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M2 Pathology > MSK (LL) Vascular, Infections, Trauma, Toxins > Flashcards

MSK (LL) Vascular, Infections, Trauma, Toxins Flashcards

1
Q

State the common vascular conditions of the lower limb

A
  1. avascular necrosis of head of femur
  2. arterial thromboembolism
  3. claudication of leg
  4. DVT
  5. varicose veins
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2
Q

State the vessels involved in blood supply to the head of femur

A

adults - trochanteric anastomosis (medial and lateral circumflex A, inferior gluteal A, superior gluteal A)

children - obturator A (found in ligamentum teres)

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3
Q

State the common cause of avascular necrosis of head of femur.

State the pathogenesis behind it.

A

fracture of neck of femur

fracture –> torn reticular A of medial circumflex A –> branch of obturator A not enough to supply head of femur –> avascular necrosis of head of femur

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4
Q

Avascular necrosis is prevalent in what demographic?

A
  • elderly
  • postmenopausal (atrophy of female reproductive organs –> decreased oestrogen –> higher risk of osteoporosis)
  • osteoporic patients
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5
Q

State the main difference between trochanteric fracture of femur and fracutre of neck of femur

A
  1. trochanteric fracture of femur does not need replacement while fracture of neck of femur requires surgical replacement of head of femur
  2. trochanteric fracture of femur does not result in avascular necrosis of femur while fracture of head of femur does
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6
Q

Name the condition associated with this x-ray.

State a feature of the x-ray.

A

Avascular necrosis of head of femur
- Head of femur is flatter and disintegrated due to destruction of bone

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7
Q

State everything associated with asvascular necrosis of head of femur

A

AVASCULAR NECROSIS OF HEAD OF FEMUR
- common in eldelrly, post-menopausal women, osteoporotic patients
- commonly due to fracture of neck of femur from trauma
- retinacular A torn –> obturator A insufficient to supply head of femur
- requires hip replacement

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8
Q

Recall virchow’s triad

A
  1. hypercoaguability
  2. endothelial damage
  3. stasis of flow
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9
Q

State the pathogenesis of arterial thromboembolism

A

ARTERIAL THROMBOEMBOLISM
- thromboemboli from AF deposits in arteries in LL

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10
Q

State the common clinical presentation, complications and treatment for ARTERIAL THROMBOEMBOLISM

A

ARTERIAL THROMBOEMBOLISM

(1) Clinical presentation
- severe pain and coldness of affected limb
- certain pulses not palpable (dorsalis pedis, posterior tibial)

(2) Complication
- ischaemia and infarction of LL

(3) Treatment
- thrombolytics (tPA) and antiplatelert (clopidogrel)

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11
Q

State the cause and pathogenesis of claudication of leg

A

CLAUDICATION OF LEG

Cause = atheroscelerosis –> hyperlipidemia prediposes vascular wall to formation of lipid plaques

Pathogenesis
- narrowing of arteries cause supply-demand mistmatch in the muscles of the leg
- build up of lactic acid from anaerobic respiration causes pain in affected muscles

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12
Q

State the clinical presentations and treatment for claudication of leg

A

**CLAUDICATION OF LEG **

Presentation
- bilateral or unilateral presentation
- diminished pulses
- pain begins with use of leg (causes demand ischaemia and lactic acid build up) and gets bettter with rest

Treatment
- pentoxyfylline
- antiplatelets (clopidogrel)
- antihypertensives (ace-i = captopril, arb = candesartan)
- antilipids (hmg-coa reducatase-i = atorvastatin)

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13
Q

State everything you know about claudication of leg
(cause, pathogensis, presentation, treatment)

A

CLAUDICATION OF LEG

Cause = atherosclerosis (hyperlipidemia predisposes vascular walls to formation of lipid plaques)

Pathogenesis
- narrowing of arteries cause supply-demand mismatch in the muscles of the leg (demand ischaemia)
- build up of lactic acid from anaeruobic respiration causes pain in affected muscles

Presentation
- bilateral or unilateral
- diminished pulses
- pain on activity, better with rest

Treatment
- antihypertensives (captopril and candesartan)
- antilipids (atorvastatin)
- antiplatelets (clopidogrel)
- pentoxyfylline

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14
Q

State the cause of deep vein thrombosis

A

VENOUS stasis when sitting for long periods of time

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15
Q

State the clinical presentation, complications and treatment of deep vein thrombosis

A

DEEP VEIN THROMBOSIS

Presentation
- pain, warmth, red discolouration of elg
- swelling of leg (compresses nerves –> weakness and numbness)

Complication
- thrombus travels to lung –> pulmonary embolism –> death

Treatment
- rivaroxaban, apixaban monotherapy
- LMWH + warfarin OR LMWH + dabigatran/rivaroxaban/edoxaban

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16
Q

State everything you know about deep vein thrombosis
(cause, clinical presentation, complication, treatment)

A

DEEP VEIN THROMBOSIS

Cause = venous stasis when sitting for long periods of time

Presentation
- pain, warmth, redness
- swelling of leg (can compress on nerves and cause numbness and weakness)

Complication
- thrombus can travel to lungs –> pulmonary embolism –> death

Treatment
- rivaroxaban/apixaban monotherapy
- LMWH + warfarin OR LMWH + rivaroxaban/dabigatran/edoxaban

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17
Q

State the cause and treatment of varicose veins

A

VARICOSE VEINS

Cause = valvular incompetency resulting in blood flowing from deep veins to the superficial veins through perforating veins

Treatment = polidocanol or mucopolysaccharide polysulfate

Common in posteromedial part of leg

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18
Q

State everything you know about poliomyelitis
(cause, presentation, treatment)

A

POLIOMYELITIS

Cause = polio virus attacks ventral horn of spinal cord

Presentation
- asymmetric flaccid paralysis without sensory loss
- reduces or absent deep tendon flexes
- systemic symptoms (fever)

TREATMENT
- 3x oral vaccination for children

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19
Q

State the pathogenesis and causes of trochanteric bursitis

A

TROCHANTERIC BURSITIS

Pathogenesis
- inflammation of the bursa which lies over the greater trochanter between the gluteus medius and gluteus minimus muscles
- thickening of the synovial membrane and increased fluid production

Causes
- friction from repetitive movement
- trauma
- RA
- septic bursitis

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20
Q

State the presentation of trochanteric bursitis

A

TROCHANTERIC BURSITIS

Presentation
- exacerbated by activity
- no reduction in ROM
- sleep disturbances
- pain on resisted adduction of hip

21
Q

State everything you know about trochanteric bursitis
(pathogenesis, causes, presentation)

A

TROCHANTERIC BURSITIS

Pathogenesis
- inflammation of the bursa which overlies the greater trochanter of femur
- thickening of synovial membrane and fluid production

Causes
- friction from repetitive movements
- trauma
- RA
- septic bursitis

Presentation
- exacerbated by actiivty
- no reduction in ROM
- sleep disturbances
- pain on resisted adduction of hip

22
Q

Recall the tendons that make up the pes anserine

A
  1. semitendinosus
  2. sartorius
  3. gracilis
23
Q

State the difference between medial joint line OA and pes anserine bursitis

A

MEDIAL JOINT LINE OA (articular)
- medial joint line palpated above pes anserine
- passive and active movements are equally painful
- tender along joint line
- pain in all planes of joint movement

PES ANSERINE BURSITIS (peri-articular)
- palpate pes anserine on medial side of knee
- passive movements less painful than active movements
- tender in structure of involvement only
- pain in certain planes of movement

24
Q

State the pathogenesis and presentation of baker’s cyst

A

BAKER’S CYST

Pathogenesis
- accumulation of synovial fluid in bursa between tendons of gastrocnemius and semitendinosus
- associated with RA, OA and meniscal tears

Presentation
- mild pain on knee flexion
- non-pulsatile swelling of popliteal fossa

25
Q

State the causes, presentation, complication and investigations of diabetic foot ulcer

A

DIABETIC FOOT ULCER

Causes
- abnormal pressure or mechanical stress chronically applied to the foot
- peripheral neuropathy and arterial diseases
- altered metabolism

Presentation
- foul smelling ulceration
- not much pain sensation (due to DM having peripheral neuropathy)

Complication
- erosion of bone and OM –> amputation

Investigation
- swab after wound debridement –> bacterial culture

26
Q

State the pathogenesis, clinical presentation and complication of dermatomyositis

A

DERMATOMYOSITIS

Pathogenesis
- inflamamtory myopathy characterised by inflammation and skin rash
- possible viral or autoimmune

Presentation
- arises in very young or old
- difficulty swallowing
- muscle weakness, stiffness, soreness
- violet-coloured upper eyelids
- violacceous skin rash
- SOB
- mechanic’s hands

Complication
- interstitial lung disease

27
Q

State the investigations and treatments used for dermatomyositis

A

DERMATOMYOSITIS

Investigation - blood test positive for anti-jo1 antibodies

Treatment - corticosteroids

28
Q

State everything you know about dermatomyositis
(pathogenesis, presentation, investigation, treatment)

A

DERMATOMYOSITIS

Pathogenesis
- inflammatory myopathy characterised by inflammation and skin rash
- possible viral or autoimmune

Presentation
- arises in very young or old
- difficulty swallowing
- muscle weakness, stiffness, soreness
- violet-coloured upper eyelids
- violacceous skin rash
- SOB
- mechanic’s hands

Complication - interstitial lung disease

Investigation - blood test positive for anti-jo1 ab

Treatment - corticosteroids

29
Q

State what PVL stands for. State what PVL is.

A

PVL = panton valentine leukocidin

PVL is the virulence factor pdocued by some strains of MRSA that cause leukocyte lysis and necrosis

30
Q

State the clinical presentation and complication of staph aureus infections for LL

A

STAPH AUREUS INFECTIONS

Clinical presentation
- systemic (fever, tachycardia, htn, low oxygen saturation)
- widespread macular rash

Complication
- septic shock –> multi-organ failure
- necrotising pneumonitis
- tissue necrosis

31
Q

State the investigations for staph aureus infection of LL

A

STAPH AUREUS INFECTION

Investigation
- elevated lft (ast/alt)
- fbc (thrombocytopenia, leukopenia)
- elevated crp (c-reactive protein)

32
Q

State the factors that maintain stability of hip joint

A
  1. depth of articular surface (acetabulum labrum deepens articular surface)
  2. surrounding muscles
  3. ligaments - ischiofemoral, iliofemoral, pubofemoral
33
Q

State the common causes of posterior dislocation of hip

A

POSTERIOR DISLOCATION OF HIP
- dashboard injury - hip dislocated posteriorly
- medial rotation of foot and foot pointed medially

34
Q

State the common presentations of posterior displacement of hip

A

POSTERIOR DISPLACEMENT OF HIP
- femoral head fracture
- compression of arteries resulting in avascular necrosis of head of femur
- post traumatic OA
- sciatica (L4-S3) –> weak knee flexion (hamstrings paralysed), muscles below knee paralysed, loss of sensation of almost whole leg, foot drop, foot inverstion (evertors paralysed), equinovarus

35
Q

State everything you know about posterior dislocation of head of femur
(causes, presentation, investigation)

A

POSTERIOR DISLOCATION OF FEMORAL HEAD

Causes
- dashboard injury –> posterior dislocation
- medial rotation of foot and foot medially pointed

Presentations
- fracture of femoral head
- compression of arteries –> AVN of femoral head
- post-traumatic OA
- sciatica (L4-S3) –> weak flexion (hamstrings paralysed), all muscles below knee paralysed, loss of sensation of almost entire leg, foot drop, foot inversion (evertors paralysed), equinovarus

Investigation - X-ray of hip, CT scan

36
Q

State the most commonly sprained ligament in the ankle.

State the less common ligaments that are also prone to sprain.

A

Most prone = anterior talofibular ligament (part of lateral collateral ligament when there is excess inversion)

Less prone
- posterior talofibular ligament
- calcaneofibular ligament

37
Q

State the factors that contribute to ankle joint stability

A
  1. medial and lateral collaterla ligaments
  2. inferior transverse tibiofibular ligament (syndesmosis)
  3. tendons anteiror and posterior to ankle
  4. tiba + 2 malleoli tightly grip the talus to allow for stronger articulation
38
Q

State the presentation and treatment of sprained ligament in ankle

A

SPRAINED LIGAMENT IN ANKLE

Presentation
- cardinal signs of inflammation (pain, loss of funtion, redness, swelling, fever)
- bruising due to hematoma in tissue surrounding joint
- patient initially able to walk but pain worsens a few hours after injury

Treatment - RICE (rest, ice, compression, elevation)

39
Q

State the pathology behind meralgia parasthetica

A

MERALGIA PARASTHETICA = compression of lateral cutaneous nerve of thigh

40
Q

State the clinical presentation of meralgia parasthetica

A

MERALGIA PARASTHETICA

Presentation
- numbness and burning sensation on lateral region of thigh
- no motor deficits since lateral cutaneous nerve is purely sensory

41
Q

State the causes and presentation of common peroneal nerve palsy

A

COMMON PERONEAL NERVE PALSY

Cause
- compression of the head of fibula due to fracture

Presentation
- paralysis of dorsiflexors and extensors
- foot drop
- paralysis of evertors
- loss of sensation on lateral leg and dorsum of foot

42
Q

State the difference between L5 radiculopathy and common peroneal nerve palsy

A

L5 RADICULOPATHY
- cannot abduct hip (L5 root involved in superiro gluteal nerve)
- cannot laterally rotate hip

COMMON PERONEAL NERVE PALSY
- press on fibular neck –> numbness and pain
- foot drop and inversion
- normal hip abduction and lateral rotation

43
Q

State the difference betweeen L3 radiculopathy and femoral nerve palsy

A

L3 RADICULOPATHY
- obturator N affected –> adduction weak
- demratome distribution numbness smaller

FEMORAL NERVE PALSY
- adduction strong
- dermatome distribution larger

44
Q

State the 7 non-traumatic causes of knee pain

A
  1. OA
  2. RA
  3. psoriatic arthritis
  4. osteomyelitis
  5. septic arthritis
  6. gout
  7. pseudogout
45
Q

State the pathogenesis of pufferfish poisoning

A

PUFFERFISH POISONING

Pathogenesis
- pufferfish carry pseudoalteromonas tetradonis bacteria which produces lethal amounts of tetradotoxin in internal organs such as liver, ovaries and skin
- TTX block voltage-gated sodium channels found in axons of CNS and PNS –> stops nerve conduction
- TTX cannot cross BBB hence only affects PNS

46
Q

State the clinical presentations and complication of pufferfish poisoning

A

PUFFERFISH POISONING

Presentation
- normal HR
- conscious
- numbness and wekaness in hands and legs
- shallow rapid breathing with low O2 saturation
- n/v + diarrhoea
- no reflexes
- hypotonia
- wasting and fasciculations

Complication - respiratory collapse

47
Q

State the pathogenesis of compartment syndrome

A

COMPARTMENT SYNDROME

Pathogenesis
- swelling of muscles –> compression of blood vessels and nerves
- causesd by = direct trauma, burns, prolonged immobilisation post surgery, dehydration, DM, rhabdomyolysis

48
Q

State presentation and treatment of compartment syndrome

A

COMPARTMENT SYNDROME

Presentation
- pain, swelling, redness, warmth
- ischaemia
- nerve damage

Treatment - fascietomy to relieve pressure and prevent further vessel and nerve damage

49
Q

State the difference between soleus injury and gastrocnemius injury

A

SOLEUS INJURY
- same pain elicited on dorsiflexing foot when knee is extended and flexed

GASTOCNEMIUS INJURY
- easier to dorsiflex foot when knee flexed

M2 Pathology (21 decks)

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