MRC Basic Science - All the shit Flashcards

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1
Q

What is the most sensitive and specific test for RA?

A

Anti-CCP

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2
Q

What is the MoA of PCN’s and Cephalosporins?

A

Cell wall inhibitors

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3
Q

What is the MoA of Vancomycin?

A

Cell wall inhibitor

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4
Q

What is the MoA of Aminoglycosides (Gentimicin, Tobrimicin, etc)

A

Inhibits protein synthesis 30s ribosome

“Buy AT 30”

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5
Q

What is the MoA of Tetracycline?

A

Inhibits protein synthesis 30s ribosome

“Buy AT 30”

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6
Q

What is the MoA of Macrolides? (Erythromycin, Azithromycin, Clarithromycin)

A

Inhibits protein synthesis 50s ribosome

“CCEL at 50”

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7
Q

What is the MoA of Clindamycin?

A

Inhibits protein synthesis 50s ribosome

“CCEL at 50”

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8
Q

What is the MoA of Linezolid?

A

Inhibits protein synthesis 50s ribosome

“CCEL at 50”

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9
Q

What is the MoA of Rifampin?

A

Inhibits RNA Polymerase

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10
Q

What is the MoA of Quinnolones (Ciprofloxacin, Levofloxicin, -floxicin)?

A

Inhibits DNA Gyrase (= Topoisomerases)

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11
Q

What signaling factors are responsible for:

  • Apical growth
  • Radial/ulnar differentiation
  • Dorsal/Ventral axis
A
  • Apical growth - Fibroblast Growth Factor (FGF..think of Achondroplasia!)
  • Radial/ulnar differentiation - Sonic Hedgehog
  • Dorsal/Ventral axis - Wnt
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12
Q
  1. ) What gene is indicated in Multiple Epiphyseal Dysplasia?
  2. ) What type of Collagen effected in MED?
  3. ) What is characteristic presentation?
A

1.) COMP
2.) Collagen IX
3.) Bilateral, effecting multiple joints; problems on both sides of the joint! NO spine involvement!
(*If has spine involvement -> then think of Spondylo-Epiphyseal Dysplasia and involvement of Collagen II…to help remember - think that nucleaus polposus is Collagen II!)

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13
Q

What is it preferable to plate on the tension side of fractures?

A

Minimizes the bending stress on the plate. When plate is on the tension side and the fracture is loaded it tends to close down so that the bone takes more of the load and there is less load on the plate. If you plate on the compression side, when the bone is loaded the tension side will open during loading and the plate will see more bending stress.

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14
Q

What does viscoelastic mean?

A

Strain varies by rate of loading

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15
Q

What is the composition of articular cartilage?

A

75% water

Next largest component is Collagen: 15%

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16
Q

What is the most common type of Collagen in Cartilage?

What other type is very common?

A

Type II Collagen
Type X Collagen (makes things hard!)
- Calcified tidemark/Hypertrophic zone/hypertrophic chondrocytes

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17
Q

What are important facts about the tangential/superficial zone of cartilage?

A

Flat tangential cartilage cells
Highest Lubricin (boundary lubricant) and Collagen%
Highest water/Least PG synthesis

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18
Q

As you go deeper in the cartilage layers what happens to the collagen?

A

Larger collagen diameter and becomes more vertical.

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19
Q

What is the main molecule associated w/ synovial fluid viscosity?

A

Hyaluronic Acid (squeeze film/fluid-film lubrication)

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20
Q

What is the difference b/t aging cartilage and cartilage in OA?

A

OA is wet and soft! (decrease modulus of elasticity, loss of proteoglycans)
Aging - dry, brittle, and stiff (Increased decorin, decreases water, increases modulus of elasticity)

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21
Q

What type of arthritis has black coloration to it? (black cartilage, urine black, black/blue sclera and ear lobe)

A

Ochronosis (due to Alkaptonuria) - get arthritis early in life.
AR defect of homogentisic acid oxidase

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22
Q
\+Viking/celtic family hx
Arthritis and liver dz
Hyperpigmented skin
Chondrocalcinosis & "hook-like" spurs on MCPs
(+) Rhomboid crystals
A

Hemochromatosis w/ CPPD

Get “bronze DM” = liver dz, DM & hyperpigmentation of skin as late finding

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23
Q

What crystals are a/w Gout?

A

Yellow Urate crystals
Negative birefringence
Needle shaped

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24
Q

What crystals are a/w pseudogout aka CPPD?

A

Blue Calcium Pyrophosphate crystal
Positive birefringence
Rhomboid shaped

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25
Q

What are the 2 common causes of Tumoral Calcinosis?

A

“Bad beans or bad genes!”

  1. ) Chronic renal failure - can’t excrete phosphate
  2. ) Genetic decrease of FGF-23 activity (*Remember FGF-23 stands for “Farewell to Fosphate”…so if have a decrease then you keep more phosphate in your serum)
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26
Q

What should you think of when you see juxta-articular erosions?

A

Rheumatoid Arthritis

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27
Q

What Ab’s are seen in RA?

A

anti-CCP (cyclic citrullinated peptide)

RF (IgM to IgG)

28
Q

What are 3 examples of a Type II Hypersensitivity Reactions (IgM or IgG)?

A

HIT -> Ab to platelet factor 4
Hemolytic transfusion rxn
Myasthenia gravis

29
Q

For SLE, what lab tests are typical?

A

ANA+
anti-dsDNA
anti-Smith

30
Q

What type of reaction is ALVAL seen in MoM prosthesis?

A

Delayed Type IV hypersensitivity reactions

31
Q

What is the cause of acute paronychia?

Chronic paronychia?

A

Acute -> staph aureus
Chronic -> Candida albicans (Fungus!). Typically see in people whose fingers stay wet all the time - dishwashers, laundry, bartenders

32
Q

What is the cause of vesicles on an erythematous base?

A

Herpetic Whitlow - viral paronychia caused by herpes simplex (see in people who put hands in mouth a lot - kids, dentist, anesthesia)

  • Tzank test
  • Rx acyclovir
  • DO NOT I&D
33
Q

What should you think about with painful erythema w/ NON-BLANCHING skin?

A

Necrotizing Fasciitis!
Group A Strep vs polymicrobial
Tx: EMERGENT DEBRIDEMENT (significant increase in mortality w/ delay!!)

34
Q

What infection under skin causes a lot of air in the tissues/soft tissue crepitance? What bug causes this?

A

Gas Gangrene
Clostridium Perfringens
(can be due to contaminated wounds)
Tx: EMERGENT DEBRIDEMENT!

35
Q

What gene confers methicillin resistance for MRSA?

What drug should be used for MRSA?

A
mecA gene (Penicillin-binding protein 2a)
Vancomycin (or Linezolid)
36
Q

What is the MoA of TXA?

A

Lysine analog that binds plasminogen preventing it from being converted to Plasmin (= pacman that breaks down fibrin clot) so fibrinolysis is inhibited

37
Q

What bug can you get after being stuck with a plant? What is tx?

A

Sporotrichosis

Debridement and antifungal

38
Q

When you see a Broadie’s Abscess on the test - what else should you be thinking about?

A

Make sure it’s not a tumor - often the answer is to culture AND biopsy the lesion!

39
Q

How do you tell acute osteomyelitis from chroninc on pathology?

A

Acute will have live bone (see osteocytes in lacunae)

Chronic will be dead bone (empty lacunae)

40
Q

Bug a/w osteomyelitis in a Newborn?

A

Group B (B for baby!) strep!

41
Q

What bug should you be thinking about in a kid with a mild infection that occurs after a URI, Cx negative?
How do you dx bug (2 possible ways)?

A

Kingella Kingae

PCR or Blood agar medium

42
Q

How do you treat Salmonella?

A

Think about in sickler’s! (MC organism still S. aureus though!)
Tx: Ceftriaxone or Ciprofloxacin

43
Q

What 2 groups do you think of pseudomonas OM in?

What is tx?

A

IV drug user
Step on a nail
(both of these S. aureus is still MC, but want to think about pseudomonas being there and covering for it!!)
Tx: Ciprofloxacin

44
Q

Lytic bone lesions in late stage AIDS w/ cat exposure = ?

What skin finding might they have?

A

Bartonella Henselae (Also look for Bacillary angiomatosis = skin lesions that bleed easily…looks like pyogenic granulomas)

45
Q

What cells make up synovial tissue?

A

Type A synoviocytes (mAcrophage-like cells)

Type B synoviocytes (fiBroBlasts) -> the B(ee)’s make the honey

46
Q

What substance is essential for bone formation and is abnormally expressed in cleidocranial dysplasia?

A

Core binding factor-1 (aka Runx2) (transcriptiion factor in osteoblastic cells)

47
Q

What is the fusion protein created in Ewings sarcoma translocation?

A

t(11:22) -> EWS:FL11 -> makes a novel chimeric transcription factor

48
Q

What bony dysplasia is caused by a mutation in Type II collagen?

A

Spondyloepiphyseal dysplasia

49
Q

What gene mutation results in multiple epiphyseal dysplasia?

A

Cartilage Oligomeric Proteiin (COMP) & COL9A1

50
Q

What is the inheritance pattern of Charcot-Marie-Tooth Dz? What other MSK findings are there besdies pes cavovarus?

A

Autosomal Dominant Duplication of Chromosome 17
Hip dysplasia
Spinal deformity

51
Q

What are the findings of fascioscapulohumeral muscular dystrophy?

A

Inability to whistle

Severe scapular winging (tx w/ scapulothoracic arthrodesis)

52
Q

What are the 5 main dz’s that are X-linked recessive?

A

Hunter’s
SED Tarda
Hemophilia A (8) & B(9)
Duchenne MD & Becker’s

53
Q

What is the one main X-linked dominant disorder? What mutated gene and what results? What is tx?

A

Hypophasphatemic Rickets (Vit D Resistant Rickets)
Mutated PHEX gene allows for increased FGF23 (PHEX typically inhibits FGF23) -> renal phosphate wasting (excrete a lot of it) -> low serum Phosphate
(To help remember think “Farewell to Fosphate”)
**
Can treat with FGF23 antibody drug!!

54
Q

What is the Carter Effect?

A

Trait threshold varies by sex (meaning that one sex needs more genes to show the dz)
*Clubfoot is an example

55
Q

What is a marker of osteoblastic differentiation?

A

Alkaline Phosphatase

56
Q

What is the only form of Rickets w/ low Alk Phosphotase?

A
Hypophosphatasia
Autosoma Recessive (duh! b/c enzyme problem!)
57
Q

What causes Fibrodysplasia ossificans progressiva?

A

AD -> gain of fxn mutatiion in Activin A Receptor Type I (ACVR1) -> over expresses BMP 4 (ligaments and muscles get extra bone everywhere!)
Also look for weird 1st toe

58
Q
  1. ) What type of differentiation is Sonich Hedgehog gene associated with?
  2. ) If have excess SHH gene expression you get?
  3. ) If have poor SHH gene expression you get?
A
  1. ) Radial/Ulnar
  2. ) Post-axial polydactyly
  3. ) Fibular hemimelia (missing whole or parts of the fibula!)
59
Q

What is the purpose of Indian Hedgehog?

A
  • Induces bone transcription factors Runx2 (aka Core binding factor) and Osterix (OsX) - turns preosteoblasts to immature osteoblasts [*Remember that Indian’s were here first - so comes before Wnt in the cascade! Wnt will help to mature the osteoblasts]
  • Matures cartilage in endochondral ossification
  • Helps to form osteophytes in OA
60
Q

What dz is a/w mutation in Core binding factor -1 (aka RunX)?

A

Cleidocranial dysplasia
Autosomal dominant
Absent clavicles and proportioned dwarf

61
Q

What is a new drug for osteoporosis that is an antibody (to something that is the chemical link to Wolff’s law)?

A

Antibody to Sclerostin (Romosozumab)

62
Q

What are the 2 main things prodecued by unloaded osteocytes? And what do they ultimately cause?

A

Sclerostin
Dickkopf
Both block Wnt/Beta-catenin pathway

63
Q

What 2 groups of Ortho patients do not need routine DVT ppx?

A

s/p knee arthroscopy

those in SLC

64
Q

What is the classic triad of Fat Emboli Syndrome?

A
  1. ) Petechial Rash
  2. ) Neuro symptoms
  3. ) ARDS/Pulmonary collapse
65
Q

What is the best clinical indicator of inadequate volume replacement in trauma pt?
What is the best lab for inadequate volume replacement?

A

Urine output < 30 cc/hr

Serum Lactate > 2.5

66
Q

What is the earliest sign of Malignant Hyperthermia?

What is it treated with?

A

Unexplained rise in end-tidal CO2

Dantrolene