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MSK Summative > Pathology of Muscle Pain > Flashcards

Pathology of Muscle Pain Flashcards

1
Q
  • What kind of disorder is dermatomyositis?
    • What is the etiology/ association?
A
  • Inflammatory disorder of the skin and skeletal muscle
    • unknown etiology
    • associated with carcinoma (gastric)
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2
Q
  • What are the 3 clinical features of Dermatomyositis?
  • What are the 3 lab findings?
    • What is seen on biopsy?
A

Inflammatory disorder of skin and skeletal muscle

  • Clinical features
    1. bilateral, proximal muscle weakness (can’t comb hair or climb stairs)
    2. Rash of the upper eyelides (helitrope rash), malar rash
    3. red papules on elbow, knuckles and knees (Gottron papules)
  • Lab findings
    • Increase creatine kinase (from muscle breakdown)
    • Positive ANA and anit-Jo-1 antibody
    • Perimysial inflammation (CD4+ T cells) with perifasicular atrophy on biopsy (i.e. closer to skin)
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3
Q
  • What kind of disorder is polymyositis?
    • How does it differ from dermatomyositis?
      • What is seen on biopsy?
A
  • Inflammatory disorder of skeletal muscle
    • resembles dermatomyositis clinically, but skin is not involved (i.e. no malar rash)
  • Endomysial inflammation (CD8+ t cells) with necrotic muscle fiber see on biopsy
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4
Q
  • McArdle Disease is what kind of disorder?
    • due to deficiency in which enzyme?
    • results in?
    • are blood glucose levels affected?
A

Glycogen storage disease:

  • Due to:
    • deficiency is skeletal muscle glycogen phosphorylase
  • Results in:
    • increase glycogen in muscle but can’t break it down
      • painful muscle cramps and myoglobinuria with strenuous exercise
  • Blood gluocse is not affected
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5
Q

Terminology:

  • Pyomyositis
  • Psoas abscess
  • Acute bacterial myositis

Which bacteria is seen with each?

A
  • Pyomyositis:
    • acute intramuscular infection that is secondary to hematogenous spread of microorganism in the body of skeletal muscle
    • S. aureus
  • Psoas abscess:
    • hematogenous bacterial spread
    • S. aureaus
    • Triad of fever, pain and limp
  • Acute bacterial myositis:
    • diffuse muscle infection without an intramuscular abscess
    • mostly gram (+) organism like MRSA
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6
Q

Streptococcus pyogenes toxins:

  • Streptolysin O
  • Exotoxin A
    • MOA
    • Cause/manifestation
A
  • Streptolysin O
    • protein that degrades cell membranes
    • lyses RBC; contributes to beta hemolysis
  • Exotoxin A:
    • Binds to MHC II and TCR outside of antigen binding site to cause overwhelming release of IL-1, IL-2, IFN alpha and TNF alpha
    • Cause toxic shock syndrome
      • fever, rash, shock
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7
Q
  • What type of bacterai is Clostridium perfringens and where is it found?
  • What toxin does Clostridium perfringens contain?
    • MOA?
    • Causes?
    • Who is at risk?
A
  • Clostridium perfringens:
    • Gram (+) found in soil, GI tract
  • Toxin:
    • Alpha toxin
  • MOA:
    • Phospholipase that degrades tissue and cell membranes
  • Manifestation:
    • degredation of phospholipids causes myonecrosis “gas gangrene” and hemolysis
      • elderly people and diabetics more at risk
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8
Q
  • Necrotizing fasciitis is caused by which bacteria?
  • What does it result in?
  • Causes?
A
  • Deeper tissue injury
    • usually from anaerobic bacteria or Strep. pyogenes
  • Results in:
    • ​creptius (grating sound of bone on bone) from methane and CO2 production
    • “flesh eating bacteria”
  • Causes:
    • ​bullae and a purple color to skin
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9
Q
  • Clostridium tetani contains which toxin?
    • MOA?
    • Causes?
A
  • Toxin:
    • Tetanospasmin
  • MOA:
    • protease that cleave SNARE a set of proteins required for neurotransmitter release via vesicular fusion
  • Cause:
    • spastic paralysis, risus sardonicus, “lockjaw”
      • prevent release of inhibitory neurotransmitter (GABA and glycine) from Renshaw cells in spinal cord

Gram (+), spore forming bacteria

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10
Q

Where (in what layer) do each of the folowing infections occur and what is each infection caused by?

  • Erypsipelas
  • Cellulitis
  • Necrotizing fasciitis
  • Myositis
  • Osteomyelitis
A
  • Erysipelas
    • Dermal papillae
      • S. pyogenes
  • Cellulitis
    • upper dermis
      • S. pyogenes
  • Necrotizing fasciitis
    • deep dermis (subcutaneous fat)
      • S. pyogenes
  • Myositis
    • muscle
      • S. aureus
  • Osteomyelitis
    • bone
      • S. aureus
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11
Q

What are 3 antimicrobials that inhibit cell wall synthesis?

A
  1. Penicillins
    • -cillin
  2. Cephalosporins
  3. Carbapenemas
    • -penem
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12
Q
  • MOA of Penicillin (G =IV, V=oral)?
    • mostly used for?
A
  • MOA:
    • Bind penicillin binding proteins (transpeptidase), block transpeptidase cross linking of peptidoglycan in cells wall
  • Used for:
    • mostly Gram (+)
      • S. pneumonia, S. pyogenes
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13
Q
  • MOA of Cephalosporins (generations I-V)
    • used for?
A
  • MOA:
    • Beta-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.
    • Bactericidal
  • Used for:
    • “Organisms typically not covered by 1st-4th generation cephalosporins are LAME”
      • Listeria
      • Atypicals (Chlamydia, Mycoplasma)
      • MRSA
      • Enterococci
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14
Q
  • MOA of Carbapenems?
    • all end in?
  • Always administer with?
  • Used for?
A
  • -penem (Imipenem, meropenem)
  • MOA:
    • broad spectrum Beta-lactamase; inhibit cell wall synthesis
    • ALWAY administered with cilastin to decrease activation of drug in renal tubule
  • Used for:
    • Gram + cocci (S. aureus, S. pyogenes)
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15
Q
  • MOA of Vancomycin?
  • Used for?
A
  • MOA:
    • inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors
    • bactericidal against most bacteria
    • not suceptible to B-lacatmases
  • Used for:
    • Gram (+) bugs only!
    • serious, multidrug resistant organisms include MRSA and sensitive Enterococcus species
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16
Q

Aminoglycosides and Tetracyclines are what kind of drugs?

A

Antimicrobials!

  • Protein synthesis inhibitors
17
Q
  • Aminoglycosides most end in?
  • MOA?
  • Used for?
A
  • -mycin (Gentamicin, Neomycin, Aminkacin, Tobramycin, Steptomycin)
  • MOA:
    • irreversible inhibition of protein synthesis by binding to 30S subunit
      • cause misreading of mRNA and translocation
  • Used for:
    • severe gram (-) rod infections
      • requires O2 for uptake so ineffective against anaerobes
18
Q
  • Tetracyclines all end in?
  • MOA?
  • Clinical use?
A
  • -cycline
  • MOA:
    • bind to 30S and prevent attachment of animoacyl-tRNA
    • proteins synthesis inhibitors
  • Used for:
    • Borrelia burgdorferi (Lyme Disease)
    • M pneumoniae
      • drug’s ability to accumulate intracellularly makes them very effective against Rickettsia and Chlamydia
19
Q

What kind of drugs are:

Macrolides (-mycins), Cholramphenicol and Linezolid?

  • Common MOA?
A

Macrolides (-omycin), Choloramphenicol, Linezolid

  • Antimicrobials that target the 50S subunit; inhibit translocation
  • proteins synthesis inhibitors
20
Q
  • MOA of Chloramphenicol?
    • Used for?
A
  • MOA:
    • blocks peptidyltransferase at 50S ribosomal subunit
  • Used for:
    • Meningitis (H. influenza, N. menigitidis, S. pneumoniae)
    • Rocky Mountain Spotted fever (Rickettsia rickettsii)
21
Q
  • MOA for Linezolid?
  • Used for?
A
  • MOA:
    • inhibit protein synthesis by binding to 50S subunit and preventing formation of the initiation complex
  • Used for:
    • Gram (+) species
      • including MRSA and VRE
22
Q
  • Macrolides all end in?
    • MOA
    • Used for
A
  • -omycin
    • Azithromycin, clarithromycin, erythromycin
  • MOA:
    • inhibit protein synthesis by blocking translocation
    • binds to the 23S rRNA of the 50S ribosomal subunit
  • Used for:
    • gram (+) cocci
      • strep. patients allergic to penicillin
    • STI (Chlamydia)
    • Atypical pneumonia (Mycoplasma)
23
Q
  • Fluoroquinolones all end in?
  • MOA?
  • Used to treat?
A
  • -oxacin
    • Ciprofloxacin, norfloxacin
  • MOA:
    • inhibit prokaryotic enzymes topoisomerase II and topoisomerase IV (mictrobutules)
  • Used for:
    • Gram (-) rods of urinary and GI tract
    • some gram (+)
24
Q
  • What do sulfonamides and Trimethoprim both inhibit?
    • How do they work together?
    • Used for?
A
  • MOA of Trimethorpim:
    • inhibits bacterial dihydrofolate reductase
  • MOA of Sulfonamides
    • inhibit dihydropteroate syntheas, thus inhibiting folate synthesis
  • Used together for:
    • Gram (+)
    • UTI
    • Nocardia, Chlamydia
25
Q

What is the treatment for TB?

“RESPI”

A
  • Rifampin
  • Ethambutol
  • Streptomycin (Aminoglycoside)
  • Pyrazinamide
  • Isoniazid
26
Q
  • What infectious agent is Leprosy caused by?
    • involves what structures?
  • 1st line treatment?
A
  • Infectious disease caused by Mycobacterium leprae
    • involves skin and peripheral nerves
  • 1st line treatment:
    • Dapsone, Rifampin, Clofazimine
27
Q

Treatment of Septic Arthritis?

“Tri Fix the Fox”

A
  • Aspiration and Effusion
  • Treatment:
    • Ceftriaxone/ Cefixime/ Cefoxitin (Cephalosporin)+ Azithromycin (macrolide)
28
Q

What are treatments of choice for MRSA?

A

Vancomycin or Daptomycin

29
Q

What class of drugs is used to treat simple Staphlococcus skin infections?

A

Penicillins

30
Q

Strep. pyogenes causes which infections?

“LINES”

A
  • Lymphagiitis
  • Impetigo
  • Necrotizing fasciitis
  • Erysipelas
  • Scarlet Fever
31
Q
  • Chlamydiae are what kind of bacteria?
    • What does Chlamydia trachomatis cause?
    • Treatment?
A
  • obligate intracellular organisms
    • can’t make their own ATP
  • C. trachomatis causes:
    • reactive arthritis (Reiter syndrome)
    • urethritis
    • follicular conjunctivitis
  • Treatment:
    • azithromycin (macrolides) or doxycycline (tetracyclines)
32
Q
  • What kind of bacteria is N. gonorrhoeae?
    • MOA
    • What does it cause?
A
  • Gram (-) diplococci
    • negative maltose utilization
  • Metabolize glucose and produce IgA protease (intracellular )
  • Causes:
    • septic arthritis
    • gonorrhea
    • osteomyelitis (in sexually active individuals)
33
Q

What is characteristic of secondary tuberculosis?

A
  • caseating granulomas with central area of necrosis and Langerhans giant cells (arrow)
34
Q

What type of bacterias is Mycobacteria tuberculosis?

A

acid fast organisms (pink rodes in picture)

35
Q
  • Who does hematogenous osteomyelitis most commonly affect?
    • most frequent site?
A
  • commonly affects:
    • children and adolescents
  • Frequent site:
    • metaphysis
      • actively growing site (increased blood flow) that favors bacterial growth and proliferation
      • lack of phagocytic properties
36
Q
  • What are the 5 main causes of acute septic arthritis?
    • who does it affect?
A
  1. S. aureus: most common
  2. Neisseria gonorrhoeae
    • sexually active, STD
  3. Borrelia borgdorferi
    • lyme disease
  4. H. influenzae
    • eldery
  5. Group B streptococcus
    • neonates
37
Q
  • What fungi is responsible for chronic arthritis?
  • What site is most commonly affected?
    • associated with?
A
  • Caused by:
    • Sporothrix schenckii
  • Common presentation:
    • knee, wrist, elbow
    • joint is boggy with decrease ROM, usually not red or tender
  • Associated with
    • gardening, outdoor activites

MSK Summative (8 decks)

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