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Patho > Exam 6 > Flashcards

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
Q

Protruded Disk Clinical Manifestations

A

Pain

Altered sensation

-Numbness

-tingling

Motor weakness

Diminished reflexes

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26
Q

Protruded disks treatment

A

-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

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27
Q

Dislocations and Subluxations: Joints etiology/pathogenesis

A

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

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28
Q

Dislocations and Subluxations: Joints clinical manifestations

A

Pain

Alteration in normal contour of the joint

Change in extremity length

Loss of normal mobility

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29
Q

Dislocations and Subluxations: Joints treatment

A

-Immobilization

-Reduction

-Pain control

-Treatment must include consideration of local soft-tissue trauma

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30
Q

Ligament injuriesetiology/pathogenesis

A

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

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31
Q

Ligament injuries clinical manifestations

A

Sudden “tearing” or “popping” sensation

Pain with weight bearing

Acute swelling

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32
Q

Ligament injuries treatment

A

Geared toward relief of symptoms

Protection of the ligament

Recovery is usually complete

May require surgery

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33
Q

Injury to muscle and tendon

A

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

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34
Q

Rotator cuff injury etiology/pathogenesis

A

Excessive use

Rupture of tendon in rotator cuff under acromion bone

Impingement syndrome: inflammation around joint causing severe characteristic pain with movement

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35
Q

Rotator cuff injury clinical manifestations/treatment

A

PAIN!

Limited range of motion

Treatment

-injected steroids

-repair

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36
Q

Fractures Etiology/Pathogenesis

A

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

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37
Q

transverse fracture

A
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38
Q

Longitudinal fracture

A
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39
Q

Oblique fracture

A
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40
Q

Comminuted fracture

A
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41
Q

Impacted fracture

A
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42
Q

Greenstick fracture

A
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43
Q

Stress fracture

A
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44
Q

Avuslion fracture

A
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45
Q

Epiphyseal injury

A
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46
Q

Classifications of fracture

A

extent and depth

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47
Q

Displaced fracture

A

End of fracture fragments separated

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48
Q

Nondisplaced fracture

A

Fracture fragments remain in alignment and position

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49
Q

Depressed fracture

A

Fracture displaced below the level of the surface of the bone (skull)

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50
Q

Complete fracture

A

Fracture line disrupts bone continuity through whole thickness

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51
Q

Incomplete fracture

A

Bone cracks but continuity is not disrupted

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52
Q

open (compound) fracture

A

Bone is broken and an external wound leads to the fracture site

Increased risk for infection

Osteomyelitis

Difficult to manage

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53
Q

closed (simple) fracture

A

Fragments do not extend through mucous membranes or skin

Skin is not broken

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54
Q

Fractures: Clinical Manifestations

A

Pain

Swelling

Loss of function

Discoloration

Deformity +/-

Muscle spasm and shortening of extremity

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55
Q

Fractures treatment

A

Main goals:

  1. Reduction

-Restoring to normal anatomical position

  1. Immobilization

-Maintain proper alignment until bone healing occurs

-External fixation

-ORIF

-Casts/splints/braces

Rehabilitation

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56
Q

External fixation

A
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57
Q

Open reduction and internal fixation(ORIF)

A
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58
Q

Fracture Complications

A

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

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59
Q

causes for Delayed healing

A

-Smoking

-Malnutrition

-Use of corticosteriods

-Poor circulation

-Infection

-Elderly

-Diabetes

-Coronary heart disease

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60
Q

Compartment syndrome

A

-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

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61
Q

Neurovascular injury

A

-Damage related to casts/splints

-Hemorrhage

-Edema

-Manipulation at the time of reduction

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62
Q

Fat emboli

A

-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

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63
Q

Hip fracture etiology

A

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

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64
Q

Hip Fracture Pathogenesis

A

Usually fracture is proximal femur

Location is important in terms of blood supply

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65
Q

Hip fracture treatment

A

Return to pre-injury function

as soon as possible

ORIF

Surgical hip replacement

-Early mobilization!

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66
Q

Scoliosis Etiology/Pathogenesis

A

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

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67
Q

Scoliosis Clinical Manifestations

A

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

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68
Q

Scoliosis treatment

A

Surgical (for 40-50 degrees curvature or greater)

-Spinal realignment

-Fusion

-Internal appliances

Non-surgical

-Braces

-Exercises

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69
Q

Osteoporosis etiology

A

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

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70
Q

Osteoporosis pathogenesis

A

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

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71
Q

Osteoporosis Clinical Manifestations

A

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

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72
Q

Osteoporosis treatment

A

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

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73
Q

Osteomalacia/Rickets etiology/pathogenesis

A

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

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74
Q

Osteomalacia/Rickets clinical manifestations

A

Kyphosis

genu valgum (“knock knee”)

genu varum (“bowleg”)

Bone pain

Fractures

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75
Q

eomalacia/Rickets treatment

A

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

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76
Q

Paget disease etiology/pathogenesis

A

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

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77
Q

Paget Disease Clinical Manifestations

A

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

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78
Q

Paget disease treatment

A

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

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79
Q

Osteomyelitis Etiology

A

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

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80
Q

Osteomyelitis pathogenesis

A

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

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81
Q

Osteomyelitis clinical manifestations

A

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

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82
Q

Osteomyelitis treatment

A

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

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83
Q

Hyperbaric Oxygen Therapy

A

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.
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84
Q

Tuberculosis of bone & joint (TB) etiology

A

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

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85
Q

Tuberculosis of bone & joint (TB) pathogenesis

A

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

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86
Q

Tuberculosis of bone & joint (TB) clinical manifestations

A

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

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87
Q

Tuberculosis of bone & joint (TB) treatment

A

Long term antibiotics/TB drugs

Surgical intervention in cases of spinal TB when severe deformities or neurologic deficits are seen

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88
Q

Bone and soft tissue tumors

A

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

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89
Q

Osteosarcoma etiology/pathogenesis

A

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

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90
Q

Osteosarcoma clinical manifestations

A

Pain-progressive to intense

Pathologic fracture

Compromised joint function

Metastasis to lung

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91
Q

Osteosarcoma treatment

A

Conservative surgery

Chemotherapy

*5 year survival rate using combination of above near 70%

Amputation

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92
Q

Chondrosarcoma etiology/pathogenesis

A

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

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93
Q

Chondrosarcoma clinical manifestations

A

Pain (but not initially)

Will eventually metastasize (usually to the lung)

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94
Q

Ewing Sarcoma etiology/pathogenesis

A

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
Q

Ewing Sarcoma clinical manifestations

A

Pain

-Because of rapid growth rate

Systemic effects

-Fever

-Anemia

-Leukocytosis

96
Q

Ewing Sarcoma treatment

A

Radiation

Possible surgery

97
Q

Multiple myeloma etiology/pathogenesis

A

Slowly growing bone marrow malignancy

Proliferation of a single clone of plasma cell

98
Q

Multiple myeloma clinical manifestations and treatment

A

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
Q

Functions of skeletal muscle

A

Enables bones to move at the joint

Provides strength, stability, and protection

Distributes loads and absorbs shock

100
Q

skeletal muscle anatomy

A

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
Q

Duchenne Muscular Dystrophy Etiology/Pathogenesis

A

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
Q

Duchenne Muscular Dystrophy clinical manifestations

A

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
Q

Duchenne Muscular Dystrophy treatment

A

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
Q

Myasthenia Gravis Etiology/Pathogenesis

A

Autoimmune disease

Affects neuromuscular function of voluntary muscles

Women affected more than men

Antibodies affect transmission of acetylcholine across neuromuscular junction

105
Q

Myasthenia Gravis clinical manifestations

A

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
Q

Myasthenia Gravis treatment

A

Corticosteriods

Anticholinesterase Inhibitors

Immunosuppressive agents

Plasmapheresis

Mechanical ventilation

Thymectomy

-Fail to respond to medications

-Usually less than 45 years old

107
Q

Fibromyalgia syndrome (FMS) etiology and pathogenesis

A

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
Q

Fibromyalgia syndrome (FMS) clinical manifestations

A

-Chronic pain often months or years in duration

-Stiffness

-Sleep dysfunction

-Fatigability

-Depression

109
Q

Fibromyalgia syndrome (FMS) treatment

A

Focus on maintaining functionality and reducing symptoms

-Exercise

-Medications

110
Q

Osteoarthritis (OA) etiology

A

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
Q

Osteoarthritis (OA) pathogenesis

A

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
Q

Osteoarthritis (OA) clinical manifestations

A

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
Q

Osteoarthritis (OA) treatment

A

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
Q

Rheumatoid Arthritis (RA) etiology

A

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
Q

Rheumatoid Arthritis (RA) pathogenesis

A

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
Q

Rheumatoid Arthritis (RA) clinical manifestations

A

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
Q

Rheumatoid Arthritis (RA) treatment

A

Alleviate pain and swelling

Disease-modifying antirheumatic drugs (DMARDS)

-methotrexate

NSAIDs

-ibuprofen

-Celebrex

Corticosteroids

Antimalarial drugs

118
Q

Swan neck deformity

A
119
Q

Boutonniere deformity

A
120
Q

Systemic Lupus Erythematosus (SLE) etiology

A

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
Q

Systemic Lupus Erythematosus (SLE) pathogenesis

A

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
Q

Systemic Lupus Erythematosus (SLE) clinical manifestation

A

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
Q

Systemic Lupus Erythematosus (SLE) diagnose/treatment

A

Lab work

-ANA+

-Anemia

-Leukopenia

-Lymphopenia

-Thrombocytopenia

-Proteinuria

-Hematuria

Treat with NSAIDs, corticosteroids, avoid sun, disease modifying anti-rheumatic drugs (DMARDs)

124
Q

Scleroderma(systemic sclerosis) etiology

A

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
Q

Scleroderma(systemic sclerosis) pathogenesis

A

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
Q

Scleroderma (systemic sclerosis) clinical manifestation

A

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
Q

Scleroderma (systemic sclerosis) treatment

A

Organ specific

Avoid cold temperatures

-Raynauds

Vasodilators

Calcium channel blockers

H2 antagonists, PPI

128
Q

Scleroderma (systemic sclerosis) contractures

A
129
Q

Lyme Disease etiology/pathogenesis

A

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
Q

Lyme disease manifestations/treatment

A

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
Q

Lyme disease bulls-eye rash

A
132
Q

Gout etiology/pathogenesis

A

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
Q

Gout clinical manifestations

A

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
Q

Gout treatment

A

Aggressive anti-inflammatory medications

-NSAIDS

-Corticosteroids

-Colchicine

-Allopurinol

135
Q

Endocrine System

A

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
Q

Hypothalamic-Pituitary-Endocrine

A

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
Q

Pituitary Hormones

A

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
Q

How to determine if the pituitary gland or the target gland is causing the problem?

A

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
Q

Growth Hormone (GH) Disorders

A

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

140
Q

Growth Hormone Deficiency etiology

A

Most relevant in children

HX of prolonged labor

Midline craniocerebral defects

Should be considered in children with nystagmus, retinal abnormalities, cleft lip or palate.

141
Q

Growth Hormone Deficiency pathogenesis

A

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

142
Q

Growth Hormone Deficiency clinical manifestations

A

Normal birth length and weight

Hypoglycemia

GH needed to maintain adequate glucose levels

Undescended testicles

Delayed dental eruption

Thin hair, poor nails

143
Q

Growth Hormone Deficiency treatment

A

hormone replacement

144
Q

Growth Hormone (giantism) Excess etiology

A

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

145
Q

Growth Hormone Excess pathogenesis

A

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

146
Q

Growth Hormone Excess clinical manifestations

A

Acromegaly

-Increased ring/shoe sz

-Lrg frontal sinus/brow

-Lrg mandible

-Internal organs increase in size

-Increased ICP

-Does NOT affect height in adults

147
Q

Growth Hormone Excess treatment

A

Surgical removal of tumor

Medications

148
Q

Thyroid Hormone Disorders

A

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

149
Q

Hypothyroidism etiology

A

Most cases are primary (thyroid gland dysfunction)

Congenital

Irradiation of the Thyroid

Surgical removal of Thyroid

Lithium inhibits TH synthesis

150
Q

Hypothyroidism pathogenesis

A

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.

151
Q

Hypothyroidism clinical manifestations

A

Goiter

Hypometabolic state

Weakness

Lethargy

Cold intolerance

Constipation

Myxedema (Facial edema)

Coarse hair

Bradycardia

152
Q

Hypothyroidism treatment

A

Return to euthyroid state

Synthroid

153
Q

Hypothyroidism in Infants(Cretinism)

A

Newborns

Congenital

↑TSH↓T4

Deficiency →mental retardation

Psychomotor deficits

Rx - thyroid replacement

154
Q

Myxedema

A

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

155
Q

Myxedema Coma

A

-Life threatening

-Older women

-Cold months

-CO2 retention & hypoxia

-F & E imbalances

-Hypothermia

156
Q

Myxedema ComaS&S

A

-Hypoventilation

-Lactic acidosis

-Hyponatremia

-Hypoglycemia

-Cardiovascular collapse

-Coma

-Hypothermia

157
Q

Myxedema ComaRx

A

-Prevention is #1

-Supportive

-No re-warming

-Thyroid replacement

158
Q

Hyperthyroidism-Graves Disease etiology

A

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

159
Q

Hyperthyroidism-Graves Disease pathogenesis

A

More common in women

In response to high circulating T3 and T4 levels, the pituitary stops producing TSH.

TSH then falls very low.

160
Q

Hyperthyroidism clinical manifestations

A

-Hypermetabolic state

-Insomnia

-Restlessness, palpitations

-Heat intolerance

-Weight loss

-Thyromegaly

-Exophthalmos-(enlarged retro-orbital muscles)

**Thyroid storm-life threatening

161
Q

Hyperthyroidism-thyroid storm

A

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

162
Q

thyroid goiters

A

Goiters are present in both hyper and hypothyroidism

163
Q

Adrenocortical Hormone (ACTH) Disorders

A

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).

164
Q

ACTH Insufficiency-Addison Dz etiology

A

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.

165
Q

ACTH Insufficiency-Addison DZ clinical manifestations

A

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

166
Q

ACTH Insufficiency-Addison DZ treatment

A

Replace the absent of deficient hormone

In adrenal crisis: give glucocorticoids IV

167
Q

Addison’s DiseasePrimary Adrenal Cortical Insufficiency

A

Hyperpigmentation of skin

-Darkened skin folds and creases

-Oral mucus membranes become bluish

168
Q

Hypercortisolism - Cushing DZ etiology

A

Hyperfunction of the adrenal cortex. Adrenal adenoma (primary)

Hyperfunction of anterior pituitary ACTH-secreting cells (secondary).

169
Q

Hypercortisolism - Cushing DZ pathogenesis

A

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

170
Q

Hypercortisolism-Cushing Dz clinical manifestations

A

-Moon face

-Weight gain

-Muscle weakness

-Cortisol increases tissue resistance to the effects of insulin and may contribute to glucose intolerance.

-HTN

-Hypokalemia

-Depression

171
Q

Hypercortisolism-Cushing Dz treatment

A

Reduce doses of steroids

Transsphenoidal

hypophysectomy or laser ablation of the pituitary tumor

172
Q

Adrenal Medulla-Pheochromocytoma etiology

A

Adrenal medulla secretes catecholamines in response to the Sympathetic Nervous System (SNS)

Malignant in 10% of patients

173
Q

Adrenal Medulla-Pheochromocytoma pathogenesis

A

Pheochromocytoma is a tumor of the adrenal medulla that results in excessive production of catecholamines

Symptoms?

174
Q

Adrenal Medulla-Pheochromocytoma clinical manifestations

A

-Intermittent or persistent HTN (most common)

-Headache

-Tachycardia

-Diaphoresis

175
Q

Adrenal Medulla-Pheochromocytoma treatment

A

Surgical removal of tumor

Beta blockers

176
Q

Parathyroid Gland Disorders

A

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

177
Q

Hyperparathyroidism etiology

A

Unclear etiology

Despite elevate serum Ca+, PTH continues to be secreted (both elevated)

Genetic

Parathyroid adenoma (MC)

178
Q

Hyperparathyroidism pathogenesis

A

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.

179
Q

Hyperparathyroidism clinical manifestations

A

-May be asymptomatic

-Prone to kidney stones. Why?

-Osteoporosis

-Bradycardia

-Cardiac arrest

-Ca+ elevated

-Phosphorus levels low

-Calcium and Phos always inversely related

180
Q

Hyperparathyroidism treatment

A

Surgery

Volume replacement

-Improve GFR

-Increase Ca+ excretion

-Diuretics

181
Q

Hypoparathyroidism etiology

A

Happens after parathyroid or thyroid surgery

May be temp or permanent

Congenital

Autoimmune

182
Q

Hypoparathyroidism clinical manifestations/treatment

A

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

183
Q

Antidiuretic Hormone (ADH) Disorders

A

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

184
Q

Diabetes Insipidus (large diuresis of inappropriately dilute urine) etiology

A

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

185
Q

Diabetes Insipidus (large diuresis of inappropriately dilute urine) pathogenesis

A

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

186
Q

Diabetes Insipidus clinical manifestations

A

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

187
Q

Diabetes Insipidus treatment

A

Give ADH

Monitor labs

-BUN

-Serum Creatinine

-Serum Electrolytes

-sodium

188
Q

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) etiology

A

Too much ADH

Tumors

Medications

189
Q

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) pathogenesis

A

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

190
Q

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) clinical manifestations

A

Increased water reabsorption

Low osmolality (too thin)

Weakness

Muscle cramps

Orthostatic hypotension

Low lab values due to dilution

Hyponatremia

-Confusion

-Lethargy

-Coma

191
Q

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) treatment

A

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

192
Q

Diabetes Statistics

A

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

193
Q

Glucose

A

broken down carbohydrates for energy. Sugar

194
Q

Glucagon

A

hormone produced by alpha cells of pancreas. Stimulates glycogenolysis and gluconeogenesis in liver

195
Q

Glycogen

A

carbohydrate consists of glucose produced in muscle and liver from stored glucose

196
Q

Insulin

A

hormone produced by beta cells of pancreas. Energy metabolism

197
Q

Glycolysis

A

breakdown of sugar so cells can use

198
Q

Glycogenolysis

A

production of glucose from breakdown of glycogen in liver and muscle tissue

199
Q

Glycogenesis

A

production of glycogen from glucose in liver in muscle tissue

200
Q

Gluconeogenesis

A

production of glucose from amino acids in liver

201
Q

Liver/muscle produce

A

Glycogen

Glycogenesis

Glycogenolysis

Gluconeogenesis

*Insulin stimulates the diffusion of glucose into adipose and muscle tissue and inhibits the production of glucose by the liver

202
Q

Pancreas produces

A

Insulin

Glucagon

203
Q

Regulation of Glucose Metabolism

A

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

204
Q

Hormonal Regulation

A

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)

205
Q

Fed State

A

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

206
Q

Fasting State

A

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

207
Q

Exercise

A

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

208
Q

Stress

A

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”

209
Q

Diabetes Mellitus (DM)

A

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

210
Q

Glucose Intolerance Disorders

A

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

211
Q

Type I Diabetes Mellitus

A

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

212
Q

Type I Diabetes Mellitus etiology

A

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

213
Q

Type I Diabetes Mellitus pathogenesis

A

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

214
Q

What are the three Ps of DM

A

-Polyuria

-Polydipsia

-Polyphagia

215
Q

Type I Diabetes Mellitus clinical manifestations

A

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

216
Q

Type II Diabetes Mellitus

A

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)

217
Q

Type II Diabetes Mellitus pathogenesis

A

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

218
Q

Type II Diabetes Mellitus etiology

A

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
219
Q

Type II Diabetes Mellitus pathogenesis

A

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

220
Q

Type II Diabetes Mellitus clinical manifestations

A

-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

221
Q

Pre-Diabetes

A

Impaired Glucose Tolerance

Impaired Fasting Glucose Tolerance

Screen every 3 years once 45 years old

222
Q

Acute Hyperglycemia etiology

A

-MC caused by alteration in nutrition, inactivity, inadequate use of antidiabetic meds

223
Q

Acute Hyperglycemia complication

A

3 P’s:

  1. Polyuria
  2. Polydipsia
  3. Polyphagia

DKA

Fluid imbalance problems

Skin infections

Blurred vision

224
Q

Hyperglycemia Signs & Symptoms

A

Nausea

Fatigue

Decreased sense of well being

Rapid deep breathing- Kussmaul respirations

225
Q

Hypoglycemia Signs & Symptoms

A

Anxiety

Tachycardia

Sweating/Diaphoresis

Constriction of the skin vessels- Cold and clammy skin

Mental confusion

Decreased LOC

226
Q

Complications of DM Macro-vascular

A

Damage to the large blood vessels providing circulation to the brain, heart, and extremities

CVD

Stroke

Risk factors

-Dyslipidemia

-HTN

-Impaired fibrinolysis

227
Q

Complications of DM-Micro-vascular

A

Retinopathy -blindness

Nephropathy-ESRD

Abnormal thickening of basement membrane in capillaries

Hyperglycemia disrupts platelet function

228
Q

Complications of DM-neuropathic

A

Diabetic neuropathy produces symptoms in 60-70% of DM

Autonomic: bladder, tachycardia, postural hypotension, erectile dysfunction

Sensory: paresthesia in feet, lower extremity amputations

229
Q

Complications of DM pregnancy

A

Type I in pregnancy has increased risk for perinatal infant mortality

Untreated in pregnancy results in macrosomia, shoulder dystocia, pre-eclampsia.

230
Q

DM Treatment and Education

A

Nutrition

-Protein

-Fat

-Carbohydrates

-Alcohol

-Obesity and Eating Disorders

Exercise

Stress Management

Assessment of Efficacy

Education

Pharmacologic Agents

-Oral antidiabetic agents

-Insulin

231
Q

DM Evaluation

A

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.

232
Q

Pediatric Considerations with diabetes

A

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

233
Q

Geriatric Considerations with diabetes

A

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

234
Q
A

Patho (10 decks)

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