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MOHD 4 Exam 5 > Thursday night highlights - high yield > Flashcards

Thursday night highlights - high yield Flashcards

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1
Q

mechanism of Guillan Barre

A

destroys myelin in patchy manner

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2
Q

Most common etiology of a mononeuropathy

A

compression of nerve –> demyelination at the site of compression (think carpal tunnel syndrome)

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3
Q

fasciculations are a ___sign (LMN/UMN)

A

LMN

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4
Q

which is more common - axonal neuropathies or demyelinating myopathies?

A

axonal, by a long shot.

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5
Q

Case: decreased sensation on right thumb, right index finnger, right middle finger, and part of ring finger. Worsened by typing / holding the steering wheel. Normal reflexes. Which nerve?

A

Median nerve - carpal tunnel.

Remember - median is mixed - sensory and motor sx

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6
Q

Radial mononeuropathy - symptoms and common cause

A

wrist drop - saturday night palsy (pass out with humerus impacted)

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7
Q

Peroneal mononeuropathy - symptoms and common cause

A

foot drop - sitting with legs crossed.

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8
Q

3 viruses that cause guillan barre

A

campylobacter, CMV, EBV

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9
Q

mechanism of guillan barre -

A

cross reaction of ab’s with gangliosides in myelin/schwann cells.

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10
Q

can improved glucose control reverse diabetic neuropathy?

A

nope. but but can prevent progress.

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11
Q

What are fasciculations?

A

visible mm twitching

LMN sign

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12
Q

cramps - LMN or UMN?

A

LMN

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13
Q

Muscle spasticity - UMN or LMN?

A

UMN

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14
Q

Atrophied tongue with fasciculations - which disease

A

hallmark of ALS

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15
Q

T/F - in diabetic neuropathy myelin is affected. In guillan barre, axons are affected.

A

False. Reverse

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16
Q

clinical characteristics of mm disorders

A

diffuse/proximal weakness - usually symmetric!!
normal sensation
normal reflexes (if mm strong enough)

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17
Q

characteristics of congenital myopathies - 3

A

inherited

  • NON-progressive/slowly progressive
  • disorders of the contractile mechanism of skeletal mm
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18
Q

What is the example disease for a muscular dystrophy caused by nuclear transcription abnormalities>

A

Fascioscapulohumeral muscular dystrophy (FSHD)

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19
Q

What is the example disease for a disorder of mm contraction?

A

Congenital fiber type disproportion.

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20
Q

Limb girdle muscle dystrophies are separated into 1s and 2s. Which one is dominant?

A

1 = dominant
2- recessive,
x linked = duchenne becker.

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21
Q

what does the dystrophin glycoprotein complex do?

A

It connects the contractile elements of the mm cell to the extracellular matrix

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22
Q

when does duchenne MD present?

A

3-5yo. wheelchair by 12

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23
Q

duchenne becker MD is x linked _____

A

recessive

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24
Q

how do people with duchenne MD typically present?

A

3-5 years old
gross motor delay
trouble walking / running

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25
Q

which type of muscle dystrophy can present in adulthood?

A

becker

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26
Q

t/f - 95% of duchenne/becker muscular dystrophy pt’s can be diagnosed by genetic testing, without mm biopsy

A

True

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27
Q

calf hypertrophy - which disease?

A

Duchenne MD

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28
Q

Mechanism of Fascioscapulohumeral muscular dystrophy (FSHD)

A

deletion within a repetitive sequence on chromosome 4 –> DUX4

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29
Q

clinical presentaiton of Fascioscapulohumeral muscular dystrophy (FSHD)

A 
young - 8 years old
-chicken wings
-trouble lifting things
-sleep w/ whites of eyes showing
-bilateral facial weakness.
"refuses to smile for family photos"
-CK normal
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30
Q

Which gene mutation is the most common culprit in congenital myopathies like nemaline, etc?

A

RYR1 (ryanodine receptor).

plays a role in excitation / contraction coupling

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31
Q

categories of congenital myopathies with characteristic path

A

Core - mitochondria extruded

nemaline - blue dots in cells

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32
Q

Lack of eye mvmts in early child - probably?

A

congenital myopathy - other diseases rarely affect eyes. - Congenial fiber disproportion!

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33
Q

What is a chronic soft tissue injury in youth?

A

osgood schlatters

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34
Q

Presentation of osgood schlatters

A

10-15 years old.
palpable bump on front of knee.
caused by overuse - jumping too much, kiddo?

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35
Q

Mechanism of osgood schlatters

A

Repeated microfractures on tibia not given a chance to heal. Tears where the patellar tendon meets the bone.

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36
Q

What does a stress fracture look like on X ray?

A

fuzzy stuff around the bone (bone attempting to reheal)

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37
Q

Imaging for proximal thigh stress fracture

A

x ray

bone scan if x ray negative.

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38
Q

definition of a sprain

A

injury to ligament

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39
Q

definition of a strain

A

injury to a tendon (sprain a joint, strain a muscle/tendon)

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40
Q

how do you classify sprains?

A

by ligament laxity.
mild- pain but no laxity
moderate - lax with an end-point (partial tear)
severe= gross laxity (feels like you could dislocate it if you want) = complete tear

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41
Q

what is the most common ankle sprain? It is due to which motion?

A

anterior talofibular ligament.

due to infersion

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42
Q

In an anterior talofibular ligament sprain tenderness will be in which area?

A

laterally, near the distal fibula and talar neck

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43
Q

what test should be done for inversion ankle sprains?

A

Anterior drawer test. If it is positive talofibular ligament broken

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44
Q

If you suspect calcaneofibular ligament injury - what test do you do?

A

Talar tilt

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45
Q

severe inversion ankle sprain - which ligaments affected?

A

anterior talofibular

calcaneofibular

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46
Q

How many ankle sprains need x rays?

A

10% if trainer present.

15-30% in Emergency room.

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47
Q

what are the indications for an x ray of an ankle? (These are the Ottowa rules)- 4

A

gross swelling
point tender over posterior or distal fibula
-crepitus
-can’t bear weight

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48
Q

Tib-fib sprain - exam findings

A

ankle external rotation painful (eversion)

  • tender above the ankle on the tibia
  • can’t walk/push off.
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49
Q

most common knee sprain

A

MCL

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50
Q

characteristics of MCL knee sprain

A
  • no joint swelling (MCL is outside the joint)

- sensitive to valgus force

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51
Q

Woman playing soccer. When she planted her foot, she heard a painful pop and then her knee shifted. Likely diagnosis?

A

ACL. Check for hemarthrosis (knee swelling)

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52
Q

A patient has hemarthrosis of the knee.(Swelling) what is the most likely injury? + 2 other less common

A

70% chance of ACL tear.
Meniscus #2
Articular surface fracture #3

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53
Q

Exam test for ACL tear?

A

Lachman (anterior drawer at 30 degrees bent.

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54
Q

What is the key physical exam finding for a meniscus tear? How sensitive / specific?

A

McMurray’s - rotate the leg around, hear a pop. Least sensitive most specific.

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55
Q

Which is worse - dislocation or subluxation?

A

Dislocation.

Subluxation is pathologic movement of the joint, short of dislocation.

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56
Q

Which upper extremity injury is associated with the positive apprehension test?

A

Shoulder dislocation (glenohumeral separation)

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57
Q

lachman’s test?

A

for ACL - similar to anterior drawer

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58
Q

Which lower extremity injury associated with apprehension sign?

A

patellar dislocation

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59
Q

In adolescent idiopathis sccoliosis (AIS), which Cobb angles should be treated with braces? What about surgery?

A

25-40 degrees = brace.

>50 degrees = surgery

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60
Q

lumbar radiculopathy at the L5 level will cause weakness where?

A

ankle/toe

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61
Q

What explains why structure does not equal function in regards to back pain?

A

Biopsychosocial model

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62
Q

Mechanism for Marfan

A

mutation in fibrillin 1 gene (auto dominant) - cannot form microfibrils - defective elastic fibers lead to more TGF-beta accessible - increased growth!!

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63
Q

major cause of death for marfan syndrome

A

thoracic aneurysm - not abdominal!`

64
Q

other side effects of Marfan

A

-myopia/glaucoma
-chest wall abnormalities
cutaneous (striae)
-long limbs

65
Q

Mechanism of Ehlers Danlos syndrome

A

mutation in collagen gene - auto dominant.

66
Q

Clinical presentation of Ehlers Danlos syndrome

A
  • fragile skin - bruising

- hypermobile/hyperelastic joints

67
Q

When does congenital scoliosis develop?

A

5-7th week of gestation - in the womb!!

68
Q

Mechanism of congenital scoliosis

A

defect of formation/ separation of vertebrae

69
Q

What does bracing do for scoliosis?

A
  • prevents progression
  • does not improve condiition
  • 25-40 degree cobb angle
70
Q

13 yo female - scoliosis with 33 degree cobb angle - what is the treatment?

A
  • Surgery

- She has a lot of growth left, so it has a high chance of progression.

71
Q

Which area gets fractured in spondylolysis.

A

Pars interarticularis.

72
Q

What is the likelihood of nerve entrapment in spondylolisthesis?

A

Low if grade 1. Higher in higher grades (4 is the worst, indicates vertebrae has slipped very far.

73
Q

Most common location for spondylolisthesis.

A

L5/S1

74
Q

treatment for spondylolisthesis?

A

Less severe - core strengthening

More severe = lumbar fixation surgery.

75
Q

Which cancers produce osteoblastic bone tumors?

A

Breast and prostate

76
Q

Which cancers produce osteolytic bone mets?

A

kidney / thyroid.

77
Q

Which cancer produces osteolytic and osteoblastic bone mets?

A

lung

78
Q

Disk Herniation at C6/C7 will produce?

A
  • triceps weakness

- middle finger sensory loss

79
Q

Disk Herniation at L4/L5 will produce?

A
  • extensor hallucis longus weakness

- sensory loss in between 2nd and 3rd toe

80
Q

Symptoms of ankylosing spondylitis + mechanism

A

Low back pain
better with exercise, worse with rest.
-inflammation–> narrowing of disc space –> fusion of spine

81
Q

___ % of low back pain is non-specific

A

85

82
Q

what are the 2 competing goals common in doing surgery on bone?

A

local control vs. functional outcomes - ie making sure you have teaken it all out but preserving function as much as possible.

83
Q

6 hallmarks of Cancer pneumonic - SARCOMA

A 
S- Self-sufficiency of growth signals
A- Apoptosis/immune evasion
R- Resistance to anti-growth factors
CO - COntinuous replication
M - metastasis
A - angiogenesis
84
Q

__% percent of cancer is caused by random mutations

A

66%

85
Q

Which is standard of care - multi agent chemotherapy or monotherapy for bone cancer?

A

multiagent - to overcome resistance to one med.

86
Q

sarcoma usually spreads via

A

blood

87
Q

definition of sarcoma

A

cancer of mesenchymal origin

  • connective tissue(bone, cartilage, muscle, fat)
  • nerve sheath
  • blood vessels
88
Q

Common sarcomas in young

A

Ewing/Osteosarcoma

89
Q

Common sarcoma in old ppl

A

Chondrosarcoma

90
Q

Why are sarcomas rare, even though they make up a large portion of mass of the human body?

A

Their stem cells don’t divide often.

91
Q

T/F sarcoma of bone is often painless

A

True

92
Q

“Red flags” for malignant tumor in soft tissue

A
  • pain
  • growing
  • deep
  • > 5cm dia
93
Q

initial imaging for all bone tumors

A

x ray

94
Q

T/F - Bone tumors rarely require bone imaging or MRI

A

True! They are highly misused. Usually you can diagnose the stage via x ray

95
Q

Every time you diagnose an osteosaarcoma, where else should you look for cancer?

A

Chest CT!! (Commonly metastasizes to lungs).

Should also get a bone scan, commonly mets to other bones.

96
Q

Chemo for osteosarcoma

A

Adriamycin-based - only approved agent!

Used pre-and post-surgery

97
Q

kid has osteosarcoma, gets pre-surgery chemo, then surgery. They look at the bone. What % of necrosis is “good response”?

A

> 90

98
Q

In what circumstances should radiation be used to extend suurgical margins?

A

if the tumor is close to bone, vessels, or nerves.

99
Q

What is an allograft?

A

Bone from a cadaver.

100
Q

Describe the RANK pathway and the “vicious cycle” of bone erosion.

A

tumors produce PTH-like protein –>
PTHrP binds to osteoblasts, makes them upregulate RANKL—->
More RANKL binds to Monocyte precursors of osteoclasts— >
osteoclasts eat up bone , releasing growth factors—>
growth factors feed tumor.

101
Q

Describe the basic work-up of patients with destructive bone lesion. Goals of management?

A

labs, CT chest/abdomen/pelvis

Surgery  Goals (if metastatic) = prevent fracture, restore function, alleviate pain (not cure)
Radiation goals == pain relief
Chemo goals = pain relief / palliative
102
Q

If you see a bone tumor, what is the likelihood it is a primary bone tumor?

A

less than 1/100. almost always metastasis!

103
Q

Pneumonic for all the types of cancer that metastasize to bone

A

=BLT with Pickles and Ketchup

Breast, Lung, thyroid, prostate, kidney

104
Q

carcinoma usually spreads via

A

lymph

105
Q

What is a really important finding for bone weakness/cancer?

A

if pain increases with weight bearing.

106
Q

What are important labs to take in bone tumors

A
  • CBC
  • Serum Ca levels.
  • SPEP / UPEP for myeloma
107
Q

MOST important study to do with bone tumor

A

CT of chest/abdomen/pelvis

-covers many organs with met to bone - breast, lung, kidneys, colon, prostate.

108
Q

bone-specific agents to reduce “vicious cycle” and inhibit osteoclasts

A
  • bisphosphonates (Zoledronic acid)
  • > induce osteoclast apoptosis

-Denosumab- binds to RANKL, blocking osteoclast maturation

109
Q

__% of primary care visits are related to Osteoarthritis

A

30

110
Q

most common Physical exam for hip osteoarthritis

A

limited internal rotation with 90deg. flexion (sitting on exam table)
also, tredelenberg gait and thomas test (contracture)

111
Q

physical exam for knee osteoarthritis

A

antalgic gait.
limited flexion/contraction
quad atrophy

112
Q

T/F - labs are commonly used in the diagnosis of osteoarthritis

A

False. Not commonly used.

113
Q

indications for surgery for osteoarthritis

A

severe pain/disability

  • advanced bone-on-bone x ray changes
  • failure of non-operative treatment
114
Q

What is the most effective non-operative treatment for osteoarthritis?

A

Weight loss = most effective

115
Q

most common surgery for osteoarthritis

A

total joint replacement.

116
Q

3 things necessary to make an informed choice about surgery

A
  • alternatives
  • benefits
  • risks
117
Q

You are counseling a patient with severe osteoarthritis. What are the chances I will be normal after the surgery, doc?

A

Hip - 95% experience 95% pain relief, 90% return to function

Knee- 85% experience 85% relief, 80% return to activities. high level sports 50/50

118
Q

Most common risk for joint replacement (arthroplasty)

A

Thromboembolic disease (DVT/PE)

119
Q

How are joints usually fixated

A

presss-fit with component ingrowth - rough surface, bone grows into it - this done 99% of the time

120
Q

3 major disease mechanisms for osteomyelitis (how you get it)

A
  • contiguous (from cut in skin)
  • hematogenous (most common mechanism in kids)
  • surgery-
121
Q

3 major disease mechanisms for septic arthritis (how you get it) - Which is most common?

A

PRIMARILY Hematogenous

  • contagious (gonorrhea)
  • surgery / trauma
122
Q

Most common microorganism that causes septic arthritis and osteomyelitis

A

staph aureus

123
Q

What is a sequestrum, and in what disease is it found?

A 
devitalized bone (from bone infection acting as a foreign body - 
osteomyelitis.
124
Q

What is the difference between gonococcal and non-gonococcal septic arthritis?

A

gonococcal = migratory, polyarthritis

non-gonococcal = monoarthritis, non-migratory

125
Q

guy has dental pain for several years, Exam shows he has caries. X ray shows lytic lesion consistent with osteomyelitis. Mechanism and bugs?

A

Contiguous.

Polymicrobial, Oral bugs (strep, anaerobes)

126
Q

septic arthritis due to osteomyelitis in the neighboring bone is classified under

A

contiguous mechanism

127
Q

Gonococcal arthritis mechanism of transmission

A

hematogenous

128
Q

DDx for a red, hot joint

A

Crystal disease vs. septic arthritis

129
Q

How to diagnose gonococcal arthritis

A

Take cultures of urethra/cervix/throat. Joint often is culture negative. Take genital fluid too. Do crystal analysis to rule out crystal joint.

130
Q

treatment for septic arthritis

A
  • joint drainage
  • IV antibiotics - 2-4 weeks
  • EARLY range of motion exercises, even if painful!! Prevents complications.
131
Q

Definition of hyperuricemia

A

> 7.0 mg/dl

132
Q

podagra =

A

pain and swelling in the big toe due to gout.

133
Q

How long does it usually take for hyperuricemia to become gout? How about for gout to become chronic/tophaceous gout?

A

10-20 years of asymptomatic hyperuricemia, usually

Once you have gout, another 10-20 years of intermittent disease, until chronic tophaceous gout.

134
Q

When is it most common for men and women, respectively to start having hyperuricemia?

A

men- puberty

women - menopause

135
Q

clinical presentation of acute gout

A

abrubt onset of acute pain and red hot joint

  • no other symptoms
  • resolves in one week without treatment.
136
Q

T/.F you can find crystals in an asymptomatic joint in gout sufferes

A

Yes. 50% chance

137
Q

T/F chronic gout is polyarticular and rate of urate deposition correlates with uric acid level.

A

tru

138
Q

chronic gout radiology

A

punched out lesions with radiodense overhanging edges (tophus)

139
Q

T/F gout affects 6% of the general population

A

False. 3% of the general population

140
Q

Uric acid = the end produce of ___ metabolism

A

Purine

141
Q

Pathophysiology of gout

A

hyperuricemia –> trigger(cold, decreased O2 tension) –> crystal deposition –> macrophages try to eat the crystals and are lysed, releasing cytokines.—> inflammatory response occurs

142
Q

gout activates the ___ arm of the immune system.

A

innate.

143
Q

What are the things that lead to hyperuricema?

A

Diet (meat)

  • alcohol (beer)
  • fructose

Underexcretion of uric acid (much more common than overproduction of uric acid)

144
Q

crystal exam of gout

A

Negatively birefringent
intracellular
parallel yellow
perpendicular to the arrow –>blue

145
Q

Mechanism of colchicine

A

inhibits assembly of NLRP3 inflammasome, turns off cytokine cascade, decreasing inflammation

146
Q

indications for urate lowering therapy

A
  • 1 gout attack and chronic kidney disease
  • presence of tophi
  • > 2 attacks / year
  • history of urolithiasis (kidney stones)
147
Q

what are the zanthine oxidase inhibitors and what are their mechanisms?

A

Allopurinol and Febuxostat

They stop purine metabolism, stopping formation of uric acid.

148
Q

2nd line gout treatment

A

Uricosurics - they increase the renal excretion of uric acid. Used in monotherapy or combination with Xanthine oxidase inhibitors.

149
Q

Difference b/t gout and CPPD

A

CPPD = big toe involvement uncommon

150
Q

Crystal diagnosis of CPPD

A

ABC
Aligned Blue Calcium
positively birefringence.

151
Q

dimensional perspective variables in psychiatry

A

continuous variables

  • intelligence
  • temperament.
152
Q

key brain area in depression

A 
limbic system/ hippocampus
Subgenual cortex (cg25) -this area is overactive in depresesd folks - goal is to inhibit activity in this area.
153
Q

glucocorticoid cascade hypothesis

A

hypothesizes that stress levels/glucocorticoids damage the hippocampus, predisposing to depression - based on work with babboons.

154
Q

neurotrophic model of depression

A

stress leads to decreased neurotropins–> decreased neuron size in hippocampus.

155
Q

examples of neurotropins

A

BDNF nd NT3

MOHD 4 Exam 5 (13 decks)

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