11 ⼀RHEUM-ORTHO/ TOX II/ Rx+ Flashcards
Diagnosis?
GOUT
juxtaarticular erosions or tophi on XR
how do you confirm acute Gout diagnosis?
Arthrocentesis showing [negatively birefringent needle crystals]
_________________
remember: serum uric acid can be normal or low during acute gout attack
Pseudogout is characterized by what findings ?-4
PRPB
1.[Pseudogout CPPD]
2.Rhomboid
3.[Positive birefringence under polarized light]
4.[Blue under parallel polarized light]
CPPD = [Ca+ Pyrophosphate Dihydrate]
What electrolyte abnormality is a risk factor for Pseudogout?
HYPERCalcemia (look for constipation!)
Pseudogout features = PRPB
[Chondrocalcinosis (calcified articular cartilage)] is seen in ⬜?
_________________
Pts with this condition should be worked up for what possible causes - 4
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?
Most Gout attacks initially occur where?
Asymmetric Inflammatory Monoarthritis
1st MTP joint = Podagra
Name the precipitants of Gout attacks(cause Hyperuricemia) -10
“CLAP.NET.SLD sold Gout”
“CLAP.NET.SLD sold Gout”
- Cyclosporine
- Lasix Furosemide
- ASA 81
- PyrazinamideTB tx
- Niacin
- EtOH
- Thiazides
- Surgery
- LARGE meals
- Dehydration
Gout or Pseudogout?
Based on answer: What type of polarized light is A ? C?
GOUT!(based on needle shape)
Since dx = Gout… then polarized light…
A = Perpendicular
C = Parallel light(GOUT is Yellow under parallel light)
Gout Etx -2
90% from underexcreted uric acid
10% from overproduction of uric acid (myeloproliferative disorders such as polycythemia vera)
Conditions associated w/Pseudogout -4
- [AOHHemochromatosis]
- hypOthyroid
- HyperParathyroid
- Osteoarthritis
AOH = Arthropathy of Hereditary
Tx for Acute Gout (3)
Also tx for Acute Pseudogout
Tx for Chronic Gout -3
- Febuxostatxanthine oxidase inhibitor
- Allopurinolxanthine oxidase inhibitor
- Probenecid
Gout [px] and [acute tx] = NSAIDs, colchicine, CTS
Px for Gout -3
- NSAIDs
- Colchicine
- CTS
Same as tx for Acute Gout
Acute PseudoGout Tx -3
- NSAIDs
- Colchicine
- CTS
Also tx for Acute Gout
what is the recommended dietary Calcium intake per day?
1200-2000
mg/day
Recommended dietary Vitamin D intake per day?
800-4000
IU/day
sunlight (15 min 2x/week)
Name the 5 groups that should receive Osteoporosis screening via ⬜
DEXA
_________________
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
[Ca+ ≥1200 mg/day]
and
[VitD ≥800 IU/day]
_________________
also [wt bearing exercise], avoid EtOH, avoid smoking,
For Women, when is Bisphosphonate therapy indicated? -3
_________________
bisphosphonate MOA = competitively binds to Bone Hydroxyapatite before osteoClast can bind ➜ prevents bone resorption
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]
There are 3 stimulators of ⬜ which ➜ bone formation. What are they?
osteoBlast
_________________
“P-E-V stimulates new bones for me!”
PTH
[E2 (EstraDiol)]
[Vitamin D]
Osteoporosis can be clinically defined as ⬜
List the 2 PRIMARY causes of Osteoporosis
([⬇︎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)]
Osteoporosis can be clinically defined as ⬜
List the 8 SECONDARY causes of Osteoporosis
([⬇︎BMD>2.5 below YAM] despite normal mineralization)
_________________
🔎BMD = [Bone Mineral DENSITY]|| 🔎YAM = [Young Adult Mean (DEXA T Score)]*
[Peak Bone Mass] occurs age ⬜ and Normal [Bone Mineral Density] = ⬜
clinically define:
osteopenia
_________________
OSTEOPOROSIS
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
clinical presentation of Osteomyelitis -3
_________________
FIF
Focal Bone Pain / Inflammatory markers / Fever
_________________
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 *}
_________________
FIFsx
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}
🔎BMD = [Bone Mineral DENSITY]|| 🔎YAM = [Young Adult Mean (DEXA T Score)]
How is the Thyroid associated with Bone?
⇪ Thyroid ➜ [⇪ osteoClast activity] ➜ [⇪ Bone Resorption] eventually→ {[2º Osteoporosis(⬇︎Bone Mass Density)}
in patients with primary hyperparathyroidism, which 2 criteria qualifiy them for Parathyroidectomy?
- PRAP[symptomatic Hypercalcemia]
- [1º hyperPTH < 50 year old (young patients are likely to get complications later)]
(PRAP: painful bones/renal stones/abd groans/psychic moans]
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)]
- [convexity >60° ] = surgical correction
- chronic pain (from Kyphosis) = surgical correction
tx for [Adhesive Capsulitis frozen shoulder syndrome] (2)
[ROM exercises] –(if severe)–> [CTS injection]
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 ➜ stifffrozen shoulder
_________________
- idiopathic
- Rotator cuff tendinopathy
- subacromial bursitis
- stroke
- DM
- humeral head fx
What is the major risk of improperly managed Scaphoid fracture? (2)
avascular necrosis ➜ NONUNION
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!
⬜ 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)]
Why do patients with Polymyositis have to be regularly monitored with ⬜ ?
PFT
_________________
Polymyositis can ➜ Pulmonary❌:
-ILD
-Infxn (from immunosuppresion)
-Pulm muscle weakness
-[MTX-inducedPneumonitis]
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)
[Polymyositis and Dermatomyositis] Tx - 2
________________
helicotrope rash in image
MTX
and
CTS (minimizes MTX side effects)
list clinical features for:
Polymyositis -4
________________
Dermatomyositis -8
Polymyositis:
-[proximal shoulder weakness symmetric]
-[pulmonary❌(ILD - ground glass on HRCT)]
-Endomysial inflammation
-CD8
________________
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.
Myasthenia is normal
PolyMyalgia Rheumatica sx -3
_________________
PMR occurs age > 50 yo
PolyMyalgia Rheumatica
[Painfully Stiff Shoulders & Hips (especially in Morning)]
[Malaise +/- wt loss]
[Really hot (Fever)]
PMR Tx =LCTS (if ⊕GCTA)–> HCTS
PMR DOESNT HAVE TO BE CONCOMITANT WITH GIANT CELL TEMPORAL ARTERITIS. CAN OCCUR ALONE</sub>
Labs for Polymyalgia Rheumatica -3
⬆︎ESR
⬆︎CRP
normal CPK
___________________________x____________________________________
PMR pts have NORMAL strength but have painful (morning) stiffness || PMR can occur independent of Giant Cell Temporal Arteritis
clinical features of FibroMyalgia 2
________________
how long do these have to be present for diagnosis?
FibroMyalgia
________________
[Fatigue +/- psych❌]
[Musculoskeletal💢 Widespread]
________________
≥3 mo
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
Mgmt for giant cell temporal arteritis(2)
- [HIGH dose CTS]*low dose CTS for PMR alone *
+
- [temporal artery biopsy]
GCTA dx confirmation = ⇪ ⇪ ⇪ ESR
[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]
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
What is [Neuropathic Charcot Arthropathy]? -4
[DM or Dorsal Column disease (B12 deficiency)]➜ impaired sensation/proprioception ➜
- acute: repetitive foot trauma and inflammation ➜
- subAcute: Osseous destruction on XR (phalangeal osteolysis, metatarsal head disappearance resembling “sucked candy”)
➜ 3. CHRONIC: IRREVERSIBLE BONE DESTRUCTION DESPITE INFLAMMATION RESOLUTION
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]
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)]
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…Means LASH Terrible*g-e-i-c-o*”
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…Means LASH Terribleg-e-i-c-o”
1. [MTX (initial DMARD)]
2. Leflunomide
3. Azathioprine
4. Sulfasalazine
5. Hydroxychloroquine
6. [TNFα inhibitorsg-e-i-c-o]
“Norris DMARD…Means LASH Terrible*g-e-i-c-o*”
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
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
Chronic MTX may ➜ ⬜ depeletion and produce a ⬜ Anemia
________________
Tx for this?
[THF] ; [mAcrocytic megaloblastic]
________________
[FH4reduced folinic acid (usually utilized by cells)] = RxLEUCOVORIN
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*
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)] =
Name the 2 treatment options for RayNAud phenomenon
Nifedipine
Amlodipine
_________________
RayNAaud phenomenon
passive smoking exacerbates this condition
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)
- CBC
- [RF & antiCCP]
- UA
- CMP
- Complement levels
- ANA
- CRP
- ESR
[RCsM] stands for ⬜
_________________
Describe MOD of [RCsM]?
RCsM : {[Renal osteodystrophy = CKD which eventually ➜ secondary hyperparathyroidism)} ➜ Mineral bone disorder] 📸
_________________
[dietary Phosphate restriction +/- phosphate binders] –(once (P) normalizes)–> [VitD supplement]
[RCsM] stands for ⬜
_________________
What is the treatment for RCsM ? (3)
RCsM = [Renal osteodystrophy = (CKD ➜ secondary hyperparathyroidism) ➜ Mineral bone disorder] 📸
_________________
[dietary Phosphate restriction +/- phosphate binders] –(Phosphate normalizes)–> [VitD supplement]
In terms of Bone physiology, elevated ALP indicates what?
[INC bone turnover (Ca+ resorption)]
[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)]
[Arthropathy of Hereditary Hemochromatosis] commonly affects which body parts? (5)
_________________
dx?
etx?
- Shoulders
- [2nd MCP]
- [3rd MCP]
- Knees
- ankles
_________________
Dx =[Pseudogout ⼀joint aspiration]
{[excess joint iron deposition] ➜ [positively birefringent rhomboid CPPD crystal] joint accumulation ➜ causes acute inflammation that resembles Gout = PSEUDOgout ➜ [Pseudogout⼀joint aspiration]dx}
Explain the extra advantage with the treatment (⬜ name tx) for Hereditary Hemochromatosis
serial phlebotomy
_________________
[serial phlebotomy] ➜ [⬇︎ cirrhosis progression] ➜ [⬇︎HepatoCellularCarcinoma]
Reiter’s Reactive Arthritis
Name the 3 inciting factors
“can’t PEE ⼀can’t see, can’t bend my knee”
- [HLA-B27 positive (is RF but only 30% develop RRA)]
- Chlamydia
- Salmonella
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
Oligoarthritis = joint pain/swelling of ⬜ in number
_________________
How do you evaluate Oligoarthritis? 📋
1-4
Nontraumatic [Acute(<4 wks) Back pain]
workup
N.I.C.U.
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)])
patient presents with lateral shoulder pain exacerbated with ABduction and/or External Rotation
diagnosis?
[(RCN) Rotator Cuff tendonitis]
+ weakness = [RC TEAR]
if→stiffness= [RC AFSS “Frozen”]
Which 3 Rx are contraindicated in patients with Gout? (3)
HCTZ / Loop diuretics / LASA
_________________
🔎LASA = [(low dose) ASA]
note: serum uric acid level can be normal in gout attack so DO NOT use to guide mgmt
which antiHTN should be used in patients with Gout?
[ARB (losartan)]
_________________
note: serum uric acid level can be normal in gout attack. DO NOT use to guide mgmt
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}]
Patient suspicious for ankylosing spondylitis
What’s the 1st step in diagnosis?
_________________
How are these patients’ disease progress monitored? (2)
Sacroiliac joint XR
_________________
- Repeat XR in 3 mo
- Acute phase reactants (ESR)
Patient suspicious for ankylosing spondylitis
What are the 3 diagnostic criteria?
ALL 3 of:
- [Low back pain/stiffness GOE3mo] that improves with activity
- Limited lumbar spine ROM
- Limited chest expansion
Patient suspicious for ankylosing spondylitis
prognosis? (3)
- GOOD PGN
- NO INC MORTALITY
- NO PHYSICAL DISABILITY
Ankylosing Spondylitis most notable sign is ⬜
List the other extraarticular manifestations (5)
[Sacroiliac (bamboo spine) fusion]
Ankylosing Spondylitis = {[5 A’s + [Sacroiliac (bamboo spine) fusion]!}
- Anterior uveitis
- [Apical lung fibrosisrestrictive lung disease& inflammed costosternal joints]
- Aortic regurgitation
- IgA nephropathy
- [Ankleplantar fasciitis]
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
How is mobility related to Calcium levels?
_________________
How can this be managed?
extended immobilization ➜ Calcium release from bones ➜ [nonPTH hypercalcemia] ;
Bisphosphonates ⬇︎ bone turnover and preserve bone mass
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]}
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]
Dupuytren Contracture
treatment (4)
- modify hand tools(padded gloves, cushion tape)
- Needle aponeurotomy
- Intralesional CTS injection
- Surgery
idiopathic Fibrotic Thickening of palmar fascia at 3rd, 4th, 5th digits ➜ nodules along flexor tendon near distal palmar crease ➜ DEC finger extension
How do you diagnose Vitamin D deficiency?
[serum (25HydroxyVitaminD)] < 20
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
What causes Osteomalacia?
Osteomalacia cp?-2
Rickets is the pediatric version of Osteomalacia
Vitamin D deficiency;
- Bone Pain
- Muscle weakness
Imaging: ⬇︎Bone Density with Looser Zone Pseudofractures
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
vitamin D? Brian Sucks Killer Penis twice!
What are the major lab findings for Osteomalacia?-5
Rickets is the pediatric version of Osteomalacia
- Vitamin D Deficiency which –>
- ⬇︎Ca+
- ⬇︎Phosphorous
- ⬆︎PTH
- ⬆︎ALP
vitamin D? Brian Sucks Killer Penis twice!
vitamin D Deficiency causes [⬜ in Adults] and [⬜ in peds]
What are the risk factors for Vitamin D deficiency? (6)
Osteomalacia ; rickets
_________________
- poor Sun Exposure
- Heavy pigmentation
- Obesity
- Malabsorption
- Advanced age
- CKD
vitamin D? Brian Sucks Killer Penis twice!
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? Brian Sucks Killer Penis twice!
- Bone: [⇪ Ca+ and PO4 Resorption → Remodeling] but also… →
- Bone: [⇪ serum Ca+ → ⇪ Mineralization]
- [Small intestineduodenum: ⇪ Ca+ absorption]❗️
- [Small intestine: ⇪ PO4 absorption]
- Kidney: [⇪ Ca+ reAbsorption]
- Kidney: [⇪ PO4- reAbsorption]
- Parathyroid = ⬇︎PTH synthesis → [⬇︎PO4 renal excretion] → [⇪ serum PO4]
- Parathyroid = ⬇︎PTH secretion
[T or F] Primary Biliary Cirrhosis is associated with Bone Disease
TRUE
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
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)]
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)
⭐ [(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)]
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]
How do you diagnose SjoGren Syndrome? (3)
_________________
why is the lab test not 100% reliable?
- [antiRo-SSa] and/or
- [antiLa-SSB]
- [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)
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
What are the Main elements of SLE-15
RASHH ORR PAINN
Lab test for SLE -4
________________
Which lab test for SLE is first line?
Remember this:
“ANA & Dana saw HIS, Mr.Smith’s rash”
Hydroxychloroquine is effective in treating the ___ and ___ from SLE.
________________
What type of drug is it? SE-2?
RASHH ORR PAINN
Rash; Arthritis
________________
Anti-Malaria drug
________________
SE = [Vision⬇︎] and Nausea
List the Immunosuppressants used to treat [SLE Lupus] -6
“Lucky needs his Charms & [SLE Lupus needs her CHARMS”]
- CycloPHOSphamide
- Hydroxychloroquine
- Azathioprine
- [Rituximab antiCD20]
- MycopPHENolate
- [Steroid prednisone]
________________
RASHH ORR PAINN
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)
ParvoB19 is transient
[Antiphospholipid syndrome] etx
Lupus anticoagulant (2/2 SLE or idiopathic) –> [⬆︎Thrombosis and spontaneous abortion]
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
RASHH ORR PAINN
Lupus Nephritis MOD
[antidsDNA] deposits in the glomerulus and forms an IMMUNE COMPLEX with circulating Complement ➜ [⬇︎complement]
antidsDNA and complement are used to monitor renal involvement in Lupus Nephritis
[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
How should you advise a patient who complains of having recurrent episodes of uncomplicated lower back pain? (3)
- physical activity actually promotes resolution of initial uLBP sx and DEC uLBP future recurrence ➜
- during acute uLBP, maintain normal/moderate physical activity
- 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
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]
[UCCR = [(UrineCa+/SerumCa+) ➗ (UrineCreatinine/SerumCreatinine)]
Familial hypOcalciuric Hypercalcemia
treatment?
NO TX NECESSARY
[UCCR = [(UrineCa+/SerumCa+) ➗ (UrineCreatinine/SerumCreatinine)]
- [fhH < (0.01–UCCR –0.02) < PHPT]
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
[UCCR = [(UrineCa+/SerumCa+) ➗ (UrineCreatinine/SerumCreatinine)]
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]
What 2 labs must be assessed before starting a patient on a bisphosphonate? Why?
Serum:
- Ca+
- [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
Name the 3 DDx for ANTERIOR KNEE PAIN in a Young Patient
list typical patient demographic for each
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)=
▶<sub>Hx:</sub> most common cause of young adult (especially women) ANT knee pain
🄲
▶<sub>Sx:</sub>subacute/chronic poorly localized ANT knee pain worst with [quadricep contraction<sub>(up/down stairs, squatting, prolonged sitting)</sub>]
▶<sub>Dx:</sub> [PatelloFemoral Compression Test<sub>(pain from [knee extension with ANT patellar pressure])</sub>]
▶<sub>Tx:</sub>[biomechanical quadricep stretching/strengthening]
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)=
briefly describe
Anserine Bursitis
Acute pain/TTP to [Anserine Bursa (medial knee, distal to joint line)] = common cause medial knee pain
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]
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
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;
“the bisphosphon DRON”
- alenDRONate
- riseDRONate
- zoleDRONic acid
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]
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]
Pelvic insufficiency fragility fracture
cp (3)
exam (3)
Pelvic insufficiency fragility fracture
dx (2)
mgmt (2)
persistent groin pain with impaired ambulation
cp of Osteoarthritis of the Hip
insidious chronic groin pain with impaired ambulation exacerbated by active AND passive ROM
⬜ 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
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
- needs opioids for pain
- Psych hx (MDD, anxiety)
- Pessimistic Recovery Expectation (rehabilitative despair, avolition)
- fxn SEVERELY impairment
How do Glucocorticoid affect Bone?
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)
- [Vitamin D daily≥800 IU/day]
- [Ca+≥1200 mg/day]
- Weight bearing exercise
- Minimal CTS dosage
- [DEXAq1-2y]
[bisphosphonate(if *High Risk for Osteoporotic Fracture* )]
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
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 (Urine:SerumCa+)➗(Urine:SerumCreatinine) Ratio] = [(UrineCa+/SerumCa+) ➗ (UrineCreatinine/SerumCreatinine)]
- [fhH < (0.01–UCCR –0.02) < PHPT]
* * *
d. fhH = reassurance | [PHPT = Parathyroidectomy > (serial monitoring)]
Transient Synovitis is a common cause of HIP pain in peds age ⬜.
Describe the clinical presentation -4
________________
Tx?
[3-8 yo]
- [Hip pain + Limp but able to bear weight still]
- often status post(viral)infection
- small hip effusions on US
- no-to-low fever
________________
NSAIDs (since self limited to 1-2 weeks)
Juvenile Idiopathic Arthritis
MOD
Juvenile Idiopathic Arthritis = [Joint Inflammation by Autoantibodies]
➜ Juvenile chronic pain/Juvenile chronic swelling of multiple joints (wrist/ankles)
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
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!
Cardiac: myocardial fibrosis|pericarditis|pericardial effusion
UroRenal: [scleroderma renal crisis(sx: HTN, oliguria, thrombocytopenia, MAHA / tx: captopril + Nitroprusside IV)]|ESRD
Lung: ILD_diffuse|PAH_Limited CREST
[Test:Topoisomerase 1_Scl70 antibody(also Anticentromere)] serology delineates SSS etx
GI:GERD|esophageal dysmotility
Integumentary: telangiectasia|sclerodactyly|digital ulcers|calcinosis cutis
Vascular: [Raynaud phenomenon], HTNcaptopril tx
Extremities: arthralgias|contractures|myalgias
Systemic: fatigue|weakness
______ = scleroderma
Dx? | Management?-2
Vetebral Compression Fracture
pain control + resume normal activity ASAP (NO unnecessary bed rest)
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)
What are the clinical features of a [Supracondylar Humeral Fracture] -2
Tx for [Supracondylar Humeral Fracture] that’s:
Nondisplaced ? (2)
________________
Displaced?
long arm splint | sling
________________
[surgical reduction with pinning]
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]
sx of Anterior Shoulder Dislocation -4
“I ASAP has ANT shoulder dislocation
-
Acromion prominent
2.Shoulder flat
3.ABduction and External Rotation of Arm
4.Prominent humeral head
________________
ANT shoulder dislocation of [glenohumeral shoulder joint]
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)
Diabetic foot infections with osteomyelitis require ⬜ to determine microbial involvement
BONE BIOPSY WITH CULTURE
How does Cyclosporine affect Gout?
Cyclosporine [⬇︎ uric acid excretion] ➜ INC GOUT
“CLAP.NET.SLD sold Gout”
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
Spondylolysis
Tx? -2
[activity modification x 90 d]
+
[symptom control x 90 d]
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)
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]
a. What sx do Marfan and Ehlers Danlos have in common? -4
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
Between Marfan and Ehlers Danlos, which is a/w
[transparent, velvety skin & easy bruising]?
ed
Between Marfan and Ehlers Danlos, which is a/w
[aortic root Dilation]?
MARFANS
Between Marfan and Ehlers Danlos, which is a/w
Lens/Retinal dislocation?
MARFANS
Between Marfan and Ehlers Danlos, which is a/w
spontaneous PTX?
MARFANS
Between Marfan and Ehlers Danlos, which is a/w
[Berry Saccular Aneurysm]?
ed
Between Marfan and Ehlers Danlos, which is a/w
[Uterine Prolapse and Hernia]?
ed
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
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)
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]
Tx for Fibromyalgia -4
1st: Aerobic Exercise
2nd: [TCAs | SNRIs | muscle relaxer]
FibroMyalgia is a clinical diagnosis
What labs are ordered to rule out other similar conditions? -3
TSH / CBC / ESR
________________
FibroMyalgia
What are the 4 most common causes of Myopathy (⬆︎ CPK)
Statins Probably hurt Muscles
- Statins
- Polymyositis vs. Dermatomyositis (autoimmune)
- Muscular Dystrophy
- hypOthyroidism (OR HYPERthyroidism)
⬜ 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
Petechial rash
Brain impairment
[SOB (respiratory insufficiency)]
_________________
Early immobilization and operative fixation of fracture
_________________
HEPARIN/ENOXAPARIN DOES NOT AFFECT FAT EMBOLUS
clinical presentation for Meniscal tear
subacute or chronic LOCKING/CATCHING sensation of the Knee
+/- ➜ gradual effusion
how are hip fractures in the elderly managed? (2)
[ambulatory/stable] = ORTHO SURGERY WITHIN 48H
[non-ambulatory/dementia/medically unstable] = Nonoperative management
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
tx = analgesics / activity cessation x 90d
Classic triad for [Spinal Epidural Abscess]
1-focal back pain
2-neuro deficits
3-fever
dx = contrast MRI
Spinal Epidural Abscess p/w ⬜ ⬜ and ⬜
_________________
How do you manage SEA? (4)
focal back pain / neuro deficits / fever
_________________
- [contrast MRI spine]
- [Infxn labs (CBCec)]
- [IV Vanc + Ceftriaxone]
- [Emergency Surgical Decompression/I&D within 24 HOURS]
___________________________x____________________________________
CBCec = infxn labs = CBC/BCx/Culture specific (i.e. spinal aspirate cx)/ESR/CRP
What are the 5 steps to appropriately transport an amputated extremity?
________________
How long will this sustain viability?
“SPLIT extremity!? wrap in… “
Saline moistened gauze. THEN put in-
Plastic bag.
Lid seal bag shut before putting it on
Ice/Saline 50/50 mix bed. to keep
Temperature ideal (33.8 - 50 F) as to NOT FREEZE extremity
________________
24 hours
In Spinal Stenosis, pts pain is usually exacerbated with _____(flexion/extension) and _____. It is accompanied with ___ symptoms
spinal stEEEnosis
EXTENSION ; Exertion (vascular claudication) ; neurological
Shopping cart sign (lEaning over for relief) = Spinal stEnosis = exacerbated with Extension and Exertion
You see an elderly patient leaning over to relieve their pain
⬜ is suspected. How is it confirmed?
management? (2)
[Spinal StEnosis secondary to Osteoarthritis joint degeneration] ; MRI spine
_________________
tx =[lumbar epidrual block] –(if persist)–> [Laminectomy surgical decompression]
Shopping cart sign (lEaning over for relief) = Spinal stEnosis = exacerbated with Extension and Exertion
In Lumbar disc herniation, pts pain is usually exacerbated with _____(flexion/extension) and accompanied with ___ symptoms
flexion ; UNILATERAL radiculopathy and neurological sx
[AOOD (avascular osteonecrosis osteochondritis dissecans)] etx
_________________
dx
osteonecrosis (from “ASEPTIC”) of [small foot/hand bones], proximal tibia, femoral head, vertebrae, humeral head ➜ bone collapse ➜ joint replacement
_________________
MRI
stage 4 AOOD ➜ Total Hip Replacement
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*
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… Means → 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.[TNFα inhibitors = g-e-i-c-o]
“Norris DMARD…Means LASH Terribleg-e-i-c-o”
Name the 6 major Treatments for Rhematoid Arthritis
DMARD (Disease Modifying AntiRheumatic Drug)
“Norris DMARD…Means LASH Terribleg-e-i-c-o”
1. [MTX (initial DMARD)]
2. Leflunomide
3. Azathioprine
4. Sulfasalazine
5. Hydroxychloroquine
6. [TNFα inhibitorsg-e-i-c-o]
Sarcoidosis Etx-2 (Etiology)
[CD4 Helper T] inappropriately respond to environmental triggers + Suppressed TRegs –> Non-Caseating Granulomas in Lung
Image showing b/l Hilar LAD
Sarcoidosis Tx-5
“Sarcoidosis is a 0-SCAM”
0bservation if asx (MAJORITY)
_________________
Steroids
Cyclosporine(Calcineurin inhibitor)
Azathioprine(Calcineurin inhibitor)
MTX
SCAM only if Sx
Major causes of Rhabdomyolysis - 4
- Immobilization prolonged (direct damage)
- Cocaine (direct damage)
- Physical restraints
- Dehydration
Muscle breakdown –> ⬆︎CPK, ⬆︎K, ⬆︎myoglobin(which causes renal damage when filtered)
causes of AOOD [Avascular Osteonecrosis Osteochondritis Dissecans]- 11
ASEPTIC
Antiphospholipid syndrome
SLE | Sickle Cell Disease | [Storage (Gaucher’s) Disease]
EtOH⭐
Pancreatitis
Trauma
InfectionHIV
CTS>20mg/day⭐ | [CKD/HD/Renal_transplant] | [Caisson’s“the bends”]
MRI = most sensitive dx
Dx for AOOD [Avascular Osteonecrosis Osteochondritis Dissecans]
MRI
etx: (“ “ASEPTIC” → AOOD)
3 Main causes of Spinal Cord Compression
- DJD Disc Herniation (Smoking risk factor)
- [Epidural Staph a. Abscess (think IV drug user vs DM)]
- Tumor (Prostate/Renal/Lung/Breast/Multiple Myeloma mets)
Dx = MRI, Positive Straight Leg, Classic S/S
DJD=Degenerative Joint Disease
[Polymyalgia Rheumatica (PMR)] affects [____(demographic)]
[> 50 yo]
tx for [PolyMyalgia rheumatica (PMR)] -2
▶LowDoseCTS(Prednisone)
▶⚠️(but if ⊕GCTA)–> HIGH_DOSECTS
[PDO] etx (3)
[PDO- Paget\Disease of bone\Osteitis deformans]
{Accelerated (and Disorganized) focal bone remodeling → [⇪ALP P.H.L.O.A.T.]}
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
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)
_________________
Platybasia(narrowing of foramen magnum)
Heart failure (from ⇪ bone vasculature → ⇪ AV shunts → high output HF]
Leontiasis Ossea(enlarged cranial bones → ⇪ hat size, hearing loss from CN8 entrapment)
OsteoFibroma vs OsteoSarcoma
Arthritis
Tibia bowing / long bone chalk-stick fractures / bone-joint pain
bx: disorganized mosaic pattern of woven & lamellar bone
tx = bisphosphonates
Lab values for PDO - 4
_________________
[PDO- Paget\Disease of bone\Osteitis deformans]
- ⬆︎ALP
- ⬆︎Urine Hydroxyproline (measures bone turnover)
- NORMAL CALCIUM
- NORMAL PHOSPHOROUS
bx: disorganized mosaic pattern of woven and lamellar bone
tx: bisphosphonates
Tx for PDO
_________________
[PDO- Paget\Disease of bone\Osteitis deformans]
Bisphosphonates
bx: disorganized mosaic pattern of woven and lamellar bone
tx: bisphosphonates
What is the most common cause of asymptomatic isolated ALP ⬆︎ in the elderly?
[PDO- _Paget\Disease of bone\Osteitis deformans_]
- bx: disorganized mosaic pattern of lamellar bone*
- tx = bisphosphonates*
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]
bx: disorganized mosaic pattern of woven and lamellar bone
tx: bisphosphonates
_____ loss is a common complication of [PDO]
________________
tx?
[PDO- Paget\Disease of bone\Osteitis deformans]
hearing
________________
Bisphosphonates
(treatment only slows progression)
Name the Conditions associated with granulomas -6
- TB
- Syphilis tertiary gummas
- Blastomycosis
- Histoplasma
- Sarcoidosis
- [Churg Strauss Eosinophilic Granulomatosis with Polyangiitis]
Dx Sarcoidosis (2)
- Endobronchial bx by Bronchoscopy
- Clinical (CCUBBEDD)
Rheumatoid Arthritis centers around the _______ treatment group, which take _______ to onset
DMARD ; weeks
“Norris DMARD…Means LASH Terrible*g-e-i-c-o*”
scoliosis
_____________
treatment -3
- [CAST GOE10°] ➜ [back brace v observation]
- [CAST GOE40°] ➜ surgery
_________________
CAST: Cobbs Angle Scoliometry Test
scoliosis
________________
dx
[CAST GOE10°]
_________________
CAST: Cobbs Angle Scoliometry Test
How do CTS impair the immune system? -3
CTS …
- ⬇︎ neutrophil’s adhesion to inflammatory sites
- sequesters eosinophils in lymph nodes
- causes lymphocyte apoptosis
How does [estrogen E2] affect bone? -2
[Estrogen E2] BUILDS BONE by…
- Blocks osteoBlast (Build bone by secreting collagen and catalyzing mineralization) apoptosis
- Causes osteoClast(Cut up/dissolve bone by secreting acid and collagenases apoptosis. (Derived from macrophage/monocyte)
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
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]
What does TNFα do? (4)
_________________
How do we stop it (3)?
“TNFα makes me C-G-S-W!”
mediates…
1.[CA Cachexia]
2.[Granulomas*(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.[Shockactivates endothelium ➜ vascular leak ➜ hypOtension]
4.[WBC recruitment(targeted by DMARD)]
[g-e-i-c-o TNFα inhibitors] = tx
Adalimumab: [anti-TNFα] monoclonal Ab
EtanerCEPT: TNFα decoy reCEPTor
Infliximab: [anti-TNFα] monoclonal Ab
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)
- Intermittent PTH → bone FORMATION
- [PTH ⇪ with mild ⬇︎ Magnesium (causes of Mg⬇︎: diarrhea, aminoglycoside, diuretics, EtOH)]
- [ PTH⬇︎ with SEVERE ⬇︎⬇︎Magnesium]
OVERALL:
[ INC serum Ca+]
[ DEC serum (P)]
[ INC urine_(P)]
PCN
A. MOA
B. which organisms are treated with PCN? (3)
contains [βlactam ring DSAD-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]
note: PCN is sensitive to [microbial βLactamASES (which cut/inactivate PCN’s [βLactam ring DSA] →inactivates PCN –> allows [microbial PBP] to cross-link Peptidoglycan Cell WALL
