Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Complete vs incomplete fracture

A

Complete is all the way through bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Potts fracture

A

Ankle-distal fibula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Colles fracture

A

Wrist-distal radius

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How are joint disorders categorized

A

Inflammatory or non

Non = no synovial membrane inflammation or system S&S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Osteoarthritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathophysiology of osteoarthritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Two nodes in OA

A

Heberden (distal interphalangeal joint)

Bouchard’s (middle joint)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

RA overview

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Systemic clinical manifestations of RA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Common RA joints

A

Fingies, hands, wrists, knees and feetsies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Pathophysiology of arthritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Gout overview

A

A group of diseases called Gout syndrome

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Gout pathogensis

A 
Uric acid (from purines -A/G) crystallizes as monosodium urate. Decreased temp increases crystals
Crystals set off inflammatory response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Gout patho 2
Microtophi (nodes of MU crystals) have chemotactic properties The inflammation destroys joint tissue Repeat attacks will eventually build up tophi (larger versions)
26
Leukocytosis
elevated WBC
27
Clinical manifestations of acute gout
Usually one joint, decreased temp increases risk. Swelling, hyperemic, warm, painful Fever, leukocytosis, tachy cardia, exhaustion
28
Clinical manifestations of chronic gout
Less inflammation, more deformities Sub q deposits in ears, arms and patella 25% have renal failure
29
Ankylosing Spondylitis definition
Ankylosis - stiffening of joint Spondylitis - vertebrae inflammation Classified as spondyloarthropathy (RF factor generally not seen)
30
Ankylosing spondylitis overiew
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
Etiology of ankylosing spondylitis
System inflammatory response, with genetic predisposition and environmental trigger
32
Pathogenesis
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
Clinical manifestations of ankylosing spondylitis
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
Characters of muscular disorders
``` Weakness (can't contract) Fatigue (can't sustain contraction) Spasm (myotonus) Fibrillation Myalgia (pain) ```
35
Neurogenic atrophy
Denervation causes muscle cells to fibrilliate, atrophy, and eventually be replaced with fibrous tissue
36
Neurogenic atrophy from upper motor neuron
Located in central cortex f brain, can be caused by injury to CNS, CVA, head injury, ALS, spinal cord trauma
37
Neurogenic atrophy lower motor neurons
Injury to peripheral nerves from intervertebral disk rupture, ankylosing spondylitis, knife wounds, ischema (the beeties) Axons regrow at 1-2mm/weel
38
Myasthenia (muscle weakness) Gravis (potent) etiology
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
Myasthenia Gravis pathophysiology
Post synaptic ACH receptors not recognized as self, so they are destroyed by helper T cells
40
Myasthenia Gravis cranial nerves which can be involved
9, 10, 11, 12
41
Clinical manifestation of myasthenia gravis
Begins with fatigue after exercise, recurrent upper resp track infections, facial weakness, airway and swallowing problems, weak resp muscles, and eventually quadriparesis
42
Fibromyalgia
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
Fibromyalgia tender points
Occiput, traps, dimples, outer lower glute | Anterior: C5-C7, second rib, elbows, knee
44
Precipitating fibromyalgia factors
Flu-like viral illnes, chronic fatigue syndrome, HIV, lime disease, trauma (physical/emotional) steroid withdrawal
45
Clinical manifestations of fibromyalgia
Diffuse and chronic, gnawing or burning pain. Fatigue without relief by sleep Headache, IBS, excess sensitivity to cold
46
Chronic fatigue syndrome
Pronounced fatigue with sudden onset, debilitating tiredness >6months and may worsen with physical and mental activity
47
CFS etiology
Unknown, neurological, psychatric and biological underpinnings Possibly secondary to viral infection 4:1 M:F ratio
48
CFS pathogenesis
Low brain stem perfusion, CNS abnormalities, immune dysfunction, increased inflammatory cytokines
49
CFS clinical manifestations
``` 6 months of symptoms Fatigue worsened by effort Muscle and joint pain Headaches Flu like symptoms with tender lymph nodes Various neurocognitive symptoms ```
50
Muscular Dystrophies
All are marked by degeneration of skeletal muscle with Genetic defect Primary muscle cell pathology Progress S&S related to muscle wasting
51
Pathophysiology of muscular dystrophies
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
Duchenne's MD
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
Beckers MD
Mild form of Duchenne's | S&S later in life and milder, live to be 35
54
Myotonic MD
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
Myotonic MD 2
``` Mental and muscle deterioration, myotonia (muscles can contract by not relax) Facial weakness (hatchet face appearance) ```
56
Cerebral palsy
Highly variable presentaiton some degree of motor impairement Non progressive S&S change with growth and maturation
57
Etiology of CP
Caused by ischemia, pre peri or immediately postnatal | Also caused by genetic mutations, infections or metabolic disorders in utero.
58
Patho of CP
Brain atrophy specific to motor function, atrophy not limited to areas of motor control
59
Clinical manifestations of CP
``` Quads, diplegia Spastic hyperreflexia/paralysis Loss of motor control Ataxic gait Loss of balance Intellectual, speech and vision problems Seizures ```
60
Subluxation
Incomplete or partial disolocation of joint or organ
61
Rhabdomyolysis
Or myoglobinuria Excessive muscle damage releases intercellular protein Myoglobin after cell destrction Commonly found first in urine
62
Etiology of rhabdo
``` Direct trauma or crush injury Infections Hyperthermia Excessive exertion Electrocution Burns NM blocking agents CNS depressants Inflammation Acidosis ```
63
Pathogenesis of rhabdo
``` 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
Compartment vs crush syndrome
Rhabdo in local scale or global
65
Rhabdo clinical manifestations
Significant amounts of myoglobin, CK in urine with red/brown pee Renal failure Shock/acidosis Lyte issues

Pathology (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions