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Clin Medicine > Mssk > Flashcards

Mssk Flashcards

1
Q

Markers of inflammation

A

CRP ESR

-go up in anything with active disease activity not specific

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2
Q

ESR

A

Rises with age, higher in women, not specific

But good suspicion of active disease process

=polymyalgia wheumatica and giant cell arteritis

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3
Q

CRP

A

Synthesized in liver
Proinflammatory cytokines increase it
Can activate complement and promote phagocytosis

-assess disease activity >8 mg/l is inflammatory

Rises and falls quicker and falls quicker than ESR

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4
Q

Active inflammatory process

A

CRP and ESR

CRP falls faster and goes up faster than ESR

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5
Q

What else goes up with inflammation

A

Leukocytosis, thrombocytosis, ferritin, fibrinogen and complement increase

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6
Q

Rheumatoid factor

A

IgM antibody to IgG

Can be IgA, IgG and IgM but it is most common

Made by B cells in synovial joints of RA patients

Not pathonomunoic
In 70% and in other diseases

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7
Q

What is have nodular RA-bump on surface or ACL

A

They have rheumatoid factor 100% of the time

NODULAR

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8
Q

What percent of healthy patients have RF

A

4%

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9
Q

RA in other conditions

A

Sjorgen, cryoglobinemia, primary biliary cirrhosis, mixed connective tissue, endocarditis, SLE, sarcoidosis, malignancy, lung diseases, LUPUS

Associated with joint erosions-higher value more aggressive disease

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10
Q

What is a positive RF

A

45 IU/ml

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11
Q

What percent RA have no RF

A

20-30

But if positive higher the more aggressive the disease process

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12
Q

Anti citrullinated proteins anti CCP

A

Specific marker -more than RF

96% specific and 78% sensitivity

Associated with aggressive erosive disease

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13
Q

If get both positive CCP and RF

A

99.5% likelihood RA

More aggressive and erosive

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14
Q

Anti nuclear antibody

A

Not pathonumonic of anything can be in 20-30% of normal ppl don’t hang hat on one test

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15
Q

Homogenous pattern ANA

A

Histone antibody >95% drug induced lupus

Drugs

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16
Q

Rim pattern ANA

A

Anti DS DNA SLE

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17
Q

Speckled ANA

A

Anti SM lupus

Anti SSA SSB in sjorgen

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18
Q

Anticentromere antibody ANA

A

Scleroderma CREST/PSS

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19
Q

Anti scl-70

A

PSS/CREST

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20
Q

ACA

A

Scleroderma

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21
Q

Labs of lupus

A

Proteinuria>500 or >3 + or casts

Neurologic-seizures psychosis

Hematologists-hemolytic anemia with reticulocytosis, coombs test positive, leukopenia, lymphopenia, thrombocytopenia
-markers!!

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22
Q

Antibodies of lupus

A 
Anti DNA
Anti SM
Syphilis
Antiphospholipid antibodies based on IgG or IgM cardiolipin
Positive lupus anticoagulant
False RPR

ASO and anti DNAase B titers-reflective of streptococcal exposure

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23
Q

ASO and DNAase B titers

A

Group A strep causes strep throat and rheumatic fever

Can target kidney-glomerular problem
Heart-valvular problem

Bones-large joints and small joints polyarticular (more than 1)
-may cause post streptococcal reactive arthritis-small joints

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24
Q

46 yo male fatigue malaise, pain in both wrists and bl swelling over MCP (symmetry)
Decreased ins trength in both hands, swollen wrists, PIP, MCP nodule on extensor surface of left arm . What lab test think abnormal

A

Positive anti CCP elevated ESR and elevated RF

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25
Q

Joint fluid analysis normal

A

Clear viscous <200 cels

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26
Q

Non inflammatory joint analysis

A

200-2000 mononuclear cells

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27
Q

Inflammatory joint aspiration

A

2000-50000 cloudy inflammatory PMN

> 50000-septic(cloudy opaque)

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28
Q

Uric acid hyperuricemia

A

> 6.8

But not all get gout

20% america has high uric acid levels

DONT TREAT HYPERURICEMIA UNLESS REASON to treat, unless starting chemo-if starting chemo be ready to treat uric acid bc chemo can raise it pretty fast

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29
Q

Gout

A

Monosodium urate crystals in joint , 1MTP podagra nocturnal awakening

Lady-postmenopausal

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30
Q

What other joints with gout

A

Knee feet anky, hot swollen puffy and tender

Tophi-deposits under skin

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31
Q

Who gets gout

A

Men 40-60, post menopausal women

Alcohol

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32
Q

Treat gout

A

NSAIDS colchicine-GI toxicity, steroids

Xanthine oxidase inhibitor, uricouric drugs
Probenecid-block tubular resorption of urate and increased uric acid excretion

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33
Q

Radiography x ray

A

OK but not high degree sensitivity for erosions

Can show b/l of involvement but digital has higher resolution of spatial quality

Look fo b/l MCP, bone density, bone mass, and erosions (imply diseaseprocess active)

Not that great

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34
Q

US

A

Sensitive for soft tissue abnormalities (synovitis, tendinitis, bursitis) and erosions

Aid in injecting/aspirating joint
No radiation

Need if aspirate and inject joint

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35
Q

MRI

A

Good for ST and spine/SI joints, tenosynovial s, erosions, joint inflammation

Gadolinium contrast taken in inflamed synovial (thickened pannus) IV can cause nephrogenic systemic fibrosis in patient with kidney disease

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36
Q

CT

A

Best for bony abnormalities (trabecular, cortical bone), erosions, fractures, degenerative or inflammatory arthritis

CT good for bone erosions! Good image to use but

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37
Q

50 year old carpenter pain and swelling and decreased range of motion into e right elbow. The elbow is swollen and very tender. He hammers and lifts boards and sawing . What study . Fluid in it looks like fluid over that joint

A

Plain film-acute fall trauma
MRI-overkill
US-YES way to go bc noninvasive, fast for ST, if really want to confirm get MRI, but US best for St involvement particularly if fluid.

MRI ok but mroe expensive
CT-erosions
But now fluid from repetitive trauma US

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38
Q

If ESR high and factor sup

A

MRI but be cautious

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39
Q

Mono

A

One

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40
Q

Oligo

A

3 or less

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41
Q

Pauci

A

5 or less

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42
Q

Poly

A

Six or more

More migratory involvement

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43
Q

First MTP toe

A

Gout until proven otherwise

Could be pseudogout

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44
Q

Penis rash with arthritis

A

Reactive arthritis

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45
Q

Bowel arthritis

A

UC
Crohn more than US
Behcets-arthritis, ocular, genital , bowel symptoms diarrhea, bloody diarrhea

Reactive arthritis-bowel infection

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46
Q

Clubbing and arthritis

A

Intestinal lung disease until proven otherwise

Clubbing arthritis

HPO——-clubbing arthritis, and pulmonary

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47
Q

Nodules

A

RA/WG/paraneoplastic

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48
Q

Effusion

A

SLE/RA

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49
Q

Hilar nodes

A

Sarcoidosis RA, lymphoma

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50
Q

Infiltrates

A

Septic WG

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51
Q

Diabetes and arthritis

A

Charcots

Cheiroarthropathy

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52
Q

Thyroid and arthritis

A

Carpal/tarsal tunnel

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53
Q

Other endocrine and arthritis

A

Hyperparathyroidism-high Ca

Acromegaly-excess growth hormone and big bones high incidence of degenerative joint disease in hips and knees

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54
Q

Eye

A

RA, SLE, SS, PSS

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55
Q

RA is a disease of what

A

The synovial tissues it is inflammatory

Diartrhodial joints-easily movable ones and small joints over large joints

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56
Q

HLA RA-multigene

A

1/3 of patients have genetic susceptibility for developing RA

HLADRB4 allele increase susceptibility to develop. RA 60% chance of gettin RA

B cells make autoantibodies, cytokines THF a IL1 and IL6 cause synovial proliferation , increase synovial fluid and lead to pannus whic destroy cartilage and tissue in region

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57
Q

Pannus

A

RA

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58
Q

27 yo male pain in both feet and hands

L hand swollen warm and tender over PIP and MCP toes are sore on plantar flexion . Diagnosis and labs

A

RA
Reactive arthritis-predisposposition to larger joints

CRP, ESR, RF, ASO, ACA, ANA, CBC, uric acid

Could start out with plain films digital radiography but plain film so not super sensitive for erosions into joint
CT better for erosions

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59
Q

Treat

A

Steroid NSAID at first and DMARD

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60
Q

RA preg

A

Improved and flares 406 weeks post partum

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61
Q

Infections RA

A

Periodontal, EBV< paro virus, B19

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62
Q

Mortality of RA

A

Significant. Disables patiets and no perfect treatment

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63
Q

Mortality RA

A

Infection, renal disease, GI disease, HD< malignancy more so than general population for people with RA

Significant mortality

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64
Q

4 components of RA

A

Large glints, small joints, serology, symmetry, synovitis

At least one joint hot tender,

6/10 high probability RA
More points for small joints of inflammation

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65
Q

RA big or small joint

A

Small

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66
Q

C1-C2 RA

A

Has predisposition for RA but spares rest of cervical vertebra, thoracic and lumbar

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67
Q

RA and bone

A

Risk of OSTEOPOROSIS

If going ot surgery and general anesthetic tell them before bc sometimes C1-C2 vulnerable to flexion or hyperextension give heads up before intubation

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68
Q

Flexion contractures

A

RA

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69
Q

GEL

A

How long take to make joints loosen up bc worse in the morning with RA

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70
Q

Pyoderma gangrenosum

A

RA effect

Tender reddish purple papule that leads to necrotic, non healing ulcer

Lower extremity

Chancge from red to purple then to dark black necrotic on LE its nota venous stasis ulcer it is an inflammatory consequence of gangrenosum of the area

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71
Q

Rheumatoid vasculitis

A

Purpura and petechia at first then nail bed with splinter hemorrhages to digital infarct

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72
Q

Wha do

A

Check peripheral pulses on RA and look at feet and fingers

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73
Q

Heart RA

A

CAD , HF< pericarditis, CAD due to chronic endothelial inflammation

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74
Q

58 yo man cough and dyspnea on exertion medical history positive for RA for 10 years and smoking 1-2 ppd for 30 years . Chest x ray nodular opacity in both lungs and diffuse hyper lucency of lungs

A

Interstitial lung disease

Hyperlucency-dark COPD with smoking

Tests-chest x ray first then if abnormal CT, sputum culture for infection gram stain culture and sensitivity aerobic and anaerobic cultures, Tb test, PFt, bronchoscope with cytology and biopsy

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75
Q

Take home

A

Rheumatoid can have nodular disease in their lung dont know if all rheumatoid or other stuff

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76
Q

Caplan

A

RA nodule, pneumoconiosis with nodular opacities,

Silicosis

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77
Q

Lung RA

A

Pleuritis most common
Nodules
Caplan syndrome-nodular densities after exposure to coal or silica dust
Pulmonary fibrosis

Caplan seen in coal miners pneumoconiosis

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78
Q

36 dry mouth decreased testing and sandy feeling under eyelids, has bright light sensitivity and been treated her for RA for 5 years

A

SLE , HIV, Sjorgen-dry feeling YES , probably sjorgen from RA

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79
Q

Text

A

Ro-ssa, la-ssb, schirmers test, slit lamp test

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80
Q

Schrimers test

A

If lack of tears or dry eye put litmus paper under upper eyelid and close eyes for 5 min if see filter paper become wet then normal if filter paper not going down 10 mm that is positive lacrimal glands not working so has dry eye syndrome Sjorgen

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81
Q

Slit lamp

A

Make sure protect macula want to know

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82
Q

Treat sjorgen

A

Lube for eyes, oral hygiene encourage water

In 35% of RA autoimmune disorder with lacrimal and salivary dysfunction 90% of women

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83
Q

What eye part involved

A

Sclera is predisposed to vulnerability

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84
Q

Uveitis

A

Eye vulnerable to RA

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85
Q

Sjorgen

A

Dry eyes dry mouth

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86
Q

Felty

A

RA splenomegaly neutropenia fever anemia thrombocytopenia RF and aCCP

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87
Q

RA CA-C2

A

Subluxation due to erosion odontological process

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88
Q

__ single finding on PE or lab test is pathognomonic for RA

A

NO

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89
Q

Synovial flud of RA

A

2/3 PMN; wbc 5000-100000

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90
Q

Low blood glucose in RA

A

Idk

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91
Q

Treat RA bc its life long

A

Want remission rheumatologist, PT, OT, rest, Treat early to prevent irreversible cartilage and bone damage

Remission possible in 50% of patients

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92
Q

Treat

A

NSAIDS1
Glucocorticoids-low dose short time
Colchicine

Can use nsaids with dmards

Dmards-takes 2-5 months tow rok start within 2-3 months of disease MTX

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93
Q

Non biologics and biological DMAD

A

Start non biological-MTX then build from there

-always monitor for AE-look at white count, kidney, liver,

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94
Q

DMARDS

A

MTX< hydroxychloroquine, lufonemide, sulfasalazine

Hydroxychloroquiine-watch eye to protect macula of eyes can cause macular damage

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95
Q

Sulfa

A

Ok in preg

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96
Q

Biological

A

Work but toxic

Lower immunity and increase infection risk and toxicities -T, neoplasia, infection

TNF stoppers, etanercept, infliximab, adalimumab, rituximab they work

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97
Q

Seronegative spondyloarthropaties

A

Axial spine and SI joints!!! Fusion , rigidity/kyphosis

B27

Enthesitis-inflammation of insertion points of tendons and ligaments

Asymmetric peripheral arthritis

Ocular inflammation

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98
Q

Axial

A

Cranium and vertebral column

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99
Q

Enthesis

A

Site of ligamentous attachment to bone

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100
Q

Enthesitis

A

Inflammatory changes of the ligament, tendinous insertion into bone, or joint capsule

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101
Q

Oligoarticular

A

Few joints

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102
Q

Osteitis

A

Inflammation of bone

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103
Q

Periarticular

A

Around a joint

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104
Q

Spondylitis

A

Inflammation of vertebrae

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105
Q

Spondylolithesis

A

ANTERIOR DISPLACEMENT OF VERTEBRAL BODY RELATIVE TO ADJACENT

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106
Q

SPONDOLOLYSIS

A

DEFEC OF PARS OF VERTEBRA

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107
Q

Which arthritis is more female

A

RA

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108
Q

Seronegative

A

Mostly males

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109
Q

Ankylosing spondylitis

A

Axial
Symmetrical
Maybe eye

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110
Q

Enteropathy arthritis

A

Axial and peripheral

Symmetrical

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111
Q

Psoriatic arthritis

A

Axial and asymmetrical and peripheral

Asymmetrical

Course non marginal

Psoriasis

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112
Q

Reactive

A

Axial and symmetrical peripheral

Asymmetrical

Iritis and conjunctivitis, keratoderma

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113
Q

B27

A 
Not positive
90% AS
80%REA
ENTEROPATHIC SPONDYLITIS 75%
Psoriatic spondylitis 50%

Not all are positive with it

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114
Q

28 yo male presents with a history of low back pain for 4 months, denies trauma, heavy lifting or unusual activity. He indicates the lower portion of the back over the lumbar-SI region, right side worse than left. He admit to morning stiffness. 9 lb weight loss, What should we ask

A
  1. Constitutional symptoms, anything help, exercise improve?(ank get better with activity)
  2. Plain fils of Ls and pelvis, if not supportive jump to CT of back, MRI is really good for SI joints and back, get B27, CRP, ESR
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115
Q

Ankylosing spondylitis

A

B27 cant diagnose, but can provide infor
Most common inflammatory disorder of axial skeleton* SI joints involvement **

905 have b27

Males more

20% have affected family member B27

2-3rd decade

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116
Q

Symptoms ank

A

Low back pain in morning stiffness and get better with activity

Fatigue, weight loss, fever

Symmetrical SI joint pain loss of mobility/flexibility; arthritis of hips

Tendinitis, plantar fasciitis(Achilles-heel pin)/enthesitis

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117
Q

Achilles tendinitis

A

Ankylosis spondylitis asymmetric in heels erosion of calcaneous from inflammatory component

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118
Q

Extra ocular ank

A

Scleritis , iritis, uveitis, photophobia

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119
Q

PE ank

A

Restriction to flexion of back with SCHOBER test stand up and drop down 5 cm below and 10 cm above and LS junctionask to bend over and measure distance between those if hasn’t changed Korea’s than 4 cm then restriction in bending

Fabere test-measure chest circumference inhale and see if change in that

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120
Q

Lab ank

A

ESR CRP
B27
Anemia
RF ACCO ANA NEGATIVE

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121
Q

SI joint x ray ank

A

Whitening sclerosis

More dense more hard

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122
Q

Syndesmophoytes

A

Bridging of vertebra causing ankylosis

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123
Q

Straightening of vertebra with white density

A

Yes

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124
Q

Tests

A

CT for erosions

MRI inflammation before changes seen on C ray and CT

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125
Q

Ank differential DISH

A

Diffuse idiopathic skeletal hyperosteosis-calcification of ligaments from one vertebra cause restriction motion in back but SI joints are ok

Calcification of 4 continuous vertebrae

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126
Q

Osteitis condensans illi and not ank

A

Young middle age females

Normal si joints x ray shows sclerosis on iliac side of SI joint

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127
Q

Cause equina from ank

A

Late complication, bowels bladder and low back pain and host of other bowel related issues, paresthesia, cant feel when have a bowel movement, bladder dont know start or stop or empty.

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128
Q

Kyphosis

A

Ank

Loss lumbar lordosis, flexion knees, severe kyphosis

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129
Q

Ank

A

Young men, insidious onset, hurting for months, morning stiffness better with activity and positive family history , better with activity, osteoarthritis does not

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130
Q

Treat ank

A

Stay mobile, PT, swim, NSAIDS< TNF inhibitors, non biologics DMARDS/

NSAID help ain but not process

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131
Q

26 yo male with pain swelling and warmth in right knee. Onset 2 weeks prior to office visit. Pain in ACL tendon and sore soles and sore soles of feet, tendons hurt feet hurt and knee hurt. No eye pain, rash, or urethral discharge

A

Aks-when worse better, trauma, sexual history, GU GI tract, oral ulcers, penile rash, IV drug, venereal disease, enteric pathogens (can cause reactive arthritis),

Reactive arthritis

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132
Q

REA

A

Autoimmune disease; asymmetric monoarthritis or oligoarthritis in lower extremities

Infection from GI/GU

Salmonella, shigella, yersinia, campylobacter jejuni, chlamydia (this one GU)

B27 in 75% of ReA and IBD

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133
Q

Reactive

A

Arthritis-asymmetrical, oligoarthritis, lower extremities

Enthesitis-Achilles tendon/plantar

Dactylitis-sausage fingers

Asymmetrical SI

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134
Q

Reiters triad

A

Urethritis, arthritis, conjunctivitis/uveitis

Can have sores in mouth circulate balantitis on penis, keratoderma blennorhagicum-painless eruption on palms and soles pustular

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135
Q

Lacs ReA

A

Same AS

WBC 2000-50000 PMN

Imaging-SI asymmetric

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136
Q

Differential for ReA

A 
GC
Sepsis
ReA HIV
Endocarditis
Viral infections -parvo
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137
Q

Reactive arthritis

A

Fever, fatigue, anorexia, asymmetric, inflammation toes fingers dacytlitis, low back pain, skin lesions, ocular, nonspecific inflammatory markers

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138
Q

Treat ReA

A

Resolve in a few months
NDSAID steroids, supportive, if chronic use DMARD

Urethritis-chlamydia, azithromycin Or doxycycline

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139
Q

Psoriatic arthritis

A

5-205
20-50% B27

Associated with SI and axial involvement

DIP, PIP, MCP, MTP also large joint,
Pitting nails, dactylitis, enthesitis, C1-C2

PSORIAtIC SKIN lesions

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140
Q

Pencil in cup

A

DIP narrowed joint space and condylar erosions

Reactive sub periosteal new bone

Pencil in cup appearance

Ankylosis if SLE joint space

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141
Q

Treat

A

NSAID pain
Dmards
Biologics

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142
Q

ENTEROPATHIC arthritis

A

1:1 male female

UC CD

Axial involvement like as but asymmetric SI joint

Parallels activity IBD, if arthritis acting up so is IBD
Large joints lower ex, small joints upper extremity

Extramanifestations more common in crohns than UC

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143
Q

Cutaneous

A

Pyoderma gangrenosum, erythema nodosum, uveitis,

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144
Q

Treat

A

Manage inflamed bowel and steroids, DMARDS, tnf alpha

Problem not a lot are handed well orally so try

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145
Q

Gout

A

Uric acid crystals engulfed and attached to synvium macrophage and inflammatory cascade and underlying etiology of all of these components to cause inflammation in joint

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146
Q

Acute gout

A

Hope red warm tender swollen

Red meat, sea food, purine, alcohol, trauma, seasonal weather extremes, dehydration, excessive exercise

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147
Q

Chronic ethicists

A

Tophi (ears, forearms, Achilles’ tendon

Renal insuffiency , radiolucent

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148
Q

Kidney stones gout

A

Uric acid

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149
Q

Treat gout

A

No best

Do not treat asymptomatic hyperuricemia
Exception-about to receive cytotoxic therapy for neoplasm

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150
Q

Chemo

A

Lysecells and increase uric acid

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151
Q

Drugs

A

Allopurinol
Uric acid inhibitor

As ingest purine get hypoxanthine

Uric acid deposited in joint or excreted in urine

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152
Q

Probenecid

A

Increase excretion

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153
Q

Colchicine Or NSAIDS

A

Inflammation inhibited

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154
Q

Acute treatment

A

NSAIDS, naproxen/indomethacin

Inc risk GI bleed/ulcer/renal disease/fluid retention/interfere with anticoagulant/HF/HT

Watch gi and kidney of nsaids

Steroids-reasonable , safe effective anti inflammatory and taper

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155
Q

Colchicine

A

Effective GI AE, liver an renal

Effective if given in first 24 hours

GI SIDE EFFECTS but worlds

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156
Q

Biologics

A

Inhibitors Il-1B antagonists anakinra for acute gout!

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157
Q

When put on uricosuric agents

A

Kidney stones, cutaneous tophi

Xanthine oxidase inhibtiors, uricouric acids (probenacid)

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158
Q

Pseudogout

A

Calcium pyrophosphate

Large joints, older, polyarticular,

Chondroma Lino’s is-calcium deposits in articular cartilage

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159
Q

CPPD crystals

A

Short blunt rods, rhomboid/cuboid

Weak positive birefringence by polarizing microscopy

associated with aging
Younger-primary hyperparathyroidism, hemochromatosis, hypomagnesemia, chronic gout, gitelman syndrome

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160
Q

Needle

A

Gout

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161
Q

Rhomboid/cuboidal

A

Pseudogout

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162
Q

Treat

A

NSAID steroid colchinie

Same treatment

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163
Q

Most common arthritis

A

OA prevelance our obesity and aging

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164
Q

Most common cause of disability to LE world wide

A

OA

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165
Q

OA improves with

A

Rest

Worse with activity and repetitive motion

Hurts a the end of the day

Destroying hyaline articular cartilage type II collagen and getting sclerosis at the joint and hardness and areas of granulation tissue

IB and TNFa that drive tissue destruction

Enurbation bone on bone joint mice no cartilage to cushion

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166
Q

Joints of OA

A

CMC 1st, DIP PIP, knees hips spine

Older

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167
Q

Spondylosis OA

A

Spine can lead to spinal stenosis

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168
Q

Crepitus

A

Decreased rang of motio effusion

COOL EFFUSION!!!!!!!

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169
Q

Cool to touch

A

OA

Effusion

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170
Q

OA

A

Bony outgrowth over DIP areas

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171
Q

Lose joint space and bone on bone

A

OA

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172
Q

Bone spur

A

OA

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173
Q

Most common OA

A

Cervical, lumbar spine, 1st cmc, pip, dip, hip, knee, 1st MTP

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174
Q

Labs OA

A

ESR up but WBC<2000 nothing diagnostic

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175
Q

Radiographically hallmarks OA

A

Asymmetry, narrow joint space, subchondral sclerosis-thickening, osteophytes and marginal lipping, bone cysts, joint mice

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176
Q

Joint mice

A

Gritty sensation

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177
Q

Most common OA

A

Idiopathic primary cause

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178
Q

Erosive OA

A

DIP and PIP more pain than typical hand of OA

PAIN
Women

Central erosions seen on radiography with seagull appearance in fingers

Pain out of proportion

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179
Q

Secondary OA

A

Underlying disorder

Trauma, infection, hemochromatosis, congenital joints like hip dysplasia

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180
Q

Charcot joints

A

Diabetics lose architectural function of joints. Joints are distorted and abnormal and lose pain sensation and position sense and really disfiguring architectural distortion

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181
Q

Osteonecrosis

A

Avascular necrosis blood supply gone -steroids cause this

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182
Q

Manage OA

A

Start immediately

Lose weight

Oral, NSAIDS< steroids, analgesics , surgery

Glucosamine and chondroitin failed to show efficacy for pain relief

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183
Q

Indications for an EDX consultation

A

Motor neuron, nerve root, plexus, peripheral nerve, neuromuscular junction

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184
Q

Symptoms of neuromuscular

A

Numbness or tingling, decreased sensation, pain, cramping or spasm

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185
Q

What is EMG

A

Test integrity of PNS

NCS-nerve conduction studies
EMG electromyography

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186
Q

How do NCS

A

Peripheral nerve stimulated with electrical stimulus and responses are recorded

Compound motor action potential (CMAP)
Sensory nerve action potential (SNAP)
F wave
H reflex

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187
Q

Three things measure emg

A

Latency, size of response, speed with which travels

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188
Q

Motor latency

A

Measure of conduction time from stimulations cross a nerve segment through the neuromuscular junction to initial activation of msucle fibers

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189
Q

Motor amplitude

A

Measure of the number of activated msucle fibers

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190
Q

Sensory latency

A

Measure of conduction time of action potential from stimulations cross a nerve segment

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191
Q

Sensory amplitude

A

Measure of the number of activated sensory axons

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192
Q

Conduction velocity

A

Measure of the velocity of the fastest conducting axons (motor and sensory)

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193
Q

Guillane

A

Loss myelin focal

Can see change in amplitude or configuration of amplitude of conduction block

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194
Q

Needle electromyography

A

Needle electrode inserted into msucle

Multiple msucles are accessible for exam

Combination of msucles tested which is dependent on clincal question

Level of discomfort is mild

C6-deltoid, brachioradialis and biceps

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195
Q

Study msucle at rest then have patient activate it a bit then exert full strength

A

Look at pattern

Needle electromyography

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196
Q

What evaluate with needle

A

Insertional activity

Spontaneous activity

Motor unit configuration

Motor unit recruitment

Interference pattern

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197
Q

Insertional activity

A

As soon as put in injur and see and hear burst of activity soon goes away then see nothing

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198
Q

Spontaneous activity

A

Fibrillation, positive sharp waves, fasciculations

Interruption in nerve supple to msucle that is not insertional

C6-see deltoid, biceps and brachioradialis see breaks
Hallmark of issue

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199
Q

Abnormal spontaneous

A

Positive sharp wave and fibrillation

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200
Q

1-4

A

0-no fib
+/1 fibs/PSW not persistent
1 persistent Fibs.PSE in at least 2 areas
2…….

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201
Q

Motor unit configuration

A

Muscle is volitionally activated at different force levels

Single motor
Then whole motor

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202
Q

Decreased recruitment

A

One unit recruited

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203
Q

Increased amplitude

A

Ok

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204
Q

Increased duration

A

Most short can be long

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205
Q

Polyphasic

A

Many turns in a motor unit

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206
Q

What is reduced recruitment, increased amplitude, increased duration, polyphasia

A

Insult and healed!

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207
Q

Anterior horn cell disease (motor neuron disease. Tell me about anterior horn

A

C6-several motor neurons contribute to that nerve

Dirosder of degeneration of motor neurons in spinal cords with or without lesions in lower brain and long tracts

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208
Q

Characterization anterior horn disease

A

Progressive wasting and weakness of the affected muscles without accompanying sensory, cerebellar or mental changes

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209
Q

Sensory cerebellar or metal changes with motor neuron

A

NO just msucle

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210
Q

Idiopathic mTOR neuron disease

A

Adult and child

ALS

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211
Q

Causes other

A

Toxins like heavy metals, polio, west Nile, HIV, a glucosidase defiency, remote effect of cancer, thyroid, POMPES disease

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212
Q

Amyotrophic lateral sclerosis

A

Most common

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213
Q

Progressive bulbar palsy

A

1/3

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214
Q

Progressive spinal muscular atrophy

A

5-10

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215
Q

Primary lateral sclerosis

A

<5%

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216
Q

Variant rare motor neuron disease

A 
Brachial amyotrophic diplopia
Leg amyotrophic diplopia
Isolated bulbar ALS
Monomelic amyotrophy Hirayama’s disease 
Familial or associated with other neurodegenerative disorders
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217
Q

Amylotrophic lateral sclerosis

A 
A-without
Myo-muscle
Tropic-nourishment
Lateral-side
Sclerosis-hardening or scarring

Nerve gives neourishmet

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218
Q

Who gets ALS

A

Males

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219
Q

Signs ALS

A

Mixed upper (spasticity, hyperflexia, babinski sign)and lower motor neuron signs (atrophy, fasciculations)

May also be bulbar involvement of the upper or lower motor neuron type

MIXED SIGNS-

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220
Q

Risk factors ALS

A

Nope

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221
Q

Fasciculations

A

Muscle twitch

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222
Q

ALS is espicially in _____

A

The same limb with mixed upper and motor neuron signs

Arm patchy msucle atrophy and fasciculations and check reflexes and hyperreflexive which dont go together

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223
Q

Pathophysiology ALS

A

Degeneration of beta, lower brainstem, descending Corticospinal tracts, and anterior horn cells

Etiology unknown -cause
Enterovirus D68 myositis flaccid in kids

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224
Q

Clincal picture ALS

A

> 50 hand clumsiness or impaired dexterity with mild wasting/weakness hand writing worse,
Spread to other limbs and leg involvement
Bulbar sucks involved

Atrophic hands, atrophic tongue tongue fasciculations

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225
Q

Anterior horn cells white

A

Sclerosed

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226
Q

Diagnose ALS

A

Spinal fluid normal

EMG-enervation and reinnervation widespread*****

Urine for heavy metals serum but not now unless reason for it

CPK normal or up

Imaging-brain , spine-normal

HIV

Muscle biopsy-only needle in confusing cases

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227
Q

Pertinent negatives

A 
No story issue
Normal mentally
No extraocular muscle involvement
Bowel or bladder symptoms not prominent
Decubitus rare
Fasciculations rarely the presenting symptoms
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228
Q

Prognosis ALS

A

No remission, progressive, death from respiratory failure, 4 years symptoms, dead 2-5 years, s

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229
Q

Treat ALS

A

Supportive

Rilutek-somewhat helpful in ppl with a lot of bulbar, a glutamate inhibitor EXPENSIVE

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230
Q

Progressive bulbar palsy

A

Presenting symtpoms in 20% of MND
Selective involvement of the motor nuclei of the lower cranial nerves
Tongue, swallowing, respiratory

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231
Q

Symptoms progressive bulbar palsy

A

Dysarthria, dysphagia, dysphagia, chewing difficulty, drooling respiratory difficulty

Usually progress to ALS but better life span

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232
Q

Progressive spinal muscular atrophy

A

5-10%
Males
64
Lower motor neuron deficits predominate from degeneration of anterior horn

No upper motor neuron invovne t

Symmetric upper extremity involvement

Weakness, atrophy, respiratory

Can become ALS but longer live

Live 15 years

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233
Q

Primary lateral sclerosis

A

2-4%
50-55
Upper motor neuron Corticospinal tract

Spasticity, hyperreflexia, babinski,

Slow progression but can become ALS

Survival better than als

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234
Q

Acquires MND

A

Polio, West Nile virus, HIV, post polio, Hopkins syndrome (follows asthma attack, usually one limb), heavy metals lead mercury, enterovirus D8 acute flaccid myelitis in kids

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235
Q

Associated with other neurodegenerative disorders

A

Familial western pacific(dementia-ALS compelx of Guan) blah blah

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236
Q

Infantile spinal muscular atrophy

A

Hypotonic, arreflexia, poor suck, breathing difficult, death in 6-12 months

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237
Q

Intermediate spinal muscular atrophy

A

Ok

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238
Q

Juvenile muscular atrophy

A

Milder than werdnig Hoffman

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239
Q

Peripheral neuropathy

A

Common
Diabetics-numbness tingling in feel

Carpal tunnel

Pinched nerve radiculopathy in back

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240
Q

Epinephrine perineureum endoneureum

A

Out ot in

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241
Q

Blood supply to nerve

A

Vaso vasorum

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242
Q

Where injure nerve

A

Cell Boyd, nerve root, plexus, peripheral nerve

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243
Q

Wallerian degeneration

A

Severed distal goes away

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244
Q

Segmental demyelination

A

Gillian demyelinating not uniform different never different places

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245
Q

Axonal degeneration

A

Nutrients/

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246
Q

Radiculopathy

A

Root where exits spinal cord

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247
Q

Single spinal nerve innervates

A

Dermatome

Myotome (group of muscles-C6 deltoid, biceps and brachioradialis)

Sclerotome-area of bone supplied by a single spinal root

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248
Q

L5

A

Head of femur

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249
Q

L4

A

Across knee

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250
Q

Radiculopathy

A

Nerve root dysfunction from structural or not (DM infections)

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251
Q

C5-C6

A

C6 nerve root compression

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252
Q

C6-C7

A

C7 nerve root compression

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253
Q

L4-L5

A

L5 nerve root compression

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254
Q

L5-S1

A

S1 nerve root compression

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255
Q

C5

A

Scapula shoulder pain
Lateral arm sensory
Weak shoulder abd

Lose biceps DTR

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256
Q

C6

A

Pain-scapula shoudler

Sensory 1st and 2nd digit lateral arm

Shoulder abd and elbow flexion weak

Lose biceps DTR

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257
Q

Cy

A

Pain-scapula shoulder arm elbow forearm

3rd digit sensory
Weak elbow ext and wrist ext

Triceps DTR loss

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258
Q

C6

A

Deep pain in forearm

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259
Q

C8

A

Pain-scapula shoudler arm medial forearm

4th 5th digit sensory

Weak finger abd and flex

DTR loss finger flexors

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260
Q

C7

A

Feel tight band around elbow

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261
Q

L4

A

Pain anteriolateral thigh knee and medial calf
Sensory medial calf

Weak hip flexion,
Loss patella DTR

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262
Q

L5

A

Pain dorsal thigh and lateral calf

Sensory lateral calf and dorsum of foot

Weakness hamstring, foot forsiflecion, inversion, eversion

No DTR loss

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263
Q

S1

A

Loss posterior thigh and calf

Sensory postlateral calf

Last foot

Weak hamstrings and foot plantarflex

Achilles reflex loss

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264
Q

L4

A

Pain band around knee

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265
Q

C6

A

Thumb index finger

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266
Q

C7

A

Middle finger

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267
Q

C8

A

Fourth fifth

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268
Q

T1

A

Medial forearm

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269
Q

T4

A

Nipple line

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270
Q

T10

A

Umbilicus

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271
Q

L1

A

Inguinal

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272
Q

L4

A

Medial calf

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273
Q

L5

A

Lateral calf

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274
Q

Brachial plexopathy

A

Routine nerve conduction not adequate to make diagnosis

paraspinal msucles must be examined

Sensory are abnormal
Rhomboids and serrated anterior may identify proximal lesions

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275
Q

SNAPS abnormal plexopathy

A

Vs radiculopathy

Bc peripheral nerve!

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276
Q

Brachial plexopathy

A

Compression or stretch injury

Inflammatory/idiopathic

Radiation injury

Neoplastic

Traumatic injury

Ischemia

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277
Q

Radiation injury

A

Upper trunk, lateral cord, painless

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278
Q

Neoplastic

A

Medial cord painful (breast lun tumor)

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279
Q

Traumatic injury

A

Traction, laceration missile

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280
Q

Ischemia

A

Diabetic usually lumbar

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281
Q

Parsonage turner

A

Unknown etiology, probably autoimmune as it often follows infections, vaccinations, surgery

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282
Q

Clincila parsonage turner

A

Severe pain in shoudler area followed within a few days by weakness and atrophy (as the pain subsides) usually involving msucles of the shoulder girdle

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283
Q

Course of parsonage turner

A

Spontaneous recovery in 6-18 months; steroids are helpful

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284
Q

Peripheral neuropathy

A

Mononeuropathy, polyneuropathy, mononeuropathy multiplex

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285
Q

Mononeuropathy

A

Single nerve

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286
Q

Polyneuropathy

A

Diffuse, symmetrical, motor and sensory

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287
Q

Mononeuropathy multiplex

A

Several single mononeuropathy

DM

288
Q

Symptoms peripheral neuropathy

A

Loss of sensation

Paresthesia-secondary to large myelinated fiber disease “pin needle:

Pain from small unmyelinated fiber
-burning

Dysestheia
Hyperalgesia
Hyperpathia

289
Q

Motor signs peripheral nerve

A

Weak, atrophy, crampons, fasciculations, decreased DTR, reduced tone

290
Q

Large fiber

A

Decrease vibration and joint position sense, areflexia, ataxia, hypotonic

Tingling pin needle numbness

291
Q

Small fiber

A

Decrease pain and temp

Burning jabbing

292
Q

Autonomic

A

Hypotension decreased sweat, impotence, urinary retention, constipathion

Hyperhydrosis, urinary frequency

293
Q

Large myelinated fibers

A

Light touch cotton swab
Two point discrimation
Vibration*
Joint position sense*

294
Q

Small unmyelinated

A

Temperature perception

Pain perception with pin prick

295
Q

Motor test

A

Atrophy weakness, depressed DTR, cramps, fasciculations

296
Q

Upper motor neuron

A

Spastic, normal bulk, weakness atrophy , hyperactive DTR, babinski sign
No fasciculations

297
Q

Lower motor

A

Hypoactive, hypotonis decreased reflexes

Distal Flacco’s atrophic fasciculations

298
Q

No sensation whole right side

A

Upper motor

299
Q

Mononeuropathies

A

Dermatomes ,

Or skin look at for innervated by a peripheral nerve

300
Q

Nerve root peripheral nerve

A

Nerve root dont split digits peripheral nerve do

301
Q

Median nerve pierces ____

A

Pronator teres can pinch there

302
Q

Median nerve and brachial artery pass below what in 20%

A

Ligamentum struthers can get pinched if have

303
Q

Pronator syndrome

A

Insidious onset of diffuse/dull ache about the proximal forearm

Pain with forced forearm pronation

Easy fatigue o the forearm muscles

Diffuse numbness of hand mostly involving the 2nd and 3rd fingers

Absence of nocturnal awakening bc of pain or numbness

-wrist down in pain sensory weakness

304
Q

Anterior interosseous syndrome

A

To long finger flexors

Ok sign

Can’t flex distal phalanxes

Now ensory loss

305
Q

Ulnar

A

Axilla elbow-between medial epicondyle and olecranon

Cubical tubule-between tendinous arch of FCU

Wrist-guyon canal

306
Q

Ulnar elbow EMG

A 
Abnormalities in 1st dorsal interosseous
Abductor digiti minimi
Adductor polices
Flexor carpi ulnaris 
Flexor digitorum profundus

Transition around elbow disturbed

307
Q

Froment sign

A

Can’t adduct thumb it is an ulnar neuropathy cant grab sheet of paper end up using distal thumb to pinch paper

308
Q

Radial mononeuropathy

A

Axilla-crutch palsy

Saturday night palsy
Supination
Wrist

309
Q

Edx features Saturday night palsy

A

Radial motor and sensory studies often normal

EMG findings in extensors of wrist and digits and perhaps brachioradialis

310
Q

Perineal

A

Fibular neck

Leg crossing , squatting

Foot drop weak evertors, sensory loss in dorsum of foot

311
Q

Sciatic

A

Sciatic notch, hip , piriformis muscle

Pain down lateral thigh, footdrop absent ankle jerk

Mainly L5-but L5 weak inversion and eversion! Distinguishing

312
Q

Posterior tibial

A

Medial amlleolus

Muscle edema
Ankle fracture, tenosymovitis

Sensory loss sole of foot

313
Q

Last fem cutaneous

A

Inguinal ligament

Tight clothing weight gain
Sensory loss in lateral thigh

Just sensory pinch over pelvic brim with belt

314
Q

Peroneal mononeuropathy

A

Stimulation at ankle toe twitch

Below knee same

Above knee-drop in amplitude

Needle-abnormalities in Tb ant, EHL, EDB, PL, TBI post and SHBF are normal

315
Q

Peripheral neuropathy

A

Usually symmetric, may be motor, sensory, autonomic or combination

Progressice, but not always

Acquired or inherited

316
Q

Motor peripheral

A

Weak, atrophy, hypo arreflexia, cramps, fasciculations

317
Q

Sensory

A

Large-position vibratory

Small-pain/temp sense

318
Q

Distribution peripheral neuropathy

A

Stalking destruction

Pain sensory loss weakness symmetrical and most usually distal portions of limbs

Legs affected first and more severely that arms

STOCKING GLOVE

319
Q

Causes peripheral neuropathy

A

MANY

Hereditary, metabolic and endocrine, infections, immune, defiency, toxins, drugs, vasculitis paraneoplastic, idiopathic

320
Q

Metabolic/endocrine

A

DM, thyroid uremia, porphyria

321
Q

Defiency

A

B1, 6, 12, E, copper

322
Q

Toxins

A

Alcohol metals, n-hexane, organophosphate

323
Q

Drug

A

Vinca alkaloids, phenytoin, isoniazid, amiodarone

Cisplastin, nitrofurantoin and a host of others

324
Q

Vincristine

A

Peripheral neuropathy

325
Q

B12 defiency

A

Combined systems degeneration

Dorsal column, Corticospinal tracts (lateral and ventral)

Neuropathy, babinski
Lose reflexes, babinski is from Corticospinal tract dysfunction,

Depressed reflexes but babinski!

326
Q

How test b12

A

Romberg

For position sense

327
Q

Vasculitis peripheral neuropathy

A

RA, SLE, polyarthritis nodosa

328
Q

Paraneoplastic peripheral neuropathy

A

Before, during after tumor

Pure sensory (dorsal ganglionopathy)

Check for antibodies

329
Q

Pure sensory polyneuropathy

A

Rare-considered sensory ganglionopathy

  • paraneoplastic
  • toxins(platinum Cisplastin)
330
Q

Small fiber polyneuropathy

A

Pain burning dysesthesias, paresthesia, temp sensation prob

Decreased pin prick and temp sensation
Dysesthesias to light touch
Normal strength reflexes, proporioception, vibratory sensation

EMG/nvc normal

331
Q

Diabetes

A

Most common cause neuropathy

-distal sensorimotor neuropathy stocking glove

But can cause cranial nerves-III most common but VI)

Nerves not operating optimally bc of DM and glucose metabolic abnormalities any little disruption may be magnified -carpal tunnel and facial neuropathies

Lumbo-sacral, radiculopathy

332
Q

Hereditary neuropathies Charcot Marie tooth neuropathies

A

Type I and II

333
Q

HMSN1

A

Most common demyelinating

334
Q

HMSNII

A

Axonal

335
Q

HMSNIII

A

Hm

336
Q

HMSN(

A

AD 10-20 with difficult walking or running just clumsy

Distal symmetric atrophy legs>arm

Arreflexia
Mild sensory loss
Skeletal deformities (high arch hammer toe scoliosis)
EMG uniform slowing of Moro’s nerve conduction (demyelination )

HIGH ARCH HAMMER TOE

337
Q

HMSN II

A 
AD adulthood
Distal symmetric atrophy
Motor nerve legs>arms
Arreflexia
Axonal not myelin EMG is normal or nearly normal
338
Q

Fairy

A

A galactosidase defiency

Kidney problems
Hereditary polyneuropathies

339
Q

Metachomiatc leukodystrohy

A

Arylsulfatase a defiency

Polyneuropathy

340
Q

Refusumdisease

A

Big orange tonsils

Phytanic acid storage disease

341
Q

Tangier disease

A

Defiency in HDL hereditary polyneuropathies

342
Q

Acquired demyelinating polyneuropathies

A

Acute-Gillian barre

Chronic-inflammatory demyelination polyneuropathy

343
Q

Gillian barre

A

Acute/subacute ascending paralysis

Antecedent illness, surgery, immunization

EBV, mycopalsma, campylobacter

HIV hodgkin can mimic

344
Q

GB onset

A

Low back pain radiating down legs

Ascending from feet

Hypo or absent DTR

Minimal sensory signs

Possible respiratory failure, autonomic involvement

Nadir-4-6 weeks improves over weeks

345
Q

Big problem GB

A

Respiratory insuffiency

346
Q

Lab GB

A

Spinal fluid increase protein normal cell and glucose

NCV-slow conduction velocity, focal conduction block, prolonged F waves

347
Q

Issue GB

A

Support and pay attention to swallowing, respiration, CVD, infection, DVT

348
Q

Treat GB

A

IVIg

349
Q

Prognosis GB

A

90% recover weeks to months
Some die, disables, lots have persistant fatigue with extremes of acute tivity

If emg shows axon involvement those areas get poor prognosis

350
Q

Miller fisher

A

GB
Kids
Ophthalmoplegia, ataxia, areflexia,
Facial weakness, dysarthria, dysphagia also possible, GQub and GT1a antibodies

351
Q

Acute motor axonal neuropathy

A

GM1, GM1b, GD1a antibodies

352
Q

Acute motor and sensory

A

GM1, GM1b, GM1a

353
Q

GB antibodies

A

None associated but variants do

354
Q

Chronic inflammatory demyelinating polyneuropathy

A

Similar to GB but slower and more persistent >2 months

Progressive or relapsing

IgM Ir IgG

Treat with IVIg, steroids, plasma exchange, immunosuppression

May occur de novo or as sequelae of GBS

355
Q

Multifocal motor neuropathy

A

Mimics peripehral but different
Slowly progressive distal weak
No UMN or sensory

GM-1 antibody ad emg show conduction block or focal demyelinating features!!!!

IVIg

356
Q

HIV neuropathies

A

Distal symmetrical polyneuropathy

357
Q

Blood tests

A

CBC, chemistry panel, fasting blood glucose, ESR< ANA, RF< thyroid function

Basophils stippling, IEP, B12 folate

358
Q

Systemic vasculitis

A

AANCA

359
Q

MGUS

A

Anti MAG

360
Q

Multifocal motor neuropathy

A

Anti GM1

361
Q

Heavy metal

A

History of exposure

362
Q

Skin biopsy

A

Small fiber neuropathy

363
Q

EMG.ncv

A

Rarely specifi except GBS, CMT1, MMN

364
Q

Presynaptic

A 
Lambert eating
Botulism
Steroids
Mg
Black widow
Congenital myasthenic
Aminoglucosides
Tetanus
Tick paralysis
A aminopyridine
365
Q

Synaptic

A

Oraganophosphates
Edrophonium
Neostigmine
Congenital

366
Q

Post synaptic

A

Myasthenia

367
Q

Myasthenia

A

Defect in neuromuscular transmission antibody to Ach receptor on membrane

368
Q

Etiology myasthenia

A

Not sure most sporadic but high frequency of HLA haplotypes B8 DR3

Seen with other autoimmune SLE RA thyroid

369
Q

Incidence

A

All age group but young women old men

370
Q

Characteristics myasthenia gravis

A

Fluctuating weakness-ptosis, dyplopia

Clinical response to cholinergic drugs

*my eyelids droop when I’m driving and squinting then in shade see droopy and i see double later in the day

Achietylcholinesterase

371
Q

Clincial history and exam myasthenia gravis

A

Acetylcholine receptor antibodies

-MUSK antibodies

372
Q

EMG myasthenia gravis

A

Decremental response on repetitive stimulation increased jitter on single fiber EMG

373
Q

Tension

A

Edrophonium test

Positive in >90% of patients

374
Q

Side effects edrophonium

A

Bradycardia, ventricular arrhythmias,

375
Q

Antibody negative myasthenia

A

Many will have MUSK antibodies

Normal have antibodies to achR

376
Q

EMG myasthenia

A

3 shocks per second see normal reproducible responses look identical even

Myasthenia each shock get decrease in force of contraction and bigggest between 1st and 2nd

DECREMENTAL RESPONSE

377
Q

Give tensiolon

A

The ptosis is gone! That’s the tension tests

Lasts 10 minutes then ptosis comes back but can run into problem ith ventricular arrhythmias

378
Q

Treat myasthenia gravis

A

Acetylcholinesterase inhibitors (mestinon)
Prednisone
Immunosuppressive agents
Plasma exchange/IVIg
Thymectomy probably helpful but without thymoma not indicated

379
Q

What drugs exacerbate or unmask myasthenia gravis

A

Neuromuscular blockers-succinylcholine, pancuronium

Excessive anticholinesterase medication
Corticosteroids and ACTH-usually with high initial dose

Thyroid supplements

Mg salts-

Antiarrhythmic-lidocaine, quinine, procainamide, verampamil, b blockers

Antibiotics-aminoglycosides

D penicillamine-may cause antibodies and stop antibodies go away and so does MG! Can get antibodies produced but not have myasthenia gravis

380
Q

Antibody myasthenia

A

10% no anti AcHR

40% MUSK

381
Q

MUSK

A

Occulopharyngeal weak
Neck shoulder respiratory weakness
Indistinguishable from antibody from positive MG

382
Q

Treat myasthenia gravis

A

Poor response to anticholinesterase medications

383
Q

Lambert Eaton

A

Autoimmune to voltage gated

SCC, breast ovarian

384
Q

Clincila lambert eaton

A

Proximal weakness, loss of deep tendon reflexes, myalgia, dry mouth, impotence,

Oropharyngeal and ocular muscles may be mildly affected but not to the degree in MG

Strength improve after exercise
May see slight response to tensilon

385
Q

Bulbar and ocular

A

MG

386
Q

Office test MG

A

Eye lids droop

Hold arms out and have them look up at finger do it for a minute
When minute it up i want you to keep arms up and shift eyes to finger

MG-they will gradually sag as msucles fatigue see ptosis !

387
Q

Antibodies lambert

A

VGCC antibodies in most

388
Q

EMG lambert

A

Low amplitude response increase with brief exercise

Incremental response on fast repetitive stimulation

389
Q

20 shocks per second lambert 50

A

BUILD UP!

390
Q

Treat lambert eaton

A

First look for malignancy

Acetylcholinesterase inhibitors-mestinon
Amifampridine
3-4 diaminopyridine helps most but AE

Guanosine hydrochloride helps LEMS but AE

Immunosuppression

IVIg

391
Q

Botulism

A

Blocks presynaptic Ach release

Mg to lambert eaton? NO Mg is +2 and Ca is +2 so Mg interfere with Ca influx at presynaptic terminal and make worse

392
Q

Clincial botulism

A

Dry, sore mouth , blurred vision, diplopia, nausea, vomiting hydros is, total external ophthalmoplegia, facial oropharyngeal limb and respiratory paralysis

393
Q

Treat botox

A

ICU monitoring with respiratory support and general medical care

-antitoxin (horse serum product which may cause serum sickness or anaphylaxis)

Guanidine hydrochloride (AE bone marrow suppression)

394
Q

Nerve gases

A

Organophosphate terrorist

Easily vaporized

Block acetlycholineesterase and overstimulation of end organ-cholinergic crisis can be to vapor or liquid

Onset is fast

Miosis, increase secretions, bronchospasm, abdominal cramps, NV, diarrhea, HR, BP,

Death by respiratory failure

395
Q

Treat nerve gas

A

Decontamination-remove clothiers, clears skin with water and Nahypochlorite

Respiratory support

Atropine

Seizures

396
Q

Connective tissue disorders

A

Ok

397
Q

22 yo arthralgia ANA 1:160 titer with a homogenous diffuse staining pattern

A

She might have an autoimmune process as the etiology for her symptoms

398
Q

ANA

A

Non specific

399
Q

1:160 ratio ANA

A

High so probably autoimmune process going on

400
Q

Homogenous diffuse staining pattern ANA

A

Everywhere

401
Q

7 yo female spot on face been there for a couple of weeks

A

Localized scleroderma

402
Q

Discoid lupus what look like

A

Ring worm

Got centralized area nothing going on raised ring

403
Q

What is this localized lesion called

A

Morphia-benign localized area of fibrosis wont progress or get worse typically in kids

404
Q

55 yo increased dry eyes, bl facial swelling, dry mouth, what most likely at risk of developing

A

Oral candidiasis

Sjorgen

405
Q

Libyan sacs

A

Lupus

406
Q

Esophageal adenocarcinoma

A

Diffuse sclerosis can lead to GERD-barret-esophageal adenocarcinoma

407
Q

Gastric antral vascular ecstasia

A

Diffuse scleroderma

408
Q

Pulmonary artery HTN

A

Limited scleroderma

409
Q

Intestinal lung disease

A

Diffuse scleroderma

410
Q

50 yo caucasion with malaise severe neck and bl shoulder stiffness and pain all day long but more in morning, weaker and cant comb hair, 7lb weight loss past 3 months, ESR up, CK normal

A

Temporal arteritis

Polymyalgia rheumatica

411
Q

Polymyalgia rheumatica

A

Pain makes them feel weak

*normal msucle strength but feels weak be of all the pain

412
Q

Smoking history

A

RA

Thromboangiotis obliterrans

413
Q

Primary raynaud syndrome

A

Hyperresponse to emotion, cold no underlying pathology

BENIGN

414
Q

Secondary raynaud

A

Secondary to scleroderma of CT process

415
Q

Hep B

A

Polyarthritis nodosum

416
Q

DVT

A

Factor V Leiden

Antiphospholipid
Lupus

Berchets-oral genital ulcer uveitis DVT!

417
Q

25 yo joint pains med student 3rd year had positive PPD and quantiferon gold put on isoniazid and B6. What serology seen

A

Histon Ab- she has drug induced lupus from isoniazid

418
Q

DsDNA

A

Lupus

419
Q

Anti Sm

A

Lupus

420
Q

Centromere

A

Limited scleroderma

421
Q

Scl70

A

Diffuse scleroderma

422
Q

37 black chest pain worse on respiration, left leg swollen , tired and 10 lb weight loss, history and psychotic episode, red hot swollen red lower extremity, bicytopenia, anemia and thrombocytopenia, DVT . ECG sinus tachycardia

A

Lupus-bc cotton wool spots, thrombocytopenia, neuropsych manifestations, african American, no insurance, DVT-antiphospholipid antibody

VDRL

423
Q

Chest pan in lupus-

A

PE orpleuritis

424
Q

If lupus heart pain change position and ECG diffuse St segment changes

A

Pericarditis

425
Q

Sinus tachycardia

A

PE

426
Q

Ecgcyclic citrulinated

A

RA

427
Q

Topoisomerase I Ab

A

Diffuse scleroderma

428
Q

Histone ab

A

Drug induced lupus

429
Q

Centromere

A

Limited scleroderma

430
Q

VDLR

A

Lupus

431
Q

Best management plan for her Lupus DVT

A

Hydrocychloroquine (mainstay treatment for lupus) and warfarin (for the DVT)

432
Q

When give warfarin

A

Bridge with enoxaparin (a low molecular wight heparin) until warfin is in therapeutic range

Warfin on own-prothrombotic

433
Q

Amlodipine

A

Ca channel blocker

Raynaud

434
Q

Omperazole

A

GERD from diffuse scleroderma

435
Q

IVIG and high dose Asprin (ASA)

A

Kalasaki

436
Q

Stop smoking

A

RA

Bergers (thromboangitis obliterrans)

437
Q

50 year old african American hashimoto thyroiditis, ANA and ds DNA , abdominal pain

A

SLE

438
Q

Interstitial lung disease

A

RA, diffuse scleroderma(cause of mortality!)

439
Q

Pulmonary artery HTN

A

Limited scleroderma (cause of mortality)

440
Q

Intestinal angina

A

Post or dial intermittent abdominal pain

Lupus but not cause of death

441
Q

Seizure disorder

A

Lupus but not cause of death

442
Q

Atherosclerosis

A

Cause of death SLE-HIGH RISK HEART ATTACK SO MODIFY ALL RISKS FOR ATHEROSCLEROSIS!!! Blood lipids, exercise program,

443
Q

45 yo white female facial numb right sided weakness ischemic stroke, no meds, vitals normal, serology and Smith, dsDNA and antiphospholipid

RRR murmur, valve thickening and Cerritos valvular

A

Libyan sacks endocarditisfrom lupus

Normal lipids and vitals bc ischemic stroke is usually froma. Vascular disease of atherosclerosis in HTN hyperlipidemia

444
Q

Infectious endocarditis

A

Blood cultures

445
Q

Murmur stroke valve lesion

A

Libyan sacks

446
Q

What murmur libman

A

Mitral regurgitation

447
Q

Pericarditis

A

Lupus with positional changes and ECG elevated st

448
Q

Rheumatic heart disease

A

Can cause endocarditis mitral valve
No recent sick so not it

Need receipt strep

449
Q

Persistent a fibrillation

A

Can cause stroke

450
Q

Which h/o bipolar disorder joint pain episodic chest pain and speckled pattern ANA and malar rash which serologic test correlated with disease state

A

Anti dsDNA -is what monitor for disease process and treat work

Sm and dsDNA both go with lupus

451
Q

CK up

A

Dermatomyositis polymyositis

452
Q

IgA deposition

A

Henoch s purpura

453
Q

Best preventative manage lupus

A

Ok

454
Q

Is my hydroxychloroquine working

A

Use dsDNA

455
Q

Dentist

A

Sjorgen risk infection and carries

456
Q

Set up EGD appointment (endoscopy)

A

Scleroderma

CREST=carcinom is raynaudys esophagility dysmotility sclarodactyly and telangiectasia ESOPHAGEAL can lead to gerd and stuff

457
Q

EDG diffuse scleroderma

A

GERD barrett to adenocarcinoma

Gastric antral vascular ectasia if irony efiency anemia!!! EGD

458
Q

Order PFT

A

Diffuse scleroderma bc has interstitial lung disease

459
Q

Schedule an echo or influenza vaccine for SLE

A

Influenza *** vaccinate, stay away from sun, regular cancer screening

Echo-pericarditis->tamponade or effusion or show libann before manifest -need something to order echo BUT echo can be preventative

460
Q

Echo preventative in which scleroderma

A

Limited bc of pulmonary artery HTN and if echo PFT no good right heart cath

461
Q

43 yo african American female no insurance fibrosis and necrosis several fingers sometimes food catches in throat

A

CREST

Dilation of small vessels causing focal red lesions

462
Q

Strawberry tongue

A

Kawasaki

463
Q

Purple red rash on eyelids

A

Heliotrope rash with dermatomyositis

464
Q

Proximal muscle weakness

A

Polymyositis, dermatoymositis, polymyalgia rheumatica (not true weakness)

465
Q

Parotid gland big

A

Sjogrens mumps infection

466
Q

Crest

A

Limited scleroderma

467
Q

29 yo Hispanic female arthralgias and depression C3 and C4 low and ds DNA and renal insuffiency

A

Type III hypersensitivity

Lupus

468
Q

Hep B

A

Hep B with polyarthritis nodosa

469
Q

Screen for cervical cancer

A

HPV , dermatomyositis typically look for occult malignancy if present dermatomyositis

Ovarian, cervical bc age , any cancer starting with age and risk factors

470
Q

Tanning bed treatment

A

No lupus decrease sun exposure

471
Q

Heliotropes rash

A

Dermatomyositis

472
Q

45 yo white female finger stiffness hard white nodules at times go blue slight perioral furrowing with red spots aon lips and tongue -telangiectasia

A

Esophageal dysmotility

Crest limited scleroderma

473
Q

Pericarditis

A

Lupus

474
Q

Malt lymphoma

A

Sjorgen! Dry mouth dry wyes MALT lymphoma

475
Q

Temporal arteritis/ giant cell arteritis

A

Polymyalgia rheumatica

DIAGNOSE WITH BIOPSY OF TEMPORAL ARTERY

476
Q

Parotid gland

A

Sjorgen

DIAGNOSE WITH LIP BIOPSY

477
Q

43 yo females dyspnea SOB GERD, raynaud, carpal tunnel, restrictive PFT, mediastinal LAD an honeycombing, topoisomeraseI ab positive, EF 50% and pulmonary artery pressure 20

A

Interstitial lung disease

478
Q

Mediastinal lymphadenopathy

A

Sarcoidosis

479
Q

Honeycombing dry Velcro crackles

A

Wet crackles-CHF

480
Q

Topoisomerase antibody

A

Diffuse scleroderma

481
Q

EF50

A

Normal

482
Q

PAP 20

A

High but not too high

> 40

483
Q

Asthma

A

Allergies, excema

Eosinophilic granulomatosis

484
Q

Emphysema

A

A1- antitrypsin

Or a lot of smoking

485
Q

CHF

A

Systolic low EF

Diastolic-cant relax

Polyarthritis nodosa

486
Q

50 yo caucasion male bl weakness having trouble getting out of bathtub and up out of a chair cant bend fingers symptoms gradual over last year. ESR CRP CK normal

Endomysial inflammation rimmed vacuoles on H and E cNIA antibodies

A

Supportive-he has inclusion body myositis , usually serology normal finger flexors serology and biopsy inclusion body

Doesn’t respond to anything but supportive

MALES

487
Q

39 yo female from India uncontrolled HTN taking 4 antihypertensive meds, fundoscopic shows copper wiring (retinal infarcts), radial and pedal pulse 1/4, narrowing renal arteries, highest risk of getting which of the following

A

Aorta rupture

Takiasku narrowing renal artery-renal artery stenosis on many anti HTN secondary cause of renal artery stenosis

Large vessel vasculitis, aorta, pulseless disease, lot of collaterals form so limb ischemia rare,

488
Q

Coronary artery aneurysm

A

Small vessel

-talk about later

489
Q

PE

A

Lupus, antiphospholipid bechet

490
Q

MI

A

Atherosclerosis, lupus

491
Q

Aortic suture

A

Large vessel

Takiatsu

492
Q

55 yo Turkish mouth and genital sores h/o DVT< HLAb51 present pustilat site of lab draw

A

Bechet

Mouth, genital sore, eye inflammation

Pustule is called pathergy

493
Q

30 yo african American male, stiffness weakness arthralgias, carpal tunnel confusion bp 212/109 , granular casts, anti centromere ab neg, RNA polymerase I and III abs are positive . What is diagnosis

A

Scleroderma renal crisis

Diffuse scleroderma

Renal crisis-predominance for males, lupus has a lot of renal studs but nocrisis like scleroderma

494
Q

Gave

A

Diffuse scleroderma

495
Q

Granulomatosis with polyangitis

A

Wegners-Upper rep and lung

496
Q

Polyarthritis nodosa

A

Vasculitis in men associated with hep B effects kidney but not in this way

497
Q

RNA p I and III ab

A

Diffuse scleroderma

498
Q

45 yo female HA wont go away with Tylenol, blurry vision for 3 days, lost 10 lb over month, painful to chew food, smoker, ESR up, temporal arteries

A
  1. Temporal arteritis perform a biopsy

1. BUT IF DELAY CORTICOSTEROIDS THEY WILL GO BLIND FOR

499
Q

Polyarthritis nodosa

A

HBC

500
Q

41 yo F weakness everyone in family healthy, weak in arms and legs, diffuse itchy skin, violacious periorbital macular erythema, papules over the dorsal MCP joints with a shawl sign noted what additional work up

A

Dermatomyositis

Heliotrope rash

Mammogram !!!!!!!!!!!!!! Look for occult malignancy

501
Q

Hep b

A

Polyarthritis odosum

502
Q

Lip biops

A

Sjorgen

503
Q

Right heart cath

A

Limited scleroderma look for pulmonary arter HTN

504
Q

PFT

A

Diffuse scleroderma for interesting lung disease

505
Q

41 yo elevated CK msucle weak last 3 weeks, muscle biopsy endomysial inflammation with invasion of non necrotic muscle fibers. PE normal 4.5 muscle strength of bl UE and LE anti jo ab on serology

A

Polymyositis

506
Q

Polymyalgia rheumatica

A

Polyarthritis

507
Q

Inclusion body myositis

A

Different muscle biopsy. More common in males and we may try steroids and immunosuppression but treatments fail and doesnt mean we should have tried them
SUPPORTIVE CARE is what we rely on heavily for inclusion body

508
Q

Giant cell arteritis

A

Persistent HA, vision changes, temporal artery biopsy showing granulomas and multinucleated giant cells

509
Q

30 yo female concerns raised rash worsen over last month tingling in arms and legs MPO ANCA positive and eosinophilia

A

Palpable purpura

(Henoch is also palpable)

Thrombocytopenia purpura not palpable

Eosinophilic granulomatosis with polyanitis (vasculitis and asthma, allergies and peripheral eosinophilia) ASTHMAAAAAAA!!!! History

510
Q

Hep B

A

Polyarthritis nodosa

511
Q

Polymyalgia

A

Terms art

512
Q

Occult malignancy

A

Dermatomyositis

513
Q

Primary biliary cirrhosis

A

Potential manifestation from diffuse scleroderma

514
Q

35 yo male chronic hep b and HTN
Has concern of fatigue and myalgia. Concerned abut numbness in hands and feet. Right foot drapes when he walks. Skin changes. What organs are effects

A

Diagnosis-polyarthritis nodosa

Hep B! Can have HTN due to renal manifestations , fatigue, myalgia, neuropathy, vasculitis neuropathy (foot drop)

Cardiac-CHF, HTN, MI , GI-intestinal postprandial abdominal pain , skin -albino reticularis skin remodeling , ulcers nodules gangrene, renal-infarcts as HTN

Pulmonary spared

515
Q

4 yo Asian female present with diffuse LDA. Fever 102 last 2 days, palmar erythema rapid strep negative, congestive eyes, and tongue papilla. What is cause of mortality in late disease

A

Kawasaki-mucucutaneous lymph node sydnrome

Childhood can resemble scarlet fever or toxic shock, strawberry tongue is the papilla , vasculitis an lead to limb ischemia as opposed to takiatsu which is collaterals, but not cause of mortality

CORONARYA RTERY ANEURYSMM (smaller vessel as opposed to tak)-causes death

516
Q

Aortic rupture

A

Takiastu

517
Q

PE

A

Bechet and antiphospholipid

518
Q

CHF

A

Polyarthritis nodosa

519
Q

50 yo WF with rashon ankles, chronic sinusitis, lung nodule on lung show necrotizing granuloma, heme analysis shows hematuria. What is also found on PE

A

Wegners(granulomatosis with polyangiitis_ Upper resp, lower resp, kidney and skin , renal manifestations, lung nodule is necrotizing granuloma and sinus disease

SADDLE NOSE

520
Q

Strawberry tong

A

Kawasaki or strep pharyngitis

521
Q

Malar rash

A

Lupus

522
Q

Got torn

A

Dermatomyositis

523
Q

Saddle nose

A

Wegners!!!!! Destruction and collapse of nasal bridge bc of process

524
Q

25 yo male finger ulcer worsening and another starting. Dad died of colon cancer, smokes a pack per day, rarely drinks alcohol, all labs are normal, most likely cause of finger ulcer

A

Bergers (thromboangiitis obliterans)

Smoking young males start losing fingers and extremities no internal organ involvement

STOP smoking or will continue to lose digits

525
Q

Type II hypersentivity

A

Lupus

526
Q

IgA

A

Henoch

527
Q

Basement membrane antibody

A

Good pastures

528
Q

Kruse skeletal msucle relaxants

A

Ok

529
Q

Two categories of skeletal muscle relaxants

A

Neuromuscular blockers-interfere with transmissiona t the neuromuscular end plate and lack CNS activity
Used as adjunct during anesthesia
No known effects on consciousness or pain threshold

Spasmolytic agents-often called centrally acting muscle relaxants
-used to reduce spasticity in a variety of neurologic conditions (chronic back pain, fibromyalgia, muscle spasm)

530
Q

Neuromuscular blockers

A

a) Nondepolarizing
i) Isoquinoline derivatives
(1) Atracurium (2) Cisatracurium (3) Doxacurium (4) Mivacurium (5) Tubocurarine
ii) Steroid derivatives (1) Pancuronium (2) Pipercuronium (3) Rocuronium (4) Vecuronium
b) Depolarizing
i) Succinylcholine

531
Q

Acetylcholinesterase inhibitors

A

a) Ambenonium b) Donepezil
c) Echothiophate d) Edrophonium e) Galantamine f) Neostigmine g) Physostigmine h) Pyridostigmine i) Rivastigmine
j) Tacrine

532
Q

Muscle relaxants spasmolytics (central and non central)

A

Central-baclofen, carisprodol, cyclobenzaprine, diazepam, tizanidine

Non centrally-dantrolene, botulinum toxin

533
Q

Antimuscarinic compounds

A

Atropine, glycopyrrolate

534
Q

Cholinesterase reactivators

A

Pralidixime

535
Q

How block end plate function

A

Nondepolarizing neuromuscular blocking agents

(1) Act as antagonists of the nicotinic acetylcholine receptor (nAChR)
(2) Prototype: d-tubocurarine
ii) Depolarizing neuromuscular blocking agents
(1) Blockade can be produced by the excess of a depolarizing agonist (e.g., excess acetylcholine (ACh), see below)
(2) Prototype: succinylcholine

536
Q

Atracurium

A

Isoquinoline

Eliminated by hydrolysis by plasma esterases

2-4 min onset

Works 30-60 min

537
Q

Cisatracurium

A

Isoquinoline

Spontaneous elimination

204 min onset

25-45 min duration (intermediate)

538
Q

Doxacurium

A

Isoquinoline

Renal elimation

4-6 min onset

90-120 min action (long action)

539
Q

Mivacurium

A

Isoquinoline

Plasma cholinesterase

Time 2-4 min

10-20 min action (short)

540
Q

Pancuronium

A

Steroid

Renal
4-5 min onset

120-180 long actin

541
Q

Pipecuronium

A

Steroid

Renal and hepatic excretion

204 min onset

80-100 long action

542
Q

Rocuronium

A

Steroid
Hepatic elimination

1-2 min onset

20-35 intermediate

543
Q

Vecuronium

A

Steroid

Renal and hepatic elimination

2-4 min onset

20-35 min intermediate

544
Q

Succinylcholine

A

Plasma cholinesterase
1-2 min onset

Ultra short duration 5-8 min

545
Q

Non depolarizing neuromuscular blocking agent pharmacokinetics

A

a) Pharmacokinetics

i) Highly polar; must be administered parenterally

546
Q

Nondepolarizing neuromuscular blocking agents pharmacodynamics

A

Pharmacodynamics
i) MOA: competitive antagonists at the nAChR
ii) As a general rule, larger muscles (abdominal, trunk, paraspinous, diaphragm) are more
resistant to blockade and recover more rapidly (the diaphragm is usually the last muscle to
be paralyzed and the quickest to recover

547
Q

Reversal of neuromuscular blockade with non depolarizing neuromuscular blocking agents

A

Reversalofneuromuscularblockade

i) Effects of nondepolarizing neuromuscular blocking agents are reversed upon the addition of acetylcholine using an acetylcholine esterase (AChE) inhibitor (larger doses of nondepolarizing agents diminish the antagonizing effects of cholinesterase inhibitors due to blockade of channel pore, which occurs at higher doses)
ii) Anticholinergic agents (e.g., atropine, glycopyrrolate) are coadministered with AChE inhibitors to minimize adverse cholinergic effects (bradycardia, bronchoconstriction, salivation, nausea, vomiting) at muscarinic AChRs

548
Q

Adverse effects of nondepolarizing agents

A

) Adverse effects of nondepolarizing agents
i) Some nondepolarizing agents produce histamine release, which can cause histamine-like
wheals to appear, bronchospasm, hypotension, and bronchial and salivary secretion
(premedication with an antihistaminic compound can attenuate these effects)
ii) At large doses, tubocurarine can produce acetylcholine receptor blockade at autonomic
ganglia and at the adrenal medulla, which can result in a fall in blood pressure and
tachycardia
iii) d-tubocurarine causes significant histamine release and has a very long duration of action,
its clinical use has declined in favor of more specific, shorter-acting neuromuscular blockers

549
Q

Nondepolarizing neuromuscular blocking agents AE

A

i) Some nondepolarizing agents produce histamine release, which can cause histamine-like
wheals to appear, bronchospasm, hypotension, and bronchial and salivary secretion
(premedication with an antihistaminic compound can attenuate these effects)
ii) At large doses, tubocurarine can produce acetylcholine receptor blockade at autonomic
ganglia and at the adrenal medulla, which can result in a fall in blood pressure and
tachycardia
iii) d-tubocurarine causes significant histamine release and has a very long duration of action,
its clinical use has declined in favor of more specific, shorter-acting neuromuscular blockers

550
Q

Drug drug interactions non depolarizing neuromuscular blocking

A

Drug-drug interactions
i) Anesthetics
(1) Inhaled anesthetics potentiate the neuromuscular blockade produced by
nondepolarizing muscle relaxants in a dose-dependent fashion
(2) Isoflurane&raquo_space; sevoflurane = desflurane = enflurane = halothane > nitrous oxide
ii) Antibiotics
(1) Aminoglycosides (gentamicin, tobramycin, amikacin, streptomycin, neomycin,
kanamycin, paromomycin, netilmicin, spectinomycin) have been shown to enhance
neuromuscular blockade
(2) Some antibiotics reduce the release of ACh in the prejunctional neuron, likely due to
blockade of specific P-type calcium channels
iii) Other agents that block signaling at the NMJ (e.g., tetrodotoxin, local anesthetics,
botulinum toxin) enhance the actions of nondepolarizing agents

551
Q

Nondepolarizing neuromuscular blocking agent effects of disease and aging on neuromuscular response

A

Prolonged duration of action from nondepolarizing relaxants occurs in elderly patients with reduced hepatic and renal function

ii) Neuromuscular blockade by nondepolarizing muscle relaxants is enhanced in patients with myasthenia gravis
iii) Patients with severe burns and those with upper motor neuron disease are resistant to nondepolarizing muscle relaxants (likely due to increased expression of nAChRs, which requires an increase in dose

552
Q

Nondepolarizing neuromuscular blocking agents : atracurium

A

Atracurium (isoquinoline derivative, intermediate acting)

(1) Inactivated by a form of spontaneous breakdown known as Hofmann elimination
(2) Less histamine release than other nondepolarizing agents
ii) Cisatracurium (isoquinoline derivative, intermediate acting

553
Q

NDM cisatracurium

A

) Cisatracurium (isoquinoline derivative, intermediate acting)

(1) Stereoisomer of atracurium with fewer side effects (less laudanosine, histamine release)
(2) Can be used even with significant renal and hepatic impairment; devoid of CV effects
iii) Doxacurium (isoquinoline derivative, long-acting

554
Q

doxacurium

A

iii) Doxacurium (isoquinoline derivative, long-acting)
(1) Not often used because of the long-lasting effects as well as high degree of elimination by the kidney (not used in patients with renal failure); devoid of CV effec

555
Q

Mivacurium

A

v) Mivacurium (isoquinoline derivative, short acting)
(1) Large doses can be associated with histamine release and subsequent CV effects (2) Metabolism by plasma cholinesterase

556
Q

Steroid derivatives

A

v) Steroid derivatives
(1) Intermediate-acting steroid muscle relaxants (vecuronium, rocuronium) tend to be
more dependent on biliary excretion or hepatic metabolism for their elimination and are more likely to be used clinically than long-acting steroid relaxants (pancuronium, pipecuronium

557
Q

The __ neuromuscular blocking agents have the least tendency to cause histamine release

A

Steroidal

558
Q

Rocurinium

A

(3) Rocuronium

(a) Rocuronium has the most rapid time of onset (60-120 seconds) (b) Alternative to succinylcholine

559
Q

Succinylcholine

A

a) Succinylcholine is the only depolarizing blocking drug used clinically

560
Q

Pharmacokinetics succinylcholine

A

Ultra-short duration of action is due to rapid hydrolysis and inactivation by butyrylcholinesterase and pseudocholinesterase in the liver and plasma, respectively
ii) Prolonged neuromuscular blockade can occur in patients with a genetically abnormal
variant of plasma cholinesterase after a dose of succinylcholine
iii) Not effectively metabolized at the synapse by acetylcholinesterase

561
Q

Pharmacokinetics succinylcholine

A

E ffects of succinylcholine are similar to ACh (i.e., succinylcholine is a nAChR agonist), but
with longer duration of action compared to ACh

562
Q

Succinylcholine phase I block

A

Phase I block (depolarizing): after activating the nAChR, depolarization of the motor end
plate spreads to adjacent membranes causing muscle contraction; the depolarized membranes remain depolarized and unresponsive to subsequent impulses (i.e., a state of depolarizing blockade); because excitation-contraction coupling requires end plate repolarization and repetitive firing to maintain muscle tension, flaccid paralysis results; phase I depolarizing block is augmented, not reversed, by cholinesterase inhibitors

563
Q

Succinylcholine phase II block

A

Phase II block (desensitizing): continued exposure to succinylcholine causes the initial end plate depolarization to decrease and the membrane becomes repolarized; the membrane is unable to be depolarized because the receptor is desensitized; although this mechanism is unclear, the channels behave as if they are in a prolonged closed state similar to nondepolarizing block; phase II desensitizing block is reversed by acetylcholinesterase inhibitors (increase in ACh at the NMJ

564
Q

Effect succinylcholine

A

iv) A standard pharmacological dose of intravenous succinylcholine causes transient muscle fasciculations (twitches) over the chest and abdomen within 30 sec; paralysis develops rapidly (<90 sec) in arm, neck, and leg muscles initially followed by respiratory muscles

565
Q

Clincial succinylcholine

A

) Succinylcholine is often used for rapid sequence induction (e.g., during emergency surgery when the objective is to secure the airway rapidly and prevent soiling of the lungs with gastric contents) and for quick surgical procedures where an ultrashort acting neuromuscular blocker is practical

566
Q

Reversal of neuromuscular blockade

A

Time due to cholinesterase degradation

567
Q

AE and contraindications succinylcholine

A

Cardiovascular effects
(1) Cardiac arrhythmias when administered during halothane anesthesia
(2) Stimulation of nAChRs and mAChRs produces negative inotropic (cardiac muscle
contraction strength) and chronotropic (heart rate) effects, which may be attenuated by
administration of an anticholinergic drug (atropine)
(3) Large doses can cause positive inotropic and chronotropic effects
ii) Hyperkalemia – patients with burns, nerve damage or neuromuscular disease, closed head injury, and other trauma can respond to succinylcholine by releasing potassium into the blood, which, on rare occasions, can cause cardiac arrest
iii) Increased intraocular pressure, increased intragastric pressure, muscle pain
iv) Contraindications include personal or familial history of malignant hyperthermia;
myopathies associated with elevated serum creatine phosphokinase (CPK) values; acute phase of injury following major burns, multiple trauma, extensive denervation of skeletal muscle or upper motor neuron injury
v) BLACKBOXWARNING(cardiacarrestrisk):rarely,acuterhabdomyolysiswith hyperkalemia followed by ventricular dysrhythmias, cardiac arrest, and death can occur after administration to apparently healthy children with an undiagnosed skeletal muscle myopathy (usually males <8 y/o but also reported in adolescents

568
Q

Black box succinylcholine

A

BLACKBOXWARNING(cardiacarrestrisk):rarely,acuterhabdomyolysiswith hyperkalemia followed by ventricular dysrhythmias, cardiac arrest, and death can occur after administration to apparently healthy children with an undiagnosed skeletal muscle myopathy (usually males <8 y/o but also reported in adolescents

569
Q

Drug drug interactions succinylcholine

A

i) Anesthetics
(1) The combination of succinylcholine and volatile anesthetics can result in malignant hyperthermia (rare)
(2) Malignant hyperthermia is caused by abnormal release of calcium from stores in skeletal muscle and is treated with dantrolene (see below)
ii) Antibiotics: See above for drug-drug interactions for nondepolarizing agents
iii) Local anesthetics and antiarrhythmic drugs (minor

570
Q

Uses of neuromuscular blocking drugs

A

) Surgical relaxation
b) Tracheal intubation
c) Controlofventilation:providesadequategasexchangeandpreventsatelectasisinpatients
who have ventilatory failure; neuromuscular blocking drugs reduce chest wall resistance and
improve thoracic compliance
d) Treatment of convulsions: attenuates the peripheral motor manifestations of convulsions
associated with status epilepticus or local anesthetic toxicity; no effect on the CNS because neuromuscular blocking agents do not cross the blood-brain barrier

571
Q

AchE inhibitors : subgroups

A

Subgroups
i) Alcohols: contain an alcohol group, positively charged; reversible (example: edrophonium)
ii) Carbamic acid esters: can be positively charged or neutral and are reversible (example:
neostigmine, pyridostigmine, physostigmine)
iii) Organophosphates: organic derivatives of phosphoric acid; neutral, highly lipid-soluble;
irreversible (examples: echothiophate, parathion, malathion, sarin, soman

572
Q

Pharmacokinetics AchE inhibtors

A

Quaternary and charged AChE inhibitors: relatively insoluble (parenteral administration), no CNS distribution (examples: neostigmine, pyridostigmine, edrophonium, echothiophate)

ii) Tertiary and uncharged AChE inhibitors: well absorbed from all sites, CNS distribution (examples: physostigmine, donepezil, tacrine, rivastigmine, galantamine)
iii) Organophosphates: lipid-soluble and readily absorbed from the skin, lung, gut, and conjunctiva, CNS distribution (except for echothiophate, which is charged); since the interaction between organophosphates and AChE is covalent and irreversible, there is virtually little metabolism and excretion via common biotransformation pathways; regeneration of AChE is required in order to reestablish the termination of ACh signaling at the neuromuscular junction (pralidoxime, see below

573
Q

MOA ache inhibtiors

A

Inhibiton of AChE

574
Q

Duration AchE inhibitors

A

Duration of action: alcohols bind weakly and reversibly resulting in short duration of action (2-
10 minutes); carbamic acid esters bind reversibly but with longer duration of (30 minutes to 8- hour duration of action); organophosphates bind covalently and reversal of binding requires rapid administration of pralidoxime to regenerate the activity of AChE

575
Q

Organ system effects ache inhibtiors

A

) Organ system effects: depending on the site of action, AChE inhibitors have the ability to
(1) stimulate mAChRs at autonomic effector organs and (2) stimulate, followed by
depression or paralysis, all autonomic ganglia and skeletal muscle (nAChRs

576
Q

CNS ache inhibitos

A

i) CNS: low concentrations: diffuse activation on EEG and a subjective altering response; high concentrations: generalized convulsions due to neuronal hyperstimulation (may be
followed by coma and respiratory arrest

577
Q

NMJ ache inhibitos

A

i) NMJ: therapeutic concentrations of AChE inhibitors prolong and intensify the actions of
ACh, which increases the strength of contraction; fibrillation of muscle fibers and fasciculations result with high concentrations; continued inhibition of AChE results in the progression of depolarizing neuromuscular blockade to nondepolarizing blockade (as seen with succinylcholine); some quaternary carbamate AChE inhibitors have additional direct nicotinic agonist effects at the NMJ (e.g., neostigmine

578
Q

AchE inhibitors eye

A 
Sphinctermuscleofiris
Contraction (miosis)
 Ciliarymuscle
Contraction for near vision (accommodation
579
Q

Heart ache inhibitors

A

 Sinoatrialnode
Decrease in rate (negative chronotropy)
 Atria
Decrease in contractile strength (negative inotropy). Decrease in refractory period
 Atrioventricularnode
Decrease in conduction velocity (negative dromotropy). Increase in refractory period
 Ventricles
Small decrease in contractile strength

580
Q

Blood vessels ache inhibitors

A

 Arteries,veins
Dilation (via EDRF). Constriction (high-dose direct effect)
 Lung
 Bronchialmuscle
Contraction (bronchoconstriction)
 Bronchialglands
Secretion

581
Q

GI ache inhibitors

A

Motility
Increase
 Sphincters
Relaxation
 Secretion
Stimulation

582
Q

Urinary bladder ache inhibitos

A

Detrusor
Contraction

 Trigoneandsphincter
Relaxation

583
Q

Glands Ache inhibitors

A

 Sweat,salivary,lacrimal,nasopharyngeal
Secretion

584
Q

Clinical ache inhibitors

A

he major therapeutic uses of agents that stimulate AChRs (direct acting or indirect acting) are for diseases of the eye (glaucoma, accommodative esotropia), GI and urinary tracts (postoperative atony, neurogenic bladder), NMJ (myasthenia gravis, curare-induced neuromuscular paralysis), heart (rarely for certain atrial arrhythmias), and Alzheimer disease

585
Q

Treat myasthenia gravis

A

Myasthenia gravis: pyridostigmine, neostigmine, and ambenonium are the standard AChE inhibitors used in the symptomatic treatment of myasthenia gravis (do not cross the blood- brain barrier); due to the relatively short duration of action of these agents, repeated dosing is required every 2-8 hours depending upon agent, dose, and clinical response
i) Edrophonium test: the short-acting agent edrophonium had been used as a diagnostic agent for myasthenia gravis (edrophonium test); replaced by ice pack test and immunologic and/or electrophysiologic testing
ii) Myasthenic vs. cholinergic crisis
(1) Myasthenic crisis is a life-threatening condition defined as weakness from acquired
myasthenia gravis that is severe enough to necessitate intubation
(2) Cholinergic crisis is a potential major side effect of excessive AChE inhibitors; the main
symptom is muscle weakness, similar to myasthenic crisis
(3) To distinguish, an AChE inhibitor (edrophonium) may delineate the cause of symptoms
(a) If the patient is in myasthenic crisis the symptoms will improve
(b) If the condition is cholinergic crisis, the symptoms will remain unchanged or worsen

586
Q

Reversal of pharmacological paralysis

A

Reversalofpharmacologicparalysis:neostigmineiscommonlyusedtoreverse
neuromuscular blocking drug-induced paralysis; AChE inhibitors may be used to treat paralytic
ileus, atony of the urinary bladder, and congenital megacolon

587
Q

Glaucoma

A

Glaucoma: AChE inhibitors reduce intraocular pressure by stimulating mAChRs of the ciliary
body and causing contraction, which facilitates outflow of aqueous humor; replaced by topical
β-blockers and prostaglandin derivatives

588
Q

Dementia

A

e) Dementia: patients with progressive dementia of the Alzheimer type have a deficiency of intact
cholinergic neurons; tacrine was approved in 1993, but due to the high incidence of hepatotoxicity newer agents are preferred (donepezil, rivastigmine, galantamine, physostigmine); patients with dementia associated with Parkinson disease also benefit

589
Q

Antidote

A

) Antidote: over 600 compounds have anticholinergic properties (e.g., anticholinergic agents (atropine), antihistamines, tricyclic antidepressants, sleep aids, cold preparations); intoxication due to anticholinergic agents can produce cutaneous vasodilation, anhidrosis, anhydrotic hyperthermia, nonreactive mydriasis, delirium, hallucinations, and a reduction or elimination of the desire to urinate, which are generally the result of reduced or blocked mAChR stimulation; physostigmine is preferred because it crosses the blood-brain barrier

590
Q

Drug drug interactions

A

a) Nondepolarizing neuromuscular blocking agents: AChE inhibitors diminish NMJ blockade
i) Exception: mivacurium (metabolized by plasma AChE), AChE inhibitors prolong blockade
b) Succinylcholine: AChE inhibitors will enhance phase 1 block and antagonize phase 2 block
c) Cholinergicagonists(direct-acting):AChEinhibitorsenhanceeffectsofcholinergicagonists
d) Beta-blockers: AChE inhibitors may enhance the bradycardic effects

591
Q

Acute intoxication

A

The dominant initial signs of AChE intoxication are those of mAChR stimulation: miosis, salivation, sweating, bronchial constriction, vomiting, and diarrhea
ii) The route of administration dictate which symptoms are noted initially
(1) After ingestion, GI symptoms occur earliest
(2) Percutaneous absorption results in early symptoms of localized sweating and muscle
fasciculations in the immediate vicinity
iii) With poisoning from lipid-soluble agents, CNS involvement follows rapidly (confusion,
ataxia, generalized convulsions, coma, and respiratory paralysis)
iv) Time of death after a single acute exposure may range 5 minutes to 24 hours and is
caused primarily by respiratory failure

592
Q

Treatment toxicity

A

i) Atropine in combination with maintenance of vital signs (respiration) and decontamination
ii) Atropine is ineffective against the peripheral neuromuscular stimulation (nAChRs)
iii) To regenerate AChE at the NMJ, cholinesterase regenerators can be administered

593
Q

Cholinesterase regenerator

A

Cholinesterase reactivators (pralidoxime) are capable of regenerating active AChE enzyme
by removal of the phosphorous group from the active site of the enzyme
ii) Restores the response to stimulation of the motor nerve within minutes
iii) Must be given soon after AChE inhibitor exposure
iv) Atropine, pralidoxime, and a benzodiazepine (anticonvulsant) are typically combined

594
Q

Skeletal msucle relaxants

A

Spasticity (muscle twitch) is characterized by an increase in tonic stretch reflexes and flexor muscle spasms (i.e., increased basal muscle tone) together with muscle weakness
b) Spasticity is associated with spinal injury, cerebral palsy, multiple sclerosis, and stroke
c) Spasmolytic agents may improve some of the symptoms of spasticity by modifying the stretch
reflex arc or by interfering directly with skeletal muscle (i.e., excitation-contraction coupling)
d) Currently available drugs can provide significant relief from painful muscle spasms, but they
are less effective in improving meaningful function (e.g., mobility, return to work

595
Q

Baclofen

A

i) Baclofen
(1) MOA: agonist at GABAB receptors; results in hyperpolarization (due to increased K+
conductance) and inhibition of excitatory neurotransmitter release in the brain and
spinal cord
(2) As effective as diazepam in reducing spasticity and causes less sedation; does not
reduce overall muscle strength as much as dantrolene
(3) Adverse effects include drowsiness and increased seizure activity in epileptic patients
(withdrawal must be done slowly); vertigo, dizziness, psychiatric disturbances,
insomnia, slurred speech, ataxia, hypotonia, and muscle weakness

596
Q

Carisprodol

A

(1) Precise mechanism of action unclear; acts as CNS depressant
(2) Schedule IV controlled substance due to addictive potential (use only short term)
(3) Adverse effects include dizziness and drowsiness
(4) Metabolized by CYP2C19; use with caution when coadministered with CYP inhibitors
(5) Metabolized to meprobamate, which has anxiolytic and sedative effects (used to
manage anxiety disorders)
iii) Chlorzoxazone
(1) MOA: Acts on the spinal cord and subcortical levels by depressing polysynaptic reflexes

597
Q

Cyclobenzaprine

A

1) Exact mechanism of action unclear; reduces tonic somatic motor activity by influencing both alpha and gamma motor neurons
(2) Structurally related to tricyclic antidepressants and produces antimuscarinic side effects (may cause significant sedation, confusion, and transient visual hallucinations)
(3) Metabolized by CYP450s; use with caution when coadministered with CYP inhibitors
(4) Adverse effects include drowsiness, dizziness, and xerostomia

598
Q

Diazepam

A

(1) Long-acting benzodiazepine; produces sedation at the doses for spasticity
(2) MOA: promote the binding of the major inhibitory neurotransmitter in the CNS - aminobutyric acid (GABA) to the GABAA receptor, enhancing GABA-induced ion currents (increase frequency of channel openings); leads to increased inhibitory
transmission and a reduction in spasticity
(3) Causes sedation, muscle relaxation, anxiolytic and anticonvulsant effects
(4) Schedule IV controlled substance

599
Q

Tizanidine

A

(1) MOA: alpha2-adrenergic agonist (similar to clonidine); decreases excitatory input to
alpha motor neurons
(2) Causes drowsiness, hypotension, dry mouth, asthenia/muscle weakness

600
Q

Dantrolene

A

(1) In contrast to the centrally acting drugs, dantrolene reduces skeletal muscle strength by interfering with excitation-contraction coupling in the muscle fibers
(2) MOA: causes inhibition of the ryanodine receptor (RyR); blocks the release of calcium through the sarcoplasmic reticulum and muscle contraction is impaired
(3) Cardiac and smooth muscle are unaffected due to a different RyR channel subtype
(4) Side effects include generalized muscle weakness, sedation, and occasionally hepatitis
(5) Used to treat spasticity associated with upper motor neuron disorders (e.g., spinal cord
injury, stroke, cerebral palsy, or multiple sclerosis) and malignant hyperthermia

601
Q

Botulism toxin

A

(1) MOA: cleaves components of the core SNARE complex involved in exocytosis, preventing the release of ACh
(2) Many clinical uses: strabismus and blepharospasm associated with dystonia; cervical dystonia; temporary improvement in the appearance of lines/wrinkles of the face; severe primary axillary hyperhidrosis; focal spasticity; prophylaxis of chronic migraine
(3) Adverse effects include focal muscle weakness in the area of injection, which may last up to several months

602
Q

Glucocorticoids for MS

A

c) Glucocorticoids
i) Monthly bolus IV glucocorticoids (typically 1000 mg of methylprednisolone) are used for
treatment of primary or secondary progressive MS alone or in combination with other
immunomodulatory or immunosuppressive medications d)

603
Q

Glatiramer acetate

A

e) Glatiramer acetate i) MOA
(1) A mixture of random polymers of four amino acids (L-alanine, L-glutamic acid, L-lysine, and L-tyrosine) that is antigenically similar to myelin basic protein, which is an important component of the myelin sheath of nerves
(2) Thought to induce and activate T-lymphocyte suppressor cells specific for a myelin antigen; also proposed to interfere with the antigen-presenting function of certain immune cells opposing pathogenic T-cell function

604
Q

Interferons

A

i) Interferon-beta-1a and interferon-beta-1b
ii) MOA: Acts on blood-brain barrier by interfering with T-cell adhesion to the endothelium by
binding VLA-4 on T cells or by inhibiting the T-cell expression of MMP
iii) Results in a reduction of relapses by one-third, a reduction of new MRI T2 lesions and the
volume of enlarging T2 lesions, a reduction in the number and volume of Gd-enhancing
lesions, and a slowing of brain atrophy

605
Q

Mitoxantrone

A

i) Antineoplastic agent used to treat MS, acute myeloid leukemia, and advanced, hormone- refractory prostate cancer
ii) MOA: intercalates into DNA resulting in cross-links and strand breaks (related to anthracycline antibiotics

606
Q

Methotrexate

A

Biological DMARD, also administered systemically to treat other autoimmune diseases such as psoriasis

607
Q

Vemurafenib

A

Inhibits the mutatedBRAF V600D MAP kinase found in 60% of melanomas

608
Q

Apremilast

A

Orally active phosphodiesterase type IV inhibitor that inhibits numerous pro inflammatory mediators, used in moderate to severe plaque psoriasis and psoriatic arthritis; severe diarrhea is AE

609
Q

Miconazole

A

Amongthe imidazole drugs commonly used to treat vulvovaginal candidiasis

610
Q

Amphotericin B

A

Antifungal agent with topical effects limited to candida infections, may temporarily stain the skin yellow (also given IV for ther fungal infections as well including aspergillus and endemic mycosis)

611
Q

C diffe

A

Common cause of diarrhea due to antibiotic associated colitis, well known example where handwashing. With soap and water is superior to alcohol based gels

612
Q

Okspironolactone

Oral contreptives

A

Canbe effective treatment for acne in women

613
Q

Biofilms?

A

Form on surfaces, very hard to kill bc resident microbes of different species help each other survive

614
Q

Polymixin B

A

Peptide antibiotic with efficacy against gram negative bacteria including pseudomonas, has a detergent like effect that damages the bacterial cell membrane

615
Q

Tetracyclines

A

Drug class useful for systemic treatment of acne, photosensitivity, GI distress and contraindication in pregnancy and young children due to gray discoloration of permanent teeth are noteworthy adverse effects

616
Q

Neomycin

A

Aminoglycosides antibioticof neosporin with activity against gram negative bacteria

617
Q

Benozyl peroxide

A

Topical antimicrobial agent commonlyused to treat acne; local skin irritate and may bleach hair or clothing

618
Q

Type IV hypersensitivity

A

Delayed hypersensitivity reaction that can be caused by substances such as latex and drugs such as neomycin and bacitracin; sometimes induced as treatment of skin disorder (psoriasis, alopecia)

619
Q

Inadequate oxygenation

A

Local vasoconstriction due to blood volume deficit, unrelieved pain, hypothermia, can impair wound healing due to an inadequate amount of this in the tissue

620
Q

Becaplermin

A

Platelet derived growth factor that promotes the cell proliferation and angiogenesis needed for diabetic ulcer repair, but must use cautiously as too much increases risk of malignancy

621
Q

Emollients

A

Refers to substance in moisturizers that form an oily layer to trap water in the skin; petrolatum, lanolin and mineral oil are among common examples

622
Q

Glycemic control

A

Control that is now considered a priority for optimal wound closure

623
Q

Naphazoline, tetrahydrozoline, phenylephrine, and oxymetazoline

A

Alpha adrenergic agonist in visine known for its ability to get the red out

624
Q

Chlorhexidine

A

Broad spectrum antimicrobial agent widely used in homes and hospitals due to efficacy on skin and oral mucosa with low irritability

625
Q

Clindamycin

A

Antibiotic that works similar to macrolides, kills anaerobes, useful for range of infections including topical treatment. Of acne and for osteomyelitis; associated with increased risk of c diffe

626
Q

Calcineurin inhibitos

A

Cyclosporine and tacrolimus are among these agents that revolutionizes transplantation therapy (didn’t cause bone marrow suppression), among theses agents that revolutionized transplantation therapy (didn’t;t cause bone marrow suppression) among other uses includes topical or systemic administration for psoriasis and topical administration for anogenital pruritis

627
Q

Moisturizers

A

Very important component of skin care for health care providers

628
Q

Tar

A

Very old remedy for psoriasis; works but color and smell create a challenge

629
Q

NYSTATIN

A

When sued to treat thrush it is held on the mouth before swallowing (has negligible GI absorption)

630
Q

Debridement

A

Important component of wound healing it conserves the local resources by limiting the need to synthesize proteases; stage when hydrogens are good wound covering

631
Q

Hand hygiene

A

Most important component of infection control

632
Q

Bacitracin

A

Peptide antibiotic with activity against gram positive organisms and some anaerobes; only applied topically to limit systemic toxicity, often causes contact dermatitis

633
Q

Ciclopirox

A

Prescription synthetic topical antimycotic agent with broad spectrum of activity against fungal skin infections such as ringworm, athletes foot, tinea versicolor, dandruff

634
Q

Azaleicacid

A

Component of plant defenses against bacteria, active against P acne

635
Q

Moist

A

To heal best, wounds should be kept clean and -_-

636
Q

Isotret

A

Retinoid administration orally for treatment of severe acne, powerful teratogen that mandates participation by young females in the iPledge program

637
Q

Horny substances (keratin softeners)

A

Urea, alpha-hydroxyl acids and allantoin are among the agents found in moisturizers to soften this and give skin a smoother feeling

638
Q

Physical interventions

A

Sometimes need to resort to things such as unna boots in the category to try to break the itch scratch cycle

639
Q

Uva

A

Radiation that may not cause erythema and sunburn but neverthe less still contribute to akin aging and phtocarcinogenesis

640
Q

Aprepitant

A

Substance P antagonist used to treat nausea and vomiting of chemotherapy also useful to treat intense itching of cutaneous T cell lymphomas (sezary syndrome)

641
Q

Anogenital pruritus

A

Itching here is far less funny than it sounds, topical calcineurin inhibitors such as tacrolimus can help treat

642
Q

5-fu topical

A

Effective topical therapy for actinic keratosis, causes fast proliferating dysplastic cells to die a thymidine-less death; necrosis/erosion gives way to re-epithelization over several weeks (no hyphen)

643
Q

Minocycline

A

Tetracycline used to treat acne, noteworthy for its ability to cause dark pigmentation in skin and sclera

644
Q

Ketoconazole

A

Imidazole antifungal drug applied topically for range of fungal infections, also noteworthy as a classic inhibitor of cytochrome P450

645
Q

Impede

A

Agents such as iodine, chorhexidine and hydrogen peroxide and potentially do this to wound healing

646
Q

Creams

A

50% water and 50% oil with a emulsifier, base that is useful for covering large and.or wet areas with a drug but preservatives, can cause allergic reactions

647
Q

Local anesthetics

A

Can be useful therapies for neuropathic pruritus

648
Q

Dacarbazine

A

FDA approved conventional therapy for malenoma

649
Q

Gabapentin

A

Antiepileptic drug used to treat neuropathic pain and itching

650
Q

Ingenolmebutate

A

Treatmentfor actinic keratosis, derived from euphorbia peplus sap, causes chemoablation with neutrophil-mediated antibody dependent cellular cytotoxicity eliminating remaining tumor cells

651
Q

Erythromycin

A

Macrolides antibiotic, among uses is for topical or systemic treatment of acne among the well known cytochrome P450 inhibtiors to remember

652
Q

Ivermectin

A

Orally administered insecticides to treat ectoparasites, binds glutamate activated Cl channels to hyprepolarize the nerve and muscle cells

653
Q

Humectants

A

Refers to agents such as glycerin, lecithin and propylene glycol found in moisturizers to draw water into the outer layer of skin

654
Q

Ustekinumab

A

Monoclonal antibody against IL12 and IL23 a biologics agent used to treat psoriasis

655
Q

Butorphanol

A

Opioid receptor agonist.a-opioid receptor antagonist administered intranasally to treat intractable.nocturnal pruritis

656
Q

Antihistamines

A

Drug class that may or may not stop itch, but associated drowsiness may help one deal with it

657
Q

Finasteride

A

Blocks the conversion of testosterone to more potent androgen dihydrotestosterone, among its uses is to treat male pattern baldness in men and second line agent in women

658
Q

Permethrin

A

Synthetic insecticide similar to that of chrysanthemums, ectoparasite therapy that binds to insect Na channels and prevents membrane repolarization

659
Q

Azithromycin

A

Macrolides among the systemic therapies used to treat acne; noteworthy bc it is not a cytochrome P450 inhibitor, has unusual pharmacokinetics in that it is taken up in phagocytes and released by them at sites of infection

660
Q

Imidazole

A

Class of antifungal drugs with a wide range of activity , blocks ergosterol synthesis

661
Q

Imiquimod

A

Topical immune response modifier used to treat actinic keratosis and basal or squamous cell carcinoma or genital warts

662
Q

Tretinoin

A

Topical retinoid administrated for the treatment of acne, alter gene expression to normalize keratinization, decrease keratinocytes cohesiveness and reduce microcomedone formation

663
Q

Griseofulvin

A

Can be given systemically to treat tinea capitis (ringworm in scalp)

664
Q

Dpcp

A

Treatment for alopecia, it is a contact allergen applied to cause dermatitis which can be followed by hair growth

665
Q

Tolnaftate

A

Among OTC drugs (tinactin) used to treat jock itch and athletes foot; like terbutaline, inactive against yeasts

666
Q

Ointment

A

Comprised of 20% water and 80% oils, best for dry skin, stay on the surface of skin and are not well absorbed , permit mor ecomplete drug absorption and less likely tocause allergic reaction skin no preservatives

667
Q

Efinaconazole

A

Antifungal applied topically that penetrates into nails to treat fungal infection

668
Q

Reservoir

A

The formation of one of thesefor a drug in the skin may prolong its half life and permit 1.day dosing

669
Q

Fluconazole

A

Example of a systemic imidazole therapy to treat tinea versicolor

670
Q

Naltrexone

A

Opoid receptor antagonist that can treat the pruritus associated with chronic kidney disease and cholestasis

671
Q

Flutamide

A

Prototypical non steroid androgen antagonist, uses besides prostate cancer include treatment of male baldness in women

672
Q

Minoxidil

A

Potent vasodilator due to hyperpolarization via activation of K channels applied topically to grow hair

673
Q

Ph

A

Lower closer to that of skin is why synthetic detergents minimize skin irritation during home skin care

674
Q

Alpha

A

Class of adrenergic agonistsadministered topically to treat rosacea or red eyes

675
Q

Newman

A

Ok

676
Q

Failed screen

A

Simply an indication for a more thorough evaluation

677
Q

Why developmental screen

A

Sooner identify delays better

678
Q

Four domains of development

A

Gross motor

Fine motor

Language

Cognitive/social emotional and behavioral

679
Q

Gross motor

A

Movements using large msucles

680
Q

Fine motor

A

Movements using hands and smaller msucles often involving daily living skills

681
Q

Language

A

Receptive and expressive communication, speech anal nonverbal communication

682
Q

Cognitive/social emotional and behavioral

A

Attachment, self regulation and interaction with others

683
Q

Myopathy domain

A

Gross motor

684
Q

6 months

A

Babbles and sits momentarily

685
Q

9 months

A

Momma/daddy
Pulls up
Cruises
Sits well without support

686
Q

1 year

A

Stands momentarily

687
Q

2 years

A

Walk up stairs

Kicks ball forward

688
Q

3 years

A

Tricycle

689
Q

4 year

A

Balance on one foot

Hop on one foot

690
Q

6 years

A

Skip

691
Q

Myopathies

A

Muscle

-muscular dystrophy, metabolic myopathies, congenital, central core

692
Q

Acquired myopathy

A

Infections, inflammatory processes , systemic diseases, toxic myopathy

693
Q

Inherited myopathy

A

Muscular dystrophy, congenital, metabolic, mitochondrial

694
Q

How do most myopathies present

A

Weakness in the proximal msucles

695
Q

Acquired muscle

A

Juvenile dermatomyositis

Statin induced myopathy

696
Q

What causes dystrophy

A

Abnormalities in dystrophin associated protein complex but not all do this

697
Q

Duchene and Becker

A

Proximal weakness
Shawl and thighs

DTR will be present

698
Q

FaCIOSCAPULOHUMERAL

A

Just proximal shawl and face

699
Q

Emery dreyfus

A

Proximal could ESR and lateral ankles and feet

700
Q

Duchene becker fascioscapulohumeral and emery Dreyfus

A

Duchene 1/3500 male
Becker 1/1845

Rare rare

701
Q

Duchene

A

Proximal weakness

Most severe childhood form

Onset early, weakness more severe

Cardiomyopathy and frameshift mutation

702
Q

Inheritance duchene

A

X linked recessive

703
Q

Prob with duchenne

A

Out of frame mutation so nothing correct and absent of muscle dystrophin

704
Q

Why boys duchene

A

X recessive

705
Q

X recessive inheritance

A

Carrier mom unaffected dad

Unaffected son, unaffected daughter, carrier daughter, and affected son

706
Q

Chance male offspring effected

A

50%

707
Q

Becker

A

Older presentation
X recessive

Less msucle damage

Can walk independently longer

Shorter lifespan 40-60

Respiratory and cardiac

708
Q

Preschool weak toe walking difficulty walking falls get what

A

CK

Family history

Involvement on moms side dystrophinopathy most common

709
Q

Baby hypotonic in nursery

A

Do a cpk get good family history and genetic testing

710
Q

Mitochondrial

A

MELAS

Mitochondrial encephalomyelitis with lactic acidosis and stroke like symptoms

711
Q

Pompe

A

Glycogen storage type II
AR

Weakness, hypotonia, build up of glycogen in lysosomes in cell

Can give enzymes that can help

712
Q

Juvenile dermatomyositis

A

Most common idiopathic inflammatory myopathy in kids

7 years

Red or purplish heliotrope rash over eyelids

Gottron papules

Thrombi or hemorrhage in peri ungual capillary beds

Acquired

713
Q

Statin induced myopathy

A

Can cause necrotizing and inflammatory myopathy

-msucle weakness pain tenderness

714
Q

Why look for myoglobin in the urine

A

Break down msucle if have heme positive urine and no blood cells look for myoglobin if muscular symtpoms it is so hard on kidney

715
Q

GGT

A

Gamma glutamyl transferase can help determine if the liver is involved
-if elevated think liver

If normal think muscle

Clin Medicine (28 decks)

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