Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Mind & Motion > Midterm 3: Buzzword Bingo > Flashcards

Midterm 3: Buzzword Bingo Flashcards

1
Q

Types of bones that use endochondral bone formation

A

Long bones (humerus, femur, metacarpals, etc); short bones (carpals, tarsals, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cartilage model of bone forms -> starts to ossify from center outward

A

Endochondral bone formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Types of bones that use intramembranous bone formation

A

Flat bones - clavicle, scapula, bones of the skull, bones of the pelvis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Embryonic mesenchymal cells cluster, differentiate into osteoblasts -> osteoblasts form spicules of bone that coalesce into bone plates

A

Intramembranous bone formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Defect in this process leads to underdeveloped or absent clavicles, dental anomalies, larger fontanelles at birth, and osteoporosis

A

Intramembranous bone formation -> the disorder described is clavicocranial dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Autosomal dominant mutation in Cbfa1/Runx2

A

Claviocranial dysplasia - these are transcription factors in genes needed for osteoblast differentiation, so the mutation has the biggest effect on intramembranous bone formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Impaired cartilage differentiation and growth may impact what kinds of bone development?

A

Endochondral bone formation, so long and short bones, but not so much flat bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Zone of the epiphyseal plate that is the most common site of fracture

A

Hypertrophic zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

AD (heterozygous) mutation leading to constitutive activation of FGFR3 at the proliferative zone of bone

A

Slows proliferation of bone -> achondroplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Part of bone responsible for increasing in length

A

Epiphyseal plate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Dense bone in diaphysis that transmits force efficiently

A

Cortical bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Type of bone found in metaphysis/epiphysis that provides cushioning

A

Cancellous/trabecular bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

“Butterfly fragment”

A

The triangular piece of bone that breaks off when a bone is broken under an axial load that is too strong. The side under tension cracks in a direction perpendicular to the axial load, but the side under compression shears, producing the triangular “butterfly fragment”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cell that controls signaling for bone remodeling, mineralizes bone, and produces type 1 collagen

A

Osteoblast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Long-lived cell embedded in bone that maintains calcium homeostasis and plays a role in mechanotransduction within the bone

A

Osteocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cell of hematopoietic origin that looks like a multinucleated giant cell and releases carbonic anhydrase to break down bone

A

Osteoclast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Bone cells of mesenchymal origin

A

Osteoblast -> osteocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Bone cells of hematopoietic origin

A

Osteoclast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Functional unit of cortical bone

A

Osteon/Haversian system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

A receptor on osteoclasts that activates signaling pathways to result in bone resorption

A

RANK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

A molecule secreted by osteoblasts that can activate osteoclasts

A

RANKL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cellular target of action of activated vitamin D/PTH (what they act on)

A

Osteoblasts -> induce release of RANKL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Consequence of continuous over-secretion of PTH

A

“Brown tumors” - a vascular, fibrous lesion that occurs when hyperparathyroidism causes too much bone resorption in order to release more calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Net action of pulses of PTH or synthetic analogue (teriparatide)

A

Building bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Drug class that mimics the structure of inorganic phosphate and leads to osteoclast apoptosis

A

Bisphosphonates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Tumor releases lots of RANKL -> what happens?

A

RANKL&raquo_space; OPG, so there is too much bone resorption -> lytic lesions. Occurs in giant cell tumors, multiple myeloma, metastatic breast cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Tumor releases lots of OPG -> what happens?

A

OPG&raquo_space; RANKL, so there is too much bone formation -> blastic lesions. Occurs in prostate cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Molecule that binds to RANKL and prevents osteoclast activation

A

OPG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

OPG knockout mouse would have bones that looked like…

A

Osteoporotic bones! Very low bone density, since OPG induces bone formation by inhibiting bone resorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

RANKL or RANK knockout mouse would have bones that looked like…

A

Hyperdense bones! Not enough RANKL/RANK action would lead to a lack of bone resorption, leading to very dense but probably structurally problematic bones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Denosumab MOA

A

RANKL Ab that essentially acts like synthetic OPG, preventing RANK/RANKL interactions and inhibiting bone resorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Osteoblasts are responsible for signaling for which aspects of bone remodeling?

A

Formation and resorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

RDA for calcium

A

1000 mg/day for most adults, more for adolescents, pregnant/lactating women, post-menopause, men over 70

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Main goal of PTH secretion

A

Raise calcium levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Blood Ca++ is low -> what does parathyroid do?

A

Secrete PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Blood Ca++ is high -> what does parathyroid do?

A

Prevent secretion of PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

If the calcium sensing receptor in the kidney senses high Ca++, what does the kidney do?

A

Excrete calcium in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

If the calcium receptor in the kidney senses low Ca++, what does the kidney do?

A

Reduce excretion of calcium in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

MOA of PTH at kidney

A

Increase Ca++ resorption, inhibit phosphate resorption (because phosphate binds Ca++ and lowers available calcium), increases activation of vitamin D by 1-a-hydroxylase because that increases gut absorption of Ca++

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

MOA of PTH at bone

A

Bind to receptors on osteoblasts -> activate osteoclasts -> increased bone turnover -> release of calcium and phosphate into blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

High PTH leads to increased secretion of what signaling molecule by osteoblasts?

A

RANKL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

If blood Ca++ is high, what should PTH levels be?

A

Lower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

If levels of 1,25-D are high, what should PTH levels be?

A

Lower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How do Ca++ and phosphate levels change in response to 1,25-D?

A

1,25-D leads to both increased Ca++ (in conjunction with PTH) and increased phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

MOA of 1,25-D at GI tract

A

Stimulate Ca++ and phosphate absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

MOA of 1,25-D at parathyroid gland

A

Decrease PTH production and cell proliferation there

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

MOA of 1,25-D at bone

A

Maintenance of adequate minerality of bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Best marker to measure vitamin D status

A

25-D -> the formation of this is unregulated so this reflects total vitamin D entering the system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Step of vitamin D activation that is most highly regulated

A

Activity of 1-a-hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Effect of PTH on 1-a-hydroxylase

A

Induces its activity in order to raise Ca++ levels by creating more 1,25-D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Inducers of 1-a-hydroxylase activity

A

PTH, low phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Inhibitors of 1-a-hydroxylase activity

A

High Ca++, 1,25-D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

This protein is structurally similar to PTH, shares a receptor, and if its levels are abnormally high (like in some cancers), it can mimic excess PTH

A

PTH-related protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Does human calcitonin have an appreciable effect on bone and calcium, as far as we know?

A

Not really

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Cells that produce calcitonin

A

C-cells of the thyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Key biomarker for determining etiology of hypercalcemia or hypocalcemia

A

PTH levels - will determine if this is a parathyroid problem or due to an external factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

High Ca++, low/normal phosphate, decreased bone density, high or inappropriately normal PTH. Urinary calcium low

A

Primary hyperparathyroidism - bones, stones, groans, and psychiatric overtones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Patient with brown tumors, abdominal pain, kidney stones, and confusion

A

Uncontrolled primary hyperparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Treatment for primary hyperparathyroidism

A

Surgical removal of affected gland - usually curative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Patient with a failed parathyroidectomy - what might you suspect?

A

Familial hypocalciuric hypercalcemia - rare AD disorder due to a LOF mutation of calcium-sensing receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Patient with malignancy (not of the parathyroid gland) and hypercalcemia - what could be causing the hypercalcemia?

A

Invasion/destruction of bone by tumor, production of PTHrP by tumor, production of vitamin D by the tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Patient with a granulomatous disease like TB or sarcoidosis and hypercalcemia - why?

A

Unregulated 1a-hydroxylase activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Hypercalcemia, renal failure, and metabolic alkalosis

A

Milk-alkali syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Hypercalcemia in a patient who has been immobilized in the ICU - why?

A

Demineralization and increased bone resorption due to prolonged immobilization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Low calcium, low or inappropriately normal PTH

A

Primary hypoparathyroidism, found in DiGeorge syndrome (22q11 deletion), post-surgical, or autoimmune

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Low or normal calcium with high PTH

A

This is normal - this is why we have parathyroid glands. Called secondary hypoparathyroidism, though.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Common causes of secondary hypoparathyroidism

A

Vitamin D deficiency, renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Effect of compressive force on bone

A

Bone growth (electronegative force)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Effect of tensile force on bone

A

Bone resorption (electropositive force)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Potential for healing in a kid with an injury to bone but not growth plate

A

Good! Can heal almost completely because an intact growth plate tends to straighten itself out over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Treatment for an injury involving growth plate

A

Recognize, reduce the fracture gently but accurately, adequate fixation (don’t fixate the physis if possible), monitor for late growth disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Bone response to low load

A

Loss of bone mass via resorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Bone response to a gradual increase in load above physiologic load

A

Increased bone mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Repetitive microdamage to bone

A

Stress fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Acute overload of bone

A

Traumatic fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

A bone healing that starts with inflammation and a hematoma, followed by formation of a soft callus made of osteoid that surrounds the hematoma, followed by a hard callus forming as fiber bone replaces the osteoid, followed by corticoremodeling

A

Secondary bone healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Bone healing after internal fixation, where cutting cones are formed by osteoblasts going in both directions to cross the break and heal the cortex

A

Primary bone healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Older patient with progressive vision loss seen over time, and straight lines do not appear straight in their vision

A

Macular degeneration - blood in the antral vision/degeneration there. The phenomenon known as metamorphopsia is seeing straight lines as curved. This is urgent but not emergent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Dark visual loss with flashes, followed by floaters, followed by a “curtain”

A

Retinal detachment - flashes are tugging of the retina due to fluid from a tear in the retina, floaters are RBCs getting behind the retina, and the curtain is retinal detachment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

If 50% or more of the retina is detached, what sign is visible?

A

Rapid afferent pupillary defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

“Smoky” vision in a diabetic

A

Vitreous hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Causes of vitreous hemorrhage

A

Proliferative diabetic retinopathy, retinal tear, valsalva maneuver, trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Urgent or emergent: Macular degeneration

A

Urgent - same day ophtho

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Urgent or emergent: retinal detachment

A

Urgent - same day ophtho

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Urgent or emergent: vitreous hemorrhage

A

Urgent - same day ophtho

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Pale or white retina with a cherry red spot and RAPD, profound visual loss

A

Central retinal artery occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Urgent or emergent: central retinal artery occlusion

A

EMERGENT! Do ocular massage to get the embolus out and page ophtho ASAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

History of hypertension; retinal exam shows “blood and thunder” (torturous vessels and multiple areas of blood in retina)

A

Central retinal vein occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Urgent or emergent: central retinal vein occclusion

A

Not as urgent - next day ophtho

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Cause of central retinal vein occlusion

A

vein gets compressed by central retinal ophtho

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Important management of central retinal vein occlusion, besides sending to ophtho next day

A

Treat hypertension to prevent this occurring in the other eye!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Corneal edema, deep eye pain, sudden decrease in vision, nausea, vomiting, halos in vision, eye is hard to the touch, pupils fixed and mid-dilated

A

Angle closure glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Urgent or emergent: angle closure glaucoma

A

EMERGENT! Call ophtho right away

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Relative afferent pupillary defect, eye pain that is worse with movement, central scotoma, and decreased color vision

A

Optic neuritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Pathophysiology of angle closure glaucoma

A

The angle of the anterior chamber gets clogged - this can occur with dilation of the pupils, especially if someone has a positive volcano sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Pathophysiology of optic neuritis

A

Swollen optic nerve in 1/3 of patients, but the symptoms are caused by optic nerve inflammation leading to demyelination. This is a common early manifestation of multiple sclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

MRI findings in optic neuritis

A

periventricular white matter lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Urgent or emergent: optic neuritis

A

Can refer next day - not all that urgent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Moderate to severe vision loss, relative afferent pupillary defect, decreased color vision, altitudinal visual field issues

A

Ischemic optic neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Urgent or emergent: ischemic optic neuropathy

A

Urgent - same day referral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Patient with ischemic optic neuropathy and scalp tenderness or jaw claudication: workup

A

Suspect giant cell arteritis - this makes it a more urgent situation. Start steroids right away, get labs (ESR, CRP), order temporal artery biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Patient with headache, homonymous hemianopia

A

Occipital lobe stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Urgent or emergent: occipital lobe stroke

A

Medical emergency!! Call the stroke team

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Patient with occipital lobe stroke: results of important CN II tests

A

Visual acuity may be 20/20… that’s because it’s not the optic nerve that’s affected! Important thing to check is visual fields, to look for deficits in one half of the visual field (homonymous hemianopia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Patient complaining of dark vision lasting for 5-10 minutes, then resolving spontaneously

A

Transient monocular visual loss (amaurosis fugax)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Pathophysiology of transient monocular visual loss

A

Small embolism in retinal vessels causes transient ischemia, leading to visual loss. It is spontaneously broken down, which is why you get the return of vision after 5-10 minutes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Important management for transient monocular visual loss

A

Workup for thromboembolic events, clots, friable plaques, heart issues, giant cell arteritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Urgent or emergent: transient monocular visual loss

A

Usually work up emergently if it occurred within the past few days, to check for underlying causes (do a carotid doppler, echo, labs, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Type of cartilage on articular surfaces, the ribs, nasal septum

A

Hyaline cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Type of cartilage on auricle of ear, trachea, auditory tube

A

Elastic cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Type of cartilage at tendon/ligament junction with bone, annulus fibrosus of intervertebral disc, menisci

A

Fibrocartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Developmental origin of cartilage in the head

A

cranial neural crest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Developmental origin of cartilage in the limbs

A

lateral plate mesoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Developmental origin of cartilage in the axial skeleton

A

Paraxial mesoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Biggest molecular component of cartilage (and the other components)

A

Main component is water, followed by collagen, then proteoglycan, then non-collagenous protein, then cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Major component of extracellular matrix dry weight

A

Collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Component of cartilage that provides its framework and tensile strength

A

Collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Component of cartilage that provides its compressive strength and attracts water

A

Proteoglycans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Function of anchorin CII

A

anchors chondrocytes to collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Function of cartilage oligomeric matrix protein

A

maintain properties and integrity of collagen network

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Function of fibronectin in cartilage

A

Matrix organization and stability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Function of tenascin in cartilage

A

Cell adhesion and cell-matrix interactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

How are nutrients transported through cartilage to chondrocytes?

A

Cartilage is avascular so nutrients are transported via diffusion in the massive amount of water that contributes to cartilage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Describe the structure of proteoglycan

A

Chondroitin sulfate molecules link onto the core protein, forming a proteoglycan. These then aggregate as attachments on hyaluronic acid through a link protein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Composition of elastic cartilage

A

Collagen type II and elastic fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Composition of hyaline cartilage

A

mostly collagen type II and aggrecan (proteoglycan), some type I collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Composition of fibrocartilage

A

Type I and II collagen, basically combined hyaline cartilage with dense connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Which types of cartilage have a perichondrium, and what is it?

A

Hyaline and elastic cartilage have a perichondrium, which is a fibrous outer layer with fibroblasts that is on top of a chondrogenic region with stem cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Cartilage that forms in the healing response to injury

A

Fibrocartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Cartilage that bests tolerates repetitive deformation

A

Elastic cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Cartilage that is strongest and best for mechanical support

A

Hyaline cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Role of hyaline cartilage in joints

A

Reduce friction and distribute loads

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

4 zones of articular hyaline cartilage

A

Superficial zone, middle zone, deep zone, calcified zone. The middle zone is the thickest.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Zone of articular cartilage with smaller, flatter cells secreting lubricin

A

Superficial or tangential zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Orientation of collagen II fibers in superficial zone

A

parallel to surface (same orientation as the flattened chondrocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Zone of articular cartilage with rounded/oval, bigger, metabolically active cells making collagen

A

Middle/transitional zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Organization of collagen fibers in middle zone

A

Less organized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Zone of articular cartilage with spherical chondrocytes arranged in columns, the most proteoglycan of any layer, and the least water

A

Deep/radial zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Orientation of collagen fibers in deep zone

A

perpendicular to surface (vertical)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Zone of articular cartilage characterized by hypertrophic chondrocytes expressing collagen X and MMPs to degrade the ECM

A

Calcified zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Tidemark

A

Line separating cartilage from subchondral zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Why is collagen X important?

A

It is a precursor to bone formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Why does the calcified zone produce MMPs?

A

To degrade ECM and allow for bone formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

A constant load on cartilage produces a time-dependent deformation - what is this called?

A

Creep behavior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

A constant deformation of cartilage results in time-dependent stress: what is this called?

A

Stress-relaxation behavior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Growth factors important for chondrogenesis

A

FGF, TGFbeta, BMP, WNT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Chondrocytes divide in lacunae of cartilage into chondroblasts, which mature into chondrocytes, leading to increasing cartilage diameter

A

Interstitial cartilage growth - embryonic process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

At the edges of the cartilage, stem cells divide into chondroblasts and then into chondrocytes in the perichondrium, leading to increased length

A

Appositional cartilage growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Changes in collagen with aging

A

Fewer but bigger chondrocytes, less water, more collagen crosslinking, less proteoglycan -> increased stiffness, more glycosylation end products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Favored type of metabolism for chondrocytes

A

Anaerobic metabolism/glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

First step in hip osteoarthritis management

A

Conservative, non-operative management - PT, weight reduction, anti-inflammation. Surgery is normally elective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Joint-sparing hip osteoarthritis surgery

A

Osteotomy, core decompression, or hip arthroscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Major limitations of total hip arthroplasty

A

Obesity, comorbidities (BMI>40 is a huge contraindication). Also poses a risk of osteolysis/bone loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

RFs for hip fracture

A

F>M, smoking, EtOH, decreased VitD, thin, caucasian, post-menopausal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Repair for an intertrochanteric hip fracture

A

Can be fixed via plates or screws depending on the fracture itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Repair for a femoral neck fracture

A

Since it damages blood supply to the femoral head, a partial or total hip replacement is needed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Morbidity for a hip fracture

A

High - around 20% within one year since many of these patients are sick or fragile to begin with

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Groin pain, restricted and painful hip ROM especially on internal rotation, Trendelenberg test, loss of joint space on XR

A

Hip osteoarthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

Back, hip, or vascular? Groin pain

A

Hip

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Back, hip, or vascular? Low back or buttock pain

A

Back

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Back, hip, or vascular? Calf pain on exercise

A

Vascular (although need to rule out neurogenic claudication as well)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Back, hip, or vascular? Not a lot of radiation of pain, if it’s present it only goes to the knee

A

Most likely hip, which doesn’t tend to have a lot of radiating pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

Back, hip, or vascular? Pain radiates down below the knee following a dermatome

A

Back - radiculopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Back, hip, or vascular? Patient has a limp and has trouble tying shoes

A

Hip

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

Back, hip, or vascular? Pain is better with back flexion

A

Back

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Back, hip, or vascular? Pain follows a particular pattern, occurs at a specific distance of walking, and gets better with rest

A

Vascular claudication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Back, hip, or vascular? Decreased hip ROM that reproduces pain

A

Hip

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

Back, hip, or vascular? Positive straight leg test and neuro findings

A

Back

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Back, hip, or vascular? Loss of leg hair

A

Neuro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

If you suspect that leg pain is due to a vascular cause, what should you do as a test?

A

Ankle-brachial index

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

Prevention of hip fracture

A

Maintain bone health with calcium, vitamin D, osteoporosis drugs as needed. Fall prevention as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

Goals for obese patients prior to elective hip or knee replacement

A

Lose weight (BMI below 40 ideally), metabolic control, optimize nutrition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

First imaging step for hip pain

A

Plain films - you don’t need MRI right away to see osteoarthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

Function of the menisci of the knee

A

Weight bearing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What’s a risk of meniscectomy that explains why it’s not really done any more?

A

Taking out the meniscus leads to increased loads on the joint and an increased risk of osteoarthritis at the knee

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

Causes of knee DJD

A

Obesity, genetics, old trauma, loss of meniscus, chronic instability, malalignment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

Imaging for diagnosis of meniscal tears

A

MRI, in addition to exam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Pain at the knee joint line

A

Meniscal tear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

Repair of meniscal tears

A

Repair via arthroscopy/joint preservation, observation, or (less commonly) meniscectomy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

Initial treatment of knee osteoarthritis

A

Decrease loads: weight loss, activity modifications, and unloader braces
PT: try to improve strength and ROM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

Purpose of a tibial osteotomy

A

Correct a bow-legged deformity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

Foreign body sensation in eye, swollen eyelids, itching, crusting

A

Blepharitis - inflammation of melbomian glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

Tx for blepharitis

A

Lid hygiene with diluted baby shampoo, ABX or steroids, lubricants. If it presents with rosacea in a severe form, treat with doxycycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

Staph infection of a melbomian gland causing cellulitis

A

Chalazion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

Tx for chalazion

A

hot compresses, massage, topical ABX and steroids, I&D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

Red, indurated, painful eyelid without proptosis or blurred vision

A

Preseptal cellulitis - caused by trauma, sinus infection, eyelid margin infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

Tx for preseptal cellulitis

A

oral ABX and monitor for orbital cellulitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

Red, indurated, painful eyelid with diplopia, vision loss/RAPD, and/or no improvement with oral ABX

A

Orbital cellulitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

Diagnostic test for orbital cellulitis

A

orbital CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

Tx for orbital cellulitis

A

IV ABX and surgical drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

Vesicles on unilateral face with involvement of the tip of the nose (pain to palpation)

A

Shingles of V1 nerve root with Hutchinson’s sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

Tx of shingles

A

Oral acyclovir

193
Q

Outturned lid

A

Ectropion

194
Q

In-turned lid

A

Entropion/trichiasis

195
Q

Dacryocystitis

A

Nasolacrimal duct infection

196
Q

Test for corneal pathology

A

Fluorescein dye - dab it on the anterior fornix and visualize with cobalt blue. It stains corneal epithelium

197
Q

In regard to eye pathology: define injection

A

Red eye

198
Q

Torn area of corneal epithelium, painful, stains with fluorescein

A

Corneal abrasion

199
Q

Tx for corneal abrasion

A

topical ABX, patching, dilating drops

200
Q

Pain and blurry vision with punctate staining of cornea with fluorescein

A

Dry eye, exposures, or contact lens overuse

201
Q

Fluorescein staining with a linear branching pattern, corneal swelling leading to clouding of cornea

A

HSV keratitis (could also be caused by VZV but that would have a rash)

202
Q

Most common cause of infectious corneal blindness

A

HSV keratitis

203
Q

Centrally located punctate staining

A

Contact lens keratitis - could be viral, bacterial, chemical, amoebic, parasitic

204
Q

Tx for contact lens keratitis

A

Discontinue use of contacts, use ABX, don’t sleep with contacts

205
Q

Tx for HSV keratitis

A

Oral antivirals

206
Q

Corneal ulcer: causes and management

A

This is an emergency! Due to pseudomonas infection, anterior chamber infection. Get ophtho consult asap

207
Q

Consider that this might be a vision-threatening cause of vision loss if you have the following symptoms:

A 
S = sudden visual loss
T = trauma (ruptured eyeball?)
O = other signs/symptoms of scary conditions
P = pain
208
Q

Red eye with sudden visual loss: DDx

A

corneal ulcer, cellulitis, angle closure glaucoma

209
Q

Management of open globe injury

A

This is an emergency! Need a shield on the eye

210
Q

Management of corneal foreign body

A

CT or XR to spot the metal, since this is most often from metal flying during activities that involve metal on metal

211
Q

Blunt injury filling the eye with blood

A

Hyphema - this is an urgent condition

212
Q

Nausea, vomiting, red eye

A

Angle closure glaucoma

213
Q

Diplopia and red eye

A

Orbital cellulitis

214
Q

Photophobia and red eye with tiny white dots on inside of cornea

A

Iritis

215
Q

Sleeps in contacts, has a red and painful eye

A

Worry about corneal ulcer

216
Q

Deep boring pain and red eye: DDx

A

Angle closure glaucoma, cellulitis, iritis, scleritis

217
Q

White of eye appears red

A

Scleritis

218
Q

Pathophys causes of scleritis

A

Dilation of vessels due to inflammation or increased flow; abnormal vessels; blood outside vessels

219
Q

Edema of conjunctiva

A

Chemosis

220
Q

Watery or clear eye discharge

A

Viral etiology or dry eye, viral will often present with palpable preauricular LNs, if viral is very contagious

221
Q

Purulent eye discharge

A

Bacterial infection - staph, strep, haemophilus. Treat with ABX

222
Q

Mucoid, white-yellow eye discharge

A

Allergic, Tx with topical antihistamines. Often itchy!

223
Q

Benign causes of subconjunctival hemorrhage

A

cough, sneeze, meds

224
Q

360 degrees of subconjunctival hemorhage

A

Globe rupture - protect eye. This is emergent! Really bad if associated with an abnormal pupil

225
Q

Abnormal wing of tissue in an area of eye exposed to UV, and red

A

Pterygium - often recurs

226
Q

Superficial and mild pain and red sclera that blanches with 2.5% phenylephrine

A

Episcleritis - caused by dilation of vessels in the vascular plexus between the conjunctiva and the sclera. Can be idiopathic

227
Q

Red sclera with a violaceous hue, with severe boring pain, often associated with autoimmune systemic disease, doesn’t blanch with phenylephrine

A

Scleritis - this can be vision-threatening. Need ophtho consult to prevent vision loss. Treated with steroids and NSAIDS.

228
Q

What is the function of the angle of the anterior chamber?

A

Drains fluid (aqueous humor) out of the anterior chamber. Usually 45 degrees

229
Q

Pathophysiology of acute angle closure glaucoma

A

A bigger, more anteriorly positioned lens pushes the iris forward, causing a narrower angle of the anterior chamber. When the pupil dilates, the peripheral iris becomes thicker, and it closes off the angle and gets stuck to the lens, so aqueous humor backs up causing an increase in eye pressure, leading to pain, nausea, and vomiting.

230
Q

Findings in acute angle closure glaucoma

A

Fixed mid-dilated pupil, dilated vessels, shallow anterior chamber, wrinkled cornea due to corneal edema

231
Q

Anterior chamber filled at least partway with blood

A

Hyphema, due to blunt trauma compressing eye in AP direction, so it expands in other directions, potentially ripping the iris off its base

232
Q

WBCs forming a hypopia in the eye, along with infection, decreased vision, severe pain

A

Endophthalmitis - often introduced during surgery

233
Q

Limbal flush, small pupil, photophobic

A

Iritis

234
Q

Pathophysiology of iritis

A

Infection and genetic predisposition lead to an autoimmune response causing vasodilation of vessels at the limbus. Also called anterior uveitis

235
Q

Fibrous connective tissue that attaches muscles to bone

A

Tendon

236
Q

Function of tendons

A

Move bones or other structures

237
Q

Fibrous connective tissue that attaches bone to bone

A

Ligament

238
Q

Function of ligaments

A

Hold structures together, provide stability

239
Q

Composition of tendons

A

Type I collagen produced by tenocytes, within a proteoglycan matrix

240
Q

How is collagen organized in tendons?

A

In response to mechanical load

241
Q

Loose connective tissue that allows longitudinal movement of tendons, binds tendon fascicles, and supports vessels and nerves as well

A

Enotenon

242
Q

Loose connective tissue that allows movement within the tendon sheath

A

Paratenon

243
Q

Synovial structure that reduces friction within the connective tissue surrounding the tendon

A

Tendon sheath

244
Q

Tendon blood supply

A

Longitudinal vessels along the tendon unit with blood supply to enotenon and paratenon; diffuses across sheath to tendon

245
Q

Innervation of tendon

A

No nerve fibers within tendon. Epi- and paratenon contain nociceptive nerve endings that terminate on the surface of the tendon, and Golgi tendon organs are at the musculotendinous junction to transmit stretch information

246
Q

What can athletes do to improve the viscoelastic relationship of their tendons?

A

Preconditioning

247
Q

Composition of ligaments

A

Collagen and matrix produced by fibroblasts

248
Q

Most common type of ligament insertion

A

Indirect insertion: superficial layer connects to periosteum, and bone is penetrated by Sharpey’s fibers

249
Q

Less common type of ligament insertion

A

Direct fibrocartilagenous insertion: tendons insert deep and superficial through four zones: ligament, fibrocartilage, mineralized fibrocartilage, bone

250
Q

Blood supply to ligaments

A

Uniform microvascularity from the ligament insertions

251
Q

Innervation of ligaments

A

Nociceptive fibers and proprioceptive fibers (these are for joint positioning sense, and are important in sprains because these take a long time to come back, so damage to these increases risk of re-injury)

252
Q

Stress-strain relationship of ligaments

A

Non-linear: non-uniform recruitment of fibers

253
Q

Pathophysiology of Achilles tendinopathy

A

The area is relatively hypovascular. Repetitive use causses microtrauma to the distal tendon (least vascularity), which probably leads to poor healing and inflammation.

254
Q

Presentation of Achilles tendinopathy

A

Gradual onset, pain over distal Achilles tendon, thickening or nodularity, bursitis.

255
Q

Painful/reduced active plantarflexion and passive dorsiflexion, but squeezing the gastrocnemius produces a passive plantarflex

A

Achilles tendinopathy. The Thompson test (squeeze the gastrocnemius) was negative (it produced passive plantarflexion) - if it didn’t produce the plantarflexion that would suggest a tendon rupture

256
Q

Do you need imaging for Achilles tendinopathy?

A

Not needed. May see Haglund’s deformity on plain films, ultrasound may help confirm diagnosis, MRI may show thickening of the tendon.

257
Q

MSK consideration with fluoroquinolones

A

Risk of tendon rupture - this is why we avoid prescribing them whenever possible

258
Q

Initial management of Achilles tendinopathy

A

Ice, NSAIDs for one week, heel lifts in shoes, avoid aggravating activities, PT

259
Q

Tx for Achilles tendinopathy with most evidence of benefit

A

Eccentric resistance-based PT, but it may take a long time and requires a lot of buy-in

260
Q

Are injections helpful for Achilles tendinopathy?

A

Evidence is mixed… steroids are helpful for reactive bursitis but may increase the risk of rupture. Injectables have no long-term outcome differences vs placebo

261
Q

When to do surgery for Achilles tendinopathy

A

If no improvement after 4-6 mo

262
Q

MOA of Achilles rupture

A

Sudden maximal plantarflexion with the ankle already fully dorsiflexed

263
Q

Will patients with Achilles rupture have previous S/Sx?

A

1/3 have Sx of tendinopathy but most probably have tendon degeneration before rupture

264
Q

Squeeze a patient’s gastrocnemius and get NO plantarflexion passively

A

Positive Thompson’s test, indicates Achilles rupture

265
Q

Imaging for achilles rupture diagnosis

A

US is ideal for showing the movement of the tendon in plantarflexion and dorsiflexion. MRI can also work

266
Q

How to manage Achilles tendon rupture

A

Surgery will lower risk of re-rupture - probably will use surgery for athletes so that they can get back to peak performance.

267
Q

2 main inflammatory causes of tenosynovitis

A

Systemic inflammation or inflammation due to overuse

268
Q

Gradual onset of reduced active motion of tendons in wrist, may have trigger finger

A

Presentation of tenosynovitis of wrist

269
Q

Tenosynovitis with acute onset, pain, redness, and decreased passive range of motion

A

Infectious etiology - need to recognize this

270
Q

Tx for inflammatory tenosynovitis

A

Ice, splinting, NSAIDs, PT, corticosteroid injections to sheath

271
Q

Tx for infectious tenosynovitis

A

ABX if identified quickly and non-suppurative, otherwise give broad-spectrum ABX and do surgical debridement

272
Q

Insidious onset of symptoms: sharp pain in heel in the morning like “stepping on a rock” with tenderness at the anteromedial calcaneus and pain with passive dorsiflexion

A

Plantar fasciitis - overuse at the proximal portion of the plantar fascia

273
Q

Relevance of a calcaneal spur on XR in a patient with plantar fasciitis?

A

Not really relevant - not the source of the pain

274
Q

Tx for plantar fasciitis

A

Rest, NSAIDs, PT, orthotics or arch support, sleeping socks that dorsiflex the ankle all night

Second line: immobilization, corticosteroids

275
Q

Grade 1 ligament tear

A

Partial tear, no laxity

276
Q

Grade 2 ligament tear

A

Partial tear with laxity but a solid endpoint

277
Q

Grade 3 ligament tear

A

Complete tear with laxity and no endpoint/soft endpoint

278
Q

Bony avulsion on a ligament tear

A

This is more common in kids - the ligament is intact but the bone has a piece come off at the ligamentous attachment

279
Q

Ligaments sprained in an inversion ankle injury

A

Anterior talofibular ligament, calcaneofibular ligament, posterior talofibular ligament - these are the ligaments on the lateral side

280
Q

MOI of a high ankle sprain

A

Dorsiflexion and external rotation lead to the talus pushing out against the fibula, causing a high ankle sprain and/or fibular fracture

281
Q

When to allow a joint injury patient to sit out of their sport but stay on the sidelines

A

Fracture (bony tenderness, crepitus, deformity) or instability without prior complications

282
Q

When to allow a joint injury patient to immediately go back in to their game

A

If joint is stable, no fracture, and they can protect themselves

283
Q

What produces a more severe injury: inversion or eversion?

A

Eversion

284
Q

Ottawa criteria for when to image ankle

A

Needs to have malleolar zone pain AND either tenderness over posterior lateral or medial malleolus OR can’t bear weight at time of injury/for 4 steps in office

285
Q

Ottawa criteria for imaging foot

A

Get foot films if there is mid-foot pain AND it is tender over the navicular or base of 5th OR the patient can’t bear weight

286
Q

Low-risk ankle rule in pediatric patients:

A

Don’t need radiographs if ankle injury is not a high-risk fracture and it meets these criteria: Acute injury (<3 days), no underlying risk of pathologic fracture (Hx of OI, bone lesion, etc), no congenital ankle or foot malformation, child can express pain or tenderness, and tenderness/swelling is limited to the distal fibula or the ligaments surrounding it below the level of the anterior tibial joint line.

*Injuries which can be managed functionally with splinting and return to activity as tolerated are deemed low-risk: sprains, nondisplaced SH I and SH II, of distal fibula, avulsions of distal fibula or lateral talus

287
Q

Best management of ankle sprains

A

RICE, walking boot or bracing, PT early and often to improve proprioception

288
Q

How to help prevent ligament injuries

A

Neuromuscular training programs - high risk reduction

289
Q

Most common direction for a GH dislocation

A

Anterior inferior direction

290
Q

Where does the long head of the biceps tendon anchor in the shoulder?

A

Superior labral cartilage

291
Q

Important stabilizers of the shoulder

A

Superior, middle, and inferior GH ligaments and the ligaments stabilizing the AC joint

292
Q

Dynamic stabilizers of the shoulder

A

Rotator cuff muscles, especially subscapularis and its tendon in the anterior direction

293
Q

MOI of a GH dislocation

A

Indirect force with arm abducted and externally rotated, OR direct force - blow from posterior shoulder

294
Q

Patient with a prominent posterior acromion and sulcus sign (skin tight over edge of acromion), in a lot of pain, arm carried in abduction/internal rotation

A

GH dislocation in anterior direction

295
Q

Ideal immediate management of GH dislocation

A

Reduce the dislocation acutely, in the ED with sedation if needed

296
Q

Tx of shoulder dislocation after reduction

A

PT necessary because there’s a high recurrence rate. Surgical stabilization is an option.

297
Q

Imaging for GH dislocation

A

Pre-reduction and post-reduction plain films from at least two views - AP and scapular Y or axillary

298
Q

Other structures that may be injured in a GH dislocation

A

Axillary nerve… But this usually resolves quickly.

Anterior inferior labrum - if this is injured, there is a particularly high recurrence rate.

299
Q

Grade 1 AC separation

A

Stretched AC ligament, no deformity, normal XR

300
Q

Grade 2 AC separation

A

Complete tear of AC ligament, may or may not have deformity or widening on XR, laxity of ligament

301
Q

Grade 3 AC separation

A

Complete tear of AC and coracoclavicular ligaments - laxity, deformity (distal clavicle elevation), widening of joint on XR, unwilling to use arm

302
Q

MOI of shoulder AC separation

A

Direct blow to lateral shoulder

303
Q

How to manage axillary neuropraxia after GH dislocation

A

Watch and wait - this is common and usually resolves in a few days

304
Q

Capsular contracture and inflammation leading to restricted passive ROM, nothing else appears to be wrong, normal MRI

A

Adhesive capsulitis aka frozen shoulder

305
Q

How to diagnose adhesive capsulitis

A

Diagnosis of exclusion - MRI will be normal

306
Q

RFs for adhesive capsulitis

A

F>M, ages 30-60, often bilaterally but usually spaced a few years apart, and never affects same shoulder twice. Can have an insidious onset or can occur if there is trauma w/o significant damage to shoulder joint that leads to inflammation and then stiffness. Diabetes and thyroid disease - may have an autoimmune component. Stroke, burn patients, Parkinson’s disease, cardiac disease, etc - again, inflammation. Hx of minor trauma, post-thoracic surgery, hyperlipidemia, drug-related. Dupuytren’s contracture is also associated with increased risk. Possible genetic component

307
Q

Pathophysiology of Adhesive Capsulitis

A

Synovial inflammation -> capsular fibrosis -> passive stiffness -> contractures of rotator interval and GH ligaments

308
Q

Work-up for adhesive capsulitis

A

Plain films to rule out bone causes, MRI as well… But this is a clinical diagnosis of exclusion

309
Q

Management of adhesive capsulitis

A

This will resolve on its own over 2-3 years. Tx is pain relief and corticosteroid injections so that the patient can tolerate PT, which is needed to restore mobility

310
Q

MOI of ACL rupture

A

Usually non-contact: quick direction change, sudden deceleration, hyperextension, valgus, or tibial torsion. Patient will usually feel a pop. Women at greater risk after puberty because it changes the angle from hip to knee.

311
Q

Felt a “pop,” pain and swelling, sudden effusion within 10 minutes, decreased range of motion in a knee injury sustained in a non-contact sport

A

ACL rupture

312
Q

PE maneuvers to test ACL

A

Lachman’s, pivot shift, anterior drawer tests

313
Q

Imaging for suspected ACL rupture

A

XR to look for bony avulsions - usually normal, but a Segond’s fracture is pathognomonic

MRI is gold standard and will show the ACL tear. The ligament will appear black. May also show contusions, indicating a pivot shift, which is also pathognomonic.

Arthrocentesis will show bloody fluid

314
Q

Terrible triad

A

ACL, MCL, and medial meniscus injuries

315
Q

Management of ACL rupture

A

Refer to ortho surgery! Most common kind of graft is an autologous bone-patellar tendon-bone autograft. This provides greater stability but may cause some patients more anterior knee pain post-op. Could also do a hamstring tendon autograft but that might cause hamstring weakness.

316
Q

MOI of MCL injury

A

Valgus force to knee, may or may not have twisted

317
Q

Management of an MCL injury

A

Normally will heal well without intervention. May place in an immobilizer brace or a more functional brace, and range of motion exercises help as well. If there is laxity, suspect an ACL injury too.

318
Q

Prevention of MCL injuries in football

A

Bracing

319
Q

MOI of patellar subluxation

A

Twisting injury

320
Q

Tenderness over medial patellar border, large and sudden knee effusion, and apprehension sign (involuntary quad contraction and dislike of lateral movement of patella)

A

Presentation of patellar subluxation

321
Q

What not to miss in a high ankle sprain

A

Fibula fracture - if this fracture has mortise widening it’s likely to require surgical repair

322
Q

Avulsion fracture of 5th metatarsal on XR

A

NO fracture line in the space between 4th and 5th metatarsal

323
Q

Jones fracture

A

Don’t miss diagnosis - fracture line is proximal to 4th and 5th metatarsal joints. Needs to be treated operatively with a fixation screw in athletes. Non-weight bearing for everyone. The challenge here is that it’s in a watershed area so there’s poor blood flow and therefore a risk of poor healing

324
Q

What is the os coxa and when does it fuse?

A

Ilium, ischium, and pubis where they come together at the hip. Fuses at age 16, until then it’s connected by the triradiate cartilage.

325
Q

Types of cartilage in SI joint

A

Sacral side is hyaline, iliac side is fibrocartilage

326
Q

Q-angle

A

Angle of femoral shaft relative to vertical axis. 13 degrees in males, 18 degrees in females

327
Q

If you do arthrocentesis from the patellofemoral joint, are you sampling the tibiofemoral joint as well?

A

Yes since the synovial cavity is continuous

328
Q

How are knee menisci tethered to the tibia?

A

Coronary ligaments made of fibrocartilage

329
Q

Where is bone deposited in the growth plate?

A

Diaphyseal end

330
Q

Which ankle ligaments prevent over-inversion?

A

Anterior talofibular, posterior talofibular, calcaneofibular

331
Q

Which ankle ligament prevents over-eversion?

A

Deltoid ligament

332
Q

Nerve roots for hip flexion

A

L2-3

333
Q

Nerve roots for hip extension

A

L4-5

334
Q

Nerve roots for knee extension

A

L3,4

335
Q

Nerve roots for knee flexion

A

L5-S1

336
Q

Nerve roots for dorsiflex ion

A

L4-5

337
Q

Nerve roots for plantar flexion

A

S1-2

338
Q

Major extensors of the hip

A

Gluteus Maximus, posterior fibers of gluteus medius

339
Q

Major flexors of the hip

A

Anterior fibers of gluteus medius, gluteus minimus, tensor fascia lata… And also iliopsoas

340
Q

Hip abductors

A

Superior fibers of gluteus Maximus, gluteus medius, gluteus minimus, tensor fascia lata

341
Q

Adductors (among the butt muscles) of the hip

A

Gluteus Maximus… But the adductor muscles do most of this

342
Q

Butt muscles that medially rotate the hip

A

Anterior fibers of gluteus medius, gluteus minimus, tensor fascia lata

343
Q

Butt muscles that laterally rotate the hip

A

Gluteus Maximus, posterior fibers of gluteus medius

344
Q

Lateral rotation contracting the piriformis could compress what nerve?

A

Sciatic nerve

345
Q

Nerve fibers in obturator nerve

A

L2-4

346
Q

Main dorsiflexor of foot

A

Tibialis anterior

347
Q

Lack of dorsiflexion

A

Foot drop, steppage gait

348
Q

Blood supply to head and neck of femur

A

Medial and lateral circumflex femoral arteries

349
Q

Blood supply to posterior compartment of thigh

A

Perforating branches of deep femoral artery

350
Q

After the femoral artery passes through the adductor hiatus and into the popliteal fossa, the popliteal artery splits into what branches?

A

Anterior tibial artery and posterior tibial artery (which then gives off the fibular artery)

351
Q

Dorsalis pedis artery comes from which artery?

A

Anterior tibial -> pierces interosseous membrane -> anterior compartment -> becomes dorsalis pedis

352
Q

Medial and lateral plantar arteries come from which bigger artery?

A

Posterior tibial artery

353
Q

What provides collaterals circulation around the hip?

A

Cruciate anastomoses - inferior gluteal artery, lateral and medial femoral circumflex arteries, first penetrating branch of deep femoral artery

354
Q

Pre axial vein of lower limb

A

Great saphenous vein - drains into femoral at the femoral triangle

355
Q

Post-axial vein of lower limb

A

Lesser saphenous vein - drains into popliteal vein

356
Q

How do valves function in the deep veins of the leg?

A

Skeletal muscle pump means that they are closed when muscles relax and open when muscles contract

357
Q

Most powerful dorsiflexor

A

Tibialis anterior

358
Q

What type of contraction does tibialis anterior do in the swing phase of the gait cycle?

A

Isometric/concentric contraction to dorsiflex foot and prepare for heel strike

359
Q

What type of contraction does tibialis anterior do in the stance phase of the gait cycle?

A

Eccentric contraction to slowly lower foot to the ground and prepare for toe-off

360
Q

Damage to which nerve produces a foot drop?

A

Common fibular

361
Q

A nerve that can’t re-establish organized nerve bundles after trauma might produce…

A

A post-traumatic neuroma

362
Q

If you lose these muscles you can’t run or jump

A

Gastrocnemius and soleus

363
Q

Fibers proliferate around the third common digital nerve of the foot, compressing it and causing pain and paresthesias in someone who wears high heels

A

Morton’s neuroma

364
Q

Describe pain sensation in neonates

A

Underdeveloped pathways, so have higher risk of hyperalgesia, immature respiratory centers so worse side effects from opioids, develop opioid tolerance more easily

365
Q

Good ways to manage pediatric acute or procedural pain

A

Comfort position (lap, or sitting up), distraction, sucrose for infants under 6 months, breastfeeding for infants, don’t reassure or apologize

366
Q

Overall goals of pain management in kids

A

Minimize opioids, minimize side effects - might use scheduled NSAIDs, acetaminophen, opioids PRN

367
Q

Analgesics that work via COX inhibition on arachidonic acid pathway

A

NSAIDs

368
Q

Analgesic that blocks central and peripheral prostaglandin synthesis

A

Acetaminophen - but avoid combo products like Vicodin or Percocet if possible, and give it IV/PO

369
Q

Which opioid is especially contraindicated in children?

A

Codeine

370
Q

Is hydromorphone or morphine safer in renal failure?

A

Hydromorphone

371
Q

Side effects of opioids and their management

A

Pruritus - nalbuphine, naloxone, ondansetron
Nausea/vomiting - ondansetron, metoclopramide
Respiratory depression - monitor for this, stop the meds, give naloxone

372
Q

Gabapentin MOA

A

Acts on presynaptic calcium channels

373
Q

IV lidocaine MOA as an analgesic

A

Anti-inflammatory, sodium channel blockade

374
Q

Ketamine MOA

A

NMDA antagonist, acts as an analgesic

375
Q

Clonidine MOA as an analgesic

A

Alpha2 agonist, augments descending modulation

376
Q

Why use regional analgesia?

A

Putting local anesthesia around a nerve - good pain control, reduced opioids, safer than epidural because there’s less risk of ileus (and if it occurs it has a shorter duration)

377
Q

What area of the spinal column do neuraxial blocks go into?

A

Meds go into the epidural space if they are done as an epidural, but a spinal block goes into the subarachnoid space (CSF) - more numbness for a shorter duration

378
Q

What is the risk of a sympathectomy in a young patient under age 8?

A

Decreased blood pressure (all patients have a risk of urinary retention)

379
Q

Which problem comes first in opioid use - sedation or respiratory depression?

A

Sedation always precedes respiratory depression

380
Q

Analgesic ceiling effect

A

In NSAIDs, etc - beyond a certain dose you don’t get improved analgesia

381
Q

A patient on patient-controlled analgesia wants more meds -> how will you alter the dose if you need to?

A

Up the demand dose, but don’t increase the basal dose

382
Q

Are opioids better for acute or chronic pain?

A

Acute

383
Q

Goals of treatment of chronic pain

A

Functional improvement at work, school, ADLs

384
Q

Tools for chronic pain management that aren’t meds

A

Patient education, CBT, DBT, mindfulness, coping skills, PT, OT, exercise, activity, treat comorbidities, improve sleep hygiene, diet, diabetes control, etc

385
Q

Considerations for acetaminophen for chronic pain

A

Lower maximum daily dose

386
Q

Considerations for NSAIDs for chronic pain

A

Watch for GI bleeds, renal function, cardiac issues

387
Q

Which low-dose antidepressants can be used for chronic pain?

A

SNRIs (duloxetine, venlafaxine) and TCAs (nortryptiline, amitryptiline)

388
Q

Which anticonvulsants are used for chronic pain?

A

Topiramate, gabapentin, pregabalin

389
Q

Initial management of back pain without worrisome symptoms

A

Rest for a few days, ice/heat, NSAIDs, muscle relaxants, PT, acupuncture

390
Q

When are epidural steroid injections beneficial for back pain?

A

May help with radicular pain or with facet joint or SI joint pain

391
Q

What is a risk of doing spine surgery to resolve back pain?

A

May continue to have back pain after the surgery

392
Q

Good prognosticators for epidural steroid injections

A

Education, radiculopathy, pain for <6mo

393
Q

Bad prognosticators for epidural steroid injections

A

Constant pain, disrupted sleep from pain, unemployed due to pain

394
Q

Presentation of facet joint pain

A

Mostly axial, often bilaterally, PE shows positive facet loading, paraspinal tenderness

395
Q

Test for SI joint pain

A

Positive FABER

396
Q

Criteria to diagnose fibromyalgia

A

Widespread pain index: 19 areas, need pain in 4 or 5 areas over past week, and severity is judged by fatigue/waking up in refreshed/cognitive symptoms, and pain needs to have lasted for over 3 months

397
Q

Management of fibromyalgia

A

NOT opioids. Anticonvulsants, dopamine agonists, SNRIs, TCAs, non-pharm management are good options

398
Q

Painless mass between the tendon of the medial gastrocnemius and distal tendon of semimembranosus, right behind the medial condyle, driven by transient increase in intraarticular pressure

A

Baker’s cyst

399
Q

Dx of Baker’s cyst

A

Ultrasound - may have internal septations, and is avascular (a vascular mass would suggest it could be sarcoma)

400
Q

Management of Baker’s cyst

A

Only aspirate if it’s bothering the patient - treat with steroid injections if symptomatic or painful. 50% will recur.

401
Q

DVT appearance on ultrasound

A

Common femoral vein has no flow or is full of stuff or doesn’t compress well

402
Q

Muscle strain appearance on MR

A

Bright on T2, focal mass with edema and contusion

403
Q

Differentiate between schwannomas and neurofibromas

A

A schwannomas is a tumor of the Schwann cell. It is intrinsic to the nerve, better encapsulated, and easier to remove. A neurofibromas is a tumor of the nerve itself, is harder to remove, and has a worse prognosis. Treat both with surgical resection.

404
Q

Benign, slow-growing fatty mesenchymal tumor that presents as a mobile, firm mass

A

Lipoma

405
Q

PNS repair rules

A

Regrowth one inch per month
If cut, maximum repair is 70% of function
If patients are older than 40, nerve recovery decreases
2-3 cm nerve gap is the maximum that’s feasible for good repair

406
Q

Myelinated neurons in a fascicle are wrapped by ___.

A

Perineurium

407
Q

Compression of nerves causes what change in signals?

A

Increased conduction time

408
Q

One nerve injured

A

Mononeuropathy

409
Q

Mononeuritis multiplex

A

Multiple nerve injuries in different locations - in vasculitis, DM, lupus, sarcoidosis

410
Q

Changes in central processing after irritation of PNS can cause what?

A

Chronic regional pain syndrome - pain, hyperalgesia, spasm

411
Q

Nerve is bruised but intact

A

Neuropraxia

412
Q

Nerve axon is transected

A

Axonotmesis

413
Q

Endoneurial tube is transected and/or fascicles ruptured

A

Neurotmesis

414
Q

Sunderland 1 nerve injury

A

Neuropraxia - localized, axons fine, conduction is preserved above and below injury. Recovery in minutes to 6-8 weeks - injury persists until local myelin repairs itself. Good prognosis

415
Q

Sunderland 2 nerve injury

A

Axonotmesis - axon transected, Wallerian degeneration dismally, acute recovery may occur but proximal lesions heal better.

416
Q

Sunderland 3 nerve injury

A

Endoneurial tube transected, Perineurium intact, Wallerian degeneration dismally, may form a neuroma

417
Q

Sunderland 4 nerve injury

A

Fascicles ruptured -> scarring, axonal misdirection, reinnervation of inappropriate targets. Usually requires resection, repair, or graft. Will form a neuroma in continuity.

418
Q

Sunderland 5 nerve injury

A

Nerve completely transected. Requires surgical repair. The proximal end forms a neuroma.

419
Q

Cut axons degenerate distally

A

Wallerian degeneration

420
Q

How long does it take the NMJ to die if a nerve is cut?

A

About a year

421
Q

Why can’t you get back 100% function with nerve repair?

A

Axons get narrower, so 100% function isn’t possible

422
Q

What’s a procedure you can do to help prevent neuroma?

A

Embed the cut end of the nerve in muscle

423
Q

Pain and numbness in lateral 3.5 fingers, worse at night, improved when shaking hands out or with wrist splints

A

Distal median nerve injury, like in carpal tunnel. There will be a sharp demarcation on the ring finger of the deficit. Positive Phalens test, Tinel sign. EMG will help show it. Tx is conservative.

424
Q

Carpal tunnel with atrophy of thenar muscles

A

Surgical release of the median nerve

425
Q

Proximal median nerve injury at the elbow presents with…

A

Benediction hand - weakness of long flexors of fingers, sensor loss in Palm

426
Q

Pain from right elbow to medial two fingers, interossei weakness

A

Ulnar neuropathy - both palmar and distal surfaces may have pain. If there’s dorsal involvement the injury is probably at the elbow, if not it’s at the wrist. If long flexion is weak that localizes injury to the elbow.

427
Q

Tx for ulnar neuropathy

A

Conservative, surgery
Surg - simple decompression or transposition. Transposition is moving the nerve medially, which is used more for recurrences since it has a higher risk of complications

428
Q

Pain and numbness of medial hand and little finger after writing

A

Hypothenar issue with ulnar neuropathy. Image here with MRI or US for ganglion cyst or Schwannoma. Treat conservatively or with decompression

429
Q

R finger drop, radial deviation with extension (loss of ulnar extension)

A

Posterior interosseous nerve palsy - a high radial nerve palsy would give wrist drop, but just the PIN would spare the radial extensors.

430
Q

Tx of PIN neuropathy

A

Have to release the Arcade of Frose to finish PIN decompression

431
Q

L hand numbness with thenar atrophy and atrophy of first dorsal interossei, all one diagnosis

A

Thoracic outlet syndrome producing Gilliat-Sumner’s hand, impinging lower trunk or medial cord of brachial plexus. Fix in surgery - make sure you don’t hit the phrenic nerve!

432
Q

Upper extremity weakness and fasciculations bilaterally with no pain or numbness

A

High suspicion for ALS

433
Q

Shoulder pain, weak abduction and external rotation, prominence of scapular spine, atrophy of supraspinatus and infraspinatus

A

Supra scapular nerve entrapment in supra scapular notch… But need to rule out brachial plexus neuritis (severe shoulder pain without provocation followed by persistent weakness)

434
Q

Winged scapula

A

Most likely long thoracic nerve, spinal accessory nerve, or dorsal scapular nerve. Conservative to

435
Q

R foot drop with decreased eversion but intact inversion

A

L5 radiculopathy or peroneal neuropathy

436
Q

Decreased sensation of dorsal 1st web space

A

Problem with deep fibular nerve

437
Q

Imaging for R foot drop

A

US or MRI to look for cysts, tumors, etc.

438
Q

Tx for tarsal tunnel syndrome

A

Tarsal tunnel release - release each nerve!

439
Q

Neuralgia paresthetica

A

Nerve trapped against iliac crest (lateral femoral cutaneous nerve) - obese patient or patient in really tight skinny jean, numbness of anterolateral thigh, worse with sitting. Tx with meds, weight loss, injection, surgery (would require snipping inguinal ligament)

440
Q

Carpal tunnel EMG results

A

Prolonged latency for median nerve compared to ulnar nerve, drop in amplitude indicating axonal loss

441
Q

Diabetic neuropathy EMG

A

Decreased amplitude

442
Q

Ulnar neuropathy nerve conduction study

A

Drop in velocity from above elbow to below, may also have decreased amplitude

443
Q

M wave on EMG

A

Stimulation of muscle fibers

444
Q

H wave on EMG

A

Stress reflex

445
Q

F wave on EMG

A

Supra maximal stimulation

446
Q

Ptosis and miosis

A

Horner syndrome

447
Q

Weak shoulder abduction

A

Axillary nerve injury

448
Q

Can’t make OK sign

A

Damage to anterior interosseous nerve (branch of median nerve)

449
Q

Can’t flex first two fingers

A

Median neuropathy

450
Q

Can’t extend last 3 fingers

A

Ulnar neuropathy

451
Q

Can’t adduct 5th finger (Wartenberg sign)

A

Ulnar nerve problem

452
Q

Pathophysiology of osteoarthritis

A

Initial injury to hyaline cartilage caused by its degeneration leads to a cascade of inflammatory response, causing increased breakdown, desiccation, loss of chondrocytes and their repair function, etc until there is no longer a smooth contour. Bone plate gets bony hypertrophy, synovial hypertrophy, inflammation, and osteophytes.

453
Q

Imaging hallmarks of osteoarthritis

A

Non-uniform joint space narrowing from cartilage loss, subchondral sclerosis, osteophytes, subchondral cysts

454
Q

Tests for nerve damage in little kids

A

Wrinkle test - skin won’t wrinkle in warm water if there’s a nerve injury
Sweat test - skin won’t demonstrate typical sweat patterns

455
Q

Pre-operative management if you are going to do a tendon transfer or nerve transfer

A

PT/OT - joint must be passively mobile. Pain management and social support also important.

456
Q

Clinical indications for nerve transfer

A

Proximal brachial plexus injury, delayed presentation or referral, trauma causing segmental nerve loss, other trauma in that area

457
Q

Principles for choosing a donor nerve

A

Purely motor, anatomically would be able to be removed without needing its own nerve graft, enough axons for the target muscle, has redundant function, has synergistic function with recipient nerve

458
Q

Neuropathy with orthostatic hypertension

A

Autonomic dysfunction

459
Q

Neuropathy with skin rash

A

Vasculitides

460
Q

Neuropathy with skeletal deformities

A

Hereditary neuropathy

461
Q

Neuropathy with nerve enlargement

A

Demyelinating neuropathy

462
Q

Neuropathy with abnormal hair and nails

A

Toxic exposure

463
Q

Diagnostic test for large fiber neuropathy

A

EMG and nerve conduction study - look at amplitude, affected motor units

464
Q

Diagnostic test for small fiber neuropathy

A

Autonomic testing, and skin punch biopsy in which you look at the density of intraepidermal nerve fibers to see if it’s reduced

465
Q

High A1c, hands and feet have neuropathy, slowly progressive with predominant sensory loss moving distal to proximal

A

Diabetic neuropathy

466
Q

Prodromal illness followed by tingling in hands and feet, ascending proximal and distal weakness, areflexia, due to Tcell driven response against peripheral myelin

A

Acute inflammatory demyelinating polyradiculopathy (Guillain-Barre syndrome, etc). LP shows increased CSF without WBCs. Tx with plasma exchange or IVIG

467
Q

Neuropathy with increased IgM, heavy chains, or light chains

A

Monoclonal gammopathy

468
Q

Length-dependent neuropathy with axonal pathology producing subacute combined degeneration of SC (corticospinal tracts, posterior columns, sensorimotor axonal polyneuropathy)

A

Vitamin B12 deficiency - test for B12 or methylmalonate

469
Q

Copper deficiency neuropathy - what should you evaluate for?

A

Excess zinc

470
Q

Low vitamin B1 and neuropathy

A

Progressive sensorimotor axonal neuropathy in beriberi

471
Q

Other toxins that can cause neuropathy

A

Alcohol, renal failure, heavy metals, chemo (vincristine, taxanes)

472
Q

Early age of onset of neuropathy,, generalized, skeletal abnormalities, symmetric, slowly progressive

A

Most common is Charcot-Marie-Tooth - high arches, hammer toes. AD, develops in first 20 yrs of life

473
Q

Sx of compartment syndrome

A

Decreased sensation in first web space - deep fibular nerve involvement
Pain with passive extension of toes, lower leg firm and tense

474
Q

Pressures diagnostic of compartment syndrome

A

Delta P <30, or absolute P>30

475
Q

6 Ps

A

Pain, pallor, pulselessness, poikilothermia, paresthesias, paralysis

476
Q

Pathophysiology of compartment syndrome

A

Increased pressure -> ischemia -> ATP decreases -> cell death -> release of CK, myoglobin, muscle enzymes, electrolytes

477
Q

CK levels posing greatest risk of rhabdomyolysis and AKI

A

CK > 15-25000

478
Q

Factors important in muscle differentiation and repair

A

Myf5, MyoD, Mrf4

479
Q

Stages of muscle repair

A

proliferation, differentiation, hypertrophy

Mind & Motion (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions