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FNP Advanced Pathophysiology > Skeletal and Muscle Systems Part 2 > Flashcards

Skeletal and Muscle Systems Part 2 Flashcards

1
Q

Congenital Diseases of Bone

A
  • Osteogenesis Imperfecta
  • Achrondoplasia
  • Osteopetrosis
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2
Q

General Terms

A

see below

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3
Q

Dysostoses

A
  • congential malformations of bone
    -Aplasia- absence of bone
    -Supernumerary- extra bones
    Abnormal fusion of bones
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4
Q

Dysplasias:

A
  • abnormalities of bone osteogenesis

- —-mutations affecting bone or cartilage growth

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5
Q

Examples of dysplasias:

A
  • Osteogenesis imperfect
  • Achrondoplasia
  • Osteopetrosis
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6
Q 
Osteogenesis Imperfecta (OI) 
Brittle bone disease
A 
● Cellular pathophysiology
-Etiology is Genetic mutation
-Defective synthesis of Collagen type 1
-----Extracellular bone matrix
-----Skin, joints, eyes
-Phenotype has broad range
-Inadequate supply of 
bone- fragile skeleton
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7
Q

4 Clinical Classifications

A

See below

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8
Q

Type 1 OI:

A

Normal lifespan
Modest increase fracture rate in childhood that decreases in puberty
Blue Sclerae so that underlying choroid visible
Hearing loss
Small misshapen teeth

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9
Q

Type II OI:

A
  • Fatal pre or immediately post-partum due to in utero fractures
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10
Q

Achrondroplasia

A

● Cellular pathophysiology

  • Etiology is genetic mutation
  • Fibroblast growth factor receptor 3 (FGFR3) is activated
  • Activated FGFR3 inhibits chondrocyte proliferation
  • Suppression of epiphyseal growth plate expansion long bones
  • Long bone growth stunted
  • All bones that develop from cartilaginous framework
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11
Q

Achrondoplasia: Clinical

A 
-Clinical 
Major Cause of Dwarfism: 
- Disproportionate shortening of proximal extremities 
-Bowed legs 
-Lordosis

Severe cases can lead to perinatal death from respiratory failure

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12
Q

Osteopetrosis (Stone Bone)

A

● Cellular pathophysiology
-Etiology is genetic mutations
-Rare
-Exact molecular cause of osteoclast dysfunction not certain.
-Defective Osteoclast-mediated bone resorption
(Normally, the cells decalcify the matrix prior to matrix digestion.)
-Bone abnormally hard and structurally unsound with tendency to break.

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13
Q

Osteopetrosis : Clinical

A
  • Fractures
  • Compression of cranial nerve that leads to related problems
  • Recurrent infections due to reduced marrow space affecting hematopoiesis
  • Hepatosplenomegaly due to extramedullary (outside the marrow) hematopoiesis
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14
Q

Osteopenia

A

• Not a disease
• Condition of Low Bone Mass
– T score between -1 and -2.5
• Diagnosed by Bone Density test
• 34 mil women and 12 mil men
• Could develop Osteoporosis if prevention strategies not taken.
– Especially if person has Osteoporosis risk factors

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15
Q

Osteoporosis

A 
• Disease
• Porous bones that are fragile
• Can be prevented and treated
• 44 million Americans, 17 billion dollars
– 80% are women
• 1 of 2 women
• 1 of 8 men
 lose trabecular bone volume (spongy interior matrix) (up to 20%)
 excess resorption
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16
Q

Types of Osteoporosis

A

See below

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17
Q

Type 1: Postmenopausal Osteoporosis

A
  • women 51-75 yr, accelerated bone loss, especially trabecular
  • common fractures of vertebrae and distal femur
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18
Q

Type II: Senile Osteoporosis

A
  • Men and women greater than 71
  • Proportional loss corticol and trabecular
  • Common fx’s of vertebrae and distal femur
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19
Q

Type III: Secondary Osteoporosis

A
  • Men and women any age

- Secondary to other such as drug therapy and diseases

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20
Q

Table 21: Broken into Categories of Generalized Osteoporosis

A

See Below

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21
Q

Primary

A
  • Post menopause: MOST COMMON

- Senile - also most common

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22
Q

Secondary

A
  • Endocrine
  • Neoplasia
  • GI disorders
  • Disease Drugs
  • Miscellaneous
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23
Q

Endocrine Disorders

A
  • Hyperparathyroidism
  • Hypogonadism
  • Pituiatry tumors
  • Diabetes type 1
  • Addison Disease
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24
Q

Neoplasia

A
  • Multiple myeloma

- Carcinomatosis

25
Q

GI Disorders

A
  • Malnutrition
  • Malabsorption
  • Hepatic insufficiency
  • Vitamin C and D deficiencies
  • Idiopathic
26
Q

Disease Drugs

A
  • Anticoagulants
  • Chemotherapy
  • Corticosteroids
  • Anticonvulsants
  • Alcohol
27
Q

Miscellaneous

A
  • Osteogenesis Imperfecta
  • Immobilization
  • Pulmonary Disease
  • Homocystinuria
  • Anemia
28
Q

Osteoporosis Risk Factors

A 
Risk Factors that can not be Changed
• Female more than male
• Age
• Body size (Small, thin) (< 21 kg/m2)
• Ethnicity (White and Asian women)
• Family history
29
Q

Osteoporosis Risk factors

A

Changeable Risk Factors
• Sex hormones. Low estrogen levels due to missing menstrual periods or to menopause can cause osteoporosis in women. Low testosterone levels can bring on osteoporosis in men.
• Calcium and vitamin D intake
• Low Exercise Activity level
• Smoking
• Drinking alcohol in excess
• Some Medications
• Glucocorticoid, steroid, antiepileptics, excess TH, chemotherapy, GRH antags.
• Chronic diseases
• Hyperthyroid, hyperparathyroidism, RA, SLE, chronic lung, malasorptive GI, eating disorders, MS, Parkinson’s, Spinal injury, hematologic/oncologic

30
Q

Osteoporosis Male Risk factors

A 
Male risk factors
• Small stature
• Prostate cancer
• Sedentary lifestyle
• Alcohol
• smoking
31
Q

Male Prevention

A 
Prevention
• Calcium and Vitamin D
• Weight bearing exercise
• No smoke
• Reduce alcohol intake
• Monitor with bone mass density
• Medications
• Fall prevention strategies
Male prevention
Same as women
32
Q

 HRT or ERT menopausal women (Not recommended as of 7/2002)

A 
Treatment
• Balanced diet:
– rich in calcium and vitamin D
• An exercise plan
• A healthy lifestyle
• Medications, if needed
33
Q

Osteopenia V Osteoporosis

A
  • if osteopenia, initiate lifestyle prevention strategies

- If osteoporosis, then continue lifestyle prevention/treatment and perhaps medications

34
Q

Outcomes of Osteoporosis

A

• Common fractures are vertebrae, forearm, hip and ribs
• Vertebrate fractures
– Height loss, spinal deformity, chronic back pain, difficult breathing
• Most common cause of hip fractures
– Disability, mortality

35
Q

Let us delve into a cellular molecular pathway

A

See Below

36
Q

Normal paracrine (localized secretion to affect activity) regulation of osteoclast and osteoblast

A

●Osteoclasts are originally macrophage precursor cells
●Receptor activator for nuclear factor ΚB (RANK)
●RANK receptors are on the Osteoclast precursor
●Stromal or osteoblasts release RANK ligand
●Stromal or osteoblasts release macrophage cell stimulating factor (M-CSF)

37
Q

The key event that leads to bone resorption

A

● The key event that leads to bone resorption
RANK ligand + RANK receptor on osteoclast precursor
+
M-CSF ligand + M-CSF receptor on osteoclast precursor
↓
activate to differentiate to osteoclast mature cell

38
Q

● COUNTER BALANCE by the Stromal or osteoblasts release osteoprotegerin (OPG)which blocks the RANK ligand + RANK receptor interaction on osteoclast precursor

A

View image in textbook if more description needed

39
Q

What changes to lead to postmenopausal pathophysiology of osteoporosis?

A

 decrease estrogen postmenopause leads to increased osteoclast activity
and a period of accelerated loss
● increased osteoclast activity
● LOW estrogen leads to increase IL-1, IL-6, and TNF which in turn leads to increase in RANK and RANK ligand and less OPG. Ultimately, will lead to more osteoclast activity

40
Q

Acquired Diseases of Bone development

A

See below

41
Q

Paget’s Disease (Osteitis Deformans):

A
  • chronic bone inflammation
    -repetitive episodic regional resorption of bone followed by rapid bone formation
    -the result is disorganized and not as strong as normal
    -cuase could be a paramyxovirus infection-not conclusive yet
    -Which bones affected?
    can be a variety of bones- see text for examples
    -numerous skeletal, neuromuscular, cardiovascular complications possible- symptoms related to bone deformations or nerve impingement
    -many cases are mild
    -sometimes during episodes, the overlying skin in warm
    -if skull proliferating, can have headache, auditory, and visual problems
    -Low back ache
  • bowing of lone bones
42
Q

Metabolic and Nutritional Bone Alterations

A

Rickets/Osteomalacia

43
Q

Rickets

A
  • Infant or growing child
  • Lack of Vitamin D
  • bowed legs and other deformities
44
Q

Osteomalacia

A
  • adults
  • calcium and or phosphorus deficiency
  • disease or nutritional
45
Q

Osteonecrosis (Avascular necrosis):

A

Ischemic necrosis followed by bone infarction
Causes:
Vascular compression or disruption such as following a fracture
 steroids
 thromboembolic disease
 primary vessel disease

46
Q

Clinical course of osteonecrosis

A
  • depends on size and location

- range from pain to osteoarthritis

47
Q

Osteomyelitis

A

inflammation of bone and marrow cavity
usually due to an infection
-most common are pyogenic bacteria and mycobacterium tuberculosis

48
Q

Joints

A

see diseases below

49
Q

Osteoarthritis

A

-degenerative joint disease
 joint damage and inflammation caused by biochemical alteration of articular cartilage in one or a few joints
 inflammation part is secondary and not always present
 etiology unknown for primary osteoarthritis
associated with age
 secondary osteoarthritis is due to trauma or infection or gender predisposition (hips in men, hands/knees in women)

50
Q

Pathophysiology of Osteoarthritis:

A
  • proliferation chondrocytes(cartilage cells) of articular cartilage
  • matrix integrity cracks
  • cartilage degraded
  • expose bone
  • stress on bone stimulates disordered growth
  • maybe synovial inflammation
51
Q

Symptoms of Osteoarthritis

A

joint pain, a.m. stiff, limit of movement

inflammatory component has been controversial:

  • whether it is primary or secondary, it occurs
  • anti-inflammatory drugs have not been able to reverse or necessarily slow disease progression
52
Q

Rheumatoid Arthritis (RA):

A 
-autoimmune
humoral and cellular
- inflammatory joint
- etiology unknown
genetic and environment likely
- Under investigation: viruses
human T-cell lymphotropic virus type I
retroviruses
Epstein-Barr virus
Herpes virus
Rubella virus
- bacteria under investigation
mycoplasma
mycobacteria
enteric bacteria
-antibodies- rheumatoid factors to synovial lymphocyte generated IgG which is considered foreign
 T lymphocytes migrate to area
CD4+ (recruit other inflammatory WBCs)
 synovial membranes joints and other tissue
 joint destruction, neuropathies, skeletal muscle inflammation, vasculitis, other
53
Q

Rheumatoid Arthritis: Active Disease

A 
ongoing joint pain
significant morning stiffness
significant fatigue
active synovitis
persistant increase in erythrocyte sedimentation rate (ESR) or C-reactive protein
54
Q

Hyperuricemia and Gout

A
  • increase serum uric acid
  • purine breakdown –> uric acid
  • recurrent attacks with urate crystals in synovial fluid
  • aggregated deposits of urate in joints -cripple and deformity
  • renal disease
55
Q

Primary Gout: (90% of cases)

enzyme defects unknown

A
  • overproduction of uric acid
  • normal excretion (majority)
  • increased excretion (minority)
  • under excretion of uric acid with normal production
56
Q

Secondary Gout: (10% of the cases)

associated with increased nucleic acid turnover - e.g. leukemia’s, chronic renal disease, inborn errors of metabolism

A
  • Overproduction of uric acid with increased urinary excretion
  • Reduced excretion of uric acid with normal production -Overproduction of uric acid with increased urinary excretion e.g.,
  • complete HGPRT deficiency (Lesch-Nyhan syndrome)
57
Q

Clinical features of Gout

A

● pain that can be severe, warmth, erythema
● 50% in big toe, 90% in instep, ankle, heal, wrist
● Systemic symptoms rare
● Acute recurring episodes of various frequencies (months to few years)
● Untreated can resolve
● over time the symptoms fail to resolve completely and develop chronic tophaceous gout

58
Q

Pseduogout (Chondrocalcinosis):

A
  • calcium pyrophosphate crystal deposits various joints

FNP Advanced Pathophysiology (6 decks)

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