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USMLE: step 1 > Muscle / Skin > Flashcards

Muscle / Skin Flashcards

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USMLE® Step 1 flashcards
1
Q

Where do ACL and PCL attach?

A

ACL: anterior tibia
PCL: posterior tibia

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2
Q

What is anterior drawer?

A

If ACL is busted, tibia moves freely anteriorly if you pull on it

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3
Q

What are varus and valgus force testing?

A

Varus: medially directed force on tibia, Testing LCL
Valgus: laterally directed force on tibia, testing MCL, if torn, will ABduct
- Think if the ligaments as a hinge, if one is broken it allows it to swing open like a door in direction of pressure away from tear

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4
Q

What is meniscus?

A

Cartilage between tibia and femur: medially it is attached to MCL making it less mobile

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5
Q

How to test for meniscal tear?

A

Mcmurray test: rotation of tibia when knee at 90

  1. Pain on internal rotation (toes to midline): lateral meniscal tear
  2. Pain in external rotation: medial meniscal tear
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6
Q

What is the unhappy triad?

A

Traumatic injury to lateral knee causing:

  1. MCL
  2. ACL
  3. Lateral meniscus “LAME” LAteral MEniscus
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7
Q

What is housemaid’s knee?

A

“Prepatellar bursitis”

- Too much kneeling = swollen / painful bursa of patella

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8
Q

What is a baker’s cyst?

A
  • Cystic lesion in knee pit area

- Can cause DVT if large enough

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9
Q

Muscles in the rotator cuff? Functions?

A

“SITS”
Supraspinatus: First 15 ABduction (deltoid after)
Infraspinatus: Lateral rotation of arm
Teres minor: ADduction / lateral rotation
Subscapularis: Medial rotation / ADduction

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10
Q

What is injury if cant abduct arm, but if you place on cheir or give it a boost then you can?

A

Tear in supraspinatus as this is responsible for first 15 degrees of lifting then the deltoid takes over

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11
Q

What muscle provides the following arm motion:

First 15 ABduction (deltoid after)

A

Supraspinatus

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12
Q

What muscle provides the following arm motion:

Lateral rotation of arm

A

Infraspinatus

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13
Q

What muscle provides the following arm motion:

ADduction / lateral rotation

A

Teres minor

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14
Q

What muscle provides the following arm motion:

Medial rotation / ADduction

A

Subscapularis

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15
Q

Cause of medial epicondylitis?

A
  1. Golf

2. Pitching

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16
Q

What causes lateral epicondylitis?

A
  1. Tennis elbow: from backhand motion
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17
Q

Bone injured when pain on snuffbox pressure?

A

Scaffoid

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18
Q

Dislocation of what bone can cause carpal tunnel?

A

Lunate can lead to median nerve compression

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19
Q

What happened if ulnar injury after fall on outstretched hand?

A

Hamate bone injury: think, you fell on your outstretched arm because you were trying to “Ham it up”

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20
Q

Where is carpal tunnel numbness experienced?

A
  1. Thumb
  2. First finger
  3. Middle finger
  4. half of ring finer
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21
Q

3 associations of carpal tunnel?

A
  1. Pregnancy
  2. RA
  3. HYPOthyroid
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22
Q

What is guyon canal syndrome and what causes?

A
  • Injury to ulnar nerve from leaning on palm
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23
Q

Nerve roots of brachial plexus?

A

C5 - T1

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24
Q

Where does C8 nerve come out?

A

Below C7, all other cervical nerves come out above their respective vertebrae

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25
Q

What does posterior cord lesion cause?

A

Problem with extension as it splits into axial and radial nerve

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26
Q

Dermatomes of hand?

A

C6 - 8 as you move from thumb to pinky

- Middle finger is C7 only

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27
Q

Sensory innervation of palm?

A

Ulnar: pinky and half of third finger

Median nerve: thumb and 2.5 fingers

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28
Q

Sensory innervation of dorsal hand?

A

Ulnar: pinky / half of third finger (same as palmar surface)
Median: tips of thumb and 2.5 fingers
Radial: lower portion thumb and 2.5 fingers down to wrist

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29
Q

What is saturday night palsy?

A
  • Fall asleep with arm over chair compressing radial nerve leading to wrist drop and numbness
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30
Q

Another name for radial never?

A

Great extensor

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31
Q

Where is radial nerve often compressed?

A

Spiral groove of humerus in the axilla

- Can be caused with arm over chair or use of crutches

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32
Q

What would direct trauma to tip of shoulder cause?

A

Upper trunk injury: “Herbs / waiter’s palsy”

  • Deltoids, biceps, brachialis paralyzed
  • Arm hangs down and medially rotated
  • No elbow flexion / supination
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33
Q

Cause of lower trunk injury?

A
  1. Grabbing branch on fall
  2. Pulling babies arm in labor
  3. Pancoast tumor of lung
  4. Additional cervical rib
    * Leads to monkeys grip
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34
Q

Where is proximal radial nerve located?

A

Axilla

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35
Q

When does radially nerve move radially?

A

Just past elbow

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36
Q

Injury in elbow dislocation?

A

Deep branch radial nerve: loss of innervation of extensor wrist muscles: wrist drop

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37
Q

Route of axillary nerve?

A

Hugs surgical neck of humerus?

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38
Q

What nerve hugs surgical neck of humerus?

A

Axillary

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39
Q

Nerve in spiral groove of humerus?

A

Radial

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40
Q

Nerve injured in fracture of humeral head?

A

Axillary

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41
Q

Nerve injury in anterior dislocation of humerus?

A

Axillary as wraps around humeral head

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42
Q

Injury if can abduct arm after 15 degrees?

A

Deltoid from anterior dislocation of shoulder injuring axially nerve

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43
Q

Nerve that innervates deltoid?

A

Axillary nerve

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44
Q

How would musculocutaneous nerve injured and what would signs be?

A
  • Carrying heavy backpack: innervates brachioradialis so you can flex arm and will have numb patch of skin on forearm
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45
Q

What compressed if supracondylar fracture of humerus?

A

Median nerve

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46
Q

What does long thoracic innervated?

A

Serratus anterior: leads to winged scapula

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47
Q

Function of lumbricals?

A
  1. Flex MCP joint

2. Extend DIP / PIP

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48
Q

What does distal lesion to median or ulnar nerve cause?

A

“Clawhand” flexion at DIP / PIP

- Lumbrical extension of DIP / PIP is loss so flexors are exaggerated

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49
Q

What is ulnar claw?

A
  • Distal ulnar injury = loss of function to medial lumbricals
    = claw of 3/4th fingers
    aka “pope’s blessing sign “
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50
Q

Injury if try to make fist and thumb, 1/2 second fingers wont close?

A

Proximal medial nerve lesion

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51
Q

Injury if you can’t extend first second fingers?

A
  1. Distal median nerve lesion
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52
Q

Injury if can’t close pinky and 4th finger?

A

Proximal ulnar nerve

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53
Q

Injury if you can’t move thumb away from hand?

A

Opponens pollicis injury innervated by proximal medial nerve

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54
Q

Lesion causing total claw?

A

Lower trunk lesions C8 - T1 of brachial plexus

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55
Q

What is thenar eminence and muscles found in it?

A

Area of palm by thumb: “OAF”

  1. Opponens pollicis
  2. Abductor pollicis
  3. Flexor pollicis brevis
    * **All innervated by medial “million dollar” nerve
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56
Q

Nerve to hypothenar eminence?

A

Ulnar

- OAF as in thenar eminence but this is digiti minimi instead of pollicis

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57
Q

What do dorsal / palmar interossei do?

A

“DAB / PAD”
Dorsal: ABduct
Palmar: ADduct

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58
Q

What gives rise to tibial and common peroneal nerves?

A

Tibial: Sciatic
Peroneal: Sciatic

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59
Q

What does obturator innervated?

A
  • Medial thigh muscles: adduct thigh

- Sensory innervation of medial thigh

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60
Q

What injury causes sensory loss of medial thigh and inability to ADduct thighs?

A

Obturator

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61
Q

Injury causing obturator injury?

A

Anterior hip dislocation

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62
Q

Injury caused by anterior hip dislocation?

A

Obturator injury causing medial thought sensory loss and inability to ADduct thighs

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63
Q

What does femoral nerve innervate?

A

Leg extensors of quad

  1. Quads
  2. Sartorius
  3. Pectineus
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64
Q

How does femoral nerve injury present?

A
  • Difficulty flexing and extending leg

- Sensory deficit on anterior thigh / medial leg

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65
Q

Which nerve injured:

  • Difficulty flexing and extending leg
  • Sensory deficit on anterior thigh / medial leg
A

Femoral

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66
Q

How is femoral nerve injured?

A

Trauma / pelvic fracture

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67
Q

Nerve injury in pelvic fracture?

A

Femoral

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68
Q

Another name for common peroneal nerve?

A

Fibular (lateral bone)

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69
Q

Peroneal innervation?

A
  • Lateral leg muscles: foot eversion

- Dorsal flexion

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70
Q

Tibial innervation?

A

“TIP”

  • Medial muscles: inversion of foot
  • Plantar flexion
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71
Q

Cause of foot drop?

A

Common peroneal injury

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72
Q

Autoimmune disease that can cause foot drop?

A

MS

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73
Q

What would happen in constantly compression fibule by sleeping on park benches and such?

A

Fibular nerve injury

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74
Q

Function of superior gluteal nerve?

A

ABduction of thigh / stabilization of hip
- Trendelenburg sign seen if injured: opposite hip drops when standing on on leg as ipsilateral hip isn’t strong enough to hold steady

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75
Q

When is trendelenburg sign seen?

A
  • Injury to superior gluteal nerve
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76
Q

Where is lesion in hip drop?

A

Contralateral superior gluteal nerve

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77
Q

Injury in posterior hip dislocation?

A

Superior gluteal nerve: contralateral hip drop

Inferior gluteal nerve:

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78
Q

Appearance of inferior gluteal nerve injury?

A

Gluteus maximus innervation: extensor of hip

  • Trouble extending hip (pushing it downward), trouble:
    1. Jumping
    2. Climbing stairs
    3. Rising from seated position
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79
Q

Function of glut max?

A

Hip extension: innervated by inf glut

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80
Q

Injury if having trouble:

  1. Jumping
  2. Climbing stairs
  3. Rising from seated position
A

Inferior gluteal nerve supplying glut max

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81
Q

Root and innervation of pudendal?

A

S2 - 4 innervating perineum

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82
Q

How to find pudendal nerve?

A

Find ischial spine to inject anesthetic in childbirth

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83
Q

Symptoms if compression at L3 - 4?

A
  1. Weak knee extension

2. Decrease patellar relfex

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84
Q

Where is lesion if:

  1. Weak knee extension
  2. Decrease patellar reflex
A

L3 - 4

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85
Q

Symptoms if compression at L4 - 5?

A
  1. Week dorsiflexion / can’t heel walk
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86
Q

Where is lesion if:

1. Week dorsiflexion / can’t heel walk

A

L4 - 5

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87
Q

Symptoms if compression at L5 - S1?

A
  1. Weak plantar flexion
  2. Cant toe walk
  3. Decrease achilles reflex
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88
Q

Where is lesion if:

  1. Weak plantar flexion
  2. Cant toe walk
  3. Decrease achilles reflex
A

L5 - S1

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89
Q

Nerve and artery along axilla on thorax?

A

Nerve: long thoracic
Artery: Lateral thoracic artery

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90
Q

Nerve and artery in surgical head of humerus?

A

Nerve: Axillary
Artery: Posterior circumflex humeral

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91
Q

Nerve and artery in radial groove at midshaft of humerus?

A

Nerve: radial
Artery: deep brachial

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92
Q

Nerve and artery in cubital fossa?

A

Nerve: medial

Artery brachial artery

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93
Q

What nerve runs with popliteal artery?

A

Tibial nerve

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94
Q

Artery with tibial nerve as wraps front of ankle?

A

Posterior tibial

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95
Q

What are DHP receptors?

A

“Dihydropyridine receptors”

- Voltage gated Ca channels on surface of myocytes

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96
Q

What are ryanodine receptors?

A

Ca induced Ca channels on surface of SR in myocyte

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97
Q

What are myofibrils composed of?

A

Sarcomeres: smallest functional unit of muscle cells

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98
Q

Extent of sarcomere?

A

Sarcomeres extend from Z line to Z line

“Z is end of sarcomere and the alphabet”

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99
Q

What comes off the Z lines?

A

Thin Actin molecules projecting in towards the M line

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100
Q

What are the lines coming off the M lines?

A

Thick Myosin molecules extending out to Z line

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101
Q

What is the H zone?

A

Stretch of myosin heavy chains not overlapping with actin light chain

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102
Q

What is the I band?

A

Part of actin light chains not overlapping my myosin heavy chains

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103
Q

When is H zone longest?

A

Relaxation

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104
Q

What is the A band?

A

Entire length of myosin heavy chain from end to end

  • **Length DOES NOT change with contraction
  • The light and heavy chain are simply sliding along each other
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105
Q

Which areas get smaller in contraction?

A

I band and H zone

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106
Q

Which areas elongate in relaxation?

A

I band and H zone

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107
Q

How do Z lines appear on EM?

A

Dark banks

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108
Q

What happens at motor end plate?

A

Depolarization via Na channels spreading down to T tubules causing DHP-r depolarization allowing Ca to flow in
- Ryanodine receptor on SR changes conformationally allowing Ca release into cytoplasm

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109
Q

Where does Ca bind once release from SR?

A

Troponin C: cause tropomyosin to move out of myosin binding groove on actin filament

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110
Q

What does myosin do when tropomyosin moves?

A

Releases ATP it was bound to allowing it to power stroke along actin

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111
Q

What is ATP necessary for?

A

Detachment of myosin head from actin filament

- This is why you get rigormortis when dead: you can no longer make ATP so can no longer release myosin from actin

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112
Q

Which fibers stain dark and light?

A

Dark: Type I, sustained contraction
Light: type II, fast twitch, thing “2 fibers = 2x as fast”

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113
Q

What do type I fibers do?

A 
"One Slow Red Ox"
Type I 
Slow Twitch 
Red Fibers
Need Oxidative phosphorylation
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114
Q

Which muscles tend to be slow twitch?

A

Postural

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115
Q

What type of muscle hypertrophies in weight training?

A

Type II: white, slow, glycolysis

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116
Q

What does Ca do when enters smooth muscle cell?

A
  • Binds calmodulin instead of RYR or troponin C
  • Calmodulin activates Myosin light chain kinase which phosphorylates myosin chains
  • Phosphorylated myosin cross bridges along actin
  • Myosin light chain phosphatase takes of P causing relaxation
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117
Q

What can cause relaxation in smooth muscle?

A
  1. Myosin light chain phosphatase

2. NO from endothelial cells

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118
Q

How does NO cause SM relaxation?

A
  1. NO activates guanylyl cyclase increasing cGMP

2. cGMP inhibits myosin light chain kinase

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119
Q

What bones are formed by endochondral ossification?

A

All the long bones in body

- Cartilage remodeling is first step on which woven and lamellar bone is formed

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120
Q

What is membranous ossification?

A
  • Woven bone directly formed with no cartilage base

* *Occurs in skull and facial bones

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121
Q

What are osteocytes?

A
  • Derived from osteoblasts

- Regulate bone repair and remodeling

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122
Q

Progenitor of Osteoclasts?

A

Monocytes

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123
Q

What is histologic marker of osteoclasts?

A

TRAP stain - same stain used in hair cell leukemia

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124
Q

What is TRAP marker for?

A

Osteoclasts

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125
Q

Impact of estrogen on bone?

A
  1. Prevents apoptosis of osteoblasts and osteocytes
  2. Promotes osteoclast death
    * Promotes bone formation
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126
Q

What is achondroplasia? Cause?

A
  • Impaired cartilage proliferation in growth plate
  • Impacts longs bones that grow via endochondral ossification
  • Caused by activating mutation of FGFR3
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127
Q

What does activation mutation in FGFR3 cause?

A

Achondroplasia

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128
Q

Presentation of achondroplasia?

A
  • Short extremities with normal head / chest

- Cartilage needed in long bones but not in bones that grow via membranous ossification such as face and chest

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129
Q

What is osteogenesis imperfecta? Cause?

A
  • Congenital defect in bone formation = weak bones

- AD defect in type I collagen

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130
Q

What type of collagen is present in bone?

A

Type ONE

- Think ONE as in “bONE”

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131
Q

Presentation of osteogenesis imperfecta?

A
  1. Bone fractures
  2. Blue sclera: exposure of choroidal veins
  3. Hearing loss
    * **Type I collagen is found in sclera and ears also
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132
Q

What is the following presentation indicative of:

  1. Bone fractures
  2. Blue sclera: exposure of choroidal veins
  3. Hearing loss
A

Osteogenica imperfect

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133
Q

What is osteopetrosis?

A

“Petros” = “rock like”

- Inherited defect in resorptive osteoclast activity = thick, heavy bone that fractures easily

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134
Q

Common cause of osteopetrosis?

A

Carbonic anhydrase deficiency

  • Acid necessary to remove Ca and resorb bone
  • Osteoclasts usually use CA to create this
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135
Q

Presentation of osteopetrosis?

A
  1. Easy fractures in abnormally thick bone
  2. Pancytopenia: marrow pushed out by bone
  3. Vision / hearing impairment: skull compressing CN
  4. Hydrocephalus: blocks foramen magnum
  5. RTA: can’t excrete acid / make bicarb in kidney
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136
Q

Treatment of osteopetrosis?

A

Bone marrow transplant: allows to you make normal monocytes which are progenitors of osteoclasts

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137
Q

Whats is rickets?

A
  • Defective osteoid mineralization due to low Vitamin D `
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138
Q

What is osteomalacia?

A

Rickets in adults

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139
Q

What is osteoid?

A

Osteoblasts make osteoid which must be mineralized with Ca and P to make final bone

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140
Q

Rickets presentation?

A
  1. Pigeon breast
  2. Bow legs
  3. Frontal bossing: osteoid deposition in skull
  4. Rachitic rosary: osteoid deposition at CV junction
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141
Q

Lab values in osteomalacia?

A
  1. Low Ca
  2. Low P
  3. Increased PTH
  4. Increased Alk phos
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142
Q

What does alk phos do?

A

Released by osteoblasts to create alkaline environment that is necessary for Ca deposition

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143
Q

What is osteoporosis?

A
  • Loss of trabecular bone mass = porous bone that easily fractures
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144
Q

What is risk of osteoporosis based on?

A
  1. Peak bone mass

2. Rate of decline after peak

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145
Q

What determines peak bone mass?

A
  1. Diet
  2. Exercise
  3. Vitamin D receptor you inherit
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146
Q

Osteoporosis presentation?

A
  1. Pain in fractures in weight bearing areas
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147
Q

How is bone density measured?

A

Dexa scan

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148
Q

Serum levels in osteoporosis?

A

Everything is normal

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149
Q

Osteoporosis therapy?

A
  1. Exercise
  2. Vitamin D / Ca
  3. Bisphosphonates
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150
Q

How do bisphosphonates work?

A
  • Attaches to bone and osteoclasts eat it leading to their death
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151
Q

What is paget’s disease of bone?

A
  • Imbalance between osteoclasts and blasts
  • Normally PTH signals blasts which activate clasts
  • In paget’s, this signalling goes awry = increase resorb
  • Blasts try to catch up but lay down weak bone
  • Result is thick sclerotic bone that easily fractures
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152
Q

Whaten is mosaic pattern of lamellar bone seen?

A

Paget’s

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153
Q

Paget’s presentation?

A
  1. Increasing hat size
  2. Bone pain
  3. Hearing loss
  4. Lion faces
  5. Elevated alk phos
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154
Q

What is following indicative of:

  1. Increasing hat size
  2. Bone pain
  3. Hearing loss
  4. Lion faces
  5. Elevated alk phos
A

Paget’s

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155
Q

Paget’s treatment?

A
  1. Calcitonin

2. Bisphosphonates

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156
Q

Paget’s complications?

A
  1. High output cardiac failure

2. Osteosarcoma: malignant blast tumor

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157
Q

How does osteomyelitis occur?

A

Hematogenous bacterial spread
Kids: seeds metaphysis
Adults: seeds epiphysis

158
Q

What are the epiphysis, metaphysis, and diaphysis?

A

From the “EMD” of the bone

- different parts of bone from its end moving down bone

159
Q

What is avascular necrosis?

A
  • Ischemic, aseptic necrosis of bone / marrow

- Leads to Osteoarthritis and fracture

160
Q

Causes of avascular necrosis?

A
  1. Trauma / fracture
  2. Steroids
  3. Sickle cell: dactylitis
  4. Caisson disease: gas emboli
161
Q

What is a osteoma?

A
  • Benign bone tumor
  • Normally on surface of facial bones
  • Seen in Gardner syndrome
162
Q

What is Gardner syndrome?

A
  1. Osteoma
  2. Familial adenomatous polyposis
  3. Fibromatosis of retroperitoneum
163
Q

What is osteoid osteoma?

A
  • Benign tumor of osteoblasts with rim of reactive bone

- Seen in

164
Q

Tumor with rim of reactive bone in long bone of 20 yo?

A

Osteoid osteoma

165
Q

What tumor has bone pain that resolves with aspirin?

A

Osteoid osteoma

166
Q

What tumor is bony mass with radiolucent core?

A

Osteoid osteoma

167
Q

Characteristics of osteoblastoma?

A
  • Benign tumor of osteoblasts
  • > 2cm
  • Found in vertebrae
  • Bone pain that does not respond to ASA
168
Q

What is the following:

  • Benign tumor of osteoblasts
  • > 2cm
  • Found in vertebrae
  • Bone pain that does not respond to ASA
A

Osteoblastoma

169
Q

What is osteochondroma?

A
  • Benign tumor of bone with cartilage cap
  • “chondro” = cartilage
  • Arises as lateral projection of growth plate
170
Q

What is the following:

  • Benign tumor of bone with cartilage cap
  • “chondro” = cartilage
  • Arises as lateral projection of growth plate
A

Osteochondroma

171
Q

What is chondrosarcoma?

A
  • Malignant transformation of cartilage camp on osteochondroma
172
Q

What is osteosarcoma?

A
  • Malignant osteoblastic tumor
  • Peak incidence in teenagers
  • In metaphysis of long bone: distal femur, proximal tibia
173
Q

Osteosarcoma risks?

A
  1. Familial retinoblastoma
  2. Pagets
  3. Radiation
174
Q

What is the following:

  • Malignant osteoblastic tumor
  • Peak incidence in teenagers
A

Osteosarcoma

175
Q

What is familial retinoblastoma?

A
  1. Bilateral retinoblastoma

2. Osteosarcoma

176
Q

Presentation of osteosarcoma?

A
  1. Pathologic fracture
  2. Bone pain with swelling
  3. Drags periosteum off bone: layer of connective tissue “Codman’s angle”
177
Q

Tumor in metaphysis of long bone?

A

Osteosarcoma

178
Q

Which tumor pulls periosteum off bone: “Codman’s angel”?

A

Osteosarcoma

179
Q

“Pleomorphic cells producing osteoid?”

A

Osteosarcoma

180
Q

What is giant cell tumor?

A
  • Tumor of giant / stromal cells in young adults
  • Arises in epiphysis
  • Locally aggressive with recurrence
    “Soap bubble sign”
181
Q

Only tumor in epiphysis?

A

Giant cell tumor

182
Q

“Soap bubble sign?”

A

Giant cell tumor

183
Q

What is ewing sarcoma?

A
  • Malignant growth of poorly differentiated cells of neuroectodermal origin
  • Male kids
  • Diaphysis of long bones
  • Onion skin on Xray
184
Q

What is following:

  • Malignant growth of poorly differentiated cells of neuroectodermal origin
  • Male kids
  • Diaphysis of long bones
  • Onion skin on Xray
A

Ewings

185
Q

Translocation in ewings?

A

11:22

186
Q

What is 11:22 translocation seen in?

A

Ewing’s sarcoma: 33 is his jersey number

187
Q

What is chondroma?

A
  • Benign tumor of cartilage

- Medulla of hands and feet

188
Q

Location of benign and malignant cartilage tumors?

A

Malignant: Pelvis / central skeleton
Benign: small bones of hands and feet

189
Q

When are punched out osteolytic lesions seen?

A

Metastasis to bones

190
Q

Presentation of prostate in bones?

A

Osteoblastic lesions

191
Q

Type of cartilage at joints?

A

Type II: think, this is where TWO bones come together

192
Q

What is synovium?

A

Lining that surrounds a joint making a capsule

- Secretes fluid of Hyaluronic acid to lubricate joint

193
Q

What is degenerative joint disease?

A
  • Degeneration of articular cartilage from wear and tear
  • Seen with age, obesity, and trauma
  • *Joint stiffness in morning that worsens throughout day
194
Q

When is stiffness worsening through day seen?

A

Degenerative joint disease

195
Q

What hand joins is degenerative joint disease in?

A

DIP

PIP

196
Q

What is eburnation?

A
  • Rubbing / polishing of bone seen in degenerative joint disease from lack of cartilage
  • Bone rubbing against bone will the to reactive osteocytes
197
Q

When are osteocytes seen in DIP and PIP?

A

Degenerative joint disease

198
Q

What are heberden and bouchard nodes?

A
  • Osteocytes seen in DIP and PIP in degenerative joint disease
199
Q

Genetic association of RA?

A

HLA-DR4

200
Q

What is HLA DR4 implicated in?

A

RA

201
Q

Hallmark of RA?

A

Synovitis leading for formation of pannus: inflamed granulation tissue

202
Q

When is this seen:

Synovitis leading for formation of pannus

A

RA

Pannus = inflamed granulation tissue

203
Q

What is occurring in the synovitis in RA?

A
  • Myofibroblasts in granulation tissue of pannus cause:
    1. Ankylosis: fusion of joint
    2. Movement of joint in different directions
    3. Destruction of articular cartilage
204
Q

What is ankylosis?

A

Fusing of joint that can be seen in RA from myofibroblast contraction

205
Q

When is morning stiffness improving during day seen?

A

RA

- Compare it to inflammation of your throat when you wake up in morning it is worse then improves during day

206
Q

Joints in RA?`

A

Symmetrical involvement of:

  1. PIP
  2. Wrists
  3. Elbows
  4. Ankles
  5. Knees
    * **Sparing DIP
207
Q

When is symmetric` joint involvement sparing DIP seen?

A

RA

208
Q

Joint disease with systemic signs?

A

RA

209
Q

What are rheumatoid nodules?

A
  • Central area of necrosis surrounded by epithelioid histiocytes
210
Q

Associated features of RA?

A
  1. Vasculitis
  2. Rheumatoid nodules
  3. Baker Cysts: seen in leg pit
211
Q

Lab findings in RA?

A
  • IgM antibody against FC portion of IgG
212
Q

When is the following seen:

- IgM antibody against FC portion of IgG

A

RA

213
Q

Sequelae of RA?

A
  1. Anemia of chronic disease

2. Secondary amyloidosis: deposition of AA

214
Q

What is deposited in secondary amyloidosis?

A
  • SAA made in liver converted to AA which is deposited in tissues
215
Q

Characteristics of seronegative spondyloarthropathies?

A
  1. Lack rheumatoid factor
  2. Axial skeleton
  3. HLA B27 association
216
Q

Joint involvement in ankylosing spondyloarthritis?

A
  1. Spine

2. SI joint

217
Q

Presentation of ankylosing spondyloarthritis?

A

Young male with:

  1. Low back pain
  2. Fusion of vertebrae: bamboo spine
  3. Uveitis
  4. Aortitis
218
Q

When is bamboo spine seen?

A

Ankylosing spondylitis

219
Q

Characteristics of psoriatic arthritis?

A
  • Psoriasis
  • Axial and distal skeleton
  • “Sausage fingers of DIP”
220
Q

When are sausage fingers seen?

A

Psoriatic arthritis

221
Q

Presentation of infectious arthritis?

A

N. gonorrhoeae or S aureus infx causing:

  1. Warm, red joint with limited motion
  2. Fever
  3. Increased WBC
  4. Increased ESR
    * **Single joint, usually knee
222
Q

What is happening in gout?

A

Monosodium urate deposition in tissues due to increased uric acid

223
Q

How do we arrive at uric acid?

A
  1. Purine degradation products AMP / GMP taken into enterocyte
  2. GMP broken to guanine, AMP to HYPOxanthine
  3. Both products broken to xanthine
  4. Xanthine oxidase converted to uric acid
  5. Uric acid filtered by kidney unless too much
224
Q

What is xanthine oxidase?

A
  • In breakdown of purines, converts xanthine to uric acid
225
Q

Causes of secondary gout?

A
  1. Leukemia and myeloproliferative: high cell turnover - increased purines
  2. Lesch nyhan
  3. Kidney failure
226
Q

What is lesch nyhan?

A

HGPRT deficiency in purine salvage pathway leading to increased uric acid causing:

  1. Gout
  2. Mental retardation
  3. Self mutilation
227
Q

What is HGPRT?

A

Salvages Hypoxanthine and guanine from purine degradation pathway
- Leads to decreased uric acid

228
Q

What is the following:

  1. Gout
  2. Mental retardation
  3. Self mutilation
A

Lesch Nyhan

229
Q

What causes inflammation in acute gout?

A

MSU crystals in joints are activating neuts

230
Q

What is podagra?

A
  • Painful arthritis of great toe seen in gout
231
Q

Why does booze cause gout?

A

Byproducts of alcohol compete with uric acid for excretion

232
Q

What are tophi?

A
  • Uric acid crystals in tissues and joints that is hallmark of chronic gout
  • Which chalky deposits on histo
233
Q

Lab in gout?

A
  • Needled shaped crystals with NEGATIVE birefringence under polarized light
  • When flat = yellow “When lay low, yellow”
234
Q

What does negative birefringence mean?

A
  • When flat = yellow “When lay low, yellow”

Seen in gout UA crystals

235
Q

What is pseudogout?

A
  • Ca pyrophosphate crystals in joints

- Rhomboid crystals with weak positive birefringence

236
Q

What is following:

- Needled shaped crystals with NEGATIVE birefringence under polarized light

A

Gout

237
Q

What is following:

- Rhomboid crystals with weak positive birefringence

A

Pseudogout

- Think pseu, positive, pyrophosphate, all begin with Ps

238
Q

What is dermatomyositis?

A
  • Inflammatory disease of skin and muscle often associated with gastric carcinoma
239
Q

Presentation of dermatomyositis?

A
  1. Proximal, bilateral muscle weakness: cant raise arms of climb stairs
  2. Rash of upper lids
  3. Malar rash
  4. Red papules on knees, knucles, elbows
240
Q

What is following:

  1. Proximal, bilateral muscle weakness: cant raise arms of climb stairs
  2. Rash of upper lids
  3. Malar rash
  4. Red papules on knees, knucles, elbows
A

Dermatomyositis

241
Q

Labs in dermatomyositis?

A
  1. Increased creatine kinase
  2. Positive ANA
  3. Anti JO-1 Ig
  4. Perimysial inflammation with perifascicular atrophy
242
Q

When is DSDNA Ig seen?

A

Lupus

243
Q

When is following seen:

Perimysial inflammation with perifascicular atrophy

A

Dermatomyositis

244
Q

What is perimysium? When is it inflamed?

A

Connective tissue surrounding muscle fascicles: inflamed in dermatomyositis
***Think, the perimysium is on outside of fiber close to skin so it must be inflamed in dermatomyositis

245
Q

What is endomysium? When is it inflamed?

A

Connective tissue between fibers

- Inflamed in polymyositis

246
Q

What is polymyositis?

A
  • Inflammatory condition of skeletal endomysium
  • No skin involvement
  • CD8 and necrotic fibers seen
247
Q

What is X linked muscular dystrophy? Caused?

A
  • Degenerative muscles wasting in which muscle is replaced by adipose tissue
  • Caused by DELETIONS of dystrophin
248
Q

What is following:

- Degenerative muscles wasting in which muscle is replaced by adipose tissue

A

Muscular dystrophy

249
Q

What is dystrophin?

A
  • Largest gene in humans:
  • DELETED in DMD
  • Anchors muscle cytoskeleton to ECM
250
Q

DMD presentation?

A
  1. Proximal muscle weakness at 1 yo
  2. Calf pseudohypertrophy
  3. Elevated CK
251
Q

Death in DMD?

A

Cardiac or respiratory failure once they become involved

252
Q

What is becker muscular dystrophy?

A
  • Mutations in dystrophin

- Similar to DMD but milder as DMD is deletion

253
Q

Transmission at NMF?

A
  • Ca channel opening allows for AcH release

- AcH binds nicotinic receptors on endplate

254
Q

What happens in myasthenia gravis?

A
  • Ig binds nicotinic receptor at NMJ endplate
  • Receptor is not destroyed, Ig just creates competition
  • With rapid firing, not enough Ach Can be released to fire muscle
  • *Classically seen in eyes = ptosis and double vision
255
Q

When is muscle weakness worse with use and better with rest seen?

A

MG

256
Q

Association of MG?

A
  1. Thymoma - improved if removed

2. Thymic hyperplasia

257
Q

What happens in eaton lambert?

A

Ig vs presynaptic Ca channel

  • Seen in small cell carcinoma of lung
  • Proximal muscles involved sparing eyes
  • Improves with use
258
Q

Muscles in MG and eatons?

A

MG: eye with ptosis is first
Eaton: eye spared, proximal muscles infected

259
Q

MG eaton improve or worsen with use?

A

MG: worsen
Eaton: improve

260
Q

When is lipoblast seen?

A

Liposarcoma

261
Q

When is cardiac rhabdomyoma seen?

A

Tuberous sclerosis

262
Q

Which tumor is desmin +?

A

Rhabdomyosarcoma

- Often seen in vagina of young girl

263
Q

What does basement membrane separate?

A

Epidermis from underlying dermis

264
Q

Layers and functions of epidermis?

A

Moving up from basement:

  1. Basalis: stem cell layer
  2. Spinosum: connected by desmosomes
  3. Granulosus: granules in cells
  4. S. corneum: keratin in cells
265
Q

What are desmosomes?

A

Connect the keratinocytes in S. basalis

266
Q

What is in dermis?

A
  1. Connective tissues
  2. Blood vessels moving up to dermis
  3. Hair cells
  4. Sebaceous glands (sweat)
267
Q

Are there blood vessels in epidermis?

A

No

268
Q

Another name for eczema?

A

“Atopic dermatitis”

269
Q

What is atopic dermatitis?

A

“Eczema”

  • Itchy, red, oozing rashing with vesicles and edema
  • Face and flexor surfaces
  • Type I HSR associated with asthma and rhinitis
270
Q

What is following:

- Itchy, red, oozing rashing with vesicles and edema on face and flexor surfaces

A

Atopic or contact

271
Q

Atopic dermatitis associations?

A

Type I HSR associated with:

  1. Asthma
  2. Allergies
272
Q

What is contact dermatitis?

A
  • Same appearance of atopic dermatitis but due to exposure to allergen: Itchy, red, oozing rashing with vesicles and edema
  • **Not a type I HSR: could be IV
273
Q

What type of HSR are nickel and IVY?

A

Type IV

274
Q

Drug causing contact dermatitis?

A

Penicillin

275
Q

Lesions seen in acne vulgaris?

A
  1. Comedones: white and black heads
  2. Nodules
  3. Pustules: pimples
276
Q

Cause and pathology of acne?

A
  • Chronic inflammation of hair follicles and sebaceous glands
  • Hormone induced increased sebum and excess keratin production in epithelial cells of follicle = blockage: comedones
  • Propionibacterium acnes = inflammation
277
Q

How does P. Acnes cause acne?

A
  • Keratin blocks follicle and excess sebum fills it = comedone
  • P. Acnes infects and releases lipases breaking down sebum releasing inflammatory FFAs = inflammation = pimple
278
Q

Acne treatment?

A
  1. Benzoyl peroxide: antibiotic

2. Isotretinoin: vitamin a derivatives block keratin production

279
Q

What is psoriasis?

A
  • Well circumscribed salmon plaques with silver scale
  • Usually on extensors and scalp
  • Pitting of nails can be seen
  • Hyperplasia and epidermal thickening: acanthosis
  • Parakeratosis
280
Q

What is following:

- Well circumscribed salmon plaques with silver scale

A

Psoriasis

281
Q

Cause of psoriasis?

A
  • Excessive keratinocyte proliferation
  • Possibly autoimmune and associated with HLA c
  • Can arise in areas of trauma
282
Q

Genetics of psoriasis?

A

HLA C: say “"”CCCCCC-riassis”

283
Q

What is hyperplasia with increased thickening of epidermis seen in?

A

Acanthosis: characteristic of pWsoriais

284
Q

When are parakeratosis and acanthosis seen?

A

Psoriasis

285
Q

When / what are munro microabscesses?

A
  • Seen in psoriasis

- Neuts deposited in excess parakeratosis

286
Q

When is elongation of dermal papillae seen?

A

Psoriasis: allows vessels to protrude into epidermal areas where not normally found which is why plaques bleed when come off

287
Q

What is auspitz sign?

A
  • Bleeding when plaques picked off in psoriais
288
Q

Psoriasis Rx?

A
  1. Steroids
  2. UVA light with psoralen: damages keratinocytes - “PUVA”
  3. Immune madulators
289
Q

What is lichen planus?

A
  • Pruritic, polygonal, planar, purple patches
  • Often have white lines on surface: Wickham striae
  • Can be seen in mouth
290
Q

What is inflammation of dermal epidermal junction with sawtooth appearance?

A

Lichen planus

291
Q

Histo of lichen planus?

A

Inflammation of dermal epidermal junction with sawtooth appearance

292
Q

Association of lichen planus?

A

Chronic HCV

293
Q

How does a blister arise?

A
  • Separation of layers of skin = bubble

- Can happen between various layers

294
Q

What is pemphigus vulgaris?

A
  • Autoimmune destruction of desmosomes: connect keratinocytes in spinosum
  • IgG vs. desmoglein
  • Fishnet on IF of IgG around keratinocytes
  • Blister is between intact basal and rest of epidermis
  • Thin epidermal wall on top of blister that easily ruptures
295
Q

What is blister on top of intact basal layer?

A

Pemphigus vulgaris: IgG against desmoglein of desmosomes

296
Q

What is acantholysis?

A

Separation of keratinocytes

297
Q

What does hemidesmosome do?

A

Attach basal cell to basement layer: attacked in bullous pemphigoid

298
Q

Where does pemphigus vulgaris present?

A

Skin AND oral mucosa

299
Q

What is bullous pemphigoid?

A
  • Autoimmune destruction of hemidesmosomes by IgG against basement membrane
  • Subepidermal blisters with oral sparing
300
Q

Which blister is on mouth?

A

Pemphigus vulgaris: think it would be “vulgar” looking to have blister on mouth

301
Q

Which Blister is thicker?

A

Bullous pemphigoid: think, it is thicker because the entire epidermal layer is on top and BM is on bottom and “Bullous” starts with B

302
Q

What is dermatitis herpetiformis?

A
  • IgA deposition at tips of dermal papillae
  • Itchy grouping of bullae and vesicles
  • Seen in celiacs
303
Q

What is erythema multiforme?

A
  • HSR withtargetoid rash and bullae

- Often seen in HSV

304
Q

What is SJS?

A
  1. Erythema multiforme with oral involvement

2. Fever

305
Q

What is TEN?

A

“Toxic epidermal necrolysis” severe SJS

  1. Sloughing of skin
  2. From drug rxn
306
Q

What causes impetigo?

A

Staph or pyogenes

307
Q

What causes cellulitis?

A

Staph or pyogenes

308
Q

What can cellulitis progress to?

A

Necrotizing fasciitis

309
Q

What is necrotizing fasciitis?

A
  1. Necrosis of sub q tissue from infx

2. CO2 production = crepitus

310
Q

Layer separated in scalded skin?

A

S. Granulosus

311
Q

Where does TEN occur?

A

Dermal / epidermal junction

312
Q

What is verruca?

A

AKA wart

313
Q

What is molluscum contagiosum?

A

Firm, pink umbilicated papule from POX virus

314
Q

What is seborrheic keratosis?

A

Benign proliferation of squamous cells common in elderly

- Raised grey plaque with stuck on appearance

315
Q

What are circular spaces with abundant pink keratin / pseudo cysts indicative of on histo?

A

Seborrheic keratosis

316
Q

What is Leser trelat sign?

A
  1. Sudden onset of multiple Seborrheic keratosis

2. Usually with GI carcinoma

317
Q

When is epidermal hyperplasia with darkening of skin seen?

A
  1. Insulin resistance

2. Malignancy

318
Q

What is xeroderma pigmentosum? What does it put you at risk for?

A

AR defect in nucleotide excision repair enzymes

- At risk for BCC

319
Q

What does UVB do to skin?

A
  • Forms pyrimidine dimers that need to be repaired by nucleotide excision repair
  • Enzyme is deficient in xeroderma pigmentosum putting you at risk for BCC
320
Q

What is following:

- Elevated nodule, central necrosis, dilated vessels surrounding

A

BCC

321
Q

Which skin cancer shows peripheral palisading?

A

BCC

322
Q

BCC prognosis?

A

Rarely metastasizes

323
Q

Risks for SCC?

A
  1. Immunosuppression
  2. Arsenic
  3. Chronic inflammation: scar from burn / draining sinus tract
  4. Actinic keratosis
324
Q

Skin cancer often appearing on scars?

A

SCC

325
Q

Which cancers present on upper and lower lip?

A

“Bull shit”
Upper: BCC
Lower: SCC

326
Q

What is actinic keratosis?

A
  • SCC precursor

- HYPERkeratotic scaly plaque

327
Q

What is a hyperkeratotic scaly plaque?

A

Actinic keratosis - risk for SCC

328
Q

What is keratoacanthoma?

A
  • Well differentiated SCC that rapidly progresses, then rapidly regresses
  • Cup shaped tumor with keratin debris in center
329
Q

What is following:

  • Well differentiated SCC that rapidly progresses, then rapidly regresses
  • Cup shaped tumor with keratin debris in center
A

Keratoacanthoma

330
Q

How do melanocytes work? Where are they found?

A
  • Found in basal layer of epidermis
  • Take tyrosine to make melanin in melanosomes
  • Melanin is passed to keratinocytes causing pigmentation
331
Q

Origin of melanocytes?

A

Neural crest in nature - S100 +

332
Q

What is vitiligo?

A

Localized autoimmune destruction of melanocytes = loss of pigmentation

333
Q

What is local autoimmune destruction of melanocytes?

A

Vitiligo

334
Q

What is albinism?

A
  • Congenital lack of pigmentation from defect in tyrosinase enzymes impairing melanin production
  • Can only involved eyes or eyes and skin
335
Q

Why do freckles darken relative to neighboring cells?

A

Increased numbers of melanosomes

336
Q

What is melasma?

A

Mask like hyperpigmentation of cheeks associated with OCPs and pregnancy

337
Q

What a nevus?

A

“mole”

- Benign neoplasm of melanocytes

338
Q

Is hair growing from mole a good sign?

A

Yes, this is not seen in melanoma as they would destroy the follicles

339
Q

Are nevis precursors to melanoma?

A

They can be if they develop dysplasia

340
Q

ABCs of melanoma?

A

Asymmetry
Border irregularity
Color changes throughout
Diameter > 6 mm

341
Q

Key feature for risk of metastasis in melanoma?

A

Depth of invasion

342
Q

4 Types of melanoma?

A
  1. Lentigo maligna
  2. Superficial spreading
  3. 4.
343
Q

What is lentigo maligna melanoma?

A 
Lentiginous proliferation (along dermal line) of melanocytes 
- Good prognosis as not much depth of invasion
344
Q

What is the following:

Melanocyte proliferation along dermal line

A

Lentigo melanoma

345
Q

What is superficial spreading melanoma?

A

Dominant early radially phase:

- Good prognosis as not going deep

346
Q

Which melanoma has dominant early radial phase?

A

Superficial spreading

347
Q

What is nodular melanoma

A
  • Early vertical phase: poor prognosis

- Pushes skin up as it goes deep which is why it is called nodular

348
Q

Which melanoma has early vertical phase?

A

Nodular

349
Q

What is acral lentiginous melanoma?

A
  • Palms and soles of dark skinned folks

- Not relation to UV light

350
Q

What is melanoma of palms and soles?

A

Acral lentiginous

351
Q

Risk for having a child with achondroplasia?

A

Advanced paternal age

352
Q

What is decrease in trabecular mass despite normal mineralization and lab values?

A

Osteoporosis

353
Q

Diagnostics of osteoporosis?

A

Osteoporotic: > 2.5 SDs from mean
Osteopenic: 1 SD from mean

354
Q

When are chalk stick fractures in long bones seen?

A

Pagets

355
Q

How will paget’s of bone kill you?

A
  1. AV shunts through bone: high output HF

2. Osteogenic sarcoma

356
Q

Increasing hat size and elevated alk phos?

A

Pagets

357
Q

2 bone diseases with normal labs?

A
  1. Osteoporosis

2. Osteopetrosis

358
Q

Labs in rickets?

A
  1. Low Ca
  2. Low P
  3. Increased Alk phos
  4. Increased PTH
359
Q

Bone tumor with homer wright rosettes?

A

Ewing sarcoma

360
Q

Characteristics of type III HSR?

A

Ig / complex mediation

361
Q

When is DIP spared?

A

RA

362
Q

What does probenecid do?

A

Cause increased uric acid excretion

363
Q

Where does pseudogout present?

A

Usually larger joints

364
Q

Presentation of sjogren’s?

A
  1. Xerophthalmia: Dry eyes / “sand in eyes”
  2. Xerostomia: dry mouth / dysphagia as makes it hard to swallow
  3. Enlarged parotids
  4. RA
    * **caused by exocrine destruction of salivary and lacrimal glands
365
Q

What is the following?

  1. Xerophthalmia
  2. Xerostomia
  3. Enlarged parotids
  4. RA
A

Sjogren

366
Q

Antibodies in sjogren’s?

A
  1. Anit RNP
  2. Anti Ro / SSA
  3. Anti La / SSB
367
Q

When is following seen:

  1. Anit RNP
  2. Anti Ro / SSA
  3. Anti La / SSB
A

Sjogrens

368
Q

Diagnosis in teenager with red hot joint?

A

Gonorrhea

369
Q

Bone disease with HLA B27?

A

Seronegative spondalropathies

370
Q

Pencil / cup deformity?

A

Psoriatic arthritis

371
Q

Joint disease caused by IBD?

A

Sacroiliitis

372
Q

What does lupus cause in heart?

A
  1. Libman sachs endocarditis

2. Pericarditis

373
Q

What is chest pain relieved by leaning forward and worse on lying down and deep breaths?

A

Pericarditis

374
Q

SLE on kidney?

A
  1. Diffuse proliferative glomerulonephritis
  2. Membranous glomerulonephritis
    * *Type III HSRs
375
Q

4 serum markers for lupus?

A
  1. Anti DSDNA
  2. Antismith
  3. ANA
  4. Antihistone: drug induced lupus
376
Q

Drugs causing drug induced lupus?

A
  1. Hydralazine
  2. Procainamide
  3. Isoniazid
377
Q

Characteristics of antiphospholipid syndrome?

A
  1. 1st semester clot or abortion
  2. False positive VDRL
  3. Falsely prolonged PTT
  4. Lupus anticoag / anticardiolipin / Anti B2
378
Q

What is following:

    • ANA
    • anti-U1-RNP
A

Mixed connective tissue disease

379
Q

Schaumann and asteroid bodies?

A

Sarcoid

380
Q

Sarcoid presentation?

A
  1. Restrictive lung disease
  2. Bell palsy
  3. Erythema nodosum
  4. Uveoparotitis
381
Q

Labs in sarcoid?

A
  1. Increased ACE
  2. Increased Ca: macs in granulomas activate vitamin D
  3. Increased CD4:8 ratio
382
Q

What is polymyalgia rheumatic?

A
  1. Pain and stiffness in hips and shoulders
383
Q

Women > 50 with muscle pain and no weakness?

A

Polymyalgia rheumatica

384
Q

Association of Polymyalgia rheumatica?

A

Giant cell arteritis

385
Q

What is polymyositis?

A
  • Progressive, symmetric, proximal muscle weakness
386
Q

What is myositis ossificans?

A

Ca deposits in muscles

387
Q

What is scleroderma?

A
  • Widespread collagen deposition in body = fibrosis

- Tight, puffy skin

388
Q

When is SCL 70 seen?

A

Diffuses scleroderma

389
Q

Lab in Diffuses scleroderma?

A

SCL 70

390
Q

What is CREST? Lab

A 
*Anticentromere Ig
Calcinosis 
Raynaud's
Esophageal dysmotility 
Sclerodactyly
Telangiectasia
391
Q

When is anticentromere Ig seen?

A

CREST

392
Q

Cause of Raynaud’s?

A

Excess Alpha receptors on vessels of hands = constriction

USMLE: step 1 (15 decks)

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