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final exam new stuff Flashcards

1
Q

osteoprogenitor cells

A

undiffertiated cells that differientiate into osteo blasts. they are found in the periosteum, endostuem, and epiphyseal growth plate of growing bones

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2
Q

osteoblasts

A

bone building cells that synthesize and secrete the organic matric of bone. osteoblasts also participate in the calcification of the organic matric

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3
Q

osteocytes

A

mature bone cells that function in the maintenance of bone matrix. osteocytes also play an active role in releasing calcium into the blood

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4
Q

osteoclasts

A

bone cells responsible for the resorption of bone matrix and the release of calcium and phosphate from bone

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5
Q

tendon

A

tendons attach muscles to bone and transmit load from muscle to bone, resulting in joint motion

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6
Q

ligament

A

attach bone to bone and augment mechanical stability of a joint

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7
Q

strain

A

stretching injury to muscle/tendon caused by mechanical overload
-results from muscle contraction or forcible stretch

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8
Q

sprain

A

involves ligamentous structures surrounding the joint
-pain and swelling subside more slowly
-ligaments torn or ruptured

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9
Q

hip injuries: dislocations

A

anterior or posterior (emergency)– tension placed on blood supply to femoral head– avascular necrosis may result

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10
Q

hip injuries: fractures

A

classified according to location
-most of femoral neck fractures
-location is important in terms of blood flow to femoral
-external rotation and shortening

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11
Q

fracture of a bone

A

a fracture is any disruption, complete or incomplete, in the continuity of a bone

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12
Q

fracture of bone causes

A

-sudden injury, stress, pathologic

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13
Q

neurovascular integrity assessment

A

-distal blood flow, pulses, and sensation

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14
Q

closed fracture

A

fracture in which bone fragments separate completely

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15
Q

open fracture

A

bone protrudes through the skin

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16
Q

spiral fracture

A

a fracture resulting from a twisting motion

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17
Q

compression fracture

A

a fracture that consists of bones that are crushed or squeezed together

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18
Q

comminuted fracture

A

a fracture with more that two pieces

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19
Q

greenstick fracture

A

fracture with a partial break in bone continuity-often seen in children

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20
Q

impacted fracture

A

fracture is wedged together

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21
Q

clinical manifestations of a fracture

A

angulation, shortening, rotation(long bones)
-pain, swelling, tenderness, loss of function
-deformity

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22
Q

bone healing stage 1

A

-hematoma formation from torn blood vessels- clot forms
-death of bone cells from blood disruption

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23
Q

bone healing stage 2

A

-inflammation–nuerovasculation–formation of fibrin meshwork
-osteoblast synthesize new bone
-granulation tissue form beginning of callus

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24
Q

bone healing stage 3

A

reparative phase: continued formation of callus of cartilage and woven bone

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25
Q

bone healing stage 4

A

remodeling phase: gives cortex time to be reestablished
-healing through continues osteoblast and osteoclast activity

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26
Q

impaired fracture healing: delayed union

A

manifestation: failure of fracture to heal within predicted time
contributing factors: large, displaces fracture

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27
Q

impaired fracture healing: malunion

A

manifestation: deformity at fracture site, deformity/angulation on XR
-inadequate immobilization, circulation, reduction or infection

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28
Q

impaired healing of fractures: nonunion

A

manifestations: failure of bone to heal before process of bone repair stops(pain)
-bone fragment separating, infection, inadequate circulation, bone necrosis, noncompliance

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29
Q

complications of musculoskeletal trauma

A

-associated with loss of skeletal continuity
-injury from bone fragments
-pressure form swelling and hemorrhage
-involvement of nerve fibers
-development of venous thromboembolism and fat embolism

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30
Q

compartment syndrome

A

pathopysiology:
-increased pressure within a limited space (abnominal and limb compartments)- compromises circulation and function of tissues
-increase in volume of contents or decreae in compartment size
-muscles/nerves enclosed in tough, non elastic fascia compartments-if pressure is too high, tissue circulation compromised- causes death of nerve and musle cells

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31
Q

compartment syndrome: causes of increased volume

A

-swelling, trauma, vascular injury, bleeding and edema post surgery, ischemic events, IV infiltration

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32
Q

compartment syndrome signs

A

hallmark sign: severe pain that is out of proportion to injury
-changes in sensation- nerve compression
-diminished reflexes or loss of motion
-necrosis occurs quickly

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33
Q

fat embolism syndrome

A

life-threatening
patho: presence of fat droplets in small vessels of lung, kidneys, brain
-long bone or pelvic fracture
-released from bone marrow or adipose tissue at fracture site into venous system

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34
Q

fat embolism syndrome clinical manifestations

A

respiratory failure, cerebral dysfunction, petechiae (little spots under skin)

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35
Q

osteomyelitis

A

acute or chronic infection of the bone caused by:
-direct penetration or contamination of open fracture/wound
-seeding through bloodstream
-extension from a contiguous site (staphylococci)
-skin infectionis in people w vascular insufficiency

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36
Q

osteomyelitis S/S

A

-bacteremia (fever, chills, warmth, malaise)
-localized erythema, edema
-pain with movement of infected extremity
-loss of ROM

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37
Q

metabolic bone disease: osteopenia

A

reduction in bone mass greater than expected for age, race, or sex
-occurs due to decrease in bone formation, inadequate bone mineralization or excessive bone deossification
-lack of bone on XR

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38
Q

osteopenia etiology

A

osteoporosis, malignancies (multiple myeloma), edocrine disorders (thryoid)

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39
Q

osteoporosis

A

loss of mineralized bone mass causing increased porosity of the skeleton
-increased risk to fractures
-reported using a T score

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40
Q

osteoporosis risk factors

A

age, women, black women, exercise, low calcium intake, estrogen, genetics, vitamin D deficiency
-exercise may prevent or delay onset by increasing peak bone mass density

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41
Q

osteoporosis patho

A

-imbalance between bone resorption and formation
-bone resorption exceeds bone formation
-bone begin to resemble fragile structe of fine porcelain vase
-loss of trabeculae, thinning of cortex– minimal stress causes fractures

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42
Q

osteoporosis hormonal factors

A

-estrogen acts to inhibit bone breakdown and stimulated bone formation
-increase loss of bone= predisposition to fractures
-decreased estrogen levels associated with increase in cytokines that stimulate prodcution of osteoclast precursors

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43
Q

osteoporosis estrogen

A

normal: estrogen stimulates production of OPG– inhibits the formation of osteoclasts
abnormal: estrogen deficiency– no inhibition of osteoclast producion which leads to excess resporption of bone
-compensatory osteoblastic activity/new bone formation occurs, but doesnt keeppace with bone that is lost

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44
Q

secondary osteoporosis

A

-malabsorption disorders
-malignancys- secret osteoclast
-alcoholism- direct inhibitor of osteoblasts-activating factor
-medications-corticosteroids cause bone loss
-female athlete triad= disorded eating, amenorrhea, OP

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45
Q

osteoporosis clinical manifestations

A

dowager hump
decrease in height
increased risk of fractures
diagnosis: DEXA scan

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46
Q

rheumatoid arthritis

A
  • systemic inflammatory disease
    -female> male
    prevalence increases with age
    etiology: genetic predisposition, development of joint inflammation that is immunologically mediated
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47
Q

rheumatoid arthritis pathogenesis

A

T-cell mediated response to immunologic trigger
-aberrant immune response that leads to synovial inflammation and destruction of he joint architecture
-activation of T-helper cells– release of cytokines (TNF-a, IL-1) and antibody formation

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48
Q

Rheumatic arthritis diagnostic lab

A

presence of rheumatoid factor (RF)
-autoimmune process– macrophages phagocytize immune complexes and release lysosomal capable of causing destructive changes to joint
-extensive new blood vessels in synovial membrane– destructive vascular granulation tissue (pannus)

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49
Q

articular manifestations

A

-joint involvement symmetric and polyarticular
-pain and stiffness> 30 minutes, lasting for an hour (fingers, hands, wrists, knees, and feet)

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50
Q

clinical manifestations of RA

A

-neck discomfort, symmetric polyarthritis, eye lesions: episcleritis, scleromalacia
-nonspecific systemic symptoms: low-grade fever, fatigue, weakness, loss of appetite
-hematologic manifestations: elevated ESR and anemia
-lymphadenopathy
-vasculitis, splenomegaly

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51
Q

extra-articular manifestations

A

-fatigue, weakness, anorexia, weightloss, low grade fever
-elavated ESR rate
-thrombocytosis/anemia
-vasculitis of arteries

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52
Q

systemic lupus erythematosus

A

chronic inflammatory disease affecting virtually any organ system
-prevalnce related to gender(female), race (african americans), age (15-44) and genetics

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53
Q

environmental triggers to lupus

A

UV light, chemicals, food, infectious agents

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54
Q

lupus pathogenesis

A

formation of autoantibodies and immune complexes
-B-cell hyperreactivity- each cell produces a different antibody (antinuclear antibodies (ANA))

55
Q

clinical manifestations of lupus

A

baldness, CNS symtoms, anemia, neurtopenia, thrombocytopenia, polyarthiritis, myositis, pleuritis pneumonitis, lupus glomerulonephritis

56
Q

osteoarthritis

A

most prevalent form of arthritis
-includes inflammatory component along with degenerative aspects
-slow, progressive destruction of cartilage of weight-bearing joint and fingers

57
Q

osteoarthritis

A

epidemiology: age, gender, race

58
Q

osteoarthritis patho

A

excess pressure on a joint gradually wears away the cartilage surface and the subchondral bone is exposed
-inflammation- degradation of cartilage
-loss of cartilage- narrowing of the joint space
at the margin of cartilage loss, osteophytes can form
-osteophytes are small bony projections that develop along the rim of bone adjacent to carilage loss- hallmark of OA

59
Q

OA clinical manifestations

A

aching joint pain, worsens with activity, relieved with rest, crepitus of the joint during motion, joint swelling (feels hard) (RA feels spongy), limited ROM

60
Q

OA physical examination

A

distal joint- herbedens nodes
proximal joint- bouchards nodes

61
Q

Gout

A

increased serum uric acid and urate crystal in kidneys and joints
severe articular inflammation
tophi-accumulation of crystalline deposits
-elevated uric acid levels
-abrupt pain
-redness, swelling
-exquisite tenderness
-increased in first metatarsophalangeal joint

62
Q

endocrine: hypofunction

A

absence or impaired development of a gland or deficiency of an enzyme needed for hormone synthesis

63
Q

endocrine: hyperfunction

A

excessive hormone production results from excessive stimulation and hyperplasia of endocrine gland

64
Q

endocrine: paraneoplastic syndrome

A

excess production from abnormal ectopic production of hormone by a malignant tumor
ex: bronchogenic tumors releasing ADH

65
Q

endocrine dysfunction:

A

may occur due to hormone resitance or receptor defects

66
Q

endocrine: primary disorders

A

-originates in the target endocrine gland in which the hormone is produced
-ex: Addison disease- autoimmune damage to adrenal cortex in underproduction of adrenal cortical hormones

67
Q

endocrine: secondary disorders

A

target endocrine gland is normal, but the gland is not producing appropriate hormone levels
-not receiving appropritate stimulation because of the dysfunction in the hypothalamus or pituitary

68
Q

pituitary gland disorders

A

-the pituitary doesn’t produce its own hormones: it stores hormones and releases when needed
-posterior lobe produces: ADH, oxytocin
-anterior lobe produces: ACTH. TSH

69
Q

hypopituitary

A

diabetes insipidus (low ADH)

70
Q

hyper pituitary

A

SIADH(symptom of inappropriate ADH: excessive ADH)
Cushing syndrome

71
Q

ACTH (anterior pituitary)

A

-controls release of cortisol from adrenal gland

72
Q

TSH (anterior pituitrary)

A

-diagnostic
-controls release of thyroid hormone from the thyroid gland

73
Q

ADH (posterior pituitary)

A
74
Q

assessment of pituitary function

A

serum cortisol, serum thyroxine and TSH, plasma osmolality, urine osmolality, MRI (osmolality is concentration)

75
Q

The thyroid gland

A

a shield shaped gland that secretes triiodothyronine, and thyroxine (T3, T4)

76
Q

Thyroid hormone

A

the regulator of the body metabolism that influences almost every body system

77
Q

Thyroid diagnosis

A

T3, t4, TSH, ultrasound, CT, MRI

78
Q

thyroid actions

A

increases MBR, CV, GI, NM function

79
Q

hypothyroidism etiology

A

radiation, surgical removal
-lithium
-iodine deficiency

80
Q

hypothyroidism pathophysiology

A

-Hashimoto’s: autoimmune destruction of thyroid gland
-TH receptor antibodies present

81
Q

hypothyroidism manifestations

A

-decrease metabolic activities
-cold intolerance
-weight gain
-lethargy
-puffy face
-hair loss
-weakness
-constipation, abdominal distention
-bradycardia

82
Q

hypothyroidism diagnosis

A

primary hypothyroidism: low hormone secretions by the thyroid gland that constantly signals pituitary to secrete TSH
-High TSH, low T3T4

83
Q

hypothyroidism complications

A

-Myxedema coma (severe hypothyroidism): hypothermia, CV collapse, hyponatremia, hypoglycemia, lactic acidosis

84
Q

hyperthyroidism etiology

A

autoimmune: Graves
-hyperthyroidism, Goiter, ophthalmopathy

85
Q

Hyperthyroidism diagnosis

A

High T3T4, low TSH

86
Q

Hyperthyroidism patho

A

Grave disease: abnormal stimulation of the thyroid by thyroid stimulating antibodies (TSH receptor antibodies)
-excessively secreting T3T4- high levels of T3T4 excerts a negative feedback inhibiting of TSH
-in the presence of low TSH, the thyroid continuously secretes hormones

87
Q

Hyperthyroidism manifestations

A

-nervousness
-tachycardia, palpitations, afib
-weight loss
-sensitivity to heat
-Goiter
-exophthalmos

88
Q

hyperthyroid manifestations: Graves ophthalmopathy

A

-periorbital edema and bulging eyes
-wide eyed stare
women more than men

89
Q

hyperthyroidism complication

A

-Thyroid storm
-overwhelming release of thyroid hormones- intense stimulus on metabolism
-precipitated by surgery, trauma, infection
-high fever, tachycardia, N/V, agitation, tremulousness, psychosis, stuporous or comatose late in progression

90
Q

Adrenal gland: cortex

A

secretes corticosteroids, also called glucocorticoids (cortisol) and mineralocorticoids (aldosterone)
-total loss of adrenal cortical function is fatal in a few days to weeks if untreated

91
Q

Adrenal gland: medulla

A

secretes epinephrine and NE

92
Q

Mineralocorticoids

A

-regulate potassium, sodium, water balance
-ALDOSTERONE (RAAS)
excess aldosterone= low potassium, muscle weakness
deficient aldosterone= hyperkalemia, cardiac toxic

93
Q

glucocorticoids

A

-corticotropin releasing factor from the hypothalamus to stimulate anterior pituitary to secrete ACTH
-CORTISOL (hyrdocortisone)
-stimulates gluconeogenesis (increase blood glucose), antiinflammatory, suppress immune responses, emotional instability

94
Q

primary adrenal insufficiency etiology

A

-Addison disease
-autoimmune destruction of adrenal glands
-adrenal hemorrhage
-stress induced
-withdrawal of exogenous glucocorticoid replacement
-TB

95
Q

Primary adrenal insufficiency manifestations

A

decreased production of adrenal cortical hormones, increase ACTH, mineralocorticoid and glucocorticoid deficiency, HYPERKALEMIA, HYPONATREMIA., HYPOGLYCEMIA
- decrease CO, FVD, weakness, fatigue
-hyperpigmentation-bronzed/tan

96
Q

secondary adrenal insufficiency

A

pituitary gland surgically removed
-rapid withdrawal of glucocorticoids
-supresses the HPA system-resulting adrenal corticoid atrophy and loss of cortisol production

97
Q

adrenal crisis

A

life threatening, exposure to a stressor

98
Q

clinical manifestations of adrenal insufficiency

A

-anorexia, weight loss, fatigue, GI issues, myalgia, arthralgia, hyponatremia, hyperkalemia, hyperpigmentation, secondary deficiencies in testost, growth hormone, thyroxine, ADH

99
Q

glucocorticoid excess etiology

A

-cushing syndrome: manifestatons of hypercortisolism from any cause
-cushing disease: excessive production of ACTH by pituitary tumor
-hypercortisolism: certain extrapituitary malignant tumors (small cell carcinoma of the lung) may secrete ACTH
-latrogenic: pharmologic admin

100
Q

glucocorticoid excess

A

-hypokalemia, HTN, increase risk of infections, emotional instability

101
Q

glucocorticoid excess manifestations

A

weight gain, redistribution of body fat to face, trunk, and abdomen
-rose colored puffy moon face
-extra subQ fat buffalo hump
-easy bruising, poor wound healing

102
Q

Antidiuretic hormone

A

-regulates: reabsorption of water by kidneys (RAAS), vasopressin, release is stimulated by increased serum osmolality -osmoreceptors
-released in stress situations: Nausea, vomitting, pain, trauma, anesthetic agents

103
Q

Diabetes insipidus

A

-caused by a deficiency or a decreased response to ADH
-central: lack of secretion (posterior)
-nephrogenic: kidneys failure to respond to ADH

104
Q

diabetes insipidus etiology

A

brain tumor, head trauma, pituitary surgery, nephrotoxic drugs, ischemia of kidney

105
Q

DI patho

A

-decreased ADH secretion
-insensitivity to ADH receptor in kidney:
. kidney does not perform antidiuresis– does not reabsorb water
.high amounts of water lost in urine (polyuria, dilute urine)
.vascular depletion causes hyperosmolality (concentrated blood): hypovolemia, dilute urine, hypernatremia

106
Q

DI manifestations

A

-frequent dilute urine, thirst/dehyrdation, confusion, disorientation, seizures, coma

107
Q

DI diagnosis

A

-serum osmolality (high)
-serum sodium (hypernatremia: due to water loss)
-urine osmolality (hypo: dilute)

108
Q

syndrome of inappropriate ADH etiology

A

-stroke, meningitis, lung/brain cancer, emphysema, pain, HIV

109
Q

SIADH patho

A

-results from failure of negative feedback system that regulated release and inhibition of ADH
-ADH secretion continues even when serum osmolality is decrease– causing marked water retention and dilutional hyponatremia
-hypervolemia, concentrated urine, dilutional hyponatremia (water retention dilutes sodium)

110
Q

SIADH clinical manifestations

A

-fluid volume overload
-hyponatremia
-fatigue
-weakness
-confusion

111
Q

SIADH diagnosis

A

serum osmolality: hypoosmolar (low)
serum sodium (hypo)
urine osmolality (hyper)

112
Q

diabetes mellitus

A

imbalance between insulin secretion and cellular responsiveness to insulin
-unable to transport glucose into cells- cells become starved-breakdown of fat/protein is increased to generate cellular energy
-high levels of blood glucose

113
Q

DM classification: type 1

A

autoantibody destruction of insulin secreting beta cells

114
Q

DM: type 2

A

cellular resistance to insulin with or without pancreatic beta cell exhaustion

115
Q

DM: Prediabetics

A

-blood glucose is elevated but doesn’t meet threshold for DM

116
Q

Other DM

A

gestations (2-3 tri), genetic, maturity, pancreatic disease, drugs

117
Q

diabetes manifestations classic triad

A

polydipsia: thirst
polyuria: peeing
polyphagia: appetite

118
Q

diabetes manifestations others

A

glycosuria, weight loss, blurred vision, fatigue, skin infections

119
Q

type 1 diabetes etiology

A

-10% of cases
-destruction of insulin secreting beta cells
-lack of insulin production
-elevated blood glucose
-breakdown of body fats for fuel
-prone to ketoacidosis
-action of insulin is inhibition of lypolyisis
-require exogenous insulin replacement

120
Q

type 2 DM

A

90% of cases
-genetics
-more in older adults, but slowly become more common in youngs
-obesity

121
Q

type 2 patho

A

insulin resitance
-deranged secretion of insulin by beta cells
-increased glucose production by liver

122
Q

type 1

A

age: young
type of onset: abrupt, symptomatic, severe ketoacidosis
body weight: normal, recent weight loss
family history: not as common
leukocyte antigen: positive
lesions: early inflammation
beta cell: reduced
circulating insulin: reduced
clinical: required insulin

123
Q

type 2

A

age: adult
onset: gradual, asymptomatic, subtle
body weight: overweight
fam history: common
leukocyte antigen: no
lesions: late fibrous amyloid
beta cell: elevated or normal
clinical: usually no insulin at first, weight loss

124
Q

metabolic syndrome

A

obestity, apple shaped, elevated glucose, dyslipidemia, evevated triglycerides, low HDL, HTN, atherosclerosis

125
Q

DM acute complications

A

hyperglycemia, hypoglycemia, DKA, type 2: hyperosmolar hyperglycemia syndrome

126
Q

diabetic ketoacidosis etiology

A

stress, infection, omission or inadequate use of insulin (type 1)

127
Q

diabetic ketoacidosis manifestations

A

osmotic diuresis, dehydration, fatigue, coma, abdominal pain, fruity breath, tachycardia, kussmaul respiration

128
Q

diabetic ketoacidosis patho

A

DKA can occur when there is no insulin secreted by pancreas
-hyperglycemia-osmotic diuresis-FVD F&E inbalance
-serum potassium normal or elevated hyperkalemia

129
Q

diabetic ketoacidosis metabolic dearangments

A

hyperglycemia, ketosis, metabolic acidosis

130
Q

hyperosmolar hyperglycemia state (type 2) patho

A

-reduce glucose utilizatoin with incresing glucagon release
-hyperglycemia leads to large volume water loss via osmotic diuresis
-dehydration more severe than DKA
-renal insufficiency
-thromboembolic

131
Q

hyperosmolar hyperglycemia state (type 2) manifestations

A

weakness, dehyrdation, polyuria, neurological alterations, hemiaparesis, seizures, coma, excessive thirst
NO ACIDOSIS
hyperglycemia, dehydration

132
Q

hypoglycemia

A

blood glucose less than 70
-with or without symptoms: error in insulin dose, not eating, increased exercise, meds, change in injection site, alcohol

133
Q
A

patho (5 decks)

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