11 ⼀RHEUM-ORTHO/ TOX II/ Rx+ Flashcards

(202 cards)

1
Q

Diagnosis?

A

GOUT

juxtaarticular erosions or tophi on XR

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2
Q

how do you confirm acute Gout diagnosis?

A

Arthrocentesis showing [negatively birefringent needle crystals]
_________________

remember: serum uric acid can be normal or low during acute gout attack

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3
Q

Pseudogout is characterized by what findings ?-4

A

PRPB

1.[Pseudogout CPPD]
2.Rhomboid
3.[Positive birefringence under polarized light]
4.[Blue under parallel polarized light]

crystals are PRPB

CPPD = [Ca+ Pyrophosphate Dihydrate]

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4
Q

What electrolyte abnormality is a risk factor for Pseudogout?

A

HYPERCalcemia (look for constipation!)

crystals are (PRPB Rhomboid, Positively birefringent (Blue under parallel birefringent light) light

Pseudogout features = PRPB

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5
Q

[Chondrocalcinosis (calcified articular cartilage)] is seen in ⬜?

_________________

Pts with this condition should be worked up for what possible causes - 4

A

Pseudogout
= PRPB which can → Chondrocalcinosis arthritis
_________________
Chondrocalcinosis 2/2 HYPERCalcemia (which may be 2/2…⬇︎)
1. HyperParathyroidism
2. hypOthyroidism
3. Hemochromatosis (dx = iron studies)
4. Osteoarthritis?

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6
Q

Most Gout attacks initially occur where?

A

Asymmetric Inflammatory Monoarthritis

1st MTP joint = Podagra

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7
Q

Name the precipitants of Gout attacks(cause Hyperuricemia) -10

A

“CLAP.NET.SLD sold Gout”

“CLAP.NET.SLD sold Gout”

  1. Cyclosporine
  2. Lasix Furosemide
  3. ASA 81
  4. PyrazinamideTB tx
  5. Niacin
  6. EtOH
  7. Thiazides
  8. Surgery
  9. LARGE meals
  10. Dehydration
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8
Q

Gout or Pseudogout?

Based on answer: What type of polarized light is A ? C?

A

GOUT!(based on needle shape)

Since dx = Gout… then polarized light…
A = Perpendicular

C = Parallel light(GOUT is Yellow under parallel light)

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9
Q

Gout Etx -2

A

90% from underexcreted uric acid

10% from overproduction of uric acid (myeloproliferative disorders such as polycythemia vera)

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10
Q

Conditions associated w/Pseudogout -4

A
  1. [AOHHemochromatosis]
  2. hypOthyroid
  3. HyperParathyroid
  4. Osteoarthritis

AOH = Arthropathy of Hereditary

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11
Q

Tx for Acute Gout (3)

A
NSAID = indomethacin

Also tx for Acute Pseudogout

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12
Q

Tx for Chronic Gout -3

A
  1. Febuxostatxanthine oxidase inhibitor
  2. Allopurinolxanthine oxidase inhibitor
  3. Probenecid

Gout [px] and [acute tx] = NSAIDs, colchicine, CTS

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13
Q

Px for Gout -3

A
  1. NSAIDs
  2. Colchicine
  3. CTS

Same as tx for Acute Gout

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14
Q

Acute PseudoGout Tx -3

A
  1. NSAIDs
  2. Colchicine
  3. CTS

Also tx for Acute Gout

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15
Q

what is the recommended dietary Calcium intake per day?

A

1200-2000

mg/day

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16
Q

Recommended dietary Vitamin D intake per day?

A

800-4000

IU/day

sunlight (15 min 2x/week)

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17
Q

Name the 5 groups that should receive Osteoporosis screening via ⬜

A

DEXA

_________________

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18
Q

What is the Calcium and Vitamin D dietary recommendation for Women with postmenopausal osteoporosis (or osteopeniaHR)?
_________________

bisphosphonate MOA = competitively binds to Bone Hydroxyapatite before osteoClast can bind ➜ prevents bone resorption

A

[Ca+ ≥1200 mg/day]

and

[VitD ≥800 IU/day]
_________________

also [wt bearing exercise], avoid EtOH, avoid smoking,

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19
Q

For Women, when is Bisphosphonate therapy indicated? -3
_________________

bisphosphonate MOA = competitively binds to Bone Hydroxyapatite before osteoClast can bind ➜ prevents bone resorption

A

postmenopausal women with:

[osteopenia + [10y FRAX probability of (major osteoporotic fx ≥20%) or (hip fx ≥3%)]
_________or________

OSTEOPOROSIS

_________or________

[Low bone mass w hx of fragility fx]

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20
Q

There are 3 stimulators of ⬜ which ➜ bone formation. What are they?

A

osteoBlast
_________________
P-E-V stimulates new bones for me!”

PTH

[E2 (EstraDiol)]

[Vitamin D]

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21
Q

Osteoporosis can be clinically defined as ⬜

List the 2 PRIMARY causes of Osteoporosis

A

([⬇︎BMD>2.5 below YAM] despite normal mineralization)

_________________

[Type 1 Postmenopausal (E2 ⬇︎)] - Female

[Type 2 Senile (Ca+ ⬇︎)] - Female and Male

🔎BMD = [Bone Mineral DENSITY]|| 🔎YAM = [Young Adult Mean (DEXA T Score)]

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22
Q

Osteoporosis can be clinically defined as ⬜

List the 8 SECONDARY causes of Osteoporosis

A

([⬇︎BMD>2.5 below YAM] despite normal mineralization)

_________________

🔎BMD = [Bone Mineral DENSITY]|| 🔎YAM = [Young Adult Mean (DEXA T Score)]*

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23
Q

[Peak Bone Mass] occurs age ⬜ and Normal [Bone Mineral Density] = ⬜

clinically define:

osteopenia
_________________

OSTEOPOROSIS

A

30
_________________
[normal: BMD 0-1 below YAM]

[osteopenia = (BMD 1 - 2.5 below YAM)] despite nml mineralization
_________or________

[OSTEOPOROSIS = (BMD >2.5 below YAM)] despite nml minerlization
________________

YAM: Young Adult Mean (DEXA T Score) || BMD: Bone Mineral Density ||PBM: Peak Bone Mass ||
below YAM = variables are negative

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24
Q

clinical presentation of Osteomyelitis -3
_________________

A

FIF

Focal Bone Pain / Inflammatory markers / Fever

_________________

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25
Which 3 organisms are usually the cause of [*pediatric* osteomyelitis]? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ and how are they treated?
① [MssA *likely*] = Nafcillin/Oxacillin|ceFAZolin ② [MRSA *likely*] = Clindamycin | Vancomycin \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ③ {*if [⊕Sickle Cell Disease]* → cover Salmonella= **ADD 3Gc**(CefTriaxone/CefoTAXime)*_to above ① |② *} \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **FIF**sx
26
*Osteoporosis can be clinically defined as ⬜* How does the Thyroid and Parathyroid affect Bone metabolism?
*([⬇︎BMD \>2.5 below YAM] despite normal mineralization)* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Hyperthyroid ➜ [⇪ osteoClast _activity_] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ HyperParathyroid ➜ [⇪ osteoClast _recruitment_] *BOTH ➜ {[ ⬇︎BMD >2.5 below YAM] **2º** OSTEOPOROSIS}* ## Footnote *🔎BMD = [Bone Mineral DENSITY]|| 🔎YAM = [Young Adult Mean (DEXA T Score)]*
27
How is the Thyroid associated with Bone?
⇪ Thyroid ➜ [⇪ osteoClast *_activity_*] ➜ [⇪ Bone Resorption] eventually→ {[Osteoporosis*(⬇︎Bone Mass Density)*}
28
in patients with primary hyperparathyroidism, which 2 criteria qualifiy them for Parathyroidectomy?
1. ***PRAP***[symptomatic Hypercalcemia] 2. [1º hyperPTH \< 50 year old (young patients are likely to get complications later)] ## Footnote (***PRAP:* p**ainful bones/**r**enal stones/**a**bd groans/**p**sychic moans]
29
Postural kyphosis is a **NORMAL** finding caused by ⬜, in the ⬜ demographic. What are the main clinical features? \_\_\_\_\_\_\_\_versus\_\_\_\_\_\_\_\_\_\_ Structural kyphosis is caused by ⬜. When is Surgical correction indicated? (2)
slouching ; teen ; [nml-slightly elevated spinal convexity] ​ [tx = voluntary back extension] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [SECONDARY SOURCE (infection, fracture, tumor or congenital)] 1. [convexity \>60° ] = surgical correction ​​ 2. chronic pain (from Kyphosis) = surgical correction
30
tx for [Adhesive Capsulitis frozen shoulder syndrome] (2)
[ROM exercises] --(if severe)--\> [CTS injection]
31
What is [Adhesive Capsulitis frozen shoulder syndrome]? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ causes? ​(6)
*[Idio/Rotator❌/CVA/DM/humeral head fx/subac bursitis] →*[contracture*(pathologic muscle contraction + hardening)* of shoulder joint capsule + inflammation and fibrosis ➜ stiff*frozen shoulder* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. idiopathic​ 2. Rotator cuff tendinopathy 3. subacromial bursitis 4. stroke 5. DM 6. humeral head fx
32
What is the major risk of improperly managed Scaphoid fracture? (2)
avascular necrosis ➜ **NONUNION**
33
management for suspected scaphoid fractures -3
XR ➜ [short arm thumb spica cast + supportive] --(1 week)--\> repeat XR *Ortho referral if Scaphoid fracture displaced* ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *Scaphoid fractures may take up to 1 week to show on XR!*
34
⬜ is the most common carpal bone fracture and clinically presents with ⬜ Describe how it's usually fractured
Scaphoid; TTP of Scaphoid within anatomic snuffbox \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [FOOSA (dorsiflexed wrist)]
35
Why do patients with *P*olymyositis have to be regularly monitored with ⬜ ?
PFT \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *P*olymyositis can ➜ *P*ulmonary❌: -ILD -Infxn (from immunosuppresion) -Pulm muscle weakness -[MTX-inducedPneumonitis]
36
Dx Labs for [Polymyositis **and** Dermatomyositis] -5 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What is the ultimate diagnostic for these?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [MUSCLE BIOPSY showing mononuclear infiltrate] is *last resort diagnostic* (if serology/diagnosis uncertain)
37
[Polymyositis **and** Dermatomyositis] Tx - 2 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *helicotrope rash in image*
MTX and CTS (minimizes MTX side effects)
38
# *list clinical features for:* Polymyositis -4 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Dermatomyositis -8
## Footnote *Polymyositis*: -[proximal shoulder weakness symmetric] -[pulmonary❌(ILD - *ground glass on HRCT*)] -Endomysial inflammation -CD8 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
39
*Myasthenia Gravis, LEMS and [Myopathies (polymyositis/dermatomyositis)] can be similar* How can you differentiate these based on reflexes?
**Myopathies[polymyositis/dermatomyositis]** and **LEMS** have ⬇︎ Reflexes. ## Footnote Myasthenia is normal
40
PolyMyalgia Rheumatica sx -3 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ## Footnote *PMR occurs age \> 50 yo*
**P**oly**M**yalgia **R**heumatica [**P**ainfully Stiff Shoulders & Hips (*especially in Morning*)] [**M**alaise +/- wt loss] [**R**eally hot (Fever)] ## Footnote *PMR Tx =LCTS (if ⊕GCTA)--> HCTS* *PMR DOESNT HAVE TO BE CONCOMITANT WITH GIANT CELL TEMPORAL ARTERITIS. CAN OCCUR ALONE*
41
Labs for Polymyalgia Rheumatica -3
⬆︎ESR ## Footnote ⬆︎CRP normal CPK \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_x\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *PMR pts have NORMAL strength but have _painful (morning) stiffness_ || PMR can occur independent of Giant Cell Temporal Arteritis*
42
clinical features of FibroMyalgia 2 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how long do these have to be present for diagnosis?
***F**ibro**M**yalgia* *\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_* [**F**atigue +/- psych❌] [**M**usculoskeletal💢 Widespread] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ≥3 mo
43
One serious complication of ⬜ is giant cell temporal arteritis ​​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ s/s of Giant cell temporal arteritis (4) ​ ​
PolyMyalgia Rheumatica ; HA ​| ​jaw pain ​| vision loss ​| temporal TTP | *GCTA dx confirmation = ⇪ ⇪ ⇪ ESR*
44
Mgmt for giant cell temporal arteritis(2)
1. [**HIGH** dose CTS]*low dose CTS for PMR alone * + 2. [temporal artery biopsy] ​ | *GCTA dx confirmation = ⇪ ⇪ ⇪ ESR*
45
[Fall Onto OutStretched Hand] **primarily** ➜ what kind of fracture? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What additional injuries should you expect? -3
[Distal radius Colles' fracture] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [ulnar styloid fx] / [scaphoid fx] / [carpal tunnel syndrome]
46
For skeletal immature patients with scoliosis, at what point is Orthopedic surgery indicated?
Cobb angle GOE40° ​ *note: skeletal mature patients (post puberty) have low risk progression and don't need any additional management*
47
What is [Neuropathic Charcot Arthropathy]? -4
[DM or Dorsal Column disease (B12 deficiency)]➜ impaired sensation/proprioception ➜ 1. acute: repetitive foot trauma and inflammation ➜ 2. subAcute: Osseous destruction on XR (phalangeal osteolysis, metatarsal head disappearance resembling "sucked candy") ➜ 3. **CHRONIC**: **IRREVERSIBLE** BONE DESTRUCTION DESPITE INFLAMMATION RESOLUTION
48
List the management for [Neuropathic Charcot Arthropathy] by stage [Acute /subAcute] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ CHRONIC
acute/subAcute= **FOOT CAST** (offload weight bearing and reduce edema) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ CHRONIC = [SURGICAL BONE REALIGNMENT]
49
What is the best way to prevent bone loss in patients **chronically** taking CTS (i.e. SLE)? -2
[Calcium supplement ( 1200-2000 mg/day)] & [Vitamin D supplement (800-4000 IU/day)]
50
*patient presents with symptoms and radiographs c/w RA but has [negative antiCCP] and [negative antiRheuamtoid Factor]* *.....* likely diagnosis and management? explain why?
[seronegative RA] = start on **DMARD** * * * *PATIENTS DON'T REQUIRE antiCCP or antiRF to have RA. When these are negative = [seronegative RA] = less aggressive course* *active RA should be started on **DMARD** maintenance ASAP to slow progression of bony erosion and cartilage loss* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ DMARD (Disease Modifying AntiRheumatic Drugs)​ | *"Norris DMARD...**M**eans **LASH** **T**errible*g-e-i-c-o*"*
51
*patient presents with symptoms and radiographs c/w RA but has [⊝ antiCCP] and [⊝antiRheuamtoid Factor]* which drugs are used to manage this?​ (6)
*[Seronegative RA]* *\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_* DMARD (Disease Modifying AntiRheumatic Drug)​ *"Norris DMARD...**M**eans **LASH** **T**erribleg-e-i-c-o"* 1. [**M**TX (initial DMARD)] 2. **L**eflunomide 3. **A**zathioprine 4. **S**ulfasalazine 5. **H**ydroxychloroquine 6. [**T**NFα inhibitors*g-e-i-c-o*] | *"Norris DMARD...**M**eans **LASH** **T**errible*g-e-i-c-o*"*
52
name the 4 drugs that cause Macrocytic Anemia by interfering with folate metabolism \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ explain how?
**DHFRi** - MTX: *👨🏻‍🦲* - phenytoin*👨🏻‍🦲* - [tMP (trimethoprim)]*🦠* - Pyrimethamine*🪱* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ inhibits [DiHydroFolate reductase] which prevents [folic acid B9] ➜ [FH4 reduced folinic acid (usually utilized by cells)] -➜ DEC [pyrimidine base] synthesis ➜ inability for RBC_[DNA *nucleus*] to condense during RBC synthesis = [macrocytic *megaloblastic* anemia] *in👨🏻‍🦲humans* *in🦠bacteria* *in🪱parasites*
53
explain how Chronic MTX causes a Macrocytic anemia
MTX inhibits [DiHydroFolate reductase] which prevents [folic acid] ➜ [FH4 reduced folinic acid (usually utilized by cells)] this [FH4 reduced folinic acid] deficiency ➜ macrocytic anemia/stomatitis/hepatotoxicity ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx = [FH4 reduced folinic acid (usually utilized by cells)] = LEUCOVORIN
54
Chronic MTX may ➜ ⬜ depeletion and produce a ⬜ Anemia \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Tx for this?
[THF] ; [mAcrocytic *megaloblastic*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [FH4reduced folinic acid (usually utilized by cells)] = Rx**LEUCOVORIN**
55
How is [gastric bypass surgery] related to chronic back pain?
[Roux-en-Y gastric bypass] often ➜ Vitamin D deficiency ➜ impairs Ca+ absorption ➜ so parathyroid hypersecretes PTH ( 2º hyperPTH) ➜ normalizes Ca+ absorption but also **depletes** **Phosphate** and Vitamin D will still be relatively low➜ IMPAIRED BONE MINERALIZATION (loss of trabeculae/cortical thinning) + INC bone resorption from PTH = OSTEOMALACIA ➜ low bone density ➜ Chronic msk Back Pain ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ * dx = [25-OHVitamin D] \< 20* * tx = [Vitamin D GOE2,000 IU/day] supplement*
56
How is primary hypOthyroidism related to Pernicious anemia? ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ MOD for Pernicious anemia?
* REMEMBER! IF THEY HAVE 1 AUTOIMMUNE DISEASE -- THEY MAY HAVE OTHER AUTOIMMUNE DISEASE!* * pt with 1º hypOthyroidism = may have Pernicious Anemia also!* ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ PA = autoimmune gastric parietal cell destruction ➜ ⬇︎ [Intrinsic Factor (and HCL)] ➜ ⬇︎ [dietary VitB12 ReAbsorption at terminal iLeum] ➜ [macrocytic anemia] + [suBACute combined degeneration (LE\>UE)] =
57
Name the 2 treatment options for RayNAud phenomenon
**N**ifedipine **A**mlodipine ​ ## Footnote \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Ray**NA**aud phenomenon *passive smoking exacerbates this condition*
58
In a patient with RayNAud phenomenon, what do you do if a patient [begins systemic symptoms (arthralgias, myalgias)] or [resistant to treatment]?
[**CRUCCACE** autoimmune labs] c/f other causes (connective tissue dz/vascular lesions/meds) ## Footnote - **C**BC - [**R**F & antiCCP] - **U**A - **C**MP - **C**omplement levels - **A**NA - **C**RP - **E**SR
59
[RCsM] stands for ⬜ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Describe MOD of [RCsM]?
**RCsM** : {[**R**enal osteodystrophy = **C**KD *which eventually* ➜ ***s***econdary hyperparathyroidism)} ➜ **M**ineral bone disorder] 📸 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *[dietary Phosphate **restriction** +/- phosphate binders] --(once (P) normalizes)--\> [VitD supplement]​*
60
[RCsM] stands for ⬜ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What is the treatment for RCsM ?​ (3)
**RCsM** = [**R**enal osteodystrophy = (**C**KD ➜ **s**econdary hyperparathyroidism) ➜ **M**ineral bone disorder] 📸 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [dietary Phosphate **restriction** +/- phosphate binders] --(*Phosphate normalizes*)--\> [VitD supplement]​
61
In terms of Bone physiology, elevated ALP indicates what?
[INC bone turnover (Ca+ resorption)]
62
[Arthropathy of Hereditary Hemochromatosis] commonly affects which body parts? (5) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Tx?
- Shoulders - [2nd MCP] - [3rd MCP] - Knees - ankles \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Tx for Hereditary Hemochromatosis = [serial phlebotomy (note: will **not** help joint pain = *NO TX for AHH*)]
63
[Arthropathy of Hereditary Hemochromatosis] commonly affects which body parts? (5) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ dx? etx?
- Shoulders - [2nd MCP] - [3rd MCP] - Knees - ankles \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Dx =[Pseudogout ⼀joint aspiration] ## Footnote *{[excess joint iron deposition] ➜ [positively birefringent rhomboid CPPD crystal] joint accumulation ➜ causes acute inflammation that resembles Gout = **PSEUDO**gout* ➜ [Pseudogout⼀joint aspiration]dx}
64
Explain the extra advantage with the treatment (⬜ *name tx*) for Hereditary Hemochromatosis
serial phlebotomy \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [serial phlebotomy] ➜ [⬇︎ cirrhosis progression] ➜ [⬇︎HepatoCellularCarcinoma]
65
Reiter's Reactive Arthritis Name the 3 inciting factors
*"can't PEE ⼀can't see, can't bend my knee"* ## Footnote 1. [HLA-B27 positive (is RF but only 30% develop RRA)] 2. Chlamydia 3. Salmonella
66
Reiter's Reactive Arthritis clinical presentation (4)
*"can't PEE ⼀can't see, can't bend my knee"* 1.[s/p GUChlamydia (or GISalmonella) infection] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\ 2.***can't PEE*** -urethritis -keratoderma blennorhagica, -circinate balanitis 3.***can't see*** -uveitis 4.***can't bend my knee*** -[**ASYMMETRIC OLIGOARTHRITIS (≤4 joints)**] -Sterile synovial joint fluid with HIGH WBC | *HLA-B27 only positive in 30% of patients*
67
Oligoarthritis = joint pain/swelling of ⬜ in number \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How do you evaluate Oligoarthritis? 📋
1-4
68
*Nontraumatic* [Acute(<4 wks) Back pain] workup
**N**.**I**.**C**.**U**.
69
*What are the 3 most common shoulder diagnosis in mid-aged patients?* How do you discern each from one another?
[(RCN) Rotator Cuff tendonitis] = Lateral shoulder pain exacerbated by ABduction or external rotation \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Rotator cuff **Tear** = (RCN **+ [weakness]**]) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [AC Frozen Shoulder Syndrome] = progression of RCN = (RCN **➜ [stiffness (dEC shoulder ROM)**])
70
*patient presents with lateral shoulder pain exacerbated with ABduction and/or External Rotation* diagnosis?
[(RCN) Rotator Cuff tendonitis] ## Footnote * * * *+ weakness = [RC _TEAR_]* *if→stiffness= [RC _AFSS_ “Frozen”]*
71
72
Which 3 Rx are contraindicated in patients with Gout? (3)
HCTZ / Loop diuretics / **L**ASA \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ | *🔎**L**ASA = [(low dose) ASA]* ## Footnote *note: serum uric acid level can be normal in gout attack so DO NOT use to guide mgmt*
73
which antiHTN should be used in patients with Gout?
[ARB (losartan)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ## Footnote *note: serum uric acid level can be normal in gout attack. DO NOT use to guide mgmt*
74
# Patient presents with acute Gout Flare Typically, 1st line treatments are ⬜ and ⬜ ⼀What do you give if an acute Gout patient has renal failure? (2)
* [Indomethacin NSAID ➜ Colchicine] ⼀both (c❌d {renal failure}) * *Renal Failure*: [{CTS local injection = monoarticular} {CTS PO = polyarticular*>2 joints*}]
75
# Patient suspicious for ankylosing spondylitis What's the 1st step in diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How are these patients' disease progress monitored? (2)
Sacroiliac joint XR \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. Repeat XR in 3 mo 2. Acute phase reactants (ESR)
76
# Patient suspicious for ankylosing spondylitis What are the 3 diagnostic criteria?
ALL 3 of: 1. [Low back pain/stiffness GOE3mo] that improves with activity 2. Limited lumbar spine ROM 3. Limited chest expansion
77
# Patient suspicious for ankylosing spondylitis prognosis? (3)
* GOOD PGN * NO INC MORTALITY * NO PHYSICAL DISABILITY
78
# Ankylosing Spondylitis most notable sign is ⬜ List the other extraarticular manifestations (5)
[Sacroiliac (bamboo spine) fusion] **A**nkylosing **S**pondylitis = {[5 **A's** + [**S**acroiliac (bamboo spine) fusion]!} - Anterior uveitis - [Apical lung fibrosis*restrictive lung disease*& inflammed costosternal joints] - Aortic regurgitation - Ig**A** nephropathy - [Ankleplantar fasciitis]
79
Why are patients with (seronegative & seropositive) rheumatologic joint disease recommended to regularly participate in ⬜ exercise?
**Aerobic** exercise (swimming/walking/bike) improves joint stability, muscle strength and overall function without exacerbating the disease
80
How is mobility related to Calcium levels? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How can this be managed?
extended immobilization ➜ Calcium release from bones ➜ [**non**PTH hypercalcemia] ; Bisphosphonates ⬇︎ bone turnover and preserve bone mass
81
# In the setting of vigorous exercise, Statins potentiate muscle injury ➜ ⇪ CPK How do you manage this? (3)
Statin holiday ➜ {[Recheck CPK]--(*if normal*)--\>[Restart Statin]}
82
# Dupuytren Contracture etx \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ risk factors (4)
idiopathic Fibrotic Thickening of palmar fascia at 3rd, 4th, 5th digits ➜ nodules along flexor tendon near distal palmar crease ➜ DEC finger extension \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ - EtOH - Smoking - DM - [White Male \>50 yo]
83
# Dupuytren Contracture treatment (4)
1. modify hand tools*(padded gloves, cushion tape)* 2. Needle aponeurotomy 3. Intralesional CTS injection 4. Surgery ## Footnote idiopathic Fibrotic Thickening of palmar fascia at 3rd, 4th, 5th digits ➜ nodules along flexor tendon near distal palmar crease ➜ DEC finger extension
84
How do you diagnose Vitamin D deficiency?
[serum (25HydroxyVitaminD)] \< 20
85
# Vertebral compression fracture clinical presentation \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ risk factors? -3 *most common cause = osteoporosis*
**acute back point TTP** after strenuous activity \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ RF: - trauma, - osteoDISEASE (osteoporosis, osteomalacia, osteomyelitis, osteocancer) - hyperparathyroidism
86
# What causes Osteomalacia? Osteomalacia cp?-2 *Rickets is the pediatric version of Osteomalacia*
Vitamin D deficiency; 1. Bone **Pain** 2. Muscle weakness *Imaging: ⬇︎Bone Density with Looser Zone Pseudofractures*
87
# Rickets is caused by \_\_\_\_in children Clinical findings for Rickets - 10
Vitamin D deficiency 1&2. [1. Delayed Fontanelle closure] *(that leads to --> [2. Wide Sutures])* 2. 3. Frontal Bossing 4. Craniotabes (softening of the skull) 5. Dental hypoplasia 6. Rachitic Rosary 7. Pes Carinatum 8. Harrison's Sulcus 9. Joint swelling 10. Bowing of Legs *Osteomalacia is Adult version of Rickets* ## Footnote *vitamin D?* **B**rian **S**ucks **K**iller **P**enis *twice!*
88
What are the major lab findings for Osteomalacia?-5 | *Rickets is the pediatric version of Osteomalacia*
1. Vitamin D Deficiency which --\> 2. ⬇︎Ca+ 3. ⬇︎Phosphorous 4. ⬆︎PTH 5. ⬆︎ALP ## Footnote *vitamin D?* **B**rian **S**ucks **K**iller **P**enis *twice!*
89
# vitamin D Deficiency causes [⬜ in Adults] and [⬜ in peds] What are the risk factors for Vitamin D deficiency? (6)
Osteomalacia ; rickets \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. poor Sun Exposure 2. Heavy pigmentation 3. Obesity 4. Malabsorption 5. Advanced age 6. CKD ## Footnote *vitamin D?* **B**rian **S**ucks **K**iller **P**enis *twice!*
90
# vitamin D Deficiency causes [⬜ in Adults] and [⬜ in peds] *Active* Vitamin D = ⬜ Name all of its functions -8
Osteomalacia ; rickets \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1,25 - dihydroxycholecalciferol \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *vitamin D?* **B**rian **S**ucks **K**iller **P**enis *twice!* 1. **B**one: [⇪ Ca+ and PO4 Resorption → Remodeling] *but also…* → 2. **B**one: [⇪ serum Ca+ → ⇪ Mineralization] 3. [**S**mall intestineduodenum: ⇪ Ca+ absorption]❗️ 4. [**S**mall intestine: ⇪ PO4 absorption] 5. **K**idney: [⇪ Ca+ reAbsorption] 6. **K**idney: [⇪ PO4- reAbsorption] 7. **P**arathyroid = ⬇︎PTH synthesis → [⬇︎PO4 renal excretion] → [⇪ serum PO4] 8. **P**arathyroid = ⬇︎PTH secretion
91
[T or F] Primary Biliary Cirrhosis is associated with Bone Disease
TRUE ## Footnote ⼀PBC*(commonly in postmenopausal women [who are at risk for osteoDISEASE anyways])* is *independently* a/w osteoDISEASE also **= warrants DEXA** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *osteoDISEASE=osteopenia/osteomalacia/osteoporosis*
92
What are the 2 [*Sicca syndrome*] sx? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What causes *Sicca*? ⼀2
[Sjogren *Sicca Syndrome*] ** [(*****_S_**ee'rs are Dry, burning & gritty*****)**= **⼀**lacrimal inflammation ➜ Xerophthalmia = *“See'rs are dry ”* ⼀ keratoconjunctivitis ➜ {prominent bulbar blood vessels with stringy eye discharge →*"burning & gritty”* ** [(*****_G_**abber is Dry***)]= ⼀parotid inflammation = BL parotid enlargement ➜ Xerostomia dry mouth {also may ➜ dental caries|MALT lymphoma} \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [SjoGren Syndrome antinuclear Abs (SSA\Ro) (SSB\La)]
93
What is Sjogren Syndrome (4)
🔲 1º or 2º _multiorgan_ autoimmune(antinuclear ab: [SSA\Ro] and [SSB\La]) inflammation of exocrine glands→ [SjoGren and [*SjoGren Sicca*]Syndrome ] (below) ## Footnote ** [(*****_S_**ee'rs are Dry, burning & gritty*****)**= **⼀**lacrimal inflammation ➜ Xerophthalmia = *“See'rs are dry ”* ⼀ keratoconjunctivitis ➜ {prominent bulbar blood vessels with stringy eye discharge →*"burning & gritty”* ** [(*****_G_**abber is Dry***)]= ⼀parotid inflammation = BL parotid enlargement ➜ Xerostomia dry mouth {also may ➜ dental caries|MALT lymphoma} ★ [(**_Swelling of Joints_**)]
94
# Sjogren syndrome is ⬜ that can cause [Sjogren Sicca syndrome (in which the ⬜ and salivary gland are attacked)] *[Xerostomia dry mouth] salivary destruction may be insidious and difficult to identify* Give 2 examples of interview questions that'll reveal *insidious* [Xerostomia dry mouth] in pts c/f [Sjogren kXkSicca syndrome] * * * What are the complications of [Xerostomia dry mouth]? (3)
multi-organ autoimmune inflammation ; lacrimal * * * “Yes/No” : ***Ever Wake up at Night feeling dry, then drink water?*** “Yes/No” : ***frequently drink water to help swallow dry food?*** * * * [dental carries, candidiasisPO, chronic esophagitis]
95
How do you diagnose SjoGren Syndrome? (3) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ why is the lab test not 100% reliable?
1. [antiRo-SSa] and/or 2. [antiLa-SSB] 3. [Schirmer test ⼀*test for inadequate tearing*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ only 50% SjoGren Syndrome pts test positive for these antibodies (*but there's no other diagnostic for SGS so we must use these)*
96
What CA is SjoGren Syndrome associated with?
[non-Hodgkin\_MALT\_Bcell lymphoma] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *chronic SICCA autoimmune inflammation ➜ B lymphocyte activation for salivary gland infiltration but this➜ INC risk for MALT\_B cell lymphoma*
97
What are the Main elements of SLE-15
***RAS***HH ***O***RR ***PAI***NN
98
Lab test for SLE -4 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Which lab test for SLE is **first line**?
*Remember this:* "**ANA** & **Dana** saw **HIS**, Mr.**Smith**'s rash"
99
Hydroxychloroquine is effective in treating the ___ and ___ from SLE. \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What type of drug is it? SE-2?
***RA******SHH ORR PAINN*** **R**ash; **A**rthritis \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Anti-Malaria drug \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ SE = [Vision⬇︎] and Nausea
100
List the Immunosuppressants used to treat [SLE Lupus] -6
"Lucky needs his Charms & [SLE Lupus needs her **CHARMS**"] 1. **C**ycloPHOSphamide 2. **H**ydroxychloroquine 3. **A**zathioprine 4. [**R**ituximab antiCD20] 5. **M**ycopPHENolate 6. [**S**teroid prednisone] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ***RASHH ORR PAINN***
101
ALERT! ParvoB19 Arthritis can resemble inflammatory arthritis (RA, SLE) How can you tell the difference?
Inflammatory Arthritis (RA, SLE) **will have ⬆︎inflammatory markers (ESR, CRP)** ## Footnote ParvoB19 is transient
102
[Antiphospholipid syndrome] etx
Lupus anticoagulant (2/2 SLE or idiopathic) --\> [⬆︎Thrombosis and spontaneous abortion]
103
Lupus Nephritis is defined as ⬜*(3)* and requires ⬜ prior to immunosuppresion treatment to guide therapy
Any SLE patient with: 1A. [proteinuria ≥ 500 mg/day] or 1B.. [hematuria *(active sediment/RBC cast)*] or 1C. [*"BADturia"*declining renal fxn] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Renal Biopsy ## Footnote ***RAS*****HH** ***O*****RR** ***PAI*****NN**
104
Lupus Nephritis MOD
[anti**dsDNA**] deposits in the glomerulus and forms an IMMUNE COMPLEX with circulating Complement ➜ [⬇︎complement] ## Footnote *antidsDNA and complement are used to monitor renal involvement in Lupus Nephritis*
105
[T or F] Lumbar support braces provide long term benefit for chronic lower back pain and decrease recurrence rate
FALSE ⼀lumbar support braces (although supported by lay media for chronic LBP) **actually have limited evidence in reducing pain, improving function or lowering recurrence rates of lumbago**
106
How should you advise a patient who complains of having recurrent episodes of uncomplicated lower back pain? (3)
1. physical activity actually promotes resolution of initial uLBP sx and DEC uLBP future recurrence ➜ 2. **during acute uLBP, maintain normal/moderate physical activity** 3. as pain improves over time, YOU MUST initiate a regular exercise program*(stretching/core strengthen /aerobic - walking)* to further DEC recurrence of uLBP in the future | *🔎uLBP = uncomplicated Lower Back Pain*
107
# Familial hypOcalciuric Hypercalcemia clinical features (4)
* Pt p/w [mild \< 12 hypercalcemia] but has normal physical exam , no sx, no complaints * [AUTO DOM *CaSR*(Calcium Sensor-Receptor) mutation] ➜[DEC sensitivity to Calcium] *and* [these defective CaSR... cause [INC Renal Ca+ reabsorption] ➜ hypOcalciuria and Hypercalcemia] * Normally, [HIGH Ca+ ➜ DEC PTH], but because of the defective CaSR in FHH = requires [**EXTRA** HIGH Ca+ to ➜ DEC PTH \ in FHH] * can be differentiated from [primary hyperparathyroidism] with urine Ca+: -[**fhH** \< (0.01--*UCCR* --0.02) \< **PHPT**] ## Footnote [UCCR = [(UrineCa+/SerumCa+) ➗ (UrineCreatinine/SerumCreatinine)]
108
# Familial hypOcalciuric Hypercalcemia treatment?
NO TX NECESSARY ## Footnote [UCCR = [(UrineCa+/SerumCa+) ➗ (UrineCreatinine/SerumCreatinine)] - [**fhH** \< (0.01--*UCCR* --0.02) \< **PHPT**]
109
# PT PRESENTS WITH HYPERCALCEMIA,, with elevated PTH How do you differentiate [primary Hyperparathyroidism] from [Familial hypOcalciuric Hypercalcemia]?
urine Ca+ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [**fhH** \< (0.01--*UCCR* --0.02) \< **PHPT**] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *FHH = no sx, no tx* ## Footnote [UCCR = [(UrineCa+/SerumCa+) ➗ (UrineCreatinine/SerumCreatinine)]
110
Recurrent bacterial infections in an adult may indicate ⬜. ⬜ helps to establish the diagnosis
[humoral immunity defect (IgA, IgG common variable immunodeficiency)]; [Quantitative measurement of serum immunoglobulin]
111
What 2 labs must be assessed before starting a patient on a bisphosphonate? Why?
Serum: 1. Ca+ 2. [25-HydroxyVitaminD] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Bisphosphonates can ➜ hypOcalcemia due to DEC bone resorption, so pt's Ca+ must be normal and [25-HydroxyVitaminD] must be normal prior to starting Bisphosphonates
112
Name the 3 DDx for ***ANTERIOR KNEE PAIN*** *in a Young Patient* * * * list typical patient demographic for each
113
There are 3 DDx for ***ANTERIOR KNEE PAIN*** *in a Young Patient* * * * ⬜ is the most common cause of young adult (especially Women) ANT knee pain. List 3 other clinical features
🄱 PFPS (PatelloFemoral Pain Syndrome)= ▶Hx: most common cause of young adult (especially women) ANT knee pain 🄲 ▶Sx:subacute/chronic poorly localized ANT knee pain worst with [quadricep contraction(up/down stairs, squatting, prolonged sitting)] ▶Dx: [PatelloFemoral Compression Test(pain from [knee extension with ANT patellar pressure])] ▶Tx:[biomechanical quadricep stretching/strengthening]
114
a. Name the 3 DDx for ***ANTERIOR KNEE PAIN*** *in a Young Patient* * * * b. ⬜ is the most common cause of young adult (especially Women) ANT knee pain. c. Briefly Describe the Clinical Features of the other 2 DDx
🄱 PFPS (PatelloFemoral Pain Syndrome)=
115
# briefly describe Anserine Bursitis
**Acute** pain/TTP to [Anserine Bursa (medial knee, distal to joint line)] = common cause medial knee pain
116
# briefly describe [Patellar tendonitis ⼀jumper's knee]
**episodic pain/TTP at margin between inferior patella and patellar tendon** 2/2 **[Jumping(volleyball, basketball)** repetition**]**
117
# briefly describe [PrePatellar Bursitis ⼀housemaid's knee]
**Acute highly localized** ANT knee pain _WITH SWELLING_, commonly complicated by [2º Staph A infection (*septic bursitis*)], and obvi seen in pts who are extensively on their knees
118
a. Why does [PDO] present with [INC Technetium uptake bone scan]? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ b. Bisphosphonates are used to treat [PDO] once ⬜. Name 3 example Bisphosphonates | [PDO- Paget\Disease of bone\Osteitis deformans]
abnl osteClast⼀followed by⼀abnl osteoBLAST → ⇪ bone turnover with _abnml remodeling_ → [⇪ALP + ⇪ technetium uptake bone scan + PHLOATsx] abnml osteoClast → [⇪ bone turnover with abnml remodeling] → [INC Technetium uptake bone scan] * * * symptoms start; ## Footnote *“the bisphosphon DRON”* 1. alen**DRON**ate 2. rise**DRON**ate 3. zole**DRON**ic acid
119
Describe 🔲 for [PDO]? a. XR b.Labs c.Tx D.Sx -2 | [PDO- Paget\Disease of bone\Osteitis deformans]
a. [**XR**: thickened cortex / bony sclerosis] b. [**Labs**: [**normal CALCIUM**] / [INC ALP] / [INC Technetium uptake bone scan]] c. [**Tx**(bisphosphonate>calcitonin) initiated once PHLOATsx start] ## Footnote d.[**SxPHLOAT**: -Platybasia*(= skull base flattening which → foramen magnum impingement & auditory foramen closure → hearing loss, neuro∆ )* -High output HF -Lentiasis Ossea*(→HA, Hat size⇪)* -Arthritis 2º *(normocalcemia +/- hypercalciuria | immobilization hyperCalcemia) * -Tibia bowing/bone pain \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_x\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *etx: abnl osteClast⼀then⼀osteoBLAST → ⇪ bone turnover with _abnml remodeling_ → [⇪ALP + ⇪ technetium uptake bone scan + PHLOATsx]*
120
# Pelvic insufficiency fragility fracture cp (3) * * * exam (3)
121
# Pelvic insufficiency fragility fracture dx (2) * * * mgmt (2)
*persistent groin pain with impaired ambulation*
122
cp of Osteoarthritis of the Hip
insidious chronic groin pain with impaired ambulation exacerbated by active AND passive ROM
123
⬜ and ⬜ are the two pillars of [acute Lumbosacral back strain]; in which patients are normally advised to ⬜
[acute low back pain] + [paraspinal TTP]; (with NSAIDs/heat/massage/spinal manipulation) maintain nml activity with gradual introduction of regular exercise as pain improves *only a small number of acute LBP → chronic LBP*
124
# Only a small number of acute LBP develop chronic LBP What are poor prognosticators for acute Lumbosacral strain? | *ie indicates poor prognosis/long term disability/chronic LBP*
1. needs opioids for pain 2. Psych hx (MDD, anxiety) 3. Pessimistic Recovery Expectation (rehabilitative despair, avolition) 4. fxn SEVERELY impairment
125
How do Glucocorticoid affect Bone?
126
Patients on long term CTS are at INC risk for Osteoporosis. How should you reduce this risk in general? (5) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [CTS Pts] who are *High Risk for Osteoporotic Fracture* should also receive ⬜. How do you determine if a patient is *High Risk for Osteoporotic Fracture* ? (3)
1. [Vitamin D daily≥800 IU/day] 2. [Ca+≥1200 mg/day] 3. Weight bearing exercise 4. Minimal CTS dosage 5. [DEXAq1-2y] * * * [bisphosphonate*(if *High Risk for Osteoporotic Fracture* )*]
127
Denosumab MOA * * * indication
monoclonal Ab that binds to [osteoBlast **RANK-L** (nuclear factor-kappa B ligand)], --BLOCKS it from interacting with [osteoclast *progenitor* **RANK**] → ⬇︎bone resorption * * * osteoporosis in patients who fail/cannot tolerate bisphosphonates
128
The most common cause of [hypercalcemia with elevated PTH] is ⬜. b. Why is it important to differentiate this from [Familial hypOcalciuric Hypercalcemia]? (2) c. How do you differentiate the two? d. what's the treatment for each?
[Primary Hyperparathyroidism (PHPT)]; * * * b. ▶fhH = auto DOM defective [Ca+ sensor (CaSR)] → {[higher levels of Ca+ are needed to suppress PTH → elevated PTH] + [defective CaSR causes INC renal reabsorption of Ca+]} = elevated Calcium and elevated PTH (similar to PHPT) ▶you must differentiate them because: fhH follows a benign course vs [PHPT has suboptimal complications (osteoporosis, nephrolithiasis, CKD)] * * * c. [UCCR (**U**rine:Serum**C**a+)➗(Urine:Serum**C**reatinine) **R**atio] = [(UrineCa+/SerumCa+) ➗ (UrineCreatinine/SerumCreatinine)] - [**fhH** \< (0.01--*UCCR* --0.02) \< **PHPT**] * * * d. fhH = reassurance | [PHPT = Parathyroidectomy \> (serial monitoring)]
129
Transient Synovitis is a common cause of HIP pain in peds age ⬜. Describe the clinical presentation -4 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Tx?
[3-8 yo] 1. [Hip pain + Limp but able to bear weight still] 2. often status **post**(viral)infection 3. small hip effusions on US 4. no-to-low fever \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ NSAIDs (since self limited to 1-2 weeks)
130
Juvenile Idiopathic Arthritis MOD
**J**uvenile **I**diopathic **A**rthritis = [**J**oint **I**nflammation by **A**utoantibodies] *➜ Juvenile chronic pain/Juvenile chronic swelling of multiple joints (wrist/ankles)*
131
Tx for [*Scleroderma Systemic Sclerosis* renal crisis] -2
Captopril (if HTN) + Nitroprusside IV (if CNS or papilledema) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *SSS etx: abnormal deposition of collagen in multiple organ systems*
132
*Scleroderma Systemic Sclerosis* = abnormal autoimmune collagen deposition in 9 organ systems Name and describe all 9 organ systems affected by *SSS*
*SSS ***CULT GIVES** *CREST* disease! **C**ardiac: myocardial fibrosis|pericarditis|pericardial effusion **U**roRenal: [_scleroderma_ renal crisis(sx: HTN, oliguria, thrombocytopenia, MAHA / tx: captopril + Nitroprusside IV)]|ESRD **L**ung: ILD\_diffuse|PAH\_Limited CREST [**T**est:Topoisomerase 1\_Scl70 antibody(also Anticentromere)] serology delineates *SSS* etx **G**I:_GERD_|esophageal dysmotility **I**ntegumentary: telangiectasia|sclerodactyly|digital ulcers|calcinosis cutis **V**ascular: [_Raynaud phenomenon_], HTNcaptopril tx **E**xtremities: arthralgias|contractures|myalgias **S**ystemic: fatigue|weakness * * * _**\_\_\_**_\_ = _scleroderma_
133
Dx? | Management?-2
Vetebral Compression Fracture pain control + resume normal activity ASAP (NO unnecessary bed rest)
134
Explain what an XR with a posterior fat pad indicates?
[*(OCCULT/nondisplaced)* Supracondylar Humeral fracture] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *fat pad = radiolucency posterior to humerus that represents displaced fat 2/2 traumatic elbow effusion (likely 2/2 an occult Supracondylar Humeral fracture)*
135
What are the clinical features of a [Supracondylar Humeral Fracture] -2
136
Tx for [Supracondylar Humeral Fracture] that's: Nondisplaced ? (2) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Displaced?
long arm splint | sling \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [surgical reduction with pinning]
137
Why are pts who've experienced 1 shoulder dislocation, at even higher risk for experiencing recurrent shoulder dislocations? -2
[residual **ligament instability/laxity**] + [incomplete healing of prior labral tears]
138
sx of Anterior Shoulder Dislocation -4
"I **ASAP** has *ANT shoulder dislocation* 1. **A**cromion prominent 2.**S**houlder flat 3.**A**Bduction and External Rotation of Arm 4.**P**rominent humeral head \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *ANT shoulder dislocation of [glenohumeral shoulder joint]*
139
What is the **best** diagnostic test for [osteomyelitis of the foot]? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Name the test used at bedside for [osteomyelitis of the foot], and why it is not the best test?
contrast MRI \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [probe-to-bone testing] (*usually done first and not sensitive...so* *if negative, still must use contrast MRI to r/o infxn)*
140
Diabetic foot infections with osteomyelitis require ⬜ to determine microbial involvement
**BONE BIOPSY WITH CULTURE**
141
How does Cyclosporine affect Gout?
**C**yclosporine [⬇︎ uric acid excretion] ➜ INC GOUT | **"CLAP.NET.SLD** *sold* Gout"
142
What is Spondylolysis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Dx?
[**FATIGUE FRACTURE of pars interarticularis**] 2/2 overuse injury ➜ [dull/achy lower back pain with radiation to butt and thigh, ⇪ with activity, ⬇︎ with rest.] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Dx = Lumbar Spine XR
143
Spondylolysis Tx? -2
[activity modification x 90 d] + [symptom control x 90 d]
144
*Septic Arthritis may lack classic signs in infants* What clinical presentation should you expect? (4)
[*infant* **Pseudoparalysis** (won't move affected joint)] [*infant* ⇪ inflammatory markers] joint effusion [aversion to being held] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *tx = debridement + IVA* *(IVA = IV antibiotics)*
145
Scoliosis is mostly caused by ⬜ What clinical features are c/f *pathologic* Scoliosis (i.e. spinal tumor)? -4
idiopathic \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Back Pain / Neuro ∆ / [rapid progressive curve] / [abnormal vertebrae]
146
a. What sx do Marfan and Ehlers Danlos have in common? -4 ## Footnote * * * b. How are the etiologies of Marfan and Ehlers Danlos different?
[MSK (joint hypermobile / Pectus excavatum / Scoliosis)] [Cardiac: MVP] * * * ed= [AUTO DOM *COl5A1/5A2 mutation*] faulty collagen synthesis vs MARFAN=[AUTO DOM *Chromo 15 FBN1 mutation*] defective fibrin(scaffold for elastin) → connective tissue disorder affecting skeleton/heart/eyes
147
Between Marfan and Ehlers Danlos, which is a/w [transparent, **velvety** skin & easy bruising]?
ed
148
Between Marfan and Ehlers Danlos, which is a/w [aortic root Dilation]?
MARFANS
149
Between Marfan and Ehlers Danlos, which is a/w Lens/Retinal dislocation?
MARFANS
150
Between Marfan and Ehlers Danlos, which is a/w spontaneous PTX?
MARFANS
151
Between Marfan and Ehlers Danlos, which is a/w [Berry Saccular Aneurysm]?
ed
152
Between Marfan and Ehlers Danlos, which is a/w [Uterine Prolapse and Hernia]?
ed
153
In [Scleroderma Systemic Sclerosis], list the 2 long term complications for SSS type: [Diffuse Cutaneous (Anti Scl70\_topoisomerase1)] -2 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [*CREST* Limited Cutaneous (AntiCentromere)] -2
[Diffuse Cutaneous (Anti Scl70\_topoisomerase1)] = Interstitial Lung Dz + Renal Crisis \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [*CREST* Limited Cutaneous (AntiCentromere)] = pulmonary htn + Renal Crisis * * *
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Why do patients with [(SSS) Scleroderma Systemic Sclerosis] receive routine Pulmonary Function Test when diagnosed ?
Both SSS types {[Diffuse\_SSS (ILD)] and [CREST Limited\_SSS (PAH)]} ➜ [⇪ Lung pathology] = PFT (to guide/track disease)
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Name and Describe the test used to diagnose [Achilles tendon complete rupture]
**Thompson test** while patient is prone, MD squeezes patient’s calf ➜ [NO plantar flexion = RUPTURE] vs [+plantar flexion = Achilles intact]
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Tx for Fibromyalgia -4
1st: Aerobic Exercise 2nd: [TCAs | SNRIs | muscle relaxer]
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***F**ibro**M**yalgia is a clinical diagnosis* What labs are ordered to rule out other similar conditions? -3
TSH / CBC / ESR \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ***F**ibro**M**yalgia*
158
What are the 4 most common causes of Myopathy (⬆︎ CPK)
**S**tatins **P**robably **h**urt **M**uscles 1. **S**tatins 2. **P**olymyositis vs. Dermatomyositis (autoimmune) 3. **M**uscular Dystrophy 4. **h**ypOthyroidism (OR HYPERthyroidism)
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⬜ should always be considered in patients with multiple complicated fractures. What is the symptom triad for this condition? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How is this prevented?
Fat Embolism ; **PBS** **P**etechial rash **B**rain impairment [**S**OB (respiratory insufficiency)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Early immobilization and operative fixation of fracture \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *HEPARIN/ENOXAPARIN DOES NOT AFFECT FAT EMBOLUS*
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clinical presentation for Meniscal tear
subacute or chronic **LOCKING/CATCHING** sensation of the Knee ## Footnote +/- ➜ gradual effusion
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how are hip fractures in the elderly managed? (2)
[ambulatory/stable] = **ORTHO SURGERY WITHIN 48H** [non-ambulatory/dementia/medically unstable] = Nonoperative management
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# define Spondylolisthesis \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ clinical presentation
ANT slippage of 1 vertebral body over another 2/2 BL **defects of the [pars interarticularis (spondylolysis)]** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Teen athlete who performs repetitive back extension and rotation ➜ low back pain exacerbated by lumbar extension ## Footnote *tx = analgesics / activity cessation x 90d*
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Classic triad for [Spinal Epidural Abscess]
1-focal back pain 2-neuro deficits 3-fever *dx = contrast MRI*
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Spinal Epidural Abscess p/w ⬜ ⬜ and ⬜ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How do you manage SEA? (4)
focal back pain / neuro deficits / fever \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ## Footnote 1. [contrast MRI spine] 2. [Infxn labs (*CBCec*)] 3. [IV Vanc + Ceftriaxone] 4. [Emergency Surgical Decompression/I&D within 24 HOURS] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_x\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ CBCec = infxn labs = CBC/BCx/Culture specific (i.e. spinal aspirate cx)/ESR/CRP
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What are the 5 steps to appropriately transport an amputated extremity? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How long will this sustain viability?
"**SPLIT** extremity!? wrap in... " **S**aline moistened gauze. THEN put in- **P**lastic bag. **L**id seal bag shut before putting it on **I**ce/Saline 50/50 mix bed. to keep **T**emperature ideal (33.8 - 50 F) as to NOT FREEZE extremity \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 24 hours
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In Spinal Stenosis, pts pain is usually exacerbated with _____(flexion/extension) and _____. It is accompanied with ___ symptoms
spinal st**EEE**nosis **E**XTENSION ; **E**xertion (vascular claudication) ; neurological ## Footnote *Shopping cart sign (l**E**aning over for relief) = Spinal st**E**nosis = exacerbated with **E**xtension and **E**xertion*
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You see an elderly patient leaning over to relieve their pain ⬜ is suspected. How is it confirmed? management? (2)
[Spinal St**E**nosis secondary to Osteoarthritis joint degeneration] ; MRI spine \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx =[lumbar epidrual block] --(if persist)--\> [Laminectomy surgical decompression] *Shopping cart sign (l**E**aning over for relief) = Spinal st**E**nosis = exacerbated with **E**xtension and **E**xertion*
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In Lumbar disc herniation, pts pain is usually exacerbated with _____(flexion/extension) and accompanied with ___ symptoms
**flexion** ; UNILATERAL radiculopathy and neurological sx
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[AOOD (avascular osteonecrosis osteochondritis dissecans)] etx \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ dx
osteonecrosis (from "**A****_S_****EPTI****_C_**") of [small foot/hand bones], proximal tibia, femoral head, vertebrae, humeral head ➜ bone collapse ➜ joint replacement \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ MRI *stage 4 AOOD ➜ Total Hip Replacement*
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*Pt jumps from a ladder, landed and now has acute R knee pain* what injury is he likely to have? why? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Describe the XR \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ management?
R patellar tendon rupture ; sudden forceful unopposed quadricep contraction (landing after jumping) ➜ patella tendon rupture = ANT knee pain/effusion , **[inability to extend knee]** or [**maintain a straight leg with flexed hip**] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ high-riding patella * requires surgery in \< 10d* * patellar stress fx conversely is gradual osnet, not sudden*
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When are [TNFα inhibitors] used in RA therapy? What's the major caution with these drugs, and how is this managed? (2)
RA patients who fail first-line therapy*"Norris DMARD... **M**eans → **LASH**"* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [a/w opportunistic infections (i.e. reactivates latent TB)] so... screen with [TB PPD] or [interferon gamma release assay] prior to [TNF inhibitors] | 6.[**T**NFα inhibitors = *g-e-i-c-o*] ## Footnote *"Norris DMARD...**M**eans **LASH** **T**erribleg-e-i-c-o"*
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Name the 6 major Treatments for Rhematoid Arthritis
DMARD (Disease Modifying AntiRheumatic Drug)​ *"Norris DMARD...**M**eans **LASH** **T**erribleg-e-i-c-o"* 1. [**M**TX (initial DMARD)] 2. **L**eflunomide 3. **A**zathioprine 4. **S**ulfasalazine 5. **H**ydroxychloroquine 6. [**T**NFα inhibitors*g-e-i-c-o*]
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Sarcoidosis Etx-2 (Etiology)
[CD4 Helper T] inappropriately respond to environmental triggers + Suppressed TRegs --\> Non-Caseating Granulomas in Lung ## Footnote *Image showing b/l Hilar LAD*
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Sarcoidosis Tx-5
"Sarcoidosis is a **0-SCAM**" **0**bservation if asx (MAJORITY) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **S**teroids **C**yclosporine(Calcineurin inhibitor) **A**zathioprine(Calcineurin inhibitor) **M**TX | **SCAM** only if Sx
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Major causes of Rhabdomyolysis - 4
1. Immobilization prolonged (direct damage) 2. Cocaine (direct damage) 3. Physical restraints 4. Dehydration ## Footnote Muscle breakdown --\> ⬆︎CPK, ⬆︎K, ⬆︎myoglobin(which causes renal damage when filtered)
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causes of AOOD [Avascular Osteonecrosis Osteochondritis Dissecans]- 11
**A****_S_****EPTI****_C_** **A**ntiphospholipid syndrome **S**LE | Sickle Cell Disease | [Storage (Gaucher's) Disease] **E**tOH **P**ancreatitis **T**rauma **I**nfection*HIV* **C**TS*>20mg/day* | [CKD/HD/Renal\_transplant] | [Caisson's*"the bends"*] *MRI = most sensitive dx*
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Dx for AOOD [Avascular Osteonecrosis Osteochondritis Dissecans]
MRI | etx: (" "**A****_S_****EPTI****_C_**" → AOOD)
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3 Main causes of Spinal Cord Compression
1. **DJD Disc Herniation** (Smoking risk factor) 2. [Epidural Staph a. Abscess (think IV drug user vs DM)] 3. Tumor (Prostate/Renal/Lung/Breast/Multiple Myeloma mets) ## Footnote Dx = MRI, Positive Straight Leg, Classic S/S *DJD=Degenerative Joint Disease*
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[Polymyalgia Rheumatica (PMR)] affects [\_\_\_\_(demographic)]
[\> 50 yo]
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tx for [PolyMyalgia rheumatica (PMR)] -2
LowDoseCTS(Prednisone) ## Footnote ▶*⚠️(but if ⊕GCTA)--> HIGH_DOSECTS*
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[PDO] etx (3) ## Footnote [PDO- Paget\Disease of bone\Osteitis deformans]
{**Accelerated (and Disorganized) _focal_ bone remodeling → [⇪ALP P.H.L.O.A.T.]}** ## Footnote 2/2 a.[ *Acclerated*/⬆︎osteoClast dysfxn ]*→ ⇪ALP and ⇪Urine HydroxyProline* f/b b. rapid subsequent osteoBlast resposne(formation of woven and lamellar bone in *disorganized mosaic pattern*) ]*→ PHLOAT* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_x\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ⚠️*tx = bisphosphonates* ⚠️Urine HydroxyProline measures bone turnover
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PDO cp -7 *most common cause of asymptomatic ALP ⬆︎ in elderly* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [PDO- Paget\Disease of bone\Osteitis deformans]
“a *PDO* [⇪ALP+ **P.H.L.O.A.T.**]” *⇪ ALP(and ⇪Urine Hydroxyproline)*✳ *(from ⇪ osteoClast resorption)* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **P**latybasia(narrowing of foramen magnum) **H**eart failure (from ⇪ bone vasculature → ⇪ AV shunts → high output HF] **L**eontiasis Ossea(enlarged cranial bones → ⇪ hat size, hearing loss from CN8 entrapment) **O**steoFibroma vs OsteoSarcoma **A**rthritis **T**ibia bowing / long bone chalk-stick fractures / bone-joint pain ## Footnote *bx: disorganized **mosaic** pattern of woven & lamellar bone* *tx = bisphosphonates*
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Lab values for PDO - 4 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [PDO- Paget\Disease of bone\Osteitis deformans]
1. ⬆︎ALP 2. ⬆︎Urine Hydroxyproline (measures bone turnover) 3. NORMAL CALCIUM 4. NORMAL PHOSPHOROUS ## Footnote *bx: disorganized **mosaic** pattern of woven and lamellar bone* *tx: bisphosphonates*
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Tx for PDO ## Footnote \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [PDO- Paget\Disease of bone\Osteitis deformans]
Bisphosphonates ## Footnote *bx: disorganized **mosaic** pattern of woven and lamellar bone* *tx: bisphosphonates*
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What is the most common cause of asymptomatic isolated ALP ⬆︎ in the elderly?
[PDO- `_Paget\Disease of bone\Osteitis deformans_`] ## Footnote * bx: disorganized **mosaic** pattern of lamellar bone* * tx = bisphosphonates*
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Dx for PDO - 2 | [PDO- Paget\Disease of bone\Osteitis deformans]
Xrays showing lesions{osteolytic or [mixed osteolytic⼀osteosclerotic]} --\> [radionuclide bone scan for confirmation] ## Footnote *bx: disorganized **mosaic** pattern of woven and lamellar bone* *tx: bisphosphonates*
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\_\_\_\_\_ loss is a common complication of [PDO] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx? | [PDO- Paget\Disease of bone\Osteitis deformans]
hearing \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Bisphosphonates *(treatment only slows progression)*
188
Name the Conditions associated with granulomas -6
1. TB 2. Syphilis tertiary gummas 3. Blastomycosis 4. Histoplasma 5. Sarcoidosis 6. [Churg Strauss Eosinophilic Granulomatosis with Polyangiitis]
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Dx Sarcoidosis (2)
1. Endobronchial bx by Bronchoscopy 2. Clinical (CCUBBEDD)
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Rheumatoid Arthritis centers around the _______ treatment group, which take _______ to onset
**DMARD** ; **weeks** ## Footnote *"Norris DMARD...**M**eans **LASH** **T**errible*g-e-i-c-o*"*
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scoliosis \_\_\_\_\_\_\_\_\_\_\_\_\_ treatment -3
* [CAST GOE10°] ➜ [back brace v observation] * [CAST GOE40°] ➜ surgery \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *CAST: Cobbs Angle Scoliometry Test*
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scoliosis \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ dx
[CAST GOE10°] ## Footnote \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *CAST: Cobbs Angle Scoliometry Test*
193
How do CTS impair the immune system? -3
CTS … - ⬇︎ **neutrophil**'s adhesion to inflammatory sites - sequesters **eosinophils** in lymph nodes - causes **lymphocyte** apoptosis
194
How does [estrogen E2] affect bone? -2
[Estrogen E2] BUILDS BONE by… - **B**locks osteo**B**last (Build bone by secreting collagen and catalyzing mineralization) apoptosis - **C**auses osteo**C**last(Cut up/dissolve bone by secreting acid and collagenases apoptosis. (Derived from macrophage/monocyte)
195
# Colchicine is used for what 2 indications? MOA? -3
[Gout **Treatment** *ACUTE*] ; [Gout **Prophylaxis**] * * * Binds and stabilizes tubulin to inhibit microtubule polymerization → DEC neutrophil chemotaxis → DEC neutrophil degranulation
196
# Define: A. Acute phase reactants B. C-reactive protein (3)
A. Liver-made proteins (induced by IL-6) whose serum concentrations significantly change in response to inflammation * * * b. CRP = Opsonin ; fixes complement and facilitates phagocytosis ; [Measured clinically as sign of ongoing inflammation = Acute Phase Reactant]
197
What does TNFα do? (4) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How do we stop it (3)?
"TNFα makes me C-G-S-W!" **mediates…** 1.[**C**A Cachexia] 2.[**G**ranulomas*(secreted by macrophages to maintain Granulomas → protects against TB! ⚠️ (always test for latent TB before starting AntiTNFα since AntiTNFα can → granuloma break-down → disseminated TB))*] 3.[**S**hock*activates endothelium ➜ vascular leak ➜ hypOtension*] 4.[**W**BC recruitment*(targeted by DMARD)*] ## Footnote [***g-e-i-c-o*** TNFα inhibitors] = tx **A**dalimumab: [anti-TNFα] monoclonal Ab **E**taner**_CEPT_**: TNFα decoy re**_CEPT_**or **I**nfliximab: [anti-TNFα] monoclonal Ab
198
# Parathyroid hormone is secreted by ⬜ cells of the ⬜ Name the functions of PTH (9)
Chief ; Parathyroid gland 1. [ kicks OUT (PO34) *(by ⬇︎renal PCT reAbsorption)*] → [ ⬇︎P] (and [⇪P{in urine}] 2. [ ⇪ renal DCT Ca+ reAbsorption] → [ ⇪Ca+] 3. [⇪ bone resorption] → [ ⇪Ca+][ ⇪ P] 4. [ ⇪ renal PCT 1α-hydroxylase activation ] → [ ⇪ 1,25VitD] → [ ⇪Ca+][ ⇪ P] 5. [ (⇪ macrophage colony stimulating factor) → ⇪ osteoclast precursor] 6. [(⇪ osteoblast_RANK-L) → ( ⇪ osteoclast activation) 7. Intermittent PTH → bone FORMATION 8. [PTH ⇪ with mild ⬇︎ Magnesium (causes of Mg⬇︎: diarrhea, aminoglycoside, diuretics, EtOH)] 9. [ PTH⬇︎ with SEVERE ⬇︎⬇︎Magnesium] OVERALL: [ INC serum Ca+] [ DEC serum (P)] [ INC urine_(P)]
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# PCN A. MOA B. which organisms are treated with PCN? (3)
contains [βlactam ring DSA*D-Ala-D-Ala* Structural Analog] which bind to [microbe's PBP] --> prevents [microbe PBP] from cont cross-linking [microbe's peptidoglycan cell WALL]→no [microbe peptidoglycan cell WALL] synthesis → microbe DEATH \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ b. [gram ⊕], [gram negative cocci], [Treponema Pallidum *Spirochete*] | *🔎PBP = [Pencillin Binding Protein transpeptidase]* ## Footnote note: PCN is sensitive to [microbial βLactam**ASES** (which cut/inactivate PCN's [βLactam ring DSA] →inactivates PCN --> allows [microbial PBP] to cross-link Peptidoglycan Cell WALL