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
- Hemochromatosis
- hypOthyroid
- HyperParathyroid
- Osteoarthritis
Tx for Acute Gout (4)
Also tx for Acute Pseudogout
Tx for Chronic Gout
- 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?
- MssA = Nafcillin|Oxacillin|ceFAZolin
- MRSA = Clindamycin | Vancomycin
- *
- [Salmonella(Sickle Cell pts)] = add 3GC(CefTriaxone/CefoTAXime)
_________________
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
_________________
[FOOSH (wrist dorsiflexed)]
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 the main sx for Polymyositis -2
________________
list sx of Dermatomyositis -6
[proximal shoulder weakness symmetric] and [pulmonary❌(ILD - ground glass on HRCT)]
________________
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 pain 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 3 drugs that cause Macrocytic Anemia by interfering with folate metabolism
________________
explain how?
- Trimethoprim
- MTX
- Phenytoin
________________
inhibits [DiHydroFolate reductase] which prevents [folic acid B9] ➜ [FH4 reduced folinic acid (usually utilized by cells)]
this folate deficiency ➜ [macrocytic megaloblastic anemia]
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?
[folate b9] ; [mAcrocytic megaloblastic]
________________
[FH4 reduced folinic acid (usually utilized by cells)] = LEUCOVORIN
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 ➜ 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 ➜ [Pseudogout⼀joint aspiration] = [positively birefringent rhomboid CPPD crystals] ➜ acute inflammation that resembles gout = Pseudogout
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. [extra-articular sx: uveitis, keratoderma blennorhagica, circinate balanitis]
3. [ASYMMETRIC OLIGOARTHRITIS (≤4 joints)]
4. Sterile synovial joint fluid with HIGH WBC
HLA-B27 only positive in 30% of patients
Oligoarthritis = joints 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 antiHTNs are contraindicated in patients with Gout? (3)
HCTZ / Loop diuretics / 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
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 pain and 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 - 9
Vitamin D deficiency
- Delayed Fontanelle closure
- Wide Sutures
- Frontal Bossing
- Craniotabes (softening of the skull)
- Dental hypoplasia
- Rachitic Rosary
- Pes Carinatum
- Joint swelling
- Bowing of Legs
Osteomalacia is the 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
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)]
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
[Antiphospholipid syndrome] etx
Lupus anticoagulant (2/2 SLE or idiopathic) –> [⬆︎Thrombosis and spontaneous abortion]
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
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)]
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)=
▶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]
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
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)
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 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]
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)
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
clinical presentation for Meniscal tear
subacute or chronic LOCKING/CATCHING sensation of the Knee
+/- ➜ gradual effusion
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
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
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
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
[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)
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
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
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)]
