Csd Ii Final

Front 1

what is the main problem in occlusive artery disease?

Back 1

Diminished perfusion

Front 2

what are three possible causes of diminished perfusion in occlusive arterial disease?

Back 2

(1) atherosclerosis
(2) thrombosis
(3) embolization

Front 3

what is the progression of endothelial dysfunction in occlusive arterial disease?

Back 3

foam cells-->fatty streak-->intermediate lesion-->atheroma-->fibrous plaque-->complicated lesion/rupture

Front 4

what is one of the largest risk factors for occlusive arterial disease?

Back 4

SMOKING

Front 5

what type of problem is vascular disease?

Back 5

systemic problem

Front 6

what are the three types of peripheral vascular disease?

Back 6

(1) arterial disease
(2) venous/lymphatic disease
(3) thoracic outlet obstruction

Front 7

what two vessels are occluded cerebrovascular disease?

Back 7

carotid arteries and vertebral arteries

Front 8

these arteries are the vessels that serve the anterior brain; serve motor and sensory cortex, frontal lobes, and are the most commonly diseased in cerebrovascular disease

Back 8

carotid

Front 9

these arteries serve the posterior portion of the brain, and symptoms of occlusion include loss of sight/balance/awareness

Back 9

vertebral

Front 10

what are two ways that a carotid plaque can cause a stroke?

Back 10

(1) arterial thromboembolism (platelet aggregates associated with obstructing plaque)
(2) hemodynamic compromise

Front 11

what is the number one cause of embolic stroke?

Back 11

carotid artery disease

Front 12

what are two treatments for people with carotid artery disease if greater than 50% of the artery is blocked?

Back 12

(1) carotid endarterectomy
(2) carotid angioplasty and stenting

Front 13

if there is a compromise of the hypoglossal nerve during carotid artery surgery, what will the tongue display?

Back 13

tongue will point to the side operated on

Front 14

if there is a compromise of the vagus nerve during carotid artery surgery, what will the patient have issues with?

Back 14

vocal cord issues (recurrent laryngeal nerve)

Front 15

in this syndrome, exercise of the ipsilateral (typically left) arm results in dizziness an in extreme cases, syncope

Back 15

subclavian steal syndrome (SSS)

Front 16

what are three signs/symptoms of chronic arterial insufficiency in LE arterial disease?

Back 16

(1) claudication
(2) rest pain
(3) gangrene/tissue loss

Front 17

what are two signs/symptoms of acute arterial insufficiency in LE arterial disease?

Back 17

(1) the cold foot
(2) distal emboli

Front 18

this is pain and cramping in a muscle group which is inducible with exercise and relieves promptly with rest; patient will sometimes describe heaviness and discomfort. Most commonly occurs in calf musculature

Back 18

claudication

Front 19

this type of claudication is when there is marginal arterial supply with exercise; the skin of foot is frequently dry but intact, and there is typically very little hair below mid lower leg

Back 19

intermittent

Front 20

what are some possible interventions for claudication?

Back 20

(1) smoking cessation
(2) diet
(3) activity
(4) pharmacologic intervention
(5) surgical intervention

Front 21

this is pain in the foot that occurs at rest, but is alleviate with dependency (because gravity helps perfusion)

Back 21

rest pain

Front 22

in this type of pain, there is marginal arterial perfusion to the foot; pain is usually in the disatl foot, particularly over the top, and it will have poor color when elevated, but become bright red when dependent

Back 22

rest pain

Front 23

this is caused by severe arterial insufficiency such that the most distal tissue become nonviable

Back 23

gangrene/tissue loss

Front 24

what four signs/symptoms must be present for someone to have acute ischemia?

Back 24

The four P's
(1) pain
(2) pulselessness
(3) pallor
(4) paresthesias

Front 25

what are the two types of occlusions in acute ischemia?

Back 25

(1) aortoiliac
(2) infrainguinal

Front 26

what type of acute ischemia is the most common?

Back 26

infrainguinal

Front 27

this type of acute ischemic occlusion is very rare, and presents with limb ischemia, acute abdominal pain, and it is extremely deadly (52% operative mortality)

Back 27

aortoiliac occlusion

Front 28

this type of acute ischemia is more common and often embolic; prognosis is good if it is treated early, and can be caused by atrial fibrillation (embolism from the heart to the leg)

Back 28

infrainguinal occlusion

Front 29

this vascular tree is located above the inguinal ligament

Back 29

inflow

Front 30

this vascular tree is located from the inguinal ligament to the knee

Back 30

outflow

Front 31

this vascular tree is located below the knee (diabetics often have complications here)

Back 31

run-off

Front 32

how many different levels of disease are there in the lower extremity vascular tree, and what are their names?

Back 32

three
inflow, outflow, and runoff

Front 33

in order to palpate a distal pulse, what is the required blood pressure?

Back 33

80-100 mm Hg systolic

Front 34

this is the ratio of blood pressurein the tibial arteries to the blood pressure in the arm

Back 34

ankle-brachial index

Front 35

what are the three imaging tests that are used to see vasculature?

Back 35

angiography, CT, MRI

Front 36

what are the two open surgical procedures used to treat vascular disease?

Back 36

(1) bypass
(2) endarterectomy

Front 37

what are the two endoluminal surgical procedures used to treat vascular disease?

Back 37

(1) angioplasty
(2) stenting

Front 38

what are two bypass options for increasing inflow?

Back 38

(1) blood flow to legs provided by axillary artery
(2) bifemoral bypass graft

Front 39

what is a possible option for improving outflow and runoff?

Back 39

venous bypass graft (connect harvested vein to arterial tree)

Front 40

this disease is defined as a 50% or greater increase in the diameter of the aorta

Back 40

abdominal aortic aneurysm

Front 41

what is the most common location for an abdominal aortic aneurysm?

Back 41

infrarenal

Front 42

are false or true abdominal aortic aneurysms more frequent?

Back 42

true

Front 43

what is the ratio of incidence of abdominal aortic aneurysm in males and females?

Back 43

4:1 males to females

Front 44

what is the average growth rate of abdominal aortic aneurysms that are less than 5 cm?

Back 44

.2-.4 cm /year

Front 45

the risk for rupture of an abdominal aortic aneurysm increases exponentially above what size?

Back 45

5.5 cm

Front 46

what is the principal problem in an abdominal aortic aneurysm?

Back 46

medial layer (elastic media) of the vessel falls apart

Front 47

what is the classic triad of symptoms for a rupture of an abdominal aortic aneurysm?

Back 47

(1) abdominal/ back pain
(2) hypotension
(3) pulsatile mass

Front 48

this type of repair of an AAA uses a balloon to place stents in an aortic graft

Back 48

endovascular repair

Front 49

which is the most common type of throacoabdominal aneurysm?

Back 49

Type II

Front 50

this is a tear into the aortic wall from blood pressure, leaving a weakened wall, and can potentially develop into an aneurysm

Back 50

aortic dissection

Front 51

this type of aortic dissection is very fatal and needs to be fixed rapidly because it will disrupt the coronary arteries

Back 51

Type A

Front 52

this type of aortic dissection is uncomplicated, and there is no operation needed

Back 52

type B

Front 53

what artery in the LE is completely aneurysm-resistant?

Back 53

external iliac artery

Front 54

what type of veins would have the most pressure with venous insufficiency?

Back 54

perforating veins

Front 55

what are two consequences of venous insufficiency?

Back 55

(1) engorged superficial veins (telangectasias (spider veins) and varicose veins)
(2) chronic venous hypertension (pain, hyperpigmentation, ulceration)

Front 56

what are three signs of chronic venous hypertension?

Back 56

(1) pain
(2) hyperpigmentation
(3) ulceration

Front 57

what is the most common thoracic outlet syndrome?

Back 57

neurogenic

Front 58

what is the least common thoracic outlet syndrome?

Back 58

arterial

Front 59

this syndrome is a compression of neurovascular structures in the thoracic outlet, causing signs and symptoms in the associated arm; majority are due to nerve compression, with relatively infrequent venous or arterial causes

Back 59

thoracic outlet syndrome

Front 60

what are seven symptoms of arterial thoracic outlet syndrome?

Back 60

(1) diminished pulses
(2) subclavian bruit
(3) pale/cool extremity
(4) fatigues rapidly with exercise
(5) pulsatile mass
(6) blue digit syndrome
(7) Raynaud's syndrome

Front 61

what are five symptoms of venous thoracic outlet syndrome?

Back 61

(1) swelling
(2) tenderness
(3) congestion
(4) distended collaterals
(5) cyanosis

Front 62

what are five symptoms of neurogenic thoracic outlet syndrome?

Back 62

(1) intermittent/vague symptoms
(2) progressive pain, paresthesias and weakness in neck, shoulder, an dhand
(3) headachers
(4) exacerbation by posture/activities
(5) muscle atrophy at end stage

Front 63

what are the four surgical interventions for thoracic outlet syndrome?

Back 63

(1) anterior and middle scalenectomy
(2) brachial plexus neurolysis
(3) first rib resection
(4) vascular reconstruction

Front 64

what part of the kidney prepares an ultrafiltrate of plasma with charge and size selectivity?

Back 64

glomeruli

Front 65

what part of the kidney adjusts the ultrafiltrate to maintain volume and electrolyt ehomeostasis, and also provides various metabolic functions (secretes erythropoeitin, vitamin D metabolism, drug metabolism and excretion)

Back 65

renal tubules

Front 66

what "type" of disease is renal failure?

Back 66

systemic

Front 67

this is a clinical syndrome of rapid decline in renal function over hours to several weeks; usually an ischemic problem that is reversible over days to weeks

Back 67

acute renal failure

Front 68

this type of renal failure is a clinical syndrome of gradual decline of renal function over months to year; usually a fibrotic scarring process that is irreversible

Back 68

chronic renal failure

Front 69

in acute renal failure, is the urine output normal or decreased?

Back 69

decreased or absent

Front 70

what are some common causes of acute renal failure?

Back 70

ischemia (low BP), drugs, toxins

Front 71

what are some common causes of chronic renal failure?

Back 71

diabetes, hypertension, autoimmune diseases, inherited diseases

Front 72

in chronic renal failure, is the urine output normal or decreased?

Back 72

normal

Front 73

what is the overall mortality rate of acute renal failure?

Back 73

50%

Front 74

in acute renal failure, what is most likely the cause of death?

Back 74

most frequently due to the underlying disorder, but kidney failure impacts this mortality

Front 75

about how much of the plasma ultrafiltrate in the renal tubules becomes reabsorbed?

Back 75

99%

Front 76

about how much of the plasma ultrafiltrate in the renal tubules becomes excreted in the urine?

Back 76

1%

Front 77

this is a concept of how much blood would be purified by the kidney over a period of time; value is standardized to body surface area to correct for different body composition

Back 77

glomerular filtration rate (GRF)

Front 78

what is the normal glomerular filtration rate?

Back 78

80-120 mL/min/1.73 m3

Front 79

what is the most common compound used to estimate glomerular filtration rate?

Back 79

creatinine

Front 80

in this phase of chronic kidney disease, a person has kidney damage with normal GFR (>/= 90)

Back 80

stage 1

Front 81

in this phase of chronic kidney disease, a perosn has a mild decrease in GFR (60-89)

Back 81

stage 2

Front 82

in this phase of chronic kidney disease, a person has a moderate drop in GFR (30-59)

Back 82

stage 3

Front 83

in this phase of chronic kidney disease, a person has a severe drop in GFR (15-29)

Back 83

stage 4

Front 84

in this phase of chronic kidney disease, a person has kidney failure and the GFR is <15

Back 84

stage 5

Front 85

diabetic nephropathy occurs in __% of both type I and type II diabetics

Back 85

30%

Front 86

what are the three functional changes in someone with diabetic nephropathy?

Back 86

(1) increase in GFR
(2) reverse albuminuria
(3) increase in kidney size

Front 87

what are the four predictors of diabetic nephropathy?

Back 87

(1) hyperfiltration
(2) microalbuminuria
(3) rising blood pressure
(4) poor glycemic control

Front 88

what are the two structural changes that occur to the kidney in diabetes?

Back 88

(1) increase in glomerular basement membrane thickening
(2) mesangial expansion

Front 89

this disease of the kidney is an inflammation of the structures (capillary endothelial cell, glomerular epithelial cell, mesangium, and basement membrane) in the glomeruli of the kidney

Back 89

glomerulonephritis

Front 90

what are two secondary causes of glomerulonephritis?

Back 90

lupus and hepatitis C

Front 91

this kidney disease is caused by a mutation in either the polycystin 1 or polycystin 2 gene; renal failure occurs in the 4th-5th decade; is the second most common kidney mutation

Back 91

autosomal dominant polycystic kidney disease

Front 92

this kidney disease is a genetic disorder in type four collagen found in the ear, eye, and kidney

Back 92

X-linked hereditary nephritis (Alport's syndrome)

Front 93

this is the incompetence of urethral valves leading to backflow from the bladder to the kidney; there is pressure damage, recurrent infections causing scarring

Back 93

reflux nephropathy

Front 94

what are the five common electrolyte disturbances in chronic kidney disease?

Back 94

(1) potassium
(2) calcium
(3) phosphorus
(4) sodium
(5) magnesium

Front 95

what disease can cause chronic kidney disease by increasing parathyroid hormone, increasing phosphate, and decreasing calcium?

Back 95

secondary hyperparathyroidism

Front 96

if parathyroid hormone is too low in patients with kidney disease, what will they develop?

Back 96

adynamic bone disease (osteoporosis)

Front 97

there is a high incidence of deficiency and insufficiency of what mineral in patients with hyperparathyroidism and resulting kidney disease?

Back 97

vitamin D

Front 98

what vascular problem develops with renal failure?

Back 98

anemia

Front 99

people born with less nephrons are more likely to have what disease?

Back 99

hypertension

Front 100

what metabolic problem often accompanies uremia (chronic kidney failure) because of the inability of the damaged kidney to augment renal ammoniagenesis?

Back 100

metabolic acidosis

Front 101

what are the adverse effects of metabolic acidosis on muscle?

Back 101

increases proteolysis, and increased cortisol, causing a decrease in lean body mass

Front 102

what are the adverse effects of metabolic acidosis on bone?

Back 102

decreased osteoblast activity, increased osteoclast activity (causes dissolution of bony matrix, physiochemical dissolution of bone mineral)

Front 103

what are the adverse effects of metabolic acidosis on the endocrine system?

Back 103

increase in PTH
decrease in Vitamin D
increase in cortisol
decrease in thyroxine
decrease in growth hormone and receptor
increase in insulin resistance

Front 104

what is the most common vascular access for hemodialysis of the kidneys?

Back 104

native arteriovenous fistula

Front 105

what is another way to get vascular access for hemodialysis of the kidneys, instead of naturally?

Back 105

polytetrafluroethylene graft (AV graft)

Front 106

this structure for hemodialysis forms a subcutaneous tunnel to the internal jugular vein and right atrium with a cuff; if rarely lasts greater than 1 year, has a low flow, and has a greater infection rate

Back 106

hemodialysis venous catheter

Front 107

the complications of dialysis are replaced by the complications of __ after kidney transplantation

Back 107

immunosuppression

Front 108

what is the current average transplant function for a cadaveric kidney?

Back 108

8-10 years

Front 109

what is the current transplant function for a living kidney?

Back 109

12-15 years

Front 110

what are six things taken into account when assessing a patient with kidney failure?

Back 110

(1) type of kidney disease and previous treatment
(2) current level of kidney function
(3) type of dialysis, length, access, and problems
(4) complications of kidney failure
(5) medications
(6) lab values

Front 111

what is the pathophysiology of deconditioning in renal failure?

Back 111

uremic myopathy

Front 112

what are six cellular mechanisms of muscle dysfunction in uremia?

Back 112

(1) decreased muscle protein synthesis and/or amino acid derangements
(2) impaired calcium flux by the sarcoplasmic reticulum
(3) skeletal muscle insulin resistance
(4) reduced intracellular inorganic phosphate
(5) reduced actomyosin ATPase
(6) numerous abnormal hormone responses

Front 113

what type of muscle fibers are slow twitch and are involved in tonic contracture and maintenance of posture?

Back 113

type I

Front 114

what type of muscle fibers are fast twitch and are involved in basic movement?

Back 114

type II

Front 115

what are six possible treatments of uremic myopathy?

Back 115

(1) androgen
(2) L-carnitine
(3) growth hormone
(4) vitamin D insufficiency
(5) exercise
(6) more dialysis

Front 116

this type of therapy in kidney patients improved their walking time, stair climbing, and lean body mass without significant changes in peak oxygen consumption or grip strength

Back 116

androgens

Front 117

this type of treatment in kidney disease acts as a shuttle across the mitochondria for fatty acid oxidation

Back 117

L-carnitine

Front 118

improving physical function in chronic kidney disease requires complete care in the form of what six things?

Back 118

(1) adequate dialysis
(2) adequate nutrition
(3) diabetic care (eyes, feet, heart, joints, etc)
(4) tobacco cessation
(5) hypertension control
(6) compliance (phosphorus, interdialytic weight gain)

Front 119

the function of this structure is to convert cholesterol into steriod hormones

Back 119

adrenal cortex

Front 120

what are the three classes of adrenocortical hormones?

Back 120

(1) glucocorticoids
(2) mineralocorticoids
(3) androgen precursors

Front 121

what are the six effects of glucocorticoids?

Back 121

(1) maintain homeostasis
(2) increase gluconeogenesis
(3) insulin resistance
(4) increase protein catabolism
(5) suppress inflammation and immune responses
(6) maintain vascular response to catecholamines

Front 122

levels of this hormone cycle with the circadian rhythm; they are low at night, then begin secreting at 4:00 am and give a big secretion first thing in the morning to "rev" you up

Back 122

cortisol

Front 123

what are the five effects of mineralocorticoids?

Back 123

(1) control salt and water balance at kidney
(2) stimulate distal renal tubules to reabsorb sodium from tubular fluid
(3) excrete more potassium and hydrogen ions
(4) increase open sodium and potassium channels in luminal membrane of tubular cells
(5) increase synthesis of basolateral membrane Na/K ATPase

Front 124

what structure in the kidney senses blood pressure, and if it is low, it begins the renin-angiotensin-aldosterone axis?

Back 124

juxtaglomerular apparatus

Front 125

what is the chain of events that occurs in the kidney/adrenal cortex if the juxtaglomerular apparatus senses a low blood pressure?

Back 125

renin-->angiotensin II-->adrenal cortex-->aldosterone-->kidney-->increase sodium-->increase BP

Front 126

what are the three causes of glucocorticoid excess?

Back 126

(1) iatrogenic (steroid use long term)
(2) ACTH excess (pituitary tumor producing it, or ectopic secretion)
(3) adrenocortical tumor making cortisol without regulation

Front 127

what are the two major causes of ACTH dependent Cushing's syndrome?

Back 127

pituitary adenoma
ectopic ACTH syndrome

Front 128

this syndrome is when there is too much glucocorticoid

Back 128

Cushing's syndrome

Front 129

what are the two major causes of ACTH independent Cushing's syndrome?

Back 129

adrenal adenoma
adrenal carcinoma

Front 130

a tumor in this gland will cause too much ACTH secretion, which shuts down the gland and ACTH will not stop being secreted

Back 130

pituitary adenoma

Front 131

what are seven effects that a cortisol excess has on the body?

Back 131

(1) increased appetite
(2) depression/psychiatric disorders
(3) hypertension
(4) muscle weakness/atrophy proximally
(5) easy bruishing, striae
(6) osteoporosis (interferes with Ca absorption)
(7) hyperglycemia

Front 132

what are 7 more specific findings in Cushing's syndrome (excess cortisol/glucocortisoid)?

Back 132

(1) thin skin
(2) easy bruising
(3) red striae
(4) facial plethora (red and puffy)
(5) muscle weakness
(6) osteoporosis
(7) growth failure (childhood cushing's)

Front 133

what are the two common screening tests for Cushing's syndrome?

Back 133

(1) overnight dexamethosone suppression test
(2) 24 hour urine cortisol

Front 134

what are the two standard tests for differential diagnosis of Cushing's syndrome?

Back 134

(1) high dose dexamethosone suppression test
(2) plasma ACTH test

Front 135

what hormone increases with increased ACTH production and changes skin color to darker?

Back 135

melanocyte stimulating hormone

Front 136

this syndrome occurs in a patient in which you remove both adrenal glands from having a pituitary tumor producing ACTH, and their skin becomes increasingly pigmented

Back 136

Nelson's syndrome

Front 137

what are the two common causes of glucocorticoid deficiency?

Back 137

(1) primary adrenal failure
(2) ACTH deficiency (secondary adrenal failure)

Front 138

what are the levels of cortisol, aldosterone, and ACTH in primary adrenal failure?

Back 138

cortisol and aldosterone both deficient, ACTH levels high

Front 139

what are the levels of cortisol, aldosterone and ACTH in ACTH deficiency (secondary renal failure)?

Back 139

cortisol and ACTH deficient, aldosterone NOT deficient

Front 140

this type of renal failure occurs when the adrenal gland is not functioning correctly (problem of adrenal gland)

Back 140

primary

Front 141

this type of renal failure occurs when there is not enough cortisol to stimulate the pituitary gland, so it atrophies (problem of pituitary gland/hypothalamus)

Back 141

secondary

Front 142

what are five clinical findings in primary and secondary renal failure (cortisol deficiency)?

Back 142

(1) weakness, fatigue, decreased BP
(2) anorexia, nausea, weight loss
(3) hyponatremia
(4) hypotension
(5) shock and death

Front 143

what are the two clinical findings that are in primary renal failure ONLY?

Back 143

(1) hyperkalemia, dehydration
(2) hyperpigmentation

Front 144

what are two diagnostic tests for adrenal failure?

Back 144

(1) cortrosyn (synthetic ACTH) stimulation test
(2) insulin induced hypoglycemia (to stress the hypothalamus)

Front 145

what are the two treatments for primary adrenal insufficiency?

Back 145

(1) glucocorticoid replacement (prednisone)
(2) mineralocorticoid replacement (fludrocortisone)

Front 146

what is the primary treatment for secondary adrenal insufficiency?

Back 146

glucocorticoid replacement

Front 147

what are the two symptoms in excess mineralocorticoids?

Back 147

(1) hypertension (increase in sodium)
(2) hypokalemic alkalosis (low blood potassium, high blood pH)

Front 148

what are the three symptoms in deficiency of mineralocorticoids?

Back 148

(1) volume depletion
(2) hypotension
(3) hyperkalemic acidosis

Front 149

what is the primary cause primary aldosteronism?

Back 149

aldosterone producing adenoma

Front 150

this type of hyperaldosteronism is when there is a tumor that is making excess aldosterone; it causes increased retention and therefore increased blood pressure in the kidney and ECF expansion

Back 150

primary

Front 151

this type of hyperaldosteronism occurs when there is decreased perfusion to the kidney, so renin is released, which makes angiotensin II which stimulates the adrenal gland to make aldosterone and the cycle continues

Back 151

secondary

Front 152

what is the screening test used for primary hyperaldosteronism?

Back 152

plasma potassium while not treated with diuretics

Front 153

whatare the two definitive tests to diagnose primary hyperaldosteronism?

Back 153

(1) plasma aldosterone/plasma renin activity ratio
(2) aldosterone supression (large dose of Na and H2O)

Front 154

adrenal androgens are the precursors for what molecules?

Back 154

major androgens: testosterone, DHT

Front 155

what are the two weak androgens?

Back 155

androstenedione and DHEA

Front 156

what are two things caused by excess adrenal androgens?

Back 156

(1) premature puberty
(2) hirsutism (in adult women)

Front 157

what are two things caused by deficiency in adrenal androgens?

Back 157

(1 ) no effect in men
(2) decreased axillary and pubic hair in women with decreased ovarian androgens (classic sign in Sheehan's syndrome)

Front 158

this is a family of disorders produced by enzymatic deficiencies of adrenal steroidogenesis and are transmitted as autosomal recessive traits

Back 158

congenital adrenal hyperplasia

Front 159

the oversecretion of steroid precursors of cortial synthesis leads to what two abnormalities in congenital adrenal hyperplasia?

Back 159

(1) excessive synthesis of the steroid precursors proximal to the enzyme defect
(2) accumulation of the products of those adrenal hormones whose synthesis is unimpaired by the enzyme deficiency

Front 160

in this disease, androgen excess leads to ambiguous genitalia in females and precocious sexual development in males; accelerated growth in both sexes, advancement of bone age, and early closure of epiphyses and ultimate short stature

Back 160

21 hydroxylase deficiency

Front 161

thi sis a block leading to androgen excess and accumulation of 11-deoxycortisone; ambiguous genitalie in females, sodium retention and hypertension

Back 161

11 beta hydroxylase deficiency

Front 162

what are the six risk factors for osteoarthritis?

Back 162

(1) AGE
(2) obesity
(3) bending occupations
(4) female sex
(5) heredity
(6) joint trauma

Front 163

what are the eight joints of the body that have primary osteoarthritis?

Back 163

(1) lower cervical spine
(2) AC joint
(3) first CMC joint
(4) PIP and DIP joints
(5) lower lumbar spine
(6) hip
(7) knee
(8) first MTP joint

Front 164

what are the six signs and symptoms of osteoarthritis?

Back 164

(1) pain with joint use, relieved with rest
(2) reduced joint ROM
(3) mild morning stiffness
(4) bony swelling
(5) little if any joint effusion
(6) joint crepitation

Front 165

this analgesic for osteoarthritis is centrally acting (binds to opioid receptors, inhibits serotonin and norepi reuptake), may be added to nsaids, but may cause dizziness, seizures, and nausea

Back 165

tramadol

Front 166

what are four types of opioid analgesics?

Back 166

(1) codeine
(2) hydrocodone
(3) oxycodone (oxycontin)
(4) fentanyl (duragesic patch)

Front 167

what are three possible side effects of taking opioids for analgesics?

Back 167

(1) dizziness
(2) sedation
(3) constipation

Front 168

this drug is approved for osteoarthritis of the knees and is administered in three weekly injections; relief comparable to naproxen, and benefit may last 6-9 months

Back 168

intraarticular hyaluronans

Front 169

what is the water content of normal cartilage?

Back 169

65-80%

Front 170

what is the calcium salt content of normal cartilage?

Back 170

5%

Front 171

what two proteins make up the rest of normal cartilage (besides water and calcium salt)?

Back 171

proteoglycans and type II collagen

Front 172

this type of material dissipiates force by compressibility and elasticity (tissue deforms gradually and reversibly); protects underlying bone from friction

Back 172

normal cartilage

Front 173

this is the predominant proteoglycan of cartilage (90%); is hydrophylic and allows it to undergo deformation

Back 173

aggrecan

Front 174

this is a compound in cartilage that is extraellular, linear, and unsulfated; binds aggrecan via a link protein, resulting in aggregation

Back 174

hyaluronan

Front 175

both of these substances are deficient and damaged in osteoarthritis

Back 175

aggrecan and hyaluronan

Front 176

it was shown in a study that joint space narrowing in osteoarthritis progressed more slowly when treated with what compound?

Back 176

glucosamine

Front 177

this is a progressive, systemic, inflammatory disorder with an unknown etiology characterized by symmetric synovitis, joint erosions, and multisystem extraarticular manifestations

Back 177

rheumatoid arthritis

Front 178

what are the three things that characterize rheumatoid arthritis?

Back 178

(1) symmetric synovitis
(2) joint erosions
(3) multisystem extra-articular manifestations

Front 179

what is the target population for the ACR classification criteria for rheumatoid arthritis in 2010?

Back 179

patients who have at least 1 joint synovitis, and with synovitis not explained by another disease

Front 180

a score of > or = __ out of 10 is needed for classification of a patient to have definite rheumatoid arthritis on the ACR classification test

Back 180

6

Front 181

definite rheumatoid arthritis is based on what two things?

Back 181

(1) confirmed presence of synovitis of at least one joint
(2) absence of alternative diagnosis that better explains that synovitis

Front 182

an achievement of a total score of >/= 6/10 on the ACR classification criteria for rheumatoid arthritis is based on what four things?

Back 182

(1) number and site of involved joints (0-5)
(2) serologic abnormality (0-3)
(3) elevated acute phase response (0-1)
(4) symptom duration (0-1)

Front 183

rheumatoid arthritis affects --% of the U.S. population

Back 183

1%

Front 184

what is the ratio of women to men that get rheumatoid arthritis?

Back 184

3:1

Front 185

what are 6 risk factors for a poor outcome for someone that has rheumatoid arthritis?

Back 185

(1) high titer rheumatoid factor
(2) nodules
(3) early erosions
(4) low education level
(5) low SES
(6) low functional status

Front 186

what are the five common drugs used in rheumatoid arthritis?

Back 186

(1) methotrexate
(2) sulfasalazine
(3) hydroxychloroquine
(4) leflunomide
(5) TNF blockers

Front 187

what are five reasons for intervening early with treatment for rheumatoid arthritis?

Back 187

(1) radiologic erosions develop in first few years of disease
(2) number of joints involved is maximal in early disease
(3) inflammation is greatest at disease onset
(4) once functional deterioration has occurred, very difficult to reverse
(5) waiting until NSAIDs prove ineffective delays inflammation suppression

Front 188

what are three TNF blocking agents?

Back 188

(1) Enbrel
(2) remicade
(3) humira

Front 189

what are five of the differences of juvenile chronic polyarthritis from rheumatoid arthritis?

Back 189

(1) occurs before the age of 16
(2) large joints>small joints
(3) less pain in the joints
(4) nodules and rheumatoid factor uncommon
(5) nonarticular symptoms (failure to grow, low grade fever, regression to infantile behavior)

Front 190

what is the ratio of female to male in juvenile chronic polyarthritis?

Back 190

2:1

Front 191

juvenile rheumatoid arthritis usually occurs in what age range?

Back 191

1-3 years

Front 192

__% of children with juvenile rheumatoid arthritis are positive for antinuclear antibody (ANA)

Back 192

40%

Front 193

__% of children with juvenile rheumatoid arthritis are positive for rheumatoid factor

Back 193

25%

Front 194

what are the four differences in children who have rheumatoid factor in juvenile rheumatoid arthritis as compared with children who do not?

Back 194

(1) later onset
(2) polyarthritis
(3) radiographic damage
(4) persistence into adulthood

Front 195

about __% of children with juvenile rheumatoid arthritis exhibit an oligoarticular pattern, with just knees and ankles affected

Back 195

60%

Front 196

this is a severe complication from juvenile rheumatoid arthritis that causes swelling in the eye that can produce glaucoma and visual loss (usually occurs in young girls with positive ANA)

Back 196

chronic uveitis

Front 197

about __% of children with juvenile rheumatoid arthritis exhibit at polyarticular pattern, with especially larger joints involved, and smaller involvement can resemble rheumatoid arthritis

Back 197

30%

Front 198

this pattern of juvenile rheumatoid arthritis affects especially large joints, and small joints affected can resemble RA; usually symmetric, low grade fever, and may persist into adulthood, especially with a positive RA factor

Back 198

polyarticular

Front 199

this pattern of jeuvenile rheumatoid arthritis is with a high spiking daily fever, anemia, rash, enlarged liver,, spleen, lymph nodes, joint involvement variable, pericarditis, and persistent severe arthritis developed in about half

Back 199

systemic pattern

Front 200

about __% of children with juvenile RA exhibit a systemic pattern

Back 200

10%

Front 201

what are the five agents used to treat juvenile RA (that are basically the same as used to treat for adult RA)?

Back 201

(1) NSAIDs
(2) prednisone
(3) methotrexate
(4) hydrochloroquine
(5) TNF blockers

Front 202

what are five characteristics of back pain in ankylosing spondylitis?

Back 202

(1) onset of back discomfort before age 40
(2) insidious onset
(3) duration longer than three months
(4) associated with morning stiffness
(5) improvement with exercise

Front 203

this describes the site where ligaments or tendons join bone

Back 203

enthesis

Front 204

this is the fundamental bony pathology in the spondylarthropathies seen in arthritis

Back 204

enthesitis

Front 205

what are the four common tendons/areas that are affected by enthesitis in spondyloarthropathies?

Back 205

(1) Achilles tendinitis
(2) plantar fascitis
(3) bamboo spine
(4) sausage digits (dactylitis)

Front 206

this is the type of arthritis that develops in someone with psoriasis

Back 206

psoriatic arthritis

Front 207

psoriasis usually precedes onset of psoriatic arthritis by an average of 10 years in about __% of people

Back 207

70%

Front 208

what are five patterns of psoriatic arthritis?

Back 208

(1) asymmetric oliogoarticular
(2) polyarticular small joint
(3) spinal involvement
(4) DIP predominant
(5) arthritis mutilans

Front 209

this type of arthritis occurs in the smaller joints of the hands and feet, in addition to larget joints; more common in women and may be difficult to clinically differentiate from RA except patients have greater evidence of erosions

Back 209

symmetric

Front 210

is spondylitis more common in males or females?

Back 210

males

Front 211

this swelling of the tendon sheath around fingers and toes occurs more frequently in psoriatic arthritis

Back 211

dactylitis

Front 212

this type of arthritis affects about 5% of PsA cases; describes the end stage condition of the small joints of the hand and feet; there are telescope digits and flail joints associated with extensive osteolysis and joint instability

Back 212

arthritis mutilans

Front 213

this type of deformity of the bones of the finger is often found in psoriatic arthritis

Back 213

pencil and cup deformity

Front 214

what is the most common drug used to treat psoriatic arthritis?

Back 214

TNF blockers

Front 215

what is the compound that is implicated in gout?

Back 215

monosodium urate

Front 216

what is the compound that is implicated in pseudogout?

Back 216

calcium pyrophosphate

Front 217

what is the compound that is implicated in Milwaukee shoulder?

Back 217

basic calcium phosphate

Front 218

what are the four basic clinical manifestations of gout?

Back 218

(1) recurrent attacks of acute arthritis
(2) tophaceous deposits
(3) gouty nephropathy
(4) kidney stones

Front 219

what transporter drives the reabsorption of urate from the proximal convoluted tubule?

Back 219

URAT1

Front 220

there is about a __% net excretion of filtered urate

Back 220

10%

Front 221

__% of hyperuricemia is from overproduction of urate (from ethanol, myeloproliferative diseases, psoriasis, overactive PRPP synthetase, deficiency of HGPRT)

Back 221

10%

Front 222

__% of hyperuricemia is from underexcretion of urate (diuretics, low dose aspirin, ethanol, lead, hypothyroidism, dehydration, starvation, ketoacidosis, renal disease)

Back 222

90%

Front 223

what are the three stages of acute gouty arthritis?

Back 223

(1) acute gouty arthritis
(2) intercritical gout
(3) chronic tophaceous gout

Front 224

this type of gout is an abrupt onset of severe inflammation (75% in MTP joint, then ankle, foot, and knee); usually monoarticular. There is intense periarticular inflammation that resembles cellulitis, thrombophlebitis

Back 224

acute gouty arthritis

Front 225

what are four triggers of acute gouty arthritis?

Back 225

trauma, surgery, medical illness, medications

Front 226

how long does it take acute gouty arthritis to resolve?

Back 226

3-10 days

Front 227

these are subcutaneous urate masses that take 10-12 years to develop and occur anywhere except the antihelix

Back 227

tophi

Front 228

where are tophi most usually found?

Back 228

antihelix of ear

Front 229

these structures erode into cartilage and bone and may resemble rheumatoid nodules; risk of development increases with higher serum urate levels

Back 229

tophi

Front 230

what are the two diagnostic criteria for chronic tophaceous gout?

Back 230

(1) identification of monosodium urate crystals in synovial fluid
(2) tophaceous erosions on radiographs

Front 231

what compound is strongly birefringent and needle shaped when shown under polarized light?

Back 231

monosodium urate crystal

Front 232

the response of this medicine is specifically for crystalline arthritis; it inhibits the polymerization of microtubules and disrupts chemotaxis and phagocytosis

Back 232

colchicine

Front 233

what are three treatments for acute gout?

Back 233

(1) colchicine
(2) NSAIDs (indomethacin)
(3) corticosteroids (systemic, articular)

Front 234

what are three things to avoid with acute gout because they decrease the clearance of uric acid?

Back 234

(1) alcohol
(2) diuretics
(3) low dose aspirin

Front 235

what is the limit of solubility of urate in serum?

Back 235

6.8 mg/dL

Front 236

this compound crystallizes as a monosodium salt in oversaturated joint tissues

Back 236

urate

Front 237

what are two urate-lowering medications that aim to reduce the serum urate level to below the limit of solubility (around 5 mg/dL)

Back 237

(1) uricosurics
(2) allopurinol

Front 238

these are weak organic acids which inhibit renal tubular resorption of urate at post-secretory site

Back 238

uricosurics

Front 239

this treatment for urate lowering is a xanthine oxidase inhibitor (blocks conversion of xanthine to uric acid)

Back 239

allopurinol

Front 240

this is the calcification of articular cartilage that is found in calcium pyrophosphate deposition disease (CPPD)

Back 240

chondrocalcinosis

Front 241

pseudogout is twice as common in what sex?

Back 241

females

Front 242

this disease is caused by the deposition of calcium pyrophosphate crystals in articular cartilage and fibrocartilage

Back 242

pseudogout

Front 243

what are two things that are used to diagnose pseudogout?

Back 243

(1) radiographic chondrocalcinosis (esp. wrist, knee, pubic symphysis)
(2) calcium pyrophosphate crystals in synovial fluid (rhomboid shape)

Front 244

acute periarthritis occurs in what four joints?

Back 244

(1) shoulder
(2) trochanter of hip
(3) epicondyle of elbow
(4) wrist

Front 245

what is a common sign seen in Milwaukee shoulder, which most commonly affects women greater than 70 years of age?

Back 245

shoulder pad sign

Front 246

acute periarthritis and Milwaukee shoulder, as well as acute arthritis are all caused by what compound?

Back 246

basic calcium phosphate

Front 247

what are four systemic connective tissue diseases?

Back 247

(1) inflammatory myopathies
(2) systemic lupus erythematosus
(3) sjogren's syndrome
(4) scleroderma

Front 248

what are five clinical features of inflammatory myopathy?

Back 248

(1) symmetric proximal muscle weakness
(2) elevated muscle enzymes (CPK)
(3) myopathic EMG abnormalities
(4) typical changes on muscle biopsy
(5) typical rash of dermatomyositis

Front 249

what is the muscle enzyme that is most often elevated in inflammatory myopathy?

Back 249

CPK (creatine phosphokinase)

Front 250

what four EMG abnormalities are seen in inflammatory myopathy?

Back 250

(1) insertional irritability
(2) positive sharp waves
(3) small amplitude, polyphasic motor unit potentials '
(4) fibrillation

Front 251

what are six clinical features of polymyositis?

Back 251

(1) proximal muscle weakness
(2) elevated CPK
(3) myopathic EMG findings
(4) diagnostic findings on muscle biopsy
(5) sometimes arthritis and interstitial lung disease
(6) no characteristic skin findings

Front 252

this disease is polymyositis plus a characteristic skin involvement

Back 252

dermatomyositis

Front 253

this type of dermatomyositis involves the skin only, not the muscles

Back 253

amyopathic

Front 254

this disease is characterized by slow, progressive muscle weakness; early involvement of distal muscles that may be asymmetric, myopathic and neuropathic changes on EMB, and responds poorly to conventional treatment

Back 254

inclusion body myositis

Front 255

what sex is usually affected more by inclusion body myositis?

Back 255

males

Front 256

what are five treatments for inclusion body myositis?

Back 256

(1) high dose prednisone
(2) methotrexate
(3) azathioprine
(4) IV IG
(5) rituximab

Front 257

what are the 1983 classification criteria for systemic lupus erythematosus?

Back 257

(1) malar rash
(2) discoid rash
(3) photosensitivity
(4) oral ulcers
(5) arthritis
(6) serositis
(7) disorders of kidneys, neurologic, hematologic, immunologic
(8) antinuclear antibody

Front 258

this type of lupus rash has fixed erythema, flat or raised, and sparing in nasolabial folds

Back 258

malar rash

Front 259

this type of lupus rash has raised patches, adherent keratotic scaling, follicular plugging, and older lesions that may cause scarring

Back 259

discoid rash

Front 260

what is a common finding in systemic lupus erythematosus that is a possible indication of kidney disease?

Back 260

red blood cell casts

Front 261

what are five clinical features of Sjogren's syndrome?

Back 261

(1) Sicca complex (dry eyes and mouth)
(2) rheumatoid arthritis or other CTD
(3) salivary gland enlargement
(4) purpura
(5) renal tubular acidosis or other tubular disorder

Front 262

what are four things that are used to diagnose Sjogren's syndrome?

Back 262

(1) xeropthalmia
(2) xerostomia
(3) anti-Ro (SSA)
(4) lip biopsy of minor salivary gland

Front 263

this test measures tear formation in order to diagnose Sjogren's syndrome

Back 263

Schirmer's test

Front 264

what are three treatments for Sjogren's syndrome?

Back 264

(1) hydroxychloroquine
(2) prednisone
(3) immunosuppressive agents

Front 265

this is hard skin in fingers that causes fingers to become contracted

Back 265

sclerodactyly

Front 266

this lung disease is the #1 cause of death in sclerederma patients; increased resistance

Back 266

basilar pulmonary fibrosis

Front 267

a condition in which cold temperatures or strong emotions cause blood vessel spasms that block blood flow to the fingers, toes, ears, and nose.

Back 267

Raynaud's phenomenon

Front 268

what is the common treatment for sclerederma?

Back 268

treatment is symptomatic, not for the actual disease (treat HTN, reflux, raynaud's and lung disease)

Front 269

this comprises a variety of systemic illnesses which are characterized by inflammation of blood vessels; clinical manifestations are determined by the size of the blood vessels and the tissues they supply; involvement of skin, muscle, nerve, kidney, lungs, etc

Back 269

vasculitis

Front 270

this vasculitis onsets at less than 20 yoa; characterized by bowel angina, granulocytes in walls of arterioles or venules, and it takes a benign course and is self-limited

Back 270

Henoch-Schonlein purpura

Front 271

this vasculitis presents with a weight loss of greater than 4 kg, testicular pain or tenderness, myalgias, weakness, or leg tenderness, and mononeuropathy or polyneuropathy

Back 271

Polyarteritis nodosa

Front 272

this type of vasculitis causes death of the bowel and loss of blood vessels in the wall

Back 272

necrotizing vasculitis

Front 273

what nerve is most commonly affected in vasculitis?

Back 273

radial nerve

Front 274

this disease is characterized by nasal or oral inflammation (oral ulcers, bloody nasal drainage), abnormal chest radiograph, nodules, urinary sediment, and granulomatous inflammation on biopsy in wall; characterized by saddle nose deformity

Back 274

Wegener's granulomatosis

Front 275

what are five common signs of relapsing polychondritis?

Back 275

(1) saddle nose deformity
(2) ear, nose inflammation
(3) scleral thinning
(4) saccular aneurysm, aorta
(5) tracheal narrowing

Front 276

what are 8 signs of cryoglobulinemia (a disease caused when proteins precipitate when they get too cold)

Back 276

(1) Raynaud's
(2) cutaneous ulceration
(3) cold-induced urticaria
(4) digital gangrene
(5) polyarthralgia
(6) purpura
(7) nephritis
(8) peripheral neuropathy

Front 277

this disease onsets at age less than 40; there is claudication of the extremities, decreased brachial artery pulse, BP difference of greater than 10 mm Hg between arms, bruit over subclavian arteries or aorta, and arteriogram abnormality

Back 277

Takayasu's arteritis

Front 278

this is a diagnosis of systemic vasculitis established by a tissue biopsy; it has serious ischemic complications, including blindness

Back 278

giant cell arteritis

Front 279

this disease is characterized by muscle pain persisting for at least 1 month in the shoulders and pelvic girdle, severe morning stiffness and gelling, and no muscle atrophy or true weakness

Back 279

polymyalgia rheumatica

Front 280

what are two ways to diagnose polymalgia rheumatica?

Back 280

(1) erythrocyte sedimentation
(2) rapid relief with small doses of glucocorticoids

Front 281

this disease is characterized by onset of greater than 50 years of age; new headache, temporal artery abnormality (tender or decreased pulse), elevated ESR, and abnormal artery biopsy

Back 281

giant cell (temporal) arteritis

Front 282

this type of vasculitis occurs with a stroke at a young age, and starting to have seizures at age 60

Back 282

isolated CNS vasculitis

Front 283

this is a common chronic widespread pain condition; often have heightened sensitivity to pain, in addition, nonnoxious stimuli may result in pain; patients my present with a wide range of additional symptoms including tenderness, sleep disturbances, fatiue, morning stifffness, and mood disorders

Back 283

fibromyalgia

Front 284

the american college of rheumatology definition of this disease is widespread pain for more than three months, on both sides of the body, above and below the waist, and axial skeleton;

Back 284

fibromyalgia

Front 285

what are the three central pain mechanisms in fibromyalgia?

Back 285

(1) CNS mechanisms (central sensitization)
(2) increased levels of excitatory neurotransmitters (glutamate)
(3) compared with normal controls, CSF levels of substance P are high

Front 286

this is a term that encompasses a group of chronic and slowly progressive respiratory conditions characterized by dyspnea and reduced airflow that is not fully reversible

Back 286

chronic obstructive pulmonary disease

Front 287

this is an anatomical term for permanent and destructive enlargement of the airspaces

Back 287

emphysema

Front 288

this disease is characterized by "pink puffers"-very thin/cachectic, barrel chested, pursed lipped breathing, less chronic cough and sputum production, less notable changes in ABGs

Back 288

emphysema

Front 289

this is a clinical term describing chronic cough and sputum production (at least 3 months/year for two consecutive years)

Back 289

chrhonic bronchitis

Front 290

this disease is characterized by blue bloaters-obese, more cough and sputum, more likely to have hypoxia, more abnormal lumg soungs, and may have right heart failure

Back 290

chronic bronchitis (classic COPD)

Front 291

this disease is characterized by chronic inflammation throughout the airways, lumg parenchyma, and pulmonary vasculature, with an increase in T cells, macrophages, and neutrophils which release chemical factors that cause lung injury and sustain inflammatory response

Back 291

COPD

Front 292

in COPD, what substances are found imbalanced?

Back 292

imbalance of oxidants and antioxidants (oxidative stress)
imbalance of proteases and antiproteases

Front 293

these enzymes, such as elastase, are capable of injuring the lung tissue

Back 293

proteases

Front 294

what airways are the major site of inflammation and airflow limitation in COPD?

Back 294

small airways

Front 295

what are four risk factors for developing COPD?

Back 295

(1) smoking
(2) air pollution
(3) occupational exposures
(4) infection

Front 296

in COPD, do the lungs underinflate or hyperinflate?

Back 296

hyperinflate

Front 297

what results from a destruction of lung tissue causing a mismatch of inspired gas and blood flow in patients with COPD?

Back 297

impaired gas exchange (V/Q mismatch)

Front 298

what does COPD generaly begin with in the 5th decade of life?

Back 298

chronic, productive cough

Front 299

what are some clinical features/physcial findings of COPD?

Back 299

(1) prolong expiratory time
(2) wheezing
(3) barrel chest
(4) distant breath sounds and heart sounds
(5) coarse inspiratory crackles and rhonchi
(6) pursed lip breathing
(7) wasting
(8) cyanosis

Front 300

what is the characteristic finding of a COPD patient's spirometry?

Back 300

a decrease in FEV1/FVC ratio

Front 301

these are infrequent and mild early in the course of CPD but become more severe and frequent as the disease progresses; impairment of gas exchange and dyspnea progress with time

Back 301

acute exacerbations of COPD

Front 302

what are the major reason for hospitalization in patients with COPD and is characterized by increased cough, increased volume/change in sputum, and increased dyspnea

Back 302

acute exacerbations of COPD

Front 303

what are five treatments for COPD?

Back 303

(1) smoking cessation
(2) bronchodilators
(3) steroids
(4) oxygen
(5) pulmonary rehabilitation

Front 304

this treatment stimulates beta two receptors in the lungs, causing bronchodilation

Back 304

bronchodilators (beta two agonists)

Front 305

these agents reduce the airway inflammation that is present in COPD

Back 305

steroids

Front 306

what is the only therapy shown to prolong life in COPD patients?

Back 306

supplemental oxygen

Front 307

what is the saturation level for oxygen that is the goal for COPD patients?

Back 307

90-92%

Front 308

patients with COPD are at a risk for what associated heart disease?

Back 308

cdoronary artery disease

Front 309

this is a chronic inflammatory disease of the airways that is characterized by increased responsiveness of the bronchial tree; is manifested by widespead episodic narrowing of the airways, and are interspersed with symptom free periods

Back 309

asthma

Front 310

what is the main feature of asthma?

Back 310

hyperresponsiveness of the airways

Front 311

asthma is thought to be cuased by __ __ __ of the airways

Back 311

chronic subacute inflammation

Front 312

what four cells infiltrate the mucosa of the airways in asthma?

Back 312

mast cells, eosinophils, neitrphils, and lymphocytes

Front 313

characteristic emphysematous changes are conpspicuously lacking in what airway disorder?

Back 313

asthma

Front 314

what are seven things that can increase airways responsiveness in asthma?

Back 314

(1) allergens
(2) drugs (aspirin)
(3) environment and air pollution
(4) occupational exposures
(5) infections
(6) exercise
(7) emotional stress

Front 315

what is the main pathophysioligic factor of asthma that leasd to increased airway resistance, reduced airlfow, air trapping, hyperinflation, etc.?

Back 315

airway narrowing

Front 316

what are the four classic symptoms of asthma?

Back 316

(1) dyspnea
(2) chest tightness
(3) nonproductive cough
(4) wheezing

Front 317

what are six treatments for asthma?

Back 317

(1) elimination of causative agents
(2) immunotherapy (allergy shots)
(3) bronchodilators
(4) steroids
(5) mast-cell stabilizing agents
(6) leukotriene modifiers

Front 318

what are the most important aspect of drug therapy for patients with mild persistent asthma and moderate or severe asthma?

Back 318

inhaled steroids

Front 319

this is an infection of the pulmonary parenchyma caused by various microorganisms, including viruses, bacteria, and mycobacteria, fungi, and parasites

Back 319

pneumonia