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LCK STEP > Week 1 UWORLD Qs > Flashcards

Week 1 UWORLD Qs Flashcards

1
Q

How do phosphatidylcholine levels impact cholesterol gallstone formation?
Name rate limiting enzyme for cholesterol break down/bile salt formation in the liver

A

Makes cholesterol MORE soluble
Cholesterol - 7 alpha hydroxylase -> cholic and chenodeoxycholic acids = bile acids
*Enzyme targeted by FIBRATES, increases risk of gallstones b/c decreasing bile acids made which changes bile acid:cholesterol ratio
Bile acids + taurine/glycine = more soluble

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2
Q

What is the pathogenic CD 4 cell in Crohn’s vs UC

A

Crohns: Th1
- Secrete IL2 + IFNg = granuloma
- Also activate macrophages which make TNF
UC: Th2 -> make cytokines/Ig that damage colon

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3
Q

Explain why Crohn’s pts are at higher risk for gall stones - which kind?

A

Cholesterol gall stones
Disease affects terminal ileum - can’t reabsorb bile acids
Bile now have less bile acid with more cholesterol - ratio changes to favor cholesterol -> cholesterol stones

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4
Q

Explain how these effect your risk for gall stones:
Statins
Spinal cord injury/total parenteral nutrition
Chronic hemolytic anemia

A

Statins decrease risk stones b/c limit cholesterol formation
Bladder hypomotility
Increase conj BR -> pigment gall stones

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5
Q

Name bugs that you see these things in STOOL:

  1. Parasite eggs
  2. Rhabditiform larvae
  3. Proglottids
  4. Trophozoites and cysts
A
  1. Schistosoma
  2. Strongyloides - eggs in GI wall
  3. Intestinal tapeworms: taneia sol + sag, diphyll
  4. Intestinal protozoans: giardia, e.histo
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6
Q

What substance has fastest rate of metabolism in glycolytic pathway: fructose, galactose, glucose, or mannose?

A 
FRUCTOSE-1-PHOSPHATE
Bypasses fructokinase = one of rate lim enzymes of glycolysis 
1. Glucose (hexo/glucokinase) -> G6P 
G1P can enter at this step
2. G6P (phosphoglucoisomerase) -> fructose 6P
Mannose 6P can enter here
3. Fructose 6P (*PFK*) -> F16bisP 
4. Separates into 2 G3P ----> pyruvate
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7
Q

What does carcinoembryonic antigen tell you about adenocarcinoma found @ sigmoid colon?

A

CEA for CRC recurrence

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8
Q

Describe why GI bacterial or helminthic infections increase risk pigment gall stones

A

Think E.Coli, Lumbricoides, or Clonorchis
Injured hepatocytes release beta glucuronidase = increases unconj BR
Pigment stones = Ca salts of unconj BR = “Cae bilirubinate”
Brown or black

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9
Q

Describe presentation and patho of lead poisoning

A

Microcytic anemia + constipation + AMS + h/o construction work
- Blue pigment at gum/tooth line
- Wrist or foot drop due to peripheral neuropathy
Lead X heme synthesis
Normal iron
BASOPHILIC STIPPLING b/c can’t degrade RNA -> ribosome aggregation

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10
Q

Describe when you see
Heinz bodies
Ring sideroblasts
Howell Jolly bodies

A

Heinz - denatured Hgb, G6PD def after oxidative stress
Ring = RBC with big purple circle in it with blue dots around the outside = defective heme synthesis including lead poisoning but @ BONE MARROW not peripheral blood
HJ bodies - DNA remnant that should be removed by spleen, if seen signals splenic dysfxn

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11
Q

What is systemic mastocytosis and how does it affect the GI?

A

Clonal mast cell prolif - tyrosine kinase KIT receptor mutation
If all these mast cell degran -> excessive histamine release
Histamine can bind H2 receptors @ stomach -> increase gastric acid
Presents: rash, rubbing, scratching, itching after hot showers, light headed after standing, syncope in hot sun

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12
Q

What are you thinking if pt presents with masses in liver + ileum w/ flushing, redness, episodes of wheezing

A

Carcinoid syndrome - flushing, watery diarrhea, bronchospasm
Dx w 5-HIAA in 24 hr urine
Medical = octreotide = SS analog = Gi to decrease cAMP = less acid
Surg

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13
Q 
Describe the colonoscopy + biopsy finding for:
Adenocarcinoma
CMV
Crypto
E.Histo
Kaposi
A

Adeno - protruding mass, glands + dysplastic mucosa cells… duh adenocarcinoma
CMV - ulcers, CMV cells w/ inclusion bodies
Crypto - inflam w/o ulcers, basophilic dots on surface of mucosal cells (google image)
E.Histo - flask shaped ulcers, trophozoites that have eaten RBCs
Kaposi - red flat maculopap lesions or hmm nodules - spindle shaped tumor w/ SV PROLIF

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14
Q

What are the 3 types of adenomas you might see in the LI?

A

All form masses and can cause occult or visible bleeding -> Fe def anemia

  1. Villous - “cauliflower like mass”, most likely to become malig, secrete watery mucus -> secretory diarrhea
  2. Tubular - colon cells form tube shaped glands
  3. Tubulovillous = mix
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15
Q

What is the manometry for achalasia vs diffuse esophageal spasm

A

Achalasia - still get peristalsis but amplitude of all the waves is smaller, incomplete LES relaxation b/c no inhibitory ganglion cells
DES - all at once waves = simultaneous contraction of the esophagus (severe, retrosternal chest pain)

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16
Q

Name the order of 5 enzymes involved in DNA base excision repair

A
  1. Glycosylase - recognizes abnormal base
  2. Endonuc - cuts 5’ end
  3. Lyase - cuts 3’ end
  4. DNA pol fills in the 1 nucleotide
  5. Ligase seals
    Think about this pathway for repair of damage due to nitrates - promotes base deamination
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17
Q

Steps of appendicitis infection formation

A

Fecal mat’l obstructs
Build up mucous products in appendix
Wall distends -> decrease venous outflow -> ischemia -> bacterial infection
If wall necrosis, may rupture causing peritonitis

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18
Q

3 histo features of Celiac - name the screening panel for this disease

A

Vilous atrophy
Crypt hyperplasia
Lymphocytes

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19
Q

Why do anal fissures (aka tears) happen at the post midline of the anal canal and run up to the dentate line?

A

Due to chronic constipation + high P when passing hard stools
Low BF at post anal canal

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20
Q

Why do Chron’s pts get kidney stones - what kind?

A
  1. Less bile acids -> less fat absorption -> Ca binds fat and goes out in feces
  2. Now nothing to compete for oxalate absorption (normally Ca ox can’t be reabsorbed)
    Think leaking GI epithelium - nothing holding back oxalate reabsorb
    Ca oxalate stones
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21
Q

What diseases increase your risk of class adenocarcinoma vs cholangiocarcinoma?

A

Adeno = chronic chole -> porcelain GB
Cholangio = fibrotic diseases
- 1ary sclerosing cholangitis
- Liver fluke chronic infection

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22
Q

Olive mass in a baby stomach you thinking….

A

Pyloric stenosis due to SM hypertrophy
Non bilious vomiting
PROJECTILE

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23
Q

What is the histo of 1ary biliary cirrhosis

A

Liver biopsy = lymphocytes + GRANULOMATOUS destruction of interlobular bile ducts
= AI liver disease
Middle aged women
Fatigue + pruritis
Can’t excrete bile from liver -> hyperchoelsterolemia w/ xanthelasma formation

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24
Q

Histo and presentation of 1ary sclerosing cholangitis

A

H/o UC + fatigue + high ALK PHOS
Inflam intra and extra hepatic bile ducts
Onion skinning round ducts

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25
Q

Histo of acute viral hepatitis

A

Ballooning degen!!

Mononuc inflam // apoptosis

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26
Q

What’s the differential for proximal vs distal duodenal ulcers (anything past duodenal bulb)? What is the difference between endogenous and exogenous secretin

A

Prox: Hpylori, NSAID use
Distal: ZE
Endogenous secretin decrease gastrin, increase bicarb from pancreas
Exogenous STIM gastrin from gastrinomas (use to def ZE from other causes hypergastrin)

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27
Q

2 big drugs to treat hyper NH4

A 
Lactalose = convert ammonia to ammonium
Rifaximin = antibiotic vs DNA dep RNA pol, decrease ammonia production by GI flora
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28
Q

What is biliary sludge?

A

Shit that accum when gallbladder isn’t contracting

Think stone precursor

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29
Q

What’s the histo of a Mallory Weiss tear

A

Repeated vomiting -> chest apin

Mucosal teal w/o acute inflam

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30
Q

What is Gilbert syndrome

A

Less UDP enzyme to cong BR in hepatocyte
No liver disese
Slightly high unconj BR aka high total bilirubin but normal direct aka conj BR
VS DUBIN JOHNSON - excess conj BR, totally normal liver tests with direct BR fraction of at least 50%

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31
Q

What are you thinking if
Fulm hepatitis w/ hepatocellular pattern of liver injury
Liver is SHRUNKEN
High serum aminotransferase levels
PRolonged prothrombin time b/c liver isn’t fxninh

A

Inhaled anesthetic heptatotox

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32
Q

Where does H Pylori colonize the stomach?

A

ANTRUM aka prepyloric area

Fundus = top, body, antrum = bottom

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33
Q

What causes Zenker diverticulum?

A

Cricopharyngeal motor dysfxn
Legit out pouching in prox esophagus - false divertic
Bad breath, choking feeling
Worried about aspiration

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34
Q

What drug interaction should you remember with XO?

A

6MCP - degraded by XO
Aka excess bone marrow suppression - super low white ct
CANCER AND GOUT WATCH OUT

35
Q

If a patient presents with rusty colored urine, increased RBC and a kidney mass - what genetic syndrome should you take the leap to think about

A

1st - recognize RCC
2nd - tie VHL
Cerebellar hemagioblastoma
Clear cell renal cancer
Pheo
3rd - know VHL: mutation chr 3 tumor suppressor gene
Even if you just have RCC alone, the likely mutation is the VHL mutation (even w/o VHL!!!)

36
Q

What is alkaptonuria?

A

AR
X homogenistic acid dioxygen = can’t breakdown tyrosine -> fumigate for TCA cycle
Symptoms:
1. Urine turns black when exposed to air
2. Black/blue face/skin
3. Ochronotic arthropathy = pigmented cartilage

37
Q

Describe how stimulants work for ADHD

A

Release more NE + D @ prefrontal cortex
Yes it is weird that a drop in NT causes hyperactivity but think: this is because these NT should also mediate concentration

38
Q

Explain mechanism by which brown fat generates body heat

A

Uncouple ETC + ATP production
H+ pumped out by ETC - back into matrix via protein thermogenin
Instead E is dissipated as heat

39
Q

Name a drug and a food that can induce oxidative stress in G6PD def

A

Fava bens
TMP SMX (dapsone)
Also think DKA, infection

40
Q

needed to harm equation

A

= 1/AR

= 1 / (a/a+b) - (c/c+d)

41
Q

Which drugs are you worried about with coronary steal?

A

Selective coronary artery vasodilators - don’t use post MI

  1. Adenosine
  2. Dipryridamole
42
Q

Explain amanita phalloides mushroom poisoning

  1. Mechanism
  2. Symptoms
  3. Dx test
A

Liver gets concentrated with amatoxin
Binds DNA dep RNA pol type 2 -> X mRNA syn -> hepatocyte apoptosis
Watery, copious diarrhea
Test urine for alpha manitin

43
Q

What is the difference between aspiration pna and pneumonitis? Discuss cause + presentation

A

Pna: oral cavity bugs (fuso, pepto, bacteroides) - DAYS after asp event
Pneumonitis: stomach bugs (HPylori) - HRS after asp event, treat supportively

44
Q

Name the types of neurons found in

  1. Striatum
  2. Locus ceruleus
  3. Nucleus baseless of Meynert
  4. Red nucleus
  5. Substantia nigra
  6. Raphi nucleus
A
  1. Caudate nucleus + putamen = striatum = motor activities; HUNTINGTONS lose Ach + GABA neurons @ striatium
  2. Locus ceruleus = NE for fight/flight
  3. Nucleus basalis of Meynert - Ach neurons; Alzheimer’s decrease Ach here
  4. Red nucleus @ ant midbrain, motor coordination of UE
  5. Substania nigra = dopamine neurons, Parkinsons
  6. Raphi nucleus - serotonin neurons
45
Q

What should you be thinking with a patient who is vomiting, tachypnic + high NH4 blood and orotic acid in urine?

A

Ornithine transcarbamylase def

46
Q

You know Huntington’s is a trinucleodtide repeat disease in the huntingtin gene - but:

  1. What is the repeat + chromosome
  2. What is the effect of this mutation on neurons
A

CAG @ chr 4

Histone de-acetylation = DNA tighter = can’t code for neuro protective genes -> neuron death

47
Q

What is the role of mull inhibiting factor vs T vs DHT in male development?

A

MIF = from stroll cells so that internal female genital regresses
T = from Leydig cells, make internal sex organs
DHT - external make sex organs

48
Q

Describe Epstein’s anomaly and the teratogenic med that can cause it

A

Lithium
1. “Atrialization of RV”
Move the tricuspid valve down
Decreases size RV

49
Q

Describe the structure and the type of injury that would aggravate it

  1. Ansernine bursa
  2. Gastroc/semi membranous bursa
  3. Supra patellar bursa
  4. Pre patellar bursa
A
  1. Anserine bursitis - (pes anserine) distal medial knee pain, obesity or athlete overuse
  2. Popliteal cyst = Baker cyst = gastrocnemius or semi-membranous bursae, OA or inflam disease that pushes synovial fluid out ofhte joint into this bursa
  3. Supra-patellar bursa = distal femur/quads, repeated quads activity (running) or direct trauma
  4. Repeated keeling
50
Q

Which CNS cell will undergo hyperplasia before making a scar after irreversible neuron damage?

A 
Glia = astrocytes 
Neuroectoderm origins, contain GFAP
1. Repair
2. Structural support 
3. BBB
4. Metabolic
51
Q

Describe where these are and what kind of injury could occur to each:

  1. Deltoid ligament
  2. Tib fib lig
  3. Ant talo-fib ligament
A
  1. Deltoid ligament - forced foot EVERSION but even then uncommon b/c so strong, harsh eversion more likely to see medial malleolus frx
  2. Tib-fib ligament can be sprained but would present w/o major swelling, instead general instability + tenderness at that pt
  3. Anterior talo-fibular ligament = sprained ankle
52
Q

What part of the muscle cellular architecture allows for uniform, all at once muscle contraction? Aka if you didn’t have these you would get uncoordinated myofibril contractions

A

T Tubules = extension of normal phospholipid bilayer w voltage gated DHP Ca channels
Triad = T-tub + A band + I band
Fxn = transmit deploy from membrane to the SR

53
Q

If you were doing a thyroidectomy and your patient had the complication of a low, harsh voice - what happened during the surgery?

A

You cut the ext laryngeal nerve to circothyroid -> now tense vocal cords
INT laryngeal nerve = afferent cough reflex = damaged if you get food stuck in piriform recess
Vs all other arytenoid muscles innervated by L recurrent laryngeal nerve

54
Q

Pseudo gout doesn’t have uric acid crystals - that’s gout. Describe pseudo gout crystals

A

INTRACELL Ca pyrophosphate crystals

Blue in parallel light, yellow in perpendicular

55
Q

What type of enzyme is telomerase?

A

RT
+ TTAGGG to 3’ end
Once you burn through this know time for that cell to die

56
Q

Cheyne Stokes breathing is seen in CHF - describe what it is

A

Period of no breathing causes drop O2 sats - must hypervent to make up for it
Then cycle restarts
No chest movement at the same time as no airflow means the 2 are still paired

57
Q

Name stain for crypto meningitis vs pna

A

Pna: mucicarmine
Meningitis: India ink

58
Q

What disease would cause 1 bout of vertigo vs recurrent?

A

Recurrent w/ change head position = benign paroxysmal positional vertigo b/c otoliths in the semicircular canals
Recurrent w/ ear ringing = Meniere disease = increase vol endolymph in inner ear
1 = vestibular neuritis

59
Q

What is the antidote for serotonin syndrome?

A

Cyrophetadine = S R antag
SS - excess S (take MAO I + SSRI)
Clonus, hyperR, HTN, confusion

60
Q

Cause of inherited vs acquired angioedema

A

Cong = C1 esterase def
Aqu = ACE I
Don’t use ACE I for adult pts w/ C1 ext def

61
Q

Presentation of aldose B def

A

Baby/kid vomiting + HYPOG after adding in normal foods

Fructose intol

62
Q

Stat + formulate for “probably pt truly does not have positive test”

A

NPV = d/c+d

63
Q

Where is the obstruction located for meconium ileus (CF) vs Hirschsprung

A

Meconium -> ileum

Hirsch -> recto sigmoid colon, + squirt signs aka rectal exam provokes forceful poop

64
Q

Name the fxn of each nerve

  1. Lingual
  2. Maxillary
  3. Phrenic
  4. Recurrent laryngeal
  5. Hypoglossal
A
  1. Lingual nerve - off trigeminal, sensory to tongue
  2. Maxillary nerve - off trigeminal, sensation to mid-face
  3. Phrenic nerve - diaphragm, refers pain to shoulder (C5) or trap ridge (C3,4)
  4. Recurrent laryngeal nerve - vocal cords
  5. Hypoglossal innervates tongue
65
Q

Explain mechanism of each for asthma treatment:

  1. Cromylin, nedocromil
  2. Omalizumab
  3. Zleuton
A

C + N: Xgranule release -> stabilize mast cells, asthma prophylaxis (seasonal triggers, exercise)
Omal - binds IgE so can’t cross link to activate mast cell
Zleuton - X lipo-oxygenase block effects of AA released from activated mast cells

66
Q

Nickel exposure increases your risk of:

A

Nasal + lung cancer

67
Q

What are CGD pts at high risk of infection with? Vs MPO def pts?

A

CGD = X NADPH oxidase (O2 => O2-) cat+ bugs: burkholderia cepacia serratia, nocardia, pseudomonas
NBT test doesn’t turn blue (abnormal)
MPO = candida infections
NBT turns blue (norm)

68
Q

What is the ductus venosus?

A

Umbilical art = high O2

Merges with IVC

69
Q

What viruses does ether target?

A

Inactivates enveloped viruses -> makes no longer infectious

70
Q

What is the drug that reduced nicotine cravings and makes smoking less pleasurable? Mechanism

A

Varenicline = partial n ACh R agonist

Less stim of downstream dopamine reward pathways

71
Q

Why is ESR an indication of inflammation?

A

APRs induced by neutrophils and macrophages

APR includes fibrinogen which causes RBCs to form Rouleaux formations -> faster sedimentation rates

72
Q

Attributable risk % in the exposed

A

Excess risk in an exposed pop that can be explained by the exposure to a risk factor
ARPe = 100 (RR-1)/R

73
Q

Describe acyl coA dehydrogenase def

A

Impaired FA oxidation => hypoketotic hypoG
FA undergo B ox -> FADH2 + NADH -> ATP prod + ACoA for the citric acid cycle + ketone bodies
Deficient enzyme = can’t use FA as E source
“1. Same presentation with Carnitine def - means can’t get FA into mito to undergo B ox, wouldn’t have to chose bet these 2 answers
2. Acetyl CoA carbox = 1st step FA SYNTHESIS aka not active during fast when breaking down
3. Acid alpha glucosidase // G-6-phosphatase // glycogen phosphorylase => gluconeogenesis “

74
Q

Med to use acutely for subarach hemm

A

Nimodipine = Ca CB to stop vasospasm

75
Q

Describe difference between
Frameshift
Missense
Nonsense mutations

A 
Frameshift = +/-
Missense = wrong AA in
Nonsense = single base *substitution* = new stop 
UAG
UAA
UGA
76
Q

SLE pts are at higher risk for what complications due to having anti-phospholipid Abs

A

Will also have false + rapid plasma reagin test

  1. Thrombo-emb duh… you know SLE is a hyper coat state
  2. RECURRENT PREG LOSS (no mechanism)
77
Q

Describe hyperPT findings vs osteoperosis

A

HyperPT
1. SUB-PERIOSTEAL resportion (@fingers)
2. Salt + pepper skull
3. Cysts in long bones = osteitis fibrosa cystica
Osteroperosis = traveler thinning with fewer interconnections

78
Q

Describe symptoms if you damage

  1. Basal pons
  2. Caudate nucleus
  3. Frontal cortex
  4. Int capsule
A

“Damage to:

  1. Base pons - contralat weakness + ataxia
  2. Caudate nucleus - behav changes, speech/lang change, movement changes
  3. Frontal cortex - social dishinhibition
  4. Int capsule - motor”
79
Q

Describe a thalamic stroke

A

R side sensory only stroke = THALAMIC STROKE
“VPL = input from spinothalamic tract + dorsal columns
VPM = input from trigeminal, projects to cortex via thalmaocortical fibers
Damage here -> complete CONTRA sensore loss
Aka sensory info gets here but doesn’t make it to the cortex to be understood/received”

80
Q

Which heart defect do you feel bounding peripheral pulses and a palpable apical thrill?

A

PDA - continuous machine like murmur alone L infraclavicular/L upper sternal border
Makes sense - think of where the problem is! High up connection pulm art + aorta

81
Q

Drug drug ints with St John’s Wart

A

“Induces cP450
Mean warfarin doesn’t work as well b/c metab too quickly -> inadequate coag”
“Inducers: carbamazepine, barbituates, phenytoin, rifampin, modafinil, cyclophos
Inhibitors: amiodarone, cimetidine, flueoro, azloes, GRAPEFRUIT JUICE, isoniazid, ritonavir”

82
Q

If you block a ureter resulting in hydronephrosis, what happens to GFR and FF?

A

Pressure from excess urine transmitted back to glomerulus - P pushing back against filtration pressure = drop GFR => drops FF

83
Q

What structures arise from the metanephric mesoderm vs ureteric bud

A

MM: Gives rise to DCTs, glomeruli, Bowman’s, PCT, loop

Uretric bud => collecting system: collecting ducts, major + minor calyces, renal pelvis, ureters

LCK STEP (27 decks)

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