Exam 6 Flashcards

1
Q

Functions of the skeletal system

A

Protection of internal organs

Provide bony attachments for muscles and ligaments

Present rigid levers to allow functional movement of the body and its separate parts

Store mineral and marrow elements for forming new blood cells

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2
Q

organic matrix of bone

A

Collagen fibers (strength and flexibility)

Ground substance (surrounds bone cells) Osteoblasts

Osteocytes

Osteoblasts

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3
Q

Inorganic mineral content

A

Mineral salts (calcium and phosphate)

Hard, rigid structure

Reservoir for calcium and phosphorus

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4
Q

Osteon (Haversion system)

A

Basic unit of bone

Haversion canals allow nutrients from blood vessels to reach the osteocytes

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5
Q

Osteoblasts

A

Lay down bone

Responsible for bone growth and repair

Estrogen secretion helps regulate

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6
Q

Osteoclasts

A

Bone resorption

Tearing down the old or excess bone

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7
Q

Cancellous bone (trabecular)

A

Spongy

Thin plates

Laid down in response to stress

Accomodates loads

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8
Q

Compact bone (cortical)

A

Resistant to compression

Dense in structure

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9
Q

Periosteum

A

Vascular

Inner layer contains

osteoblasts

Covers the entire bone except for the ends

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10
Q

long bone

A
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11
Q

Wolff’s law

A

Bone is laid down where it is needed and resorbed where it is not needed

Why is this important?

Immobilized bone or persons on bedrest are not subject to stress

Bone-resorbing activity

increases (osteoclasts)

Increased risk for fractures

Increased risk for falls

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12
Q

Geriatric Considerations

A

Increased bone resorption and decreased bone formation

-Osteoporosis

Increased bone circumference

-Pelvis widening

Dehydration of intravertebral disks

-Kyphosis

-Decreased height

Erosion and thinning of cartilage

-Synovial membrane fibrosis

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13
Q

Cartilage

A

Dense connective tissue

Supports, shapes, and cushions body structures

Avascular

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14
Q

Tendons

A

Attach bones to muscles

Allow movement

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15
Q

Ligaments

A

Connect bones to bones

Provide stability to joints

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16
Q

Bursea

A

Small sac synovial fluid around joints & between tendons, ligaments, bone

Located in areas of high friction-acts as a cushion

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17
Q

Types of joints which determine the ROM of a joint

A
  1. Synarthroses
  2. Diarthroses
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18
Q

Synarthroses

A

Fibrous - stabilize and fuse to surfaces and allow little movement (skull)

Cartilaginous - stabilize, transmit stress and allow little movement (symphysis pubis)

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19
Q

Diarthroses

A

Synovial or diarthroses - mobile joints

-Incapsulated with synovial fluid, cartilage, menisci

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20
Q

typical synovial joint

A
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21
Q

Torn Meniscus Etiology/Pathogenesis

A

Made of tough cartilage

Shock absorbers in knee

Menisci are often torn by rotation of the femur when the knee is flexed

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22
Q

Torn Meniscus Clinical Manifestations

A

Pain

Swelling

Tenderness when pressing on the meniscus

Popping or clicking within the knee

“Joint locking” or inability to completely straighten out the joint

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23
Q

Torn Meniscus Treatment

A

Anti-inflammatory medications, joint stabilization,

physical therapy

possible surgery

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24
Q

Protruded Disks Etiology

A

Padlike structures between vertebrae

-Annulus fibrosis

-Nucleus pulposus

Allow slight movement

Age related wear and tear

Lifting heavy objects/Twisting

Trauma

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25
Protruded Disk Clinical Manifestations
Pain Altered sensation -Numbness -tingling Motor weakness Diminished reflexes
26
Protruded disks treatment
-Bedrest -Narcotic pain medications -Muscle relaxers -Cortisone injections -Heat or ice -Traction -Ultrasound -Electrical stimulation -Short-term bracing for the neck or lower back -Surgery
27
Dislocations and Subluxations: Joints etiology/pathogenesis
Considerable tissue damage -Possible ligament tear -Rupture Subluxation: displacement from normal position; not as severe as a dislocation Dislocation: Articulating surface loses contact Commonly dislocated joints -Fingers -Patella -Shoulder
28
Dislocations and Subluxations: Joints clinical manifestations
Pain Alteration in normal contour of the joint Change in extremity length Loss of normal mobility
29
Dislocations and Subluxations: Joints treatment
-Immobilization -Reduction -Pain control -Treatment must include consideration of local soft-tissue trauma
30
Ligament injuries etiology/pathogenesis
Often occur when range of motion is exceeded Damage to surrounding tissue may occur Classified by the extent of tear Common site of injury is the knee (anterior cruciate ligament -ACL) -athletes
31
Ligament injuries clinical manifestations
Sudden "tearing" or "popping" sensation Pain with weight bearing Acute swelling
32
Ligament injuries treatment
Geared toward relief of symptoms Protection of the ligament Recovery is usually complete May require surgery
33
Injury to muscle and tendon
Minor strain -A few fibers of the tendons/muscle are torn -Usually from excessive physical effort Sprain -Traumatic injury to tendons, muscles, or ligaments >>>Pain >>>Swelling >>>Treatment varies with extent of injury TREATMENT: RICE: -R-EST -I-CE -C-OMPRESSION -E-LEVATION
34
Rotator cuff injury etiology/pathogenesis
Excessive use Rupture of tendon in rotator cuff under acromion bone Impingement syndrome: inflammation around joint causing severe characteristic pain with movement
35
Rotator cuff injury clinical manifestations/treatment
PAIN! Limited range of motion Treatment -injected steroids -repair
36
Fractures Etiology/Pathogenesis
A break in the continuity of bone, an epiphyseal plate, or a cartilaginous joint surface Trauma generates enough energy to fracture a bone also produces force enough to traumatize adjacent soft tissue Types of fractures -Transverse -Spiral -Longitudinal -Oblique -Comminuted -Impacted -Greenstick -Stress -Avulsion
37
transverse fracture
38
Longitudinal fracture
39
Oblique fracture
40
Comminuted fracture
41
Impacted fracture
42
Greenstick fracture
43
Stress fracture
44
Avuslion fracture
45
Epiphyseal injury
46
Classifications of fracture
extent and depth
47
Displaced fracture
End of fracture fragments separated
48
Nondisplaced fracture
Fracture fragments remain in alignment and position
49
Depressed fracture
Fracture displaced below the level of the surface of the bone (skull)
50
Complete fracture
Fracture line disrupts bone continuity through whole thickness
51
Incomplete fracture
Bone cracks but continuity is not disrupted
52
open (compound) fracture
Bone is broken and an external wound leads to the fracture site Increased risk for infection Osteomyelitis Difficult to manage
53
closed (simple) fracture
Fragments do not extend through mucous membranes or skin Skin is not broken
54
Fractures: Clinical Manifestations
Pain Swelling Loss of function Discoloration Deformity +/- Muscle spasm and shortening of extremity
55
Fractures treatment
Main goals: 1. Reduction -Restoring to normal anatomical position 2. Immobilization -Maintain proper alignment until bone healing occurs -External fixation -ORIF -Casts/splints/braces Rehabilitation
56
External fixation
57
Open reduction and internal fixation (ORIF)
58
Fracture Complications
Delayed healing Compartment syndrome Neurovascular injury Fat emboli Deep Vein Thrombosis (DVT) -Pulmonary embolus Osteomyelitis -Severe bone infection Osteonecrosis -Avascular necrosis -Compromised circulation-> ischemia->bone death
59
causes for Delayed healing
-Smoking -Malnutrition -Use of corticosteriods -Poor circulation -Infection -Elderly -Diabetes -Coronary heart disease
60
Compartment syndrome
-Triggered by injury to the tissues surrounding bone leading to inflammation, swelling, and sometimes hemorrhage -High pressure in a muscle compartment in the closed fascial space -Leads to decreased blood flow -Tissue hypoxia -Tissue death >>>Pain >>>Paralysis >>>Paresthesia >>>Pallor >>>Pulselessness
61
Neurovascular injury
-Damage related to casts/splints -Hemorrhage -Edema -Manipulation at the time of reduction
62
Fat emboli
-Fat from bone or adipose enters the venous system -Most common in long bone factures -Within 24 to 72 hours of trauma -Can affect any organ system -S&S: depend on system affected
63
Hip fracture etiology
Major health problem of elderly Female/Caucasian Most result from falls Risk Factors -Alcohol & caffeine -Inactivity -Tall stature -Low body weight -Psychotropic drugs -Dementia -Osteoporosis
64
Hip Fracture Pathogenesis
Usually fracture is proximal femur Location is important in terms of blood supply
65
Hip fracture treatment
Return to pre-injury function as soon as possible ORIF Surgical hip replacement -Early mobilization!
66
Scoliosis Etiology/Pathogenesis
Lateral curvature of the spine resulting in an S or a C-shaped spinal column Detected from asymmetry of the shoulders, hips, and chest wall Consequence of congenital, connective tissue, or neuromuscular disorder Majority ideopathic
67
Scoliosis Clinical Manifestations
Structural -Fails to correct on forced bending -More serious-progressive -Involves deformity of vertebrae and changes in hip, shoulder, and rib cage positions Nonstructural -Resolves when the patient bends to the affected side -Condition not progressive Related to postural problems Body image disturbances -Uneven shoulders of hips -Shoulder or scapular prominence -Rib or chest hump when bending over -C or S shaped spine Respiratory difficulties Pain
68
Scoliosis treatment
Surgical (for 40-50 degrees curvature or greater) -Spinal realignment -Fusion -Internal appliances Non-surgical -Braces -Exercises
69
Osteoporosis etiology
Most common metabolic bone disease 10 million people >50 Fractures of hip & spine -Increased mortality -740,000 deaths annually Specific cause unknown Contributing factors -Age -Risk Factors: >>>Low body weight >>>Smoking >>>Alcoholism >>>Low calcium intake >>>Prolonged immobilization -Genetics -Estrogen >>>Stimulating bone resorption over bone formation
70
Osteoporosis pathogenesis
Rate of bone resorption accelerates and the rate of bone formation decelerates Decreased density and loss of trabeculae A reduction in bone mass predisposes to fractures (brittle, porous bones) Bone Mineral Density (BMD) by Dual-energy absorptiometry (DXA) -T score <2.5
71
Osteoporosis Clinical Manifestations
May be asymptomatic until fracture occurs Bone fractures Kyphosis (Dowager's hump) Shortened stature Muscle wasting or spasms of back muscles Difficulty bending over May complain of impaired breathing
72
Osteoporosis treatment
Exercise -Moderate, regular -Walking, stationary bike -PT Calcium and Vitamin D -1000-1500 mg daily (calcium) -D3 400-1000 IU Antiresorptive Agents -bisphosphonates Prevent falls
73
Osteomalacia/Rickets etiology/pathogenesis
Inadequate and delayed bone mineralization results in spongy bone -Growing skeleton-Rickets -Mature skeleton-Osteomalacia Due to Vitamin D deficiency Deficient vitamin D → ↑Ca++ pulled from the bone Characterized by soft, weak bones
74
Osteomalacia/Rickets clinical manifestations
Kyphosis genu valgum ("knock knee") genu varum ("bowleg") Bone pain Fractures
75
eomalacia/Rickets treatment
Correction of underlying deficiency -Vitamin D supplements >>>Especially D3 -Adequate intake of calcium and phosphate -Exposure to sunlight >>>Increases Vitamin D absorption especially for elderly individuals
76
Paget disease etiology/pathogenesis
Slowly progressive metabolic bone disease characterized by an initial phase of excessive bone resportion (osteoclasts) followed by excessive bone formation Disorganized laying down of bone End result-new bone that is less compact, more vascular, and more fragile Cause unknown -May be genetic -May be a viral infection
77
Paget Disease Clinical Manifestations
Early in the disease no symptoms Severe and persistent pain Initial phase- affected bones soften and bend Later phase-bones hard and thick -Thick cranial bones result in vertigo, blindness, deafness, headaches and facial paralysis
78
Paget disease treatment
Reduce pain Preventing deformity and fracture -Calcitonin -Bisphosphonates These medications have been shown to decrease bone resorption, stabilize the fragile bone lesions, reduce pain, and the risk for fractures
79
Osteomyelitis Etiology
Severe infection of bone and local tissue requiring immediate attention May be acute or chronic More common in children Organisms reach bone by -Bloodstream (hematogenous) -Adjacent tissue (contiguous) -Direct introduction of organism into the bone >>>Trauma >>>Surgery >>>Hardware
80
Osteomyelitis pathogenesis
Organisms may begin to grow in a hematoma (from a recent trauma) or a weakened area (site of localized infection) Pathogen provokes inflammation → thrombosis of small distal vessels seal canaliculi→exudate enters the marrow → lifting of the periosteum →deprivation of underlying bone of O2 →necrosis and death of the infected tissue (sequestrum) Lifting also stimulates osteoblastic activity → deposition of new bone (involucrum) over the sequestrum Even after meticulous treatment the organism can appear years later
81
Osteomyelitis clinical manifestations
Acute Children -High fever -Pain at the site -Muscle spasms, redness, swelling -May not move the limb Adults -Fever -Malaise -Anorexia -Night sweats -Weight loss -Pain at rest
82
Osteomyelitis treatment
Acute 4-6 weeks of parenteral antibiotics for acute phase Analgesics Intracavity instillation of antibiotics Antibiotic choice based on C&S Debridement -Abscesses or extensive necrosis -Dead space filled with packing, bone grafts, muscle pedicles, or skin grafts Removal of infected hardware More chronic -Hyperbaric oxygen -Placement of antibiotic beads -Possible amputation
83
Hyperbaric Oxygen Therapy
Oxygen under greater than atmospheric pressure. Because of the heightened pressure, the pure oxygen is taken in by the body more rapidly. The oxygen is saturated into the blood at a much higher rate and is absorbed by every single muscle, tissue and cell of the body HBO2 has six actions which have been used to combat clinical infection: 1. Tissue rendered hypoxic by infection is supported 2. Neutrophils are activated and rendered more efficient 3. Macrophage activity is enhanced 4. Bacterial growth is inhibited 5. Release of certain bacterial endotoxins is inhibited 6. The effect of antibiotics is potentiated.
84
Tuberculosis of bone & joint (TB) etiology
Extrapulmonary Infection is spread via lung or lymphohematogenous drainage NOT communicable UNLESS an open wound exists Patients with skeletal TB may have a history of: -Pulmonary TB -Drug abuse -Crowded and poor living conditions -Immunosuppressive diseases -Immigration to US before 1991
85
Tuberculosis of bone & joint (TB) pathogenesis
Mycobacterium tuberculosis is the organism responsible for bone and joint destruction Organism initially transmitted via airborne route Infectious droplets are inhaled and infect lungs M. tuberculosis spreads hematogenously from lung or lymphatic drainage to bone May lie dormant before it is detected
86
Tuberculosis of bone & joint (TB) clinical manifestations
Most common site of infection is vertebral column-particularly thoracic and lumbar Other common sites -Hips -Knees -Ankles Symptoms -Pain -Joint swelling -Low-grade fever -Possible neurologic symptoms from impingement
87
Tuberculosis of bone & joint (TB) treatment
Long term antibiotics/TB drugs Surgical intervention in cases of spinal TB when severe deformities or neurologic deficits are seen
88
Bone and soft tissue tumors
May be malignant or benign Benign tumors often go undiagnosed because there is no pain Malignant tumors are called sarcomas Most bone tumors are secondary to metastasis from another site most commonly from: -Breast -Prostate -Lung -Kidney
89
Osteosarcoma etiology/pathogenesis
Most common primary bone cancer Rapid growth-destroys cortex Extremely malignant Formation of bone by tumor cells Common sites of involvement are active epiphyseal growth areas -Distal end of femur -Proximal end of tibia, fibula -Proximal end of humerus Occurs most in adolescents and young adults...from 20-30 years
90
Osteosarcoma clinical manifestations
Pain-progressive to intense Pathologic fracture Compromised joint function Metastasis to lung
91
Osteosarcoma treatment
Conservative surgery Chemotherapy *5 year survival rate using combination of above near 70% Amputation
92
Chondrosarcoma etiology/pathogenesis
Primary malignant cartilage forming tumor Diagnosed in 30-60 year old age group Slow rate of development Formation of cartilage by tumor cells Tend to develop in proximal ends of long bones
93
Chondrosarcoma clinical manifestations
Pain (but not initially) Will eventually metastasize (usually to the lung)
94
Ewing Sarcoma etiology/pathogenesis
Rapidly growing round cell primary tumor Most common in long bones of children and young adults 5-25 Metastasizes early to the lungs and other bones Tumor perforates the cortex of the shaft producing a painful soft tissue mass overlying the affected bone Tumor favors: -Femur -Tibia -Proximal fibula -Humerus
95
Ewing Sarcoma clinical manifestations
Pain -Because of rapid growth rate Systemic effects -Fever -Anemia -Leukocytosis
96
Ewing Sarcoma treatment
Radiation Possible surgery
97
Multiple myeloma etiology/pathogenesis
Slowly growing bone marrow malignancy Proliferation of a single clone of plasma cell
98
Multiple myeloma clinical manifestations and treatment
Takes a long time to be symptomatic because of slow growth Bone pain: -Chest & back -Excessive accumulation of abnormal plasma cells I the bone marrow Hypercalcemia Pathologic fractures TREATMENT -Aggressive combination chemotherapy -Local radiation -Bisphosphonates <10% survival 2-3 years
99
Functions of skeletal muscle
Enables bones to move at the joint Provides strength, stability, and protection Distributes loads and absorbs shock
100
skeletal muscle anatomy
Composed of thousands of muscle fibers Each fiber is a single muscle cell (myofibril) Muscle fibers are grouped together in bundles call fasciculi Individual muscles are composed of many fasciculi
101
Duchenne Muscular Dystrophy Etiology/Pathogenesis
Most common and most severe Affects only males-X-linked 1 in 5,000 live births A weakened muscle cell membrane allows extracellular fluid to leak into the cell -Due to genetic mutation -Deficiency in dystrophin Inflammatory processes lead to muscle fiber necrosis and muscle degeneration Disease begins at birth and is usually apparent by the age of 3
102
Duchenne Muscular Dystrophy clinical manifestations
Calf muscles are notably enlarged Distal muscle involvement leads to frequent falls by the age of 5-6 years Wheelchair by 12-14 years Survival to 20s early 30s Muscles of hands, face, jaw, pharynx, larynx, eyes are usually spared to the end Death usually from cardiac failure or pulmonary complications
103
Duchenne Muscular Dystrophy treatment
Education of patient and family Preservation of function as long as possible Prevention of contractures In some cases, corticosteriod therapy may prolong muscle strength and independent ambulation
104
Myasthenia Gravis Etiology/Pathogenesis
Autoimmune disease Affects neuromuscular function of voluntary muscles Women affected more than men Antibodies affect transmission of acetylcholine across neuromuscular junction
105
Myasthenia Gravis clinical manifestations
Profound muscle weakness -Ocular and cranial muscles first-drooping eyelids -Then proximal limb muscles -Exacerbated by repetitive muscle use -Improves with rest Fatigability Respiratory muscles may be involved during times of stress
106
Myasthenia Gravis treatment
Corticosteriods Anticholinesterase Inhibitors Immunosuppressive agents Plasmapheresis Mechanical ventilation Thymectomy -Fail to respond to medications -Usually less than 45 years old
107
Fibromyalgia syndrome (FMS) etiology and pathogenesis
Cause unknown -No abnormal labs -Muscle biopsy non-specific -Normal psychological testing More females "Pain syndrome" -Changes in central nervous system may lead to amplification of pain fiber impulses
108
Fibromyalgia syndrome (FMS) clinical manifestations
-Chronic pain often months or years in duration -Stiffness -Sleep dysfunction -Fatigability -Depression
109
Fibromyalgia syndrome (FMS) treatment
Focus on maintaining functionality and reducing symptoms -Exercise -Medications
110
Osteoarthritis (OA) etiology
Degenerative joint disease Most common arthritis worldwide Progressive loss of articular cartridge Etiology varies: -Abnormal wear and tear -Repetitive stress -Obesity -Joint trauma -Congenital disorders Occupation (stress to joints) Age Postmenopausal -Knees -Hands Genetic predisposition
111
Osteoarthritis (OA) pathogenesis
Initial injury release of proteolytic enzymes Breakdown of collagen Decreased hydration of cartilage (aging) Microfracture with weight bearing Ability to absorb shock decreased Fissures and erosion Bone spur formation Synovium inflamed causes joints to distend (weight bearing joints often affected
112
Osteoarthritis (OA) clinical manifestations
Localized: NOT systemic Crepitus with movement Morning stiffness less than 30 minutes (improves with mobility) Pain with function Weight bearing joints most affected Bouchard nodes: -Proximal interphalangeal joint bone spur Heberden nodes: -Distal interphalangeal joint bone spur
113
Osteoarthritis (OA) treatment
Decrease stress on joint -Weight loss -Crutches, braces, canes, shoes insoles, heel lifts Pain relief -Acetaminophen (DOC) -NSAIDS Physical therapy -Strengthening exercises Surgery -Severe cases
114
Rheumatoid Arthritis (RA) etiology
Systemic/chronic autoimmune inflammatory disease Affects all races More women Specific cause idiopathic -80% test rheumatoid factor (RF) positive Most likely an abnormal autoimmune response triggered by a bacterial or viral antigen Marked by remissions and exacerbations Potentially crippling disease
115
Rheumatoid Arthritis (RA) pathogenesis
T and B cell lymphocytes are activated by antigen and develop altered IgG antibodies The body does not recognize these antibodies as "self" so B cells produce rheumatoid factor (RF) antibodies Inflammatory response occurs in the synovium which creates Cytokines (inflammation & growth factor) Pannus occurs -Thickened layer of granulation tissue -Accumulation of cells erode and destroy articular cartilage Destruction of joint -Bone erosion -Bone cysts -Fissures
116
Rheumatoid Arthritis (RA) clinical manifestations
Morning stiffness lasting at least one hour Malaise Fatigue Diffuse musculoskeletal pain Soft-tissue swelling Usually bilateral/Symmetrical swelling of wrists, fingers, elbows, knees, ankles, hands Presence of rheumatoid factor Swan-neck deformity Boutonniere deformity
117
Rheumatoid Arthritis (RA) treatment
Alleviate pain and swelling Disease-modifying antirheumatic drugs (DMARDS) -methotrexate NSAIDs -ibuprofen -Celebrex Corticosteroids Antimalarial drugs
118
Swan neck deformity
119
Boutonniere deformity
120
Systemic Lupus Erythematosus (SLE) etiology
Chronic, multisystem inflammatory autoimmune disease affecting connective tissues Genetic More common in women between 15-40 Environmental: sunlight may initiate the development Abnormal immune reaction of the body against its own tissues, cells, and serum proteins No cure/may affect multiple organs/may be fatal
121
Systemic Lupus Erythematosus (SLE) pathogenesis
B-lymphocyte overactivity leads to excessive autoantibody production Antinuclear antibodies (ANA) found in 98% of patients Antigen-antibody complexes form within the membranes of the kidneys, heart, skin, brain, and joints Trigger inflammatory response which destroys tissue
122
Systemic Lupus Erythematosus (SLE) clinical manifestation
Exacerbation and remission Arthralgias Morning stiffness Sunlight worsens Neurologic -Seizures -Confusion Renal -Renal failure -UTI and renal failure-leading cause of death Cardiopulmonary -Chest pain -Pericarditis -Atherosclerosis -Pleuritis -Pleural effusions Skin lesions -Classic butterfly (malar) rash in 80% -Patchy alopecia
123
Systemic Lupus Erythematosus (SLE) diagnose/treatment
Lab work -ANA+ -Anemia -Leukopenia -Lymphopenia -Thrombocytopenia -Proteinuria -Hematuria Treat with NSAIDs, corticosteroids, avoid sun, disease modifying anti-rheumatic drugs (DMARDs)
124
Scleroderma(systemic sclerosis) etiology
Multisystem inflammatory connective tissue disease characterized by skin thickening and large amt of collagen deposits which cause fibrosis Can affect skin, blood vessels, synovium, skeletal muscle, and microvasculature of internal organs Etiology unknown
125
Scleroderma(systemic sclerosis) pathogenesis
Inflammation and immune cell infiltration can be found in skin, lungs, and tissues Vascular wall thickening and lumen obliteration of small arteries, arterioles, capillaries Tissue ischemia Tissue fibrosis Cytokines cause increased collagen and other connective tissue components
126
Scleroderma (systemic sclerosis) clinical manifestation
Raynaud phenomenon (early) Thick, tight skin begins distally and progresses proximally (sclerodactyly) Contractures (from tight skin) Polyarthritis Gastrointestinal -Difficulty swallowing -Gastric reflux -Malabsorption/constipation Atrophy of muscles -Decreased movement Pulmonary fibrosis CHF Renal
127
Scleroderma (systemic sclerosis) treatment
Organ specific Avoid cold temperatures -Raynauds Vasodilators Calcium channel blockers H2 antagonists, PPI
128
Scleroderma (systemic sclerosis) contractures
129
Lyme Disease etiology/pathogenesis
Most often in summer months Caused by the Borrelia burgdorferi tick-borne spirochete Carried by the deer tick Antigenic fragments of the dead organism trigger the inflammatory responses The initial infection stimulates an autoimmune inflammatory response
130
Lyme disease manifestations/treatment
Red macule or papule -Expand to annular lesion Flulike illness Headache Stiff neck Splenomegaly More than 10% develop chronic arthritis Neurologic and Cardiac -Meningitis -LV dysfunction -Cardiomegaly Treat with antibiotics -Oral or parenteral
131
Lyme disease bulls-eye rash
132
Gout etiology/pathogenesis
Underlying cause unknown Risk increases with age Disturbance of uric acid metabolism leads to deposition of urate salts in articular, periarticular, and subcutaneous tissue Hyperuricemia-hallmark of gout Lack of enzyme to metabolize uric acid Uric acid is a normal waste product filtered by kidneys When production of uric acid exceeds removal, hyperuricemia results Often triggered by: -Traumatic event -Surgical procedure -Acute illness -Starvation -Alcohol -Medications
133
Gout clinical manifestations
Middle-aged men Postmenopausal women Manifestations Acute gouty arthritis: -Great toe! (podagra) -Articular inflammation >>>Extreme pain >>>Swelling >>>Tenderness >>>Hyperuricemia Chronic(advanced stage) -Accumulation of tophi (crystalline deposits) in bony connective tissue -Complications: >>>Renal impairment >>>Deforming arthritis >>>Uric acid calculi
134
Gout treatment
Aggressive anti-inflammatory medications -NSAIDS -Corticosteroids -Colchicine -Allopurinol
135
Endocrine System
Together with the nervous system, the endocrine system (the glands and the hormones they secrete) regulates body processes involving growth, maturation, metabolism, fluid balance, responses to stress, and reproduction. Hormones: chemical messengers that travel though the bloodstream to exert physiologic effects on specific target cells and tissues In the healthy state, hormones are released by endocrine glands when their action is needed and inhibited when their effect is attained. Hyperfunction -excessively high blood concentration hormone Hypofunction -Depressed levels of concentrated hormone
136
Hypothalamic-Pituitary-Endocrine
May originate in: Hypothalamus (Releasing hormones) -Secondary endocrine disease Pituitary (Stimulating hormones) -Secondary endocrine disease Hormone producing gland (i.e. pancreas, thyroid) -Primary endocrine disease
137
Pituitary Hormones
Posterior Lobe Pituitary: -Antidiuretic hormone (ADH): Kidneys, osmolality -Oxytocin: Uterus and breast Anterior Lobe Pituitary: -Somatotropes: secrete growth hormone (GH): Liver, bones, muscle, metabolism -Gonadotropes: secrete luteinizing and follicle-stimulating hormone (LH and FSH): Ovaries, estrogen -Thyrotropes: secrete thyroid stimulating hormone (TSH): Thyroid gland, T3 T4 -Corticotropes: secrete adrenocorticotropic hormone (ACTH): Adrenal Cortex, Cortisol -Lactotropes: secrete prolactin (PRL):Breast, lactation
138
How to determine if the pituitary gland or the target gland is causing the problem?
Pituitary gland secretes stimulating hormones In response to the stimulating hormones, the target gland responds by secreting its hormone. So... If there are normal to high levels of stimulating hormone present and low levels of target gland hormone available, the cause is the target gland because the target gland is not responding.
139
Growth Hormone (GH) Disorders
Produced in the anterior pituitary gland under the influence of hypothalamic releasing (growth hormone-releasing hormone) and inhibiting (somatostatin) factors. Primary target organ is the liver Affects body mass Causes liver to release glucose Induces lipolysis Increases rate of protein synthesis Hypoglycemia stimulates the release of GH
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Growth Hormone Deficiency etiology
Most relevant in children HX of prolonged labor Midline craniocerebral defects Should be considered in children with nystagmus, retinal abnormalities, cleft lip or palate.
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Growth Hormone Deficiency pathogenesis
Variety of presentations Depend on the age at onset May be caused by failure of hypothalamus to stimulate pituitary GH secretions or failure of the pituitary to produce GH Midline brain tumors common cause
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Growth Hormone Deficiency clinical manifestations
Normal birth length and weight Hypoglycemia GH needed to maintain adequate glucose levels Undescended testicles Delayed dental eruption Thin hair, poor nails
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Growth Hormone Deficiency treatment
hormone replacement
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Growth Hormone (giantism) Excess etiology
Nearly always due to uncontrolled production of the hormone by a benign somatotropic tumor in the pituitary gland. GH stimulates the liver and this causes an upregulated growth of soft and bony tissues
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Growth Hormone Excess pathogenesis
Tumor present in childhood before epiphyses are closed: giantism. Rapid growth. Exceed 95% on growth charts. May be taller than 8 feet. May have heart failure or die Tumor present after epiphyses are closed: acromegaly. Fourth or fifth decade. Growth of short bones
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Growth Hormone Excess clinical manifestations
Acromegaly -Increased ring/shoe sz -Lrg frontal sinus/brow -Lrg mandible -Internal organs increase in size -Increased ICP -Does NOT affect height in adults
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Growth Hormone Excess treatment
Surgical removal of tumor Medications
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Thyroid Hormone Disorders
Secretion of thyroid hormones T3 and T4 is under control of thyroid-stimulating hormone (TSH) secretion from the anterior pituitary gland Thyroid hormones are important for metabolism Needed for normal growth and development of tissues
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Hypothyroidism etiology
Most cases are primary (thyroid gland dysfunction) Congenital Irradiation of the Thyroid Surgical removal of Thyroid Lithium inhibits TH synthesis
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Hypothyroidism pathogenesis
Lymphocytic thyroiditis (Hashimoto thyroiditis) most common -Characterized by an enlarged thyroid gland (Goiter) due to lymphocytic infiltration. TH decreased producing increased TSH from pituitary gland.
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Hypothyroidism clinical manifestations
Goiter Hypometabolic state Weakness Lethargy Cold intolerance Constipation Myxedema (Facial edema) Coarse hair Bradycardia
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Hypothyroidism treatment
Return to euthyroid state Synthroid
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Hypothyroidism in Infants (Cretinism)
Newborns Congenital ↑TSH↓T4 Deficiency →mental retardation Psychomotor deficits Rx - thyroid replacement
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Myxedema
Occurs in severe prolonged thyroid deficiency Generalized, non-pitting edema Fluid retention due to accumulation of glycosaminoglycans in interstitial spaces Present to emergency room with: -AMS, thermoregulation problems -Hx of sepsis, trauma, certain medication use "Myxedema coma" happens if left untreated -Medical emergency -60% mortality rate
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Myxedema Coma
-Life threatening -Older women -Cold months -CO2 retention & hypoxia -F & E imbalances -Hypothermia
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Myxedema Coma S&S
-Hypoventilation -Lactic acidosis -Hyponatremia -Hypoglycemia -Cardiovascular collapse -Coma -Hypothermia
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Myxedema Coma Rx
-Prevention is #1 -Supportive -No re-warming -Thyroid replacement
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Hyperthyroidism-Graves Disease etiology
Thyroid gland hyperfunction with increased synthesis and secretion of T4 and T3 MC is from autoantibodies that stimulate TSH. This causes toxic goiter. End result-Graves Disease
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Hyperthyroidism-Graves Disease pathogenesis
More common in women In response to high circulating T3 and T4 levels, the pituitary stops producing TSH. TSH then falls very low.
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Hyperthyroidism clinical manifestations
-Hypermetabolic state -Insomnia -Restlessness, palpitations -Heat intolerance -Weight loss -Thyromegaly -Exophthalmos-(enlarged retro-orbital muscles) **Thyroid storm-life threatening
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Hyperthyroidism-thyroid storm
When excessive amounts of hormone are released in circulation. -Increased temperature -Severe tachycardia -Cardiac dysrhythmias -N/V/D Treatment: Beta Blockers Surgical removal of thyroid Life threatening surge of TH Stress response -DKA -Trauma (physical or emotional) -Thyroid manipulation during surgery Life threatening- hypermetabolic state Rx - cooling, supportive measures, βblockers, steroids, antithyroid meds
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thyroid goiters
Goiters are present in both hyper and hypothyroidism
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Adrenocortical Hormone (ACTH) Disorders
The adrenal cortex synthesizes three different classes of steroid hormones: -Glucocorticoids (Cortisol) -Mineralocorticoids (Aldosterone) -Sex Steroids (Androgens) -Sugar, Salt, Sex Steroid hormones: provide negative feedback regulation of the hypothalamus and pituitary gland to suppress "turn off" adrenocorticotropic hormone (ACTH).
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ACTH Insufficiency-Addison Dz etiology
Hyposecretion of adrenocortical hormones (ACTH) can result from disease of the adrenal cortex (primary adrenocortical insufficiency, Addison disease) Inadequate secretion of ACTH from the anterior pituitary. (secondary) OR Lack of releasing hormone from the hypothalamus Caused by destruction of the adrenal gland through idiopathic or autoimmune mechanisms (trauma or hemorrhage) Addisonian crisis or acute adrenal insufficiency is a true emergency. Could be severe in patients who take corticosteroids routinely and then abruptly stop.
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ACTH Insufficiency-Addison DZ clinical manifestations
Most severe manifestations are r/t inadequate levels of circulation cortisol and aldosterone. Reduced CO Diminished vascular tone Inadequate circulating volume Early signs: -Weight loss, weakness, malaise, apathy, electrolyte imbalances
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ACTH Insufficiency-Addison DZ treatment
Replace the absent of deficient hormone In adrenal crisis: give glucocorticoids IV
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Addison's Disease Primary Adrenal Cortical Insufficiency
Hyperpigmentation of skin -Darkened skin folds and creases -Oral mucus membranes become bluish
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Hypercortisolism - Cushing DZ etiology
Hyperfunction of the adrenal cortex. Adrenal adenoma (primary) Hyperfunction of anterior pituitary ACTH-secreting cells (secondary).
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Hypercortisolism - Cushing DZ pathogenesis
Excessive production of pituitary ACTH by adenomas stimulate the adrenal glands to overproduce hormones In the US, exogenous steroids used in respiratory disease is the most common cause of Cushing syndrome
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Hypercortisolism-Cushing Dz clinical manifestations
-Moon face -Weight gain -Muscle weakness -Cortisol increases tissue resistance to the effects of insulin and may contribute to glucose intolerance. -HTN -Hypokalemia -Depression
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Hypercortisolism-Cushing Dz treatment
Reduce doses of steroids Transsphenoidal hypophysectomy or laser ablation of the pituitary tumor
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Adrenal Medulla-Pheochromocytoma etiology
Adrenal medulla secretes catecholamines in response to the Sympathetic Nervous System (SNS) Malignant in 10% of patients
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Adrenal Medulla-Pheochromocytoma pathogenesis
Pheochromocytoma is a tumor of the adrenal medulla that results in excessive production of catecholamines Symptoms?
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Adrenal Medulla-Pheochromocytoma clinical manifestations
-Intermittent or persistent HTN (most common) -Headache -Tachycardia -Diaphoresis
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Adrenal Medulla-Pheochromocytoma treatment
Surgical removal of tumor Beta blockers
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Parathyroid Gland Disorders
Four, small glands located at the upper and lower poles of the thyroid. Detect serum calcium (Ca+) concentrations in serum Regulate calcium absorption and resorption from bone Serum Ca+ levels provide feedback to regulate the parathyroid hormone (PTH) Normal (for me and you) relationship: -Decrease in serum Ca+ causes a release of PTH -Elevated serum Ca+ leads to suppression PTH -Normally inverse to one another PTH is not under the control of the hypothalamic-pituitary system like the others PTH acts on bones, intestines, and renal tubules
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Hyperparathyroidism etiology
Unclear etiology Despite elevate serum Ca+, PTH continues to be secreted (both elevated) Genetic Parathyroid adenoma (MC)
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Hyperparathyroidism pathogenesis
Bone resorption and formation rates are increased In chronic RF, hyperparathyroidism results from reduced production of Vitamin D (needed for Ca+ absorption) from impaired GFR. Lithium may increase Ca+ levels.
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Hyperparathyroidism clinical manifestations
-May be asymptomatic -Prone to kidney stones. Why? -Osteoporosis -Bradycardia -Cardiac arrest -Ca+ elevated -Phosphorus levels low -Calcium and Phos always inversely related
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Hyperparathyroidism treatment
Surgery Volume replacement -Improve GFR -Increase Ca+ excretion -Diuretics
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Hypoparathyroidism etiology
Happens after parathyroid or thyroid surgery May be temp or permanent Congenital Autoimmune
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Hypoparathyroidism clinical manifestations/treatment
Low serum Ca+ (<7mg/dl) Neuromuscular irritability -Paresthesia, cramps, seizure Chvostek sign -Tetany of the facial nerve. When facial nerve is tapped, causes muscle contraction Trousseau sign -BP cuff is place to obliterate arterial flow. Hand/forearm flexes due to hypoxia and neuromuscular irritability Tx: Give IV CALCIUM
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Antidiuretic Hormone (ADH) Disorders
ADH (vasopressin) is secreted from the posterior pituitary gland in response to changes in blood osmolality. ADH does not affect Na+ regulation ADH does affect water regulation When body water "too thick" -Pituitary release ADH When body water "too thin" -Pituitary suppress ADH
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Diabetes Insipidus (large diuresis of inappropriately dilute urine) etiology
Disorder of insufficient ADH Excessive loss of water in urine ADH acts directly on distal tubules Damage to the hypothalamus in head injuries 30 % idiopathic in adults Surgical treatment of brain tumors Brain trauma
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Diabetes Insipidus (large diuresis of inappropriately dilute urine) pathogenesis
Damage to posterior pituitary gland →deficient ADH Urine cannot concentrate without ADH Free water is lost Hyperosmolality (thick) Hypernatremia -Cells shrivel -Increased concentration of extracellular fluid causes water to move out of cells by osmosis
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Diabetes Insipidus clinical manifestations
Polyuria Polydipsia May void 15 L per day Specific gravity decreased Drink up to 15 L to correct Hypernatremia (due to water loss) -Thirst -Dry mouth
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Diabetes Insipidus treatment
Give ADH Monitor labs -BUN -Serum Creatinine -Serum Electrolytes -sodium
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Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) etiology
Too much ADH Tumors Medications
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Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) pathogenesis
Results in hyponatremia (water overload) Free water dilutes sodium Hyponatremia -Cells swell -Decreased concentration of extracellular fluid causes water to move into cells by osmosis
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Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) clinical manifestations
Increased water reabsorption Low osmolality (too thin) Weakness Muscle cramps Orthostatic hypotension Low lab values due to dilution Hyponatremia -Confusion -Lethargy -Coma
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Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) treatment
Free water restriction will result in slow increase in serum Na+ levels and increased osmolality (concentration) Treat hyponatremia slowly to avoid rapid changes in brain cell volume from fluid compartment shifts
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Diabetes Statistics
21 million people in US - Diabetes Mellitus (DM) Only 70% aware they have it Costs healthcare $176 billion per year 6th leading cause of death With dx of DM there is increase risk: -Heart disease -End Stage Renal Disease (ESRD) -Blindness -Amputation -Pregnancy complications
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Glucose
broken down carbohydrates for energy. Sugar
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Glucagon
hormone produced by alpha cells of pancreas. Stimulates glycogenolysis and gluconeogenesis in liver
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Glycogen
carbohydrate consists of glucose produced in muscle and liver from stored glucose
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Insulin
hormone produced by beta cells of pancreas. Energy metabolism
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Glycolysis
breakdown of sugar so cells can use
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Glycogenolysis
production of glucose from breakdown of glycogen in liver and muscle tissue
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Glycogenesis
production of glycogen from glucose in liver in muscle tissue
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Gluconeogenesis
production of glucose from amino acids in liver
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Liver/muscle produce
Glycogen Glycogenesis Glycogenolysis Gluconeogenesis *Insulin stimulates the diffusion of glucose into adipose and muscle tissue and inhibits the production of glucose by the liver
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Pancreas produces
Insulin Glucagon
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Regulation of Glucose Metabolism
DM affects utilization of ALL energy Glucose and fats= human energy Glucose is produced by: -Glycogen stores in muscles and liver -Amino acids and lactate Glucose is supplied to blood stream by GI tract and liver Glucose enters cell through diffusion and semipermeable membrane Heart, adipose, and skeletal muscle possess insulin receptors
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Hormonal Regulation
Protein and fat metabolism are regulated by the effects of insulin Insulin is synthesized in pancreas in Beta cells of the islets of Langerhans Normal glucose metabolism is describe as fed and fasting state (absorptive and post absorptive)
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Fed State
After eating, rise in blood glucose and insulin Presence of insulin stimulates glucose diffusion into adipose and muscle tissue and inhibits production of glucose by liver Glycolysis (sugar is broken down)-energy use for cell Glycogenesis-glycogen production muscle/liver
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Fasting State
Fasting state: dominated by glucagon Glucose is produced: -by glycogenolysis (breakdown of stored glycogen) in liver and muscles -By gluconeogenesis (production of glucose in liver) Glucagon-stimulated glycogenolysis and gluconeogenesis responsible for 75% of glucose production Lipolysis, stimulated by the fall in plasma insulin, is primary source of energy to muscles
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Exercise
Increase activity requires increase fuel Onset of exercise insulin drops and glucagon rises Glycogenolysis is stimulated due to above Muscle switch to using stored glycogen After 10-40 minutes, glucose use by muscles increase 7 to 20 times Muscle contraction increases insulin sensitivity for up to 16 hours
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Stress
Injury, illness, pain and stress hormones: All increase production of glucose Catecholamines and corticosteroids increase: -Glucagon levels -Liver production of glucose -But decreases the use of glucose in muscle/fat tissue -"Stress hyperglycemia"
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Diabetes Mellitus (DM)
Normal Blood Glucose level: -FPG 70-110 mg/dl (this varies per resource) Diagnosing Pre-Diabetes -Impaired fasting glucose tolerance test >>>FPG 100-125 mg/dl -Impaired glucose tolerance test >>>2 hours post glucose ingestion 140-200mg/dl Diagnosing DM -Fasting Plasma Glucose (FPG) >126 OR -Symptoms of hyperglycemia or random >200 OR -2-hour plasma glucose during an Oral Glucose Tolerance Test (OGTT) after drinking 75g sugar
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Glucose Intolerance Disorders
Diabetes Mellitus - disease in which the body doesn't produce enough insulin—hyperglycemia Normally insulin allows glucose into cells Then it can be used for energy or stored as glycogen -Type I -Type II -Gestational -Pre-Diabetes
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Type I Diabetes Mellitus
Characterized by destruction of the Beta cells of the pancreas Can occur at any age: Most common between 5 and 20 years of age Affect 5% to 10% of people with diabetes Caucasian most prevalent
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Type I Diabetes Mellitus etiology
Immune-mediated: result of autoimmune attack on the beta cells of the pancreas Presence of hyperglycemia indicates that autoimmune destruction of beta cells has reached the point at which insulin secretion is inadequate
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Type I Diabetes Mellitus pathogenesis
Absolute insulin deficiency Thus glucose cannot enter muscle and adipose tissue Liver glucose production is no longer opposed by insulin Overproduction of glucagon by pancreatic alpha cells stimulates glycogenolysis and gluconeogenesis Plasma glucose levels rise When the maximal tubular absorptive capacity (renal threshold) of the kidney is exceeded, glucose is lost in the urine Glycosuria and osmotic fluid loss leads to hypovolemia Neural tissue in the brain responds to this emergency by promoting eating behavior Metabolic acidosis ensues as bicarbonate concentration decreases Diabetic Ketoacidosis (DKA) occurs Hyperkalemia due to excretion of fluid Lactic acid, a product of glucose metabolism, in excess Hypovolemic shock Respiratory compensation: Kussmaul respirations Continued insulin deficiency leads to lipolysis in the body tissues Metabolism of fats from storage leads to fatty acid production These are turned into keto acids in the liver PH falls below normal Ketone bodies in urine which causes osmotic fluid loss
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What are the three Ps of DM
-Polyuria -Polydipsia -Polyphagia
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Type I Diabetes Mellitus clinical manifestations
Decreased -Bicarbonate ions -Sodium -Magnesium -Phosphorus -Total body water (hypovolemia) >>>Leads to increased K=, H&H, protein, creatinine, lactic acid. Kussmaul respiration to correct metabolic acidosis "fruity breath" Classic Triad: Polydipsia, Polyuria, Polyphagia
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Type II Diabetes Mellitus
Normally insulin levels rise in response to high glucose levels In DM II, insufficient insulin is produced or the cells resist insulin. This makes it difficult for glucose to enter the cell. Cells don't get energy and glucose builds up in the blood stream and blood vessels (this is why we have organ and vessel damage)
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Type II Diabetes Mellitus pathogenesis
Relative lack of insulin Insulin resistance and beta-cell dysfunction A requirement for more insulin Decreased number of insulin receptors Impaired glycogen syntheses Impaired production of insulin by pancreas
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Type II Diabetes Mellitus etiology
Resistant to the action of insulin on peripheral tissues 90-95% of affected individuals Non-caucasian and elderly Obese teenagers Risk factors -Sedentary lifestyle -Obesity -Abdominal adipose -c/o 3 "P's": 1. Polyuria 2. Polydipsia 3. Polyphagia
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Type II Diabetes Mellitus pathogenesis
Insulin deficient Insulin resistance Progressive disease-at first it is compensated by increased insulin production and hyperinsulinemia Impaired Beta cells are unable to produce sufficient insulin to overcome insulin resistance
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Type II Diabetes Mellitus clinical manifestations
-Polyuria -Polydipsia -Polyphagia DKA uncommon: due to endogenous insulin which suppresses the lipolysis that leads to ketone body formation Nonketotic hyperglycemic hyperosmolar coma -Severe hyperglycemia and dehydration W/O ketones
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Pre-Diabetes
Impaired Glucose Tolerance Impaired Fasting Glucose Tolerance Screen every 3 years once 45 years old
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Acute Hyperglycemia etiology
-MC caused by alteration in nutrition, inactivity, inadequate use of antidiabetic meds
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Acute Hyperglycemia complication
3 P's: 1. Polyuria 2. Polydipsia 3. Polyphagia DKA Fluid imbalance problems Skin infections Blurred vision
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Hyperglycemia Signs & Symptoms
Nausea Fatigue Decreased sense of well being Rapid deep breathing- Kussmaul respirations
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Hypoglycemia Signs & Symptoms
Anxiety Tachycardia Sweating/Diaphoresis Constriction of the skin vessels- Cold and clammy skin Mental confusion Decreased LOC
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Complications of DM Macro-vascular
Damage to the large blood vessels providing circulation to the brain, heart, and extremities CVD Stroke Risk factors -Dyslipidemia -HTN -Impaired fibrinolysis
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Complications of DM-Micro-vascular
Retinopathy -blindness Nephropathy-ESRD Abnormal thickening of basement membrane in capillaries Hyperglycemia disrupts platelet function
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Complications of DM-neuropathic
Diabetic neuropathy produces symptoms in 60-70% of DM Autonomic: bladder, tachycardia, postural hypotension, erectile dysfunction Sensory: paresthesia in feet, lower extremity amputations
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Complications of DM pregnancy
Type I in pregnancy has increased risk for perinatal infant mortality Untreated in pregnancy results in macrosomia, shoulder dystocia, pre-eclampsia.
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DM Treatment and Education
Nutrition -Protein -Fat -Carbohydrates -Alcohol -Obesity and Eating Disorders Exercise Stress Management Assessment of Efficacy Education Pharmacologic Agents -Oral antidiabetic agents -Insulin
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DM Evaluation
HbA1c is a measure of glycosylated Hgb Glycosylated Hgb is hemoglobin(Hgb) that has glucose attached to it. The glucose attaches to the Hgb only when blood glucose levels are high. The amount of glucose that attaches to Hgb is proportional to the amount of glucose in the blood. HbA1c reflects the average blood glucose levels over the previous 100-120 days. HbA1c is used to measure long term control of blood sugar levels. A HbA1c of 7 or less indicates good blood glucose control for the 100-120 day period.
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Pediatric Considerations with diabetes
Diabetes has been diagnosed in 176,500 children and adolescents younger than 20 years old One in every 400 to 600 children have Type I DM Goal: achieve normal growth and development, avoiding acute and chronic complications, addressing psychosocial issues, and educating children regarding self-care. Insulin requirements are 1.0 unit per Kg per day. Diet Counseling
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Geriatric Considerations with diabetes
The prevalence of type II DM increases with age Adults older than 60 years old constitute 50 % of the diabetic population in the United States Goal: prevention of acute complications, prevention and management of chronic complications, attention to psychosocial issues, and education regarding self-care Treatment -Oral antidiabetic agents -Insulin
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