Clinical Patterns Flashcards
Explaint the numeric and the TMN cancer staging systems.
T - extent/size of tumour. T0 in situ. T1-4.
N - N0 no lymph nodes, N1-3
M - M0 no mets, M1 (distant mets present).
I - no lymph, no mets, <2cm
II - 2-5cm, maybe lymph, no mets
III - >5cm, yes lymph, no mets
IV - mets, all other details do not matter.
List the involved PT treatment of symptoms of post-op tumour removal.
i) scar mobilization
ii) ROM
iii) post-op pain and fatigue
iv) deconditioning training
v) infection and wound healing.
List the involved PT treatment of symptoms of chemotherapy.
i) desensitization techniques for peripheral neuropathy.
ii) TREATMENT-RELATED FATIGUE
iii) deconditioning
Note: mindful of possible presence of OP, renal failure or pulmonary fibrosis
List the involved PT treatment of symptoms of radiation therapy. When is it safe to begin stretching and manual therapy post radiation?
i) Tissue fibrosis (contracture & ROM release)
ii) TREATMENT-RELATED FATIGUE
iii) deconditioning
Stretch 4**-6 weeks after last dose as it often becomes strongest 2-3 weeks after administration.
By what mechanism does cancer treatment cause treatment-related fatigue?
Bone marrow suppression, reduced RBCs, reduced capacity to produce energy.
Increased HR and CV effort to meet O2 needs causes increased energy consumption - even at rest.
Which blood test levels would be altered in patients with cancer?
i) Hb - pt anemic, cannot exercise if <8g/dL
ii) Neutrophils - reduced WBCs, increased infection risk,
iii) thrombocytopenia - low platelet, increased risk of bruising and bleeding, cannot exercise if <10,000MCL
Describe the two types of lymphodema.
Primary: rare, inherited d/t problem with teh lymph vessels
Secondary: damage or obstruction of lymph vessels
What are the risk factors for developing lymphodema?
i) radiation
ii) axillary dissection (breast cancer)
iii) infection
iv) older age
v) obesity
vi) post-op weight gain
Describe the stages of lymphodema.
0 - transport reduced, not yet visible, c/o “heaviness”
I - reversible, pitting, no fibrosis
II - irreversible, less pitting, fibrosis present
III - lymphostatic elephantiasis, excessive fibrosis, sclerosis and skin changes.
Describe the manual therapy treatment aimed towards improving lymphodema symptoms.
Manual lymphatic drainage massage to re-route damaged lymph pathways. Can teach this to patient themselves.
Describe the physical aid treatments that can be used for lymphodema.
i) compression garments
ii) k-taping to provide compression
What education is necessary to for patients with lymphodema?
i) Increased risk of infection due to stasis - important for pt to do skin checks.
ii) signs of infection
iii) role of exercise important to promote flow.
iv) keep cool as heat will exacerbate
v) S/S to watch out for
Note: do not use BP cuffs on affected side
What is the lab evidence required for a diagnosis of AIDS?
i) HIV-1 virus +ve
ii) CD4 < 200mL
OR
- 14% lymphocytes
OR
-diagnosis of 1 of 26 conditions found in HIV (in lieu of CD4 count, but still HIV+ve).
List conditions that HIV+ individuals are more at risk of experiencing.
i) pneumonia
ii) TB
iii) cancer
iv) meningitis
v) encephalitis
vi) dementia
vii) herpes
- distal and leuko neuropathies common
Explain the pathophysiology of Guillian-Barre syndrome.
Autoimmune response, following recent respiratory illness, that demyelinates Shwann cells in the peripheral nervous system causing widespread flaccid paralysis. Onset peaks at 4 weeks.
What are the two options for medical treatment of G-B syndrome?
i) plasmaphoresis
ii) immunoglobin therapy
Describe the pathophysiology of systemic lupus erythematosus.
A systemic rheumatoid, inflammatory disease in which the body creates antibodies against its own cells (RBCs, lymphocytes, etc.). Most commonly involved tissues and organs include skin, kidney, CNS, cardiac, pulmonary, and arthritis.
Describe common S/S associated with SLE.
i) butterfly (malar) rash
ii) mouth and genital ulcers,
iii) photosensitivity
iv) anemia and thrombocytopenia
v) kidney and liver decline
vii) seizures/CNS involvement
vi) +ve or abnormal antinuclear antibodies (ANA) indicative of symmetric arthritis.
- localized edema
- alopecia
Raynaud’s
What are the most important considerations in treatment of SLE for PTs.
i) education re: skin break down and risk prevention
ii) aerobic exercise
iii) energy conservation training.
Describe the pathophys of scleroderma.
A connective tissue disease that can cause fibrotic changes to the skin primarily as well as blood vessels and organs. Caused by sclerosis (hardening of the skin secondary to massive fibrotic tissue response). It can be systemic or localized.
List some of the associated complications with scleroderma.
i) joint contractures
ii) pulmonary fibrosis
iii) HTN
iv) renal
v) GI dysmobility
vi) Raynaud’s
Describe the pathophys of polymyositis (muscle only) and dermatomyositis (muscle & skin). List some common signs and symptoms.
A chronic inflammatory disease of muscle (+/- skin), particuarly proximal limb girdle muscles, especially of the UEs. Common occurs with photosensitive skin rash, and purple erythematous on the face.
Describe the pathophys of haemophilia.
A congenital x-linked recessive disorder causing reduced clotting factor of blood or (hemostasis). Hemophiliacs do not bleed FASTER than others, they bleed longer. Comes in Type A and B - just difference deficiency in clotting factor. Treated with Factor Replacement Therapy by infusion ( though some pt develop antibodies to fight this). Or desmopressin if mild.
REVIEW AVERAGE LAB VALUES!
SERIOUSLY!
What are the signs and symptoms of hemophilia?
i) excessive bleeding after post-birth circumcision.
ii) excessive bruising (ex. under arm from lifting)
iii) bleeding in joints and muscles
iv) excessive bleeding after minor trauma (Ex. losing a tooth)
RARE: but be aware of possibility of hemorrhaging into the CNS
What is the main concern for hemophiliacs?
Joint bleeds (hemoarthosis most common!) and muscle bleeds. CANNOT TAKE IBUPROFEN OR ASPIRIN AS THEY ARE BLOOD THINNERS.
Describe the PT management of hemophilia.
i) movement to prevent disuse atrophy, joint contractures and arthritis (all of which contribute to increased bleeding).
ii) Acute joint/muscle bleed management
- factor replacement if indicated (joint)
- RICE
- painfree ROM
iii) Do not overtrain or do max strength testing!
iv) treat complications (ex. peripheral neuropathy 2’ hematoma compression).
What questions/red flags do you need to ask re: someone with potential rheumatic disease?
- Acute or chronic (>6weeks)
- Focal or widespread (>3 joints)
- Inflammation IN or AROUND the joint?
- Red flgs: #, septic arthritis, malignancy, central cord S/S, focal/diffuse muscle weakness, burning/numbness/parasthesias.
Describe the pathophys of rheumatoid arthritis.
Chronic, systemic, autoimmune, inflammatory disease causing persistent synovitis. However, structures around the joint (tendon, bursa etc.) can also be affected. Causes swelling, muscle weakness, limited ROM and major disability over time. May extend to affect multiple organs and systems. 40-50% genetic.
Describe how rheumatoid arthritis can affect a joint.
Synovitis cause proliferation and thickening of this membrane. A dense cellular membrane known as a pannus proliferates and invades the joint surface(s). It spreads over articular cartilage and releases enzymes that destroy the cartilage and bone. It may also affect tendons and ligaments the end results being:
i) fibrous scar tissue
ii) adhesions
iii) bony ankylosing (fusion)
iv) joint instability
List risk factors for RA.
i) family Hx
ii) smoking
iii) female (esp. post-menopause and post-partum)
iv) poor diet (esp. low vitD & antioxidants, high sodium)
v) obesity
vi) high alcohol intake
vii) statins
List the criteria for RA Dx.
Note: the first four must have persisted for at least 6 weeks. PATIENT MUST HAVE AT LEAST 4/7 CRITERIA 1. Morning stiffness (>1hr) 2. Arthritis >/=3 joints 3. Arthritis of hand joints 4. Symmetric Arthritis 5. Rheumatoid nodules 6. Serum rheumatoid factor 7. Radiographic changes ** abnormal antibody HLA-DR4 common (80%) as well, but not specific to RA.
Describe the S/S of rheumatoid arthritis.
i) joint swelling/stiffness (esp. hands and feet)
ii) fatigue
iii) pain
iv) joint deformity
v) muscle atrophy
vii) MORNING STIFFNESS > 1hr
Which joints are most commonly affected by rheumatoid arthritis in early presentation?
i) MTPs
ii) MCPs
iii) radiocarpal/DRUJ (wrist)
iv) proximal IPs
Explain the medical management of RA.
i) DMARDs (disease-modifying anti-rheumatic drugs) to slow disease process
ii) statins (to reduce CV risk, although controversial since they also increase auttoimmunity).
iii) radiosynovectomy - inject radioactive particles to treat synovitis.
iv) methotrexate - reduce inflammation but may cause liver damage
v) joint surgeries
Explain the PT role in treating RA in the acute phase (flare up).
i) energy conservation
ii) pain relief (ice+ other strategies)
iii) gentle ROM maintenance
iv) joint protection: splints, orthoses, gloves
v) ISOMETRIC exercise only
vi) NO STRETCHING - CAN CAUSE DAMAGE
vii) AVOID STAIRS AND LIFTING IF IN KNEES
Explain the PT role in treating RA in the chronic phase.
i) relieve pain (modalities, education etc.)
ii) splints and gentle ROM for joint protection
iii) aerobic exercise (aquatics for this population great!)
iv) compression gloves
v) CONTRACTURES CAN BE HELD FOR 6S AND REPEATED 5-10 TIMES DAILY.
vi) fall prevention
vii) functional activities
What are the main types of surgeries performed on RA patients?
Remove (MTP resection)
Re-align (tendon rupture)
Rest (arthrodesis - fusion)
Replace (arthroplasty)
What joints are most commonly affected by RA?
i) atlanto-axial (transverse ligament - +ve sharp pursor test, cord signs).
ii) TMJ - fusion
iii) shoulder - HOH superior
iv) AC joint
v) elbow - reduced extension (PRUJ, radial head erosion)
vi) hip - groin P, flexion deformity
vii) knee - baker’s cyst, valgus, flexion deformity
Explain how to conduct an active joint count.
i) joint effusion
ii) joint tenderness: over collateral ligaments, press hard enough to blanch fingernail
iii) stress pain: PROM w/ OP - Ax for pain.
* *these are assessed sequentially in this order. If one iis +ve then do not need to test the next one. But need to test all of them to rule out an active joint.
Explain the difference between a two thumb and finger technique for measuring joint effusion.
i) Two thumb: one directs pressure around the joint the other senses for fluid movement. They must be offset a little to prevent just pushing the joint into the thumb.
ii) Four finger: sensor fingers must be DORSAL to the collateral ligaments and PROXIMAL to the joint line. Other two fingers squeeze AP (sensors feel for fluid movement on the sides of the joint).
- IPs usually!
- bursh-stroke-bulge for knee. Hip cannot Ax effusion.
Explain hallux valgus (RA).
Valgus at the 1st MTP 2’ ligamentous laxity.
Explain MTP subluxation (RA).
synovitis causes displacement of flexors and erosion of plantar ligament. Extensors pull 1st MTP into hyperextension due to unopposed force. Callouses are often a sign. Causes lateral drift of toes.
Explain claw toe (RA).
MTP hypextension causing PIP and DIP flexion. Often this occurs in all toes except for the big toe (plantar plate again).
Explain hammer toe (RA).
Due to MTP and PIP synovitis. Causes flexion of PIP an extension of DIP (similar to boutennieres in hand). usually 2nd toe - may be 3rd or fourth too. Callouses.
Explain mallet toe (RA).
flexion of the DIP joint only - usually affects the longest toe.
Explain swan neck deformity (RA).
MCP in flexion
PIP in extension
DIP in flexion
Caused by volar plate erosion or tear of flexor tendons to the middle phalanx.
Ax: Bunnel Littler (PIP flexion first w/ MCP extendended, then with MCP flexed. If same - capsular. If more w/ flexed - lumbricals limiting ROM).
Explain Boutinniere deformity (RA).
PIP flexion
DIP extension
Caused by rupture of central slip of extensor expansion (often w/ compromised transverse ligaments of extensor expansion).
Ax: central slip tenodesis test (flex PIP 90’, ask pt to extend DIP, feel for middle phalanx - +ve if low to no pressure over middle phalanx.)
Explain ulnar drift deformity (RA).
MOST COMMON
MCP synovitis causes laxity/rupture of volar plate and radial collateral ligaments. Phalanges oriented towards ulnar side. 1st dorsal interossei compromise (turns into flexor when capsule stretched).
Ax: radial collateral ligament stress test (w/ MCP in 90’ flexion), extensor tendon subluxation test.
Rx: radial finger walking, splinting, prevent ulnar forces in daily use (Ex. getting up from chair).
Explain DRUJ instability in the context of RA.
ulnar collateral ligament at the wrist becomes lax causing dorsal displacement of ulnar head. ECU will become volarly displaced and act as more of a flexor.
Ax: Balottement test/Piano Key Test
Explain Swan neck deformity of the thumb (RA).
CMC flexion
MCP extension
IP flexion
(Swan neck, just starting at MCP)
Explain Boutenniere deformity of the thumb.
90/90 position MCP flexed IP extended hitchhiker's thumb/z-deformity Ax: grind & crank test (Thumb CMC grind test)
Explain Gamekeeper’s thumb deformity (RA).
Note: skier’s thumb if traumatic.
Rupture of UCL of the 1st MCP causing a radially deviated 1st phalanx.
Stener lesion - if adductor becomes interposed betw/ UCL and supposed attachment on prox phalanx.
Explain Ape hand deformity (RA).
Median nerve palsy/dysfunction. Thenar wasting.
Explain Dupuytren’s contracture (RA).
Contracture of palmar aponeurosis. 4th and 5th digits most affected (MCP and PIP). Involves nodules formation.
Explain Mallet finger (RA).
Avulsion or rupture of extensor expansion/lateral bands at distal attachment on distal phalanx. DIP flexion.
Explain the pathophysiology of gout and the PT role.
A purine (protein) metabolic disorder resulting in crystal-induced arthritis (uric acid crystals). May be inherited (primary), secondary to another pathology or idiopathic. Attacks will reccur and tend to become more severe as they do. - pseudogout: primarily knee, similar episodic nature but less frequent.
Explain the medical and PT management of gout.
1.NSAIDS (daily low dose to prevent, analgesia during), COX2 inhibitors
2. uricosuric drugs
3. dietary changes
PT:
- weight loss
- control inflammation
- ROM/spinting as needed
