PathTest 3 Flashcards
(216 cards)
1
Q
What is the normal mechanism of Achondroplasia?
A
Activation of FGFR3.
2
Q
What will the FGFR3 do once activated?
A
Inhibit cartilage proliferation.
3
Q
Osteopetrosis is caused by what?
A
A genetic deficiency of carbonic anhydrase II.
4
Q
What can x-rays of osteopetrosis show?
A
Erlenmeyer flask bones.
5
Q
Erlenmeyer flask bones that flare out can result in what?
A
Cranial nerve impingment, and palsies due to narrowed foramina.
6
Q
What is the most common fracture with aseptic bone necrosis?
A
Femoral head.
7
Q
What is the most common fracture with aseptic bone necrosis in the carpal bones?
A
Navicular (scaphoid).
8
Q
Eosinophilic fascitis often begins after what?
A
Strenuous activity.
9
Q
What is a common sign of eosinophilic fascitis?
A
Orange-peel configuration.
10
Q
Cutaneous manifestiations with eospinophilic fasciitis may suggest what?
A
Systemic sclerosis.
11
Q
Patients with systemic sclerosis usually also have what?
A
Raynaud’s syndrome, acral involvment, telangiectasia, and visceral changes.
12
Q
Will patients with eosinophilic fascitis also have Raynaud’s syndrome, acral involvment, telangiectasia, and visceral changes?
A
No.
13
Q
What will blood tests show with a patient with eosinophilic fasciitis?
A
Serum protein electrophoresis shows polyclonal hypergammaglobulinemia.
14
Q
What % of females and males get Mixed connective tissue disease (MCTD)?
A
females-80%. Males-20%.
15
Q
With mixed connective tissue disease what signs and symptoms may precede other manifestations by years?
A
Raynaud’s syndrome.
16
Q
Some of the first manifestations of mixed connective tissue disease resemble what?
A
Early SLE, Sytemic sclerosis, polymyositis, dermatomyositis, or RA.
17
Q
What is the most frequent finding with mixed connective tissue disease?
A
Sausage-like appearance of the fingers.
18
Q
Renal disease happens how often and how serious with mixed connective tissue disease?
A
10% (rare) and is often mild.
19
Q
Mixed connective tissue is diagnosed how (without doing labs)?
A
Overlapping features are present in patients appearing to have SLE, systemic sclerosis, polymyositis, or RA.
20
Q
What will lab work show with a patient that has mixed connective tissue disease?
A
RNP antibodies very high, positive ANA.
21
Q
What type of antibodies are present with mixed connective tissue disease?
A
ENA.
22
Q
85% of mixed connective tissue disease patients have what else involved?
A
Lungs.
23
Q
What are some possible ways polymyositis and dermatomyositis are incited?
A
Viral myositis and underlying cancer.
24
Q
Dermatomyositis is considered what?
A
A complement-mediated vasculopathy (disease of blood vessels).
25
What is the abnormality in polymyositis?
Direct T-cell mediated muscle injury.
26
What skin changes occur with dermatomyositis?
Periorbital edema with a purplish appearance (heliotrope rash).
27
What would another relatively specific finding be with a patient that has dermatomyositis?
Gottron's papules (pink patches on the knuckles).
28
What is a way to diagnose someone who has polymyositis?
Proximal muscle weakness with or without muscle tenderness.
29
What is a way to diagnose someone who has dermatomyositis?
Heliotropic rash or gottron's papules.
30
polymyositis and dermatomyositis share clinical findings with systemic scerosis or less frequently SLE or vasculitis so what should be done to diagnose polymyositis and dermatomyositis correctly?
Include as many of the following 5 criteria as possible: 1. proximal muscle weakness. 2. Characteristic skin rash. 3. Elevated serum muscle enzymes. 4. Characteristic electromyographic or MRI abnormalities. 5. Muscle biopsy changes.
31
Of the 5 tests to determine if a patient has polymyositis and dermatomyositis which one is the definitive test?
Muscle biopsy changes.
32
What else should be tested with polymyositis and dermatomyositis patients?
Cancer screening is recommended.
33
Relapsing polychondritis has what signs and symptoms?
Acute pain, erythema and swelling.
34
What is the most common and second most common place for acute pain, erythmea, and swelling with relapsing polychondritis?
1st pinna cartilage. 2nd- nasal cartilage.
35
What joints will have arthritis with relapsing polychondritis?
Costochondral joints.
36
Bouts of inflammation in relapsing polychondritis heal over what time frame?
Over weeks to months with recurrences over several years.
37
Sjogren's syndrome occurs most frequently amoung who?
Middle-aged women.
38
What happens with sjogren's syndrome?
Salivary, lacrimal, and other exocrine glands become infiltrated with CD4+ T helper cells and with some B cells.
39
What happens to the exocrine glands once infiltrated with CD4+ T cells and some B cells?
They are damaged and atrophy.
40
What will lacrimal glands that are damaged and atrophy cause to happen?
Keratoconjunctivitis sicca.
41
What is a way to diagnose sjogren's syndrome?
Gritty or dry eyes or dry mouth.
42
What is needed to officialy diagnose someone with sjogren's syndrome?
3 or more of 6 manifestations.
43
What are the 6 manifestations of sjogren's syndrome?
1. Eye symptoms. 2. Oral symptoms. 3. positive eye tests. 4. Salivary gland involvment. 5. autoantibodies. 6. Histopathology.
44
How is histopathology of sjogren's syndrome done?
Biopsy of minor salivary glands.
45
How is a histopathology of sjogren's syndrome confirmed?
LabialmMinor salivary gland will show multiple large foci of lymphocytes with atrophy of acinar tissue
46
What type of people will get Systemic Lupus erythematosus (SLE)?
70-90% in females. More common amoung blacks, and Asians than Whites.
47
How quickly will SLE develop?
Abruptly or insidiously.
48
SLE will develop with episodes of what?
Arthralgias (joint pain), and Malaise (General body weakness or discomfort).
49
What are some of the initial findings of SLE?
Vascular headaches, epilepsy, or psychoses (Mental disorder).
50
What happens to the skin with SLE?
Malar butterfly erythema.
51
What is the most common cardiac problem with SLE?
pericarditis (inflammation of pericardium).
52
What type of endocarditis is seen with SLE patients?
Libman-Sacks endocarditis.
53
Name the 11 clincal findings of SLE?
1. Malar rash. 2. Discoid rash. 3. Photosensitivity. 4. Oral ulcers. 5. Arthritis. 6. Serositis. 7. Renal disorder. 8. Leukopenia. 9. Neurolgic disorder. 10. Positive Anti-DNA or anti-smith antibodies. 1.. Antinuclear antibodies ANA ih high titers.
54
How many of the 11 criteria for calssification of SLE are needed to classify the patient as having SLE?
At least 4.
55
What will anti-Sm and Anti-double-stranded DNA antibodies tell us about SLE?
They are very specific but not sensitive.
56
What will blood tests be like for SLE?
Serum complement levels (C3-C4) are often depressed. ESR is elevated.
57
Renal involvment with SLE will be screened with a urinalysis and it will show what?
RBC and WBC casts suggest active nephritis.
58
What will the prognosis of SLE be?
Chronic relapsing and unpredictable.
59
Improvments of SLE often take how long?
4-12 weeks.
60
What should be tested on pregnant women with SLE?
Antiphospholipid antibodies.
61
Discoid lupus erythematosus will lead to skin changes as part of lupus and the skin changes will cluster where?
In light-exposed areas of the skin. Such as face scalp and ears
62
Drug-Induced lupus erythematosus will show what in lab work?
Extremely high antihistone antibodies.
63
Systemic sclerosis pathophysiology involves what?
Vascular damage.
64
What is pathophysiology?
Study of normal changing to abnormal caused by a disease.
65
Systemic sclerosis is aka?
Scleroderma.
66
What happens to the skin with systemic sclerosis aka scleroderma?
More compact collagen fibers in the reticular dermis, epidermal thinning, loss of rete pegs, and atrophy of dermal appendages.
67
What is systemic sclerosis called that is isolated to skin involvment?
Limited cutaneous scleroderma or Crest syndrome.
68
What is a sign of systemic sclerosis aka scleroderma?
Raynaud's syndrome, and swelling of distal extremities.
69
What is Raynaud's syndrome?
Cold hands.
70
How will Systemic sclerosis aka scleroderma affect the joints?
Polyarthralgias, or mild arthritis, flexion contractures.
71
What is a common cause of death from systemic sclerosis aka scleroderma?
Lung involvment, and pulmonary hypertension.
72
What is the prognosis of systemic sclerosis?
unperdictable.
73
What is the 10 year survival rate like with systemic sclerosis?
65%.
74
What type of systemic sclerosis can be limited and nonprogressive for long periods?
Crest syndrome which is aka cutaneous scleroderma.
75
Calcium pyrophosphate dihydrate crystal deposition disease is transmitted in an autosomal dominant pattern with complete penetration by when?
Age 40.
76
With Gout what is the most common cause of hyperuricemia?
Decreased renal excretion.
77
What is lesch-Nyhan syndrome?
A complete deficiency of the enzyme called hypoxanthine-guanine phosphoribosyltransferase.
78
Lesch-nyhan syndrome is associated with what disorder?
Gout.
79
With gout urate crystals will precipitate out as what
Needle-shaped monosodium urate.
80
What is podagra?
Gouty inflammation of the metatarsophalangeal joint of the great toe.
81
What is tophi?
Firm yellow or white papules or nodules that occur in patients who have had chronic gout or who have never had gout.
82
How will tophi be present in gout?
Single or multiple.
83
About 20% of chronic gout patients will develop what?
urolithiasis with uric acid stones or Ca oxalate stones.
84
Palindromic rheumatism (gout) is acute, recurrent attacks of inflammation in or near one or several joints and these attacks happen how?
Attacks subside spontaneously and completely in 1 to 3 days.
85
What are serum urate levels like with an acute attack of gout?
at leaste 30% of patients have normal serum urate at time of attack.
86
With new gout patients the serum urate levels should be measured 2 or 3 times to establish a baseline if it is elevated what can also be measured?
24-h urinary urate excretion.
87
What is the normal amount of urinary urate excretion in 24 hours?
600-900.
88
X-rays of gout patients are taken to look for what?
Tophi.
89
What is the shape of monosodium urate (gout crystal)?
Needle- or rod-shaped.
90
What is the shape of Ca pyrophosphate dihydrate (gout crystal)?
Rhomboid- or rod-shaped.
91
What is the shape of Ca oxalate (a rare gout crystal)?
bipyramidal.
92
What is the shape of Basic Ca Phosphate (gout crystal)?
Shiny, coinlike or slightly irregular.
93
With achilles tendon enthesopathy what can be done to minimize stress to the achilles tendon?
Night splints, Heel lifts.
94
What are the signs and symptoms of anterior achilles tendon bursitis?
Pain, swelling, and warmth around the heel are common.
95
What will cause pain to a patient with anterior achilles tendon bursitis?
Use thumb and index finger, side to side compression anterior to achilles tendon will cause pain.
96
A bunion is what?
A adventitious bursa due to pressure from tight shoes.
97
A bunion is often caused by what?
Hallux valgus.
98
a bunion that has swelling and mild inflammation that affects the entire joint would be called what?
Osteoarthritic synovitis.
99
Osteoarthritic synovitis is more what?
Circumferential.
100
Epiphysitis of the calcaneus is aka?
Sever's disease.
101
What is ephiphysitis of calcaneus aka sever's disease?
Cartilaginous disruption in calcaneal epiphysitis.
102
When will Pain will develop for people with epiphysitis of the calcaneus aka sever's disease?
between 9-14 usually.
103
What is the usual cause of Hammer toe deformity?
Misalignment of the joint surface due to genetic predisposition toward aberrant foot biomechanics and tendon contractures
104
What is another cause of Hammer Toe Deformity?
Charcot-Marie-Tooth disease.
105
What is the most common digit affected with hammer toe deformity?
2nd.
106
Painful corns often develop from hammer toe and they affect what toe?
5th.
107
Inferior calcaneal bursitis can develop at the inferior calcaneous near what?
the insertion of the plantar fascia.
108
What is a symptom or sign of medial plantar nerve entrapment?
Almost constant pain.
109
What is a treatment of medial plantar nerve entrapment?
Physical therapy and cryotherapy (treatment by means of application of cold).
110
What is the most common cause of metatarsalgia?
Freibergs disease, interdigital nerve pain, Morton's neuroma
111
What is morton's neuroma?
It includes Freiberg's disease and interdigital nerve pain.
112
What is Freiberg's disease?
avascular necrosis of the metatarsal head.
113
What disease is Freiberg's disease seen with?
Metatarsalgia.
114
How is metatarsalgia diagnosed?
With X-rays.
115
What will be seen on X-rays of a metatarsalgia patient?
head of 2nd metatarsal is widened and flattened.
116
What are the signs and symptoms of metatarsalgia?
Burning or lancinating(stabing) quality or paresthesias.
117
What can’t patients do with metatarsalgia?
Wear most shoes.
118
What causes tissue changes with metatarsalgia?
Tissue changes due to aberrant foot biomechanics.
119
To diagnose metatarsalgia take the patients foot and 1st toe is dorsiflexed and then inspect the metatarsal head and palpate each sesamoid. Tenderness is localized where?
To a sesamoid usually the tibial sesamoid.
120
Plantar fasciosis is caused by a shortening or contracture of the calf muscles and plantar fascia and what are the things that can lead to this?
Sedentary lifestyle.
121
Plantar fasciosis is common amoung sedentary people and who?
People who are standing or walking on hard surfaces for prolonged periods.
122
What is a sign or symptom of plantar fasciosis?
Pain at the bottom of the heel on weight bearing particularly when first arising in the morning.
123
What happens to pain at the bottom of the heel for plantar fasciosis in the morning?
It usually improves within 5 to 10 minutes only to return later in the day.
124
How is plantar fasciosis diagnosed?
Confirmed if firm thumb pressure applied to calcaneus when the foot is dorsiflexed elicits pain.
125
What are the most effective treatments of plantar fasciosis?
in-shoe heel and arch cushioning, calf stretching exercises, and night splinting devices that stretch the calf and plantar fascia.
126
With plantar fibromatosis what is seen while the foot is dorsiflexed?
Nodules.
127
What is Haglund's deformity?
bony prominence on the calcaneous seen with many posterior achilles tendon bursitis patients.
128
what are the signs and symptoms of posterior achilles tendon bursitis?
Cystic nodules 1-3 cm in diameter.
129
Enthesopathy(A disease occurring at the site of attachment of muscle tendons and ligaments to bones or joint capsules) is differentiated from posterior achilles tendon bursitis how?
by the absence of a soft-tissue lesion.
130
What are the signs and symptoms of tarsal tunnel syndrome?
Pain (occasionally buring and tingling).
131
Where will pain be at with tarsal tunnel syndrome?
Retroballeolar and sometimes in the plantar medial heel and may extend along the plantar surface as far as the toes.
132
How is tarsal tunnel syndrome diagnosed?
TAPPING or palpating the posterior tibial nerve below the medial malleolus at the site of compression or injury, and this will often cause distal tingling.
133
When tapping of the posterior tibial nerve to diagnose tarsal tunnel syndrome and the patient gets distal tingling what is this called?
Tinel's sign.
134
With tibialis posterior tendinosis a treatment could be corticosteroid injections what will this do?
Exacerbate the degenerative process.
135
What is the cause of juvenile idopathic arthritis?
Unknown.
136
What seems to be the cause of Juvenile idopathic arthritis?
Genetic predisoposition and autoimmune pathophysiology.
137
How many possible patterns are there of Juvenile idiopathic arthritis?
three.
138
What are the 3 possible patterns of Juvenile idiopathic arthritis?
1. Systemic onset. 2. Pauciarticular onset aka oligoarticular. 3. Polyarticular onset.
139
Systemic onset of juvenile idiopathic arthritis is aka?
Still's disease.
140
What is the difference between pauciarticular (oligoarticular) and polyarticular onset of juvenile idiopathic arthritis?
Pauciarticular (oligoarticular) onset- less than 4 joints are involved. Polyarticular onset- more than 5 and often more than 20 joints are invovled.
141
How will Still's disease be diagnosed by lab work?
RF and ANA are absent.
142
What will lab work show for pauciarticular onset JIA?
ANA are present in up to 75% and RF is absent.
143
What will the lab work show for polyarticular-onset?
RF usually negative.
144
What type of patients with polyarticular-onset JIA will RF be positive?
Adolescent girls.
145
What is the pathophysiology of neurogenic arthropathy?
Impaired deep pain sensation or proprioception.
146
What are the signs and symptoms of neurogenic arthropathy?
Pain is the first symptom, but ability to sense pain is impaired and therefore the degree of pain is often unexpectedly mild for the degree of joint damage.
147
What are some of the late signs and symptoms of neurogenic arthropathy?
Fractures and bony healing may produce many loose pieces of cartilage or bone BAG OF BONES.
148
What will neurogenic arthropathy simulate in its early stages?
Osteoarthrisits.
149
How can neurogneic arthropathy be distinguished from osteoarthritis?
Neurogenic arthropathy progresses more rapidly than OA and frequently causes proportionately less pain.
150
How is neurogenic arthropathy treated?
Treatment of the underlying neurologic condition may slow progression.
151
What is the most common joint disorder?
Osteoarthritis (OA).
152
Osteoarthritis results from what?
Trauma.
153
What will a primary OA that involves multiple joints be classified as?
A primary generalized OA.
154
Osteoarthritis aka OA begins with what?
Mechanical injury transmission of inflammatory mediators from the synovium into cartilage or defects in cartilage emtabolism.
155
What happens to synovial fluid with OA?
The synovium becomes inflamed and thickened and produces synovial fluid with less viscosity and greater volume.
156
What is symptom or sign of OA?
Pain is usually worsened by weight bearing and relived by rest but can eventually become constant.
157
Stiffness following awaking with OA lasts how long?
less than 30 minutes.
158
What are the joints most often affected by OA?
DIP and PIP.
159
What is DIP and PIP and what is another name for them?
DIP- distal interphalangeal aka Heberden's nodes. PIP-proximal interphalangeal aka Bouchards nodes.
160
How can OA affect back pain?
Lower back or leg pain that is worsened by walking or back extension
161
What is a treatment of OA of the hip?
Prolotherapy.
162
What are 2 treatments of OA?
Rehabilitation techniques and weight loss.
163
What is a cause of Rheumatoid arthritis?
Autoimmune reactions.
164
What happens to the synovium with Rheumatoid arthritis aka RA?
normally thin synovium thickens.
165
Lots of inflammatory mediators are released with Rheumatoid arthritis and they are released by what?
Hyperplastic synovial tissue.
166
What is a symptom or sign of Rheumatoid arthritis?
Symmetric joint symptoms, stiffness that lasts 60 minutes or more after rising in the morning, and the stiffness may occur after any prolonged inactivity.
167
How can Rhematiod arthritis be diagnosed?
Check for Anti-ccp antibodies.
168
Anti-ccp is more sensitive for RA than what?
RF.
169
You need 4 of 7 criteria to diagnose someone with RA what are the 7 criteria?
1. Arthritis in 3 or more joints. 2. Arthritis in hand joints. 3. Morning stiffness for more than 1 hour. 4. Rheumatoid nodules. 5. Serum rheumatoid factor. 6. Symmetric arthritis. 7. Imaging changes.
170
What would the Rheumatoid factor aka RF be like in labs of a patient that has seronegative spondyloarthropathies?
RF is negative.
171
What disorders will be included in seronegative spondyloarthropathies?
Ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and others.
172
What is common in untreated ankylosing spondylitis patients?
Kyphosis.
173
What is the spine like with ankylosing spondylitis?
Bamboo spine.
174
Reactive arthritis is aka?
Reiter's syndrome.
175
What can't you do with reactive arthritis?
can't see, can't pee, and can't dance with me.
176
What is joint involvment like with reactive arthritis aka reiter's syndrome?
generally asymmetric.
177
With reactive arthritis when would urethritis develop?
7-14 days after sexual contact.
178
What else might develop over the next few weeks with reactive arthritis after sexual contact?
Conjunctivitis.
179
How is reactive arthritis diagnosed?
Asymmetric arthritis affecting the large joints of the lower extremities or toes.
180
Disseminated gonococcal infections can closely simulate reactive arthritis so how can they be distinguished?
Disseminated gonococcal infection tends to involve upper and lower extremities equally, and reactive arthritis affects the lower extremities or toes.
181
What else can simulate reactive arthritis?
Psoriatic arthritis.
182
How can we distinguish between psoriatic arthritis and reactive arthritis?
psoriatic arthritis affects mostly upper extremities and RA-affects lower extremities.
183
Psoriatic arthritis develops in 5-40% of patients with what?
Psoriasis.
184
The next 11 questions I will give the autoantibody and you give the associated disorder.
ok
185
antinuclear antibodies (ANA)?
SLE, but not exclusive.
186
anti-ds(double stranded)DNA and anti-smith?
Specific for SLE.
187
Antihistone?
Drug-induced lupus.
188
Anti-IgG?
Rheumatoid arthritis.
189
Anticentromere?
Scleroderma (CREST).
190
Anti-Scl-70?
Scleroderma (Diffuse).
191
anti-jo-1?
Polymyositis, dermatomyositis.
192
Anti-SS-A?
Sjogren's syndrome.
193
Anti-SS-B?
Sjogren's syndrome.
194
Anti-U1 RNP?
Mixed connective tissue disease.
195
Anti CCP?
Rheumatoid arthritis.
196
What is another name for Anti-IgG antibody?
Rheumatoid factor.
197
What will osteoporosis do to bone?
Cortical thickness and number and size of trabeculae decrease resulting in increased porosity.
198
What will decrease with osteoporosis?
Total bone mass.
199
What type of deficiency in men and women is linked with osteoporosis?
Estrogen deficiency.
200
Osteoporosis is impaired formation response during bone remodeling probalby caused by what?
Age-related decline in the number and activity of osteoblasts.
201
Where is the most common site for fragility fractures with osteoporosis?
Distal radius and vertebral compression fractures.
202
What are some risk factors associated with osteoporosis?
Ciagrette smoking and excessive caffeine or alcohol use.
203
What will be seen on X-ray with osteoporosis?
Loss of horizontally oriented trabeculae increases the prominence of the cortical end plates and of vertically oriented weight bearing trabeculae.
204
What is DEXA and what is it used for?
Dual-energy x-ray absorptiometry used to measure bone density often with osteoporosis.
205
About 80% of osteomyelitis results from what?
contiguous spread or from open wounds it is often polymicrobial.
206
What are some of the common infecting organims with osteomyelitis?
S. aureus, MRSA(methicillin-resistant S. aureus), Pseudomonas aeruginosa, serratia sp, salmonella sp, histoplasmosis, blastomycosis, or coccidioidomycosis.
207
What are x-rays like for osteomyelitis?
they become abnormal after 2-4 weeks showing periosteal elevation, bone destruction, soft-tissue swelling, and in the vertebrae it shows loss of body height or narrowing of the adjacent infected intervertebral disk space, and destruction of end plates above and below the disk.
208
What will show abnormalities earlyer than x-rays with osteomyelitis?
Bone scans.
209
Paget's disease is aka?
Osteitis deformans.
210
What is the histologic hallmark of paget's disease aka osteitis deformans?
Mosaic bone pattern.
211
What type of bone tumor will be found in the epiphysis both benign and malignant?
Benign- giant cell tumor. Malignant-none.
212
Gian cell tumor is aka?
Osteoclastoma.
213
What type of bone tumor will be found at the metaphysis both benign and malignant?
benign- osteochondroma. Malignant- Osteosarcoma.
214
What type of bone tumor will be found at the diaphysis both benign and mallignant?
Benign- osteoid osteoma. Malignant- Ewing's sarcoma.
215
What type of bone tumor will be found at the intramedullary area both benign and mallignant?
Benign- enchondroma. Malignant- chondrosarcoma.
216
With osteosarcoma the periosteum has been lifted and laid down a shell of reactive bone known as what?
Codman triangle.
