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237 Cards in this Set
- Front
- Back
|
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
|
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what is the 5-lipoxygenase inhibitor used in the tx of asthma?
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zileuton
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what are the adverse effects of zafirlukast and montelukast?
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churg-strauss syndrome
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what are the adverse effects of zileuton?
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hepatoxicity
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what drug is not utilized much in asthma management?
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theophylline
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what are the MOAs of theophylline?
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MOA-1: phosphodiesterase inhibitor; relaxation of smooth muscle, decrease release of inflammatory mediators
MOA-2: adenosine antagonist; relaxation of smooth muscle |
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what is the therapeutic blood level of theophylline?
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5-15 micrograms/mL
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what are the adverse effects of theophylline?
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-tachycardia
-nausea/vomiting -h/a -seizures |
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what drugs decrease the clearance of theophylline?
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-cimetidine
-macrolides -quinolones -zileuton |
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what drugs increase the clearance of theophylline?
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-rifampin
-phenobarbital -phenytoin -smoking |
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what is the IgE inhibitor used in the tx of asthma?
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omalizumab
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what are the indications of IgE inhibitor use?
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-pts > 12 y/o
-moderate to severe disease -failed traditional anti-inflammatory agents |
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what is the MOA of IgE inhibitors?
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forms complexes with IgE and prevents binding to receptors limiting inflammatory mediator release
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what is used as the tx for mild intermittent, mild persistent, moderate persistent, and severe persistent asthma FOR QUICK RELIEF?
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short-acting b2-agonists as needed for symptoms
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what long-term control is used to treat mild intermittent asthma?
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no daily med needed
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what long-term control is used to tx mild persistent asthma?
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low-dose inhaled corticosteroids
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what long-term control is used to tx moderate persistent asthma?
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low-med-dose inhaled corticosteroids AND long-acting inhaled b2-agonists
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what long-term control is used to tx severe persistent asthma?
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high-dose inhaled corticosteroids AND long-acting inhaled b-agonists
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what is the pathophysiology of COPD?
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-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 |
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what are the risk factors for COPD?
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-smoking
-age -male gender -occupational -alpha-1 antitrypsin deficiency |
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what are the sxs of COPD?
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-chronic cough
-chronic sputum production -dyspnea |
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the FEV1/FVC spirometry reading in COPD is what?
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< 70%
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what are the COPD guidelines?
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-prevent disease progression
-relieve symptoms -improve exercise tolerance -improve health status -prevent and treat exacerbations -reduce mortality |
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is it normally possible to reduce the intensity of therapy while maintaining optimal therapeutic effects?
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No, it is not
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T/F: progression of underlying lung disease will generally require further intensification of treatments.
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TRUE
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what are the non-pharmacologic interventions of COPD?
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-smoking cessation
-reduce or eliminate occupational exposures -reduce or eliminate env. exposures -pt education -pulmonary rehabilitation |
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how can COPD be treated?
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-non-pharmacologic therapy
-smoking cessation |
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what can aid in smoking cessation for COPD pts?
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-behavioral counseling
-NRT -patch -gum -lozenge -inhalers -bupropion |
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T/F: none of the COPD existing meds have been shown to modify the long-term decline in lung function
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TRUE
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what is the essential symptomatic management of COPD?
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bronchodilators
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what are the common short-acting bronchodilators used for COPD?
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b2-agonists: albuterol, pirbuterol
anticholinergic agents: ipratropium bromide |
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what are the common long-acting bronchodilators used for COPD?
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b2-agonists: salmeterol, formoterol
anticholinergic agents: tiotropium bromide |
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tiotropium v. ipratropium
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tiotropium significantly improved FEV1, increased PEF
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albuterol + ipratropium
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wheezing and shortness of breath significantly better with combo
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salmeterol + ipratropium
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wheezing and shortness of breath significantly better with combo
no difference in adverse events |
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T/F: oral or inhaled corticosteroids are only beneficial to a minority of COPD pts
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true
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what are the inflammatory mediators of asthma?
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-eosinophils
-sm increase in macrophages -mast cells -IL-4, IL-5 |
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what are the inflammatory mediators of COPD?
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-neutrophils
-large increase in macrophages -TNF-alpha -IL-8 |
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in what kind of pts should oxygen be given?
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-pts who have a resting PaO2 < 55
-pts who desaturate following exercise or at night |
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what is the goal of oxygen therapy?
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to maintain a PaO2 > 60, which correlates with an oxygen saturation of > 90%
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what has oxygen therapy been shown to do?
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reduce mortality in COPD pts
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T/F: it is inconsitent to provide health care and -- at the same time --- remain silent (or inactive) about a major health risk.
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TRUE!!
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