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LCK STEP > Week 3 UWORLD Qs > Flashcards

Week 3 UWORLD Qs Flashcards

1
Q

Describe the difference between CRC associated with Lynch syndrome vs FAP?

A

Lynch - inherited defect DNA mismatch repair genes (MSH, MLH, PMS)
Be on the lookout for relatives for GYN + CR cancers (adenocarcinoma CRC)
FAP - APC gene mutation so likely to develop tumors by adenoma-carcinoma sequence, will present with MANY polyps
APC mutation is also most common mutation in sporadic colon cancers

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2
Q

What kind of tumor are you thinking + what are the risk factors:
Weight loss, anorexia - 3 mos
Jaundice, dark urine, pale stools
Enlarged GB, non-tender

A

You were thinking porcelain GB but NO - is pancreatic cancer @ head causing back up of bile into the GB distending it
It’s not a horrible idea b/c porcelain are not painful, but no h/o recurrent GB infections here like you’d need (chronic cholecystits)
RF pancreatic cancer:
1. Age - old people
2. Smoking!!!!
3. Chronic pancreatitis (think 20 yrs) associated with h/o alcoholism
4. Diabetes
5. Genetics: MEN1 (ant pit, paraT, pancreas)

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3
Q

Name the 2 main causes of acute pancreatitis and other clues that would tip you off to this dx

A
  1. Gall stones - see stones on scans, jaundice
  2. Alcohol - 2 AST > ALT, macrocytic RBC (even if not anemic)
    Possible EFFECTS of acute pancreatitis
  3. HypoCa if Ca deposits on necrotic tissue that was self digested
  4. HyperG if islets got destroyed
  5. HyperNa due to acute pancreatitis induced hypovol
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4
Q

What is the difference between biliary atresia and Gilbert syndrome?

A

Biliary atresia = normal bile duct at birth that gets obliterated, baby w/ jaundice, dark urine, pale stool
*Hepatomegaly that would show liver fibrosis and intrahepatic duct profile if biopsied, urgent treat to prevent progression to cirrhosis
Gilbert syndrome = less UDP glucuronosyltransferase than normal to conjugated BR but generally no symptoms - see small increase BR in blood w/ stress
Don’t confuse with Crippler Najjar which has NO UDP enzyme so babies present with jaundice too - but this is fatal b/c will deposit in brain (ketonicturus)

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5
Q

2 enzymes reflect biliary injury

A

Alk phos

GGT = gamma glytamyl transpeptidase

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6
Q

What 3 measures determine cirrhosis prognosis

A

Albumin
BR (but not all phos or GGT)
PT

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7
Q

3 major complications of UC

A
  1. Toxic megacolon - XR is best for colonic dilation (NO barium enema or colonoscopy b/c higher risk to perf thin wall of dilated bowel)
  2. Fulminant colitis
  3. Perforation
    Do contrast CT for obstructions
    Do US for kidney stones and free fluid aka blood w/ trauma (FAST exam)
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8
Q

If a patient presents with pain w/ swallowing but no dysphagia, what esophageal path are you thinking?

A

ULCER

Vs dysphagia think stricture (+obstruction) or Barrett’s metaplasia w/ chronic GERD (weight loss b/c cancer)

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9
Q

What are the 2 watershed areas of the colon/

A

Splenic flexure - between SMA + IMA supplied by marginal artery
Recto-sigmoid jxn - between sigmoid artery (SMA) and superior rectal artery (int iliac)

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10
Q

Describe histo for the esophagus with:
Changes due GERD
Adenocarcinoma (Barrett’s)
SCC

A

GERD - longer papillae, basal cell hypertrophy, intraepi eosinophils
Barretts - look for GOBLET cells (intestinal metaplasia)
SCC - keratin pearls + no intercell bridges

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11
Q

Who gets Cdiff?

A

People on ANTIBIOTICS - esp those in hospital b/c more likely to exposed
This is because normal GI flora prevents infection
Why you don’t see any IC canes in sketch

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12
Q

Which disease has the IgA vs tissue transglutaminase, endomysial, and deamidated gladden peptide? Where do you see it specifically, what are other symptoms?

A

Celiac - HLA DQ 2, 8
Screen w/ IgA test or d-xylose test - are things gets absorbed in the prox SI
Confirm with duodenum (some jejunum) biopsy
Dermatitis herpetiformis - IgA vs tips of dermal papillae, looks ulcerative on skin

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13
Q

Name the symptoms and possible causes of vit A def

A

Need vit A for vision + cell differentiation
Symptoms: night blind, dry skin (SE of using retinoid face creams)
Causes
1. Pancreatic insuff - A is fat sol it
2. Intestinal mal absorb
3. Biliary disorder = PRIMARY BILIARY CIRRHOSIS
AI destroy intra-hepatic bile ducts (+ANA)
- Vit A def b/c no bile to emulsify fat for absorption
- PRURITIS b/c build up BR
- Xanthomas
- High alk phos (bile problem) + cholesterol in blood

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14
Q

What is the presentation and patho of familial hypercholesterolemia

A

AD mutate LDL R
Most effects b/c liver can’t use this R well to remove LDL + IDL
See atherosclerosis at v/ young age

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15
Q

You know RAS as a TF. Explain how RAS exists in cells, gets activated, and works

A 
RAS = protein
Exists in cytoplasm
Inactive: RAS + GDP
Active: RAS + GTP
Something binds cell TK -> activates RAS -> activates MAPK mitogen activated protein kinase = what goes into nucleus to change gene transcription
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16
Q

What is Wilson’s disease

A

Can’t excrete Cu into bile (excretion)/blood (transport)
AR (chr 13) mutate Cu transporting ATPase -> accumulates in TISSUES and damges via free rad prod
Lover
Brain - neuro + psych disease
Eyes - Kayser Fleisher rings
Renal - Fanconi syndrome (increase U Cu)

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17
Q

Describe the presentation and treatment of arsenic poisoning

A

Mechanism: X cell resp (X pyruvate deH)
Sources: insecticide, well water, pressure treated wood
Acute symp: garlic breath, QT prolong, watery diarrhea, vomit
Chronic symp: hypo/hyperpigment, stocking/glove neuropathy
+ DIMERCAPROL - pee out metals
Or DMSA

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18
Q 
Describe what you use each anti-dote for
CaNa2 EDTA
Deferoxamine
Hydroxycobalamin
Methylene blue
A
  1. Acute lead poisoning - urine excretion - constipation, anemia, irritability, confusion
  2. Fe OD due to multiple transfusions - urine excretion
  3. Cyanide poisoning - cherry red skin - urine excretion
  4. Anti-freeze (methemoglobinemia) - use as artificial e- transporter to reduce methemoglobin in NADPH pathway - gray/blue skin, SOB, chocolate colored blood
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19
Q

Describe Dubin Johnson syndrome

A

You can conj BR - but you can’t get it out of hepatocytes
Asymptomatic - decreased excretion BR glucuronides
+ Stress see increase direct = conj BR
BLACK LIVER incidental finding

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20
Q

What does the D-xylose test tell you?

A

SI absorptive fxn index of pancreatic fun

Since this molecule should be absorbed directly

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21
Q

Explain mechanism of HMG CoA reductase

A

X cholesterol synthesis = decrease levels cholesterol @ liver
Upreg LDL R -> take more LDL/IDL out of circulation to get the cholesterol you need to do things in the liver

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22
Q

Explain mechanism of cholestyramine

A

= bile acid binder aka don’t let them be reabsorbed so now have to use more cholesterol to make new ones
Therefore you much increase hepatic cholesterol synthesis

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23
Q

Describe symptoms, people at risk, and effects of riboflavin def

A

= Vit B2 = FAD
Alcoholics, malnourished
Needed for ETC (complex 2 in ETC = succinate dehydrogenase [also TCA enzyme])
Cheilosis = inflam lips, scaling at corners mouth
Corneal vasculaization

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24
Q

Describe presentation of peau d’orange

A

Red, itchy breast
Can see axilla lymphadenopathy
Cancerous cell obstruct lymphatics

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25
Q

Describe the process of making and the significance of Barr bodies

A

“Condensed body of heaving methylated DNA”
Embryo: X inactivation = lyonization
Each cell suppress either mom or dad X - mosaic pattern of which one is suppressed means X recessive carriers don’t have symptoms
Barr body = heterochromatin @ periphery of nucleus
1. Hyper meth DNA
2. DE acetylated histones
Aka low (not no) transcriptional activity

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26
Q

Describe mechanism + use of proteasome Is

A

Bortezomib
Proteosome = protein breakdown/recycle
Mechanism = boronic acid dipeptide @ proteasome catalytic site => cause cell apoptosis
Use for multiple myeloma b/c plasma cells v sensitive due to constant protein production (Ig)
Recognize MM: low back pain (bone pain), hyperCa, anemia, high creatinine (kidney disease)

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27
Q

How does HIV become resistant to the normal HAART regimen?

A

Mutations to POL
Change proteases - protease I resistance
Change RT - N and nonNRT Is
Vs env mutations allow escape neutralizing Abs
Vs high intrinsic mutation rate - cell mediate immune responses don’t work vs HIV

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28
Q

Describe when you use fibrinolytics for MI and the CIs to doing so

A 
Fibrin specific fibrinolytics only cleave recently formed clot w/o systemic activation (tPA, reteplase)
Vs non-fibrin specific streptokinase
Use WITHIN 6 HRS STEMI
CI
1. Hemm stroke
2. Ischemic stroke within 1 yr
2. BP > 180/110
Dissecting aneurysm + active internal bleeding
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29
Q

Name the LNs these structures drain to

  1. Bladder dome
  2. Lateral lobe prostate
  3. Orifice anal canal
  4. Upper pole testes
  5. Upper 1/3 rectum
A
  1. Superior bladder -> external iliac (vs inferior portion pladder -> internal iliac)
  2. Prostate -> internal iliac (mainly) also ext iliac and sacral
  3. Anal canal BELOW dentate line -> inf rectal nodes -> superficial inguinal nodes
    *Sup inguinal LNs drain all CUTANEOUS lymph from the belly button down including scrotum
    Exception: testes, glans penis (deep inguinal), skin of post CALF
  4. Testes -> para aortic LNs
  5. Above dentate line -> inf mesenteric LNs
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30
Q

Why do we keep increasing ionizing radiation doses with each treatment?

A

B/c initial dose = plateau
Higher dose + more treatments -> more dsDNA breaks + ROS -> cancer cell survival drops dramatically
As does normal actively replication cells
Vs UV radiation = mades prymidine dimers

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31
Q

Describe RNA interference

A

Changes mRNA TRANSLATION
+non-coding RNA (siRNA or miRNA) to cause post-transcription gene silencing
miRNA -> nucleus to make ds precursor -> out to cytoplasm -> cleave into RNA helix via dicer -> individual strands separated + incorporated into RNA induced silencing complex
Uses miRNA to bind complementary seq on target mRNA

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32
Q

What is HgF’s relationship to 2,3 BPG?

A

Binds BPG with lower affinity that normal B globin
Good in a fetus b/c binds O2 more tightly than mom’s Hg so can take the O2 @ placental transfer
Hg S - reduced O2 affinity
Hg H (alpha thal -> Beta tetramers) - higher O2 affinity
Hg C - no change
Hg A1c - reduced 2,3 BPG affinity but due to methylation (not replacing AA in the binding site like Hg F)

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33
Q

Where is heme made in cells

A

Mitochondria + cytoplasm

@ Bone marrow + liver via RBC precursors

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34
Q

How do Gardos channel blockers help sickle cell patients

A

Sickle cell treatment

  1. Hydroxyurea increase HgF
  2. Gardos channel blockers X K + H2O efflux -> prevent dehydration so less change sickle (polymerize Hb S)
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35
Q

Mechanism and rescue treatment for MTX

A

MTX - DHF reductase - no THF for purine synthesis in rapidly dividing cells
Rescue w/ leucovorin (foilinic acid) = reduced folic acid that does NOT require DHF-R
Often adding together to rescue cells normally hit by MTX toxicity
Remember, leucovorin potentiates 5-FU (X thymidylate synthase) - making more portent treatment for CRC

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36
Q

What accumulates in cells due to MTX use

A

X DHF reductase so precursors build up in cells: folic acid + DHF polyglutamate (aka recycled)
MTX is brought into cells and polyglutamated to keep it in cells - same with folate and recycled DHF
Think about this in the context of using MTX for ectopic preg

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37
Q

Name + describe mechanism of integrase Is for HIV

A

Raltegravir
X HIV dsDNA from integrating into host chromosomes
Vs protease Is = ritonavir, saquinavir = X cleavage of polyprotein precursor into fxnal proteins
Vs fusion Is = enfuvirtide = bind gp41
Vs RT Is = efavirenz, tenofavir, lamivudine
Vs CCR5 antag = maraviroc

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38
Q

Describe 5 steps of T cell maturation

A

Double neg (no CD4/8) = pro-T cells arrive @ thymus
TCR rearragement
1. Rearrange b chain = both CD4 + CD8 expressed = double positive T cells (immature T cells)
2. Rearrange a chain
3. Positive selection @ cortex - do you work vs antigen
4. Negative selection @ medulla - do you recognize self
5. Lose either 4 or 8

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39
Q

Mechanism etoposide

A

Major uses: testicular cancer + small cell lung cancer
X topo 2 -> can’t seal the ds DNA breaks it induces -> breaks accum -> cell death
Topo 2 induces dsDNA breaks to relieve both positive and negative supercoiling
Same idea = podophyllin - use for genital warts
Vs topo 1 - ss nicks to relieve negative supercoil (drugs here are irinotecan and topotecan)

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40
Q

What is released during placental abruption that cause cause maternal DIC

A

Tissue factor = thromboplastin
- Hypertension may have cause the abruption
Also DIC w acute fatty liver of pregnancy but presents w/ N/V, ab pain, elevated liver enzymes
Can also get DIC from amniotic fluid emoblism but this is seen with hypotension and cardiogenic shock

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41
Q

Difference between unfract and LMW heparin

A

Unfract - can bind antithrombin 3 + F10a or AT3 + thrombin

LMW - binds only AT3 + 10a

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42
Q

Yeah sure cancer can met to the adrenals, but how would this present

A

Asymptomatic or w/ adrenal INSUFF

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43
Q

What is the fusion product in non small cell lung cancer vs CML

A

NSSLC = EML4-ALK fusion, active TK -> malignancy, treat with TK I = crizotinib
CML t 9,22 = philadephila = Bcr-Abl fusion = TK activity causes profile granulocyte precursors, treat with TK I = imatinib

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44
Q

Describe changes to carboxyHgb, PaO2, and methemoglobin w/ CO poisoning

A

Normal PaO2 = O2 dissolved in blood doesn’t change unless vent/prof changes
Increase carboxyHgb = CO bd Hgb = INCREASES makes sense b/c Co binds Hgb with greater affinity than O2
No change methemoglobin - does not cause precipitation (when Fe2+ -> Fe3+, changes w/ drug exposure, enzyme def, hemoglobinopathies)

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45
Q

Which is a DNA vs RNA virus: Hep B vs C

A 
B = RNA - incorporates into host genome so risk HCC stays high even after infectivity ceases/liver damage tapers off as you develop anti-viral Abs
C = DNA - no RT, won't integrate into host genome
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46
Q

Explain why a person with B thal trait may have skewed diabetic control via HbA1c

A

B thal trait - B globin underproduced -> decreased Hgb A (2a,2b) and increase HgA2 (2a,2d)
HbA1c is talking and HgA NOT A2
Therefore less A to begin with will skew your readings if you are a diabetic

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47
Q

Pt has megaloblastic anemia - describe what happens if you start B12 or folate supplement

A

Start folate -> still have symptoms or develop new ones (neuro) then it was actually b/c B12 def
Treating B12 def /w folate will worsen demyelination by depleting [unmethylated cobalamin] for MM CoA processing

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48
Q

Describe PCR

A

Goal = amplify small DNA fragments
You need to know DNA segments flanking your target region to make the primers to start PCR
The target region doesn’t need to be known b/c may be mutated - that’s one of the reasons your doing PCR
+thermo stable DNA pol to repl DNA template from supplied pool of DNA bases
1. Denature via heat
2. Anneal - primers combine w/ ss or target region
3. Elongation - DNA pol forms new daughter DNA strands 5 -> 3 prime starting from 3’ end

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49
Q

Effects of adding TMP/SMX to ganciclovir

A

Gan SE = neutropenia, anemia, TCP, etc
For CMV infections in advanced HIV
TMP/SMX xs formation THF acid for purine/pyrmidine synthesis SE = bone marrow suppression
Together even higher risk bone marrow suppression (neutropenia)
Another one you’d want to watch in this scenario = zidovudine

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50
Q

What is heteroplasmy

A

= coexistence of distinct versions of mitochondrial genomes in 1 cell
Each cell has many mitochondria - each mitochondria has own DNA (you know that)
Varies the expression of mitochondrial diseases
Vs mosaicism = 2+ cells ones w/ unique nuclear genome in the same person

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51
Q

Describe inherited mitochondrial encephalopathy

A

Mito disease therefore

  1. Lactic acidosis - mito should do ox phos but here don’t have enough fxning mito
  2. Ragged skeletal muscle fibers - makes sense, mito dense tissues are muscle + neuro
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52
Q

What is one of the main differences in COX 1 and 2 besides their function?

A

COX 1 = constitutively expressed

COX 2 = induced by inflammatory states to release PGs

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53
Q

Mutation and presentation of alkaptonuria

A

Mutation in tyrosine breakdown to products for the TCA cycle
X homogentisic acid dioxygenase - build up homogentisate at:
1. Joints - darkening of articular cartilage
2. Deposits in eye: blue black spots in eye
3. Urine goes black on standing

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54
Q 
Motor and sensory innervation of 
Tibial nerve 
Femoral n
Superficial fibular nerve
Deep fibular nerve
A

T: plantarflex, invert ankle, toe flex, sense plantar foot
*Prox injury to this nerve presents as dorsiflex + eversion w/ sensory loss, distal injury @ tarsal tunnel may be just sensory loss
F: hip flex, knee extend, sensory to medial thigh + ant knee + medial calf
SF: eversion, lateral calf + lat dorsal foot
DF: dorsiflex, extend toes, sensory to area between big toe and 2nd toe
Common tibial - think wrapping around fibular head

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55
Q

Describe presentation of parvoB19 in kids vs adults

A 
Kids = 5th disease = erythema infectiosum = bright red rash in circle on cheeks
Adults = acute arthritis in multiple joints that resolves on own
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56
Q

Depolarizing vs non-depol NMJ block

A

Non-depol = vecuronium = compete for post synpatic ACh R, train of four shows fading as less ACh is released with each impulse
Depol = SCh
Phase 1: TOF shows equal in all 4 twitches b/c presynaptic ACh R stim helps mobilize presynaptic ACh vesicle release
Phase 2: Persistant SCh exposure causes ACh R to become desensitized//inactivated (aka basically same as non deploy block)

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57
Q

Match up: ACL/PCL insertions on medial/lateral femoral epicondyle

A

ACL onto lat

PCL onto med

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58
Q

2 factors required for osteoclast differentiation vs osteoblast

A

M-CSF macrophage colony stim factor
RANK L = receptor for activated nuclear factor kappa B ligand
vs
Fibroblast growth factor

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59
Q

Mutation and presentation of McCune Albright Syndrome

A

Gs receptor mutation in alpha subunit -> always on adenylate cyclase

  1. Cafe au last spots - melanin production
  2. Endocrine problems: hyperT, early puberty
  3. Fibrous dysplasia - IL 6 production + osteoclast activation = many lesions throughout bone
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60
Q

What is Legg Calve Perthes disease? NF1?

A 
LCP = idiopathic osteonec of hip in KIDS
NF1 = cafe au lait, neurofibromas, tibial bowing // pseudoarthosis
61
Q

“-Dronate” drugs are for what disease? What are they analogs of?

A

= bisphosphonates
Osteoporosis etc
Pyrophosphate analogs

62
Q

Describe the 3 phases of symptoms and treatment for Lyme disease

A

Borrelia burgdorferi
Early local = target rash (erythema chonicum migrans)
Early disseminated = CNS involve (facial palsy) or cardiac involve (heart block)
Late
1. Asymmetric arthritis (knee, swelling + pain)
2. Encephalopathy - decrease memory, more sleepy, mood changes
Treat: doxycycline or ceftriaxone

63
Q

2 diuretics that effects Ca

A

Loop - more Ca excretion

Thiazide - more Ca reabsorbed

64
Q

Histo giant cell arteritis

A 
SCATTERED granulomatous inflam 
Intimal thickening 
Elastic lamina fragmentation 
Giant cells (w/o granuloma)
IL 6 production from lymphocytes (mostly CD4 T cells) correlates with disease severity - why use toclizumab = Av vs IL 6
65
Q

Describe the lab findings for SLE

A

Anemia, leukopenia, TCP
ANA -> anti dsDNA or antiSM (snRNP)
Low complement C3/4

66
Q

What is the Ab for RA? For 1ary biliary cirrhosis?

A

RA: anti cyclic citrullinated peptide Abs
PBC: anti mito Ab

67
Q

Name the contents of the 4 pharyngeal pouches in embryo

A
  1. Epithelium of middle ear + auditory tube
    Pharyngeal membrane here becomes tympanic membrane
    Pharyngeal groove here becomes epi of ext ear canal
  2. Epi of palatine tonsil crypts
  3. Thymus, inf paraT
  4. Sup paraT
68
Q

What connects osteocytes

A

Gap jxns in Haversian system

69
Q

What infection is associated with polyarteritis nodosa

A 
Hep V
Biopsy shows TRANSMURAL inflam
Symptoms
1. Renal - GN, HTN
2. Nervous - peripheral neuropathy, mononeuritis
3. GI - bowel ischemia/infarct
4. MSK - myositis, arthritis 
cANCA med/small artery disease of any organ (EXCEPT lung)
70
Q

Supracondylar frx will impair what nerve

A

Anterolat displacement - RADIAL nerve

Anteromedial displacement - median nerve

71
Q

By what mechanism can a large blood transfusion cause hypoCa vs hyperK

A

HypoCa: citrate anti-coag is a preservative added, can chelate Ca already in pts blood
HyperK: stored RBC gradually lose K to plasma

72
Q

Inheritance pattern hemophilia + probability that a 50% chance carrier will have kid with it

A

X linked recessive
1/2 chance carrier
1/2 chance female carrier will pass down the mutated vs normal X
1/2 chance she’ll have a boy = only sex that can be effected by X R

73
Q

Mechanism, presentation, inheritance, treatment of acute intermittent porphyria

A 
AD X porphobilinogen deaminase 
Porphobilinogen (PBG) and ALA build up
5 Ps = symptoms
1. Pain ab
2. Port wine urine
3. Polyneuropathy
4. Psychological disturbances 
5. Precipitated by CYP 45- inducers, alc, starvation *often times the mutation alone isn't enough to create porphyria attack, need the med too*
Treat by decreasing ALAS = enzyme that starts the entire heme synthesis pathway
Via glucose or hemin
74
Q

Difference between tamoxifen and raloxifene

A

Ralox
1. Antag at breast + uterus
2. Agonist at bone = continue benefits of E at bone to prevent osteoporosis
Tamox
1. Antag @ breast
2. Agonist at bone AND endometrium - no bone protective effects, increase risk ENDO HYPERPLASIA + CANCER

75
Q

What is the difference in structure and fxn of golgi tendon organ vs muscle spindles

A

GTO connected in SERIES w/ contracting (extrafusal muscle fibers)
- Goal = prevent muscle damage (sudden relax when you’re holding weight too heavy)
- Afferent: 1b sensory - changes in muscle lengths when there is TENSION (contracting)
- Connect to inhibitor interneuron @ spinal cord
- Alpha motor neurons back
GTO don’t sense muscle length b/c lengthen happens in muscle fibers not tendon
Muscle spindles (intrafusal) connected in parallel with extrafusal
- Goal = sense changes in length aka stretch reflex
- Afferent = groups 1a + 2
- Direct synapse onto alpha motor neuron
- When muscle stretched, contraction induced by reflex resists that stretch

76
Q 
Describe problem and presentation of
SCID
DiGeorge
CVID
Wiskott Aldrich
X L Agamma
A

SCID = ADA def, cytokine R defect -> no T or B cells +/- no thymus, bact + viral infect, chronic diarrhea, cutaneous candida (bubble boy)
DiGeorge = 22q11 delete, X T cells or PT -> craniofacial, heart problems, hypoCa
CVID = low Ab due to B or CD 4 T cells
1. Bact 2. Enterov 3. Giardia infections + increased risk AI + lymphoma
XL AG = B TK mut, no Ig same 3 infections
WA = X linked WASP gene, triad: TCP (easy bleed), eczema, infection (worsen w/ age)

77
Q

Name bugs that cause diarrhea w/

  1. RBC + some WBC
  2. WBC - mainly eos
  3. WBC - mainly monocytes
  4. WBC - mainly neutrophils
A
  1. Invasive aka bloody diarrhea: Ecoli, Campy, Salmonella, Shigella (EHEC is blood w/o WBC b/c toxin mediated)
  2. Intestinal parasites if Charcot Leyden crystals
    Diarrhea w/ peripheral eos: Strong, Ancylo, Ascaris, Toxocara, Trichinella
  3. Salmonella via typhoid fever
  4. Dysentery/inflam diarrhea: Shigella, Salmonella, Camp
78
Q

Which area is damaged if you have word salad?

A

Wernicke: meaningless but able to talk

Vs Broca’s aphasia

79
Q

Mutation for early vs late Alzheimer’s

A 
Early
1. APP - chr 21
2. Presilin 1 - chr 14
2. PResilin 2 - chr 1
Late: apolipo E4
80
Q

Equation for t1/2, MD, LD

A 
t1/2 = (Vd X 0.7) / Cl
LD = target [plasma] X Vd / bioavail
MD = target [plasma] x Cl x time bet doses / bioavail
81
Q

2 mechanisms of loop diuretics

A

FUROSEMIDE

  1. X Na/K/2Cl
  2. Increase PG release = vasodilate = increase RBF -> increase GFR
82
Q

Why does a pt w/ 1ary hyper aldo have normal Na levels?

A

Will have low K + high bicarb for known reasons
Low K = paresthesia + muscle weakness
“Aldosterone escape” - increase intra vasc volume due to Na reabsorption triggers reflex ANP release -> limits net Na retention and prevent development of overt vol overload (edema)/hyperNa

83
Q 
Describe histo changes to neurons w/ ischemic stroke at:
12-24 hrs
24-72 hrs
3-7 days
1-2 wks
> 2 wks
A

12-24 hrs: red neurons - increase eosinophilic cytoplasm + lose Nissl substance
24-72 hrs: neutrophils infiltrate
3-7 days: macrophage + microglia come in for phagocytosis
1-2 wks: reactive gliosis + vasc prolif = liquefactive necrosis
> 2 wks: glial scar = cystic area + dense glia around

84
Q

Name ovarian tumors that increase levels of:

  1. BhCG + LDH
  2. AFP
  3. E + inhibin
  4. Androgens
  5. CA 125
A

Dysgerminoma high BhCG + LDH: teens, fried egg
Endodermal sinus/yolk sac: high AFP, Schiller Duval bodies
Granuloma tumor - E + I, Call Exner bodies + coffee bean nuclei
Sertoli/Leydig - androgens = hirsutism, clitoromegaly
Epithelial cancers: serous or mucinous

85
Q

Name mechanism + SE
Statins
Fibrates: gemfibrozil, bezafibrate, fenofibrate
Bile acid resins: cholestyramine, cholestipol, colesevelam
Ezetimibe
Niacin = Vit B3

A
  1. X HMG CoA R aka can’t make mevalonte - major drop TG, drop LDL, increase HDL - myopathy + hepatitis (hepatotox)
  2. Fibrates increase LPL aka cleave fat to move it out of the blood into storage sites - really drop TGs, drop LDL, increase HDL - myopathy (WHY DON’T USE W/ STATINS, cholesterol stones)
  3. Resins block absorption bile acids at term ileum - you must use cholesterol to make more - drop LDL - maybe decrease in GI absorption (fat sol vitamins)
  4. Ezetimibe blocks absorption @ SI brush border SE GI upset
  5. Niacin blocks lipolysis/formation of VLDL - aka keep fat where it is - SE red face b/c increase PGs (+ NSAID), hyperG, hyperuricemia
86
Q

What is the disease if a female presents b/c she hasn’t had her first period and you discover she doesn’t have internal female report but instead cryptorchid testes

A

Androgen insensitivity syndrome: 46 XY but defective T receptor

87
Q

Ambiguous genitalia and salt wasting at birth makes you think what deficiency

A

21 OH def - congenital adrenal hyperplasia

88
Q

2 ways get resistance to drugs in M.TB

A
  1. Downregulate catalase peroxidase vs isoniazid

2. Alter DNA dep RNA pol vs rifampin

89
Q

What compartments do the sup fibular, deep fibular, and the tibial nerve run in the lower leg - name all 4 compartments

A

Ant, lat, deep + superficial post compartments (4)
Sup fib @ very front lat comport
Deep fib @ back of ant compartment (on the membrane between tub + fib) w/ ant tibial art + vein
- Sensory between big toe + 2nd toe
- Dorsiflexion - lose get foot drop + claw foot
Tibial nerve in back of deep post compartment w/ post tib art + vein

90
Q

What type of bond links AA in peptide chain vs holds in alpha vs beta structures

A

Peptide bonds link
H bonds form 2ary structures
Vs ionic, H, disulfide bonds and hydrophobic ints for 3ary structure

91
Q

Describe the para + sympa innervation of peeing

A

Sympa: contract internal urethral sphincter, inhibit detrusor contraction
Para: relax sphincter, contract detrusor
External urethral sphincter is mostly pelvic floor skeletal muscle and thus under vol control

92
Q

What murmur may result from dilation of the LV in response to increased preload

A

Think CHF pre-diuretics = vol overload
S3 + mitral regurg (holosystolic @ apex)
Vs perm MR murmur due to rupture chordae tendinae post MI
Vs non-acute onset with MR of endocarditis or CT disease

93
Q

Describe genital presentation of

  1. Chlamydia
  2. H.ducreyi
  3. HSV
  4. Kleb
  5. Syphillis
A
  1. Chlamydia serotypes L1-3 cause lymphogranuloma venereum: starts painless ulcers -> heal -> painful coalescing LNs (buboes), worried about these not healing causing fibrosis -> lymphatic obstruction
  2. Painful red papules -> tender ulcers, regional LNs swell
  3. Shallow ulcers, painful, heal in 10 days
  4. Painless genital papule that eventually ulcerates
  5. Painless lesion heals on own
94
Q

Describe the structures and nerves from each pharyngeal arches

A

Each pharyngeal arch has associated CN
1 - CN 5 trigeminal + maxilla, zygoma, mandible, incus, malleus + muscles of mastication
2 - CN 7 facial - styloid process temporal bone, less horn hyoid, stapes, muscles of facial expression
3 - CN 9 glossopharyngeal (problems w/ gag reflex) greater horn hyoid + stylopharyngeus
Arch 4 + 6: CN 10 vagus - larynx

95
Q

What is Treacher Collins syndrome

A

X 1 + 2 pharyngeal arches
Bones malformed
- Compromise airway and feeding problems
- Conductive hearing loss

96
Q

What is the difference between capitation, discounted fee for service, patient centered medical home and point of service health care plans?

A

Capitation - company pays pre-det fixed fee that limits which physicians you might go to, requires vary doc referred for specialists and offering services only on evidence base practice standards
Global payment - single payment to cover all associated expenses, ex: elective surg + pre and post op reqs
Fee for service - each service paid for w/ pre-arranged discounted rate
Point of service - require pts to have vary referral for specialties and can pay more to see outside docs (vs HMO)
Pt centered medical home - personal physician who sees pt through all aspects of care (captiated or fee for service)

97
Q

What lung disease can be seen with RA

A

Pulm fibrosis
Restrictive
Hear: crackles at end of inspo
Treat w/ MTX

98
Q

Mechanism of fibrates

A

Increases LPL - increased FA oxidation

X cholesterol 7 alpha OH - less bile acids made, more cholesterol into bile itself -> increases risk cholesterol stones

99
Q

What kind of transporter are the GLUT receptors

A

Carrier-mediated transporters
Do facilitated diffusion: glucose moves down concentration gradient into cell (w/o E), but GLUT changes conformation as the substrate is transported
Same idea w/ GLUT2 but now moving from high concentration in liver OUT into circulation

100
Q

Medications to treat muscle spasticity (think in relation to MS)

A
  1. Baclofen = GABA B agonist
  2. Tizanidine = alpha 2 agonist (centrally) = Gi -> IP3/DAG -> decrease cAMP
    Decrease NT release
101
Q

Describe how you generate TH peripherally

A

Most secreted at T4
Converted to T3 peripherally
T4 specifically is inactivate to rT3

102
Q

What is Guillain Barre mechanism - sure it’s ascending paralysis after infection - but HOW

A

Ab vs myelin -> segmental demyelination or peripheral nerves
Muscle weakness
Lose DTR
+ endoneural inflam infiltrate
Vs Beriberi (thiamine def) - demyelination peripheral nerves w/o perineural inflam

103
Q

Patho of DMD

A

XR mutation to dystrophin = muscle structural protein
Light micro: change in muscle fiber shape/size, regen fibers, increased CT
Fibrofatty infiltrate of calf (pseudo hypertrophy)

104
Q

Describe patho, clinical presentation, labs for dx and treatment of Wilson’s ds

A

AR ATP7B mutation -> hepatic Cu accum -> damages hepatocytes -> leak free Cu -> deposits in other tissues
Clinical
1. Change attitude, depression
2. Neuro: gait changes, tremor (Parkinsonism), dysarthria
3. Hepatic cirrhosis, acute liver fail
4. Kayser Fleischer rings
Low ceruloplasmin
More Ucu
Trt: D penicillamine (chelates Cu to make H2O sol)

105
Q

What is the coinfection with gonorrhea and why do you care?

A

B/c you’ll treat the gonorrhea w/ ceftriaxone but the patient won’t get better!
B/c you’re not treating co-infection of chlamydia - need to add PO azithromycin (doxycycline or macrolide)
And you won’t see chlamydia b/c intra cellular
Same symptoms: dysuria w/ mucopurulent discharge so always treat for both

106
Q

Describe when you would use mannitol, how it works, and SE

A

Massive osmotic diuresis when you’re worried about ICP/cerebral edema
SE: headache, N/V
Worry about excessive vol deplete -> hyperNa
*Pulm edema
So you’re pulling out a ton of water meaning plasma oncotic pressure increases - increases the fluid in the vasculature as you pull water out of tissues -> further vol expansion and can worsen pulm edema
Why don’t use osmotic diuretics in pts w/ CHF or pre-existing edema

107
Q

Define
Reassortment
Recombination
Transformation

A 
Reassortment = (genetic shift) mixing genome segments in segment viruses that infect the same host cell (flu)
Recomb = gene exchange via crossing over 2 dsDNA so progeny have recombined genomes with traits not in either parent 
Transformation = uptake naked DNA into pro/eukaryotic cell or incorporate viral DNA into host cell - alters host cell by not the progeny viruses
108
Q

Describe the PTH, Pca, P phos of a celiac pt

A

Destroy SI lumen - decrease vit D absorption (weird since you get a lot from sun anyways)
Hypophos + hypoCa -> increase PTH
PTH reabsorbs Ca from bone but the Pca stays low!!! B/c even with bone sources, PTH isn’t 100% effective w/o its action through vit D

109
Q

What is the difference in presentation between decerebrate and decorticate postures - what brain structures are damaged in each

A

Decerebrate = extensor posture
Due to lesion below red nucleus (since red nucleus activates flexors) leaving unopposed extension via vestibulospinal tract
Think @ midbrain, pons
Decorticate = flexor posture
Lesions above the red nucleus (cerebral hemisphere) b/c lose descending inhibition of red nucleus -> flexion only

110
Q

Which chamber of the heart lies on the esophagus and aorta

A

RA

RH disease causes either regurg or stenosis of the mitral valve -> RA ENLARGEMENT

111
Q

Name CYP 450 Is aka things that would increase [ ] drugs metabolized this way

A 
Cimetidine - H2 block for gastric ulcers 
Ciprofloxacin - fluoroquinolone
Erythromycin (macrolide)
Azole antifungals
Grape fruit juice
Isoniazid - TB
Ritonavir - protease I for HIV
Note: azuthromycin does NOT have sig effect on p450, if a pt have a p450 I on board you can use pravastatin for cholesterol control
**Watch out w/ phenytoin - P450 metab
112
Q

Name CYP 450 inducers

A 
Carbamazepine - anti-epilectic b/c prolong Na channel refract period
Phenobarbital 
Phenytoin
Rifampin 
Griseofulvin - anti fungal
**Watch out w/ phenytoin - P450 metab
113
Q

Mutation and presentation of Friedreich Ataxia

A

AR
GAA trinuc repeat in frataxin gene - codes for iron-sulfur enzymes in the mitochondria
Decrease mito E pro + more ox stress -> degen neural tracts + peripheral nerves
1. Gait ataxia - spinocerebellar
2. Spastic weakness - lat corticospinal tract
3. Lose position/vibration - dorsal columns, DRG
4. Kyphosis + high arches
5. Hypertrophic CM
5. Diabetes
Don’t confuse for Charcot Marie Tooth which AD demyelin peripheral nerves - leg weakness/atrophy w/ calf + foot findings

114
Q

Describe 4 ways a lacunar infarct caused by chronic HTN would present

A

Penetrating vessels supply deep structures (basal gang, pons) + subcortical white matter (int cap, corona radiate)
Small infants - may not see on first round imaging, will grow with time
1. Pure motor hemiparesis - infarct post limb of int cap or basal pons
2. Pure sensory stroke - VPL or VPM thalamus
3. Ataxia-hemiplegia syndrome - same as 1
4. Dysarthria clumsy hand syndrome - same

115
Q

Describe changes to heart with normal aging

A

Think: “smaller heart b/c stuff has gotten into the muscle including brown ish!!!”
Smaller ventricles causes sigmoid shape inter ventricular septum (really just looks hypertrophy b/c does obstruct outflow tract)
More CT due to myocardium atrophy
Accum lipofuscin = yellow brown peri-nuc cytoplasmic inclusions (wear + tear pigment)

116
Q

What cell in the alveoli have “parallel stack of membrane lamellae” - what are these and what do they do

A

Lamellar bodies that carry surfactant for exocytosis into the alveoli
T2 pneumocytes produce and recycle old surfactant
W/o surfactant - neonatal RDS

117
Q

Describe when you can use a long acting GnRH agonist + flutamide to treat prostate cancer

A

Prostate cancer = T dependent
Normally, GnRH release PULSITILE causing LH secretion from ant pit to get T from leydig cells
+ constant agonist - LH receptors on ant pit downregulated so net decrease LH - decrease T
BUT you must add med to cover the transient rise in T until the downreg happens = androgen receptor antagonist
1. Flutamide
2. Cyproterone
3. Spironolactone

118
Q

What SE would you see if you put a kid on an H1 R antag for allergies

A 
M antagonist (anti cholinergic)
Flushed cheeks = X eccrine sweat gland secretions causing fever -> comp vasodilation of skin to release heat
Dilated pupils = X pupillary constrictor + ciliary muscles
119
Q

What is the antidote for

  1. Warfarin
  2. Heparin
  3. Fibrinolytics
A
  1. Fresh frozen plasma has all coat factors - rapid, + vit K but takes time
  2. Protamine binds heparin inactivating it
  3. Aminocapric acid inhibits plasminogen activators
120
Q

Define merocrine, apocrine and holocrine exocrine secretions

A 
Holocrine = cell lyses and all contents release (skin oil glands aka acne)
Apocrine = secrete via membrane bound vesicles (mammary glands)
Merocrine = watery, exocytosis for secretion (sweat and salivary glands)
121
Q

Describe patho of migraines and treat

A

Activate trigeminal gang afferents that innervate meninges
Release substance P + calcitonin gene related peptide (CGRP) -> vasodilation w/ plasma proteins moving out of the blood -> inflam
+ Nerve fibers become more sensitized
TRIPTANS = S agonists that inhibit release of those sub P/CGRP, use to ABORT migraines
SE: cardiac events + rise BP

122
Q

Name the steps of pre and post gang synpasing in the para + sympa systems - name the NT released and the receptor it binds - plus 2 sympa exceptions

A

PARA
Long pre-gang - ACh @ N in ganglia near target
Short post - ACh @ M on target
SYMPA
Short pregang - ACh @ N in sympa chain gang
Long post - NE onto alpha/beta R at target
2 exceptions
1. Direct pre-gang synapse onto adrenal medulla to release E > NE into blood
2. Release ACh at sweat glands post gang

123
Q

Name cause of fetal hydronephrosis if

  1. Obstructive, unilat
  2. Non-obstructive, unilat
  3. Bilateral in a boy
A
  1. Kink uretro pelvic jxn (last to canalize so most common site of obstruction)
  2. Incomplete closure of vesicouretral jxn
  3. Posterior urethral valves aka obstructive, persistent urogenital membrane @ jxn of bladder + urethra
124
Q

Why is one of the SE of isoniazid peripheral neuropathy?

A

Structurally similar to B6 (pyridoxine)
1. Competes for NT synthesis -> defective products
2. Increase urine excretion of B6
Therefore supplement w/ B6

125
Q

Describe the presentation of a unilateral schwannoma forming intracranially at the cerebellopontine angle

A

Where CN 8 exists the brainstem
Remember CN 8 has 2 parts: cochlear for hearing and vestibular
Schwannoma directly both causing sensorineual hearing loss + ear ringing (tines) and vertigo, nystagmus
ALSO damage CN 5 + 7 b/c in that area leaving the brain stem
CN 5: lose facial sensation + paralysis of muscle of mastication
CN 7: facial muscle paralysis, lose taste on ant 2/3, less tears and saliva, loud sounds b/c paralyze stapedius

126
Q

What’s another name for insulin like growth factor 1

A

Somatomedin C

127
Q

Describe the symptoms and RF for neonatal abstinence syndrome aka baby born addicted to opiates

A

Tachypnea, irritably, diarrhea
Hours after birth
RF: mom h/o mental health, hep C infection, or no prenatal care
Treat with morphine or methadone until off

128
Q

What value should you use to determine alveolar ventilation: PaCO2 or PaO2

A

PaCO2
If low you should be thinking hyper ventilation (PE, pna) doesn’t resolve when you can’t get your PaO2 back up so maintain hyper vent and hypocapnea
Eventually resp muscle will fail causing hypo vent w/ hypercap and hypoxemia

129
Q

What molecule is used to est RPF

A

PAH b/c fitlered and secreted at prox tubule
Secretion is b/c taken up from capillaries running next to lumen via carrier proteins (can be saturated)
If you increase the blood levels enough, you will overwhelm these 2 excretion methods

130
Q

You know lipofuschin is the wear and tear pigment but what is it actually

A

Product of free rad injury and lipid peroxidation

131
Q

You know that glucose gets trapped as sorbitol in cells during high BG states of diabetes to cause damage - but why does this occur? What accumulates?

A

Sorbitol accum b/c most tissues CANNOT convert into fructose
Seminal vesicles can b/c 1ary E source for sperm is fructose
Otherwise Schwann, retina, renal papilla can’t
Lens ability to do so overwhelmed

132
Q

How does vision from the nasal visual field of the L eye travel?

A

Via L temporal hemirentina - aka when talking about heme retina talking about eye NOT visual field
Straight back (no optic chiasm)
LGN -> thalamus -> 1ary visual cortex

133
Q

Name 2 mechanism to help hear S3

A

LLD + end of inspiration

Normal in young or deoamp HF

134
Q

Name all the conditions associated with DOWNS

A 
Early onset Alz - extra copy amyloid precursor protein on chr 21
AV septal defect
VSD
ASD
Duodenal atresia
Hirschsprung
HypoT
T1D
Obesity
Acute leukemia
Atlantoaxial instability
135
Q

What is the difference between med + lat LE drainage

A 
SUPERFICIAL ONLY (not noting deep that runs w/ arteries)
Medial bypasses - drains with long saphenous being - sup inguinal LN
Lateral goes through popliteal the to sup inguinal
136
Q 
Name the protein involved and the fxn of each:
Gap jxn
Tight jxn
Adherens jxn
Desmosomes 
Hemi-desmosomes
A

Gap = connexins - intercell comm
Tight = claudins, occludin - parcel barrier
Adherens = cadherins - cell anchor
Desmosomes “ “
Hemidesmosomes = integrins - cell anchor @ basement membrane

137
Q

Name the fxn and structures than insert onto the perineal body

A

Perineal body = pelvic floor integrity, separates urogenital + anal triangles, anchor:
1. Bulbospongiosus (outer most muscle circle of vaginal)
2. Ext anal sphincter - do episiotomy to avoid large lacerations to this structure
3. Sup + deep transverse perineal muscles - cut during med/lat episiotomy
4. Some of ext urethral sphincter, levator ani, muscles of rectum
Cut this during midline episiotomy

138
Q

You know you can use finasteride (5a reductase I) for BPH, but name 2 other med classes to

  1. SM tone in bladder neck, prostate capsule and prostatic urethra
  2. Overactive bladder
A
  1. Alpha ad antag = terazosin, tamsulosin = alpha 1 specific to relax urethra + prostate SM (1st line)
    SE: orthostatic hypotension, dizzy
  2. Anti-M - vs M3 R to relax SM of bladder and ureter
    SE: urine retention, dry mouth (anti-cholinergic)
    SE of finasteride = less libido, erectile dysfxn
139
Q

What is the mechanism of OCP vs local acting P vs copper IUD

A

OCP = E + P = X GnRH - no ovulation
Local P = thicken cervical mucous
Cu IUD = chronic inflam, X sperm migration “intrauterine enviro toxic to sperm”

140
Q

Pathophys of PCOS

A

Multifactorial
Rise LH + insulin
LH @ theca interna -> increase cholesterol (desmolase) -> androgens
Increase androgens: anov (increasing risk endo cancer), oligomen, enlarged cystic ovaries, acne, hirstuism
+ OCP to reduce symptoms and decrease endo prolif
+ Clomiphene (SERM - no neg FB) if trying to get preg
2nd line = spironolactone = androgen R antag for the excess if don’t respond to OCP + not trying to get preg

141
Q

Describe 2 reasons why you might get polyhydramnios

A
  1. Swallowing not right - GI obstruction (atresia), anencephaly (defective CN tube)
    Look for anti-epileptics as RF for neural tube defects
  2. More urine - high fetal CO (anemia, twin-twin transfusion)
    Maternal diabetes and multiple gestations can cause it too but to a lesser extent
142
Q

What is the Robertsonian translocation

A

Downs: 46 XX or XY, t(14,21)

143
Q

What is the least common cause of Down’s

A

Mosaicism = individual w/ 2 different cell lines
1 normal genotype
1 w/ trisomy 21
Means a nondisjxn event happened early in embryo life
Risk of recurrence is based on maternal age

144
Q

Describe the how testes descend through the ab

A
  1. Out deep inguinal ring - opening in transversals fascia - anywhere past here you can feel the testes
    Enter inguinal canal
  2. Exit canal vis sup inguinal ring = opening in ext oblique muscle aponeurosis (medial to pubic tubercle)
145
Q

What hormone induces normal insulin resistance in 2nd + 3rd trimesters

A

Human placental lactogen from syncytio-trophoblast
Simultaneously increases insulin RELEASE from B cells while also causing resistance
Have high glucose levels for E for fetus
Also high ketones (proteolysis) and FFA (lipolysis)

146
Q

What artery supplies the testes and where does it originate from

A

Gonadal arteries right off the abdominal aorta (below the renal arteries)

147
Q

What structure causes an imperforate hymen

A

Incomplete deign of the central portion of the fibrous tissue band connecting the walls of the vagina
Think - usually this ruptures on own but if not all the period blood would get stuck behind it

148
Q

How does prostate cancer spread via blood

A

Drains into the prostatic venous plexus -> vertebral venous plexus -> runs up entire spinal column + connects w/ venous supply of brain
Valveless system
Why prostate can met to the lumbosacral spine

149
Q

Describe what happens in postpartum hemmorhage

A

Delivery -> uterine atony = boggy uterus = can’t contract to stop bleeding
Bilat ligate int iliac arteries to prevent hysterectomy
Colat BF from ovarian arteries will be enough to keep uterus supplied (off abdominal aorta)

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