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NYCC Loia final ad

NYCC Loia Exam 3 Evi. Based Clin Case Mgmt Sp2012

QuestionAnswer
Abducts and externally rotates thigh piriformis
piriformis syndrome PAIN from sciatic n. irritation DEEP in buttocks, worse by SITTING, CLIMBING, SQUATS
Patient presentation = PIRFORMIS syndrome (+) LASAGUES, INTERNAL rotation pain, HYPESTHESIA over S1/2 dermatomes, diffuse MOTOR WEAKNESS = pain in the SACRAL or GLUTEAL region is MOST CONSTANT SYMPTOM
Medical mgmt of piriformis syndrome Stretch – Ice/heat – PT – Meds – Injections – Electrotherapy
PT for piriformis syndrome Deep massage, ROM exercises
CHIRO treatment options for piriformis syndrome Ischemic compress – Spray n stretch – Active myofascial release – manip/adj of associated joint dysfunction – Exercise
Claudication 'limping' – can be neurogenic from stenosis or vascular from atherosclerosis
Will all patients with spinal stenosis (ss) or foraminal encroach have neuro sx? No. Only have symptoms when there is IRRITATION
Leading PRE-OPERATIVE DX for adults >65 LUMBAR SPINAL STENOSIS [LSS] = neurogenic claudication
Why is LSS more frequent in lower lumbar area Increased DORSAL ROOT GANGLION DIAMETER then decreased foramen
Younger population has disc herniation and congenital... canal STENOSIS (young = LDH + SS)
Structure which presses on DORSAL COLUMNS in lumbar ss: Hypertrophied LIGAMENTUM FLAVUM
When should SURGERY for LSS be considered? UNREMITTING pain or PROGRESSIVE NEURO defect = CAUDA EQUINA
Non-surgically, ______ management for LSS is encouraged. Conservative – intention is to reduce inflammation
Conservative mgmt for LSS medically Anti-inflammatory meds, pain relievers, steroid injections, laminectomy
Complications of LSS (3) Injury from LACK OF SENSATION, INFECTIONS, CHANGES from nerve compression
Ligamentum flavum hypertrophy in LSS affects the DORSAL COLUMNS = less proprioreception, wide based gait, loss of sense of vibration
TESTS for LSS REFLEXES (asymmetry of lower), NEUROLOGIC (hypesthesia and leg WEAKNESS), X-RAY/CT (degeneration and stenosis), MRI (stenosis and ligamentum flavum hypertrophy), EMG
What will you see on LSS imaging? Disc space NARROWING, Prominent OSTEOPHYTES, Hypertrophied LIGAMENTUM FLAVUM, Facet ARTHROSIS
Who should decide if chiropractic manipulation should be applied to LSS patient? The chiropractor!
What kind of spinal manipulation does KIRKALDY-WILLIS rec. for LSS FLEXION & ROTATION
Flaccid weakness and hyporeflexive... Lumbar RADIC!
Why is LSS relieved by FLEXION? Creates a tensile pull on the ligamentum flavum, instead of buckling it
Prominent sx of BOTH neurogenic and vascular claudication LEG pain on WALKING
Claudication RELIEVED BY FLEXION NEUROGENIC
NEUROGENIC claudication big 3: RELIEVED by FLEXION, Walking UPHILL EASIER, Riding a BICYCLE EASIER (all flexed postures)
Claudication WORSENED by STANDING VASCULAR (severe cramp due to back up of fluid)
PAIN of vascular claudication SEVERE CRAMP (versus tingling and numbness of neurogenic claudication)
PAIN of neurogenic claud TINGLING, NUMBNESS
CLASSIC presentation of Lumbar Spinal Stenosis LSS BILATERAL NEUROGENIC claudication
Kind of stenosis that causes unilateral neurogenic claudication Lateral recess stenosis or foraminal stenosis
INTERMITTENT, DIFFUSE radiating thigh or leg pain w/ assoc parasthesias NEUROGENIC claudication
Affects 90% of patients with LSS LEG PAIN
ALLEVIATES neurogenic claudication (LSS) Lying SUPINE, SITTING, SQUATTING, FLEXION lumbar
Neurogenic claudication (LSS) 80% pain diminution with... SITTING and 75% relief w/ forward BENDING/FLEXION
Physical EXAM findings in LSS Often NORMAL – WIDE BASED GAIT, EXTENSION causes thigh pain, RHOMBERG test (+), loss of lumbar LORDOSIS, MRS abnormalities L4-L5 MOST COMMON
ASYMMETRIC muscle stretch and focal myotomal weakness LATERAL recess stenosis
These symptoms are NEGATIVE for neurogenic LSS VASCULAR (skin color/temp/turgor, bruits, pulses) & Lumbar segment MOBILIZATION fails to reproduce pain. NO mftp's.
Can you ADJUST a pt w/ neurogenic claudication LSS Yes, even elderly. Just reduce the flexion and pre-load.
Describe sx of CAUDA EQUINA syndrome SADDLE, BLADDER, NEURO DEFICIT lower ex
LONG TERM effects of cauda equina syndrome Bladder infection – Decubitis ulcer – Venous thromboemboli
CAUSES of vascular claudication ATHEROSCLEROSIS + HEART disease
EXACERBATED by PHYSICAL activity, RELIEVED by REST VASCULAR claudication – no positional component
If the dorsal pedal pulse is patent, then … no vascular component. OKAY. Helps d/dx vascular from neuro lesion
3 arteries of lower extremity Femoral – Popliteal – Dorsalis pedis (most impt)
TESTS for vascular claudication DORSALIS PEDIS PULSE – CAPILLARY REFILL – BRUGGER'S dorsi/plantar flex
Bifurcation level of abdominal aorta into common iliac a. L4
Average diameter of aorta? Evaluation diameter of aorta? Normal 2.0-2.5 cm, EVALUATE if 3.5 cm or greater!
More than 90% of AAA are associated with? ATHEROSCLEROSIS and can cause CLAUDICATION as LEG: PAIN - NUMBNESS - FATIGUE
An artery may be sclerosed but if the lumen isn't altered, there is NO aneurysm.
CHIEF SIGNS of AAA (when there are any): 1. PULSATING MASS 2. BRUIT 3. symptoms from continuous PRESSURE (ie, abdominal and back pain)
Most AAA do NOT produce symptoms but the pt can feel a pulsating sensation in abdominal
AAA on CT Calcium is bright/white on CT
How can PULSATIONS of AAA cause a spinal problem? EROSION of vertebrae, LOW BACK PAIN due to pounding on vertebral endplate (nociceptors), also THINS aorta (rupture)
How to PALPATE an AAA Hooklying position, relaxed abs, pulsation to RIGHT of midline = surgical eval
Renal artery aneurysm causing hypertension NOSEBLEED relieves the headache
D/dx AAA PSOAS SPASM will angulate spine, RENAL A. aneurysm will cause HIGH b.p.
INNER THIGH PAIN can be triggered by
TESTS for AAA KIDNEY PUNCH, LABS (inflammation/infection/stones + kidney fcn) =but there is NO LAB TEST for AAA
90% chance of AAA rupture if what 2 comorbidities HYPERTENSION & COPD
Is there a lab test for AAA? No.
IMAGING for AAA FILMS, ULTRASOUND, MRI, CT, ANGIOGRAPHY
Hemothorax ruptured AAA on xray as cloudy (full of blood)
Sx of RUPTURE of AAA PULSATING, PAIN, RIGIDITY,LBP, PALE, RAPID pulse, DRY, THIRST, cannot concentrate!!, TACHYCARDIA
Plethysmography BP CUFFS on ankles -recorded by pulse volume
Visible signs of AAA on LEGS HAIR LOSS patches
Imaging technique to measure abmormal arterial blood flow DOPPLER ultrasound
When NOT to use b.p. Cuff on ankles to detect AAA THROMBOPHLEBITIS – possible embolus
RED flags of LBP Severe MORNING stiffness as CC – Pain Unrelieved by posture and unchanged over 2-4 wks – Bowel/bladder dysfcn – Failed back surgery
LBP w/ bilateral leg pain. Difficult to stand or walk up stairs. Biking good. Neurogenic claudication LSS
#1 cause of disability in America ARTHRITIS
Chronic dz causing break down of JOINT CARTILAGE and sclerosis Osteoarthritis
OA occurs in Athletes and more Women after age 55
Primary CAUSE of OA MECHANICAL
Labs for OA none. Can use them to monitor tx
X-RAYS of OA LOSS of cartilage and NARROWING of joint space
CHIRO OFFICE mgmt for OA ADJUST & MODALITIES to control pain + reduce inflammation
CHIRO HOME mgmt for OA Weight loss, Nutrition, Heat/Cold, EXERCISE (water)
MOST common form of INFLAMMATORY ARTHRITIS RHEUMATOID = most debilitating
3 stages of RA 1. SWELL 2. PANNUS 3. DEFORMITY/misalignment
Who gets RA (excepting JRA) Women b/w ages 20 – 50
22 yo male LBP getting progressively worse. Rough in morning, better, then stiff/achy Ankylosing spondylitis
D/dx for 22 yo male w/ progressive LBP worse in morning + night AS and Reiter's
LABS for AS and REITER REACTIVE HLA-B27 (both)
LABS for LUPUS (SLE) ANA
LABS for GOUT URIC acid
LABS for PSORIATIC arthritis ESR and Rf+
LABS for RA and Sjogren syndrome ANA and Rf+
When is adjustment for RA contraindicated? ACUTE inflammatory stage or wherever there is ankylosis
Spinal FUSION terms for AS SYNDESMOPHYTES >> BAMBOO SPINE
Difference b/w AS and Reiter's reactive arthritis EYE AS – no conjunctivitis, just uveitis. No exudate.
MOST common SYMPTOMS of AS Ages 17-35, males: STIFF lower back & buttocks, GRADUAL onset, DULL/DIFFUSE, worse in MORNING & NIGHT
HALLMARK feature of AS SACROILIAC involvement
GASTROINTESTINAL feature of AS Bowel inflammation, assoc w/ Crohn's or Ulcerative colitis
PERIPHERAL JOINT involvement is more common in ______ w/ AS. JUVENILES
AS often accompanied by IRITIS or UEVITIS (non-exudative) will see injection, watery
D/Dx AS PHYSICAL EXAM, RADIOGRAPHS, HISTORY, FAMILY hx of AS, LAB = include HLA-B27
Radiograph finding of AS SACROILITIS (can take 7-10 years to show so not best imaging choice)
3 predisposing factors for AS: 1. FAMILY HX 2. Freqent GI INFECTION 3. HLA-B27 (+) marker
CHIRO mgmt of AS EXERCISE – ADJUST – LIFESTYLE chg.
MD mgmt of AS PT and Meds
Causes of FATIGUE in AS ANEMIA, inflammation (exercise may increase fatigue)
3 sx of REITER'S/REACTIVE arthritis 1. ARTHRITIS 2. UEVITIS (redness) 3. URINARY TRACT infection
Name the SERONEGATIVE spondyloarthropathies REITERS – PSORIATIC – ANKYLOSING SPONDYLITIS – INFLAMMATORY BOWEL syndrome
Why is Reiter's called REACTIVE Apart from Dr. Reiter being a known Nazi, REACTIVE implies an etiology due to infection elsewhere in the body
2 modes of infectious transmission in REITER/REACTIVE 1. SEXUAL (genitourinary) 2. GI/ENTERIC (food ingest that is tainted by bacteria)
#1 cause of REITERs/REACTIVE arthritis CHLAMYDIA trachomatis (sex), then CAMPYLOBACTER (food), salmonella, shigella, yersinia
GENETIC factor for reactive arthritis HLA-B27 (*80% of people w/ Reiter's have the HLA-B27 factor)
MOST common type of ARTHRITIS to affect young men (20-40) REITER'S /REACTIVE arthritis because of sexual transmission
JOINT sx of reactive arthritis knees, ankles, feet = ENTHESOPHYTES leading to HEEL SPUR (can't dance with me)
SPINAL effects of reactive arthritis SPONDYLITIS (inflammation of vertebrae) & SACROILITIS
EYE effects of reactive arthritis CONJUNCTIVITIS (exudative uevitis)
What 2 tests are NORMAL in reactive arthritis 1. ANA 2. Rf factor {both negative in Reiters/Reactive}
2 tests that are normally positive in Reiter's/Reactive arthritis CHALMYDIA & HLA-B27
LAB for temporal arteritis or polymyalgia rheumatica ESR
LAB for Inflammatory Bowel disease
Defining characteristics of SLE for d/dx malar rash, thrombocytopenia, arthritis, and (+) ANA test
LAB for scleroderma, Sjogren's, and Raynaud syndrome (not dz) ANA
Characteristics for RA d/dx nodules and (+) RF and ANA and CRP
Stiffness in joints in morning, nodules, swelling, xray joint capsule evidence RA = RF+
characteristics for Sjogren's syndrome Xerostomia (dry mouth) and Kertoconjunctivitis sicca (dry eye) due to lymphocyte infiltration = RF +
Why would there be a connection b/w Sjogren's and lymphoma Sjogren's is due to lymphocyte infiltration of glands, caused by genetics and exposure to virus or bacteria
NEGATIVE Rf can mean: NO RA, too early in dz to diagnose, patient in remission phase
Arthritis char by sudden, severe attacks of pain, red, tender joints GOUT
Chronic gouty arthritis due to Overproduction of URIC acid or reduced ability to ELIMINATE it via kidneys
Populations at highest risk for gout Men and post-menopausal women (Diabetes II, Sickle cell, Kidney dz)
TEST for GOUT Best: aspiration SYNOVIAL fluid analysis, URIC acid, KIDNEY FCN, X-RAY affected jts
DRUG tx for GOUT Allopurinol, cholchicine, Probenecid, and increasing fluid
TREATMENT for Inflammatory arthritides MOVEMENT THERAPY (gentle – tai chi, yoga), WEIGHT LOSS & STRENGTH (pain reduction), RELAXATION therapy (meditation, biofeedback, guided viz)
Created by: hecutler