Exam 1

Question 1

When does bone formation begin?

Answer 1

bone formation begins in two phases at approx 6 weeks gestation

Question 2

What does bone formation consist of?

Answer 2

-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)

Question 3

Ossification occurs in 2 long bone centers:

Answer 3

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

Question 4

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

Answer 4

epiphyseal plate

Question 5

Eipiphyseal closure

Answer 5

unites the metaphysis and epiphysis

Question 6

Eipiphyseal closure occurs earlier in_______.

Answer 6

girls than boys because of earlier puberty in girls

Question 7

Factors affect bone growth

Answer 7

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

Question 8

Peak bone mass is achieved by when?

Answer 8

middle to late 20s

Question 9

How is the spine shaped in the newborn?

Answer 9

concave anteriorly (kyphosed)

Question 10

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

Answer 10

first 3 months of life

Question 11

How does the spine differ in the adult vs newborn?

Answer 11

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

Question 12

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

Answer 12

1 year
8 years

Question 13

What is Genu Varum?

Answer 13

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

Question 14

What is genu valgum?

Answer 14

-knock knees
-peaks by 5-6 years

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

Question 15

Composition and size of muscles vary with age

Answer 15

-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

Question 15

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

Answer 15

14
10

Question 16

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

Answer 16

25% infants
40% adults

Question 17

Where is the majority of weight in the infant?

Answer 17

axial musculature (55% in an adults lower limbs)

Question 18

What is syndactyly?

Answer 18

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

Question 19

Complex Syndactyly

Answer 19

also includes fusion of the bones and nails

Question 20

Vestigial tabs

Answer 20

Extra digit

Question 21

Developmental dysplasia of hip (congenital dislocation of the hip)

Answer 21

abnormality of the proximal femur, acetabulum or both

Question 22

What are risk factors for developmental dysplasia of hip?

Answer 22

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

Question 23

Clinical manifestations of developmental dysplasia of hip

Answer 23

-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

Question 24

treatment for developmental dysplasia of hip younger than 4 months

Answer 24

pavlik harness

Question 25

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

Answer 25

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

Question 26

treatment for developmental dysplasia of hip after 12 months of age

Answer 26

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

Question 27

Metatarsus adductus (forefoot adduction)

Answer 27

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

Question 28

treatment of metatarsus adductus

Answer 28

serial casts during first 6 months of life

Question 29

Clubfoot

Answer 29

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

Question 30

Positional equinovarus

Answer 30

serial casts

Question 31

Idiopathic Congenital equinovarus

Answer 31

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

Question 32

tetratologic equinovarus

Answer 32

always required surgical correction and/or muscle balancing procedures

Question 33

pes planus

Answer 33

flat foot: if painless, then feet are normal

Question 34

Osteogenesis Imperfecta

Answer 34

"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)

Question 35

Tx for Osteogenesis imperfecta

Answer 35

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

Question 36

What is Rickets?

Answer 36

disorder causing mineralization failure, "soft" bones and skeletal deformity

Question 37

Causes of rickets

Answer 37

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

Question 38

Clinical manifestations of Rickets

Answer 38

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

Question 39

Treatment of Rickets

Answer 39

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

Question 40

Non-structural scoliosis

Answer 40

curvature from a cause other than the spine

Question 41

Structural scoliosis

Answer 41

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

Question 42

Idiopathic scolioisis

Answer 42

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

Question 43

Clinical manifestation of nonstructural scoliosis

Answer 43

mild spinal curvature with prominence of one hip or rounded shoulders

Question 44

treatment of scoliosis

Answer 44

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

Question 45

Structural scoliosis clinical manifestations

Answer 45

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

Question 46

Osteomyelitis

Answer 46

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

Question 47

When is osteomyelitis less common?

Answer 47

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

Question 48

Clinical manifestations of osteomyelitis in infants

Answer 48

fever and failure to move affected limb (pseudoparalysis)

Question 49

Clinical manifestations of osteomyelitis in children

Answer 49

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

Question 50

Clinical manifestations of osteomyelitis in adolescents

Answer 50

back pain for several weeks: may be only complaint

Question 51

Treatment of osteomyelitis

Answer 51

-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.

Question 52

Juvenile Idiopathic Arthritis (JIA)

Answer 52

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

Question 53

Tx of JIA

Answer 53

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

Question 54

Differences in JIA and adult RA

Answer 54

-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

Question 55

Osteochondrosis

Answer 55

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

Question 56

Treatment of osteochondrosis

Answer 56

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

Question 57

Legg-Calve-Perthes disease

Answer 57

-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

Question 58

Clinical manifestations of Perthes Disease

Answer 58

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

Question 59

Treatment of Perthes disease

Answer 59

-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

Question 60

Osgood-Schlatter disease

Answer 60

-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

Question 61

Clinical manifestations of Osgood-Schlatter disease

Answer 61

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

Question 62

Treatment of Osgood-Schlatter disease

Answer 62

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

Question 63

What is cerebral palsy?

Answer 63

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

Question 64

Clinical manifestations of Cerebral Palsy

Answer 64

motor milestones are not met

Question 65

Treatment for Cerebral palsy

Answer 65

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

Question 66

Muscular dystrophies

Answer 66

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

Question 67

What is the most common muscular dystrophy?

Answer 67

duchenne muscular dystrophy

Question 68

What is Duchenne muscular dystrophy?

Answer 68

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

Question 69

Duchenne muscular dystrophy gene

Answer 69

-encodes for dystrophin protein

Question 70

What does dystrophin mediate?

Answer 70

-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

Question 71

When do clinical manifestations appear in DMD?

Answer 71

3 years of age

Question 72

Clinical manifestations of DMD

Answer 72

-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

Question 73

Treatment of DMD

Answer 73

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

Question 74

Becker muscular dystrophy

Answer 74

-similar but milder clinical features as compared with DMD

Question 75

Facioscapulohumeral muscular dystrophy

Answer 75

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

Question 76

Limb girdle muscular dystrophy

Answer 76

pelvic and shoulder girdles involved

Question 77

Nonossifying fibroma

Answer 77

benign bone tumor fibrocytes that have replaced normal bone

Question 78

Simple bone cysts

Answer 78

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

Question 79

Aneurysmal bone cysts

Answer 79

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

Question 80

Osteoid osteoma

Answer 80

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

Question 81

What is osteochondroma also called?

Answer 81

exostosis

Question 82

What is osteochondroma?

Answer 82

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

Question 83

Fibrous dysplasia

Answer 83

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

Question 84

Albright syndrome triad

Answer 84

1. polyostotic fibrous dysplasia 2. precocious puberty 3. cutaneous pigmentation

Question 85

Osteosarcoma

Answer 85

-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

Question 86

Clinical manifestations of osteosarcoma

Answer 86

pain

Question 87

treatment of osteosarcoma

Answer 87

-surgery and multiagent chemotherapy -radiation

Question 88

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

Answer 88

ewing sarcoma

Question 89

What is ewing sarcoma?

Answer 89

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

Question 90

clinical manifestations of ewing sarcoma

Answer 90

pain, soft-tissue mass

Question 91

treatment of ewing sarcoma

Answer 91

-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

Question 92

Rhabdomyosarcoma

Answer 92

malignant bone tumor -arises from embryonal rhabdomyoblasts

Question 93

clinical manifestations of rhabdomyosarcoma

Answer 93

painless palpable, visible mass

Question 94

treatment of rhabdomyosarcoma

Answer 94

surgery, radiation, chemotherapy

Question 95

complete fracture

Answer 95

bone broken all the way through

Question 96

incomplete fracture

Answer 96

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

Question 97

comminuted fracture

Answer 97

-bone breaks into more than 2 fragments

Question 98

linear fracture

Answer 98

fracture runs parallel to long axis of bone

Question 99

oblique fracture

Answer 99

fracture of shaft of bone is slanted

Question 100

spiral fracture

Answer 100

encircles bone

Question 101

transverse fracture

Answer 101

occurs straight across bone

Question 102

greenstick fracture

Answer 102

perforates one cortex and splinters spongy bone

Question 103

torus fracture

Answer 103

cortex buckles but does not break

Question 104

bowing fracture

Answer 104

longitudinal force is applied to bone

Question 105

pathologic fracture

Answer 105

break occurs at the site of a preexisting abnormality

Question 106

stress fracture

Answer 106

fatigue and insufficiency transchondral

Question 107

Bone fracture inflammatory phase

Answer 107

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

Question 108

Repair phase of bone fractures

Answer 108

-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

Question 109

Remodeling phase of bone fractures

Answer 109

-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

Question 110

bone fracture clinical manifestations

Answer 110

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

Question 111

treatment of bone fractures

Answer 111

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

Question 112

nonunion

Answer 112

-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

Question 113

malunion

Answer 113

healing of bone in an nonanatomic position

Question 114

delayed union

Answer 114

does not occur until 8-9 months after fracture

Question 115

Dislocation

Answer 115

temporary displacement of bone from its joint

Question 116

subluxation

Answer 116

contact between the bones in the joint only partially lost

Question 117

treatment of dislocation and subluxation

Answer 117

-reduction and immobilization for 2-6 weeks -exercises

Question 118

strain

Answer 118

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

Question 119

sprain

Answer 119

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

Question 120

avulsion

Answer 120

complete separation of tendon or ligament from its bony attachment site

Question 121

tendinitis

Answer 121

inflammation of a tendon

Question 122

tendinosis

Answer 122

painful degradation of collagen fibers

Question 123

bursitis

Answer 123

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

Question 124

Epicondylitis

Answer 124

inflammation of a tendon where it attaches to a bone

Question 125

tennis elbow

Answer 125

lateral epicondylitis

Question 126

golfer's elbow

Answer 126

medial epicondylitis

Question 127

treatment for tendinopathy and bursitis

Answer 127

-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

Question 128

muscle strain

Answer 128

-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

Question 129

myositis ossificans

Answer 129

-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

Question 130

rhabdomyolysis

Answer 130

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

Question 131

classic triad of rhabdomyolysis

Answer 131

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

Question 132

treatment of rhabdo

Answer 132

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

Question 133

compartment syndrome

Answer 133

-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

Question 134

Clinical manifestations of compartment syndrome

Answer 134

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

Question 135

treatment of compartment snydrome

Answer 135

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

Question 136

osteoporosis

Answer 136

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

Question 137

normal bone density

Answer 137

833 mg/cm2

Question 138

osteopenic bone

Answer 138

-decreased bone mass -833-648 mg/cm2

Question 139

Causes of osteoporosis

Answer 139

-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)

Question 140

postmenopausal osteoporosis

Answer 140

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

Question 141

glucocorticoids effect on bone density

Answer 141

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

Question 142

types of osteoporosis

Answer 142

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

Question 143

clinical manifestations of osteoporosis

Answer 143

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

Question 144

prevention of osteoporosis

Answer 144

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

Question 145

treatment of osteoporosis

Answer 145

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

Question 146

osteomalacia

Answer 146

-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

Question 147

clinical manifestations of osteomalacia

Answer 147

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

Question 148

treatment of osteomalacia

Answer 148

-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

Question 149

Pagets disease (osteitis deformans)

Answer 149

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

Question 150

clinical manifestations of Paget disease

Answer 150

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

Question 151

treatment of paget disease

Answer 151

bisphosphonates and calcitonin

Question 152

osteomyelitis

Answer 152

-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

Question 153

clinical manifestations of osteomyelitis

Answer 153

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

Question 154

treatment of osteomyelitis

Answer 154

-abx -debridement -surgery -hyperbaric O2 therapy

Question 155

Malignant bone tumors

Answer 155

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

Question 156

Geographic bone destruction

Answer 156

well-defined margins of lytic bone with normal bone

Question 157

moth-eaten bone destruction

Answer 157

areas of partially destroyed bone adjacent to completely lytic areas

Question 158

permeative bone destruction

Answer 158

-abnormal lytic bone imperceptibly merges with surrounding normal bone

Question 159

38% of all bone tumors

Answer 159

osteosarcoma

Question 160

What is osteosarcoma located?

Answer 160

in metaphyses of long bones 50% occur around knees

Question 161

Osteosarcoma is predominant in:

Answer 161

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

Question 162

contain masses of osteoids: bone-forming tumors

Answer 162

osteosarcoma streamers: noncalcified bone matrix and callus

Question 163

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

Answer 163

chondrosarcoma

Question 164

Chondrosarcoma

Answer 164

-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

Question 165

chondrosarcoma treatment

Answer 165

wide-surgical excision-damaged area and surrounding area

Question 166

fibrosarcoma

Answer 166

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

Question 167

fibrosarcoma clinical manifestations

Answer 167

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

Question 168

tx of fibrosarcoma

Answer 168

radical sx and amputation

Question 169

giant cell tumor

Answer 169

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

Question 170

where is giant cell tumor located?

Answer 170

epiphyses of femur, tibia, radius or humerus

Question 171

clinical manifestations of giant cell tumor

Answer 171

-pain -local swelling -limitation of movement

Question 172

tx of giant cell tumor

Answer 172

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

Question 173

noninflammatory joint disease is differentiated by:

Answer 173

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

Question 174

arthropathies

Answer 174

disease of joints

Question 175

Osteoarthritis (degenerative joint disease)

Answer 175

-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

Question 176

clinical manifestations of OA

Answer 176

-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

Question 177

treatment of OA

Answer 177

-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

Question 178

Arthritis

Answer 178

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

Question 179

Rheumatoid arthritis (RA)

Answer 179

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

Question 180

clinical manifestations of RA

Answer 180

-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

Question 181

RA evaluation (four or more of the following):

Answer 181

-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

Question 182

treatment of RA

Answer 182

-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

Question 183

Ankylosing spondylitis

Answer 183

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

Question 184

what is ankylosing spondylitis strongly associated with?

Answer 184

human leukocyte antigen B27 (HLA-B27)

Question 185

clinical manifestations of ankylosing spondylitis

Answer 185

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

Question 186

treatment of ankylosing spondylitis

Answer 186

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

Question 187

gout

Answer 187

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

Question 188

what are precursors of gout?

Answer 188

purines

Question 189

causes of gout

Answer 189

purine synthesis or breakdown accelerated poor uric acid secretion in kidneys

Question 190

mechanisms for crystal deposition in gout

Answer 190

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

Question 191

asymptomatic hyperuricemia

Answer 191

urate level high with no symptoms

Question 192

tophaceous gout

Answer 192

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

Question 193

clinical manifestations of gout

Answer 193

-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

Question 194

treatment of gout

Answer 194

-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

Question 195

physiologic contracture

Answer 195

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

Question 196

pathologic contracture

Answer 196

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

Question 197

fibromyalgia

Answer 197

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

Question 198

fibromyalgia symptoms

Answer 198

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

Question 199

possible factors of fibromyalgia

Answer 199

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

Question 200

treatment of fibromyalgia

Answer 200

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

Question 201

chronic fatigue syndrome (myalgic encephalomyelitis)

Answer 201

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

Question 202

chronic fatigue syndrome possible causes

Answer 202

-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

Question 203

clinical manifestations of chronic fatigue syndrome

Answer 203

-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

Question 204

treatment of chronic fatigue syndrome

Answer 204

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

Question 205

Disuse atrophy

Answer 205

-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

Question 206

myotonia

Answer 206

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

Question 207

periodic paralysis

Answer 207

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

Question 208

hypokalemic periodic paralysis

Answer 208

alteration in potassium ion channels regulated by T3

Question 209

Treatment of hypokalemic periodic paralysis

Answer 209

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

Question 210

hyperkalemic periodic paralysis

Answer 210

-genetic mutation of sodium channels

Question 211

treatment of hyperkalemic periodic paralysis

Answer 211

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

Question 212

thyrotoxicosis

Answer 212

proximal weakness, paresis of extraocular muscles (exophthalmic ophthalmoplegia)

Question 213

hypothyroidism

Answer 213

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

Question 214

familial hypomagnesemia

Answer 214

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

Question 215

mcArdle disease

Answer 215

-disease of energy metabolism -myophosphorylase deficiency

Question 216

Acid maltase deficiency or Pompe disease

Answer 216

-disease of energy metabolism -glycogen

Question 217

myoadenylate deaminase deficiency

Answer 217

disease of energy metabolism

Question 218

myositis

Answer 218

-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

Question 219

myopathy

Answer 219

-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)

Question 220

treatment of polymyositis, dermatomyositis and inclusion body myositis

Answer 220

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

Question 221

inclusion body myositis

Answer 221

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

Question 222

polymyositis

Answer 222

generalized muscle inflammation mediated by T cells

Question 223

dermatomyositis

Answer 223

polymyositis, accompanied with skin rash, humorally mediated

Question 224

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

Answer 224

polymyositis dermatomyositis inclusion body myositis

Question 225

Gold mechanism of action

Answer 225

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

Question 226

T1/2 gold

Answer 226

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

Question 227

only gold salt available as parenteral preparation for IM administration

Answer 227

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

Question 228

Orally effective gold preparation

Answer 228

Auranofin (Ridaura)

Question 229

What is the most common side effect of Gold?

Answer 229

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

Question 230

Other side effects of gold

Answer 230

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

Question 231

More serious toxicities of gold

Answer 231

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

Question 232

MOA of hydroxychloroquine (Plaquenil)

Answer 232

-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.

Question 233

Side effects of Hydroxychloroquine

Answer 233

-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

Question 234

Anti-rheumatic drug that is a chelator

Answer 234

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

Question 235

problems with the use of D-Penicillamine

Answer 235

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

Question 236

cytotoxic agents which are anti-rheumatic drugs

Answer 236

Azathioprine (Imuran) Methotrexate drugs may have direct anti-inflammatory effects in addition to their ability to suppress or modify immune responses

Question 237

Serious side effects of azathioprine and methotrexate

Answer 237

-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

Question 238

TNF blockers

Answer 238

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

Question 239

How do TNF blockers work?

Answer 239

-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

Question 240

SE of TNF blockers

Answer 240

-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)

Question 241

JAK1,JAK2, JAK 3

Answer 241

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.

Question 242

Janus Kinase inhibitors

Answer 242

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

Question 243

gout

Answer 243

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

Question 244

uric acid is the end product of _______

Answer 244

purine metabolism is poorly soluble especially in acidic environments

Question 245

causes of hyperuricemia and acute arthritic episodes

Answer 245

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

Question 246

drug therapy of gout has 2 primary aims:

Answer 246

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

Question 247

treatment of gout

Answer 247

-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

Question 248

Drugs used in therapy of acute gout attacks

Answer 248

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

Question 249

drugs that increase urate excretion (uricosurics)

Answer 249

probenecid

Question 250

drugs that decrease uric acid production

Answer 250

1. allopurinol (Zyloprim) 2. Febuxostat (Uloric)

Question 251

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

Answer 251

Colchicine

Question 252

What is the mechanism of action of Colchicine?

Answer 252

-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.

Question 253

Colchicine uses

Answer 253

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)

Question 254

Colchicine toxicity and interactions

Answer 254

-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

Question 255

serious symptom of overose with Colchicine

Answer 255

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

Question 256

Colchicine dosing

Answer 256

-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

Question 257

Colchicine can be used with _____ and ______.

Answer 257

probenecid and allopurinol

Question 258

Other drugs used for acute gout attacks

Answer 258

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

Question 259

MOA of probenecid

Answer 259

-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

Question 260

with what agents is there a paradoxical effect?

Answer 260

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

Question 261

uses of probenecid

Answer 261

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

Question 262

toxicity and interactions

Answer 262

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

Question 263

dose of probenecid

Answer 263

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

Question 264

Lesinurad (Zurampic) MOA

Answer 264

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

Question 265

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

Answer 265

Lesinurad (Zurampic)

Question 266

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

Answer 266

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

Question 267

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

Answer 267

CYP3A4 Warfarin

Question 268

Allopurinol (Zyloprim) and Febuxostat (Uloric) MOA

Answer 268

-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

Question 269

Xanthine oxidase converts ____ to _______ to ________.

Answer 269

converys hypoxanthine to xasnthine and xanthine to uric acid

Question 270

Which drug is an irreversible "suicide-substrate" inhibitor of XO

Answer 270

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

Question 271

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

Answer 271

Febuxostat

Question 272

Half-life of allopurinol is ______.

Answer 272

2-3 hours

Question 273

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

Answer 273

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

Question 274

Half life of Febuxostat is _______.

Answer 274

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

Question 275

Plasma protein binding of Febuxostat

Answer 275

99.2%

Question 276

VD of Febuxostat

Answer 276

0.7 l/kg

Question 277

Uses of Allopurinol and Febuxostat

Answer 277

-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

Question 278

toxicity and problems with allopurinol

Answer 278

-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

Question 279

Febuxostat toxicity and problems

Answer 279

-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

Question 280

Interactions of Allopurinol and Febuxostat

Answer 280

-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

Question 281

Pegloticase (Krystexxa)

Answer 281

-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

Question 282

SE of Pegloticase

Answer 282

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

Question 283

Pegloticase contraindicated in patients with _____

Answer 283

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

Question 284

tremor

Answer 284

rhythmic/oscillatory movement around joint

Question 285

Resting tremor (Parkinson's) associated with:

Answer 285

-rigidity -impairment of volitional movement

Question 286

essential tremor

Answer 286

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

Question 287

intentional tremor

Answer 287

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

Question 288

Chorea

Answer 288

-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

Question 289

Athetosis

Answer 289

slow, writhing abnormal movement

Question 290

dystonia

Answer 290

postural abnormality-associated with sustained abnormal movement

Question 291

athetosis/dystonias causes

Answer 291

-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

Question 292

Tics

Answer 292

sudden, abnormal coordinated movements common: shoulder shrugging repetitive sniffing

Question 293

characteristics of tics

Answer 293

-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

Question 294

symptoms of parkinsons

Answer 294

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

Question 295

disease characteristics of parkinsons

Answer 295

-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

Question 296

physiology of parkinsons

Answer 296

-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)

Question 297

causes of parkinsons

Answer 297

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

Question 298

clinical manifestations of parkinsons

Answer 298

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

Question 299

does dopamine cross BBB?

Answer 299

no, ineffective if administered peripherally

Question 300

L-DOPA

Answer 300

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

Question 301

D1

Answer 301

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

Question 302

D2

Answer 302

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

Question 302

How much Levodopa reaches the brain?

Answer 302

1-3%

Question 303

How do you achieve therapeutic brain levels of levodopa?

Answer 303

-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.

Question 304

With carbidopa (Lodosyn):

Answer 304

-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

Question 305

Levodopa with Entacapone (Comtan)

Answer 305

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

Question 306

Does L-dopa stop disease progression?

Answer 306

no, may reduce Parkinson's disease mortality rate

Question 307

L-dopa most effective in diminishing _______.

Answer 307

bradykinesia

Question 308

Adverse effects of Levodopa

Answer 308

-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

Question 309

with long term tx of Levodopa ________ is most frequent.

Answer 309

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

Question 310

most common dyskinesia

Answer 310

choreoathetosis (twisting, writhing activity)

Question 311

dyskinesias include:

Answer 311

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

Question 312

management of dyskinesias

Answer 312

-dose reduction -drug holidays

Question 313

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

Answer 313

Selegiline (Eldepryl)

Question 314

Other therapeutics used in parkinsons

Answer 314

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

Question 315

Physiologic postural tremor increased by:

Answer 315

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

Question 316

drug induced increase in normal physiologic tremor

Answer 316

-bronchodilators -TCA -lithium

Question 317

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

Answer 317

propanolol (sometimes not blocked by metoprolol B1)

Question 318

drug/drug classes useful in management of essential tremor

Answer 318

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

Question 319

intentional tremor

Answer 319

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

Question 320

Huntington's disease

Answer 320

-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

Question 321

possibilities of huntington's disease

Answer 321

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

Question 322

what drugs reduce chorea

Answer 322

anti-dopaminergic agents reserpine phenothiazines and butyrophenones (haloperidol)

Question 323

What drugs increase chorea?

Answer 323

dopaminergic drugs (i.e. levodopa)

Question 324

chorea

Answer 324

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

Question 325

drug-induced chorea

Answer 325

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

Question 326

Ballismus tx

Answer 326

dopamine-blocking drugs-perphenazine, haldol

Question 327

athetosis and dystonia-tx

Answer 327

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

Question 328

treatment of tic (tourette's snydrome)

Answer 328

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

Question 329

Phenothiazine induced dyskinesia tx

Answer 329

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

Question 330

tardive dyskinesia

Answer 330

-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

Question 331

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

Answer 331

olanzapine and risperidone

Question 332

Wilson's disease

Answer 332

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

Question 333

clinical presentation of Wilson's disease

Answer 333

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

Question 334

What is Diabetes insipidus?

Answer 334

-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

Question 335

What can cause DI?

Answer 335

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

Question 336

Uses of Arginine Vasopressin (ADH)

Answer 336

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

Question 337

Metabolism of Arginine vasopressin

Answer 337

-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

Question 338

Desmopressin (DDAVP)

Answer 338

-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

Question 338

SE of Arginine Vasopressin

Answer 338

-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

Question 339

What is the 1/2 life of desopressin?

Answer 339

3-4 hrs

Question 340

Other uses of Demopressin (DDAVP)

Answer 340

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

Question 341

Diabetes Mellitus

Answer 341

-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)

Question 342

Insulin

Answer 342

-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

Question 343

Insulin structure

Answer 343

51 AA in 2 chains

Question 344

what is the primary insulin replacement used?

Answer 344

human recombinant insulin (Humulin)

Question 345

__________ 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.

Answer 345

Insulin Lispro (Humalog)

Question 346

Mechanism of insulin

Answer 346

-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

Question 347

What is the half life of insulin

Answer 347

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.

Question 348

Lispro (Humalog)

Answer 348

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

Question 349

Synthetic similar to Lispro

Answer 349

insulin aspart (Novolog)

Question 350

24 hour long-acting analog

Answer 350

Glargine (Lantus)

Question 351

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

Answer 351

ISophane Insulin (humulin N)

Question 352

Humulin 70/30 is a mixture of

Answer 352

Humulin N 70% R 30%

Question 353

Afrezza

Answer 353

-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

Question 354

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

Answer 354

Afrezza

Question 355

Side effects of insulin

Answer 355

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

Question 356

Which drugs counteract the hypoglycemic effects of insulin?

Answer 356

-AGE ACTH Glucagon Estrogens

Question 357

Which drugs may increase the duration of action of insulin?

Answer 357

Tetracyclines Chloramphenicol Salicylates MAOI's may potentiate effects

Question 358

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

Answer 358

T-BAMS Thiazolidinediones Biguanides Alpha-Glucosidase Inhibitors Meglitinides Sulfonylureas

Question 359

MOA of sulfonylureas

Answer 359

-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

Question 360

What is the longest duration of the sufonylureas?

Answer 360

chlorpropamide 2-3 days may effect takes up to 2 weeks (half life 1.5 days)

Question 361

SE of Chlorpropamide

Answer 361

severe hyponatremia -can cause disulfiram-like reaction

Question 362

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

Question 363

What are the names of the sulfonylureas?

Answer 363

Glyburide Glipizide Glimepiride Chlorpropamide Tolbutamide

Question 364

Glyburide (Glynase and Generic)

Answer 364

increases insulin sensitivity somewhat inhibits liver gluconeogenesis

Question 365

Glipizide (Glucotrol & Generic)

Answer 365

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

Question 366

Glimepiride (amaryl & Generic)

Answer 366

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

Question 367

What are the drugs that are Meglitinides?

Answer 367

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

Question 368

What are the Alpha-Glucosidase inhibitors

Answer 368

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

Question 369

What is the MOA of Miglitol (Glyset)

Answer 369

-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

Question 370

What is a biguanide drug?

Answer 370

Metformin (Glucophage & Generic)

Question 371

Which drug is effective in cases where sulfonylureas have failed?

Answer 371

Metformin

Question 372

MOA Metformin

Answer 372

-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

Question 373

SE Metformin

Answer 373

-anorexia -nausea -diarrhea

Question 374

What drugs are Thiazolidinediones?

Answer 374

-Rosiglitazone (Avandia) -Pioglitazone (Actos)

Question 375

What is the MOA of Pioglitazone?

Answer 375

-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

Question 376

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

Answer 376

Pioglitazone

Question 377

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?

Answer 377

Rosiglitazone (Avandia)

Question 378

What is incretin?

Answer 378

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

Question 379

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

Answer 379

exenatide (Byetta)

Question 380

How are incretin analogs administered?

Answer 380

SQ not oral

Question 381

Name the incretin analogs

Answer 381

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

Question 382

Are incretin analogs continued through peri-op period?

Answer 382

yes

Question 383

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

Answer 383

-Liraglutide (Victoza) reported serious SE such as pancreatitis, thyroid cancer and pancreatic cancer may limit potential benefits

Question 384

MOA of dipeptidyl peptidase 4 (DPP-4) inhibitor

Answer 384

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

Question 385

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

Answer 385

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

Question 386

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

Answer 386

Arthralgia

Question 387

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

Answer 387

saxagliptin (onglyza)

Question 388

What is Janumet a combination of?

Answer 388

Metformin +Sitagliptin (Januvia)

Question 389

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

Answer 389

no

Question 390

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

Answer 390

true

Question 391

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

Answer 391

sodium/glucose transporter 2 (SGLT-2)

Question 392

MOA of SGLT-2 inhibitors

Answer 392

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

Question 393

What are the SGLT--2 inhibitors?

Answer 393

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

Question 394

Side effects of SGLT--2 inhibitors

Answer 394

-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

Question 395

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

Answer 395

decrease

Question 396

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

Answer 396

SGLT-2 inhibitors

Question 397

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

Answer 397

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

Question 398

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

Answer 398

lower

Question 399

GLP-1 agonists

Answer 399

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)

Question 400

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

Answer 400

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

Question 401

Receptor-associated disorders due to:

Answer 401

-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

Question 402

What does the posterior pituitary arise from?

Answer 402

neuroendocrine tissue (neurohypophysis)

Question 403

What is produced from the posterior pituitary?

Answer 403

oxytocin ADH -vasopressin both nonapeptides (9AA)

Question 404

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

Answer 404

-SIADH

Question 405

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

Answer 405

diabetes insipidus neurogenic nephrogenic dipsogenic

Question 406

SIADH

Answer 406

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

Question 407

What is the most common cause of SIADH

Answer 407

ectopic secretion of ADH also common after surgery and some cancers

Question 408

Clinical manifestations of SIADH

Answer 408

-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

Question 409

Treatment of SIADH

Answer 409

-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

Question 410

Which medication is used for resistant or chronic SIADH

Answer 410

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

Question 411

DI (Diabetes Insipidus)

Answer 411

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

Question 412

Neurogenic DI

Answer 412

insufficient amounts of ADH

Question 413

Nephrogenic DI

Answer 413

insensitivity of the renal collecting tubules to ADH

Question 414

Dipsogenic DI

Answer 414

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

Question 415

Diabetes insipidus is characterized by:

Answer 415

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

Question 416

S/S of DI

Answer 416

-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

Question 417

Treatment of neurogenic DI

Answer 417

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

Question 418

Treatment of Nephrogenic DI

Answer 418

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

Question 419

Treatment of dipsogenic DI

Answer 419

effective management of water ingestion

Question 420

Hormone effects of hyper functioning anterior pituitary

Answer 420

-hyperpituitarism -hypersecretion of growth hormone -hypersecretion of prolactin

Question 421

Diseases of hyperfunctioning anterior pituitary

Answer 421

-primary adenoma -acromegaly -prolactinoma

Question 422

What hormone effects are seen with a hypofunctioning anterior pituitary?

Answer 422

hypopituitarism

Question 423

What are diseases caused by a hypofunctioning anterior pituitary?

Answer 423

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

Question 424

Hypopituitarism is characterized by:

Answer 424

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

Question 425

Causes of hypopituitarism

Answer 425

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

Question 426

Panhypopituitarism (all hormones affected)

Answer 426

Adrenocorticotropic hormone deficiency -Thyroid stimulating hormone deficiency Follicle-stimulating hormone and luteinizing hormone deficiency growth hormone deficiency Tx: replacement of deficient hormones

Question 427

ACTH deficiency leads to:

Answer 427

cortisol deficiency

Question 428

TSH deficiency leads to

Answer 428

-altered metabolism -thyroid hormones critical for maintaining homeostasis

Question 429

FSH and LH deficiency

Answer 429

-lack of secondary sex characteristics

Question 430

Growth hormone deficiency

Answer 430

-lack of growth in children -short stature, dwarfism

Question 431

Hyperpituitarism is commonly from

Answer 431

benign, slow-growing pituitary adenoma

Question 432

Clinical manifestations of Hyperpituitarism

Answer 432

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

Question 433

Tx of Hyperpituitarism

Answer 433

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

Question 434

Hypersecretion of GH

Answer 434

-giantism -GH hypersecretion in children and adolescents

Question 435

Acromegaly

Answer 435

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

Question 436

Clnical manifestations of acromegaly

Answer 436

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

Question 437

Treatment of acromegaly

Answer 437

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

Question 438

Hypersecretion of prolactin caused by:

Answer 438

prolactinomas -most common hormonally active pituitary tumor Women: amenorrhea, galatorrhea, hirsutism, osteoporosis men: hypogonadism, erectile dysfunction

Question 439

Treatment of hypersecretion of prolactin

Answer 439

-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

Question 440

Diseases of hyperthyroidism

Answer 440

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

Question 441

Disease of hypothyroidism

Answer 441

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

Question 442

Primary thyroid disease

Answer 442

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

Question 443

Secondary hypothyroidism

Answer 443

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

Question 444

Thyrotoxicosis

Answer 444

-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

Question 445

Clinical manifestations of thyrotoxicosis

Answer 445

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

Question 446

treatment of thyrotoxicosis

Answer 446

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

Question 447

Graves disease

Answer 447

autoimmune disease develops autoantibodies cant turn of secretion of thyroid hormone

Question 448

Clinical manifestations of graves disease

Answer 448

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

Question 449

What is pretibial myxedema?

Answer 449

Graves dermopathy leg swelling due to increased deposition of mucopolysaccharides not just specific to graves disease

Question 450

Treatment of graves disease

Answer 450

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

Question 451

Thyrotoxic crisis (thyroid storm)

Answer 451

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

Question 452

clinical manifestations of thyroid storm

Answer 452

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

Question 453

Treatment of thyroid storm

Answer 453

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

Question 454

Hypothyroidism

Answer 454

-deficient production of thyroid hormone by the thyroid gland

Question 455

most common cause of hypothyroidism WORLDWIDE

Answer 455

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

Question 456

Most common cause of hypothyroidism in the US

Answer 456

autoimmune thyroiditis (Hashimoto's disease)

Question 457

primary hypothyroidism causes

Answer 457

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

Question 458

Congenital hypothyroidism

Answer 458

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

Question 459

What is the most common endocrine malignancy from ionizing radiation?

Answer 459

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

Question 460

Secondary hypothyroidism

Answer 460

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

Question 461

Clinical manifestations of hypothyroidism

Answer 461

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

Question 462

Myxedema

Answer 462

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

Question 463

Myxedema coma

Answer 463

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

Question 464

treatment of hypothyroidism

Answer 464

Levothyroxine

Question 465

tx of myxedema coma

Answer 465

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

Question 466

Primary hyperparathyroidism

Answer 466

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

Question 467

Secondary hyperparathyroidism

Answer 467

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

Question 468

Tertiary hyperparathyroidism

Answer 468

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

Question 469

Pseudohypoparathyroidism

Answer 469

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

Question 470

clinical manifestations of hyperparathyroidism

Answer 470

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

Question 471

Treatment hyperparathyroidism

Answer 471

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

Question 472

hypoparathyroidism

Answer 472

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

Question 473

Clinical manifestations of hypoparathyroidism

Answer 473

-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

Question 474

treatment of hypoparathyroidism

Answer 474

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

Question 475

Diabetes mellitus

Answer 475

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

Question 476

Dx of DM

Answer 476

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

Question 477

What is Glycosylated Hemoglobin (HgA1C)?

Answer 477

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

Question 478

Categories at risk for diabetes

Answer 478

-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

Question 479

Type 1 DM

Answer 479

pancreatic atrophy and loss of beta cells

Question 480

Types of Type 1 DM

Answer 480

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)

Question 481

Type 1 DM genetic susceptibility

Answer 481

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

Question 482

Environmental factors in type 1 DM

Answer 482

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

Question 483

Patho type 1 DM

Answer 483

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

Question 484

Clinical manifestations type 1 DM

Answer 484

-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

Question 485

treatment of type 1 DM

Answer 485

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

Question 486

Risk factors of type 2 DM

Answer 486

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

Question 487

Metabolic syndrome

Answer 487

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

Question 488

major mechanisms of type 2 DM

Answer 488

insulin resistance decreased insulin secretion from beta cells

Question 489

Mechanisms of type 2 DM

Answer 489

-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

Question 490

Amylin and Ghrelin in DM

Answer 490

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

Question 491

clinical manifestation of type 2 DM

Answer 491

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

Question 492

treatment of Type 2 DM

Answer 492

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

Question 493

Maturity onset diabetes of youth (MODY)

Answer 493

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

Question 494

Gestational DM

Answer 494

-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

Question 495

-complications of DM

Answer 495

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

Question 496

somogyi effect

Answer 496

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

Question 497

dawn phenomenon

Answer 497

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

Question 498

hypoglycemia

Answer 498

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

Question 499

clinical manifestations of hypoglycemia

Answer 499

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

Question 500

treatment of hypoglycemia

Answer 500

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

Question 501

Diabetic ketoacidosis

Answer 501

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

Question 502

DKA most common in __________

Answer 502

type 1 DM

Question 503

precipitating factors DKA

Answer 503

-illness -trauma -surgery -MI increased fat mobilization with the release of fatty acids, leading to DKA

Question 504

Clinical manifestations of DKA

Answer 504

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

Question 505

lab values for DKA

Answer 505

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

Question 506

treatment of DKA

Answer 506

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

Question 507

Hyperosmolar Hyperglycemic nonketotic syndrome (HHS)

Answer 507

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

Question 508

HHS associated with ______________

Answer 508

type 2 DM

Question 509

HHS precipitated by:

Answer 509

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

Question 510

Clinical manifestations of Nonketotic Syndrome

Answer 510

-glycosuria -polyuria -dehydration -coma

Question 511

Treatment of nonketotic snydrome

Answer 511

-insulin infusion with fluid repletion -electrolyte replacement

Question 512

lab findings nonketotic syndrome

Answer 512

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

Question 513

Somogyi effect

Answer 513

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

Question 514

Dawn phenomenon

Answer 514

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

Question 515

Microvascular disease of DM

Answer 515

-diabetic retinopathy -diabetic nephropathy -diabetic neuropathies

Question 516

macrovascular disease associated with DM

Answer 516

-coronary artery disease -stroke -peripheral arterial disease

Question 517

Microvascular disease

Answer 517

-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

Question 518

diabetic retinopathy

Answer 518

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

Question 519

Maculopathy

Answer 519

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

Question 520

Macular edema

Answer 520

-fluid accumulation -retinal thickening

Question 521

tx for diabetic retinopathy

Answer 521

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

Question 522

Diabetic nephropathy

Answer 522

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

Question 523

progressive changes of diabetic neuropathy

Answer 523

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

Question 524

Treatment of diabetic nephropathy

Answer 524

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

Question 525

what is the most common complication of DM

Answer 525

diabetic neuropathies

Question 526

Diabetic neuropathy

Answer 526

-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

Question 527

macrovascular disease

Answer 527

-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

Question 528

Coronary artery disease

Answer 528

-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

Question 529

stroke

Answer 529

-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

Question 530

Peripheral arterial disease

Answer 530

-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

Question 531

Risk for infection with DM increases for several reasons:

Answer 531

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

Question 532

hyperfunction of the adrenal cortex :

Answer 532

increases cortisol -cushings disease/syndrome

Question 533

hyperfunction that increases androgens and estrogen

Answer 533

virilization feminization

Question 534

hyperfunction of adrenal cortex that increases aldosterone

Answer 534

primary or secondary hyperaldosteronism

Question 535

hypofunction of the adrenal cortex

Answer 535

-addisons disease -secondary hypocortisolism

Question 536

cushing syndrome

Answer 536

chronic excessive cortisol level, regardless of cause

Question 537

cushing disease

Answer 537

-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

Question 538

Cushing-like syndrome

Answer 538

exogenous administration of glucocorticoids

Question 539

Clinical manifestations of Cushings

Answer 539

-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

Question 540

Congenital adrenal hyperplasia

Answer 540

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

Question 541

causes of adrenal hyperplasia

Answer 541

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

Question 542

Primary hyperaldosteronism

Answer 542

conn disease usually a single benign aldosterone-producing adrenal adenoma

Question 543

secondary aldosteronism

Answer 543

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

Question 544

clinical manifestations of hyperaldosteronism

Answer 544

-HTN -hypokalemia, renal potassium wasting -neuromuscular manifestations

Question 545

treatment of hyperaldosteronism

Answer 545

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

Question 546

hypersecretion of estrogens

Answer 546

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

Question 547

hypersecretion of androgens

Answer 547

-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

Question 548

Addisons disease

Answer 548

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

Question 549

Clinical manifestations of addisons disease

Answer 549

-hypocortisolism and hypoaldosteronism -weakness, hyperpigmentation, vitiligo

Question 550

treatment of addisons

Answer 550

lifetime glucocorticoid and mineralocorticoid replacement therapy 150meq sodium per day

Question 551

patho of secondary hypocortisolism

Answer 551

prolonged administration of exogenous glucocorticoids which suppress ACTH secretion

Question 552

clinical manifestation of secondary hypocortisolism

Answer 552

similar to Addisons hyperpigmentation does not occur

Question 554

hyperfunction of the adrenal medulla

Answer 554

tumor of adrenal medulla-pheochromocytoma

Question 555

is there a hypofunction of the adrenal medulla identified?

Answer 555

no

Question 556

Pheochromocytoma

Answer 556

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

Question 557

clinical manifestations of pheochromocytoma

Answer 557

-HTN -diaphoresis -tachycardia -palpitations severe headache