sodium+[glucose/18]+[BUN/2.8] →
increased osmolar gap when there’s an
unmeasured solute, such as alcohol
(ethylene glycol, ethanol)
● PCR: first you heat it (denatures DNA,
into two separate single strands), then
when you cool the mixture, the primer
binds to the single-strand DNA - this
is the ‘reannealing’; after this, the
solution is heated again and that’s when
the Taq DNA polymerase can start to
synthesize new complementary DNA
● Sarcomere: when it relaxes, the width
of the I and H bands both increase (I =
just actin, H = just myosin); the areas of
overlap shorten during relaxation
○ A band (the myosin filament)
Always stays the same

58
59
PHYSIO:
● Pt with asx HFrEF: he would still have increased NE, ANP and ATII, even though he doesn’t have
symptoms
● Pt with sx HTN and LA enlargement, LV h.t., EF 67%: LV compliance is low (thus you have S4
sound), while ATII signaling and cardiac myosin heavy chain beta expression is increased (bc genes
for contractile proteins of the sarcomere are upregulated)
● Pt with h/o infective endocarditis has a new heart murmur with rapid rise and fall of arterial pulse
in carotids and a systolic-diastolic bruit when the femoral aa. are partially compressed: aortic
regurgitation
○ decreased pressure of aorta during diastole, and backflow → LV dilation, with increased EDV
and eccentric h.t.;
○ widened PP: high-amplitude, rapid rise-rapid fall pulsation with each ventricular contraction
○ Corrigan sign: rapid distension and collapse of carotid arteries
○ Duroziez sign: to-fro bruit seen in femoral aa.
● Pt is given nitrates: peripheral venous capacitance increases, SVR decreases, and LVEDP
decreases too (because they decrease preload by increased venous capacitance)
● Pt with heart sx is given dobutamine infusion → before infusion EF = 60%, during EF = 45%, 5
mins after infusion, EF = 60% again; during infusion, the apical contractility was decreased. Pt is
undergoing pharmacologic stress testing to dx CAD, which he has, because when the drug should
increase his contractility, it cannot (due to some occlusion); dobutamine unmasks that by changing the
supply/demand
● Pt treated for AF and he undergoes stress testing. His pre-test QRS duration was 95ms (corrected
410), and at maximal HR was 125ms (QTc 400); what AF drug was he on?
○ FLECAINIDE: explanation is that during exercise, QRS complex should decrease, but this
pt’s actually increased, which suggests that the drug lengthens QRS in a rate-dependent
manner
● Pt age 37 has intermittent palpitations, and he’s started on a drug that works on both atrial and
ventricular arrhythmias; the medication prolongs QRS with minimal increase in QT interval duration.
Which phase of the AP does it affect? Class IC, so affects phase 0
● Pt age 30 comes in with generalized weakness, paresthesias, and HTN; plasma renin is low,
seCreatinine is normal. CT shows adrenal mass → levels of Na/K+/bicarb are?
○ Sodium: normal -- pt has hyperaldosteronism, and you’d think that the sodium would be
high due to aldosterone retention of Na/water, but aldosterone escape
○ Potassium is low, bicarb is high (to offset the loss of H+ ions → metabolic alkalosis)
● Oxygen content of arterial blood ≄ partial pressure of oxygen in arterial blood
○ O2 content: both dissolved and O2 attached to Hb
○ Partial pressure of O2: the dissolved O2
○ In methemoglobinemia, O2 content is decreased, b/c metHb cannot bind oxygen; but the
partial pressure of O2 doesn’t change, because that’s the amount of O2 dissolved in the
plasma
● Pulse pressure is directly proportional to SV and inversely proportional to arterial compliance
● Low/narrow pulse pressure due to: ↓ SV (e.g., congestive heart failure, shock, cardiac
tamponade, aortic stenosis)
● High/wide pulse pressure due to: ↑ SV (e.g., exercise, hyperthyroidism, aortic regurgitation) or
stiff arteries
● Hypovolemia results in activation of the RAAS system, and the increased angiotensin II stimulates the
release of endothelin 1 and aldosterone
○ Endothelin is a potent VC and is produced by the vascular endothelial cells
● Pt is given a drug that increases BP, decreases PP, decreases HR and increases peripheral vascular
resistance: it’s phenylephrine (alpha 1 agonist) → VC and resultant reflex bradycardia
○ Besides use in rhinitis and ocular procedures (bc its mydriatic), it also treats ischemic
priapism (not sure how)

60
● Peripartum dCMP may be due to impaired angiogenic GFs
● COMPLIANCE explained once and for all: something that’s easily stretchable/flexible is more
compliant
○ Dilated CMP → more compliant, due to the eccentric h.t.
○ htCMP → less compliant, due to thickened walls
● ATII preferentially constricts the EFFERENT arteriole, therefore increasing glomerular filtration; thus
when ACEi are given, the filtration pressure decreases → decreased GFR
● The single most important limiting factor for LV myocardial blood supply during exercise stress test is
the duration of diastole
● Narcoleptic pt gets a new drug that ‘promotes the release of DA and NE in the CNS’ -- which of the
following autonomic efferents would be most affected by the use of this drug?
○ NOT eccrine sweat glands, because they are controlled by SYMP system, using Ach via
musc R
○ NOT adrenal medulla, because that is controlled also by Ach via nicotinic R
● 35yo female has worsening SOB → ABG shows PaO2 and O2 sat are normal, and oxygen content is
low so diagnosis = chronic blood loss (of the options given); def not high altitude, because PaO2 is
normal
○ If both the PaO2 and SaO2 are normal, the lower total blood oxygen content is most likely
due to low Hb concentration, which in young females is often due to chronic blood loss 2ndary
to menstruation
● Woman is stuck in an elevator; she was anxious and got dizzy → panic attack causes
hyperventilation, thus low PaCO2 (hypocapnia), which can cause decreased cerebral perfusion and
thus neuro consequences (blurred vision, presyncope, syncope, weakness)
○ note that hypercapnia triggers an INCREASE of CBF, to aid in the removal of toxins
● Air-trapping, as seen in COPD, increases functional residual capacity
● Calcium binds to troponinC, which displaces the tropomyosin (that is covering the myosin binding
sites) → now myosin binding sites are exposed to the actin filaments
● FRC: volume of air present in the lungs at the end of passive expiration —> at this point, the opposing
elastic recoil and the chest wall are in equilibrium
○ Elevated in emphysema: b/c the lungs are more compliant, due to the decreased elasticity, so
there is a decreased collapsing pressure created by the lungs to expel air —> chest wall
expands outward to balance out the increased lung volume (b/c increased compliance) and
increased collapsing pressure, and this new equilibrium is at a higher lung volume ie higher
FRC (note that RV also increased)
○ Lowered FRC in obesity
○ UNCHANGED in pulmonary embolism
○ Positioning plays a big role in FRC (highest in upright position)
● In muscle contraction and excitation-contraction coupling:
○ Trigger: calcium influx via L-type voltage gated calcium channels
○ Massive influx of calcium: via RyR in the sarcoplasmic reticulum, which releases stored Ca2+
○ Removal of calcium: via NaCa exchange pump (NCX) and SERCA (sarcoplasmic reticular
Ca-ATP
● 2 days at high altitude allows the body to compensate for the respiratory alkalosis, but not back to
baseline —> therefore you will continue to see some alkalosis but the pH is slightly normalized;
however, the PaO2 will not normalize (around 60 in the
example given) because hypoxemia will persist, and
somewhat low HCO3
● Question: pt has daily loose stools, greasy and malodorous;
pancreatic insuff is suspected, so bicarb levels are
measured from the duodenum as drug A is infused; what is
Drug A? Secretin - aims to increase bicarb secretion;
stimulated by intraluminal acidity
○

61
● Dead space is any volume that does not participate in gas exchange: i.e. in a pulm embolism, there
are several alveoli that now have no access to blood (ventilated but not perfused), thus V/Q mismatch
and increased dead space ventilation
● MECHANICAL VENTILATION:
○ When pts are weaned off, they breathe at LOW tidal volumes, with a compensatory increase
in respiratory rate to maintain minute ventilation
■ b/c at low TV a higher proportion of each breath is composed of dead space, this type
of breathing leads to inefficient breathing (wasted ventilation)
■ See ipad pic (to print)
○ Pt is on ventilator → meant to provide minute ventilation of 6L/min, but the calculated alveolar
ventilation is 4.2L/min: why? dead space
■ QID 1563
● ACEi initiated in RAD patients:
○ Yes, ACEi cause decreased filtration fraction and decreased intraglomerular pressure due to
the inhibition of ATII-VCing-efferent-arteriole, BUT it’s important to realize that renal perfusion
DROPS, because previously the patient had hypertension, which was high enough pressure
to perfuse the kidneys, but now with his new heart medications, the pressure isn’t high
enough
● In severe hypoglycemia, administering glucagon works on liver to induce gluconeogenesis and
glycogenolysis
○ Epinephrine, unlike glucagon, would work on more tissues (sk. muscle, adipose tissue, renal
cortex)
○ Note that glucagon also stimulates insulin release from
pancreatic beta cells (???)
● Hb-O2 dissociation curve → during the movement from 1 to 2, Hb
molecules release more H+, because in the lungs, the binding of
O2 to Hb drives the release of CO2 and H+ = this is called the
Haldane effect
○ (whereas in the peripheral tissue, high CO2 and H+
concentrations facilitate O2 unloading from Hb, called
Bohr effect)

● Carotid massage will increase pressure on carotid sinus, which is

perceived as an increase in BP via increased ‘stretch’, so the
baroreceptors increase their firing → activate PSY and thus increase AVN refractory period to
decrease HR (used to treat PSVT) - it’s counterintuitive: increased baroreceptor firing decreases HR
● Work of breathing: the amount of work required to overcome both elastic and airflow resistances; in
pathologies, the goal is to minimize the WOB QID 8260
○ In obstructive diseases: there is increased airflow resistance, so pt breath with lower
respiratory rate, but higher tidal volume (aka slow, deep breaths); goiter is another type of
obstruction
○ In restrictive diseases: there is increased elastic resistance (like pulm fibrosis), so the resp
rate is high and TV is low (aka fast, shallow breaths)
○ PANIC attack: rapid, shallow breathing, yes,
but the lungs function normally so the WOB
vs respiratory rate curve is normal
● Equilibrium potential: at -70 mV QID 11755
○ Na +60 // K+ -90 // Cl -75 // Ca +125
● QID 1625 In a chronic AV fistula/malformation, the
kidneys/symp system compensate for the chronic
fistula by increasing cardiac contractility, vascular
tone and circulating blood → these increase the
cardiac function curve and the MAP (right shift of
venous return on x-axis)

62
-----------
● Central aortic pressure is higher than RV pressure at ALL phases of the cardiac cycle → in a
fistula between the two, the flow of blood from aorta would be constant (aorta 120/80 // RV 25/5)
● Coronary vasodilation is maintained by local mediators (mainly NO and adenosine); ANS
stimulation (epinephrine/Ach) plays a relatively small part
● In septic shock, you would see the following changes: v SVR (third spacing) and decreased PCWP
(because of peripheral venous dilation → decreased CVP and thus decreased PCWP)
○ Cardiac index (the cardiac output per body
surface area) would increase -- due to the
initial sympathetic compensatory increase
○ High mixed venous O2 saturation -- meaning
that there is incomplete extraction of O2 by
the tissues due to the high flow rates
● PV loop (QID 1652): VIP -- giving a patient
nitroprusside decreases both preload and afterload
● Epinephrine decreases insulin secretion, but after
pretreatment with a certain Drug A, epi increases
insulin secretion; what’s drug A? an alpha2 R ATG --
bc epinephrine activates both alpha2 and beta2
receptors (but alpha2 more, thus overall there is a
decreased insulin secretion)
● Vascular function curve (venous return vs CO):
change is explained by myocardial infarction →
Other option choices given:
○ excessive hydration / hemorrhage
○ chronic anemia (increases cardiac output, and
the VR increases very slightly due to decreased
viscosity)
○ anaphylaxis (widespread venous, arteriolar
dilation, increased capillary permeability and 3rd
spacing) → VR drops a lot, while contractility
increases
● When calculating FF, we don’t use renal blood flow (RBF), because RBF includes the volume of
blood that is occupied by RBCs, and this volume is not available for filtration across glomerular
capillaries; therefore we use RPF, which is the volume of plasma that can pass through the glomerular
capillaries
○ RBF = RPF/(1-hematocrit)
● ANP has three major effects: increases GFR by afferent VD and efferent VC; decreasing proximal
sodium reabsorption, and decreasing renin secretion
● FVC: can decrease in airway obstruction (ie in emphysema); FEV1 would see an even greater
decrease, resulting in a decreased FEV1/FVC ratio
● Where is the concentration of PAH lowest in the nephron tubule? In the Bowman capsule (recall
that some PAH is freely filtered by the glomerulus into the Bowman’s space, but the majority is
secreted by the PT via active transport) - don’t really understand QID 1588; see pic on iPad too
● S3 sound is best heard at end expiration; it’s a low-frequency sound heard right after S2 (during
diastole) -- seen in decompensated HF; end expiration helps because it decreases lung volume and
brings the heart closer to the chest (this is also true for S3)
○ Anything that decreases VR (like phase 2/straining phase of Valsalva, or anything that
vasodilates, or leads to diuresis) would all decrease the intensity of S3
● LV failure leads to an INCREASED right atrial pressure (in advanced HF), and an increased
LVEDV → this makes sense b/c the cardiac output decreases (dead tissue), so the heart can’t pump
out the volume (incr. LVEDV, which backs up into the pulmonary veins → pulmonary edema)
○ Think of RAP as central venous pressure, which is elevated due to volume overload; also
secondary right-sided HF can contribute to the elevated RAP

63
 ○ Increased RAP with normal or decreased LVEDP suggests RV HF
○ KEY for differential: pulmonary crackles, yes or no? If yes → LV HF; if lungs are clear, more
likely to be RV HF
●

64
● QID 1617: Concentrations of PAH, creatinine, inulin, urea --
increase as fluid passes along PT; concentrations of
bicarb, glucose, AA -- all decrease
○ Urea is freely filtered from glomerular capillaries
and poorly reabsorbed → it’s secreted in very high
concentrations (waste product)
○ PAH/creatinine/inulin: they’re all freely filtered
from the capillary and are poorly reabsorbed in the
PT → water is reabsorbed faster, so their
concentration in the PT increases
● Carotid body is innervated by CN IX, whereas aortic body
is by CN X (Picmonic: aortic-orca with the chemo-keys in
his mouth, jumping from the baro-barrel in Las Vagus)
● Gq = IP3/DAG pathway (think of the Q-tie doggies “dags”)
● NE is the TOC for septic shock, bc it doesn’t affect B3
○ Alpha1: VC via IP3 system - note that it’s not in the
heart muscles (!)
○ Alpha2: results in a decrease of cAMP in the
pancreatic beta cells, but note that central alpha 2
receptors are not stimulated by IV NE bc it doesn’t
cross the BBB
○ Beta1: increases cardiac contractility, conduction, heart rate via cAMP
● In metabolic acidosis, renal metabolism of GLUTAMINE is really helpful for maximizing acid
excretion; when you have ischemia → lactate accumulation → acidosis, which induces renal
ammoniagenesis (epithelial cells in kidney metabolize glutamine to generate ammonium and bicarb →
ammonium is excreted and bicarb is reabsorb to buffer acids)
● Regardless of hydration status, the majority of water reabsorption occurs in the PT (passively,
with reabs of solutes!)
● Hypovolemic shock will cause an increased urea reabsorption: this is done via ADH, which is
released in response to thirst; ADH increases urea permeability in the inner medullary collecting duct
● Pt with 30-pack-year history is saturating at 88% on room air; expiratory wheezes are heard; they give
her high-flow O2 → she becomes lethargic and confused: this is due to ventilation perfusion
mismatch
○ O2-induced hypercapnia: hypoxia causes VC of the pulmonary arterioles, so blood is
shunted toward alveoli with the highest ventilation (minimizes dead-space) → when you given
oxygen, there is a reversal of the vasoconstriction of the
previously poorly ventilated areas and suddenly you’re
increasing the physiologic dead space (bc the blood is
redistributed away from well-ventilated alveoli)
● If you give a patient with macrocytic anemia cyanocobalamin,
here’s what you see: when you give the vitB12, erythrocyte
precursors start to transform from megaloblastic to normoblastic
→ erythropoietic rate increases and the reticulocytes are
released from BM into blood → this rise peaks at about 1 week;
note that anemia takes 8 weeks to correct bc hemoglobin levels
are steady but slower to rise
● CO can be calculated in two ways: (1) CO = SV * HR, and (2) CO
= rate of O2 consumption / arteriovenous O2 content difference; the second way can be determined
with a Swan-Ganz catheter using Fick principle
●

65
● Amboss: creatine kinase is made from
arginine + glycine; physio question
about CK experient is below:
○ Ans: Creatine is synthesized 
from arginine and glycine in two 
steps that take place in the 
kidney and liver. Creatine 
phosphate is then transported to 
cells, where it is converted to 
creatinine through the removal 
of phosphate residues. Arginine 
is considered a nonessential 
amino acid, but it can become an 
essential amino acid in phases of 
high demand (periods of growth 
or physical recovery).

● In muscle, ‘sparse transverse tubules’ leads to uncoordinated contraction of myofibrils →

manifest as muscle weakness (in this particular disease, a limb girdle muscular dystrophy due to
mutated sarcolemma protein like caveolin manifested as a teenager unable to play basketball)
● TIME vs LENGTH constant: the speed of conduction along axon depends on these two constant
(velocity = =length/time)
○ Myelination INCREASES length constant, DECREASES time constant → these speed up
the speed
○ Length aka space constant: measures how far along an axon the impulse can travel without
requiring active regeneration (so myelin increases this, which makes sense)
○ Time constant: the time it takes for the membrane potential to respond to a change in
permeability (based on membrane resistance and capacitance): myelin reduces time constant
(allows membrane potential to change faster)
■ myelin decreased capacitance
■ myelin increased membrane resistance (meaning less charge leaked through
membrane)
○ Demyelination: decreases velocity by decreasing the length constant and increasing the time
● Intestinal influences down-regulate gastric acid secretion after a meal (intestinal is the 3rd stage
of acid secretion in the stomach, but it begins when protein-containing food enters the duodenum and
the ileum/colon release peptide YY → simulate ECLS → inhibits histamine release from ECLs)
○ Alkaline tide has nothing to do with downregulating acid; it’s just when the surge of acid in
the gastric lumen is accompanied with an increased plasma bicarb)

66
● Recall that ACTH affects only the F and R layers of the cortex (G aka glomerulosa is stimulated by
ATII); therefore, in excess ACTH production, both cortisol and androgen production increases, and
ACTH has trophic effects on the F and R layers (so they undergo hyperplasia via ACTH upregulating
RNA/protein synthesis)
○ Atrophy of the entire adrenal cortex is seen in autoimmune adrenalitis (presents as chronic
adrenal insufficiency aka Addison); cortisol would not be elevated
● Blood flow per minute must be the same between systemic and pulmonary circulation
● In HOCM: LV mass is increased, but cavity is decreased; EF is preserved, but LV relaxation is
impaired; the reason EF is mostly preserved is because the outflow obstruction is dynamic and
usually only presents with exercise, buuuut the impaired relaxation does lead to diastolic dysfunction
● Pt in shock had low PCWP but high RAP; this shows that the blood flow is likely impaired from RV to
the left side of the heart aka right-sided heart failure
○ Septic or anaphylactic shock would result in decreased RAP and PCWP (bc of the
widespread peripheral VD)
● Alpha 1 agonists result in increased systolic and diastolic pressures (VC of both arteries, which
increases preload) and veins (increases afterload → diastolic BP increases); this results in reflex
bradycardia via a VAGAL response (thus decreased conduction thru AV node)
● Ddx hemorrhagic from distributive shock (like septic shock) requires looking at the SVR: if it’s low,
then it’s due to the peripheral vasodilation we see in sepsis (low SVR, low CVP, low PCWP, but high
CO (compensatory sympathetic activation)
○ Whereas hypovolemic shock would have a compensatory increase in SVR!!
● Highest osmolarity of the renal tubule is at the bottom of the loop of Henle (in the absence of
ADH); lowest is at the start of the DCT -- PenguinProf video was EXCELLENt
● Aortic stenosis is heard loudest at the point of maximum pressure difference between the LV and
the aorta (which is not right when the aortic valve opens! ~ approx at the peak of LV pressure)
● Level of what is higher in pulmonary vein than the pulmonary artery? Angiotensin II → recall:
ACE converts AT1 to AT2 in the lungs
● Isoproterenol has equal B1 and B2 activity, so via beta1 it increases contractility and via beta2 it
causes VSMC relaxation → decreased SVR (on the graph of contractility you’d see an increase after
IV; on SVR graph you see gradual decrease)
○ Contrast with phenylephrine: only has alpha activity, which causes VC → increased SVR
● Cardiorenal syndrome: essentially, decompensated HF will lead to activate of RAAS (low cardiac
output → renal hypoperfusion → RAAS/ADH/sympathetic activity → more water is retained,
peripheral VC is initiated → worsens LV systolic function, further worsening CO and renal perfusion
● Dobutamine: beta1 > beta2 (“just do bugling” shirt on girl with crank-up-heart-flashlight and 1 bugle)
→ used in cardiogenic shock; it’s a beta agonist so it’s coupled to Gs (adenylyl cyclase, cAMP)
○ Beta 1 fx: heart effects so increased contractility, increased HR, more renin release
○ Beta 2 fx: would cause VD, bronchodil, metabolic fx
● BUN/creatinine ratio should be 15 (that’s the normal, also sometimes in postrenal AKI)
○ In prerenal AKI, the pt is attempting to conserve water (hypovolemia, etc) so they reabsorb
more urea → increases urea, but creatinine is excreted as usual, so BUN/Cr > 20 (incr.)
■ Urine sodium decreases to <20mEq/L bc we reabsorb more tubular sodium; we
also reabsorb lots of water, so this results in high urine osmolarity
○ In intrinsic AKI, the pt is unable to reabsorb urea, so the BUN/creatinine ratio <15
●

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ANAT:
● UPPER LIMB:
○ Trapezius injury: during resection of cervical LN in posterior triangle, results in difficulty with
overhead activity and shoulder droop (due to damage to CN XI, which also innervates SCM)
■ CNXI is very superficial and is vulnerable to penetrating trauma and surgical error
○ Serratus anterior injury:
■ Long thoracic nerve, like in mastectomy → winging of the scapula, impaired
abduction
■
○ INFRASPINATUS injury:
■ Landed on posterior shoulder; cannot externally rotate against resistance but
abduction is preserved
○ RADIAL n. Injury:
■ Screwdriver use: supinator canal → due to repetitive pronation/supination, the
posterior interosseous nerve is damaged, causing finger and thumb extension
problems
■ Crutch palsy: injury at axilla
○ MUSCULOCUTANEOUS n. Injury: LATERAL CORD
■ Usually due to trauma (qstem: pitcher)
■ Inn. biceps and brachialis and coracobrachialis —> decreased flexion
■ Inn. lateral cutaneous nerve —> lateral forearm
○ AXILLARY n. Injury: usually due to trauma
■ Deltoid muscle → arm weakness, atrophy of deltoid, impaired abduction
○ ULNAR n. Injury:
■ Office-worker pt w/o h/o trauma has pins and needles on his right hand, worse at
night; loss of sensation over fifth digit; diagnosis = ulnar n. injury due to compression
(resting hand on sfc while using computer) → in severe cases, impaired wrist
flexion and adduction (ulnar deviation)
■ Woman has intermittent tingling, numbness of left hand involving 4th, 5th digits, esp
when driving a car; due to ulnar mononeuropathy —> focal compression, usually at
elbow, which causes ischemia and apoptosis/damage to Schwann cells (dx this
demyelinating disease via nerve conduction study, where signal is slow, delayed)
● Ddx from axonal neuropathy, due to damage to nerve axon, which results in
reduced signal amplitude - causes = DM, CTX rx, hypothyroidism, Vit B12
def, vasculitis
○ MEDIAN n. Injury:
■ Meat LOAF: median nerve innervates the two Lumbricals, the Opponens pollicis and
the Abductor pollicis brevis, Flexor pollicis brevis
● LOWER LIMB:
○ Iliopsoas m. helps sit up from supine position (along with external abdominal obliques, rectus
abdominis and hip flexors)
○ Compartments: anterior - deep peroneal nerve → most common site of anterior compartment
syndrome; sx would be decreased sensation b/w first and second toes, decreased
dorsiflexion/foot drop and claw foot
○ Great saphenous vein: when it’s harvested for CABG, it’s taken from the MEDIAL leg, or,
less frequently, from just below the pubic tubercle ie in the femoral triangle
○ High velocity trauma or trauma during a fall (onto hip) can cause greater trochanter avulsion
and impaired gluteus medius
○ Hip surgery can result in LL weakness → pt presents with impaired dorsiflexion, plantar
flexion and impaired knee flexion, because there’s a good chance that the sciatic nerve was
injured (either during femoral fracture or during arthroplasty); sciatic gives branches to
common peroneal (dorsi) and tibial (plantar

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 ○ Overuse injury of the quadriceps (OsgoodSchlatter) (rectus femoris, vastus intermedius,
medialis, lateralis), which attaches to the tibial tubercle via the patellar ligament, can occur in
youth undergoing a rapid growth spurt; since the tubercle forms as a secondary ossification
center, it is weaker than ossified adult bone, so any repetitive quad contraction or
extension/jumping can cause pain due to chronic avulsion
○ Common peroneal nerve injury: due to laying for a long time on side (i.e. hip surgery) or
proximal fibular fracture
■ Deep —> foot drop *dorsiflexion
■ Superficial —> eversion (due to peroneus longus, brevis damage) and loss of
sensation over lateral lag and dorsolateral foot
■ Note: question mentioned intact ankle inversion - that’s a trick!
○ Fibula is LATERAL, tibia is medial → fibuLA = LAteral
■ Fracture at the neck of the fibula results in damage to the common peroneal (aka
fibular) nerve → loss of dorsal foot sensation and Eversion (dropPED)
○ Pseudoarthrosis is a FALSE joint, i.e. when a fracture breaks and doesn’t heal properly; may
be a/w NF1
○ Cruciate ligaments are defined by their attachment to the tibia
○
● General anatomy:
○ During abdominal aorta aneurysm repair, reconnecting the IMA is not always necessary b/c
the SMA anastomoses are pretty strong
○ Upper 2/3rd of the esophagus is squamous cell cancer, but the adenocarcinoma of the distal
1/3rd is more common
○ Chest tube placement at 5th ICS at midaxillary line dissects the serratus anterior muscle
(thorax)
■ FA: needle positioning for tension PTX: ICS 2nd
○ Abdominal trauma: spleen is the most commonly injured organ with blunt abdominal trauma
■ Splenic laceration → may cause Kehr sign (referred pain to the shoulder), hiccups
(C3-C5)
■ Splenic damage → question may hint that spleen was removed in surgery
post-trauma, and pt might be asplenic
○ Bladder is EXTRAperitoneal, so when doing a suprapubic catheter/cystostomy, you don’t
have to pierce the peritoneal cavity, only the aponeurosis of the abdominal wall muscles,
along with the layers of superficial and transversalis fascias, and the aponeurosis
○ During thyroid surgery and ligation of inferior thyroid artery, recurrent laryngeal nerve may be
damaged
■ External brand of superior laryngeal nerve may be misligated instead of the superior
thyroid artery
○ Lunate is the more medial of the two bones that articulate with the radius (the other being the
scaphoid)
■ Volar dislocation (like in FOOSH) can compress the median nerve in the carpal tunnel
○ Right arm numbness in 15 yo boy who pitches for his team; h/o extra rib —> patient has a
cervical rib that results in thoracic outlet syndrome, which is compression of the brachial
plexus within the scalene triangle, and may or may not involve the subclavian vein and
artery; weakness and tingling sx
worsen with repetitive overhead arm
movements (pitching)
■ Other muscle involved in
‘pitching’ injury is
infraspinatus
○ Left 12th rib fracture/trauma:
injures the left kidney
■ Visceral pleura damaged
during fracture of ribs 1-6

69
 ○ Erosion of the posterior wall of the duodenum by an ulcer would result in bleeding from the
gastroduodenal artery, which is directly behind it (note that the gastroepiploic runs along the
greater curve, and the inferior pancreaticoduodenal is a branch of the SMA)
○ Prostate on CT is seen behind the bladder (especially if BPH) and in front of the rectum
(DRE)
■ Imagine the CT x-section at the level of his finger
■ Also suprapubic bladder catheter, so obviously the bladder has to be closer to the
abdominal wall
○ Thyroidectomy injures the external branch of the superior laryngeal nerve, which innervates
the cricothyroid (remember, it is very close to the superior thyroid artery)
○ Trauma resulting in full bladder sensation → injury to the membranous segment of the
posterior urethra, which is found in the perineal muscles
○ Inferior orbital fissure: home to CNV2 and infraorbital
vessels, sphenopalatine nerves → do not enter orbit
■ Superior orbital fissure: CN III, IV, V1, VI and
superior ophthalmic vein → enter orbit
■ Note that ALL these nerves first pass through the
cavernous sinus (except the sphenopalatine
ganglion branches)
● Abducens is most susceptible to damage
○ Kiesselbach plexus is located on the nasal SEPTUM (thus
that’s where you would cauterize a bleeding nose with
silver nitrate)
■ Anastomosis of anterior ethmoidal,
sphenopalatine, and facial (superior labial artery)
○ Chest CT: esophagus is between trachea and vertebral
column (may be off to the side, close to the descending
aorta) and the arch of the azygos vein is to the RIGHT of
the esophagus -- don’t get them confused
○ Bronchial arteries are derived from the thoracic aorta, via
the posterior intercostal artery (on the right side)

----------------------------------------------------------------------------------------------------
● Both gonadal arteries are directly from abdominal aorta, but venous drainage is different: the right
gonadal vein → IVC, while the left goes into the left renal vein
● Thoracocentesis locations: 6-8 at MCL, 8-10 at midaxillary, 10-12 paravertebrally
○ In qstem, they did it above 10th rib midaxillary → risk of puncturing the right hepatic lobe
● Obturator nerve travels through obturator canal and functions to adduct the thigh; such injury usually
from pelvic trauma/surgery/bladder cancer
● Hiatal hernia ddx → the sliding one is due to membrane laxity (ie weakness of the
phrenoesophageal membrane), can be caused by repetitive stress like coughing, vomiting; the
paraesophageal hernia (rarer) is due to membrane defect in the phrenoesophageal membrane
● Patellar bursitis: suprapatellar -- due to blow to distal thigh or prolong/repetitive quad activity such
as running; prepatellar is housemaid’s knee, found above patella, under skin
● HEART ABLATION hotspots: buzzwords for each of the key spots
○ SA node: opening of SVC+crista terminalis
○ AV node: interatrial septum/tricuspid+coronary sinus
○ Atrial flutter: isthmus between tricuspid+IVC
○ Atrial fibrillation: pulmonary vein ostia
● Anterior humerus dislocations: often seen due to blunt force when you’re throwing a ball (externally
rotated, abducted arm) → axillary nerve injury (deltoid and teres minor muscles)
● Lateral epicondylitis → extensor (LATex), whereas medial epicondylitis is flexor surface
○ To remember that lateral is tennis elbow: latex grips on the tennis rackets

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● Mastectomy can injure the long thoracic nerve → serratus anterior problem (patient can’t rotate the
scapula upward aka can’t lift arm above horizontal)
● Patient can’t tiptoe (tibial nerve injured), so loses sensation over plantar surface of the foot!
○ Other innervations: Lateral leg/dorsum of foot = superficiaL // skin between great and second
toe = deep peroneal nerve // anterior thigh = femoral nerve // medial leg = saphenous n.
● Duodenum:
○ Damage to 2nd part: in posterior peptic ulcer → rupture of gastroduodenal art.
○ Damage to 3rd part: like due to a mass → damage to SMA
● Hypothenar atrophy and decreased sensation over little finger is likely due to ulnar nerve injury at the
hook of hamate (Guyon canal)
○ Damage at the head of the radius (subluxation) → deep branch of radial nerve in supinator
canal, causes finger/thumb extension weakness (aka finger drop)
● Femoral nerve block: at inguinal crease → anesthetizes anterior thigh (skin, muscles), knee and
saphenous nerve (medial leg)
● Anatomical location for LP: iliac crest
● Midline episiotomy: cuts the perineal body, not the external anal sphincter
○ The anal sphincter is usually damaged in tears of the perineum
● Trauma (stab wound) at 5th ICS, MCL, results in damage to the LEFT LUNG (not the right ventricle)
- the anterior surface of the heart is partially covered by the lungs
○ Note that a deeper/more medially direct puncture could have injured the LEFT ventricle (not
the right), whose apex can lie at the MCL (all other heart structures are way medial to the
MCL)
● Pulling a child upwards by the arm results in radial head subluxation → annular ligament can slip
over the head of the radius and become entrapped in the radiohumeral joint (very painful: pt holds
arm close to the body with elbow flexed, forearm pronated): this is aka nursemaid’s elbow
○ Reduced by hyperpronation or supination of the forearm while elbow is flexed
● Blunt trauma to the aorta: tears at aortic isthmus (ligamentum arteriosum keeps it fixed and
immobile, so sudden deceleration can cause extreme stretching)
● Anatomy of cryptorchidism: first they enter through the deep inguinal ring (opening in the
transversalis fascia) → superficial inguinal ring (external oblique muscle aponeurosis) → scrotum
○ Question asked what structure do you have to pull the malpositioned testis through, if you
could palpate the mass ‘medial to the right-mid-inguinal point’; this was meant to suggest that
the testis was already in the inguinal canal, thus you’d have to pull it through only the
superficial inguinal ring
● Latissimus dorsi (inn. thoracodorsal nerve) is huge (originates from iliac crest), and thus
vulnerable to injury from external trauma (sports that require forceful downward movement of the
humerus - throwing, climbing, overhead tennis swing);
issue would be with internal rotation (and
extension/adduction) of the humerus
● Sciatic foramen: split into greater and lesser sciatic
foramen by the sacrospinous ligament
○ PIRIFORMIS (external hip rotation) occupies
the majority of the greater sciatic foramen
→ accompanied by the superior gluteal
vessels and nerve (above the muscle); and
inferior gluteal vessels, internal pudendal
vessels and sciatic nerve (below the muscle)
○ Piriformis syndrome: Piriformis muscle
hypertrophy or damage can compress the
sciatic nerve → sciatica-like symptoms
● Femoral artery access (above the inguinal ligament)
is the optimal site for cardiac catheterization, which
cause increase the risk of RETROPERITONEAL

71
 hemorrhage significantly (bc if you look closely, there is a tiny space above the inguinal ligament,
below the peritoneum
● Main branches of external iliac artery: inferior epigastric, which takes off immediately proximal to
inguinal ligament, and the deep circumflex iliac artery (branches more laterally); both supply the lower
anterior abdominal wall → then the external iliac becomes the femoral under the inguinal ligament (at
which point the first branch is the superficial epigastric)
● Nerve routes:
○ Median - between flexor digitorum superficialis and
flexor digitorum profundus
■ Courses b/w the humeral and ulnar
heads of the pronator teres muscle
○ Ulnar - flexor carpi ulnaris and between flexor
digitorum profundus (they tricked me!)
● Quadratus lumborum is posterior to the psoas;
contraction of this muscle assists in extension and lateral
flexion of vertebral column
● SVC on CT would appear in front of the pulmonary trunk, right by the ascending aorta; the thing
closest to the descending aorta will be the esophagus
● Patellar fracture will make it difficult to extend the knee against gravity
● Orbital floor fracture can affect 2 things: 1) infraorbital nerve, which is a branch of maxillary → lesion
results in numbness and paresthesia of upper cheek, upper lip/gingiva, or 2) the inferior rectus muscle
(if trapped, limits vertical gaze)
● In an image of the median brain, these are ANTERIOR: hypothal, mamillary body, pituitary gland;
the pineal gland is the only structure of pathological interest that it posterior (directly above 4th
ventricle)
● The MMA is a branch of the maxillary artery → seen at the pterion (fusion of sphenoid, parietal,
temporal, frontal)
● Supraspinatus tendon is MOST COMMONLY affected; qstem - man was helping daughter move out
of her dorm; empty can test was positive (impingement!)
● Mucormycosis dx: mucosal biopsy
● Phrenic nerve innervates the fibrinous pericardium also (thus pericarditis can refer pain to
shoulder) (Amboss)
● Bullous pemphigoid presents with itchy blisters on palms, soles, LL, inguinal folds; it is Nikolsky (-)
● Left-dominant circulation of heart: pt has an MI -- where is the stenosis if it’s just before the origin of
the artery supplying the AV node? LCX
○ Usually the AV nodal branch comes from the PDA, which is the vessel that determines
dominance; in LEFT dominance, the PDA arises from the LCA → LCX
○ QID 11837
● Peptic ulcer on proximal lesser curvature endangers the left gastric artery (note that the splenic
artery is separated from the posterior wall of the stomach by the pancreas, despite how it may look on
pictures)
● Cricothyrotomy: passes through superficial cervical fascia, pretracheal fascia, cricothyroid membrane
● Supracondylar humeral fracture laterally → radial nerve (with deep brachial artery); medially →
median nerve + brachial artery (check if the pt has intact radial pulses)
● CONSTIPATION is due to pelvic splanchnic nerve dysfunction (PSY innervation); can be caused by
cauda equina syndrome (sx: progressive lower back pain, bilateral LL weakness, bowel/bladder
dysfunction, impaired perineal sensation)
○ Cause may be epidural metastasis, most commonly from lung cancer (pt had 60 pack years,
dry cough)
○ Note that the greater and lesser splanchnic nerves are SYMPATHETIC innervation (i.e. they
slow GI peristalsis)
● Emissary veins in the skull connect the intra- and extracranial venous systems
● ANKLE LIGAMENTS:
○ deLtoid = mediaL → it’s a complex of three ligaments and it’s strongest, so rarely injured

72
 ○ Lateral ligaments are much weaker, and ATL is most commonly injured
● Medial to inferior epigastric vessel = DIRECT hernia, due to weakness in the transversalis fascia
(don’t let them confuse you with talk of abdominal muscles separating; that’s a diastasis)
○ MDs dont LIe - medial/direct -- lateral/indirect
● Pelvic surgery neuropathies:
○ Pudendal nerve S2-S4: epidural anesthesia by the ischial spines/sacrospinous ligament (note
that internal pudendal artery and inferior gluteal artery are close by, so they can also be
injured → hematoma)
○ Genitofemoral L1-L2: abdominal retractors during
laparotomy → labial/scrotal anesthesia
○ Iliohypogastric T12-L1: closure of Pfannenstiel incision
like in C-section → suprapubic skin
○ Obturator L3-L4: retroperitoneal pelvic LN dissection →
medial thigh sensation/adduction
○ OTHER:
■ Lateral femoral cutaneous nerve L2-L3:
hyperflexion of thighs in lithotomy position →
anterior/lateral thigh numbness aka meralgia
paresthetica
■ Inferior gluteal nerve L5-S2: hip surgery → innervates gluteus maximus
● Common peroneal nerve injury: neck of fibula → lateral trauma to knee/tight cast
○ Food drop, impaired dorsal foot sensation (deep is for the space bw the 1st and 2nd toes;
superficial is for all else)
● Femoral nerve damage: secondary to spontaneous retroperitoneal hematoma (like with patients on
warfarin), or abscess, or trauma during surgery/childbirth
○ Quad weakness → hard to climb stairs, knees buckle a lot (falling), decreased patellar reflex,
sensory loss over anterior and MEDIAL thigh/leg
● Interscalene nerve block of the cervical and brachial plexuses can be used for procedures involving
the shoulder and upper arm, but since it blocks everything from C3-C7, can also cause ipsilateral
diaphragmatic paralysis; thus it’s CI in pts with chronic lung disease or contralat phrenic nerve
dysfunction (C3-C5)
○ Bw anterior and middle scalene muscles, aka in scalene triangle
●
○
●

73
●

BIOCHEM:
● Experiment isolates nucleic acids → incubated with short sequence of repeated deoxythymidine
residues fixed to latex beads; which of the following types of nucleic acid is most likely to bind the
strongest to the latex beads in this experiment?

74
 ○ >> Mature mRNA << first think of what the deoxythymidine would bind → A (adenine)
residues are bound, aka the poly-A tail, which describes mature mRNA (post-transcription
mRNA)
● Methylmalonic acidemia: AR disease secondary to methylmalonyl-CoA mutase deficiency; since the
MM and propionic acids build up, you get metabolic acidosis; increased metabolic rate results in more
glucose utilization and hypoglycemia, and thus ketone production → futhers AG MA; and since the
organic acids directly inhibit the urea cycle, you have hyperammonemia
○ Presents as dehydration, difficulty feeding, history of sibling with similar disease, tachypnea
(acidosis), and low level of consciousness
○ Urine: high MM acid, high propionic acid, high ketones
○ Serum: low glucose, increased ammonia
○ Propionyl coa → MM coa → enzyme deficient → X succinyl coa
● A company is making new treatment for Burkitt; a short (21bp) dsRNA molecule which has a region
complementary to mRNA encoding c-myc; introducing this RNA molecule causes decreased cell
growth, and they show the Western blot: which process is inhibited?
○ They are describing RNA interference (a short ds RNA sequence induces post-transcriptional
gene silencing); this siRNA and miRNA can cause mRNA degradation (exact match) or
translational repression (partial match) → this interferes with mRNA translation (correct
answer)
● RBCs and the liver are the only tissues that cannot use ketone bodies, because they lack
mitochondria (RBCs) and succinyl CoA-acetoacetate CoA transferase (liver)
● Ddx between the peroxisome disorders: all cause accumulation of VLCFAs like phytanic acid, due to
impaired oxidation
○ Refsum: alpha oxidation
○ Adrenoleukodystrophy: beta oxidation
○ Zellweger: defective peroxisomal biogenesis (presents with widened sutures and large
anterior fontanelle)
● Acetyl-CoA is what directly stimulates the first enzyme involved in raising glucose level during the fast
(activates pyruvate carboxylase, which then converts pyruvate to oxaloacetate)
○ Citrate also activates gluconeogenesis, BUT it does so at the F1,6bisphosphatase step
● Ethanol inhibits gluconeogenesis —> can cause hypoglycemia when hepatic glycogen stores are
depleted; the mechanism of this is that ethanol metabolism (by alcohol/aldehyde DHase) reduces
NAD+ to NADH, thereby increasing the NADH/NAD ratio. This inhibits all other paths that require
NAD+ (including gluconeogenesis), and lactate —> pyruvate conversion (thus lactic acidosis). OAA is
also made into malate, thus inhibiting gluconeogenesis; and ketoacidosis is seen b/c acetyl-CoA is
sent toward ketogenesis rather than the TCA cycle
● In experiment, pts are placed on high-carb, high-protein diet —> enzymes of FA metabolism are
measured, and its noted that beta oxidation is inhibited, due to what? Malonyl CoA, which inhibits
carnitine acyltransferase (shuttle) so acyl groups cannot be transported into the mitochondria
● Glycolysis in certain cells will always yield pyruvate, but may generate no net ATP: this is specifically
true for RBCs, which can shunt pathway away from normal glycolysis by activating BPG mutase,
which converts 1,3 BPG to 2,3BPG; in states of hypoxia, more 2,3BPG allosterically decreases Hb’s
affinity for O2 →in this way, RBCs sacrifice ATP for more O2 delivery to peripheral tissues
● FASTING:
○ Processes that maintain glucose between meals are glycogenolysis (12-18 hours) and
gluconeogenesis (when glycogen stores run out)
● Zinc finger motifs (muo AA such as cysteine and histidine) are utilized by transcription factors;
steroids, thyroid hormones and fat-soluble vitamins bind the IC receptors and alter the activity of the
genes
● Since galactokinase def is not nearly as severe as GALT def, cataracts may be the only manifestation
in an otherwise healthy child (in qstem, pt presented with blurry vision only at age 11)
● Out of the heme drugs, note that only 2 major enzymes (that get tested) are in the mito: ALA-S and
ferrochelatase
------------------------------------------------------------------------------------------------------------

75
● Purpose of NADPH: to regenerate reduced glutathione (anti-oxidant) and for use in reductive
biosynthesis (FA, cholesterol, steroid synthesis and P450 metabolism)
○ NOTE: Niacin is required for the synthesis of NAD and NADP both; they’re used in many
dehydrogenase and reductase enzymes -- niacin deficiency would therefore result in a
decrease in these enzymes
■ NAD: for catabolic reactions -- glycolysis, beta-oxidation, TCA (isocitrate DHase,
alpha-ketoglutarate DHase, malate DHase)
■ NADP: for anabolic reactions -- fatty acid and cholesterol synthesis
○ Notable exception: succinate dehydrogenase is unique because it uses FADH2 instead
● PKU due to BH4 issues (like secondary to dihydrobiopterin reductase deficiency) will result in
hyperphenylalaninemia and low dopamine (which results in increased PRL); the child will still have
neuro symptoms (even if dietary restrictions are kept and tyrosine is supplemented) because the pt
will have lower-than-necessary levels of DA, NE, 5HT, etc.
○ Note that tyrosine’s conversion to DOPA also requires the conversion of BH4 back to BH2 via
the enzyme DHP reductase
● Transcription initiators: CAAT and TATA (not enhancers)
● Type 1 muscle fibers are found in postural muscles (soleus, parasternal), and since they rely mainly
on aerobic metabolism, they have high myoglobin content (RED! for max O2 storage) and lots of
mitochondria (for aerobic respiration)
○ Type 2 muscles are the ‘fast twitch’ ones - they usually get energy from anaerobic
glycogenolysis and glycolysis
(great for rapid, forceful pulses
of movement)
● “Glutamate labeled with nitrogen
isotopes; researcher finds that the
isotopes are transferred to OAA,
forming aspartate in the process” → this
is describing a transamination; all of
these reactions require pyridoxine
(transam reactions occur between AA (glutamate) and an alpha-keto acid (OAA))
● FASTING: a starving woman (2 days) has a blood glucose of 72mg/dL and positive urine ketones:
which enzymes have increased activity? Hormone sensitive lipase - break down TGs into glycerol
(→ glucose) and FAs (→ ketone bodies); it’s stimulated by the stress hormones (catecholamines,
glucagon, ACTH)
● I-cell disease: required for transferring proteins to lysosomes (hint: it IS a lysosomal storage
disease); the Golgi body has a phosphotransferase enzyme that catalyzes the phosph of mannose
residues
● Ehlers-Danlos: deficient procollagen peptidase → should cleave terminal propeptides from
procollagen in the EC space
● Western blot and ELISA are very similar: main difference is that in ELISA, the serum is tested
directly, whereas in Western blotting, the proteins are first separated by electrophoresis
● Study showed that a cancer making a soluble Fas protein which was shorter and lacked the
transmembrane domain was able to escape the IS; DNA analysis revealed NO FAS gene mutations;
this can be explained by alternative splicing → lots of cancers can use alternative splicing to
evade innate defense mechanisms, and in this case, cancer cells can splice out a particular exon that
codes for the TM domain of FasR (so its soluble and not seen on the cell surface → cell won’t
undergo apoptosis)
● Polyadenylation (post-transcriptional mod) is necessary for nuclear export AND cytoplasmic stability
of mRNA
● Klebsiella can also cause staghorn caliculi
● ACE works to convert angiotensin I to II
● HBV vaccine has recombinant HBsAG that makes body generate anti-HBs antibodies; the HBsAG
is muo envelope glycoproteins that are found on the surface of HBV → they mediate ATTACHMENT
of virus to hepatocytes and thus viral entry

76
● Nucleolus is the primary site of ribosomal RNA transcription; this is done by RNAP I
● First generation H1 R ATGs (diphenhydramine and chlorpheniramine) should not be used together
with benzos or other drugs that cause CNS depression (alcohol, barbs, neuroleptics, etc.)
○ VIP to remember that ranitidine is not an H2 antagonist; and loratadine is a 2nd gen H1 ATG
● In MSUD, BCK acids like leucine, valine and isoleucine cannot be metabolized into substrates for
entry into the TCA; meaning that leucine, which usually gets turned into acetyl-coa, and val/ile
(which are usually converted into propionyl-coa) cannot be broken down by BCKDHase → they
should be restricted from the diet!
● In DNA replication, the MAJOR difference between the lagging and leading strands is the work of
the DNA ligase, which has to act many more times on the lagging strand than the leading strand
● DNAP I → besides synth and proofreading, it ALSO removes RNA primer, bc it has the 5’ to 3’
exonuclease activity; DNAP III cannot do this, so it just synthesizes and proofreads
● ROS: the antioxidant enzymes are superoxide dismutase, glutathione peroxidase, catalase → their
job is to convert ROS to oxygen and water
● Experiment studying insulin receptor shows that pre-treatment with TNFalpha → decreased insulin
glucose uptake; this is due to the fact that TNF-alpha upregulates serine residue phosphorylation;
this results in insulin resistance; note that catecholamines, GCs and glucagon can all lead to insulin
resistance via this type of phosphorylation
○ Serine phosphorylation INHIBITS the tyrosine/autophosphorylation of the IRS, which is why
this occurs
● Linkage disequilibrium example: gene A has frequency of 0.3; gene B has frequency of 0.2, so the
expected probability of the two alleles from separate loci appearing together = multiplying their
occurrence rate, in this case A x B = 0.06; but the frequency of both alleles being inherited together
is found to be 0.2 → this is due to linkage diseq. (their frequency together is greater than just the
expected random pairing -- often seen when genes are in close physical proximity)
● Lactose is muo glucose+galactose (‘that gal lacks some nice gluts’); thus sucrose = fructose +
glucose
● Enteropeptidase deficiency (duodenal brush border enzyme) is needed to activate trypsin, and
trypsin is required for both protein and fat absorption
○ Sx of enteropeptidase deficiency: diarrhea, failure to thrive and edema (hypoproteinemia)
● A drug inhibits enzymatic adenosine to inosine conversion, causing DNA strand breaks and
apoptosis; what cancer is being treated with this new drug?
○ ADA converts adenosine to inosine; it’s really important in purine metabolism; when it’s
inhibited, the metabolism of deoxyadenosine follows another pathway → it’s phosphorylated
into a toxic metabolite (deoxyadenosine triphosphate), which activates the caspase system
and inhibits RR (so ribonucleotides can’t become deoxyribonucleotides, thus DNA precursors
run out) → ultimately, this leads to DNA synth/repair issues and apoptosis
■ Since lymphocytes are very
mitotically active, they are very
damaged, so lymphocyte-derived
cancers (such as hairy cell
leukemia) are especially targeted
■ Suddenly, SCID makes a lot more
sense!
○ TLDR; if ADA isn’t working, adenosine is
made into a toxic metabolite that causes
lymphocyte apoptosis; which cancer has
lots of lymphocytes? (out of the options
given) hairy cell leukemia!
● P-bodies are cytoplasmic elements that bind the
mRNA after it leaves the nucleus; it’s role includes
translation repression, mRNA decay, quality control,
etc.; the key is that it’s in the cytoplasm, unlike all the post-transcriptional mods (capping, poly-A tail,
splicing, etc, which all occur in the nucleus)

77
 ● Scientists are studying Ecoli: two strains, one which has beta galactosidase, and the other that
doesn’t; the one that doesn’t contains a mutation that inhibits the binding of a protein to its regulatory
sequence → where is that mutation happening specifically? QID 1479 ← dont understand
○ Answer: mutation is at operator locus
● Degree of gene transcription can be determined with a NORTHERN blot, which analyzes for the
presence of mRNA
● Uracil is found only in RNA; so if uracils are seen somewhere in association with bacterial DNA,
during replication, the only place that could be is in the primer - an RNA sequence, which is made by
primase (an RNA polymerase)
● Cell cycle: a stimulus X increases the activity of many enzymes, including DHFR and DNA
polymerase → this stimulus must be something like the phosphorylation of retinoblastoma; recall that
Rb is active when it’s hypophosphorylated and inactive when it’s HYPERphosphorylated, but when it’s
active it blocks the cell cycle transition from G1 to S → therefore, when it’s phosphorylated, Rb is
inactive, and allows the synthesis of DNA
○ Mnemonic: activated Rb (hypophosph) is like a sad Robocop ⇒ stops traffic (hypo = sad)
○ P27 is a cell-cycle inhibitor, so if it’s upregulated, no cell cycle
● In MSUD, the branch-chained ketoacids should be avoided (leucine, isoleucine, valine), but
BCKDHase requires the TLCFN coenzymes, thus thiamine supplementation can help
● Giving B12 in pt with hyperhomocysteinemia can lower homocysteine levels (which is good since it’s a
prothrombotic substance)
●
●

ETHICS:
● Patient asks you out: decline, say it would be unethical
● Patient gives you a card and free Knicks tickets: decline, but say you’ll treasure the card
● Elderly patient seems to be submissive to caretaker daughter → attempt to interview him/her alone
● Med student mentions patient status in public setting, resident says, “Let’s wait til the morning signout
to discuss all the patients.”
● All adolescents (WHO describes that as b/w ages 10-19) should be asked to be interviewed alone, to
ask about drugs, sex, etc.
○ Teens CAN be treated for STDs without parental notification/consent, but may NOT receive
an abortion unless they are emancipated
● Healthcare proxy overrules ALL surrogate decision makers, including husband
● Prevention: primary = prevent (i.e. health promotion)
● Physician fatigue errors: after working 17+ hours, cognitive performance and motor skills are
decreased → whereas physician burnout = callousness, lack of concern, emotional exhaustion, etc.
● End of life/advanced directive should be included as part of the admission process for all patients, not
just “elderly” or “sick” ones; they must be discussed at an initial encounter with a patient
○ Things like diet, exercise, smoking cessation do not have to be talked about initially
● Malpractice is NOT a type of medical error -- it is a legal determination; it’s a consequence of a few
different types of medical errors that result in harm
● “Adverse event” in ethics is defined not as a “side effect” of the procedure, dx, etc., but rather as the
“failure to follow evidence-based best practice protocols -- can be preventable or non-preventable)
------------------------------------------------------------------------------------------------
● Pt living at home with daughter seems to not be taking his medication, even though she lays them out
before leaving for work. Patient thinks he’s taking them; what to do? Involve a social worker in
discharge planning -- they can see if the daughter is still willing/able to supervise his medications
○ A mini mental state examination screens cognitive function (orientation, attention,
calculation, recall, language and motor skills), not assessment of functional status (whether
he can perform self-care, take meds, etc.)

78
 ● If mom refuses to treat baby’s meningitis, no need to convene an ethics committee: get a court order
or involve CPS
● Pt seems to be addicted to opioids, how to proceed? Obtain confirmation of the patient’s
prescription history
● If a patient is illiterate, use visual aids (UW says re-explaining the procedure slowly, clearly, isn’t
good enough, bc many with low literacy also have trouble with spoken language)
● HMO is the cheapest (HMO-be-not-payin’-the-bill -- ZDoggMD)
● Doc shouldn’t prescribe a drug that would be harmful to pt even if pt asks for it: non-maleficence

BIOSTATS:
● NNH: how many people must be exposed to the risk (i.e. smoking) for one person to develop lung
cancer? = 1/AR (attributable risk, i.e. the difference in risk of the exposed vs the non-exposed group)
● In study, pts taking vitamins less than 5 years have no increased protection from MI, but those taking
it longer than 5 years are protected → might be explained by ‘accumulation’ effect, i.e. the risk
reducer may need to be accumulated in order to have an effect
--------------------------------------------------------------------------------------------------------
● In correlation graphs, the closer the value is to -1 or +1, the stronger the association (aka more
correlated); therefore -0.8 is more linear of a fit than, say, -0.2
● Standard error measures variability around the mean; if you increase sample size → decrease SE
○ SE = STD/sqrt(n)
● Lead time vs. length time: lead time = early diagnosis; length of time = length of survival (in patient
with slowly progressive disease, you might detect a false increase in survival)
● HIGHEST RF of coronary heart disease: atherosclerosis elsewhere, DM, CKD → COD = MI
○ For a person with DM2, the risk of dying from CAD exceeds the risk of dying from most other
diseases
● A result is considered statistically significant if the 95% CI does not cross the null value (which
corresponds to a p value < 0.05); in this question, RR was 1.2 and the CI was 1-1.85, thus the p value
could be 0.03 (but not the values given as options, b/c they were >0.05)
● Smoking cessation is by far the most effective preventative intervention in almost all patients,
especially in those with diabetes
● Attrition bias is a type of SELECTION bias (which is a type of systematic error); loss to follow-up
between exposed and unexposed groups = attrition
● Attack rate (in an outbreak, ie food poisoning at a party): the number of people who got sick from
food X/ the number of people who ate food X
● In a metanalysis, if the pooled estimate (aka the total/end determined finding) was statistically
significant, then the findings are considered statistically significant → meaning that you disregard the
fact that some of the studies in the metanalysis were statistically insignificant (if, for ex, the null value
of 0 was included in the CI)
● BIASES:
○ Hawthorne effect = observer effect (“he watched her like a hawk”)
○ Berkson bias = choosing hospitalized patients as control group is poor selection
○ Pygmalion effect = researcher’s beliefs in efficacy of treatment can affect outcome (ie. belief
that a student is smart will make teacher act differently toward student → student has better
test scores as a result)

79
80
 BEHAV SCI:
● Under age of 6, normal for kids not to understand death (may have stomach pains when mom tries to
explain)
● High risk of suicide (bolded UW questions): 1) remove firearm 2) hospital sequestration
○ HIGHEST risk of completed suicide: previous attempt
● In adolescents, ddx oppositional defiant disorder (ODD) from normal adolescent behavior and
disruptive mood dysregulation disorder and conduct disorder:
○ ODD: angry, argumentative, vindictive, deliberately annoys others like brother, authority
figures, doesn’t follow rules; defiant but doesn’t violate the rights of others (unlike
conduct/antisocial)
○ DMDD: irritable mood accompanied by temper outbursts that are >> stimulus; manifests
before age 10; increased “baseline” irritability (aka irritable b/w tantrums too)
○ Conduct disorder: the childhood version of anti-social
● Ddx schizoaffective, bipolar or MDD with psychotic features, and schizophrenia disorders:
○ Schizoaffective: major depressive OR mania episode CONCURRENT with symptoms of
schizophrenia, with history of delusions or hallucinations in the absence of MD or manic
episode -- this may be seen as a psychotic sx without mood sx in between hospitalizations
○ Bipolar with psychotic: psychotic sx are EXCLUSIVELY during manic episodes, as in MDD
with psychotic features, psychotic sx are only seen during episodes
○ Schizophrenia does NOT include prominent mood symptoms that would meet the criteria for
manic/dep episodes
● Although counterintuitive, sublimation and suppression are both considered mature defense
mechanisms; sub = channeling impulses into socially acceptable things instead and suppression,
putting unwanted feelings aside temporarily to cope with reality
○ Undoing (immature): symbolically nullifying a guilt-provoking feeling by confession or
atonement (bringing gift to doc to negate angry feelings); commonly seen in OCD
● Children and grief: until the age of 6, children do not understand the finality of death, and
hallucinations of a loved one may be part of normal grief
● Specific phobia, the treatment of choice is CBT - involves repeated exposure; this is the case even if
the patient’s phobia “dates back to childhood”
○ not psychodynamic (developing insight into unresolved conflicts and influences of past
relationships)
○ Not supportive (bolsters adaptive psychological defenses to help pt cope with acute crisis or
chronic psych illness)
● Antidepressants can precipitate mania in patients who present with depression therefore very
important to screen depressed people for episodes of mania
● Opioid SE that you do NOT develop tolerance to: constipation (worsening with increased dose) and
miosis
● DOC for alcohol addiction is opioid receptor antagonist (naltrexone): inhibits the rewarding and
reinforcing effects of alcohol; given in depot form (esp. useful for pts with nonadherence)
○ Acamprosate (another option) modulates glutamate neurotransmission at
N-methyl-D-aspartate R
○ 2nd line: aldehyde dehydrogenase inhibitor (disulfiram) - poor efficacy (requires supervised
administration); works by allowing accumulation of acetaldehyde which causes unpleasant
“hangover-like” effects
------------------------------------------------------------------------------------
● Acute stress vs. PSTD: time frame -- PTSD requires only 1 month of symptoms (ASD is 3 days to 1
month)
● MDD vs. adjustment disorder with depressed mood -- MDD requires only 2 weeks of symptoms; AD
with depressed mood would only be diagnosable if the pt did not meet the criteria for MDD
● ADHD diagnosis requires lack of attention in 2+ settings, therefore if child has sx at home, should
interview the teachers as well

81
● Pt with panic disorder can be given SSRIs or BZDs; while BZDs are good in acute settings, if pt is
currently well (or if s/he has a history of substance abuse - check vignette) then BZDs are CI
● Treatment-resistant depression is MDD with atypical features, such as mood reactivity (mood is
better in response to positive things), leaden paralysis (when arms/legs feel heavy), rejection
sensitivity (overly sensitive to slight critique), increased sleep and appetite (reversed vegetative
signs) → treatment: MAOIs like phenelzine
● Ddx between disruptive mood dysregulation and intermittent explosive disorder: disruptive is
CHILDHOOD (age of onset is <10), and there is persistent irritability/anger between episodes
○ In intermittent, there is an impulse control issue (so mood between episodes is fine, it’s
normally a reaction that’s out of proportion to the provocation)
● Majority of OD deaths are due to opioids (both prescription and heroin)
● GAD can be treated with SSRIs, yes, but if patient isn’t full ‘cured,’ can add short-or-medium acting
BZDs such as lorazepam (will lower anxiety, treat insomnia but without impairing daytime cognition)
○ BZDs which have long half life (diazepam, chlordiazepoxide) are not great because they have
daytime sedation
● Social anxiety disorder can have somatic symptoms (i.e. stomachache) - school refusal is common
● Do not confuse schizoid with paranoid; this patient’s focused on the idea that the hospital was
taking advantage of his insurance / hadn’t talked to his family in years / no friends
● Persistent depressive disorder aka dysthymia: chronic depressed mood for 2+ years plus at least two
other depressive symptoms
○ UW: “the presence of depressive symptoms for more than 2 years rules out a dx of MDD --
persistent depressive disorder can occur as a pure dysthymic syndrome or with persistent or
intermittent major depressive episodes)” ← I don’t understand the distinction QID1347, 80%
● White coat HTN could be explained by classical conditioning
● 2nd drug if SSRIs have bad sexual side effects: bupropion
○ Trazodone can also cause sexual dysfunction (incl. priapism), and is v. sedative (good for
insomniac depressed people)
● Delusional disorder: more than 1 delusion for 1+ month
● Premature ejaculation is based ONLY on partnered sexual activity, which means if the pt is
ejaculating normally when masturbating, it doesn’t negate the diagnosis (req. Ejaculation in <1min, for
more than 6 months)
● Drunk patient wants to leave: wait until he is sober, and re-evaluate (logic: he temporarily lacks
capacity)
● Acutely panicking pt (i.e. one that is tremulous and says, “I feel like I’m going to die”) can be given
BZDs even if his vitals are ok-to-normal (also note that most ERs aren’t going to initiate SSRIs…)
● MesoLIMBIC is for POSITIVE symptoms (excess dopamine): “mnemonic - I went out on a limb for
her and it was a positive experience!”
● Atheroma: endothelial injury is FIRST; then smooth muscle cells directly cause secretion of
collagen (forms fibrous cap)
● Post-stroke, myelin debris can remain in place for months, even years (microglia are very slow)
● It seemed like patient had schizophreniform disorder, bc he was experiencing voices 2 weeks ago,
and got fired/broke up with his girlfriend “last month,” but UW only considers the 2 weeks as the start
of the true psychotic symptoms, so it’s considered brief psychotic disorder (>1 day, <1 month)
● Postpartum mood changes (blues) should resolve within 14 days (!!); 6-month follow-up, as
suggested in the qstem, is too long, so reassurance and monitoring is key
○ PP depression: within 4-6 weeks but can be up to a YEAR (more than 2 weeks of depi
symptoms); treat pharmacologically
○ PP psychosis: days to weeks later, do not leave mom with babe
● ALWAYS ask general open-ended questions: “what can you tell me about your pain?” is way better
than “what do you think causes your pain?”
● Mental tests:
○ Months backwards = concentration
○ 3-step command = comprehension
○ Recalling 3 words after 5 mins = short term memory

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 ○ Drawing clock oriented to time/place = executive function
● Separation anxiety: big hint is if child had repeated nightmares about losing parents; common to
have physical sx when separation occurs or is anticipated (i.e. stomach aches, nausea during
sleepover)
● Stages of ‘change’:
○ Precontemplation: not even thinking about behavioral modification
○ Contemplation: thinking about it
○ Preparation: planning
○ Action
○ Maintenance
● Medication compliance is better when teens see peers using them too → i.e. a child with an inhaler
will benefit from seeing classmates using inhalers
● Panic disorder (without tx) can lead to agoraphobia!
● Transference: shifting of emotions from a person in the past to one in the present
○ Note that if the pt didn’t express anger to this person of the past, and instead placed it on
someone/something in the present (i.e. the doctor), then it would be considered displacement
● Wernicke-Korsakoff syndrome: treatment will result in improvement of most of the sx (oculomotor
problems, ataxia, confusion) except memory loss: that is permanent

EXERCISE:
● QRS complex decreases slightly (in response to the increase in cardiac conduction velocity that we
get with increased heart rates)
● PaO2 and PaCO2 levels remain close to resting levels due to lung/circulation adaptations, as well as
hyperventilation and improved ventilation perfusion matching
● In exercise, calcium (due to muscle contraction) is the STRONGEST activator of glycogen
phosphorylase (and thus glycogenolysis)
● Athlete’s heart (cardiac adaptation) would be enlarged LV cavity due to eccentric hypertrophy with
some concentric components; uniformly increased LV wall thickness
------------------------------------------------------------
● When you exercise, which parameter decreases? Total systemic vascular resistance → massive
arteriolar dilation within active muscles; there is an increase in CO so that you can perfuse the
exercising muscles more, but the overall rise in mean arterial pressure is much lower, due to this
decrease in systemic vascular resistance (despite massive increase in CO and splanchnic
vasoconstriction)
○ Vasodilation is mediated within active skeletal muscles by adenosine, K+, ATP, CO2 and
lactate
● Athlete’s heart: physiological → endurance exercise results in eccentric h.t. (bigger cavity allows for
better diastolic function) and some concentric h.t. (increases systolic function); enhanced coronary
capillary system, and decreased resting HR → all these improve efficiency of heart pumping (LV EF
was 70% in this patient)
●

83
 AGING:
● Renal function decline: beware of toxicity (i.e. digoxin)
○ Note that creatinine may not rise b/c creatinine is derived from muscle tissue, and lean body
mass may also decrease with age
● Respiratory:
○ Since these two counterbalance each out, TLC is unchanged
■ Decreased chest wall compliance —> due to stiffening from rib calcification/increased
curvature of thoracic spine due to osteoporosis, osteoarthritis
■ Increased lung compliance due to loss of elastic recoil, especially at alveolar ducts
○ RV is increased because of diminished elastic recoil and collapse of supporting tissues
around the airways
○ FVC decreases, b/c RV becomes a larger portion of the TLC

● Neuro:
○ Slight decrease in fluid intelligence and ability to process new information quickly
○ Normal functioning in all activities of daily living
● UWorld chart
○ Cardio: decreased maximum HR, hypertension
○ GI: more acid reflux, less colonic motility (thus GERD, constipation)
○ Urinary: less able to concentrate urine, and impaired emptying → dehydration, UTIs,
incontinence
○ Immune: fewer B and T cells
○ MSK: less muscle mass, more mineral loss → more falls, more fractures
○ Skin: atrophy, less subdermal fat → more fragile, WRINKLING
○ Sensory: ocular lens hardening and auditory path degeneration
■ By this mechanism, myopia can be “corrected’
--------------------------------------------------------------------------------------------------------------
● Sleep: decreased total sleep time, increased night awakenings, earlier wakeup, more naps
● AV node dysfunction (age-related fibrosis and cell degeneration) can actually result in 3rd degree
AV block
● Increased arterial stiffness, which is due to endothelial dysfunction and changes in ECM
composition (less elastin, more collagen, etc) → this can actually lead to increased stiffness of the
aorta and thus causes elevated systolic pressures (you may see isolated systolic hypertension,
which is pretty common in the elderly)
● Gradual decline of lung function starts at age 30; measured with FEV1 (and smoking accelerates
this greatly; smoking cessation can help slow the smoking-associated decline of FEV1 in COPD pts)

84
● WRINKLES: due to decreased collagen fibril production → UVA causes photoaging by producing
ROS, which activate inflamm cell surface R’s and nuclear TFs → decreased production of collagen
fibrils AND upregulation of matrix metalloproteinases, incl. collagenases, and INCREASED
cross-linking

85
 EYE/ophthalmology:

→ random:
● Trochlear n. is the longest nerve, has the smallest caliber -- more susceptible to injury
→ AGE-related MACULAR DEGENERATION (most common cause of blindness in industrialized
countries)
● DRY: gradual, likely due to chronic oxidative damage; Drusen deposits (subretinal) with pigment
abnormalities
● WET - acute; progression from the dry (due to the chronic retinal hypoxia, local VEGF is produced):
blurry, distorted vision (metamorphopsia, when straight lines appear curved),
→ GLAUCOMA:
● Increased cup:disc ratio, along with a significantly paler disc (ratio >0.6) → pale because of
progressive loss of ganglion cell axons
● OPEN ANGLE: increased pressure or decreased aqueous humor outflow
○ Peripheral visual field loss, progressively
○ Tx: latanoprost (PG agonist) - first line, increases outflow
■ Decrease production:
● CAi like dorzolamide decrease formation of bicarb in ciliary body → thus
decreased production of aq.humor
● Alpha agonists like brimonidine cause VC → decreased production
● BB like timolol also decrease production → acts on ciliary epithelium to
decrease aqueous humor secretion
■ Increase outflow: PG agonists
■ Trabecular outflow: muscarinic agonists
● ACUTE ANGLE CLOSURE:
○ Treatment: CAi - how does that help? Because carbonic anhydrase modulates bicarb
formation in the aqueous humor, so by inhibiting it, we decrease both bicarb and aqueous
humor formation → relieves intraocular pressure

86
-------------------------------------------------------------------------------------------------------------------------------------------
● Transient loss of vision when bending forward/lifting → pseudotumor cerebri, which increases
pressure and thus impairs axoplasmic flow within optic nerves
○ Female TOAD: tetracyclines, obesity, vit A excess, danazol
○ Sx: transient vision loss, daily headaches, bilateral symmetrical papilledema (fundoscopy)
● Choroidal inflammation: posterior uveitis, a/w inflammatory diseases like IBD, ankylosing
spondylitis; painless vision loss and floaters
● New onset diplopia + down and out right eye in diabetic pt: lesion is due to nerve ischemia,
secondary to diabetic ophthalmoplegia (central infarction); unilateral CN III involvement is the most
common, and presents with acute onset diplopia
○ Nerve compression is due to aneurysm, and is accompanied with pupillary dysfunction
(unlike in DM eye, in which there is no pupil involvement, since the superficial PSY fibers are
spared); note that the down-and-out pupil would be seen in both
● Small yellow retinal lesions clustered in the macula → central scotoma; any lesion of the macula
will impair central visions, causing central scotoma (i.e. in macular degeneration, you could develop a
central scotoma due to fatty tissue (Drusen) deposits behind the retina)
○ Arcuate scotoma occurs when the defect follows arcuate shape on nerve fiber pattern
○

87
88
 NBME Reviews:
● 23:
○ Fecal incontinence due to S2-S4 issues -- thus associated with impotence (pudendal nerve -
external anal sphincter)
○
○
○
○

NBME 24: please do not read if you haven’t done this yet
● Horseback riding man develops painful, swollen mass in left inner thigh → circumscribed, very firm:
myositis ossificans (a type of metaplasia, in which bone forms after trauma), esp. after repetitive
injury to the same area
● TGF-beta is really important fibroblast migration/proliferation promoter
● Granulation tissue is characterized by angiogenesis: happens day 3-weeks after MI
● Pt with small cell carcinoma develops hypertension, hypokalemia has ectopic ACTH secretion:
tricky question, ACTH has two fx: activates cortisol, which increases BP, and increases
aldosterone, which accounts for the hypokalemia
○ Note that in SIADH, BP may be high or normal, and body responds to the increased fluid
volume with decreasing aldosterone
● Tricky question: child has + immunoreactive trypsin test, and later + sweat chloride test: analysis of
the 70 most common CF TM gene mutations shows mutation in one allele; why is that? It is likely that
the patient has another mutation hat wasn’t included in the 70
● Vit E deficiency might present very similarly to VitB12, without the megaloblastic anemia
● 13 yo boy MAY grow some breast buds (Tanner stage 3): reassure them that this is normal, and will
resolve in 12-18 months
● Child with jaundice, large fontanelles, hypotonia, hepatomegaly and increased VLCFAs: likely has
Zellweger syndrome (issue with peroxisomes)
● Women uses finger to support vaginal wall in order to defecate (called ‘splinting’) → likely has a
rectocele, due to damage to the rectovaginal septum (often seen in multiparity; note that she had
extensive diverticuli - did not seem related); this is also seen in large subserosal fibroids
● Bare lymphocyte syndrome: two types, this one was due to absence of class I MHC cells (NK cells
function normally) - mutation in TAP; other type is due to defect in HLAII (MHCII)
○ Issue with Fas ligand results in autoimmune lymphoproliferative syndrome (extrinsic
death pathway)
● Radiation: ionizing (radiotherapy → dsDNA breaks and free radical formation) and non-ionizing
(sun → pyrimidine dimers)
● Sleep apnea is accompanied by a decrease in oxygen saturation (episodic)
○ Ddx between OHS and OSA: in OHS, there is increase in PaCO2 during waking hours (due
to retention)
● Factitious disorder: CHF patient with exacerbation is placed on fluid restriction, but is seen drinking
water
● Fibromuscular dysplasia (distal 2/3rd) vs atherosclerosis (proximal 1/3rd)
○ NBME 22: it causes tubular atrophy
● RUDIMENTARY VAGINA aka blind vaginal pouch:
○ Androgen insensitivity syndrome: scant pubic hair, increased testosterone, no uterus
○ Mullerian agenesis: no pubic hair
● Mitotic cyclins are synthesized in the G2 phase (!)
● NEURO:

89
 ○ Right dorsolateral medullary injury: loss of P/T on right side of face, left side of body; vocal
cord paralysis on right, absence of gag reflex on right -- PICA damage causing Lateral
Medullary Syndrome aka Wallenberg
○ Second question about Wallenberg: dysarthria, dysphagia, dizziness, decreased pain on
right side of face, loss of pain on left side of body → PICA occlusion
● BMS due to high dose CTX can be treated with G-CSF
● Acral lentigous melanoma is found on the palms and
soles; most common in AA
● Breakdown of dipeptides and tripeptides to free AA
occurs in the intestinal mucosa, aka the brush border
○ In the duodenal lumen, it’s the pancreatic
enzymes/proteases that cleave large
polypeptides into smaller bits
● Obstruction in the renal tubule leads to backup
(hydronephrosis) → causes increased hydrostatic
pressure in Bowman space
● ASA decreases the risk of thrombosis via decreasing the
adherence of platelets (weird question, bc according to wiki, ASA acts on platelet aggregation by
inhibiting production of TXA2)
○ Note that ASA’s COX-1 inhibition also results in decreased PG synthesis → antiinflamm,
analgesic, antipyretic fx
● TRICKY: Changes in alcohol withdrawal (note: patient suffered from seizure): hypokalemia, urine
potassium 40mEq/L, high BP -- in DT, the
sympathetic system is often activated →
catecholamine-mediated intracellular shifts of K+,
increased BP
● Reduction of TMJ requires the relaxation of the
lateral pterygoid muscle
● Crohn disease patient has anemia, due to ‘failure of
conversion of 5MTHF to THF)
○ Note: pic showed macrocytic anemia
without the hypersegmented neutrophils
(tricky, tricky) → key is to realize that the
lymphocyte, which are usually way smaller than RBCs, were the same size

● Oophorectomy: woman is in greatest danger of injury ureter when cutting suspensory ligament
(ovarian vessels)
Block 2:
● Young boy with metabolic acidosis + phosphaturia → PT affected (Fanconi)
● Transfusion rxn 45 minutes after initiation is due to acute lung injury aka TRALI - sx were
hypotension with no JVD, only minimal ascites/edema; bilateral diffuse airspace disease w/o pleural

90
 effusions or cardiomegaly (FA writes that TRALI sx are respiratory distress and non-cardiogenic
pulmonary edema); cause: donor anti-leukocyte antibodies against recipient PMNs, pulmo
endothelial cells
○ Not acute hemolytic reaction, as I put, which would present with the following: fever, flank
pain, hemoglobinuria, jaundice
● In DKA, the loss of consciousness is due to “intra and extracellular dehydration,” likely to do with
the osmotic diuresis that is caused by the high glucose concentration
● POMC makes a protein that serves as a precursor of ACTH and beta-lipotropin: this is a result of
post-translational modification → key is that it’s already a protein, that is cleaved (POMC makes a
pro-protein)
● HMG-Coa reductase results in decrease of cholesterol via increased LDL Rs
● HIV pt has diarrhea refractory to all standard oral therapies, but resolves after IV SST: reddit says
this is because increased gastrin leads to increased GI motility; by blocking that with octreotide,
you fix it
● Flexor digitorum profundus
muscle function can be tested by
flexion at DISTAL
interphalangeal joint
● Drug tx for atrial and ventricular
arrhythmia that results in normal
sinus rhythm with prolonged QT
interval: likely sotalol
● In XR inheritance, there is NO
male to male transmission; in this
q, it could have been AD
(incomplete penetrance)
● Man kicked by a horse → most likely cause of his low hematocrit = ruptured spleen (of the options)
● In LV failure: SV decreases, LVEDV increases, CO decreases
● Injecting histamine into the brachial artery → increases lymph flow (histamine increases
microvascular permeability)
● SIADH: urine osmolality will be greater than plasma (think of it in terms of solute: you’re reabsorbing a
lot of fluid → dilutes the plasma (low osmolality); you’re leaving all the salt in the urine (high
osmolality))
● PSGN is aka ‘proliferative’ GN, according to answer
● Beta thalassemia question: man and woman both have microcytic anemia and increased HbA2;
man = heterozygous null mutation of beta globin, whereas woman has heterozygous mutation
known to cause 50% decrease in beta globin gene function of one allele: what is their child going to
have?
○ One in four will have 25% beta globin function; may req occasional transfusion: genotype
would be B0B+ (see notes page 411)
● Inhaled B2 adrenergic agonist results in tremor as a SE
● DM1 patient complains of burning sensation of feet; allodynia is seen bilaterally, with decreased
sensation to pinprick (motor, DTRs, proprioception and vibration are all normal); due to persistent
activation of VGSC in the nociceptor
● Allergy is associated with increased eosinophils (nothing to do with mast cells)
● NTD (small tuft of hair on midline) in this case is due to failure of fusion of sclerotomes aka
neuropores (not development of the notochord, because then you would not have developed any
part of the CNS!)
● Breast cxc mets travels to vertebrae via INTERCOSTAL veins (they are posterior; they arise from
the azygous system, which meets with the Batson plexus)
● Hemodynamic changes in MI: man with chest pain, nausea, vomiting (he appears to be having an
MI) → increased PCWP, decreased CO, increased SVR

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 ○ PCWP is increased by anything that elevates LAP (mitral stenosis, LV failure, AS, AR, MR); in
cardiogenic shock, PCWP can increase or decrease depending on where the infarct is (reddit
says that if LV, then increased; if RV, then decreases)
● In urothelial cancer of the bladder, you see PAPILLARY growth (main RF is smoking); in SCC of
the bladder, you’d see squamous cells (not these papillae)
● Child at age 3 starts to develop epigastric pain and bile-stained vomitus: annular pancreas
● Obturator nerve innervates adductor brevis;
○ Adductor muscles and gracilis are innervated by the obturator nerve
○ External oblique is innervated by the iliohypogastric nerve
○ Obturator internus is innervated by the obturator internus nerve (L5–S2)
○ Piriformis is innervated by the sciatic nerve (L5-S3)
● AML treatment: GM-CSF
● Thyroid hormone in pregnancy: woman has increased serum T4 at 16 weeks’ gestation - that is
because the liver produces more T4-binding protein: recall that in pregnancy, FREE T4 decreases
but total increases, bc estrogen stimulates liver to make more TBG
● CD8 T cells are the atypical lymphocytes we see in mono
● Parotid duct pierces the BUCCINATOR muscle
● Blood loss stimulates bone marrow to synthesize delta-aminolevulinate!
● Carpal bones - some lovers try positions that they can’t handle; from FOOSH, scaphoid is most likely
to be fractured; lunate is most likely to be dislocated
○ Lunate dislocation → acute carpal tunnel syndrome
● Genes of embryology mnemonic: Sonic Wants a Friendly Home(obox)
● 37-year old male: gradually progressive weakness, anorexia, weight loss over 6 months; BP is low,
skin is hyperpigmented; morning cortisol level was low → AUTOIMMUNE ADRENALITIS
○ According to FA: adrenocortical carcinoma, mets is not even a cause of chronic adrenal
insufficiency, which is what this patient has (low cortisol stimulates ACTH → causes
hyperpigmentation)
○ Hallmarks of adrenal insuff:
low cortisol AND low
aldosterone
● T4 = levothyroxine: preferred
treatment for hypothyroidism, bc
more physiological
○ Active hormone is T3, thus
T4 must be converted to
T3 → if we give exogenous
T4, both T4 and T3
increase, and TSH/thyroid
iodine uptake decrease
(thyroid needs to make less
thyroid hormone)
○ If we give T3 exogenously,
your T3 would increase but
T4 would remain low (and
TSH/TIU would be low)
● Nuclear membrane has a
fibrous protein that forms a
two-dimensional network on
the inner surface: lamin
(intermediate filament type 4,
important for assembling/
disassembling the nuclear
membrane)

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● Fibronectin/laminin: part of the ECM; they bind to cell membranes via integrins

93
● Pt on bedrest for 3 weeks (previously healthy) will likely develop DECREASED blood volume;
physiological, bc when you’re lying supine, more venous return → body then switches off the RAAS
system and you end up diuresing fluid out
● When you inflate a BP cuff for 2 mins, then remove it, blood flow increases by 50%: this is due to
adenosine; CHALK mnemonic = things that increase VD in sk.muscle (C - Co2, H - H+, A- adenosine, L
- lactate K- K+)
● Most EFFECTIVE birth control: IUD
● In osteogenesis imperfecta, scar formation is affected (not granulation tissue deposition), bc OI
affects type 1 collagen, which is the predominant collagen in scars (recall that the initial type 3
collagen is turned into type 1 in the last stage of wound healing)
● Ethics: woman with a burka doesn’t want a male physician examining her → ask if she would allow
the exam if her husband was present at all times
●
●

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NBME 23: please do not read if you haven’t done this exam yourself!
Test date: October 1st week

Block 3:
● Tissue that’s able to regenerate without scarring: liver
● Granulocytes are most rapidly decreased in cyclophosphamide therapy
○ Pathoma: most susceptible to alkylating agents: WBCs, specifically neutrophils // most
susceptible to whole body radiation = lymphocytes
● Pt is given NSAIDs for RA, but develops PUD; what is the MOA of the 2nd drug given, which causes
diarrhea as a SE? Misoprostol, a PG analog (diarrhea is indeed a common SE)
● Ethics: a close friend of a patient who seems to have no family can still help in the decision making;
correct answer was, “Thank you for telling me this, it will be helpful.”
● Pt with severe right sided back pain should get a shot involving the LEFT spinothalamic tract
(remember that the fibers cross at the level of the SC); lateral spinothalamic tract = pain, temperature
● Child with yellow-tinged skin, but normal sclera and stool, likely has carotene excess; change diet!
● Coloboma in the eye is a bit of embryonic tissue missing; if it occurs in the iris, there is no vision
loss; if it occurs elsewhere, patient might suffer different degrees of vision loss (i.e. macula, retina)
● Recall that BUN/creatinine ratio is important → in prerenal, you’re reabsorbing more BUN (urea
follows the water), so the ratio becomes higher (>20)
● In tracheal obstruction, all values (FEV, FVC, expiratory and inspiratory rates) decrease
● Pt with 30+ pack history and white patch on lateral border of tongue (seen on histo): the lesion,
which was leukoplakia, will likely
invade the submucosa as it
transforms
○ Ddx from oral hairy
leukoplakia (caused by
EBV, associated with HIV,
often first sign)
● Fluoxetine has its fx on neurons
arising from raphe nuclei -- home
of serotonin, in the medulla
● Subscapularis muscle: does
medial rotation
● Inspiratory pause when
palpating abdomen is MURPHY
sign; seen in cholecystitis
● Stress urinary incontinence can
be treated with alpha R agonist
bc it increases sphincteric contraction (alpha1 specifically, p. 238); note that beta agonists would
cause bladder relaxation (not a desired effect)
● Mechanical ventilation question: if patient is put on PEEP → all of the following increase:

○
○ This is bc in ‘PEEP, bc of how mechanical ventilation works, all the inspiration part of
breathing is done by the machine actively pushing air into the lungs. As a result,
there is no negative pressures in the system compared to the normal lung which
needs the negative inter-pleural pressure to draw air in’
● Action potential in demyelinating diseases is impaired due to increased axonal capacitance → the
higher the capacitance, the slower the impulse is transmitted
○ Myelin LOWERS capacitance and thus speeds up impulse transmission
○ Note that transport is not stopped, just slowed down

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● NMDA receptors use CALCIUM
●

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NBME 22: please do not read if you haven’t done it yet
● Narcotic medication: key is to control his pain (self-pump)
● Fibromuscular dysplasia leads to tubular atrophy
● Calorie consumption > energy expenditure: can lead to obesity (child in question)
● Compliance = [volume/pressure] → pressure end-expiratory - end-inspiratory
● Parvovirus results in interruption of RBC production (attacks the BM)
● In I-cell disease, the mannose-6-phosphate makes the proteins get secreted EXTRACELLULARLY
instead of being sent to lysosomes
● Pt says he’s not ready for smoking cessation, even though he says, “I know it can hurt me,” ask pt to
identify pros and cons
● Woman is angry that her family wasn’t helping her with the kids; now she does kickboxing and she’s
happy; this is considered displacement
● Maxillary and medial nasal prominence = cleft PALATE
● Pancreatic beta cells are endoderm (derived from gut tube)
● Statins + fibrates: myopathy!
● Left 12th rib: puncture inferior pole of kidney injures splenic flexure

● Case control: you can’t get incidence

● Meningioma in interhemispheric fissure (central sulcus region)
● Woman with Leydig cell tumor → she has increased hemoglobin, due to increased testosterone
● Insulin is secreted in vesicles
● Pneumococcal pneumonia heals without scarring because the BM integrity is maintained
● Horseshoe kidney makes aneurysm repair tough because anomalous origins of multiple renal
arteries to each kidney (note that the # of ureters is absolutely the same!)
● If a virus causes encephalitis and it contains an RNA-dependent DNA polymerase, what kind of virus
genome is it?
● Nicotinic acid = niacin = it inhibits the formation of VLDL and
decreases lipolysis
● Woman had 69,XXY pregnancy: how to discover if she had an
embryo within this conceptus → the presence of HSC
○ Villus are seen in both complete (all hydropic) and
incomplete (few) ← only partial has 69,XXY
● Pt has lots of diarrhea → what fluids would you give?
○ Treatment for dehydration: glucose and sodium,
because water follows it
○ Also you need both for the SGLT

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● Reduuvid bug causes Chagas → unilateral eye swelling
● Satellite cells: found in PNS, supportive cells of the PNS (kind of like astrocytes)
○ If a nerve is injured, the Schwann cells might actually be blocking reinnervation
● Third degree AV block: pacemaker!
● Nerve that lies on the external surface of the spermatic cord at the superficial inguinal ring:
responsible for the anterior surface of the scrotum (probably ilioinguinal)
● Hypopigmented lesion helps ddx between NF1 (cafe au lait), Sturge-Weber (port wine stains),
tuberous sclerosis (ashleaf = hypopigmented!)
● Acute hemolytic transfusion reaction: mediated by antibodies and complement C5-C9
● Sjogren’s multifactorial
● Contrast xray of small and large bowel shows that the small bowel is more “feathery” in appearance
→ this is because the small intestine has more villi, which gives the small intestine a greater
mucosal surface area
● Prostatectomy causes pelvic parasympathetic nerve damage
● Gs subunit mutation (lacking GTPase activity) leads to increased adenylyl cyclase activity
● Y. entercolitica grows at cold temperatures
● Note the substantia nigra

● Phase variation: microbe has pilli outside the human body, but no pilli once inside the CSF → phase
variation process shuts it off
○ Transposon mutagenesis ortransposition mutagenesis, is a biological process
that allows genes to be transferred to a host organism's chromosome,
interrupting or modifying the function of an extant gene on the chromosome
and causing mutation.
● Hypocalcemia can TC seizures and diffuse hyperreflexia

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● Wasting of interosseous muscles and inability to abduct fingers + plantar flexion problem: ulnar + tibial
injury
● Ranitidine is an H2 antagonist; it acts on H2, which is Gs coupled → increases cAMP
● Antimuscarinic fx are often the cause of noncompliance in TCAs
● In COPD, you retain pCO2 → therefore your body will compensate by increasing serum bicarb
● In ED, think about DEPRESSION as a possible cause: if you’re depressed, your libido is low
(depression), but nocturnal emissions are normal
● In angiogenesis, you might have erythema and slight warmth; if no pain/drainage, its unlikely to be
an infection → most likely due to angiogenesis
● Cachexia/low albumin = negative nitrogen balance explains the edema
● In CO poisoning, the removal of all CO-carrying RBCs will take 4 months → until the RBCs die
● Child immersed in 60F water up to his neck for 20 mins: what would you see in central blood
volume, ADH, ANP: this is cold water → you VC peripheral vessels, which results in increased central
blood volume, and therefore increased preload → ANP increases; ADH responds to the fact that we
have ‘enough’ blood volume, so it decreases
○ ANP inhibits RAAS btw
● Trauma patient had hypotension, but not too severe → until
surgeon slides his hand behind the liver, and there’s a massive
hemorrhage: likely due to avulsion of hepatic veins from the IVC
● Dextromethorphan: no constipation as a side effect
● Contents of the cell:
○ Hi K+ in // high Na+ outside // high calcium outside the
cell
■ You can’t have free Ca2+ inside the cells, bc it
would activate caspase, etc.
● Graft rejection months after transplant -- histology would show
lymphocytes infiltrating tubular epithelium (likely acute)
● PCOS: LH/FSH ratio is high, bc your body is producing LOTS of
LH, for reasons unknown (mnemonic: Ladies Love PCs)
● SLE is mostly an HS III (organ damage is mediated via IC), but
also party HS II
● Fibularis brevis vs tertius: how to know which one is damaged? In qstem, it was the BREVIS: fracture
of the fibula above the distal tibiofibular
● Pt at high altitude takes CAi → this causes acidosis, and urinary volume goes down
● Bruton XLA: no tonsillar tissue is seen
○ IgG2 deficiency: most common IgG deficiency; leads to recurrent encapsulated bacteria
infections
● If you have GIB or even variceal bleeding/vomiting → can trigger encephalopathy
● Increase sample size only affects the Type II error → higher sample size, decreased type II error
● Chi-square is categorical AND is used to check differences between two or more PERCENTAGES or
proportions
● Adrenal failure → both adrenal glands are normal on CT but seem smaller; the most likely dx is
autoimmune adrenalitis
● Romberg sign is positive:

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 ○ Pt had numbness in both legs, sensation to vibration is decreased and DTRs are low, +
romberg → sensory neuropathy
● MPTP exposure is toxic to substantia nigra → Parkinson disease
● Synthesis of glucosamine from F6-phosphate requires glutamine
○ Hexosamine pathway → it’s required to make polysaccharides
● Child with dilation of left ureter and renal pelvis, with decreased kidney function → nephrectomy,
shows diminished cortex and dilation: likely VUR → interstitial inflammation
● Morphine is metabolized to active metabolites that accumulate: can lead to severe respiratory
depression → especially a problem with renal impairment
● Breast cancer mx → via intercostal veins, connects to vertebral plexus → mx
● Antithrombin deficiency: no change in PT, PTT, thrombin time (!); diagnosis would require you to see
that the PTT following a heparin IV would not increase as much
● Consequence of CKD is MAD HUNGER, so Metabolic acidosis is one of the things that happens →
this is bc kidney can’t excrete H+ ions, so as a result, you would have a decrease of bicarb (tries to
compensate by buffering the H+ so it’s depleted)
● Orlistat inhibits gastric/pancreatic lipase → causes diarrhea as a SE in the beginning
● Kaposi sarcoma: spindle-shaped stromal cells with slit-like vascular spaces
● Triceps is MAINLY by C7 (not C6); C7 is apparently more commonly injured
● Alpha actinin, which is a microfilament that connects the actin to the Z-lines; it’s found in the gap
junctions
● Surfactant = dipalmitoyl lecithin / phosphatidylcholine
● Transection of the SC superior to the level of the sympathetic nervous outflow → what will happen if
he develops a systemic infection? He will have alteration of the thermostatic set point
○ “Alteration of the thermostatic set point is a hypothalamic process mediated by prostaglandins
and is independent of the sympathetic nervous system.”
● Give baby in
● IV administered cholera vaccines aren’t effective, because the vaccine can’t elicit secretory antibody
at the epithelial surface
● Fine crackles ⇒ pulmonary fibrosis
● Cervical rib: girl has tinging in left hand when she goes backpacking → caused by compression of
backpack (it resolves a few minutes after she takes it off)
○ Diastematomyelia: congenital dsr in which part of the SC is split longitudinally
○ Hemivertebra: atype of vertebral anomaly and results from a lack of formation of
one half of a vertebral body. It is a common cause of congenital scoliosis
● Fecal elastase levels: decreased in pancreatic insufficiency, bc normally its secreted by the pancreas
(give pancrelipase combo drug to treat)
● DIC: decrease plasma fibrinogen concentration
● Olfactory cortex is in the TEMPORAL LOBE
● Polycystin is defective in ADPKD
● Superior hemorrhoids BLEED, whereas inferior ones thrombose
● Calculation: man has an aneurysm with cross-sectional area of aneurysm of 2cm^2 and mean velocity
of blood flow → see ipad pic

100
● Increased risk of avascular necrosis in alcoholism (!): mnemonic CASTS bend LEGS)
● Histamine is infused in the left brachial artery: what happens to arteriolar resistance, cap hydrostatic
pressure, cap filtration rate? Histamine is an
○ Resistance decreases, and so hydrostatic P and filtration both increase
● Stenting the renal artery → from femoral access, you go up the aorta and insert into the artery right
above the testicular artery
● Cerebral blood flow decreases when you hyper
● In laxative use → hypokalemia: stool contains a lot bicarb and K+

● Burns: first degree → best kind of burn, no blisters (opposite of murder, where 1st degree is the worst
kind)
○ Rhus dermatitis = urushiol-induced reaction aka poison oak, etc
● Loperamide OD can be treated with naloxone
● Treatment of nephrogenic DI = TZDs, amiloride and indomethacin
● Hemorrhagic shock → weak pulse due to decreased stroke volume

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Treatment algorithm for community acquired pneumonia (esp with suspected pseudomonas) - Amboss

Courtesy of @slayusmle

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