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MS2 All > Everything Ever > Flashcards

Everything Ever Flashcards

1
Q

<p>What is indomethicin used for?</p>

A

<p>Like naproxen, NSAID

| Long-term relief of symptoms in RA and other musculoskeletal disorders</p>

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2
Q

<p>Why are COX-2 inhibitors being used more than NSAIDs?</p>

A

<p>Cox-2 inhibitors decrease the incidence of gastric and duodenal ulcers by 50% as compared with traditional NSAIDs

Provide therapeutic relief until a DMARD takes effect.</p>

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3
Q

<p>What is sulfasalazine used for?</p>

A

<p>Oldest DMARD
Fast-acting (1 month)
Mechanism not understood, may inhibit IL-1 and TNF-alpha release
Adverse effects - nausea, rashes, headaches, neutropenia</p>

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4
Q

<p>What is one advantage of using antimalarials to treat rheumatic disorders?</p>

A

<p>Less efficacious than other DMARDs but also less toxic</p>

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5
Q

<p>What is the gold-standard DMARD therapy?</p>

A

<p>Methotrexate</p>

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6
Q

<p>Why is cyclosporine A not used more often as a DMARD?</p>

A

<p>Toxic</p>

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7
Q

<p>What is leflunomide?</p>

A

<p>Similar effects to sulfasalazine and methotrexate
DMARD
Newest
prevents de novo pyrimidine synthesis
Side effects are diarrhea, alopecia and hepatotoxicity</p>

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8
Q

<p>What is the mechanism of action of prednisone?</p>

A

<p>Glucocorticoids in general:
inhibit phospholipase A2 activity --> inhibits release of arachadonic acid from cell membranes --> inhibits formation of prostaglandins

Glucocorticoids also inhibit production of numerous cytokines which prevent induction of COX-2. </p>

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9
Q

<p>What are the long term effects of glucocorticoid use?</p>

A

<p>Hyperglycemia
Osteoporosis
Poor wound healing
Though usually benefits outweigh complications
Use glucocorticoids to induce remission while slower-acting DMARD takes effect</p>

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10
Q

<p>What are examples of antimalarials in use as DMARDs?</p>

A

<p>Chloroquine (can cause irreversible retinal damage if used long term)

Hydroxychloroquine (better tolerated) for RA, lupus

Overall, less efficacious than other DMARDs

Act by inhibiting chemotaxis</p>

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11
Q

<p>What is the most commonly used DMARD (is also immunosuppressive)?</p>

A

<p>Methotrexate
Folate analog
Inhibits reaction catalyzed by dihydrofolate reductase that is essential for DNA synthesis
Also used as anticancer agent
Major complication is hepatotoxicity
At low doses (for rheumatic diseases) --> inhibition of aminoimidazolecarbomide transformylase and thymidylate synthetase with secondary effects on polymorphonuclear chemotaxis --> AMP then accumulates and is converted to adenosine, which inhibits inflammation</p>

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12
Q

<p>What are the TNF-alpha antagonists?</p>

A 
<p>Etanercept
Infliximab
Adalimumab
Golimumab
Certolizumab</p>
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13
Q

<p>How does Etanercept (Enbrel) work?</p>

A

<p>TNF-alpha antagonist --> less inflammation systemically
Binds to TNF and prevents its binding to receptors
example of an antagonist that binds a receptor but does not activate it
SubQ 2x/wk</p>

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14
Q

<p>What is Infliximab (Remicade)?</p>

A

<p>TNF-alpha antagonist --> less inflammation systemically
Monoclonal antibody (chimeric mouse-human)
TNF-alpha antagonist
Effective within 1 week of injection
Antigenic</p>

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15
Q

<p>Why is Adalimumab favored over etanercept?</p>

A

<p>TNF-alpha antagonist --> less inflammation systemically
More convenient dosing regimen (2x/monthly)
Fully human anti-tnf-alpha mab
Not antigenic</p>

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16
Q

<p>How does Golimumab work?</p>

A

<p>TNF-alpha antagonist --> less inflammation systemically
Once monthly dosing
human mab, binds to both membrane bound and soluble tnf-alpha
Opportunistic pathogen infection risk is increased (ie TB) **which is generally true of all TNF-alpha blockers</p>

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17
Q

<p>How is Certolizumab different from other TNF-alpha antagonists?</p>

A

<p>TNF-alpha antagonist --> less inflammation systemically

| It's a humanized Fab fragment congugated to polyethylene glycol to delay metabolism and elimination</p>

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18
Q

<p>What is Anakinra?</p>

A

<p>Cytokine antagonist (IL-1)
Soluble human IL-1 receptor antagonist
Short half life necessitates frequent daily treatment in high doses</p>

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19
Q

<p>What IL-6 receptor antagonist has had serious issues with opportunistic infections?</p>

A

<p>Tocilizumab

| Approved as "Actemra"</p>

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20
Q

<p>What is the MOA of Abatacept?</p>

A

<p>Inhibits T-cell activation and induces T-cell apoptosis
Name brand: Orencia
approved for RA refractory to TNF-alpha inhibitors
Side effects - headaches, infections</p>

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21
Q

<p>What is Rituximab?</p>

A

<p>Anti-CD20 mAb that reduces circulating B cells
considered a "costimulation modulator"
approved for RA refractory to TNF-alpha inhibitors</p>

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22
Q

<p>What signaling pathway inhibitor is used for RA treatment?</p>

A

<p>Tofacitinib
inhibitor is JAK kinase 1 and 3
inhibits production of inflammatory mediators</p>

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23
Q

<p>RA is characterized by chronic inflammation of the synovial membrane and infiltration by blood-derived cells, for example....</p>

A

<p>CD4+ T-cells, which produce inflammatory cytokines</p>

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24
Q

<p>T/F: TNF-alpha and IL-1 play a central role in RA.</p>

A

<p>True

IL-6 also plays a role in pro-inflammatory plathways.</p>

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25
Q

<p>What is the rheumatoid pannus?</p>

A

<p>Synovial membrane --> inflammatory tissue (the pannus) which destroys surrounding cartilage and bone
Pannus: type A and B synoviocytes and plasma cells</p>

26
Q

<p>Uric acid, which accumulates and crystallizes in the joints in gout, is the major end product of what metabolic process?</p>

A

<p>Purine metabolism (catablolism)

| hypoxanthine --> xanthine --> uric acid (xanthine oxidase used to catalyze both steps)</p>

27
Q

<p>Normal serum uric acid concentration is:</p>

A

<p>40-50 mg/L

| Uric acid precipitates at > 100 mg/L</p>

28
Q

<p>Name some causes of hyperuricemia:</p>

A

<p>Alcohol use (beer)
Obesity (high fructose corn syrup)
Renal disease (less excretion)
Diabetes
HTN
Drugs is thiazide diuretics, aspirin, diuretics, levodopa, pyrazinimide, cytotoxic drugs, cyclosporine
Cancers - diseases associated with rapid production and destruction of cells ie Hodgkins disease</p>

29
Q

<p>What is podagra?</p>

A

<p>Gouty arthritis attack of metatarsaophalangeal joint of the big toe

Tophi (deposits of urate)</p>

30
Q

<p>What is the MOA of colchicine?</p>

A

<p>Inhibits spindle formation --> neutrophils can't travel --> lowers inflammatory response

**Low therapeutic index means than the diff between therapeutic dose and toxicity is small

Side effects: nausea, diarrhea, vomiting...long term can cause peripheral neuropathy, neutropenia</p>

31
Q

<p>What are the commonly used NSAIDs for gout?</p>

A

<p>Naproxen
indomethicin
sulindac
celecoxib (selective COX-2 inhibitors)</p>

32
Q

<p>Uricosuric agents act by:</p>

A

<p>Increasing the rate of excretion of uric acid
Normally, only 10% of uric acid is excreted
Uricosuric acids compete with uric acid in the renal tubule to prevent reabsorption

Example: Probenecid (developed as an adjunct to penicillin to increase its effectiveness)
--can also have the effect of increasing urate crystal mobilization</p>

33
Q

<p>What is the MOA of Allopurinol?</p>

A

<p>Inhibits xanthine oxidase competitively AFTER being metabolized to its active form (alloxanthine) by xanthine oxidase itself
Used much more often than probenecid

Maculopapular rash in 2% of patients</p>

34
Q

<p>What is the other xanthine oxidase antagonist besides allopurinol?</p>

A

<p>Febuxostate
New
Non-purine, non-competitive antagonist of xanthine oxidase
Cardiovascular safety still under investigation</p>

35
Q

<p>T/F: Developing gout without hyperuricemia is possible.</p>

A

<p>True</p>

36
Q

<p>Why are pubic lice called crabs?</p>

A

<p>Their body shape is longer than body and head lice. Presence of pubic lice warrants screening for all STIs</p>

37
Q

<p>How do you stain for treponema?</p>

A

<p>Darkfield, no gram staining
in the "poorly staining bacteria" category
cannot be cultured
they are too small to be seen by standard light microscopy</p>

38
Q

<p>What is the result of immune evasion with treponema?</p>

A

<p>Low virulence but persisting symptoms that worsen over time
Humans raise mostly useless antibodies against the infection
T pallidum enters lymphatics ans bloodstream immediately and does not need to build up numbers for symptoms to begin</p>

39
Q

<p>What is the infection caused by treponema palladum?</p>

A

<p>Syphilis, transmitted sexually and congenitally</p>

40
Q

<p>What is the Argyll-Robertson pupil?</p>

A

<p>The prostitute will accomodate but not react...

| tertiary (neuro) syphilis</p>

41
Q

<p>What are the stages of syphilis?</p>

A

<p>1. primary chancre,

2. secondary body-wide rashes, condylomata lata (Reddish-brown papular lesions on the penis or anogenital area) and patchy alopecia,
3. latent period - 2/3 patients progress only to here
4. tertiary gummas, neurosyphilis, cardiac involvement - 1/3 of patients progress to tertiary syphilis</p>

42
Q

<p>Neurosyphilis may includes what sequelae?</p>

A

<p>meningitis,
tabes dorsalis (damage to spinal cord → impaired sensation, wide-based gait),
general paresis,
check for Argyll-Robertson pupil</p>

43
Q

<p>Why is congenital syphilis dangerous?</p>

A

<p>kills 50% fetus/newborn, survivors are infected, bone deformities, interstitial keratitis, progress rapidly to symptoms of secondary&amp;amp;tertiary syphilis if untreated</p>

44
Q

<p>Why are body lice (pediculus humanus) dangerous?</p>

A

<p>Can transmit typhus and relapsing fever, trench fever</p>

45
Q

<p>What is the relationship between syphilis and HIV?</p>

A

<p>Ulcerations of syphilis facilitate HIV infection

| HIV immunosuppression accelerates syphilis course, and reduces efficacy of treatment</p>

46
Q

<p>What is the treatment for syphilis?</p>

A

<p>Penicillin G IV (same for yaws and pinta which are also treponema)</p>

47
Q

<p>How do you test for syphilis?</p>

A

<p>Syphilis serology for reagin (VDRL, RPR) is best test for disease-in-progress and for efficacy of treatment;
confirm exposure with tests for treponeme-specific antibodies;
histo of lesions shows infiltrate rich in plasma cells</p>

48
Q

<p>What kind of organism is Neisseria gonorrhea?</p>

A

<p>Gram (-) diplococci
oxidase +
catalase +</p>

49
Q

<p>How does gonorrhea present in males, females and neonates?</p>

A

<p>Males - urethritis
Females - asymptomatic or cervicitis or PID
Neonates - purulent conjunctivitis - can treat with prophylactic eye ointment</p>

50
Q

<p>T/F: Gonorrheal infection is a marker for sexual abuse in children.</p>

A

<p>True</p>

51
Q

<p>What are virulence factors for gonorrhea?</p>

A

<p>IgA protease - clears IgA from mucosal surfaces to facilitate colonization
Pili
LOS (less immunogenic than LPS) - local inflammation
Opa - opacity-associated proteins enhance binding</p>

52
Q

<p>Arthritis/dermatitis can be signs of what disseminated infection?</p>

A

<p>N. gonorrhea

| Other complications are DGI, meningitis, endocarditis</p>

53
Q

<p>What is the best way to test for gonorrhea?</p>

A

<p>Nucleic acid amplification tests (NAAT) - same for chlamydia
gram stain (-)
organism is delicate
culture on Thayer-Martin (chocolate agar)</p>

54
Q

<p>What are important similarities between N. meningitides and N. gonorrhea?</p>

A

<p>Culture on Thayer-Martin
Septic arthritis as a complication
IgA protease as a virulence factor</p>

55
Q

<p>What are the treatment options for gonorrhea?</p>

A

<p>Ceftriaxone

| Cefotaxime</p>

56
Q

<p>What are the treatment options for C. trachomatis?</p>

A

<p>Doxycyline (or azithromycin) unless pregnant, then use erythromycin
these drugs must penetrate cell membrane bc chlamydia is intracellular</p>

57
Q

<p>What is the known virulence factor for chlamydia that is involved in inclusion body formation?</p>

A

<p>T3SS
Reticulate bodies form intracellular inclusions that are visible on microscopy; within the inclusions they multiply by binary fission, forming new reticulate bodies and later new elementary bodies.</p>

58
Q

<p>What are the symptoms of chlamydia in women?</p>

A 
<p>May be asymptomatic
Easily induced endocervical bleeding 
Mucopurulent endocervical discharge 
Intermenstrual bleeding 
Dysuria 
Abdominal pain 
can cause PID
Men: can be asymptomatic reservoirs
Urethral discharge 
Urinary frequency and/or urgency 
Dysuria 
Scrotal pain/tenderness 
Perineal fullness </p>
59
Q

<p>What causes reactive arthritis?</p>

A

<p>Defined as Conjunctivitis + Urethritis + Arthritis

| From chlamydia infection - aka Reiter's syndrome</p>

60
Q

<p>What is lymphogranuloma venereum?</p>

A

<p>Painless ulcer leads to swollen lymph nodes (buboes)
caused by chlamydia bacterium (diff serovar than genital)
</p>

61
Q

<p>What is blinding trachoma?</p>

A

<p>Leading cause of preventable blindness worldwide

| Serovar of chlamydia</p>

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