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Pathopharm 2 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

When does bone formation begin?

A

bone formation begins in two phases at approx 6 weeks gestation

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2
Q

What does bone formation consist of?

A

-delivery of bone cell precursors to sites of bone formation
-aggregation of the bone cell precursors at the primary centers of ossification (are mature and begin to secrete osteoid)

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3
Q

Ossification occurs in 2 long bone centers:

A
  1. primary center=diaphysis-long, central portion of bone
  2. secondary center=epiphysis-end portions of bones
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4
Q

Until adult stature is achieved, bone growth occurs at _______ through endochondral ossification

A

epiphyseal plate

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5
Q

Eipiphyseal closure

A

unites the metaphysis and epiphysis

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6
Q

Eipiphyseal closure occurs earlier in_______.

A

girls than boys because of earlier puberty in girls

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7
Q

Factors affect bone growth

A

-growth hormone (secreted by the pituitary)
-nutrition
-general health
-many growth factors and regulators: fibroblast growth factor

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8
Q

Peak bone mass is achieved by when?

A

middle to late 20s

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9
Q

How is the spine shaped in the newborn?

A

concave anteriorly (kyphosed)

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10
Q

When does the cervical spine begin to arch (lordotic)?

A

first 3 months of life

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11
Q

How does the spine differ in the adult vs newborn?

A

compared with the adult, a newborn has a large head, long spine and short extremities

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12
Q

By _______, 50% of total growth of spine has occurred and is more than 70% complete by ________ years of age.

A

1 year
8 years

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13
Q

What is Genu Varum?

A

Bowleg
-occurs in all newborns as a result of intrauterine stress
-peaks by 2 1/2 years

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14
Q

What is genu valgum?

A

-knock knees
-peaks by 5-6 years

if varum and valgum persist past their respective ages: pathologic cause

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15
Q

Composition and size of muscles vary with age

A

-growth in length occurs at the ends of muscles
-increase in length is accompanied by an increase in the number of nuclei in the fibers
-muscle fibers increase in diameter as the fibrils become more numerous
-fibrils themselves do not increase in diameter

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15
Q

Between birth and maturity, muscle nuclei in the body increases _____ times in boys and ______ times in girls.

A

14
10

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16
Q

What percent of total body weight is muscle in infants vs. adults?

A

25% infants
40% adults

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17
Q

Where is the majority of weight in the infant?

A

axial musculature (55% in an adults lower limbs)

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18
Q

What is syndactyly?

A

-webbing of fingers
-fusion of soft tissues of the fingers

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19
Q

Complex Syndactyly

A

also includes fusion of the bones and nails

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20
Q

Vestigial tabs

A

Extra digit

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21
Q

Developmental dysplasia of hip (congenital dislocation of the hip)

A

abnormality of the proximal femur, acetabulum or both

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22
Q

What are risk factors for developmental dysplasia of hip?

A

-family history
-female
-metatarsus adductus
-torticollis
-oligohydramnios
-first pregnancy
-breech presentation

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23
Q

Clinical manifestations of developmental dysplasia of hip

A

-asymmetry of gluteal or thigh folds
-limb length discrepancy: Galeazzi sign
-limitation of hip abduction
-positive ortolani sign: hip dislocated but reducible
-positive Barlow maneuver: hip reduced but dislocatable
-positive trendelenburg gait: waddling
-pain=very late

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24
Q

treatment for developmental dysplasia of hip younger than 4 months

A

pavlik harness

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25
Q

treatment for developmental dysplasia of hip up to 12 months of age

A

closed reduction (without opening of the joint), followed by spica or body casting for up to 3 months

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26
Q

treatment for developmental dysplasia of hip after 12 months of age

A

surgical intervention, including opening of the joint and cutting and realigning the femur and/or acetabulum

up to 70% of children treated surgically after 3 yrs develop osteoarthritis

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27
Q

Metatarsus adductus (forefoot adduction)

A

Degree of deformity
mild=heel bisection line passes medial to third toe
moderate-through the third and fourth toes
severe=lateral to fourth toe

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28
Q

treatment of metatarsus adductus

A

serial casts during first 6 months of life

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29
Q

Clubfoot

A

equinovarus deformity: heel positioned varus (inwardly deviated) and equinus (plantar flexed)

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30
Q

Positional equinovarus

A

serial casts

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31
Q

Idiopathic Congenital equinovarus

A

cast correction, followed by surgical intervention of resistant deformities, braces may be used

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32
Q

tetratologic equinovarus

A

always required surgical correction and/or muscle balancing procedures

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33
Q

pes planus

A

flat foot: if painless, then feet are normal

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34
Q

Osteogenesis Imperfecta

A

“brittle bone” disesase
-defect in bone and/or vessel collagen production
-sillence classification (types I-IV)
-results in osteoporosis, bowed and deformed limbs, spine curvature and bluish sclera, fractures (even utero fractures)

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35
Q

Tx for Osteogenesis imperfecta

A

prompt fx care
careful handling and positioning
telescoping rodes
bisphosphonate therapy (ex. alendronate (fosamax)
genetic counseling

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36
Q

What is Rickets?

A

disorder causing mineralization failure, “soft” bones and skeletal deformity

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37
Q

Causes of rickets

A

-insufficient Vitamin D
-insensitivity to Vitamin D
-renal wasting of vitamin D
-inability to absorb calcium or vitamin D in the gut

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38
Q

Clinical manifestations of Rickets

A

-short stature
-bowing of the limbs with hypotonia and muscle weakness

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39
Q

Treatment of Rickets

A

-calcium, phosphorus and Vitamin D levels must be optimized before surgical intervention

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40
Q

Non-structural scoliosis

A

curvature from a cause other than the spine

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41
Q

Structural scoliosis

A

-curvature associated with vertebral rotation
-skeletal abn, neuromuscular dz, trauma, extraspinal contractures,, bone infections of the vertebrae, metabolic bone disorders, joint dz and tumors

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42
Q

Idiopathic scolioisis

A

-no known cause
-onset: infant, juvenile, adolescent

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43
Q

Clinical manifestation of nonstructural scoliosis

A

mild spinal curvature with prominence of one hip or rounded shoulders

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44
Q

treatment of scoliosis

A

Bracing: prevents progression, does not cure
-surgical fusion of spine

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45
Q

Structural scoliosis clinical manifestations

A

asymmetry of hip height, shoulder height, shoulder and scapular (shoulder blade) prominences and rib prominence

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46
Q

Osteomyelitis

A

infection in bone
-often associated with septic arthritis because an infant’s bone has blood vessels that perforate the growth plate
-begins as a bloody abcess in the metaphysics of the bone
-vertebae may be involved in adolescents and adults-these age groups are affected less often than younger populations
-infection spreads under the periosteum and along the bone shaft or into the bone marrow
-sequestra-sections of dead bone from periosteal separation
-involucrum-periosteal new bone

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47
Q

When is osteomyelitis less common?

A

after the epiphyseal plates are closed, except in the vertebral body
-infection may develop in any part of a bone and abscesses spread slowly
-destruction of the cortex in a localized area may result in a pathologic fracture

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48
Q

Clinical manifestations of osteomyelitis in infants

A

fever and failure to move affected limb (pseudoparalysis)

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49
Q

Clinical manifestations of osteomyelitis in children

A

-fever and systemic signs of toxicitiy
-swelling, fever, tenderness, and decreasing ability to bear weight on or move affected area
-onset can be abrupt

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50
Q

Clinical manifestations of osteomyelitis in adolescents

A

back pain for several weeks: may be only complaint

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51
Q

Treatment of osteomyelitis

A

-IV antibiotics or in highly reliable children and families, a combination of IV and oral abx for 6 weeks.
- drainage and imagination of bone: for abscess
-immobilization: for pain control
-if a joint is infected (septic arthritis): it is a surgical emergency: Lysozymes released from the involved neutrophils cause damage to the articular cartilage.

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52
Q

Juvenile Idiopathic Arthritis (JIA)

A

childhood form of RA
basic pathophysiology: same as adult form
one difference=mode of onset
fewer than 5 joints: pauciarticular arthritis
-more than 5 joints: polyarticular arthritis
-systemic: still disease

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53
Q

Tx of JIA

A

no cure
DMARDs-used to tx arthritis but not great at eliminating the cause

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54
Q

Differences in JIA and adult RA

A

-large joints are affected
-spinal changes include subluxation and ankylosis of the cervical spine
-joint pain is not as severe
-antinuclear antibody test is positive
-chronic uveitis is common
-rheumatoid factor is seldom detected
-rheumatoid nodules are common in the heart, lungs, eyes and other organs
-is positive for cyclic citrullinated peptide antibody-antibody we tend to see in RA, autoimmune common that causes destruction of joints

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55
Q

Osteochondrosis

A

-avascular disease of the bone; insufficient blood supply to growing bones
-several types
-activity-related pain of the affected region that improves with rest

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56
Q

Treatment of osteochondrosis

A

-antiinflammatory medications
-modification of activites and even immobilization
-reparative correction by revascularization

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57
Q

Legg-Calve-Perthes disease

A

-blood supply to femoral head is interrupted
-self-limiting
-if left untreated leads to destruction of femoral head and dislocation of hip joint
-ossification center first becomes necrotic, collapses and then is gradually remodeled by live bone

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58
Q

Clinical manifestations of Perthes Disease

A

-knee pain
-spasm on inward rotation of hip and a limitation of internal rotation flexion and abduction
-abnormal gait: Trendelenburg gait or abductor lurch

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59
Q

Treatment of Perthes disease

A

-containment: keep ball completely in socket
-motion: maintain articular cartilage
-administer antiinflammatory medications and use crutches: for episodes of synovitis and activity modification
–avoid jumping activities that place increased stress on hip during active phase
-serial roentgenograms: to monitor hip placement/degree of damage
-intraarticular injection of bisphosphonates
-surgery may be necessary/complete joint replacement

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60
Q

Osgood-Schlatter disease

A

-tendinitis of the anterior patellar tendon and osteochondrosis of the tubercle of the tibia
-mild tendinitis to a complete separation of the anterior extension of the tibial epiphysis

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61
Q

Clinical manifestations of Osgood-Schlatter disease

A

-pain and swelling in affected area, becoming prominent and tender to direct pressure, especially after physical activity

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62
Q

Treatment of Osgood-Schlatter disease

A

-restriction from strenuous physical activity: 4-8 weeks
-if pain relief is not achieved: cast or brace
-return to unrestricted athletic participation

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63
Q

What is cerebral palsy?

A

-congenital muscular disorder
-nonprogressive disorder of movement and posture caused by an ischemic insult to the brain
-disease patterns: hemiplegia, diplegia, quadriplegia

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64
Q

Clinical manifestations of Cerebral Palsy

A

motor milestones are not met

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65
Q

Treatment for Cerebral palsy

A

-no cure: multidisciplinary approach; surgery
-physical and occupational therapies
-orthotics
-spasticity reduction (selected dorsal rhizotomy, baclofen)
-botulinum-A (Botox) injections

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66
Q

Muscular dystrophies

A

-group of inherited disorders that cause degeneration of skeletal muscle fiber
-cause progressive symmetric weakness and wasting of skeletal muscle groups

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67
Q

What is the most common muscular dystrophy?

A

duchenne muscular dystrophy

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68
Q

What is Duchenne muscular dystrophy?

A

X-linked recessive inheritance (males only)
-deletion of a segment of DNA or single gene defect on the short arm of the X chromosome

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69
Q

Duchenne muscular dystrophy gene

A

-encodes for dystrophin protein

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70
Q

What does dystrophin mediate?

A

-mediates the anchorage of the actin cyto-skeleton of the skeletal muscle fiber to the basement membrane
-poorly anchored fibers tear apart under the repeated stress of contraction; free calcium then enters the muscle cells, causing cell death and fiber necrosis

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71
Q

When do clinical manifestations appear in DMD?

A

3 years of age

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72
Q

Clinical manifestations of DMD

A

-slow motor development
-progressive weakness
-muscle wasting
-delayed sitting and standing
-calf hypertrophy
-clumsy, frequently falls, difficulty climbing stairs
-waddling gait
-gower sign: climbing up the legs when rising

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73
Q

Treatment of DMD

A

-genetic counseling
-oral steroids early in the disease
-range-of-motion exercises, bracing and surgical release of contracture deformities
-multidisciplinary approach

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74
Q

Becker muscular dystrophy

A

-similar but milder clinical features as compared with DMD

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75
Q

Facioscapulohumeral muscular dystrophy

A

-mild form of progressive, autosomal dominant
-facial and shoulder girdles involved

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76
Q

Limb girdle muscular dystrophy

A

pelvic and shoulder girdles involved

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77
Q

Nonossifying fibroma

A

benign bone tumor
fibrocytes that have replaced normal bone

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78
Q

Simple bone cysts

A

benign bone tumor
cystic lesions of central region of the metaphyseal region

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79
Q

Aneurysmal bone cysts

A

-metaphyseal lesions that occur in a slightly older population than simple bone cysts
-benign bone tumors

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80
Q

Osteoid osteoma

A

-painful lesions of the diaphysis or metadiaphysis of long bones
-benign bone tumors

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81
Q

What is osteochondroma also called?

A

exostosis

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82
Q

What is osteochondroma?

A

bony protuberance of bone, growing near the growth plate can lead to painful deformity
-solitary lesion or inherited syndrome

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83
Q

Fibrous dysplasia

A

-bone thinning, growths or lesions that can occur in one bone (monostotic) or in multiple bones (polyostotic)

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84
Q

Albright syndrome triad

A
  1. polyostotic fibrous dysplasia
  2. precocious puberty
  3. cutaneous pigmentation
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85
Q

Osteosarcoma

A

-malignant bone tumor
-originates from bone-producing mesenchymal cells
-makes osteoid tissue
-deletion of genetic material on the long arm of chromosome 13
-most occurring between 10 and 18 years old

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86
Q

Clinical manifestations of osteosarcoma

A

pain

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87
Q

treatment of osteosarcoma

A

-surgery and multiagent chemotherapy
-radiation

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88
Q

What is the most lethal malignant bone tumor that can occur?

A

ewing sarcoma

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89
Q

What is ewing sarcoma?

A

–malignant round cell tumor of bone and soft tissue
-occurs in the diaphysis of long bones or in flat bones

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90
Q

clinical manifestations of ewing sarcoma

A

pain, soft-tissue mass

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91
Q

treatment of ewing sarcoma

A

-preop chemotherapy followed by radiation or surgical resection or both, with continuation of chemotherapy for 12-18 months
-surgical resection: essential, must get tissues out before they spread

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92
Q

Rhabdomyosarcoma

A

malignant bone tumor
-arises from embryonal rhabdomyoblasts

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93
Q

clinical manifestations of rhabdomyosarcoma

A

painless palpable, visible mass

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94
Q

treatment of rhabdomyosarcoma

A

surgery, radiation, chemotherapy

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95
Q

complete fracture

A

bone broken all the way through

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96
Q

incomplete fracture

A

bone damaged but still in one piece
closed or simple (complete or incomplete)-skin intact
open or compound (complete or incomplete): skin is broken

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97
Q

comminuted fracture

A

-bone breaks into more than 2 fragments

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98
Q

linear fracture

A

fracture runs parallel to long axis of bone

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99
Q

oblique fracture

A

fracture of shaft of bone is slanted

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100
Q

spiral fracture

A

encircles bone

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101
Q

transverse fracture

A

occurs straight across bone

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102
Q

greenstick fracture

A

perforates one cortex and splinters spongy bone

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103
Q

torus fracture

A

cortex buckles but does not break

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104
Q

bowing fracture

A

longitudinal force is applied to bone

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105
Q

pathologic fracture

A

break occurs at the site of a preexisting abnormality

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106
Q

stress fracture

A

fatigue and insufficiency
transchondral

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107
Q

Bone fracture inflammatory phase

A

-lasts 3-4 days
-bone tissue destruction tiggers an inflammatory response
-hematoma formation-blood vessels that were ruptured

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108
Q

Repair phase of bone fractures

A

-lasts several days
-capillary ingrowth, mononuclear cells, and fibroblasts transforms hematoma into granulation tissue
-osteoblasts within the procallus (early stage of repair) synthesize collagen and matrix to form callus

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109
Q

Remodeling phase of bone fractures

A

-lasts months to years
-unnecessary callus is resorbed and trabeculae are formed
-at the end, bone can withstand normal stresses
-structure of bone follows function necessary. remodels itself back to original shape for normal function

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110
Q

bone fracture clinical manifestations

A

-unnatural alignment
-swelling
-muscle spasm
-tenderness, pain
-impaired sensation

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111
Q

treatment of bone fractures

A

-closed manipulation, traction (skeletal or skin), open reduction, internal fixation, external fixation
-splints and casts

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112
Q

nonunion

A

-failure of bone ends to grow together
-gap between broken ends of the bone fills with dense fibrous and fibrocartilaginous tissue
-occasionally, fibrous tissue contains a fluid-filled space that resembles a joint: referred to as false joint or pseudoarthrosis

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113
Q

malunion

A

healing of bone in an nonanatomic position

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114
Q

delayed union

A

does not occur until 8-9 months after fracture

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115
Q

Dislocation

A

temporary displacement of bone from its joint

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116
Q

subluxation

A

contact between the bones in the joint only partially lost

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117
Q

treatment of dislocation and subluxation

A

-reduction and immobilization for 2-6 weeks
-exercises

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118
Q

strain

A

tear or injury to a tendon (fibrous connective tissue that attaches skeletal muscle to bone)

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119
Q

sprain

A

tear or injury to a ligament (fibrous connective tissue that connects bones)

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120
Q

avulsion

A

complete separation of tendon or ligament from its bony attachment site

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121
Q

tendinitis

A

inflammation of a tendon

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122
Q

tendinosis

A

painful degradation of collagen fibers

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123
Q

bursitis

A

inflammation of a bursa (inflamed fluid filled sac around area)
-sacs lines with synovial membrane and filled with synovial fluid
-caused by repeated trauma
-septic bursitis: caused by a wound infection

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124
Q

Epicondylitis

A

inflammation of a tendon where it attaches to a bone

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125
Q

tennis elbow

A

lateral epicondylitis

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126
Q

golfer’s elbow

A

medial epicondylitis

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127
Q

treatment for tendinopathy and bursitis

A

-systemic analgesics, ice or heat applications, or local injection of an anesthetic and a corticosteroid to reduce inflammation
-bursitis: aspiration to drain excess fluid
-physical therapy

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128
Q

muscle strain

A

-sudden, forced motion, causing muscle to become stretched beyond its normal capacity
-causes local muscle damage
-can also involve tendons
-regardless of the cause of trauma, muscle cells can usually regenerate
-may take up to 6 weeks

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129
Q

myositis ossificans

A

-also called heterotopic ossification
-complication of local muscle injury
-inflammation of muscular tissue with subsequent calcification and ossification of muscle
-rider’s bone in equestrians
-drill bone in infantry soldiers
-thigh muscles in football players
-muscles that are overused, build up of calcium deposits

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130
Q

rhabdomyolysis

A

life-threatening complication of severe muscle trauma with muscle cell loss
-crush syndrome vs. crush injury
-compartment syndrome
-rapid breakdown of muscle that causes release of intracellular contents-toxic to tissues leading to inflammation in space
-protein pigment myoglobin into extracellular space and bloodstream

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131
Q

classic triad of rhabdomyolysis

A
  1. muscle pain
  2. weakness
  3. dark urine (from myoglobin)
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132
Q

treatment of rhabdo

A

rapid IV hydration to maintain adequate kidney flow
hyperkalemia-may require temporary hemodialysis

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133
Q

compartment syndrome

A

-a complication of fractures
-blood flow to affected area is comprised because of increased venous pressure, leading to decreased arterial inflow, ischemia, and edema-increases pressure on blood vessels and shuts off blood flow can lead to permanent necrosis

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134
Q

Clinical manifestations of compartment syndrome

A

pain: out of proportion to injury
paresthesia
pallor
pulsenessness
paralysis (late sign)

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135
Q

treatment of compartment snydrome

A

immediate fasciotomy and debridement
emergency treatment may be required to safe affected limb

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136
Q

osteoporosis

A

-porous bone
-poorly mineralized bone
bone density <648mg/cm2

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137
Q

normal bone density

A

833 mg/cm2

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138
Q

osteopenic bone

A

-decreased bone mass
-833-648 mg/cm2

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139
Q

Causes of osteoporosis

A

-decreased levels of estrogen and testosterone
-decreased activity level
-inadequate levels of vitamins d and calcium or mag
-alterations in osteoprotegerin (OPG), receptor activator of nuclear factor kappa B ligand (RANKL), and receptor activator of nuclear factor kB (RANK)

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140
Q

postmenopausal osteoporosis

A

increased osteoclast activity
changes in OPG
insulin-like growth factor (IGF)
family history

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141
Q

glucocorticoids effect on bone density

A

increase RANKL expression and inhibit OPG production by osteoblasts, leading to lower bone density

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142
Q

types of osteoporosis

A

Perimenopausal
iatrogenic-drug cause
regional-osteo at particular region from trauma in area
postmenopausal-estrogen levels way down
-glucocorticoid induced
-age-related bone loss

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143
Q

clinical manifestations of osteoporosis

A

-pain
-bone deformity
-fractures
-kyphosis (hunchback)
diminished height

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144
Q

prevention of osteoporosis

A

-regular moderate weight bearing exercises
-calcium intake sufficient to maintain normal calcium balance during adolescence
-sufficient intake of magnesium

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145
Q

treatment of osteoporosis

A

-estrogen
-biphosphonates, denosumab (Prolia), teriparatide (Forteo), parathyroid hormone (PTH) 1-84

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146
Q

osteomalacia

A

-deficiency of vitamin D lowers the absorption of calcium from the intestines
-mineralization is inadequate or delayed
-bone formation progresses to osteoid formation but calcification does not occur, result is soft bones

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147
Q

clinical manifestations of osteomalacia

A

-pain
-bone fractures
-vertebral collapse
-bone malformation
-waddling gait

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148
Q

treatment of osteomalacia

A

-adjust serum calcium and phosphorus levels to normal
-suppress secondary hyperthyroidism
–chelate bone aluminum
-administer calcium carbonate to decrease hyperphosphatemia
-administer dietary supplements of vitamin D
-use renal dialysis
-renal transplantation for renal osteodystrophy

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149
Q

Pagets disease (osteitis deformans)

A

state of increase metabolic activity of bone
-is abnormal and bone resorption and formation are excessive
-enlarges and softens the affected bones
-most often affects axial skeleton

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150
Q

clinical manifestations of Paget disease

A

-brain compression
-impaired motor function
-deafness
-atrophy of optic nerve

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151
Q

treatment of paget disease

A

bisphosphonates and calcitonin

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152
Q

osteomyelitis

A

-usually caused by staphylococcal infxn
-often outside the body (exogenous); can be from bloodborne (endogenous) infection
-infection spreads under the periosteum and along the bone shaft or into bone marrow
-in adults: affects cortex
-sequestra: sections of dead bone from periosteal separation
-involucrum: periosteal new bone

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153
Q

clinical manifestations of osteomyelitis

A

-acute and chronic inflammation
-fever
-pain
-necrotic bone

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154
Q

treatment of osteomyelitis

A

-abx
-debridement
-surgery
-hyperbaric O2 therapy

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155
Q

Malignant bone tumors

A

increased nuclear-cytoplasmic ratio
-irregular borders
-excess chromatin
-prominent nucleolus
-increase in mitotic rate-hallmark of cancer cells

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156
Q

Geographic bone destruction

A

well-defined margins of lytic bone with normal bone

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157
Q

moth-eaten bone destruction

A

areas of partially destroyed bone adjacent to completely lytic areas

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158
Q

permeative bone destruction

A

-abnormal lytic bone imperceptibly merges with surrounding normal bone

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159
Q

38% of all bone tumors

A

osteosarcoma

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160
Q

What is osteosarcoma located?

A

in metaphyses of long bones
50% occur around knees

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161
Q

Osteosarcoma is predominant in:

A

adolescents and young adults
occurs in seniors with history of radiation therapy

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162
Q

contain masses of osteoids: bone-forming tumors

A

osteosarcoma
streamers: noncalcified bone matrix and callus

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163
Q

What is a tumor of middle-ages and older adults?

A

chondrosarcoma

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164
Q

Chondrosarcoma

A

-produces cartilage or chondroid
-infiltrates trabeculae in spongy bone; is frequently in the metaphyses or diaphysis of long bones
-contains lobules of hyaline cartilage that expand and enlarge the bone with no ossification
-causes erosion of the cortex and can expand into the neighboring soft tissues

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165
Q

chondrosarcoma treatment

A

wide-surgical excision-damaged area and surrounding area

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166
Q

fibrosarcoma

A

-firm, fibrous masses of collagen, malignant fibroblasts and osteoclast-like cells
-usually affects metaphyses of femur or tibia
-metastasis to lungs is common

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167
Q

fibrosarcoma clinical manifestations

A

-pain
-swelling
-local tenderness
-palpable mass
-limitation of motion
-pathologic fracture

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168
Q

tx of fibrosarcoma

A

radical sx and amputation

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169
Q

giant cell tumor

A

-causes extensive bone resorption as a result of osteoclastic origin
-slow relentless growth rate; metastasis rare

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170
Q

where is giant cell tumor located?

A

epiphyses of femur, tibia, radius or humerus

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171
Q

clinical manifestations of giant cell tumor

A

-pain
-local swelling
-limitation of movement

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172
Q

tx of giant cell tumor

A

cryosurgery and resection with adjuvant polymethylmethacrylate (PMMA) for bone grafts

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173
Q

noninflammatory joint disease is differentiated by:

A

-absence of synovial membrane inflammation
-lack of systemic s/s
-normal synovial fluid

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174
Q

arthropathies

A

disease of joints

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175
Q

Osteoarthritis (degenerative joint disease)

A

-common age-related disorder of synovial joints
-inflammatory joint disease
-loss of articular cartilage, sclerosis of underlying bone, formation of bone spurs (osteophytes)
-incidence increases with age

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176
Q

clinical manifestations of OA

A

-pain, stiffness, enlargement of the joint, tenderness, limited motion, deformity
-joint swelling in the fingers: heberden and bouchard nodes
-joint effusion: exudate or blood entering the joint

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177
Q

treatment of OA

A

-rest of involved joint until inflammation subsides
-aerobic exercise of ROM
-cane, crutches or walker
-weight loss if obese
-analgesic and antiinflammatory drugs
-magnetic bracelets and acupuncture
-intraarticular injection of high-molecular weight viscosupplements to increase joint fluid particularly hyaluronic acid
-sx:joint replacement

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178
Q

Arthritis

A

-inflammatory damage or destruction in the synovial membrane or articular cartilage
-systemic signs of inflammation: fever, leukocytosis, malaise, anorexia and hyperfibrinogenemia

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179
Q

Rheumatoid arthritis (RA)

A

inflammatory joint disease
-systemic autoimmune destruction to synovial membranes and joints
-presence of rheumatoid factors: RA or RF test
-antibodies (IgG and IgM against antibodies)
-joint fluid with inflammatory exudate

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180
Q

clinical manifestations of RA

A

-symmetric joint swelling, joint deformities
-rheumatoid nodules in organs
caplan syndrome
-autoantibodies RF
-significantly more specific serum marker, anticitrullinated protein antibody (ACPA)
-present for years to decades before synovial or radiographic changes become apparent

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181
Q

RA evaluation (four or more of the following):

A

-morning joint stiffness lasting atleast 1 hour
-arthritis of 3 or more joint areas
-arthritis of the hand joints
-symmetric arthritis
-rheumatoid nodules
-abnormal amounts of serum RF
-radiographic changes

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182
Q

treatment of RA

A

-DMARDs such as:
methotrexate-first line
azathioprine
sulfasalazine
-hydroxychloroquine
-leflunomide
cyclosporine

biologic DMARDS: meds affect specific processes in the development of RA: tumor necrosis factor inhibitors
-monoclonal antibodies
-NSAIDS
-glucocorticoids and intraarticular steroid inj.
-sx: synovectomy or joint replacement

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183
Q

Ankylosing spondylitis

A

chronic inflammatory joint disease of spine or sacroiliac joints, causing stiffening and fusion of joints
-uncontrolled bone formation
-enthesis: primary proposed site where ligaments, tendons, and joint capsule are inserted into bone

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184
Q

what is ankylosing spondylitis strongly associated with?

A

human leukocyte antigen B27 (HLA-B27)

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185
Q

clinical manifestations of ankylosing spondylitis

A

-low back pain
-stiffness
-pain
-restricted motion
-bamboo spine
-loss of normal lumbar curvature

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186
Q

treatment of ankylosing spondylitis

A

physical therapy: maintenance of skeletal mobility and prevention of natural progression of contractures
-support groups
-NSAIDS
corticosteroids

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187
Q

gout

A

metabolic disorder that disrupts the body’s control of uric acid production or excretion
-exhibits high levels of uric acid in the blood and other body fluids
-occurs when uric acid concentration increases to high enough levels to crystallize
-crystals deposit in connective tissue throughout the body
if prolonged in joints: gouty arthritis
tophi: small, white visible nodules

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188
Q

what are precursors of gout?

A

purines

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189
Q

causes of gout

A

purine synthesis or breakdown accelerated
poor uric acid secretion in kidneys

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190
Q

mechanisms for crystal deposition in gout

A

-low body temps
-decreased albumin or glycosaminoglycan levels
-changes in ion concentration and pH
-trauma
-low pH

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191
Q

asymptomatic hyperuricemia

A

urate level high with no symptoms

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192
Q

tophaceous gout

A

urate crystal deposits (tophi) appear in cartilage, synovial membranes, tendons and soft tissues

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193
Q

clinical manifestations of gout

A

-pain in great toe
-worse at night
-increase in serum urate concentration-hyperuricemia
-recurrent attacks of monoarticular arthritis: inflammation of a single joint
-deposits of monosodium urate monohydrate (tophi) in and around joints
-renal dz, involving glomerular, tubular and interstitial tissues and blood vessels
-formation of renal stones

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194
Q

treatment of gout

A

-NSAIDS and xanthine oxidase inhibitors (block formation of uric acid) : Allopurinol and febuxostat
-acute attacks: colchicine and NSAIDS
-hydrocortisone: may be injected into joint
-ice: for inflammation of joint
-avoidance of weight-bearing movements on involved joint until acute attack subsides
-weight reduction
-avoidance of alcohol
-consumption of low-fat dairy products, cherries, soybeans and vegetable sources of protein

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195
Q

physiologic contracture

A

muscle fiber shortening without an action potential
cause: failure of the SR (calcium pump) even with available ATP
-usually temporary
-ex eye twitch

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196
Q

pathologic contracture

A

muscle shortening caused by muscle spasm or weakness
-plentiful ATP and occurs despite a normal action potential
-permanent

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197
Q

fibromyalgia

A

chronic widespread joint and muscle pain, fatigue and tender points
-CNS dysfunction: amplified pain transmission and interpretation-central sensitization

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198
Q

fibromyalgia symptoms

A

increased sensitivity to touch, absence of inflammation, fatigue and sleep disturbances
diffuse, chronic pain
-9 pairs (18) of tender points; must have tenderness in 11 of these tender points

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199
Q

possible factors of fibromyalgia

A

-flu-like viral illness
-chronic fatigue snydrome
-HIV
-lyme dz
-meds
-physical or emotional trauma

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200
Q

treatment of fibromyalgia

A

medications that improve sleep and vitamin D supplementation
-pregabalin
CBT, exercise, meds, education

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201
Q

chronic fatigue syndrome (myalgic encephalomyelitis)

A

-debilitating and complex disorder
-profound fatigue, neurologic energy production and immune impairments

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202
Q

chronic fatigue syndrome possible causes

A

-CNS dysregulation
-cardiovascular and immune system abnormalities
-immune system abnormalities
-chronic proinflammatory cytokines
-dysfunction of cellular energy metabolism
-dysfunction of ion transport
-people with lyme disease

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203
Q

clinical manifestations of chronic fatigue syndrome

A

-unrestful sleep
-debilitating fatigue made worse by physical or mental exercise (postexertional fatigue)
-muscle pain
-noninflammatory joint pain
-headaches
-flu-like symptoms
-memory or concentration problems

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204
Q

treatment of chronic fatigue syndrome

A

-consider psychosocial factors and symptomatic and supportive care
-acupuncture, massage and therapeutic touch

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205
Q

Disuse atrophy

A

-normal size of muscle cells are reduced as a result of prolonged inactivity
-bed rest, trauma, casting or nerve damage
-oxidative stress causes decreased protein synthesis and increased proteolysis
-prevention and tx: isometric movements and passive lengthening exercises

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206
Q

myotonia

A

delayed muscle relaxation after voluntary contractions
Cause: lack of chloride
treatment: medication to reduce muscle fiber excitability

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207
Q

periodic paralysis

A

-autosomal dominant inherited mutations of the skeletal muscle channels; muscle cannot contract

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208
Q

hypokalemic periodic paralysis

A

alteration in potassium ion channels regulated by T3

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209
Q

Treatment of hypokalemic periodic paralysis

A

potassium-sparing diuretics; high salt diet
long term: acetazolamide, dichlorphenamide, low-salt diet

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210
Q

hyperkalemic periodic paralysis

A

-genetic mutation of sodium channels

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211
Q

treatment of hyperkalemic periodic paralysis

A

small carb-rich meals, light exercise, and IV calcium gluconate

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212
Q

thyrotoxicosis

A

proximal weakness, paresis of extraocular muscles (exophthalmic ophthalmoplegia)

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213
Q

hypothyroidism

A

decrease in muscle mass and strenth with weak, flabby skeletal muscles and sluggish movements

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214
Q

familial hypomagnesemia

A

autosomal recessive disease, affecting the renal system causing hypomagnesemia and secondary hypocalcemia

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215
Q

mcArdle disease

A

-disease of energy metabolism
-myophosphorylase deficiency

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216
Q

Acid maltase deficiency or Pompe disease

A

-disease of energy metabolism
-glycogen

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217
Q

myoadenylate deaminase deficiency

A

disease of energy metabolism

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218
Q

myositis

A

-viral, bacterial and parasitic myositis
tuberculosis and sarcoidosis: granulomas found in muscle
trichinellosis: muscle stiffness; tx: corticosteroids and antiparasitic agents
viral infections: acute myositis–>muscle pain, tenderness, signs of inflammation and CK elevation

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219
Q

myopathy

A

-term applied to a primary muscle disorder
-affects muscle strength, tone and bulk
-associated with weakness-usually significant weakness and atrophy
-injections of drugs can affect muscle fibers (local trauma to the muscle fibers from direct effects of the needle)

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220
Q

treatment of polymyositis, dermatomyositis and inclusion body myositis

A

-immunosuppressive drugs
-corticosteroids initially
-high dose IVIG
-azathioprine and methotrexate
-creatine supplements
-physical therapy

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221
Q

inclusion body myositis

A

degenerative changes of muscle
accumulation of multiple proteins with muscle fibers
-evidence of Endoplasmic reticular stress with misfolding of proteins
-weakness of the wrist and finger flexors as well as asymmetric atrophy and quad weakness

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222
Q

polymyositis

A

generalized muscle inflammation mediated by T cells

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223
Q

dermatomyositis

A

polymyositis, accompanied with skin rash, humorally mediated

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224
Q

autoimmune diseases targeting skeletal muscle, characterized by symmetric proximal muscle (pelvic and shoulder girdle) weakness and myalgia that develops over weeks to

A

polymyositis
dermatomyositis
inclusion body myositis

225
Q

Gold mechanism of action

A

-anti-rheumatic drug
-unknown, but may alter functions and morphology of macrophage; appears to selectively accumulate in macrophages in inflamed synovium

226
Q

T1/2 gold

A

7 days
increases to weeks or months within successive dosing
avidly binds to tissues (found in liver and skin several years after therapy is Dcd)
excreted in urine and feces

227
Q

only gold salt available as parenteral preparation for IM administration

A

gold sodium thiomalate (Myochrysine)
-not in US but in canada

228
Q

Orally effective gold preparation

A

Auranofin (Ridaura)

229
Q

What is the most common side effect of Gold?

A

Dermatitis. Puritis is a warning signal
mucous membrane reactions also common

230
Q

Other side effects of gold

A

-stomatitis and ulcers on the buccal membranes and tongue
-skin toxicities include a bluish-gray pigmentation (chrysiasis)
-effects seen in 15-20% of patients

231
Q

More serious toxicities of gold

A

-bone marrow depression (blood counts mandatory)
-renal reactions such as nephrotic syndrome
-auranofin is better tolerated but causes a high incidence of GI disturbances

232
Q

MOA of hydroxychloroquine (Plaquenil)

A

-antimalarial
-unknown, but effects may be, in part, to stabilize lysosomal membranes
-use as an anti-inflammatory agent requires large doses for long periods of time.

233
Q

Side effects of Hydroxychloroquine

A

-drugs is deposited in tissues and can cause serious damage to the retina where the drug is preferentially concentrated (periodic ophthalmological tests are recommended). The retinal damage may be irreversible and may progress after the drug is discontinued
-can also cause dermatitis, ototoxicity and neuromyopathy

234
Q

Anti-rheumatic drug that is a chelator

A

D-Penicillamine (Cupramine)-helps bind and eliminate metals
-effective chelator of copper and other metals. Inhibitos enzymes that are pyridoxal-dependent; increases pyridoxine requirement
Mechanism unknown but may affect immune system

235
Q

problems with the use of D-Penicillamine

A

-loss of taste perception
-nephrotoxicity
-myasthenia-like syndrome
-rash
-thrombocytopenia
-leukopenia

236
Q

cytotoxic agents which are anti-rheumatic drugs

A

Azathioprine (Imuran)
Methotrexate

drugs may have direct anti-inflammatory effects in addition to their ability to suppress or modify immune responses

237
Q

Serious side effects of azathioprine and methotrexate

A

-bone marrow depression
-sterility
-carcinogenic and mutagenic effects
in spit of these effects, aggressive early tx with methotrexate can prevent major manifestations of RA before irreversible damage becomes prevalent.
-methotrexate has best-benefit to risk ratio
-methotrexate used ONCE a week in small doses (low dose pulse therapy). mucosal ulcers common at this dose

238
Q

TNF blockers

A

I-CAGE
Infliximab (Remicade)
Certolizumab (Cimzia)
Adalimumab (Humira)
Golimumab (simponi)
Etanercept (Enbrel)

239
Q

How do TNF blockers work?

A

-proteins that block TNF which is a large group of cytokines at its receptor
-TNF responsible for triggering immune response and is present in larger amounts in patients with RA and some other immune disorders such as ankylosing spondylitis and psoriasis. TNF increase body inflammatory reactions

240
Q

SE of TNF blockers

A

-increased risk of infections due to inhibited immune function
-occasional fatal blood dyscrasias, nervous system disorders, seizures and increased risk of some cancers (i.e. lymphoma)

241
Q

JAK1,JAK2, JAK 3

A

enzymes play a part in the signaling pathways that start by the action of cytokines at cytokine receptors
-inhibition of JAK enzymes thus block cytokine signaling and can decrease various immune and inflammatory responses; decrease overall ability to cytokines to interact at receptor.

242
Q

Janus Kinase inhibitors

A

Ruxolitinib (Jakafi)-JAK1/JAK2 inhibitor for RA
Baricitinib (Olumiant)-a JAK 1/JAK2 inhibitor for RA
Tofacitinib (Xeljanz)-JAK 3 inhibitor for moderate to severe RA not responding to methotrexate

243
Q

gout

A

chronic disease characterized biochemically as a disorder of uric acid metabolism and clinically by hyperuricemia and recurrent attacks of acute arthritis caused by deposition of crystals of sodium urate in tissues especially joints and the kidney
-leads to acute inflammatory reactions and tophi or inflamed swellings.
when blood uric acid level becomes saturated, neutrophils phagocytize crystals
-when crystals are phagocytized by these cells, they fuse with lysosomes which eventually rupture and cause the cell to lyse, releasing lysosomal enzymes and inflammatory and chemotacic mediators such as PGs, IL-1 and lactate (which decreases pH so solubility of urate decreases)
-these mediators attract PMNs (polymorphonuclear neutrophils) to the site
-these also release mediators and increase inflammation. more macrophages are called into the site, ingest the crystals and release more mediators

244
Q

uric acid is the end product of _______

A

purine metabolism
is poorly soluble especially in acidic environments

245
Q

causes of hyperuricemia and acute arthritic episodes

A

-drug effects
-renal damage
-metabolic
-increased nucleic acid turnover
-enzyme defects
-local decrease in urate solubility
-increased urate production

246
Q

drug therapy of gout has 2 primary aims:

A
  1. prevent and reduce the inflammation and pain of the acute attack
  2. reduce blood urate levels (below 6mg/dl) either by increasing urate excretion or by increasing urate production
247
Q

treatment of gout

A

-dietary changes-diet high in purines (meats) can trigger a gouty attack in susceptible individuals (also inherited disease- inability to properly handle uric acid)
-weight reduction
-adequate fluid intake
-limitation of alcohol consumption
-drug therapy

248
Q

Drugs used in therapy of acute gout attacks

A
  1. colchicine (most effective but potentially toxic)
  2. NSAIDs
249
Q

drugs that increase urate excretion (uricosurics)

A

probenecid

250
Q

drugs that decrease uric acid production

A
  1. allopurinol (Zyloprim)
  2. Febuxostat (Uloric)
251
Q

Which drug is a plant alkaloid of colchicum autumnale (automn crocus, meadow saffron)

A

Colchicine

252
Q

What is the mechanism of action of Colchicine?

A

-binds to tubulin and disrupts mitotic spindles causes depolymerization, microtubules in granulocytes and inflammatory cells are affected and granulocytes then cannot migrate to inflamed area. Their phagocytic activity is inhibited and importantly, net effect is to decrease release of lactic acid Thus inflammation is decreased and further urate deposition caused by the lactate-induced low pH is prevented.

253
Q

Colchicine uses

A

effective at the onset of symptoms and gives prompt relief of symptoms.
-pain, swelling, redness usually subside within 12 hours and are completely gone within 48-72 hours
-useful as a prophylactic agent in very low doses at the initiation of treatment with other anti-gout drugs to decrease risk of acute attacks of gout (0.5mg 2-4 times/wk)

254
Q

Colchicine toxicity and interactions

A

-since mitotic spindles cant form, mitosis is arrested at metaphase and cells with high rates of division are affected ex. rapidly proliferating cells of GI tract. Therefore GI symptoms of N/V, abd pain and diarrhea are common

255
Q

serious symptom of overose with Colchicine

A

-hemorrhagic gastroenteritis–stop taking
if not stopped can progress to vascular damage, renal toxicity, muscular depression and paralysis

256
Q

Colchicine dosing

A

-can be used orally (pushing the dose until pain relief or diarrhea) but not current practice to give IV (works faster and can avoid GI SE)
-take care not to cause extravasation which can cause severe tissue necrosis

257
Q

Colchicine can be used with _____ and ______.

A

probenecid and allopurinol

258
Q

Other drugs used for acute gout attacks

A

-NSAIDS
-steroids-used to decrease localized inflammation and therefore some of the pain of gouty attack

259
Q

MOA of probenecid

A

-organic acid
-in the kidneys uric acid is filtered, reabsorbed and then secreted. Probenecid blocks reabsorption of urate in the renal proximal tubule. Also blocks urate secretion but effects on reabsorption predominate and the net result is increased urate excretion in the urine-a uricosuric effect
-it is a prototype inhibitor of organic anion secretion (used to increase t 1/2 of penicillin by decreasing its secretion) but when used in sufficient amounts it interferes with uric acid reabsorption
-carrier causes blockate of secretion method of acid from blood into urine. Initially increase in uric acid concentration in blood, carrier can also move acid from the urine side back into the blood

260
Q

with what agents is there a paradoxical effect?

A

uricosuric agents (probenecid)
-small doses can compete with uric acid for tubular secretion and may even increase uric acid concentration.
-initiation of therapy may precipitate an acute gout attack
-prophylactic use of colchicine of an NSAID can prevent the acute attack.
-best not to start tx with uricosuric until 1-2 weeks after an acute gout attack

261
Q

uses of probenecid

A

-to decrease excretion of penicillin (competitive inhibition of renal organic acid carrier)

262
Q

toxicity and interactions

A

inhibits elimination of organic acid type drugs (PCN. cephalosporin etc)

263
Q

dose of probenecid

A

250 BID x 1 week, then 500mg BID (to max 2g/day)
take with plenty of water to minimized production of uric acid stones

264
Q

Lesinurad (Zurampic) MOA

A

-blocks uric acid transporter in the kidneys responsible for uric acid reabsorption. Does not block secretion

265
Q

which medication is only approved for use with a xanthine oxidase inhibitor (allopurinol)

A

Lesinurad (Zurampic)

266
Q

Lesinurad (Zurampic) should be avoided in patients with _______.

A

severely decreased kidney function
-may decrease normal kidney function and has been linked to kidney failure in some patients

267
Q

Lesinurad (Zurampic) induces ______ which may decrease effectiveness of some drugs such as __________.

A

CYP3A4
Warfarin

268
Q

Allopurinol (Zyloprim) and Febuxostat (Uloric) MOA

A

-major action is to inhibit xanthine oxidase (XO)
-both drugs result in increased concentrations of the more water soluble hypoxanthine and xanthine and decreased concentrations of the less soluble uric acid. It is thus less likely that uric acid crystals will precipitate in joints and tissues

269
Q

Xanthine oxidase converts ____ to _______ to ________.

A

converys hypoxanthine to xasnthine and xanthine to uric acid

270
Q

Which drug is an irreversible “suicide-substrate” inhibitor of XO

A

allopurinol
oxidized by XO to oxypurinol (alloxanthine) which is an irreversible suicide substrate inhibitor of XO

271
Q

what is a non-competitive inhibitor of XO, blocking ability of hypoxanthine and xanthine from getting to the site of enzyme action on XO.

A

Febuxostat

272
Q

Half-life of allopurinol is ______.

A

2-3 hours

273
Q

Allopurinol is metabolized to _______ which has a t1/2 of ______.

A

oxypurinol (alloxanthine)
18-30 hours
because the metabolite also inhibits xanthine oxidase. accumulation of the metabolite during chronic therapy contributes to the total therapeutic effect

274
Q

Half life of Febuxostat is _______.

A

5-8 hours, becuase it is non-competititive its dosing is normally once a day

275
Q

Plasma protein binding of Febuxostat

A

99.2%

276
Q

VD of Febuxostat

A

0.7 l/kg

277
Q

Uses of Allopurinol and Febuxostat

A

-severe chronic gout characterized by one or more of the following:
-renal stones and or impaired renal functioning
-tophaceous deposits
-gouty neuropathy
-hyperuricemia not controlled by uricosuric drugs
-allopurinol is also useful in prevention of hyperuricemia in patients with leukemia and some other cancers undergoing chemotherapy with cytotoxic agents

278
Q

toxicity and problems with allopurinol

A

-common SE is skin rash that can become serious is therapy is continued
-GI problems occur occasionally
-bone marrow depression has been reported but rare
-acute attacks may be observed during initiation of therapy and may be treated with colchicine or an NSAID
-may require dosage adjustments in kidney disease

279
Q

Febuxostat toxicity and problems

A

-greatest concern is increase in plasma liver enzymes indicative of liver damage (seen in up to 1% of patients)
-other SE include: rash, nausea, joint pain and headache

280
Q

Interactions of Allopurinol and Febuxostat

A

-Xanthine oxidase inactivates 6-mercaptopurine (6-MP or Purinethol)- an immunosuppresant and anti-cancer agent and azathioprine (Imuran) used in RA
-doses of these drugs must be reduced to 1/3-1/4 of usual dose
-inhibits metabolism of oral anticoagulants by inhibition of hepatic microsomal enzymes
-use of ampicillin in allopurinol treated patients is associated with a higher incidence of ampicillin rash

281
Q

Pegloticase (Krystexxa)

A

-drug used in refractory gout
-modified porcine-type uricase
-metabolizes uric acid to a more water soluble compound
-peptide so must be administered by injection
-only approved for patients not responding to other available chronic gout tx

282
Q

SE of Pegloticase

A

life threatening allergic reactions (anaphylaxis) possible 5%
-n/v
-chest pain
-possible CHF aggravation
-early gout exacerbation

283
Q

Pegloticase contraindicated in patients with _____

A

glucose-6-phosphate dehydrogenase (G6pD) deficiency due to increased risk of methemoglobinemia and hemolysis (care in Mediterranean and African heritage)

284
Q

tremor

A

rhythmic/oscillatory movement around joint

285
Q

Resting tremor (Parkinson’s) associated with:

A

-rigidity
-impairment of volitional movement

286
Q

essential tremor

A

one muscle stronger than other
-postural tremor-opposing gravity
-kinetic tremor-during movement

287
Q

intentional tremor

A

-most common at the end of movement
-brain stem/cerebellar lesion or MS
-may also be associated with alcohol/other drug toxicities

288
Q

Chorea

A

-involuntary muscle jerks; unpredictable
-hereditary link
-secondary to drug tx/various physiological disorders
-volitional activity impairment
-different parts of the body affected
-limb proximal muscles-most severely affected
-violent movements-ballismus

289
Q

Athetosis

A

slow, writhing abnormal movement

290
Q

dystonia

A

postural abnormality-associated with sustained abnormal movement

291
Q

athetosis/dystonias causes

A

-brain damage (perinatal)
-focal/generalized cortical lesions
-adverse effect associated with certain drugs (i.e. antipsychotics)
-associated with various neuro disorders
-unknown causes: idiopathic torsion dystonia also known as dystonia musculorum deformans

292
Q

Tics

A

sudden, abnormal coordinated movements
common:
shoulder shrugging
repetitive sniffing

293
Q

characteristics of tics

A

-single/multiple; transient/chronic
-repetitive (esp around head/face, in children)
-voluntary suppression: for limited amount of time
-most will resolve during puberty as well epilepsy but not always

294
Q

symptoms of parkinsons

A

-tremor
-bradykinesia
-rigidity
-characteristic gait/postural abnormality
-pill rolling, hand tremor early sign

295
Q

disease characteristics of parkinsons

A

-chronic, progressive
-begins in middle/late life and leads to progressive disability
-affects all ethnic groups
-equal gender distribution
frequency
general population: 1-2/1000, increase numbers as we age
>65 years: 1/100 persons
65-74 yrs: 15% of all cases
>85 years >50% of all cases

296
Q

physiology of parkinsons

A

-cell bodies from the substantia nigra pars compact provides dopaminergic input to the striatum (basal ganglia)
-dopaminergic neurons + cholinergic striatal interneurons modulate monosynaptic GABA inhibitory output to the globus palludis internus and pars reticulata of the substantial nigra
-globus pallidus internus transmits GABA-mediated inhibition to the ventrolateral/ventroanterior thalamic nuclei (direct pathway, striatal D1 mediated) loss of inhibition inhibits GABA pathway leading to increase in GABA release, decreases inhibition in motor center
-globus pallidus externus transmits via subthalamic nuclear (indirect pathway, striatal D2 mediated) excitatory (glutamate) input to the globus pallidus internus
-loss of substantial nigra pars compact cells cause reduced nigral-striatal dopamine input to the putamen
2 effects:
loss of striatal excitatory dopamine input (D1 mediated direct pathway)
loss of straital inhibitory dopamine input (D2 mediated indirect pathway)

297
Q

causes of parkinsons

A

-unknown
-environmental toxin
-endogenous toxins
-genetic aspect (uncertain)

298
Q

clinical manifestations of parkinsons

A

tremor:
-frequency usually 4-6 Hz (4-6 cycles per second)
-7-8 Hz in 10-15%
-resting tremor
-initially rhythmic flexion-extension of fingers, hand, foot
-may be associated with one limb or two limbs ipsilateral initially then becoming more widespread
-rigidity: increased resistance to passive movement
-bradykinesia:most disabling disease manifestation
-severest form-akinesia
-voluntary movement-slowness
-flat affect;infrequent blinking
other effects:
-blepharoclonus: closed eyelid fluttering
-blepharospasm (eyelid closure-involuntary)
-drooling
-voice: hypophonic/poorly modulated
-handwriting: small, tremulous, perhaps illegible
-Walking: difficulty in initiation, small, shuffling steps, no arm-swing, stooping difficulty
-festinating gait
-reflexees: tendon-unaltered
tapping over glabella: sustained blink reflex (Myerson’s sign)
-deression
-impaired cognitive function

299
Q

does dopamine cross BBB?

A

no, ineffective if administered peripherally

300
Q

L-DOPA

A

-crosses BBB
-metabolic precursor dopamine
-enters neuronal cells and is decarboxylated to dopamine

301
Q

D1

A

-adenyl cyclase stimulation
-increases cyclic AMP levels
-located in high concentration in substantial nigra zona compacta

302
Q

D2

A

-adenyl cyclase inhibition
-decreases cyclic AMP levels
-postsynaptic localization on striatal neurons–>region that tends to control movement activity

302
Q

How much Levodopa reaches the brain?

A

1-3%

303
Q

How do you achieve therapeutic brain levels of levodopa?

A

-large quantities of levodopa must be given or
-must be given along with dopa decarboxylase inhibitor such as carbidopa (does not penetrate brain) will block peripheral metabolism. Will only affect conversion of L-dopa to dopamine in periphery and reach BBB with lower dose and less SE.

304
Q

With carbidopa (Lodosyn):

A

-peripheral decarboxylation of levodopa is lessened
-levodopa plama 1/2 life=longer
-more levodopa available for brain entry
-levodopa + carbidopa =sinemet
-Rytary-extended release formulation

305
Q

Levodopa with Entacapone (Comtan)

A

a COMT inhibitor
-works similar to carbidopa in that it decreases metabolism of L-dopa which increases the amount that can cross BBB
-levodopa + carbidopa + entacapone=stavelo
-use of a peripheral dopa decarboxylase inhibitor allows 75% reduction in daily levodopa dose

306
Q

Does L-dopa stop disease progression?

A

no, may reduce Parkinson’s disease mortality rate

307
Q

L-dopa most effective in diminishing _______.

A

bradykinesia

308
Q

Adverse effects of Levodopa

A

-GI
20% frequency when administered with carbidopa
80% frequency when administered as monotherapy
-vomiting–>stimulation of brain stem emetic center (tolerance develops)
-avoid phenothiazines–>reduce efficacy of levodopa/disease exacerbation

309
Q

with long term tx of Levodopa ________ is most frequent.

A

dyskinesias 80%
-dose-related
-more common with combination tx (L-dopa plus carbidopa)

310
Q

most common dyskinesia

A

choreoathetosis (twisting, writhing activity)

311
Q

dyskinesias include:

A

-chorea
-ballismus
-athetosis
-dystonia
-myoclonus
-shakes
-tremor

312
Q

management of dyskinesias

A

-dose reduction
-drug holidays

313
Q

What is a selective monoamine oxidase B inhibitor that prolongs levodopa effect (inhibits metabolism)

A

Selegiline (Eldepryl)

314
Q

Other therapeutics used in parkinsons

A

Amantadine: antiviral drug; may influence dopamine release/reuptake/synthesis; may also be in part due to its anticholinergic activity
-anticholinergics: benztropine (Cogentin), Biperiden (akineton), orphenadrine (norflex), Trihexyphenidyl Hcl

315
Q

Physiologic postural tremor increased by:

A

-thyroitoxicosis
-isoproterenol (Isuprel)/epinephrine (IV)
-anxiety
-fatigue

316
Q

drug induced increase in normal physiologic tremor

A

-bronchodilators
-TCA
-lithium

317
Q

tremors induced/enhanced b sympathomimetics blocked by ______ suggesting tremor may be due to B2 receptor activation.

A

propanolol (sometimes not blocked by metoprolol B1)

318
Q

drug/drug classes useful in management of essential tremor

A

-beta-adrenergic receptor blockers
-primidone (Mysoline)
-alprazolam (xanax)

319
Q

intentional tremor

A

-may be caused by toxic reactions to alcohol and other drugs (i.e. phenytoin)
-withdrawal of causative agents alleviates symptoms

320
Q

Huntington’s disease

A

-dominant, inherited genetic disorder
-progressive chorea in dementia (typically adult onset)
-chorea: dpamine/acetylcholine/GABA basal ganglia imbalance
mechanism: chorea, difficulty slowing/stopping motion
-dopaminergic nigrostriatal pathway overactivity

321
Q

possibilities of huntington’s disease

A

-postsynaptic dopamine receptor hypersensitivity
-reduction in dopamine antagonizing neurotransmitter concentration

322
Q

what drugs reduce chorea

A

anti-dopaminergic agents
reserpine
phenothiazines and butyrophenones (haloperidol)

323
Q

What drugs increase chorea?

A

dopaminergic drugs (i.e. levodopa)

324
Q

chorea

A

complication of non-neurological disorder:
-thyrotoxicosis, hypocalcemia, lupus erythematosus, hepatic cirrhosis, polycythemia vera rubra

325
Q

drug-induced chorea

A

-levodopa
-antimuscarinics
-lithium
-phenytoin
-oral contraceptives
-amphetamine

326
Q

Ballismus tx

A

dopamine-blocking drugs-perphenazine, haldol

327
Q

athetosis and dystonia-tx

A

pharmacological tx usually not satisfactory
agents to try: diazepam, high-dose antimuscarinic agents. levodopa, baclofen, phenothiazines, amantadine

328
Q

treatment of tic (tourette’s snydrome)

A

haldol most effective
other: temazepam (restoril), carbamazepine (tegretol), clonidine (catapres), fluphenzine (prolixin)

329
Q

Phenothiazine induced dyskinesia tx

A

anti-muscarinic agents:
benztropine (congentin) IV
Benedryl IV
diperiden (Akiton) IM/IV
Valium IV

330
Q

tardive dyskinesia

A

-consequence of long-term antipsychotic drug tx
characteristics:

dosage reduction: worsens symptoms
dosage increase: suppresses symptoms
difficult to treat, in adults may well be irreversible

331
Q

new agents: _______& _____________ do not appear to cause tardive dyskinesia

A

olanzapine and risperidone

332
Q

Wilson’s disease

A

-recessive, inherited copper metabolism error
-reduced serum copper/ceruloplasmin
-increased copper concentration : brain, viscera

333
Q

clinical presentation of Wilson’s disease

A

-hepatic dysfunction
-neurologic dysfunction (dystonias, spasticity, seizures)

334
Q

What is Diabetes insipidus?

A

-inability to properly respond to ADH (arginine vasopressin-AVP) which is secreted by the post- pit (may be nephrogenic, gestational, or neurogenic
-results in polyuria and hypernatremia
-ADH acts on renal collecting ducts to increase permeability to water, thus further concentrating urine and conserving water
-nephrogenic not responsible to exogenous AVAP or other congeners such as desmopressin or lypressin
-gestational may be due to rapid metabolism by placenta

335
Q

What can cause DI?

A

trauma or surgery in area of post. pit. can cause deficiency which can be corrected by exogenous application

336
Q

Uses of Arginine Vasopressin (ADH)

A

-tx and dx of DI
-uncontrolled bleeding from esophageal varices
-hemodynamic stabilization in hemorrhagic shock
-refractory cardiac arrest (alternative to epi)

337
Q

Metabolism of Arginine vasopressin

A

-not orally active (destroyed in GIT)
-IV effects brief due to rapid tissue enzymatic breakdown, especially by the kidneys
-longer duration effects achieved by administration IM in oil vehicle

338
Q

Desmopressin (DDAVP)

A

-synthetic analog of AVP
-more potent antidiuretic (V2) than pressor (V1)
-also triggers cellular release of prostaglandins and von Willebrand factor
-fewer SE than AVP (N/V mostly)
-DOC for DI due to inadequate to inadequate post. pit production of AVP

338
Q

SE of Arginine Vasopressin

A

-vasoconstriction only in large doses
-angina pectoris (due to vasoconstriction-even in small doses)
-N/V d/t stimulation of GI smooth muscle
-stimulation of uterine contractions (Avoid in pregnancy?)
-decreased platelet count due to stimulation of platelet aggregation
-allergic reactions
-prolonged use may increase antibodies and decrease 1/2 life

339
Q

What is the 1/2 life of desopressin?

A

3-4 hrs

340
Q

Other uses of Demopressin (DDAVP)

A

hemostasis in hemophilia and chronic liver disease
-decreased blood loss during cardiac surgery

341
Q

Diabetes Mellitus

A

-characterized by hyperglycemia and ‘spilling’ of glucose into urine (sweet urine) which leads to osmotic diuresis
-due to defective insulin secretion (type 1-insulin dependant) or (Type 2-noninsulin dependent)
-believed due to excessive consumption leading to overstimulation of insulin release leading to insulin resistance at cells (type 2)

342
Q

Insulin

A

-peptide hormone produces as proinsulin (86 AAs) that loops and self-links via several disulfide bridges
-a center section (C peptide) is clipped out leaving what appears to be two peptide chains (a and b chains) linked by disulfide bridges
-both compounds (insulin and C protein) stored in granules for release as needed
-C protein plasma concentration can be used as a guide of beta cell

343
Q

Insulin structure

A

51 AA in 2 chains

344
Q

what is the primary insulin replacement used?

A

human recombinant insulin (Humulin)

345
Q

__________ is an insulin analog at position 28 & 29 allowing more rapid onset of action and shorter duration more like release of insulin in the body following a meal.

A

Insulin Lispro (Humalog)

346
Q

Mechanism of insulin

A

-binds to insulin receptors on cells, leading to increased intracellular phosphorylation of specific enzymes
-leads to increase in Glut-4 transporter proteins on cell surface and increased glucose transport into cells

347
Q

What is the half life of insulin

A

5-10 min
can be increased by either renal or hepatic disease (eliminated by both liver and kidneys)
-normal low level secretion by pancreatic beta cells, that is increased 5-10 times after meal
-best therapy is slow constant release (pump) but larger single dose is mainly bound and has increased duration.

348
Q

Lispro (Humalog)

A

-synthetic analog
-swap lysine and proline at positions 28 and 29 which blocks normal insulin hexamer formation with zinc, leading to more rapid onset

349
Q

Synthetic similar to Lispro

A

insulin aspart (Novolog)

350
Q

24 hour long-acting analog

A

Glargine (Lantus)

351
Q

Insulin that contains protamine and zinc in crystallized form that increases duration

A

ISophane Insulin (humulin N)

352
Q

Humulin 70/30 is a mixture of

A

Humulin N 70%
R 30%

353
Q

Afrezza

A

-inhalational powder form of recombinant human insulin
-approved in 2014
-removed from market in 2016 due to slow sales
–only available in 4, 8, or 12 unit cartridges. Many patients require higher doses thus requiring multiple cartridge administration to obtain needed dose

354
Q

Which medication required spirometer testing of patient lung strength prior to prescribing?

A

Afrezza

355
Q

Side effects of insulin

A

-hypoglycemia=greatest risk
-allergic reactions (reduced risk with recombinant preps)
-lipidemias
-insulin resistance
-drug interactions

356
Q

Which drugs counteract the hypoglycemic effects of insulin?

A

-AGE

ACTH
Glucagon
Estrogens

357
Q

Which drugs may increase the duration of action of insulin?

A

Tetracyclines
Chloramphenicol
Salicylates

MAOI’s may potentiate effects

358
Q

What are the oral hypoglycemics used to treat DM 2 (not Type 1)?

A

T-BAMS

Thiazolidinediones
Biguanides
Alpha-Glucosidase Inhibitors
Meglitinides
Sulfonylureas

359
Q

MOA of sulfonylureas

A

-can lower blood glucose to hypoglycemic levels
-inhibit ATP-sensitive potassium-ion channels on beta cells in the pancreas resulting in increased calcium influx and increased exocytosis of insulin storage granules
-also seem to decrease insulin-resistance, but not believed to be a major mechanism
-main differences between compounds is elimination rate
-largely metabolized by the liver
-greatest risk is hypoglycemia, especially with agents with longer durations
-decrease ischemic preconditioning which is cardioprotective thus may be dc’d 24-48 hours prior to surgery

360
Q

What is the longest duration of the sufonylureas?

A

chlorpropamide 2-3 days

may effect takes up to 2 weeks (half life 1.5 days)

361
Q

SE of Chlorpropamide

A

severe hyponatremia
-can cause disulfiram-like reaction

362
Q

Which is the shortest duration, least potent, and least risk of SE among Sulfonylureas?

A
363
Q

What are the names of the sulfonylureas?

A

Glyburide
Glipizide
Glimepiride
Chlorpropamide
Tolbutamide

364
Q

Glyburide (Glynase and Generic)

A

increases insulin sensitivity somewhat
inhibits liver gluconeogenesis

365
Q

Glipizide (Glucotrol & Generic)

A

-increases glucose uptake
-inhibits liver gluconeogenesis
-appears to show little tolerance development

366
Q

Glimepiride (amaryl & Generic)

A

-stimulates insulin release and decreases gluconeogenesis
-used in combo with insulin in cases of sulfonylurea failure

367
Q

What are the drugs that are Meglitinides?

A

-Repaglinide (Prandin & Generic)
-Nateglinide (Starlix & Generic)
-similar mech to sulfonylureas but has shorter duration of action and more rapid onset

368
Q

What are the Alpha-Glucosidase inhibitors

A

-Acarbose (Precose & Generic)
-Miglitol (Glyset)

369
Q

What is the MOA of Miglitol (Glyset)

A

-inhibits intestinal glucosidase thus decreasing disaccharide convertion to monosaccharides and decreasing GI absorption, thus lowering blood sugar
-hypoglycemia not likely unless combined with other therapy

370
Q

What is a biguanide drug?

A

Metformin (Glucophage & Generic)

371
Q

Which drug is effective in cases where sulfonylureas have failed?

A

Metformin

372
Q

MOA Metformin

A

-inhibits hepatic and renal gluconeogenesis
-considered an insulin sensitizer since insulin presence is required for effects
-low risk for hypoglycemia
-recommend to be D/c’d 48 hours prior to sx due to metabolic shift in glucose metabolism to anaerobic, with an increase in lactic acid production

373
Q

SE Metformin

A

-anorexia
-nausea
-diarrhea

374
Q

What drugs are Thiazolidinediones?

A

-Rosiglitazone (Avandia)
-Pioglitazone (Actos)

375
Q

What is the MOA of Pioglitazone?

A

-decrease insulin resistance at skeletal muscle and adipose tissue
-required insulin presence to be effective
-very effective in obese patients but may cause weight gain in part due to extracellular fluid accumulation which may aggravate CHF

376
Q

Which drug causes drug induced liver dysfunction so transaminases must be monitored?

A

Pioglitazone

377
Q

Which drug did the FDA issue a warning about in 2007 advising caution in patients with cardiac disease because of an increased risk of cardiac incidents?

A

Rosiglitazone (Avandia)

378
Q

What is incretin?

A

-peptide released from the GI mucosal cells which triggers pancreatic beta cells to release insulin

379
Q

Which medication is an incretin analog with a longer half life than incretin?

A

exenatide (Byetta)

380
Q

How are incretin analogs administered?

A

SQ not oral

381
Q

Name the incretin analogs

A

ALE

Albiglutide (Tanzeum)
Liraglutide (Victoza)
Exenatide (Byetta)

382
Q

Are incretin analogs continued through peri-op period?

A

yes

383
Q

Which incretin analogs are shown to decrease risk of heart attack, stroke and CV related deaths?

A

-Liraglutide (Victoza)

reported serious SE such as pancreatitis, thyroid cancer and pancreatic cancer may limit potential benefits

384
Q

MOA of dipeptidyl peptidase 4 (DPP-4) inhibitor

A

inhibits metabolism of incretin, which stimulates pancreatic beta cells to release insulin

385
Q

What are the names for the Dipeptidyl Peptidase -4 inhibitors?

A

Sitagliptin (Januvia)
Saxagliptin (Onglyza)
Alogliptin (Nesina)
Linagliptin (Tradjenta)

386
Q

FDA warns of increased risk of what with DPP-4 inhibitor use?

A

Arthralgia

387
Q

Which medication has a 27% increase in hospitalizations for heart failure?

A

saxagliptin (onglyza)

388
Q

What is Janumet a combination of?

A

Metformin +Sitagliptin (Januvia)

389
Q

Does Sitagliptin (Januvia) decrease risk of heart attacks or CV events?

A

no

390
Q

True/false: Sitagliptin (Januvia) is used alone or in combination with other Type 2 hypoglycemic.

A

true

391
Q

What is the primary glucose transporter for glucose reabsorption in the kidney?

A

sodium/glucose transporter 2 (SGLT-2)

392
Q

MOA of SGLT-2 inhibitors

A

inhibition of this transporter lowers blood sugar by increasing urinary glucose elimination

393
Q

What are the SGLT–2 inhibitors?

A

CEED
Canagliflozin (Invokana)
Empagliflozin (Jardiance)
Ertugliflozin (Steglatro)
Dapagliflozin (Farxiga)

394
Q

Side effects of SGLT–2 inhibitors

A

-cause some diuresis which lowers BP
-causes weight loss (Calories)
-ketoacidosis
-increased risk of yeast infections due to sugar in urine
-rare link to Fournier’s gangrene (perinuem)
-family referred to as the glifozins

395
Q

Empagliflozin (Jardiance) has been shown to ______ heart attacks, strokes and CV related deaths.

A

decrease

396
Q

what class is considered the best new type-2 diabetic therapy in many years?

A

SGLT-2 inhibitors

397
Q

MOA of GLP-1 agonists (Glucagon like peptide-1)

A

gut protein analop (GLP-1) that is release on eating and triggers insulin release.
They also decrease glucose production in liver and make patient feel sated.GL

398
Q

GLP-1 agonists have been shown to _____MACE risk in cardiac disease.

A

lower

399
Q

GLP-1 agonists

A

T-SLED
Tirzepatide (Mounjaro) Zepbound for weight loss
Semaglutide (Ozempic) (wegovy for weight loss)
Liraglutide (Victoza) (Saxenda for weight loss)
Exenatide (Byetta) first in class
Dulaglutide (Trulicity)

400
Q

Patients taking GLP-1 agonists should hold them for how long?

A

last weekly or last daily dose due to increased risk of vomiting and aspiration

401
Q

Receptor-associated disorders due to:

A

-decrease in the number of receptors
-impaired receptor function
-presence of antibodies against specific receptors
-antibodies that mimic hormone action
-unusual expression of receptor function

402
Q

What does the posterior pituitary arise from?

A

neuroendocrine tissue (neurohypophysis)

403
Q

What is produced from the posterior pituitary?

A

oxytocin
ADH -vasopressin
both nonapeptides (9AA)

404
Q

Examples of diseases with too much antidiuretic hormone effects and posterior pituitary functioning

A

-SIADH

405
Q

Example of disease with too little antidiuretic hormone effects and hypofunctioning posterior pituitary

A

diabetes insipidus
neurogenic
nephrogenic
dipsogenic

406
Q

SIADH

A

levels of antidiuretic hormone abnormally high
-water retention: action of ADH on renal collecting ducts increases permeability to water, thus increasing water reabsorption by kidneys
-for dx normal renal, adrenal, and thyroid function must exist

407
Q

What is the most common cause of SIADH

A

ectopic secretion of ADH
also common after surgery and some cancers

408
Q

Clinical manifestations of SIADH

A

-hyponatremia: Na <135mEq/L
-Hypoosmolality: <280mOsm/kg
-urine hyperosmolality: higher than serum osmolality
-hypervolemia
-weight gain
-serum sodium levels below 110-115mEq/L: can cause severe and sometimes irreversible neuro damage

409
Q

Treatment of SIADH

A

-correction of underlying causal problems
-emergency correction of severe hyponatremia by the administration of hypertonic saline
-Conivaptan (Vaprisol)-ADH receptor blocker
*most important: fluid restriction between 800-1000mL/day

410
Q

Which medication is used for resistant or chronic SIADH

A

Demeclocycline-tetracycline analog with a known SE of causing nephrogenic diabetes insipidus by blocking normal ADH activity

is an abx

411
Q

DI (Diabetes Insipidus)

A

-insufficiency of ADH
-polyuria and polydypsia
-partial or total inability to concentrate urine

412
Q

Neurogenic DI

A

insufficient amounts of ADH

413
Q

Nephrogenic DI

A

insensitivity of the renal collecting tubules to ADH

414
Q

Dipsogenic DI

A

excessive fluid intake lowering plasma osmolarity to the point that it falls below the threshold for ADH secretion

415
Q

Diabetes insipidus is characterized by:

A

inability of the kidney to increase permeability to water
-ADH not acting properly on distal tubules and collecting ducts

416
Q

S/S of DI

A

-excretion of large volumes of dilute urine
-increase in plasma osmolality: 300mOsm or more, depending on adequate water intake
-urine output: 8-12 L/day (normal is 1-2 L/day)
-polyuria, nocturia, continual thirst
-urine specific gravity <1.010
-low urine osmolality (<200mOsml/kg)
-hypernatremia

417
Q

Treatment of neurogenic DI

A

administration of synthetic vasopressin analog desmopressin acetate (DDAVP)-similar to arginine vasopressin but longer 1/2 life

418
Q

Treatment of Nephrogenic DI

A

tx of any reversible underlying disorders
-discontinuation of etiologic medications
-correction of associated electrolyte disorders
-administration of thiazide diuretic

419
Q

Treatment of dipsogenic DI

A

effective management of water ingestion

420
Q

Hormone effects of hyper functioning anterior pituitary

A

-hyperpituitarism
-hypersecretion of growth hormone
-hypersecretion of prolactin

421
Q

Diseases of hyperfunctioning anterior pituitary

A

-primary adenoma
-acromegaly
-prolactinoma

422
Q

What hormone effects are seen with a hypofunctioning anterior pituitary?

A

hypopituitarism

423
Q

What are diseases caused by a hypofunctioning anterior pituitary?

A

-panhypopituitarism
-ACTH (adrenocorticotropic) deficiency
-TSH deficiency
-FSH and LH deficiency
-Growth hormone deficiency

424
Q

Hypopituitarism is characterized by:

A

absence of selective pituitary hormones or complete failure of all pituitary hormone functions
-pituitary is vascular and therefore vulnerable to ischemia and infarction

425
Q

Causes of hypopituitarism

A

-inadequate supply of hypothalamic-releasing hormones
-damage to pituitary stalk
-inability of the gland to produce hormones
-pituitary infarction
-tumor or surgical removal

426
Q

Panhypopituitarism (all hormones affected)

A

Adrenocorticotropic hormone deficiency
-Thyroid stimulating hormone deficiency
Follicle-stimulating hormone and luteinizing hormone deficiency
growth hormone deficiency

Tx: replacement of deficient hormones

427
Q

ACTH deficiency leads to:

A

cortisol deficiency

428
Q

TSH deficiency leads to

A

-altered metabolism
-thyroid hormones critical for maintaining homeostasis

429
Q

FSH and LH deficiency

A

-lack of secondary sex characteristics

430
Q

Growth hormone deficiency

A

-lack of growth in children
-short stature, dwarfism

431
Q

Hyperpituitarism is commonly from

A

benign, slow-growing pituitary adenoma

432
Q

Clinical manifestations of Hyperpituitarism

A

-headache and fatigue
-visual changes
-hypersecretion of pituitary hormones from tumor
-hyposecretion of neighboring anterior pituitary hormones

433
Q

Tx of Hyperpituitarism

A

-specific meds to suppress tumor growth
-transsphenoidal tumor resection
-radiation therapy/chemotherapy
-hormone regulation

434
Q

Hypersecretion of GH

A

-giantism
-GH hypersecretion in children and adolescents

435
Q

Acromegaly

A

-hypersecretion of GH during adulthood
-slowly progressive pituitary adenoma
Mortaility: cardiac hypertrophy, HTN, atherosclerosis, type 2 DM, leading to CAD

436
Q

Clnical manifestations of acromegaly

A

Connective tissue proliferation-englarged tongue, interstitial edema, increased in size and function of sebaceous and sweat glands, coarse skin and body hair
boney proliferation-large joint arthropathy, kyphosis, enlargement of facial bones and hands and feet, protrusion of lower jaw and forehead, need for increasingly larger shoes, hats, rings and gloves
-symptoms of DM -polyuria and polydipsia
-CNS symptoms-headache, seizure activity, visual disturbances, papilledema

437
Q

Treatment of acromegaly

A

primary treatment:transspenoidal surgery or endonasal endoscopic sx for removal of the GH-secretion adenoma
-octreotide (Sandostatin), Octreotide long acting and Lanreiotide (Somatuline) Somatostatin analogs to lower GH levels
-Cabergoline (Dopaminergic agonists) to lower prolactin levels
-pegvisomant (Somavert) to block GH reeptor

438
Q

Hypersecretion of prolactin caused by:

A

prolactinomas
-most common hormonally active pituitary tumor

Women: amenorrhea, galatorrhea, hirsutism, osteoporosis
men: hypogonadism, erectile dysfunction

439
Q

Treatment of hypersecretion of prolactin

A

-Bromocriptine (Parlodel)
-Carbergoline
-pergolide
these are dopamine agonists–>rapid reduction in the size of the tumor and a reversal of the gonadal effects
-resistant or intolerant to meds: transsphenoidal surgery, endonasal endoscopic surgery and radiotherapy

440
Q

Diseases of hyperthyroidism

A

thyrotoxicosis
Graves disease
hyperthyroidism resulting from nodular thyroid disease
-thyroid storm

441
Q

Disease of hypothyroidism

A

-primary hypothyroidism
-Hashimoto disease
-secondary hypothyroidism
-subclinical hypothyroidism
-congenital hypothyroidism
-thyroid carcinoma

442
Q

Primary thyroid disease

A

-dysfunction or disease of the thyroid gland
-alters thyroid hormone production

443
Q

Secondary hypothyroidism

A

-conditions that cause alterations in pituitary or hypothalamic functioning
-alters TSH or TRH production

444
Q

Thyrotoxicosis

A

-condition that results from any cause of increase level of thyroid hormone
-excess amounts of thyroid hormone are secreted from the thyroid gland
-continuous stimulation of cells causing hyperplasia and goiter

445
Q

Clinical manifestations of thyrotoxicosis

A

-increased metabolic rate with heat intolerance and increased tissue sensitivity to stimulation by the sympathetic nervous system
-enlargement of the thyroid gland (goiter)

446
Q

treatment of thyrotoxicosis

A

-methimazole (Tapazole) or propylthiouracil: antithyroid drugs
-radioactive iodine therapy
-surgery

447
Q

Graves disease

A

autoimmune disease
develops autoantibodies cant turn of secretion of thyroid hormone

448
Q

Clinical manifestations of graves disease

A

opthalmopathy
exophthalmos: increased secretion of hyaluronic acid, orbital fat accumulation, inflammation and edema of the orbital contents
-diplopia: double vision
-pretibial myxedema (Graves dermopathy): leg swelling due to increased deposition of mucopolysaccharides

449
Q

What is pretibial myxedema?

A

Graves dermopathy
leg swelling due to increased deposition of mucopolysaccharides

not just specific to graves disease

450
Q

Treatment of graves disease

A

-antithyroid drugs, radioactive iodine, surgery
-does not reverse infiltrative opthalmopathy or pretibial myxedema

451
Q

Thyrotoxic crisis (thyroid storm)

A

results from excess stress
increased action of thyroxine (T4) and triiodothyronine (T3)

452
Q

clinical manifestations of thyroid storm

A

-hyperthermia
-tachycardia
-atrial tachydysrythmias
-high-output failure
-agitation or delirum
-N/v
-diarrhea

453
Q

Treatment of thyroid storm

A

-propylthiouracil or methimazole (Tapazole): blocks thyroid hormone synthesis
-beta-blockers to control cardiovascular symptoms, corticosteroids, potassium iodide)
-supportive

454
Q

Hypothyroidism

A

-deficient production of thyroid hormone by the thyroid gland

455
Q

most common cause of hypothyroidism WORLDWIDE

A

iodine deficiency (endemic goiter)
soil deficiency of iodine west of Mississippi river

456
Q

Most common cause of hypothyroidism in the US

A

autoimmune thyroiditis (Hashimoto’s disease)

457
Q

primary hypothyroidism causes

A

iodine deficiency
autoimmune thyroiditis
subacute thyroiditis
painless thyroiditis
iatrogenic thyroiditis
postpartum thyroiditis

458
Q

Congenital hypothyroidism

A

-thyroid hormone deficiency present at birth
-if not treated, cretinism develops
-neonatal screening to reduce incidents
-administration of T4

459
Q

What is the most common endocrine malignancy from ionizing radiation?

A

thyroid carcinoma
changes in voice and swallowing and difficulting in breathing related to a tumor growth impinging the trachea or esophagus
some may have normal T3 and T4 levels

460
Q

Secondary hypothyroidism

A

conditions that cause either pituitary or hypothaamic failure with deficiency of thyrotropin-releasing hormone and TSH

461
Q

Clinical manifestations of hypothyroidism

A

-low basal metabolic rate
-cold intolerance
-lethargy
-tiredness
-slightly lowered basal body temp
-diastolic hypertension

462
Q

Myxedema

A

-nonpitting, boggy edema especially around the eyes, hands, and feet
-thickening of the tongue

463
Q

Myxedema coma

A

medical emergency!
-diminished LOC
-hypothermia without shivering
-hypoventilation
-hypotension
-hypoglycemia
-lactic acidosis
-coma

464
Q

treatment of hypothyroidism

A

Levothyroxine

465
Q

tx of myxedema coma

A

-thyoid hormone
-combined with circulatory and ventilatory support
-management of hyponatremia and hypothermia

466
Q

Primary hyperparathyroidism

A

-excess secretion of PTH from one or more parathyroid glands and hypercalcemia
-80-85% caused by parathyroid adenomas

467
Q

Secondary hyperparathyroidism

A

-increase in PTH, secondary to a chronic disease
-chronic renal failure
-dietary deficiency of Vitamin D, calcium
-hypercalcemia does not occur

468
Q

Tertiary hyperparathyroidism

A

-excessive secretion of PTH and hypercalcemia from long-standing secondary hyperparathyroidism

469
Q

Pseudohypoparathyroidism

A

inherited condition
resistance to PTH
-familial hypocalciuric hypercalcemia-benign autosomal dominant condition

470
Q

clinical manifestations of hyperparathyroidism

A

-most asymptomatic
-hypercalcemia and hypophasphatemia, possible kidney stones from hypercalciuria, alkaline urine, ,pathologic fractures
secondary: low serum calcium but elevated PTH

471
Q

Treatment hyperparathyroidism

A

-surgery
-biphosphonates -block osteoclast activity ex. Aldrenoate (fosamax)
-corticosteroids
-calcimimetics (lower calcium and PTH levels ex. Cinacalcet (Sensipar)

472
Q

hypoparathyroidism

A

-abnormally low PTH levels
-depressed serum calcium
increased serum phosphate level
usual causes: parathyroid damage in thyroid surgery, autoimmunity or genetic mechanisms

473
Q

Clinical manifestations of hypoparathyroidism

A

-hypocalcemia
-lowering of the threshold for nerve and muscle excitation making it easier to fire nerves
-muscle spasms
-hyperreflexia
-tonic-clonic convulsions
-laryngeal spasms
-death from asphyxiation
-cvostek and trousseau signs
-phosphate retention

474
Q

treatment of hypoparathyroidism

A

calcium and vitamin D
phosphate binders if needed ex. Calcium Acetate (PhosLo)

475
Q

Diabetes mellitus

A

dysfunction of the endocrine pancreas, beta cells
-affects metabolism of fat, protein and carbs
-characterized by hyperglycemia resulting from defects in insulin secretion, insulin action or both

476
Q

Dx of DM

A

-glycosylated hemoglobin A1C levels
-fasting plasma glucose levels
-two our plasma glucose during oral glucose tolerance testing using a 75 gm glucose load

477
Q

What is Glycosylated Hemoglobin (HgA1C)?

A

permanent attachment of glucose to hemoglobin molecules reflects average glucose exposure over life of RBC (approx 120 days)

478
Q

Categories at risk for diabetes

A

-nondiabetic elevations of HgA1c, FPG or 2 hour plasma glucose value during OGTT
-impaired glucose tolerance: from diminished insulin secretion
-impaired fasting glucose: from enhanced hepatic glucose output
-prediabetic, you have risk factors for DM and blood glucose levels increasing closer to diabetic levels

479
Q

Type 1 DM

A

pancreatic atrophy and loss of beta cells

480
Q

Types of Type 1 DM

A

Autimmune
-environmental and genetic factors are thought to trigger cell-mediated destruction of pancreatic beta cells (Type 1A)
-autoantibody, T-cell and macrophage destruction of pancreatic beta cells (Type 1A) occur with a loss of insulin production and a relative excess of glucagon

Nonimmune
occurs secondary to other diseases such as pancreatitis or secondary to a more fulminant disorder termed idiopathic diabetes (Type 1B)

481
Q

Type 1 DM genetic susceptibility

A

first degree relative (parent or sibling) with type 1 DM (esp 1B)
-strongest association with major histocompatibility complex (MHC)

482
Q

Environmental factors in type 1 DM

A

-viral infection
-Helicobacter pylori
-exposure to cow’s milk proteins
-relative lack of vitamin D

483
Q

Patho type 1 DM

A

immunologically mediated destruction of beta cells
–lymphocyte and macrophage infiltrate islets, resulting inflammation (insulinitis) and islet beta cell death
-autoantibodies are produced against islet cells, insulin, glutamic acid decarboxylase (GAD) and other cytoplasmic proteins
-hyperglycemia, glucagon, hyperketonemia
-both alpha and beta functions are abnormal and both lack insulin and amylin and have a relative excess of glucagon ,contributing to hyperglycemia

484
Q

Clinical manifestations type 1 DM

A

-long preclinical period with gradual beta cell destruction, leading to insulin deficiency and hyperglycemia
-80-90% loss of function of the insulin-secreting beta-cells in the islets of Langerhans occurs before hyperglycemia develops
-polydipsia, polyuria
-polyphagia
-weight loss
-fatigue

485
Q

treatment of type 1 DM

A

-combination of insulin, meal planning, exercise and self monitoring of blood glucose
-transplant: islet cells and whole pancreas

486
Q

Risk factors of type 2 DM

A

-age
-obestiy
-HTN
-physical inactivity
-family history
-metabolic syndrome

487
Q

Metabolic syndrome

A

DOPE
Dyslipidemia
Obesity (central)
Prehypertension
-elevated fasting blood glucose level

488
Q

major mechanisms of type 2 DM

A

insulin resistance
decreased insulin secretion from beta cells

489
Q

Mechanisms of type 2 DM

A

-alteration in the production of adipokines by adipose tissue: leptin resistance
-elevated serum free fatty acids and intracellular lipid deposits
-reduced insulin-stimulated mitochondrial activity
-obesity-associated insulin resistance
insulin resistance
-beta cell dysfunction-beta cell mass is decreased
-glucagon-pancreatic alpha cells less responsive to glucose inhibition

490
Q

Amylin and Ghrelin in DM

A

Amylin-decreased in type 1/2
Ghrelin-decreased in type 2

491
Q

clinical manifestation of type 2 DM

A

-fatigue
-prutritis
-recurrent infections
-visual changes
-symptoms of neuropathy (paresthesia or weakness)

492
Q

treatment of Type 2 DM

A

-exercise
-diet
-tx of obesity
-oral hypoglycemics
-bariatric surgery
-decreased body fat may lead to decreased sensitivity

493
Q

Maturity onset diabetes of youth (MODY)

A

includes six specific autosomal dominant mutations occuring before 25 years of age

494
Q

Gestational DM

A

-any degree of glucose intolerance with the onset or first recognition occurring during pregnancy
-contributing factors-insulin resistance and inadequate insulin secretion
-recommendation: high-risk women who are found to have diabetes at their initial prenatal visit receive a diagnosis of overt diabetes

495
Q

-complications of DM

A

-hypoglycemia
-hyperosmolar hyperglycemic nonketotic syndrome
-somogyi effect
-dawn phenomenon

496
Q

somogyi effect

A

overuse of insulin results in rebound effect, excessive morning blood sugar

497
Q

dawn phenomenon

A

increased blood sugar early morning without nocturnal hypoglycemia seen in somogyi effect

498
Q

hypoglycemia

A

newborns <35 mg/dl
children and adults: <45-60mg/dl

499
Q

clinical manifestations of hypoglycemia

A

-tachycardia
-palpitations
-diaphoresis
-tremors
-pallor
-arousal anxiety

500
Q

treatment of hypoglycemia

A

-glucose (15-20g): conscious
-glucagon; emergency use

501
Q

Diabetic ketoacidosis

A

absolute or relative deficiency of insulin and an increase in insulin couterregulatory hormones

502
Q

DKA most common in __________

A

type 1 DM

503
Q

precipitating factors DKA

A

-illness
-trauma
-surgery
-MI

increased fat mobilization with the release of fatty acids, leading to DKA

504
Q

Clinical manifestations of DKA

A

-polyuria and dehydration
-Kussmaul respirations
-sweet or fruity breath odor

505
Q

lab values for DKA

A

-serum glucose level >250mg/dl
-serum pH <7.30
-urine ketones
-total body (not serum) potassium depletion

506
Q

treatment of DKA

A

-administration of insulin to decrease glucose levels
-fluids
-replacement of electrolytes

507
Q

Hyperosmolar Hyperglycemic nonketotic syndrome (HHS)

A

-life threatening emergency
-some insulin deficiency: more profound in DKA
-fluid deficiency: more marked than DKA
-elevated glucose levels: more marked than DKA

508
Q

HHS associated with ______________

A

type 2 DM

509
Q

HHS precipitated by:

A

-infection
-medication
-nonadherence to DM tx
-coexisting disease

510
Q

Clinical manifestations of Nonketotic Syndrome

A

-glycosuria
-polyuria
-dehydration
-coma

511
Q

Treatment of nonketotic snydrome

A

-insulin infusion with fluid repletion
-electrolyte replacement

512
Q

lab findings nonketotic syndrome

A

Glucose >600mg/dl
-absent or low urine ketones

513
Q

Somogyi effect

A

-hypoglycemia with rebound hyperglycemia
-counterregulatory hormones cause gluconeogenesis
-most common in Type 1 and children

514
Q

Dawn phenomenon

A

-early morning glucose elevation without nocturnal hypoglycemia
-related to nocturnal growth hormone elevation
-tx: alter timing and dose of insulin

515
Q

Microvascular disease of DM

A

-diabetic retinopathy
-diabetic nephropathy
-diabetic neuropathies

516
Q

macrovascular disease associated with DM

A

-coronary artery disease
-stroke
-peripheral arterial disease

517
Q

Microvascular disease

A

-disease in the capillaries caused by Diabetes
Characteristics:
-thickening of capillary basement membrane, endothelial cell hyperplasia, thrombosis, and pericyte degeneration
-hyperglycemia (must be present)
-hypoxia and ischemia

518
Q

diabetic retinopathy

A

-leading cause of blindness worldwide
-develops more rapidly in type 2 DM

519
Q

Maculopathy

A

progressive process that accompanies retinal capillary permeability, vessel occlusion, ischemia

520
Q

Macular edema

A

-fluid accumulation
-retinal thickening

521
Q

tx for diabetic retinopathy

A

-laster tx
-vitrectomy
-intravitreal steroids
-antivascular endothelial growth factor
-renin-angiotensin system inhibitors

522
Q

Diabetic nephropathy

A

-most common cause of end-stage kidney disease in the western owrld

523
Q

progressive changes of diabetic neuropathy

A

-glomerular enlargement
-glomerular basement membrane thickening
-membrane thickening
-microalbuminuria

524
Q

Treatment of diabetic nephropathy

A

-has decreased from tight glucose control and ACE inhibitors or Angiotensin II receptor blockers
-aggressive treatment of HTN

525
Q

what is the most common complication of DM

A

diabetic neuropathies

526
Q

Diabetic neuropathy

A

-sensory deficits generally precede motor involvement
-form of “dying back” neuropathy: distal portions of the neurons are initially and eventually more severely affected
-axonal and schwann cell degeneration
-distal symmetrical polyneuropathy: includes large and small nerve fibers
small: neuropathic pain, loss of sensation
large: sensory loss of proprioception

527
Q

macrovascular disease

A

-lesions develop in large and medium sizes arteries from hyperglycemia
-advanced glycation end-products (AGE) attach to their receptor from AGE (RAGE) in the walls of blood vessels
-fat beings to accumulate and promotes oxidative stress, inflammation, endothelial and vascular smooth muscle dysfunction and hyperlipidemia. PRoduce fatty streaks and plaques leading to clots and blockage in vessels

528
Q

Coronary artery disease

A

-most common cause of morbidity and mortality (up to 75%) in both men and women with DM
-increases with duration but not the severity of DM
-consequence of accelerated atherosclerosis, HTN, increased risk for thrombus formation
-can result in MI
-cardiomyopathy is higher in people with DM

529
Q

stroke

A

-twice as common in those with DM esp type 2
-survival rate for people with diabetes after a massive stroke is typically shorter than for person without DM
-consequence of accelerated atherosclerosis, HTN and increased risk for thrombus

530
Q

Peripheral arterial disease

A

-incidence increases in those with diabetes for PAD, neuropathy, gangrene and amputation
-atherosclerosis combined with peripheral neuropathy: occlusions, ulcers and gangrenous changes off the lower extremities

531
Q

Risk for infection with DM increases for several reasons:

A

-impaired senses
-hypoxia-rapid replication of pathogens from increased glucose
-decreased blood supply
-suppressed immune response
-delayed wound healing

532
Q

hyperfunction of the adrenal cortex :

A

increases cortisol
-cushings disease/syndrome

533
Q

hyperfunction that increases androgens and estrogen

A

virilization
feminization

534
Q

hyperfunction of adrenal cortex that increases aldosterone

A

primary or secondary hyperaldosteronism

535
Q

hypofunction of the adrenal cortex

A

-addisons disease
-secondary hypocortisolism

536
Q

cushing syndrome

A

chronic excessive cortisol level, regardless of cause

537
Q

cushing disease

A

-overproduction of pituitary ACTH by pituitary adenoma
-lose diurnal and circadian patterns of ACTH and cortisol secretion
-lack ability to increase ACTH and cortisol in response to stressors

538
Q

Cushing-like syndrome

A

exogenous administration of glucocorticoids

539
Q

Clinical manifestations of Cushings

A

-weight gain of adipose tissue in the trunk, facial, cervical areas (truncal obesity, moon face, buffalo hump
-sodium and water retention
glucose intolerance
protein wasting
-renal stones
-purple striae
-bronze or brownish hyperpigmentation of the skin

540
Q

Congenital adrenal hyperplasia

A

-autosomal recessive disorder: enzyme for cortisol biosynthesis is deficient
-cortisol production is low
-ACTH is increased

541
Q

causes of adrenal hyperplasia

A

-overproduction of either mineralocorticoids or androgens
affected female infants are virilized
-infants of both genders exhibit salt wasting

542
Q

Primary hyperaldosteronism

A

conn disease
usually a single benign aldosterone-producing adrenal adenoma

543
Q

secondary aldosteronism

A

from a extraadrenal stimulus most often angiotensin II, through a renin-dependent mechanism

544
Q

clinical manifestations of hyperaldosteronism

A

-HTN
-hypokalemia, renal potassium wasting
-neuromuscular manifestations

545
Q

treatment of hyperaldosteronism

A

management of HTN and hypokalemia
surgery for adenoma
-administration of aldosterone-receptor antagonists such as spironolactone or eplerenone

546
Q

hypersecretion of estrogens

A

leads to feminization and development of female sex characteristics
-most evident in men, results in gynecomastia, testicular atrophy and decreased libido
leads to early development of secondary sex characteristics in female chidren

547
Q

hypersecretion of androgens

A

-leads to virilization and development of male sex characteristics
-changes more easily observed in women and include:
-hirsutism
-clitoral enlargement
-deep voice
-amenorrhea
-acne
breast atrophy
-virilizing tumors promote precocious sexual development and bone aging in children

tx:surgical excision

548
Q

Addisons disease

A

-primary adrenal insufficiency
-hypocortisolism
-rare, autoimmune mechanisms
-inadequate corticosteroid and mineralocorticoid synthesis
elevated ACTH

549
Q

Clinical manifestations of addisons disease

A

-hypocortisolism and hypoaldosteronism
-weakness, hyperpigmentation, vitiligo

550
Q

treatment of addisons

A

lifetime glucocorticoid and mineralocorticoid replacement therapy
150meq sodium per day

551
Q

patho of secondary hypocortisolism

A

prolonged administration of exogenous glucocorticoids which suppress ACTH secretion

552
Q

clinical manifestation of secondary hypocortisolism

A

similar to Addisons
hyperpigmentation does not occur

553
Q
A
554
Q

hyperfunction of the adrenal medulla

A

tumor of adrenal medulla-pheochromocytoma

555
Q

is there a hypofunction of the adrenal medulla identified?

A

no

556
Q

Pheochromocytoma

A

-caused by tumors derived from chromaffin cells of adrenal medulla
-secrete catecholamines

557
Q

clinical manifestations of pheochromocytoma

A

-HTN
-diaphoresis
-tachycardia
-palpitations
severe headache

558
Q
A

Pathopharm 2 (4 decks)

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