NBME Form 30 Incorrects Flashcards

1
Q

Frank-Starling mechanism of the cardiomyocytes. Frank starling curve for CO curve has shifted down. what does this indicate?

A

for any given preload, there is reduced CO compared to normal» occurs in decreased inotropic states like CHF, negative inotropes, increased afterload.

cardiac tamponade had decreased filling (via compression), in absence of other factors affecting afterload/contractility, it would not be depressed. **cardiac tamponade would affect the VR curve, apparently?

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2
Q

57yr man dies 5 days s/p stroke. He refused tx for his progressively severe HTN over the past 2yrs. BP just prior to stroke was 220/110. Which of the following is the most likely histology of his kidneys at autopsy?

A

hyperplastic arteriolitis> chronic HTN associated w/ arteriosclerosis- thickened vessel walls, w/ loss of elasticity> either hyaline or hyperplastic.
hyaline= protein deposition in the vessel walls
hyperplastic= concentric thickening of the vessel wall w/ proliferation of smooth muscle cells

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3
Q

chronic pyelonephritis develops in the setting of

A

recurrent infections of the GU tract w/ reflux into the renal pelvis.

obstructive uropathy, nephrlithiasis, vesicoureteral reflux> kindeys atrophy, calyceal deformities, fibrosis of renal parenchyma

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4
Q

nodular glomerulosclerosis is associated with

A

diabetic nephropathy, amyloidosis> nephrotic syndrome

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5
Q

renal papillary necrosis associated with

A

severe ischemic injury to the kidney» sickle cell disease, obstructive nephropathy, NSAIDs, DM, severe pyelonephritis.

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6
Q

transgenic animal containing targeted mutation in the gene coding for macrophage-CSF is prepared. What is the generalized skeletal abnormalities expected in this animal?

A

osteopetrosis» imbalance in the fxn of osteoclasts:osteoblasts, given excess bone mineral deposition w/ dense, abnormally mineralized bones.
osteoclasts originate from the monocyte/macrophage lineage> inhibition here would prevent differentiation of these cells.

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7
Q

what are the genetic abnormalities associated with osteopetrosis?

A

RANKL, RANKr, CLCN7 (channelopathies), CA2 (carbonic anhydrase 2) deficiencies.

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8
Q

osteoblast arise from

A

mesenchymal stem cells (unlike osteoclasts that arise from macrophages lineage)

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9
Q

4yr old boy has viral URI for the past 3 days. clearance of the virus is most dependant on?

A

MHC class I= CD8 T cells most likely clear the virus.
virus: obligate intracellular pathogen.
CD8 T realease granzyme, perforin= pore formation to apoptosis the infected cell.
also release cytokines INFg TNFa

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10
Q

which cytokines activate macrophages

A

IL 12, INFg

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11
Q

what is the role of CD4 T

A

assist B cells in making antibodies, recruit macrophages, activates CD8+, and leukocytes to site of activation.
…they do contribute to viral clearance, but are incapable of DIRECTLY killing infected cells (unlike CD8)

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12
Q

23yr old F comes to the doc b/c 1wk history of intermittent episodes of fever/chills w/ rash. She had 4 operations to correct scoliosis, w/ tonsilectomy, appendectomy, removal of lipoma, dermabrasion for acne. She admited 1yr ago with n/v of unexplained origin. Pt has 12 evenly spaced punctate marks in linear pattern on abdomen and upper/lower extremities. No marks on face, or back. most likely diagnosis?

A

factitious disorder> pts consciously produce symtoms for primary gain> generally to be cared far, which is an unconscious motivator for pt’s conscious production of symptoms.
elective surgery history + linear, spaced marks= self inflicted pattern of care seeking

tx: regular f/u with doc who oversees mangement, possible psychotherapy

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13
Q

immune thrombocytopenic purpura presents in what areas

A

dependent body area> feet, legs, hands

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14
Q

53yr M comes to doc b/c 6day history of SOB, cough, pleuritic chest pain. 102T, respirations 35/min. Sputum is rust colored, gram+ diplococci, L side lobar consolidation. Which of the following anatomical structures allowed rapid spread of organisms btw alveoli to involve entire L lobe?

A

pores of Kohn> connections btw alveoli
consists of type 2 alveolar cells that allow for air passage, fluid, phagocytes, and w/ pneumo bacteria to adj alveoli
»really useful in allowing equilibration of adj alveoli, aid normal oxygenation, and prevention of atelectasis.

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15
Q

do alveolar capillaries provide direct connect btw adj alveoli (has intact beings)

A

no» they surround each alveolus and cruical for gas exchange, but not for bacteria/air/fluid/phagocytes

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16
Q

20yr M w/ 4hr history of abd pain, n/v. Had been drinking ethanol all weekend, took 3 doses of actaminophen w/in 2hr after onset of severe headache mon morning. Patient at increased risk for liver injury…

A

via induction of cyp450 enzymes that activate actea to hepatotoxic metabolities> acetamin poisoning is SUPER common w/ alcohol/hepatotoxic drugs.

alcohol makes more NAPQI from acetamin> drastically depleting glutathione» give N-acetylcysteine.

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17
Q

decreased acetaminophen clearance via glucuronidation does not occur w/ alcohol exposure» alcohol doesn’t effect capacity of liver to perform glucuronidation

A

alcohol increases the capacity of liver to produce NAPQI thru induction of p450 enzymes

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18
Q

Study conducted to assess the accuracy of new rapid test to detect a virulent infection. Infections has 80% mortality rate if it’s not identified early; prompt antibiotics is 5%. The graph shows distribution of infected and non-infected according to results of test. what is the optimal diagnostic cut point? *graph shows bimodal distribution where the two curves touch in middle.

A

the cut point of test should be set that all persons w/ infection result as positive so there’s few false negatives= set to optimize sensitivity, specificity, or both depending on the clinical utility of test. a sensitive test should be employed when ruling out significantly mortal diagnosis. pt B shows the max #pts without disease, so select this point to all for “catching” early if you will

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19
Q

4yr old girl has aggressive, non-responsive ALL. Doc recommends palliative care and suggests parents talk to their daughter about impending death. The parents ask doc to help them respond to her questions; the parents should understand that child will understand death as

A

view death as temporary and reversible.
age 5: begin to understand that death is inevitable/irreversible, often incomplete due to lack of experience of death, and media images of ghosts.
age 10: general understanding death is universal, irreversible, and renders people inanimate (vs ghosts idea)

…infants have no understanding of death. toddlers begin to understand and aware of death over time

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20
Q

who is a 4yr in pallative care likely to blame for death

A

parents> unlikely to blame God for illness or death (very abstract concept). depending on parent’s religious beliefs she may believe death represents in going to Heaven, without the abstract understanding of heaven itself.

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21
Q

An investigator studying effects of a new spider venom. Isolated nerve bathed in solution with venom, decreased end plate potential amplitude following stimulation. The presence of venom doesn’t change amp of nerve AP or potential in response to Ach at NMJ. Blockade of what by venom is the reason for dec end plate potential amplitude?

A

presynaptic, voltage gated Ca2+ channel> which would then lead to subsequent downstream decreased synaptic Ach concentration> decreased end plate amplitude.

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22
Q

Investigator studies PO2 in experimental animal. Found PO2 in renal vein higher compared to other organs. Why?

A

blood flow/g tissue is greater in kidneys than other organs
kidney has low metabolic demands compared to other organs, matched with high flow> small differences in renal arterial/venous PO2. other organs depend on flow to meet metabolic demands

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23
Q

Do fenestrations in glomerular capillaries do not promote the convective transport of O2 from BS to efferent arteriole…fenestrations in glomerulus function to filter plasma solutes and water, creating ultrafiltrate in BS

A

-

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24
Q

29yr F w/ 6 day hx rash, joint pain, fatigue. BP 150/90. Raised, red, blotchy malar rash and mild peripheral edema. Tenderness and swelling of several joints. Labs show ANA+, antidsDNA+, protein, RBC casts. What is likely to produce a false positive in this patient?

A

rapid plama reagin> which is test for syphillis (RPR) the test looks for antibodies against cardiolipin-cholesterol-lecithin agent= “reagin” antibodies.
pt has SLE, potentially antiphospholipid antibodies, anticardiolipin antibodies, lupus anticoagulant…predisposes to venous/arterial thrombosis, recurrent preggo loss» antibodies also interfere with the test.

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25
Q

Solution of mixed fatty acids is injected into the duodenum of experimental animal. Clearance rate of IV glucose load is doubled. Vs injection of 0.9% saline into duodenum has less effect on duodenum. This is caused by secretion of which horomone?

A

glucose-dependend-insulinotropic peptide (GIP) secreted by K cells in duodenum and jejunum, to decreased gastric acid, stimulate insulin release from pancreas. secretion is promoted by fatty acids/AA/glucose.
**gastrin has no effect on serum glucose concentration

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26
Q

35yr M with 3yr history of enlaring nose, coarsening facial features, increased hand/foot size. Pt has increased IGF1, triglycerides. Increased serum GH doesn’t decrease s/p oral glucose. What best describes metabolic changes in this patient?

A

pt has acromegaly via pituitary adenoma that gives off IGF1> deranges glucose hemeostatis (increases peripheral insulin resistance), impairs muscle & adipse glucose uptake, increasing adipose lipolysis, increasing hepatic gluconeo.
50% of acromegaly pts had DM w/ hypertriglyceridemia.

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27
Q

Local health people studying acute HepA outbreak in 2 cities by reviewing medical records. Plan to analyze clinical/epidemiologic characteristics of pts who tested positive for IgM antibody compared to those who tested negative. What is the study design?

A

case-control study» analyzing the odds of exopsure to potential hazard.
**not retrospective cohort since pts are not grouped based on disease outcome status (would be grouped on exposure status for cohort)

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28
Q

12yr girl in ER 15mins after accidentally sliced her palm open. 2cm laceration over the L palm. The wound is cleansed and sutured. One week later, the sutures are removed. At this time, which of the following factors is most instrumental in migration of fibroblasts for wound healing?

A

fibronectin
early: platelet aggregation and plug formation
1-7days: neutrophils, macrophages infiltrate to stimulate fibroblast proliferation. Fibronectin is essential for fibroblast migration> they bind peptide sequences within to guide to healing site.
**collagen is what is synthesized by fibroblasts

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29
Q

88yr M LOC when neck is palpated during routine health exam. PMH 40yr HTN well controlled with HCTZ, 20yr degenerative OA w/ anti-inflammatory meds. What caused his syncope?

A

sinus bradycardia> carotid sinus syndrome, an exaggerated response to carotid baroreceptor stimulation w/ low BP, brady, syncope. this is often common w/ volume depletion (HCTZ)

Baroreceptors are sensitive to mechanical pressure> inc BP + baroreceptor> +parasymp> slow pulse, dec peripheral vascular resistance (-sympathetic too)

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30
Q

does peripheral arteriole constriction result in syncope?

A

no> it occurs w/ inc sympathetic activity & signaling at vascular adrenergic receptors> giving inc BP

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31
Q

where are baroreceptors located

A

carotid sinus, aortic arch

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32
Q

32yr M begins to laugh while eating dinner w/ friends. A small particle of food irritates his larynx and provokes him to cough. What is the following best position of his vocal cords thru this sequence: while swallow, immediately after irritation, while coughing.

A

swallowing: closed> prevent food into lungs
irritation: closed> while resp muscles contract to generate pressure in airways, traps air in lungs
coughing: open> allows for forceful exhalation of air to remove the irritant.
**respiratory muscle weakness and neuromuscular disorders interfere w/ mechanism, inc risk of aspiration–>and pneumonia.

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33
Q

27yr F delivers monozygotic twins at 34wk’s gestation. Larger twin has hematocrit of 68%, smaller twin is pale, hematocrit 25%. What likely happened to account for these findings?

A

artery-to-artery chorionic surface anastomoses (more commonly it’s arteriovenous anastomoses in chorion of placenta, leading to blood passing to other)> twin-twin transfusion syndrome, twin anemia polycythemia sequence= common complications of monochorionic gestations. HIGH mortality/morbidity.
** at u/s look for unequal amniotic fluid btw two sacs, or anemia in one/polycythemia in other.

management: laser ablation of anastomoses, amnioreduction, and/or selective fetal reduction.

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34
Q

what happens with knotting of the umbilical cord?

A

cord compression> fetal hypoxemia> compression during fetal descent thru the vaginal canal; generally rare, but would likely occur in monochorionic monoamniotic twins.
**unlikely to affect hematocrit in either twin.

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35
Q

what are the complications of twin-twin transfusion?

A

twin anemia polycythemia sequence, discordant amniotic fluid indices, congenital anatomic abnormalities, hydrops fetalis, HF, intrauterine growth restriction.

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36
Q

51yr M develops diaphoresis, tachy, BP 155/100 24hrs s/p abdominal operation. 2hrs later he has a general tonic-clonic seizure. Which of the following is most likely responsuble for these adverse effects?

A

alcohol withdrawal> chronic use changes expression of NMDA/GABA receptors> discontinuation leads to sympathetic overdrive , in severe cases causes seizures.
early> hyperexcitability, tremors, anxiety, sweating, HTN, tachy, n/v.
late> hallucinations, confusion, seizures.
life-threatening> delirum tremens: severe confusion, disorentiation, LOC, agitation, visual hallucinations, autonomic instability (pulse flux, BP flux, hyperthermia)

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37
Q

what is the typical feature of anaphylactic reaction?

A

acute, life-threatening low BP via increased vascular permeability via histamine (mast cell degranulation). seizures would be atypical of rxn

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38
Q

acute renal failure, anaphylatic reaction, narcotic pain meds, and sepsis all have what feature in common?

A

all lead to low BP.

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39
Q

27yr M weightlifter comes for routine f/u. He’s on synthetic androgens for 1yr to increase muscle mass. Increased scalp hair loss, mid testicular atrophy. Why does he have small testicles?

A

increased negative feedback on GnRH secretion> downregulation of FSH/LH> less release of endogenous T.
read the entire answer downregulation of LH receptors would be accurate for the gonadal regions, but LH receptors are not expressed really in the pituitary. damn.

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40
Q

28yr F has had restlessness, exercise intolerance, palpitations, diarrhea, and excessive sweating for the past 3 days. URI 3wks ago. Thyroid gland is diffusely enlarged and tender. Total T3/T4 increased, free T4 increased; TSH, radioactive iodine uptake decreased. What is the most likely cause of her condition?

A

subacute granulomatous thyroiditis (deQuervain)» self-limited inflammatory condition s/p acute viral illness. Pt presents as hyperthyroid, be they can become hypothyroid/euthyroid following hyperthyroid phase.
**separate from hyperthyroid w/ PAINFUL thyroid (generally not painful in Graves)

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41
Q

Physician prescribes recently marketed drug for 20pts. After months, several pts have adverse symptoms. Doc discontinues drug for all pts and reports to FDA. Which of the following phases of testing is this drug in?

A

phase 4» the reporting to FDA is characteristic of s/p distribution and s/p prescription surveillance following tx approval.
**this is how long-term, rare adverse effects are often identified= failure during this phase results in discontinuation of drug from market/loss of FDA approval.

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42
Q

Clinical Trial Phases Purposes:
Phase 1, Phase 2, Phase 3, Phase 4

A

Phase 1: assesses safety/toxicity in HEALTHY pts; pharmacodynamics/kinetics, adverse effects
Phase 2: assesses efficacy/dosing in small # of SICK pts
Phase 3: generally LARGE, randomized trails comparing intervention to placebo/standard; approval here leads to commercial use.
Phase 4: s/p marketing surveillance for long-term, rare effects

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43
Q

55yr homeless man ER PMH fevers, cough bloody, night sweats, fatigue for 2months. Weight loss, decreased appetite, cachectic, w/ chronic cough on exam. Rhonchi RUL. XR shows cavitation in RUL. What likely caused this tissue injury in patient?

A

type 4 hypersensitivity> pt has TB, via CD4/CD8 cells» +macrophages become histiocytes, form caseating granulomas> local inflammation at site in attempt to encapsulate/destroy TB, but local response results in substantial damage in surrounding lung parenchyma.

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44
Q

70 yr F for pelvic exam. During exam, valsalva leads to ant bulge of vaginal wall. What is the cause of this finding>

A

cystocele> via pelvic floor support defects.
presents as vaginal mass, vaginal pressure, perineal discomfort, urinary/fecal retention, incontinence.

ant> bladder (correct w/ vaginal pessary, surg)
post> rectum
lower cervix> uterine prolapse

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45
Q

what are the risk factors for pelvic organ prolapse?

A

weakness in pelvic floor muscles> previous vaginal deliveries, connective tissue disorders, PMH pelvic surgery
menopause
increased intra-abdominal pressure

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46
Q

66yr M ER 30mins s/p sudden substernal chest pain radiating to neck/L arm. Pain associated w/ weakness, n/v, profuse sweating. Jogging when pain started. PMH HTN w/ indapamide. BP 150/90, pulse 90/min. Cardio S4. Tx with nitroglycerin resolves pain w/in 2mins. ECG has 2mm ST elevation in anterior leads. Tx w/ fibrinolytic drug is beneficial to this patient b/c of what MOA?

A

catalyzing the formation of plasmin, via thrombolytics> pt has STEMI leading to LV dysfxn (S4)

tx requires antiplatelets (aspirin, clopidogrel) + anticoagulants (heparin) + pain control + revascularzation via angioplasty, thrombolysis, CABG. Unable to get percutaneous coronary intervention timely= thrombolytics, which convert plasminogen-> plasmin, a serine protease that cleaves fibrin clots.

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47
Q

what is the MOA of heparin

A

inhibition of conversion of fibrinogen to fibrin> increases the binding affinity of antithrombin 3, inactivating thrombin (direct thrombin inhibitors: lepirudin, bivalirudin just inactivate thrombin)

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48
Q

36yr M PMH HIV+ 4yrs for f/u. Takes AZT, etc meds. CD4 count 410; 6 months ago 720. RT PCR tests show his remaining CD4 are CCR5+. Based on this expression, which cell types are likely also infected?

A

macrophages> CD4, CCR5+ on cell surfaces
*CCR5 is also present on dendritic cells.

macrophages serve to perpetuate infection: present in high numbers at sites of viral entry, resistant to cytotoxic effects of HIV infection allowing for HIV persistence & replication, remarkably long life span w/ ability to survive for months (even years!) in peripheral tissues, and able to distribute thru body (hence CNS later concerns)

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49
Q

21yr F college student comes to severe L headache, n/v for 1hr. Symtoms began w/ flashing lights in both eyes while study. Physical exam shows no abnormalities. Most app tx is a drug that acts on what endogenous mediator?

A

serotonin> pt presents with migraine headache, treated with triptans, SEROTONIN agonists.
**postulated to arise from deficient serotonin inhibition of descending pain pathways.

tx: triptans (serotonin agonists), dopamine inhibitors, antiemetics, acetamin, and/or NSAIDs. Disabling/frequent migraines require prophylaxtic tx> beta blockers, antidepressants (SSRIs, TCAs), anticonvulsants

50
Q

what is the typical presentation of a migraine?

A

unilateral, pulsating headaches w/ n/v, photophobia, phonophobia, +- visual/sensory auras.

51
Q

1 day after hospital admission w/ peritonitis, 42yr M progressive SOB and moderate distress. Pulse Ox 53%. B/l basilar crackles. Pt is intubated and mech vent w/ 90% oxygen at TV 550mL and respirations at 16/min. PEEP is also added, why?

A

to prevent absorption atelectasis> prevent pressure in the alveoli from dropping to zero/becoming negative during respiratory cycle> allows to be open, participate in gas exchange.
**pt has acute lung injury, impaired gas exchange caused w/ fluid filling alveoli, which results in absorption atelectasis.
“The application of PEEP has been employed in postoperative patients in an effort to prevent atelectasis and atelectrauma that can occur in injured lung when undergoing ventilation”– UpToDate

52
Q

what are the advantages of PEEP

A

increased airway pressure> incr oxygenation
increased FRC> prevention of airway collapse
incr artieral O2 (PaO2)> inc interface for gas exchange
**MAX recruitment alveoli
dec airway resistance

53
Q

62yr M brought by wife for inc confusion for 6 months. Lost twice when going to work, difficulty finding objects, can only name current president even though watching news daily, cannot recall children’s names. Neuro exam shows no abnormalities. Mini-mental 19/30. Tx w/ AchEsterase inhibitor (donepezil) is most likely to improve patient’s memory because of it’s ability to target synaptic connections btw?

A

the basal forebrain & neurons in cerebral cortex> pt has dementia Alzheimer’s type, which results from dec cholinergic signal in these areas.
**cholinergic neurons originate from locus coeruleus, mediate attention, learning, memory.
**Alzheimer’s: progressive cognitive decline begins w/ short term impairment, progresses to language changes, then personality changes heavily interfering w/ daily living.
no meds are curative, only modestly improve fxn/cognitive decline

54
Q

the synaptic connections btw thalamus & layer 4 of cerebral cortex mediate the transmission of

A

sensory info to the primary sensory cortices. sensory domains are unlikely affected in Alzheimer’s dementia.

55
Q

16yr M in ER 30mins after he dove into a 3ft deep swimming pool at night. Unable to move R lower or upper extremities. Most likely cause of movement deficits in pt is damage to what region of spinal cord?

A

R lateral corticospinal tract in C spine (the C spine cord picture is more ovoid, and heavily white matter predominance); most likely C5 or higher via vertebral column fracture-> cord compression
*UMN of corticospinal tract originate in 1 motor cortex, descend i/l thru internal capsule/midbrain, decussate in caudal medulla, then descend c/l in spinal cord until synapse at c/l LMN.
**lesions involving the lateral corticospinal tract w/in C spine lead to i/l motor weakness, with UMN patterns (increased muscle tone, hyperreflexias, Babinski reflex).

56
Q

where are the spinothalamic tracts in relation to the spinal horns? injury pattern?

A

ant to ventral horns
injury in C spine results in changes in c/l pain, temp, crude touch, pressure sensations.
decussation of tract happens at ant white commissure immediately after the peripheral sensory nerve synapses w/ 2nd order neuron in i/l dorsal horn

57
Q

where are the corticospinal tracts in relation to the spinal horns?

A

lateral to the lateral horns
injury in C spine results in UMN pattern dysfunction of i/l upper and/or lower extremities.

58
Q

where are the fascicili cuneatus, fascicili gracilis in relation to the spinal horns?

A

dorsal medial to dorsal horns; gracilis more medial than cuneatus (think gracilus muscle in leg, sensory from lower body)
injury in C spine results in i/l deficits in pressure, vibration, fine touch, and proprioception
tract decussates in the medulla at nucleus of name

59
Q

25yr M unable to conceive for 2yrs. Wife is fine. Pt has autoantibodies to sperm. Dysfunction of what cell is most likely the cause?

A

Sertoli cells> they line the seminiferous tubules, creating the blood-testis-barrier.
**LH acts on Leydig cells> testosterone.

**sertoli, seminiferous tubules, sperm= all S

60
Q

2mon F 2 days s/p complete blood count was found abnormal. Her blood group is A, Rh+. She was born term to 23yr O, Rh+ mom. 8lb,9oz, uncomplicated prego/delivery. Pt is active & feeding well. Vitals stable. Leukocyte total 17,200, neutro 4%, eosin 4%, basophil 4%, lymph 69%, monocytes 19%, platelets/Hb in normal range. Exam shows no abnormalities. What is the diagnosis?

A

congenital neutropenia> defined as ANC less than 1500, most have less 1000. Extremely high risk bacterial infections, though most patients remain largely asymptomatic (this pt)
**neutropenia is common in Chediak-Higashi, X-linked agammaglobulinemia, von Gierke> must diff from bone marrow arrest.

61
Q

Describe alloimmune hemolytic disease of the newborn.

A

occurs in pts who are Rh+ born to Rh- moms, who were sensitive by prior birth or blood transfusions with Rh+, and now have anti-Rh antibodies.
**repeat again, Rh- mom w/ 2nd child that’s Rh+.

62
Q

presentation of congenital CMV

A

hearing loss
seizures
petechial rash
intracranial Ca2+
^^all transmitted via placenta.
splenomegaly, hepatomegaly also common

63
Q

presentation of DiGeorge syndrome

A

22q11 deletion> failure of 3rd/4th brachial pouches develop> no thymus, no parathyroid glands. FISH to see DNA segment missing

hypocalcemia
thymic aplasia
cardiac defects
craniofacial deformities
**making susceptible to viral & fungal infections

64
Q

presentation of SCID

A

recurrent bacterial, viral, fungal infections.
severe impairment of B & T cells

65
Q

4yr M PMH 3month of hyperactivity and decreased attention span. Exam shows no abnormalities. Labs show: low Hb, low Hct, low MCH, low MCV. Smear shows basophilic stippling, ring sideroblasts w/in bone marrow. What is the most likely cause of these findings?

A

inhibition of ferrochelatase> via lead poisoning.
affects CNS/PNS, heme synthesis, GI/kidney fxn

children often demonstrate neurobehavioral symptoms (which can become permanent), actue hearing loss, peripheral neuropathy, n/v, abd pain, anemia, interstitial nephritis.

66
Q

Basophilic stippling vs Howell-Jolly bodies vs Heniz bodies

A

basophilic: ribosomal inclusion in RBCs (lead poison, thalassemia, myelodysplastic syndromes, sickle cell)
Howell-Jolly: DNA remnants in RBCs (asplenia)
Heniz: denatured, precipitated Hb (G6PD)

67
Q

25yr M w/ abd pain, vomit for 1 day. Greasy yellow plaques on skin, recurrent abd pain following ingestion of fatty meals since infancy. Exam shows xanthomas over the trunk and lupemia retinalis. Tenderness over the epigastrum, dec bowel sounds. Labs show leukocytosis, increased serum amylase. The plasma appears milky. Which is most likely increased in patient’s serum?

A

chylomicrons> pt has familial hyperchylomicronemia, genetic lipid disorder caused by LPL deficiency, eliminating the conversion of TGs on chylomicrons into FFA in extrahepatic tissues.

LPL deficiency: increased chylomicrons, TGs> present w/ abd pain following fatty meals, steatosis, eruptive xanthomas, lipemia retinalis» all leading to milky appearances, increased amylase.

68
Q

Does deficiency of Apo A2 result in hyperchylomicronemia?

A

no, but Apo C2 does> VLDL-cholesterol and chylomicrons transport, also activates LPL> deficiency leads to typical familial hyperchylomicronemia presentation

69
Q

what lipoproteins are in HDL-cholesterol?

A

ApoA1, ApoC2, ApoE

70
Q

what lipoproteins are in LDL-cholesterol?

A

ApoB100

71
Q

What is the implication of degeneracy of the genetic code?

A

multiple species of tRNAs exist for most amino acids> aka different codons can encode for the same individual amino acid

**the amino acid sequence of a protein derived from a given mRNA can vary is incorrect via the unambiguous of genetic code: each codon designates only 1 AA

72
Q

In a patient of HIV1 infection, the viral genome is most likely found in T helper cells and what other cell?

A

macrophages» remember the persistence of infection with CD4+, CCR5+.
**damn literal repeat question….at least I gave the same answer. lol
NOTE: all T helper cells will have infection, CD4 & suppressor T cells (regulatory T cells, are subset of T-helper)

73
Q

20yr M ER 30mins fainting while playing basketball. He has felt tired for hx 3 mon. Systolic murmur heard at L sternal border. Murmur increases with valsalva. Diagnosis?

A

idiopathic hypertrophic obstructive cardiomyopathy> key here is that the murmur increased with valsalva.
tx: beta blockers, dihydropyridine CCBs mainstay (need to increase diastolic filling, reduce pulse)

LV thickened, leads to outflow tract obstruction> diastolic dysfxn> decrease preload (valsalva) will accentuate murmur with increased incursion of the septum, further obstructing that outflow.
classically presents in dyspnea/chest pain/syncope/sudden death in exercising, young athletes +- family history w/ same events.
**murmur differs from tri regurg since valsalva would make for less preload over the valve> less issues over the crappy valve> softer murmur.

74
Q

Which of the following labeled structures in the sagittal MRI of knee is largly responsible for preventing excessive posterior movement of the tibia with respect to femur?

A

looking for PCL, connects the medial condyle of femur to posterior tibia (intercondylar); think knees striking dashboard of car in rapid deceleration of MVA
MRI of knee is choice study.
**in a sagittal MRI, it will always be posterior closes to the leg muscles. sagittal view will mostly highlight ACL.

75
Q

23yr M presents w/ pain in L leg for 3 days. 9yr PMH alcoholism. Court hearing next day while DUI, and another next week for fighting in bar. He blames the “overzealous police” for his problems, and says that most people are stupid for not seeing things his way…the right way. Physical exam shows no abnormalities of L leg. Patient most likely has what personality disorder?

A

antisocial personality> cluster B personality disorders (the emotional/dramatic cluster), arising from deficit in empathy, resulting in pervasive violations of others’ rights, aggression, and hostile manipulative attitudes towards others.
pts are often chronically bored, sensation seeking (hence high substance abuse/gambling). deficits in personal (extreme ego-centrism), and interpersonal (empathy, intimacy) fxn; maladaptive ways of relating to self and others, appearing in early adulthood.

76
Q

what is the presenation of avoidant personality disorder?

A

avoidant personality disorder> cluster C (anxious, fearful)
avoidance of interpersonal contact caused by feelings of social inadequacy/hypersensitive to rejections, unwilling to be involved, extreme embarrassment is feared emotion, **longs for attachment

77
Q

what is the presentation of histrionic personality disorder?

A

histrionic personality disorder> cluster B (emotional, dramatic)
theatrical, superficial expressions of emotion that unconsciously serve to garner attention from other to fulfill emotional needs; dressing seductive, crazy stories.

78
Q

what is the presentation of paranoid personality disorder?

A

paranoid personality disorder> cluster A (odd, eccentric)
pervasive mistrust of others & viewing others as possessing malicious intent, assumes others talk behind back/lie/disappoint, generally suspicious

79
Q

what is the presentation of schizoid personality disorder?

A

schizoid personality disorder> cluster A (odd, eccentric)
extreme social detachment, cold/restricted affect, solitary lifestyle, indifferent to praise/criticism, not interested in sexual experiences, lacks friends, no enjoyment from activities.

80
Q

what personality disorders are in Cluster A

A

paranoid, schizoid, schiotypical

81
Q

what personality disorders are in cluster B

A

antisocial, borderline, histrionic, narcissistic

82
Q

what personality disorders are in cluster C

A

avoidant, dependent, OCD personality

83
Q

The GI contractive effects of drug X alone, drug X + cholinesterase (same level of contract as drug alone), and drug X + atropine (barely any contractions). Drug X is most likely what?

A

bethanechol> direct cholinergic agonist at muscarinic receptors (but not nicotinic receptors)» commonly used to tx urinary retention, gastric dysmotility.
it would not be metabolized by cholinesterase, but it is blocked by atropine (competitive inhibitor of M receptors)
**direct agonist of nicotine only affects nicotinic receptors…which there are none in GI tract, only muscarinic

84
Q

Newborn F delivered at 26wks develops grunting and chest retractions shortly after birth. She is intubated, mechanically ventilated. CXR 8hrs later shows b/l pulm infiltrates. Newborn dies the following day, at autopsy what is microscopic exam of lung show?

A

proteinaceous alveolar debris and atelectasis (and hyaline material)» pt has neonatal RDS, from inadequate amt of surfactant (type 2 pneumocytes)» high tension w/o surfactant leads to pulm collapse. protein debris= PAS+
neonate at high risk when lecithin, sphingomyelin ratio is low. surfactant is high in phospholipids, and indicative of fetal lung development, measured in amniotic fluid.

tx: give glucocorticoids prior to delivery, during NRDS

85
Q

what is the histological presentation of viral pneumonia in neonate?

A

dense lymphocytic infiltrates, interstitial edema

86
Q

65yr F w/ stage 1 ER+ breast carcinoma undergoes mastectomy and radiation. Upon completion, she’s given tamoxifen. The initial site of binding of this agent to it’s receptor most likely occurs in which part of the tumor cell?

A

cytosol> while it is a steroid (and thus exerts effects on DNA), it’s receptor is found in cytosol.
**estrogens, androgens, glucocorticoids all bind intracellular, cytosolic receptors, then translocate to nucleus for DNA effects
***T3/T4 bind nuclear receptors, DNA effects

87
Q

A paper says “we chose the sample size to have an 80% power of detecting mean difference w/ significance level (two-sided) of 5%”. If there is really no difference btw groups overall, which of the following best respresents the chance that the study will find a statistically significant difference, and what is the error called?

A

5%, type 1 error» the significance level is equivalent to the p value, which is synonymous with type 1 error rate.

88
Q

42yr F finds nodule on L side of neck for 2wk, asymptomatic. Undergoes thyroid scan. After 1wk, where is the largest amount of I-123 found?

A

T4 bound to T4-binding globulin» most amt of thyroid hormone exists as T4 (even tho T3 more potent)
**free T3/T4 low
**T3/T4 bound to transthyretin is low, more abundant amt of globulins

89
Q

43yr man comes for f/u after a 10yr cardiac valve replacement. Based on CXR, what valve was replaced?

A

**aortic & mitral valves most commonly replaced.
based on CXR, the valve replaced would be above the “imaginary” line btw the L appendage & R diaphragmatic crus; on the lateral CXR, you can see the valve is pointed up, and in the R heart field= aortic valve

(silly questions..)

90
Q

30yr F f/u with 10yr PMH recurrent renal calculi, primarily calcium oxalate. Exam shows no abnormalities. Serum Ca2+/PO4 WNL. 24hr urine Ca increased. Pt recommends increased water intake, decreased sodium/protein intake. Also recommends drug that decreases urinary calcium, what is the MOA of this drug?

A

increases Ca2+ resorb in distal tubule (reduce Na, Cl via inhibit NaCl transport, BUT inc Ca)» most likely prescribes a HCTZ.
**can also tx w/ oral citric acid: reduces the formation of crystals forming SOLUBLE complexes w/ Ca

91
Q

do phosphate concentration have a significant impact on formation of calcium oxalate stones?

A

no» increased PO43- resorb in PCT would be with dec PTH, acts to inc intestinal absorption/renal reabsorption of Ca to decrease PCT reabsorption of PO43-, BUT don’t have anything to do with calcium oxalate stones.

92
Q

55yr F w/ 6mon progressive difficulty walking. Neuro exam shows spasticity, hyperreflexia, and clonus in lower extremities. Babinski+ b/l. A drug with what MOA will decrease the spasticity of patient?

A

activation of GABA receptors in muscle spindle afferents (baclofen)» muscle spindles are stretch receptors located w/in the muscle which sense changes in the length of a muscle fiber, this pt has loss of UMN inhibitory control of spinal reflex arcs= exaggerated muscle stretch.

93
Q

55yr DM1 male has intermittent burning pain of his feet during last 4 months. Exam of feet shows allodynia b/l. Sensation to pinprick is decreased. Motor strength, DTR, joint position, vibration WNL. Which of following most likely cause of the pain in pt?

A

persistent activation of voltage gated Na channels in nociceptor» poorly controlled DM1 leads to advanced glycation end products in vascular endothelium> capillary damage> esp vasa nervorum= diabetic neuropathy, neuropathic pain> inc production of AP causing sensation of pain
tx: TCAs, carbamazepine (Na blockade)

94
Q

what is the general pathophys for neuropathic pain?

A

increased activation of glutamate receptors in DRG» BUT key this is not in poorly controlled diabetes (peripheral neuropathy)
increased activity of voltage-gated K+ channels in thalamus» increased central processing of nociceptive stimuli

95
Q

54yr M w/ 3day hx LBP. 101T, 75/min, BP 120/80. Exam shows R sided flank tenderness to percussion. CT scan of the abdomen has lesion consistent with abscess along the post-medial aspect of the R kidney. Extension into the pelvis is most likely to occur along which surface?

A

psoas fascia» pt has perinephric abscess (via perirenal fat necrosis, contained within Gerota’s fascia) as complication of pyelonephritis (think EColi); less commonly will hematogenous spread in bacteremia (S. aureus)
**psoas & transveralis m most common extension places
**the quad lumborum fascia is lateral to psoas, post border of iliac crest & inserts to 12th rib/L spine.

96
Q

1yr boy receives L cochlear implant that gives electrodes. 6 months earlier dx w/ severe b/l hearing deficit. What must remain intact for this pt to perceive auditory stimulation via activation of the electrodes in the implant?

A

auditory nerve> cochlear implants directly stimulate the auditory n endings in the cochlea, thus require fxn nerve.
sensorineural hearing loss typically results from damage to the hair cells in the cochlea» implants bypass the damaged cochlea.
**auditory hair cells, round window= cochlea components, and thus don’t need fxn here
**implant has external mic, so don’t rely on inner/middle ear apparatus either

97
Q

21yr F is participating in study of experimental drug. Various cardio before/after. No changes in pulse. CVP 1-> 6. Mean arterial P 100-> 90. PCWP 3-> 12. Aortic P 134/83-> 110/80. Assuming no reflex adjustments, what is the MOA of drug?

A

decreased cardiac contractility» no change in pulse, inc CVP/PCWP, dec MAP–> dec SV, dec forward blood flow. Systolic pressure dec w/ preservation of diastolic= argues for reduced volume of blood ejected during systole w/o impairment of vascular tone.

98
Q

what happens with dec compliance of aorta?

A

compliance: volume/pressure

**if we dec compliance aorta, would give inc aortic systolic pressure s/p drug, as volume entering aorta remains same.

99
Q

what happens with inc TPR?

A

increased total peripheral resistance= increased systolic and diastolic pressures, increase MAP as flow is equal to driving pressure/resistance.
**if our flow remains equal, pressure increases as resistance increases.

100
Q

what happens with increased ventricular compliance?

A

increased ventricular compliance would give decreased CVP, dec PCWP s/p drug» less driving pressure to fill the ventricles with same amount of blood.

101
Q

21yr M ER 30min s/p gunshot wound to leg. Pt unconscious. Pulse 150/min, resp 26/min but spontaneous, BP 80/60. Exam shows pallor. How pt’s condition compare to his baseline: AV PO2 diff, plasma lactic acid, plasma ADH, systemic capillary fluid transfer?

A

pt in hypovolemic shock 2/2 signficant reduction in intravascular volume via hemorrhage» dec preload> dec SV> dec CO (so pulse inc)> arteriolar vasoconstrict to inc TPR to inc MAP> when it fails you get low BP, inadequate perfusion.
AV PO2 diff: increased (O2 extraction in tissues is increased, giving more AV PO2 diff)
plasma lactic acid: increased
plasma ADH: increased
systemic capillary fluid transfer: favors reabsorption

102
Q

when do you see a dec AV PO2 difference?

A

in states with less O2 extraction, septic shock, hyperthyroidism, high CO output states, AV fistulas

103
Q

23yr F 3wk history of frequent thirst & urination, weight loss, dehydration, tachypnea. Glucose labs 330, 2+ ketones, pH 7.2. Following insulin and IV fluids, marked improve. The activity of which enzyme is most likely increased in pt hepatocytes b/c of tx?

A

glucokinase> pt has in DKA prior to insulin tx, insulin promotes peripheral tissue glucose uptake, glycolysis, hepatic glucose storage as glycogen= all decreasing serum glucose.
**glucokinase is 1st step of hepatic glycolysis, glycogen synthesis
G6Phophatase downregulated (gluconeo, glycogen degrade that releases glucose into blood)
glycogen phosphorylase downregulated (stimulated by glucagon, fxn in glycogenolysis)
PEP carboxykinase downregulated (OAA to PEP in gluconeo)
phophorylase kinase (stimulated by glucagon, counteracts insulin giving incr glucose)

104
Q

24yr M w/ 3day hx of progressive numbness in b/l feet now ascended to his thighs, and today his hands. Exam shows ataxic gait. Sensation to vibration/joint position is absent in fingertips/feet b/l. Mild weakness of distal upper extremities, moderate weakness of lower extremities. A process involving what structure most likely explanation for sensory findings?

A

myelinated primary afferents» pt has acute inflammatory demyelinating polyradiculopathy, subtype Guillain-Barre syndrome.
**generally preceded by C. jejuni infection leading to immuno mediate cross-reactivity w/ myelin of nerve roots exiting spinal cord; generally ventral (motor, symp efferents common +- DRG sensory afferents)

DX: increased CSF protein w/ normal cell counts, “albuminocytologic dissociation”= generalized inflammation.
TX: respiratory support, plasma exchange/IV immunoglobulin tx

105
Q

5yr girl w/ 4day hx stumbling gait, muscle rigidity, slurred speech, dec cognition. Exam shows dec visual acuity, inability to discern colors. Assays of isolated mito show dec ability to oxidize NADH but normal FADH2. What complex is likely impaired in ETC?

A

complex 1> “NADH oxireductase”, most common site of electron leakage and free radical generation. mutations in this complex is commonly implicated in in LHON syndrome (Leber Hereditary Optic Neuropathy).
**can have a neurodegenerative component w/ spasiticity, ataxia, tremors, and cardiac arrythmias.
** mito inheritance means all kids will be affected.

complex 2= FAHD2
complex 3= just proton gradient
complex 4= final transfer to H20

106
Q

36yr man sustains burns in fire. BMI 25. Exam shows 2nd burns over approx 40% body surface area. IV fluids administered, admit to ICU. Compared to healthy, pt’s nutrition & fluid requirements are?

A

increased both nutrition, fluids
»severe partial (2nd)/full (3rd) burns compromise skin’s ability to maintain fluid balance> body T is high so body creates inseible evaporative fluid losses + general 3rd spacing from burns (dermal edema)> pt needs isotonic crystalloid fluids
»burn injury causes hypermetabolic state w/ incr stress response + proper nutrition is essential for wound healing, limiting infections, organ dysfxn

107
Q

25yr man w/ 3day hx abd cramps, dirrhea. Appears anxious. Exam shows piloerections, diffuse abd tenderness. Neuro exam shows no abnormalities. Oriented to person, place, time (not event). Most likely pt in withdrawal from?

A

heroin» opiates CNS depressants, intoxication causes sedation, brady, low BP, depressed resp drive, constricted pupils» commonly use for analgesia, acting on GI ro reduce gut motility, causing constipation.
**withdrawal presents w/ restlessness, cramps, n/v, dirrhea, lacrimation/rhinorrhea, yawning, piloerection (this doesn’t occur in alcohol nor benzo withdrawl)

NOTE: withdraw is fatal & unpleasant, support w/ benzo, antiemetics, clonidine (acutely); ideally w/ buprenorphine for transitional period, methadone long term to prevent relapse.

108
Q

A screening program was instituted for detection of depressive symotoms among college students. At first exam, 250/1250 evidence of depression. The following year, an additional 100 developed depression. What is the annual incidence of depression in this population?

A

10%» incidence is the rate of new disease in an at-risk population.
incidence= (#new cases)/(#at risk)
250/1250 initial incidence year.
100/1000 2nd year (250 already developed it, so #at risk changed)

109
Q

Protectio against paralytic poliomyelitis can be achieved by oral Sabin (live attenuated) vaccine or parenteral Salk (killed) vaccine. The common features of the vaccine, is their ability to induce what polio-specific immune response?

A

neutralizing antibodies in circulation» production of neutral antibodies is the goal of vaccination, regardless of route, poliovirus is endocytosed by APCs> sampled by B cells directly> binding to Fab region>somatic hypermutation of Fab region>differentiation to plasma cells> specific neutralizing IGs (process is further augmented by costimulation of T cells via CD4/MHC2)
**neutralizing secretory IgA antibodies in gut are likely present in pts w/ oral vaccine, but unlikely in parenteral vaccine. Specific neutralizing antibodies are more likely, also, to be IgG in both cases.

110
Q

25yr F w/ 7yr hx of 5-10min episodes of inc HR, sweaty, trembling, dizzy, derealization, intense fear occuring almost daily. She feels well btw attacks, but does worry about when next attack will occur. What is the most likely dx?

A

panic disorder» pt is experiencing recurrent panic attacks consistent w/ panic disorder; attacks feature acute fear/axiety that peaks w/in mins and is assoicated with 4 addn phsycial symptoms.

tx: psychotheraphy, long-term SSRIs, short term benzos
**not GAD, characterized by generalized worrying that may be assoicated with sympathetic hyperactivity. Panic attacks can occur in GAD, though anxiety symptoms are more constant/persistent compared to episodic like panic disorder.

111
Q

An experimental animal has blood flow of 4mL/sec in a small arterial segment of the mesenteric circulation. Which of the following best describes the blood flow if the diameter of the vessel is dec be 1/2 with no change in perfusion pressure gradient?

A

flow= pressure/resistance
resistance= (8cylinder lengthfluid viscosity)/(pi*r^4).
if the vessel length & blood viscosity remain constant, a change in diameter of the vessel by factor of 2>inverse change in resistance by 16» flow rate of 4 thru vessel will decrease to 0.25mL/sec if decreased by half (4/16= .025mL/sec)

112
Q

45yr M w/ wosening heartburn which has been present for past 15 months. Pain is more frequent and severe in the past month, no longer relieved by antacids. Occasionally has trouble swallowing. Biopsies of area show basal zone hyperplasia & eosinophilic infiltrate of squamous mucosa. Most likely diagnosis?

A

reflux esophagitis (GERD)» typically presents as burning epigastric pain & lower chest pain, w/ large meals or “trigger foods”; largely worse when supine» all causes mucosal irritation: mucosal erythema, hyperplasia, eosinophilic infiltrate, and erosions in reflux esophagitis.
overtime, if left untreated, GERD leads to metaplasia (Barretts esophagus)> which then leads to esophageal adenocarcinoma.
**there’s no noted intestinal metaplasia here–would say goblet cells or something if wanted Barretts esophagus. questionable timeline on when you’d develop Barretts s/p untx GERD.

113
Q

23yr F for prenatal care. She appears euthyroid & thyroid gland is not palpable. Uterine size is consistent w/ dates, and fetal pulse is normal. Serum T4 14, TSH 2. Changes in which of the following horomones during preggo is primarily responsible for the thyroid test results?

A

estrogens» via the production of the placenta; increased estrogen increases concentration of transport proteins (like TBG)» decreased metabolism of TBG allows more TH to be bound by protein plasma
**free concentration of thyroxine is unchanged, keeping TSH WNL as result of feedback

114
Q

29yr F in ER 1hr after being injured in MVA. Abd exam shows tenderness w/ rebound. Vitals stable. CT shows small amt of intraperitoneal fluid. After 6hrs of observation, pt denotes servere abd pain, an exploratory laparotomy is done. No abnormalities are see until the surgeon gently slides his hand behind the liver; there is a sudden massive hemorrhage from the region of the hand, and the patient’s blood pressure becomes undetectable w/in 1min. Which of the following underlying lesions is most likely associated w/ the hemorrhage?

A

avulsion of hepatic veins from the IVC» the source of occult & slow bleeding posterior to the hepatic veins of IVC, creating an auto-tamponade from the weight of the liver, once the hand went, hemorrhage.
Tx: immediate pressure, packing, clamping, and vascular repair, emergent infusion of blood products.
**can be rapidly fatal b/c transfusion-refractory hypotension & hemorrhagic shock.

115
Q

what is the presentation of traumatic transection of the portal vein?

A

unlikely to have posterior hemorrhage (located ant to liver, adj to hepatic artery)» bleeding is generally present w/ obvious intraperitoneal hemm.

116
Q

10yr boy with cerebral palsy begins benzo treatment. The MOA of diazepam interacts with the GABA ion channel complex. What is the nature of the ion flux that occurs?

A

GABA & BZ binding sites are separate (they are positive allosteric modulators of the GABAa receptor, increasing the freq that the ion channel opens when GABA is bound)» Cl- would move intracellularly.
**CP is a non-progressive central motor dysfxn resulting from several potential prenatal causes, typically presenting with UMN signs like muscle spasticity. tx with benzos and baclofen will increase GABA and dec muscle contraction, giving relief of spasticity.

117
Q

60yr M comes for routine maintenance. Exam shows no abnormalities. UA shows pH 6.0, specificity gravity 1.018, blood 3+, glucose negative, protein 1+. Micro examination of urine shows atypical cells. CT scan shows a lesion in R kidney. What compound is most significant predisposing risk factor for patient’s condition?

A

2-naphthylamine» papillary transitional cell carcinoma is tumor of urinary tract & typically presents with painless gross hematuria> develops in renal collecting tubules, calyx, renal pelvis, ureter, urethra, or bladder (all same origin of epithelium).
**strong risk factor is smoking
*other carcinogens: phenacetin, cyclophosphamide, 2-naphthalamine> all are excreted in the urine causing concentrated exposure to mucosal surfaces

118
Q

what chemical predisposes to hepatic angiosarcoma?

A

vinyl chloride

119
Q

22yr M in ER 15 s/p gunshot. Pulse is 110, resp 20, BP 100/60. Abd exam shows entrace wound in LUQ, but no exit wound. CT shows bullet lodged in what organ?

A

spleen»hyperdense, solid organ with shiny penetrating trauma
structures in LUQ are stomach, spleen, tail of pancreas

120
Q

53yr M w/ progressive fever, cough, SOB, fatigue for 3days. 102.6T, resp 21, sweaty man. increased tactile fremitus, dullness to percussion, and weird breath sounds over the LL hemithorax posteriorly. ABG on 2L/min oxygen give: pH (7.46), PCO2 (22), PO2 (70), HCO3 (15.3). What is the primary cause of hypoxemia in pt?

A

pulmonary arterial blood transversing poorly aerated alveoli»pt has aquired bacterial pneumonia (S pneumo, H influ)> generally lobar type, shows increased consolidation caused by inflammatory infiltration of neutrophils and edema into the alveoli» impairing gas exchange w/in the affected parenchyma, hypoxia 2/2 pulmonary arterial blood transfusing poorly.

121
Q

27yr F PMH 15yr recurrent UTIs develops HTN, proteinuria, and renal failure. XR shows irregular scarring of the kidneys & blunting of renal calyces, most prominent in the upper/lower poles. What is the most likely cause of the renal abnormalities?

A

reflux nephropathy» pt has renal damage 2/2 vesicoureteral reflux (VUR) where retrograde flow of urine from bladder into the ureters & renal calyces.
**VUR begins in childhood
** actue pyelonephritis can lead to inflammation of renal parenchyma & cause complications (renal papillary necrosis), and while calyceal blunt/scar is sometimes observed in chronic pyelonephritis, it’s more suggestive of VUR, reflux nephropathy

122
Q

18yr M 101T sore throat and C lymph node enlargement for 8 days. EBV+. Atypical cells w/ abundant lacey cytoplasm in peripheral blood smear are most likely derived from which of the following cell types?

A

T cells> atypical cells seen in peripheral smear in pts with mono are T cells, infectious mono is a viral illness. EBV infects via CD21, but the T cells seen on smear are the cytotoxic CD8+ reacting to virus.
tx is supportive and pts should be counseled on limiting sports activities due to spleen rupture.
*lacey thing sounded like plasma cells, but that would indicate plasma cell leukemia (multiple myeloma variant), not mono.