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Pathology > Muscoskeletal part 1 > Flashcards

Muscoskeletal part 1 Flashcards

1
Q

Sudden injury fractures

A

Could be compression, shearing and tension. Human bones have low tolerance for tension.

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2
Q

Complete vs incomplete fracture

A

Complete is all the way through bone

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3
Q

Potts fracture

A

Ankle-distal fibula

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4
Q

Colles fracture

A

Wrist-distal radius

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5
Q

How are joint disorders categorized

A

Inflammatory or non

Non = no synovial membrane inflammation or system S&S

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6
Q

Osteoarthritis

A

Non-inflammatory degenerative with loss of articular cartilage in synovial joints
The most common joint disease

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7
Q

Types of osetoarthritis

A

Primary with an unknown etiology, age is a factor and maybe wear and tear
Secondary from congenital defects, trauma, or inflammation

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8
Q

Pathophysiology of osteoarthritis

A

Articular cartilage erodes, bone underneath thickens, spurs form and it mainly affects weight bearing joints

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9
Q

Clinical manifestations of OA

A

Hip, knee, foot, hand, lumbar and C-spine affected commonly
Aching, diffuse pain exacerbated by USE
Stiffness, reduced mobility, crepitus, swelling, deformed joints.
New bone formation causes areas of enlargement in OA to feel hard, in RA they feel soft

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10
Q

Two nodes in OA

A

Heberden (distal interphalangeal joint)

Bouchard’s (middle joint)

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11
Q

RA definition

A

Rheumatism is an disease process or condition involving joints and connective tissue
Arthritis is joint swelling (a descriptive term not a diagnosis)

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12
Q

RA overview

A

A chronic, systemic autoimmune disease which causes connective tissue inflammation (mainly joints) with no known cause
Family predisposition

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13
Q

RA etiology

A

Autoimmune mediated
70-80% have RF factor (self produced antibody IgRF)
Activation of T-cells by a microbial agent, from a genetic predisposition and environmental trigger

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14
Q

RA pathogenisis

A

Begins as synovitis, immune system has inflammatory response which destroys surrounding joint structures.
Normal inflammation mechanisms lead to tissue destruction (phagocytes, lysosomal enzymes, vasodilation, increased vascular permeability)
Chronic inflammation causes hyperplasia of synovial cells and surrounding tissue

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15
Q

RA pathogenesis part 2

A

Extensive angiogenesis within synovium
New granulated vessel tissue (pannus) extends between cartilage and subchondral bone
Inflammatory cells within Pannus have a destructive effect on the cartilage and bone

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16
Q

Local clinical manifestation of RA

A

5 cardinal signs of inflammation

Rheumatoid nodules - granulomatous lesions that develop around small blood vessels, usually over pressure points

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17
Q

Systemic clinical manifestations of RA

A

Immune mediated fatigue, weakness, weight loss, anorexia, fever
Generalized aching and stiffness
Exacerbations and remissions

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18
Q

Common RA joints

A

Fingies, hands, wrists, knees and feetsies

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19
Q

Infectious arthritis

A

Results from spread of pathogens during sepsis from adjacent bone infections
From surgery or removing joint fluid, most commonly lyme disease

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20
Q

Pathophysiology of arthritis

A

Knee or other weight bearing joints
Transient exudation of fluid into joint cavity
S&S of synovitis

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21
Q

Gout overview

A

A group of diseases called Gout syndrome

We focus on acute gouty arthritis, men over 40 most common

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22
Q

Gout physiology

A

Problem with uric acid production or excretion, too much of it means it is deposited in joint cavaties where it crystallizes
90% in big toe

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23
Q

Gout classifications

A

Primary gout:
Genetic defect leading to abrnomal purine metabolism or decreased excretion of uric acid
Secondary gout:
From an underlying condition like a tumor elevating nucleic acid breakdown or renal disease leading to decreased exretion

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24
Q

Gout pathogensis

A 
Uric acid (from purines -A/G) crystallizes as monosodium urate. Decreased temp increases crystals
Crystals set off inflammatory response
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25
Q

Gout patho 2

A

Microtophi (nodes of MU crystals) have chemotactic properties
The inflammation destroys joint tissue
Repeat attacks will eventually build up tophi (larger versions)

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26
Q

Leukocytosis

A

elevated WBC

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27
Q

Clinical manifestations of acute gout

A

Usually one joint, decreased temp increases risk.
Swelling, hyperemic, warm, painful
Fever, leukocytosis, tachy cardia, exhaustion

28
Q

Clinical manifestations of chronic gout

A

Less inflammation, more deformities
Sub q deposits in ears, arms and patella
25% have renal failure

29
Q

Ankylosing Spondylitis definition

A

Ankylosis - stiffening of joint
Spondylitis - vertebrae inflammation
Classified as spondyloarthropathy (RF factor generally not seen)

30
Q

Ankylosing spondylitis overiew

A

A chronic inflammatory joint disease with thickening of the spine and SI joints (males) and peripheral joints (females)
Onset is 20-30 years old
Marked by remission and exacerbation

31
Q

Etiology of ankylosing spondylitis

A

System inflammatory response, with genetic predisposition and environmental trigger

32
Q

Pathogenesis

A

Immune mediated, inflammatory erosion of sites where tendons and ligaments attach to bone
Begins in SI joints and travels up
Vertebral inflammation leads to fibrosis, ossification, and fusion of joints

33
Q

Clinical manifestations of ankylosing spondylitis

A

Kyphosis, osteoporosis, hip and back pain (exacerbated by REST)
may restrict chest wall movement because of costovertebral joint involvement
Similar systemic S&S of RA

34
Q

Characters of muscular disorders

A 
Weakness (can't contract)
Fatigue (can't sustain contraction)
Spasm (myotonus)
Fibrillation
Myalgia (pain)
35
Q

Neurogenic atrophy

A

Denervation causes muscle cells to fibrilliate, atrophy, and eventually be replaced with fibrous tissue

36
Q

Neurogenic atrophy from upper motor neuron

A

Located in central cortex f brain, can be caused by injury to CNS, CVA, head injury, ALS, spinal cord trauma

37
Q

Neurogenic atrophy lower motor neurons

A

Injury to peripheral nerves from intervertebral disk rupture, ankylosing spondylitis, knife wounds, ischema (the beeties)
Axons regrow at 1-2mm/weel

38
Q

Myasthenia (muscle weakness) Gravis (potent) etiology

A

Autoimmune mediated, believed to be caused by sensitizes helper T cells which leads to attack on ACH receptors in NMJ
Often associated with lupius, RA)

39
Q

Myasthenia Gravis pathophysiology

A

Post synaptic ACH receptors not recognized as self, so they are destroyed by helper T cells

40
Q

Myasthenia Gravis cranial nerves which can be involved

A

9, 10, 11, 12

41
Q

Clinical manifestation of myasthenia gravis

A

Begins with fatigue after exercise, recurrent upper resp track infections, facial weakness, airway and swallowing problems, weak resp muscles, and eventually quadriparesis

42
Q

Fibromyalgia

A

10:1 ratio to women, widespread joint and muscle pain with fatigue and tender points plus nonrestorative sleep
Noninflammatory
Can co exist with other muscular disorders
Characterized by pain in all areas, especially ‘tender points’ <3 months

43
Q

Fibromyalgia tender points

A

Occiput, traps, dimples, outer lower glute

Anterior: C5-C7, second rib, elbows, knee

44
Q

Precipitating fibromyalgia factors

A

Flu-like viral illnes, chronic fatigue syndrome, HIV, lime disease, trauma (physical/emotional) steroid withdrawal

45
Q

Clinical manifestations of fibromyalgia

A

Diffuse and chronic, gnawing or burning pain.
Fatigue without relief by sleep
Headache, IBS, excess sensitivity to cold

46
Q

Chronic fatigue syndrome

A

Pronounced fatigue with sudden onset, debilitating tiredness >6months and may worsen with physical and mental activity

47
Q

CFS etiology

A

Unknown, neurological, psychatric and biological underpinnings
Possibly secondary to viral infection
4:1 M:F ratio

48
Q

CFS pathogenesis

A

Low brain stem perfusion, CNS abnormalities, immune dysfunction, increased inflammatory cytokines

49
Q

CFS clinical manifestations

A 
6 months of symptoms
Fatigue worsened by effort
Muscle and joint pain
Headaches
Flu like symptoms with tender lymph nodes
Various neurocognitive symptoms
50
Q

Muscular Dystrophies

A

All are marked by degeneration of skeletal muscle with
Genetic defect
Primary muscle cell pathology
Progress S&S related to muscle wasting

51
Q

Pathophysiology of muscular dystrophies

A

Abnormality in intracellular metabolism of muscle fibers, deficiency of dytrophin ( a muscle cell protein membrane which binds actin to cell membrane and part of NMJ)
The deficiency leads to degeneration and necrosis of cell, replacement of fiber with fat and other CT, and release of CK enzymes

52
Q

Duchenne’s MD

A

x-linked recessive (more common in males)
Most common MD
Usually die before 21
First noted at 3 (clumsy/falls)
Slow motor development, progressive weakness, muscle wasting, waddling gait, walk on toes, kyphoscoliosis
1 in 3 retarded
Die from resp insufficiency

53
Q

Beckers MD

A

Mild form of Duchenne’s

S&S later in life and milder, live to be 35

54
Q

Myotonic MD

A

Second most common, chromosome 19 autosomal (M and F equally)
S&S appear in adulthood with slow progression
Insulin resistance in muscle cells is common

55
Q

Myotonic MD 2

A 
Mental and muscle deterioration, myotonia (muscles can contract by not relax)
Facial weakness (hatchet face appearance)
56
Q

Cerebral palsy

A

Highly variable presentaiton some degree of motor impairement
Non progressive
S&S change with growth and maturation

57
Q

Etiology of CP

A

Caused by ischemia, pre peri or immediately postnatal

Also caused by genetic mutations, infections or metabolic disorders in utero.

58
Q

Patho of CP

A

Brain atrophy specific to motor function, atrophy not limited to areas of motor control

59
Q

Clinical manifestations of CP

A 
Quads, diplegia 
Spastic hyperreflexia/paralysis
Loss of motor control
Ataxic gait
Loss of balance
Intellectual, speech and vision problems
Seizures
60
Q

Subluxation

A

Incomplete or partial disolocation of joint or organ

61
Q

Rhabdomyolysis

A

Or myoglobinuria
Excessive muscle damage releases intercellular protein Myoglobin after cell destrction
Commonly found first in urine

62
Q

Etiology of rhabdo

A 
Direct trauma or crush injury
Infections
Hyperthermia
Excessive exertion
Electrocution
Burns
NM blocking agents
CNS depressants
Inflammation
Acidosis
63
Q

Pathogenesis of rhabdo

A 
Injury causes ischemia, edema, compartment pressure and tamponade so muscle infarcts
A limp extremity can cause rhabdo
Cell contents released:
Myoglobin
CK
Phosphate
Potassium
Calcium
64
Q

Compartment vs crush syndrome

A

Rhabdo in local scale or global

65
Q

Rhabdo clinical manifestations

A

Significant amounts of myoglobin, CK in urine with red/brown pee
Renal failure
Shock/acidosis
Lyte issues

Pathology (24 decks)

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