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237 Cards in this Set

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what are the most common diabetes related symptoms?
polyuria, polydipsia, polyphagia
rapid weight loss
weakness
extreme fatigue
noctural enuresis
urinalysis: (+) glucose, (+) ketones
what are the other symptoms associated with diabetes?
recurrent blurred vision
vulvovaginitis or pruritis
peripheral neuropathy
Diabetes is the _____ leading cause of death.
sixth
diabetes is the number one cause of what?
renal failure
new cases of blindness
nontraumatic amputations
what is diabetes?
a group of metabolic diseases characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both.
what are the metabolic disturbances that are associated with diabetes?
carbohydrate
fats
protein
what are the hormone imbalances that are associated with diabetes?
insulin
glucagon
amylin
what are the hormones that affect blood glucose?
insulin
amylin
glucagon
epi
glucocorticoids
growth hormone
progesterone, HCS, cortisol
what are the effects of the hormones that affect blood glucose?
decrease blood glucose
who produces insulin and where?
produced by beta cells in the pancreatic islets of langerhans
what does free insulin promote?
glucose utilization
accelerates transport of blood glucose into cells
decreases release of free fatty acids (FFA)
suppresses glucose production by the liver
what are the different types of diabetes?
Type 1
LADA - latent autoimmune diabetes
Type 2
gestational diabetes mellitus (GDM)
pre-diabetes
how can diabetes be diagnosed?
symptoms of DM + casual plasma glucose concentraion >/= 200 mg/dL
OR
fasting plasma glucose (FPG) >/= 126 mg/dL
OR
2-hr plasma glucose >/= 200 mg/dL during an oral glucose tolerance test (OGTT)
what is pre-diabetes?
-intermediate between NL glucose homeostasis and diabetes
-impaired fasting glucose (IFG) of >/= 100 and < 126
-impaired glucose tolerance (IGT) of 2hr PPG >/= 140 and < 200
pt who are diagonosed with pre-diabetes are at an increased risk for what type of diabetes?
Type 2
pre-diabetes has a higher _____/______
morbidity/mortality
what is the diabetes control and complications trial (DCCT)?
it was a randomized study of type 1 diabetes pts
-they assessed the effect of intensive glycemic control vs conventional therapy on: development and progression of retinopathy and other long-term microvascular complications
what did the results of the DCCT lead to?
led to similar studies of type 2 diabetes pts
intensive control of blood glucose reduced the risk of:
retinopathy 34-70%
nephropathy 56%
neuropathy 60%
but there's a 2-3 fold greater incidence of severe hypoglycemia
what is the UKPDS key message?
for every % point decrease in A1c there was a decrease of:
35% in microvascular disease
25% in diabetes related deaths
18% in myocardial infarction
what are the educational initiatives for DM?
-glycemic control using insulin and self monitoring blood glucose (SMBG)
-medical nutrition therapy
-diet
-exercise
-reduction of co-morbidities
what is an essential component of diabetes care?
medical nutrition therapy and insulin administration -- DM can't be treated with diet alone
what is carbohydrate counting?
-it's useful for all pts with DM
-used to determine rapid-short-acting insulin doses for those on intensive therapy or insulin pump
1 carb serving = ______ carbs
15g
1 unit of insulin covers ~ ______ carbs
10-15g
a typical meal plan includes how many carb choices per meal for women and men?
3-4 for women
4-5 for men
what are the human insulin: rapid acting drugs?
aspart (Novolog), Lispro (Humalog), and Glulisine (ApidraTM)
what are the human insulin: short acting drugs?
regular (Humulin R, Novolin R)
what are the human insulin: intermediate acting drugs?
NPH (Humulin N, Novolin N)
what are the human insulin: long acting drugs?
detemir (Levemir) and Glargine (Lantus)
what is the onset, peak, and duration of fast acting insulin?
onset: 15 min
peak: 0.5-1.5
duration: 2-4 (hr?)
what is the onset, peak, and duration of short acting insulin?
onset: 30-60 min
peak: 2-4
duration: 12-24 (hr?)
what is the onset, peak, and duration of intermediate acting insulin?
onset: 1-3
peak: 6-12
duration: 12-24
what is the onset, peak, and duration of long acting insulin?
onset: 1-2
peak: -
duration: 24
what are the side effects of insulin?
-weight gain
-hypoglycemia
-lipohypertrophy
-lipoatrophy
what is the general dosing of rapid acting insulin?
0-15 min before meals
what is the general dosing of regular insulin?
30 min before meals
what is the general dosing of NPH insulin?
dosed with short/rapid either QD or BID
what is the general dosing of glargine (Lantus)?
QD, at the same time every day
the 2-injection regimen is best for what type of pts?
best in Type 2 and early Type 1
what are the disadvantages of the 2-injection regimen?
-poor peaking of noon insulin and excess insulin at night
how is the problem of poor peaking of noon insulin and excess insulin at night solved in the 2-injection regimen?
limit noon meal and eat a bedtime snack.
what are the advantages of the 3-injection regimen?
-less nighttime hypoglycemia
-better control of AM hyperglycemia
what are the disadvantages of the 3-injection regimen?
-poor peaking of noon insulin
T/F: the 4-injection regimen is typicall not a starting regimen
TRUE
what are the disadvantages of the 4-injection regimen?
no more than 4-6 hours can transpire between meals
what are the advantages of the insulin pen?
dial dosing
convinient
discreet
what are the disadvantages of the insulin pen?
cost
can't mix insulins
the ______ _______ delivers a _______ basal amount of insulin
insulin pump; continuous
the insulin pump is indicated for?
-pts who aren't controlled with multiple daily injections
-pts who desire a high level of control
what most closely mimics endogenous insulin production?
insulin pump
what are the advantages of the external insulin pump?
-most physiologic mode of insulin delivery
-increased predictability of insulin absorption
-increased lifestyle flexibility
what are the disadvantages of the external insulin pump?
-extensive pt education
-expensive
-more frequent BG monitoring
-routine infusion site care
-periodic reprogramming required to accomodate lifestyle changes
what are the advantages of the implantable insulin pump?
-insulin delivered intra-peritoneally is absorbed rapidly and predictably
-most closely mimics normal physiology
what are the disadvantages of the implantable insulin pump?
-minor surgery to implant
-needs refill in clinic or hospital
-potential for infx
what has been shown to be the least effective TX in DM?
inhaled insulin
what are the advantages of inhaled insulin?
-no unusual episodes of hypoglycemia
-popular concept with pts
what are the disadvantages of inhaled insulin?
-expensive: more insulin is required to achieve the same effect as injected insulin
-injections of intermediate/long acting insulin still required
-difficult to titrate dose
T/F: a lesser concentration of inhaled insulin is required to achieve the same effect as injected insulin because it is readily absorb in the airway.
FALSE!!
Type 2 DM is characterized by what type of pancreatic function?
< NL
NL
> NL
what is the most common type of DM?
Type 2 -- ~90% of all cases
T/F: obesity is common in Type 2 DM
TRUE
what is the clinical presentation of type 2?
mild sxs
gradual in onset
what is the prevalence of type 2 diabetes, in order from most to least?
1) american indians/alaska natives
2) non-hispanic blacks
3) hispanic/latino americans
4) non-hispanic whites
what are the goals for co-morbidities in type 2 diabetes?
-smoking cessation
-weight control
-blood pressure < 130/80
-lipids: LDL < 100
what is the tx for HTN in type 2 diabetes?
-drug of choice: ACEi
-alternative: ARB and non-DHP calcium channel blocker (Dilitiazem)
what is the drug of choice for tx dyslipidemia?
statins
what is the drug of choice for cardio-protection?
aspirin
for fasting plasma glucose (FPG) what is the normal and goal?
NL: < 100
goal: 90-130
for postprandial what is the NL and goal?
NL: <140
goal: <180
for bedtime what is the NL and goal?
NL: <120
goal: 110-150
for HgA1c what is the NL and goal?
NL: <6
goal: <7
what are some of the predisposing factors of Type 2 diabetes?
obesity, sedentary, aging, genetic factors
what factors influence insulin resistance?
aging, genetics, obesity/sedentary lifestyle, acromegaly, Cushing's, lipodystrophy, antireceptor, medications
what are the 1st generation sulfonylurea?
acetohexamide
chlorpropamide
tolazamide
tolbutamide
what are the 2nd generation sulfonylurea?
glimeperide
glipizide
glyburide
can sulfonylurea be used for mono or combo therapy for type 2 DM?
YES
what is the MOA for sulfonylurea?
increase B-cell secretion of insulin by binding to SU receptor on beta-cell, causing influx of Ca and release of insulin
what is the primary and secondary failure of sulfonylurea?
primary: doesn't respond initially
secondary: 10% pts/yr, failure to follow diet, stressful conditions, and worsening of disease
what is the dosing and administration of sulfonylurea?
-~30 min prior to meal
-start low and go slow
-lowest effective dose, especially in the elderly
what are the adverse effect of sulfonylurea?
-hypoglycemia
-wgt gain
-GI distress
-photosensitivity
-disulfiram reaction (mostly with chlorpropamide)
what are the contraindications of sulfonylurea?
-pregnancy (use insulin)
-severe hepatic or renal dysfunction
-sulfa allergy
can metformin be used in a mono or combo therapy?
YES
what is the MOA of metformin?
-inhibits hepatic glucose production
-enhances peripheral muscle glucose uptake
in what types of pts should metformin be used?
-obese
-UKPDS (United Kingdom perspective diabetes study)-34
what is the response rate of metformin?
80-90%
what is the response rate of sulfonylurea?
60-70%
what are the adverse effects of metformin?
-GI distress
-alterations in taste
-lactic acidosis
what are the contraindications of metformin?
-SrCr >/= 1.4 females
-SrCr >/= 1.5 males
-active liver disease
-active alcoholic
-H/O lactic acidosis
-heart failure
-procedures requiring IV contrast dye (stop prior to and hold for 48 hrs after)
what are the advantages of metformin?
-neutral effect on lipid profile
-neutral or possible wgt loss
-doesn't cause hypoglycemia when used as monotherapy
-possible prevention option
what are the thiazolidinediones (glitazones)?
troglitazone
pioglitazone
rosiglitazone
which of the thiazolidinediones was removed from the market in 1997 due to hepatic failure?
troglitazone
can thiazolidinediones be used in mono or combo therapy?
YES
what is the MOA of thiazolidinediones?
-enhances peripheral muscle glucose uptake: activation of PPAR-gamma receptors, increases glucose utilization
-inhibits hepatic glucose production
what is the response rate of thiazolidinediones?
50-60%
what are the adverse effects of thiazolidinediones?
-hepatic failure death
-GI distress
-hematologic
-wgt gain
-edema
what are the contraindications of thiazolidinediones?
-active liver disease: ALT > 2.5X upper limit of NL
-severe heart failure
what are the advantages of thiazolidinediones?
-lower insulin requirements
-DO NOT cause hypoglycemia when used as a monotherapy
-pioglitazone neutral on lipid profile
what are the disadvantages of thiazolidinediones?
-cost
-wgt gain
-maximum response at 12 weeks
-rosiglitazone may increase LDL
what do you have to monitor when using thiazolidinediones?
-LFT's
-baseline
-periodically thereafter
what are the alpha-glucosidase inhibitors?
-acarbose
-miglitol
can alpha-glucosidase inhibitors be used in mono or combo therapy?
YES
what is the MOA of alpha-glucosidase inhibitors?
-inhibits action of intestinal alpha-glucosidase
-delays breakdown of ingested carbs
-reduces postprandial hyperglycemia
what are the adverse effects of alpha-glucosidase inhibitors?
-GI distress
-hepatoxicity (dose related)
what are the drug interactions of alpha-glucosidase inhibitors?
-digestive enzymes
-intestinal absorbents
what are the advantages of alpha-glucosidase inhibitors?
-DO NOT cause hypoglycemia
-DO NOT cause hyperinsulinemia
-possible prevention option
what are the disadvantages of alpha-glucosidase inhibitors?
-less effective than other agents
-GI distress
-method of treating hypoglycemia if occurs with combo therapy
what are the meglitinides?
-repaglinide
-netaglinide
can meglitinides be used in mono or combo therapy?
YES
what is the MOA of meglitinides?
similar to sulfonylurea (short) acting
what are the adverse effects of meglitinides?
hypoglycemia (slightly < sulfonylurea)
headache
meglitinides have to be cautioned when used in pts with ______
liver dysfunction
______ is a synthetic analogue of amylin
pramlintide
where is pramlintide released from?
beta-cells of pancreas
pramlintide suppresses ______ release
glucagon
T/F: pramlintide slows gastric empyting
TRUE
T/F: pramlintide can be used as an adjunctive therapy in Type 1 and Type 2 DM
TRUE
T/F: pramlintide targets regular hyperglycemia
FALSE, it targets postprandial hyperglycemia
what are the adverse effects of pramlintide?
nausea
hypoglycemia
incretin hormone (GLP-1) is secreted by?
small intestines in response to food intake
GLP-1 binds to receptors in the ____ _____ of the _______
beta cells; pancreas
T/F: GLP-1 has a long half life
FALSE
what is the MOA of GLP-1?
enhances glucose dependent insulin secretion, suppresses inappropriate glucagon secretion, delays gastric emptying, and reduces food intake
what is the first in a new class of meds known as incretin mimetics?
Byetta (Exenatide)
Byetta is a synthetic form of?
exendin-4 (a hormone discovered in the venom of a large reptile called the Gila monster)
what are the indications for Byetta?
adjunctive therapy in pts with Type 2 diabetes who are taking metformin, a sulfonylurea, or both but have not achieved adequate glycemic control
what is the MOA of Byetta?
-binds to GLP-1 receptors which:
* increase glucose dependent insulin secretion
* moderate glucagon secretion
* delay gastric emptying
* reduce food intake
T/F: in a study performed, Byetta (Exenatide) significantly increased A1c in pts with Type 2 diabetes.
FALSE, it significantly decreased A1c in pts
T/F: if a pts glycemic control is reached by lifestyle modications, no drug therapy is needed, only pt monitoring every 3 months.
TRUE
T/F: if a pts goal is not achieved within 2 months, a monotherapy (sulfonylurea or metformin) is initiated.
TRUE
what are examples of artifical sweeters?
saccharin and aspartame
cholesterol intake in type 2 DM should be limited to how much/day?
< 300 mg/day
T/F: exercise decreases utilization of glucose
FALSE, increases utilization
T/F: exercise increases insulin sensitivity
TRUE
_______ is an integral part of the diabetes management
self monitoring blood glucose (SMBG)
which of the following agents DO NOT cause hypoglycemia when used as a monotherapy?
-metformin
-pioglitazone
-miglitol
-all of the above
all of the above
which of the following agents are useful in lowering postprandial hyperglycemia?
-glyburide
-acarbose
-repaglinide
-both B and C
both B and C
what interventions could be done to prevent the progression to diabetes mellitus?
-lifestyle modifications
-metformin
-acarbose
what are the therapeutic options for DM in a white male, PMH of HTN, s/p MI, HgA1c 10.5%, SrCr 1.7 mg/dL, LFT's wnl?
-diet
-exercise
-thiazolidinedione
obstructive lung disease implies...
an inability to move gas out of the airways.
in obstructive lung disease, there is an _______ in airway resistance
increase
what are the obstructive lung diseases?
-asthma
-chronic bronchitis
-emphysema
restrictive lung disease implies...
an inability to move gas into the lungs and maintain NL lung volumes.
there is no ______ in airway resistance in restrictive lung disease
increase
what are the restrictive lung diseases?
-interstitial lung diseases
-infiltrative lung diseases
-pleural lung diseases
-chest wall diseases
what is asthma?
chronic inflammatory disorder of the airways with variable, and reversible, obstruction
what is asthma characterized by?
recurrent episodes of wheezing, breathlessness, cough, chest tightness - especially at night or early morning
increased bronchial hyper-responsiveness to a variety of stimuli (exogenous, endogenous)
what is COPD?
chronic obstruction in expiratory airflow that may be accompanied by airway hyperresponsiveness and may be partially reversible
what are the example diseases of COPD?
emphysema and chronic bronchitis
what is chronic bronchitis?
presence of cough and increased respiratory secretions for at least 3 months in each of two successive years.
chronic bronchitis is what % of COPD cases?
75%
what is emphysema?
abnormal, permanent enlargement of air spaces distal to the terminal bronchiole.
definition based on anatomical defect.
the official diagnosis of emphysema can only be made at autopsy.
emphysema is what % of COPD cases?
25%
T/F: It is NOT common to find characteristics of both chronic bronchitis and emphysema in the same pt.
FALSE, it's common
that is the factor that differentiates COPD and asthma?
-pts with COPD have disease that is irreversible or only partially reversible.
-pts with asthma have a reversible airway obstruction
what is a common feature of chronic bronchitis?
chronic productive cough
individuals with asthma exposed to chronic irritation, such as cigarette smoke suffer from what?
asthmatic bronchitis
how would a clinician know if a pt has reversible airway obstruction?
-pulmonary function testing (PFT's)
-pre-post bronchodilator testing
what does carbon monoxide diffusing capacity measure?
the ability of a gas to diffuse across the alveolar-capillary membrane
what is DLCO directly related to?
alveolar volume
A reduced DLCO value suggests a loss of functioning _______-______ units.
alveolar-capillary
what are some of the agents that trigger asthma?
-respiratory infection
-RSV
-allergens
-grass, trees, dander
-environment
-cold air, smoke
-emotions
-stress
-exercise
-drugs
-aspirin, NSAIDS
-occupational stimuli
what are the diagnosing criteria for asthma?
-episodic symptoms of airflow obstruction (SOB, wheezing, chest tightness)
-obstruction is at least partially reversible
-alternative diagnoses are excluded
T/F: all that wheezes is asthma.
FALSE
what are the treatment goals for asthma?
-reduce chronic symptoms and exacerbations
-eliminate limitations on activities
-maintain pulmonary function near normal
-limit medication use and adverse effects
what are the quick relief drugs of asthma?
b2-agonists and anticholinergics
what are the b2-agonists used in asthma tx?
-albuterol
-pirbuterol
-levalbuterol
what are the anticholinergics used in asthma tx?
ipratropium
what are the long-term control drugs used in asthma tx?
-corticosteroids
-long-acting b2-agonists
-mast cell stabilizers
-leukotriene modifiers
-theophylline
-anti-IgE antibody
what is the MOA of short-acting b2-agonists?
stimulate adenyl cyclase and increase the formation of cAMP
what is the result of short-acting b2-agonists?
relaxation of airway smooth muscle and bronchodilation
what are the systemic adverse reactions of b2-agonists?
-tachycardia
-skeletal muscle tremor
-hypokalemia
-headache
what are the inhaled adverse reactions of b2-agonists?
-tachycardia
-skeletal muscle temor
what are the long acting b2-agonists?
-salmeterol
-formoterol
T/F: long acting b2-agonists can be used for acute attacks.
FASLE
what is the MOA of long acting b2-agonists?
stimulate adenyl cyclase and increase the formation of cAMP
what is the result of long-acting b2-agonists?
relaxation of airway smooth muscle and bronchodilation
what is the anticholinergic agent used in asthma tx?
ipratropium
ipratropium is typically reserved for...
ED and inpatient settings, limited role in outpatient asthma therapy
what is the MOA of anticholinergic agents?
competitive inhibitor of muscarinic cholinergic receptors
what is the result of anticholinergic agents?
bronchodilation
what are the adverse reactions of anticholinergic agents?
-dry mouth
-blurred vision
cortiosteroids are for the ______-_______ control therapy of persistent asthma
long-term
T/F: corticosteroids are used for acute exacerbations only
TRUE
what are the short-term adverse effects of corticosteroids?
-cough
-dysphonia
-thrush
-fluid retention
-wgt gain
-mood alteration
what are the long-term adverse effects of corticosteroids?
-adrenal axis suppression
-growth suppression
-HTN
-diabetes
-cataracts
-osteoporosis
what are the inhaled steroids used to tx asthma?
-beclomethasone
-budesonide
-flunisolide
-fluticasone
-triamcinolone
what are the mast cell stabilizers used in the tx of asthma?
-cromolyn
-nedocromil
are mast cell stabilizers used to tx acute asthma attacks?
NEVER!!
what is the MOA of mast cell stabilizers?
alteration in the function of delayed chloride channels, inhibiting cellular activation
what is the result of mast cell stabilizers?
decrease release of pro-inflammatory cytokines
T/F: mast cell stabilizers have a very potent anti-inflammatory action.
FALSE, less potent
what are the adverse reactions of mast cell stabilizers?
-very well tolerated
-unpleasant taste from neodocromil
what are the leukotriene antagonists used in the tx of asthma?
-zufirlukast
-montelukast
are leukotriene modifiers used in acute attacks?
NEVER
T/F: leukotriene modifiers have a very potent anti-inflammatory action.
FALSE, less potent
what is the 5-lipoxygenase inhibitor used in the tx of asthma?
zileuton
what are the adverse effects of zafirlukast and montelukast?
churg-strauss syndrome
what are the adverse effects of zileuton?
hepatoxicity
what drug is not utilized much in asthma management?
theophylline
what are the MOAs of theophylline?
MOA-1: phosphodiesterase inhibitor; relaxation of smooth muscle, decrease release of inflammatory mediators
MOA-2: adenosine antagonist; relaxation of smooth muscle
what is the therapeutic blood level of theophylline?
5-15 micrograms/mL
what are the adverse effects of theophylline?
-tachycardia
-nausea/vomiting
-h/a
-seizures
what drugs decrease the clearance of theophylline?
-cimetidine
-macrolides
-quinolones
-zileuton
what drugs increase the clearance of theophylline?
-rifampin
-phenobarbital
-phenytoin
-smoking
what is the IgE inhibitor used in the tx of asthma?
omalizumab
what are the indications of IgE inhibitor use?
-pts > 12 y/o
-moderate to severe disease
-failed traditional anti-inflammatory agents
what is the MOA of IgE inhibitors?
forms complexes with IgE and prevents binding to receptors limiting inflammatory mediator release
what is used as the tx for mild intermittent, mild persistent, moderate persistent, and severe persistent asthma FOR QUICK RELIEF?
short-acting b2-agonists as needed for symptoms
what long-term control is used to treat mild intermittent asthma?
no daily med needed
what long-term control is used to tx mild persistent asthma?
low-dose inhaled corticosteroids
what long-term control is used to tx moderate persistent asthma?
low-med-dose inhaled corticosteroids AND long-acting inhaled b2-agonists
what long-term control is used to tx severe persistent asthma?
high-dose inhaled corticosteroids AND long-acting inhaled b-agonists
what is the pathophysiology of COPD?
-hypersecretion of mucous in the large airway
-hypertrophy of the submucosal glands
-increase in goblet cells, leading to increase mucous production and obstruction of the airway
what are the risk factors for COPD?
-smoking
-age
-male gender
-occupational
-alpha-1 antitrypsin deficiency
what are the sxs of COPD?
-chronic cough
-chronic sputum production
-dyspnea
the FEV1/FVC spirometry reading in COPD is what?
< 70%
what are the COPD guidelines?
-prevent disease progression
-relieve symptoms
-improve exercise tolerance
-improve health status
-prevent and treat exacerbations
-reduce mortality
is it normally possible to reduce the intensity of therapy while maintaining optimal therapeutic effects?
No, it is not
T/F: progression of underlying lung disease will generally require further intensification of treatments.
TRUE
what are the non-pharmacologic interventions of COPD?
-smoking cessation
-reduce or eliminate occupational exposures
-reduce or eliminate env. exposures
-pt education
-pulmonary rehabilitation
how can COPD be treated?
-non-pharmacologic therapy
-smoking cessation
what can aid in smoking cessation for COPD pts?
-behavioral counseling
-NRT
-patch
-gum
-lozenge
-inhalers
-bupropion
T/F: none of the COPD existing meds have been shown to modify the long-term decline in lung function
TRUE
what is the essential symptomatic management of COPD?
bronchodilators
what are the common short-acting bronchodilators used for COPD?
b2-agonists: albuterol, pirbuterol
anticholinergic agents: ipratropium bromide
what are the common long-acting bronchodilators used for COPD?
b2-agonists: salmeterol, formoterol
anticholinergic agents: tiotropium bromide
tiotropium v. ipratropium
tiotropium significantly improved FEV1, increased PEF
albuterol + ipratropium
wheezing and shortness of breath significantly better with combo
salmeterol + ipratropium
wheezing and shortness of breath significantly better with combo
no difference in adverse events
T/F: oral or inhaled corticosteroids are only beneficial to a minority of COPD pts
true
what are the inflammatory mediators of asthma?
-eosinophils
-sm increase in macrophages
-mast cells
-IL-4, IL-5
what are the inflammatory mediators of COPD?
-neutrophils
-large increase in macrophages
-TNF-alpha
-IL-8
in what kind of pts should oxygen be given?
-pts who have a resting PaO2 < 55
-pts who desaturate following exercise or at night
what is the goal of oxygen therapy?
to maintain a PaO2 > 60, which correlates with an oxygen saturation of > 90%
what has oxygen therapy been shown to do?
reduce mortality in COPD pts
T/F: it is inconsitent to provide health care and -- at the same time --- remain silent (or inactive) about a major health risk.
TRUE!!