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
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
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
4
Q
osteoclasts
A
bone cells responsible for the resorption of bone matrix and the release of calcium and phosphate from bone
5
Q
tendon
A
tendons attach muscles to bone and transmit load from muscle to bone, resulting in joint motion
6
Q
ligament
A
attach bone to bone and augment mechanical stability of a joint
7
Q
strain
A
stretching injury to muscle/tendon caused by mechanical overload
-results from muscle contraction or forcible stretch
8
Q
sprain
A
involves ligamentous structures surrounding the joint
-pain and swelling subside more slowly
-ligaments torn or ruptured
9
Q
hip injuries: dislocations
A
anterior or posterior (emergency)– tension placed on blood supply to femoral head– avascular necrosis may result
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
11
Q
fracture of a bone
A
a fracture is any disruption, complete or incomplete, in the continuity of a bone
12
Q
fracture of bone causes
A
-sudden injury, stress, pathologic
13
Q
neurovascular integrity assessment
A
-distal blood flow, pulses, and sensation
14
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closed fracture
A
fracture in which bone fragments separate completely
15
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open fracture
A
bone protrudes through the skin
16
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spiral fracture
A
a fracture resulting from a twisting motion
17
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compression fracture
A
a fracture that consists of bones that are crushed or squeezed together
18
Q
comminuted fracture
A
a fracture with more that two pieces
19
Q
greenstick fracture
A
fracture with a partial break in bone continuity-often seen in children
20
Q
impacted fracture
A
fracture is wedged together
21
Q
clinical manifestations of a fracture
A
angulation, shortening, rotation(long bones)
-pain, swelling, tenderness, loss of function
-deformity
22
Q
bone healing stage 1
A
-hematoma formation from torn blood vessels- clot forms
-death of bone cells from blood disruption
23
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bone healing stage 2
A
-inflammation–nuerovasculation–formation of fibrin meshwork
-osteoblast synthesize new bone
-granulation tissue form beginning of callus
24
Q
bone healing stage 3
A
reparative phase: continued formation of callus of cartilage and woven bone
25
bone healing stage 4
remodeling phase: gives cortex time to be reestablished
-healing through continues osteoblast and osteoclast activity
26
impaired fracture healing: delayed union
manifestation: failure of fracture to heal within predicted time
contributing factors: large, displaces fracture
27
impaired fracture healing: malunion
manifestation: deformity at fracture site, deformity/angulation on XR
-inadequate immobilization, circulation, reduction or infection
28
impaired healing of fractures: nonunion
manifestations: failure of bone to heal before process of bone repair stops(pain)
-bone fragment separating, infection, inadequate circulation, bone necrosis, noncompliance
29
complications of musculoskeletal trauma
-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
30
compartment syndrome
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
31
compartment syndrome: causes of increased volume
-swelling, trauma, vascular injury, bleeding and edema post surgery, ischemic events, IV infiltration
32
compartment syndrome signs
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
33
fat embolism syndrome
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
34
fat embolism syndrome clinical manifestations
respiratory failure, cerebral dysfunction, petechiae (little spots under skin)
35
osteomyelitis
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
36
osteomyelitis S/S
-bacteremia (fever, chills, warmth, malaise)
-localized erythema, edema
-pain with movement of infected extremity
-loss of ROM
37
metabolic bone disease: osteopenia
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
38
osteopenia etiology
osteoporosis, malignancies (multiple myeloma), edocrine disorders (thryoid)
39
osteoporosis
loss of mineralized bone mass causing increased porosity of the skeleton
-increased risk to fractures
-reported using a T score
40
osteoporosis risk factors
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
41
osteoporosis patho
-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
42
osteoporosis hormonal factors
-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
43
osteoporosis estrogen
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
44
secondary osteoporosis
-malabsorption disorders
-malignancys- secret osteoclast
-alcoholism- direct inhibitor of osteoblasts-activating factor
-medications-corticosteroids cause bone loss
-female athlete triad= disorded eating, amenorrhea, OP
45
osteoporosis clinical manifestations
dowager hump
decrease in height
increased risk of fractures
diagnosis: DEXA scan
46
rheumatoid arthritis
- systemic inflammatory disease
-female> male
prevalence increases with age
etiology: genetic predisposition, development of joint inflammation that is immunologically mediated
47
rheumatoid arthritis pathogenesis
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
48
Rheumatic arthritis diagnostic lab
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)
49
articular manifestations
-joint involvement symmetric and polyarticular
-pain and stiffness> 30 minutes, lasting for an hour (fingers, hands, wrists, knees, and feet)
50
clinical manifestations of RA
-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
51
extra-articular manifestations
-fatigue, weakness, anorexia, weightloss, low grade fever
-elavated ESR rate
-thrombocytosis/anemia
-vasculitis of arteries
52
systemic lupus erythematosus
chronic inflammatory disease affecting virtually any organ system
-prevalnce related to gender(female), race (african americans), age (15-44) and genetics
53
environmental triggers to lupus
UV light, chemicals, food, infectious agents
54
lupus pathogenesis
formation of autoantibodies and immune complexes
-B-cell hyperreactivity- each cell produces a different antibody (antinuclear antibodies (ANA))
55
clinical manifestations of lupus
baldness, CNS symtoms, anemia, neurtopenia, thrombocytopenia, polyarthiritis, myositis, pleuritis pneumonitis, lupus glomerulonephritis
56
osteoarthritis
most prevalent form of arthritis
-includes inflammatory component along with degenerative aspects
-slow, progressive destruction of cartilage of weight-bearing joint and fingers
57
osteoarthritis
epidemiology: age, gender, race
58
osteoarthritis patho
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
OA clinical manifestations
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
OA physical examination
distal joint- herbedens nodes
proximal joint- bouchards nodes
61
Gout
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
endocrine: hypofunction
absence or impaired development of a gland or deficiency of an enzyme needed for hormone synthesis
63
endocrine: hyperfunction
excessive hormone production results from excessive stimulation and hyperplasia of endocrine gland
64
endocrine: paraneoplastic syndrome
excess production from abnormal ectopic production of hormone by a malignant tumor
ex: bronchogenic tumors releasing ADH
65
endocrine dysfunction:
may occur due to hormone resitance or receptor defects
66
endocrine: primary disorders
-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
endocrine: secondary disorders
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
pituitary gland disorders
-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
hypopituitary
diabetes insipidus (low ADH)
70
hyper pituitary
SIADH(symptom of inappropriate ADH: excessive ADH)
Cushing syndrome
71
ACTH (anterior pituitary)
-controls release of cortisol from adrenal gland
72
TSH (anterior pituitrary)
-diagnostic
-controls release of thyroid hormone from the thyroid gland
73
ADH (posterior pituitary)
74
assessment of pituitary function
serum cortisol, serum thyroxine and TSH, plasma osmolality, urine osmolality, MRI (osmolality is concentration)
75
The thyroid gland
a shield shaped gland that secretes triiodothyronine, and thyroxine (T3, T4)
76
Thyroid hormone
the regulator of the body metabolism that influences almost every body system
77
Thyroid diagnosis
T3, t4, TSH, ultrasound, CT, MRI
78
thyroid actions
increases MBR, CV, GI, NM function
79
hypothyroidism etiology
radiation, surgical removal
-lithium
-iodine deficiency
80
hypothyroidism pathophysiology
-Hashimoto's: autoimmune destruction of thyroid gland
-TH receptor antibodies present
81
hypothyroidism manifestations
-decrease metabolic activities
-cold intolerance
-weight gain
-lethargy
-puffy face
-hair loss
-weakness
-constipation, abdominal distention
-bradycardia
82
hypothyroidism diagnosis
primary hypothyroidism: low hormone secretions by the thyroid gland that constantly signals pituitary to secrete TSH
-High TSH, low T3T4
83
hypothyroidism complications
-Myxedema coma (severe hypothyroidism): hypothermia, CV collapse, hyponatremia, hypoglycemia, lactic acidosis
84
hyperthyroidism etiology
autoimmune: Graves
-hyperthyroidism, Goiter, ophthalmopathy
85
Hyperthyroidism diagnosis
High T3T4, low TSH
86
Hyperthyroidism patho
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
Hyperthyroidism manifestations
-nervousness
-tachycardia, palpitations, afib
-weight loss
-sensitivity to heat
-Goiter
-exophthalmos
88
hyperthyroid manifestations: Graves ophthalmopathy
-periorbital edema and bulging eyes
-wide eyed stare
women more than men
89
hyperthyroidism complication
-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
Adrenal gland: cortex
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
Adrenal gland: medulla
secretes epinephrine and NE
92
Mineralocorticoids
-regulate potassium, sodium, water balance
-ALDOSTERONE (RAAS)
excess aldosterone= low potassium, muscle weakness
deficient aldosterone= hyperkalemia, cardiac toxic
93
glucocorticoids
-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
primary adrenal insufficiency etiology
-Addison disease
-autoimmune destruction of adrenal glands
-adrenal hemorrhage
-stress induced
-withdrawal of exogenous glucocorticoid replacement
-TB
95
Primary adrenal insufficiency manifestations
decreased production of adrenal cortical hormones, increase ACTH, mineralocorticoid and glucocorticoid deficiency, HYPERKALEMIA, HYPONATREMIA., HYPOGLYCEMIA
- decrease CO, FVD, weakness, fatigue
-hyperpigmentation-bronzed/tan
96
secondary adrenal insufficiency
pituitary gland surgically removed
-rapid withdrawal of glucocorticoids
-supresses the HPA system-resulting adrenal corticoid atrophy and loss of cortisol production
97
adrenal crisis
life threatening, exposure to a stressor
98
clinical manifestations of adrenal insufficiency
-anorexia, weight loss, fatigue, GI issues, myalgia, arthralgia, hyponatremia, hyperkalemia, hyperpigmentation, secondary deficiencies in testost, growth hormone, thyroxine, ADH
99
glucocorticoid excess etiology
-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
glucocorticoid excess
-hypokalemia, HTN, increase risk of infections, emotional instability
101
glucocorticoid excess manifestations
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
Antidiuretic hormone
-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
Diabetes insipidus
-caused by a deficiency or a decreased response to ADH
-central: lack of secretion (posterior)
-nephrogenic: kidneys failure to respond to ADH
104
diabetes insipidus etiology
brain tumor, head trauma, pituitary surgery, nephrotoxic drugs, ischemia of kidney
105
DI patho
-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
DI manifestations
-frequent dilute urine, thirst/dehyrdation, confusion, disorientation, seizures, coma
107
DI diagnosis
-serum osmolality (high)
-serum sodium (hypernatremia: due to water loss)
-urine osmolality (hypo: dilute)
108
syndrome of inappropriate ADH etiology
-stroke, meningitis, lung/brain cancer, emphysema, pain, HIV
109
SIADH patho
-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
SIADH clinical manifestations
-fluid volume overload
-hyponatremia
-fatigue
-weakness
-confusion
111
SIADH diagnosis
serum osmolality: hypoosmolar (low)
serum sodium (hypo)
urine osmolality (hyper)
112
diabetes mellitus
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
DM classification: type 1
autoantibody destruction of insulin secreting beta cells
114
DM: type 2
cellular resistance to insulin with or without pancreatic beta cell exhaustion
115
DM: Prediabetics
-blood glucose is elevated but doesn't meet threshold for DM
116
Other DM
gestations (2-3 tri), genetic, maturity, pancreatic disease, drugs
117
diabetes manifestations classic triad
polydipsia: thirst
polyuria: peeing
polyphagia: appetite
118
diabetes manifestations others
glycosuria, weight loss, blurred vision, fatigue, skin infections
119
type 1 diabetes etiology
-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
type 2 DM
90% of cases
-genetics
-more in older adults, but slowly become more common in youngs
-obesity
121
type 2 patho
insulin resitance
-deranged secretion of insulin by beta cells
-increased glucose production by liver
122
type 1
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
type 2
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
metabolic syndrome
obestity, apple shaped, elevated glucose, dyslipidemia, evevated triglycerides, low HDL, HTN, atherosclerosis
125
DM acute complications
hyperglycemia, hypoglycemia, DKA, type 2: hyperosmolar hyperglycemia syndrome
126
diabetic ketoacidosis etiology
stress, infection, omission or inadequate use of insulin (type 1)
127
diabetic ketoacidosis manifestations
osmotic diuresis, dehydration, fatigue, coma, abdominal pain, fruity breath, tachycardia, kussmaul respiration
128
diabetic ketoacidosis patho
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
diabetic ketoacidosis metabolic dearangments
hyperglycemia, ketosis, metabolic acidosis
130
hyperosmolar hyperglycemia state (type 2) patho
-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
hyperosmolar hyperglycemia state (type 2) manifestations
weakness, dehyrdation, polyuria, neurological alterations, hemiaparesis, seizures, coma, excessive thirst
NO ACIDOSIS
hyperglycemia, dehydration
132
hypoglycemia
blood glucose less than 70
-with or without symptoms: error in insulin dose, not eating, increased exercise, meds, change in injection site, alcohol
133
